95
MANAGEMENT OF ACUTE RENAL FAILURE PROF.DR M.ABDELAZIZ CLINICAL PHARMACOLOGY COLLEGE OF MEDICINE
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MANAGEMENT OF ACUTE RENAL FAILURE
PROFDR MABDELAZIZ CLINICAL PHARMACOLOGYCOLLEGE OF MEDICINE
Human beings are essentially big bags of water the volume of which must be kept under tight control to prevent us from either drying out or drowninghellip
Highlightshellip
FOLLOWING THE TRENDShellip
CAPTURE THE KEYS TO OPEN THE DOOR
HOW TO PREVENT ARF
REPLACING KIDNEY [hellipvery difficult]
lsquoACUTE KIDNEY INJURYrsquo
Abrupt reduction [lt48 hrs] in kidney function defined as an absolute increase in S creatinine of ge03 mgdLA percentage increase in S creatinine of ge 50 [15 fold from baseline] or a reduction in urine output-- documented oliguria of lt 05 mlkghr for more than six hours
STAGING SYSTEM FOR AKISTAGE SCREATININE
CRITERIAURINE OUTPUT CRITERIA
1 INCREASE IN SCREATININE ge03mgdL OR INCREASE TO ge 150-200 FROM BASELINE
lt05 mlkghr FOR gt6HRS
2 INCREASE IN SCREATININE TO gt200-300[2-3 FOLD] FROM BASELINE
lt05 mlkghr FOR gt12 HRS
3 INCREASE IN S CREATININE TO gt300[gt3 FOLD] FROM BASELINE OR SCREATININE OF ge4mgdL WITH AN ACUTE INCREASE OF ATLEAST 05 mgdL
lt03mlkghr FOR 24 HRS OR ANURIA FOR 12 HRS
RIFLE criteria
CLASSIFICATION
PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Human beings are essentially big bags of water the volume of which must be kept under tight control to prevent us from either drying out or drowninghellip
Highlightshellip
FOLLOWING THE TRENDShellip
CAPTURE THE KEYS TO OPEN THE DOOR
HOW TO PREVENT ARF
REPLACING KIDNEY [hellipvery difficult]
lsquoACUTE KIDNEY INJURYrsquo
Abrupt reduction [lt48 hrs] in kidney function defined as an absolute increase in S creatinine of ge03 mgdLA percentage increase in S creatinine of ge 50 [15 fold from baseline] or a reduction in urine output-- documented oliguria of lt 05 mlkghr for more than six hours
STAGING SYSTEM FOR AKISTAGE SCREATININE
CRITERIAURINE OUTPUT CRITERIA
1 INCREASE IN SCREATININE ge03mgdL OR INCREASE TO ge 150-200 FROM BASELINE
lt05 mlkghr FOR gt6HRS
2 INCREASE IN SCREATININE TO gt200-300[2-3 FOLD] FROM BASELINE
lt05 mlkghr FOR gt12 HRS
3 INCREASE IN S CREATININE TO gt300[gt3 FOLD] FROM BASELINE OR SCREATININE OF ge4mgdL WITH AN ACUTE INCREASE OF ATLEAST 05 mgdL
lt03mlkghr FOR 24 HRS OR ANURIA FOR 12 HRS
RIFLE criteria
CLASSIFICATION
PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Highlightshellip
FOLLOWING THE TRENDShellip
CAPTURE THE KEYS TO OPEN THE DOOR
HOW TO PREVENT ARF
REPLACING KIDNEY [hellipvery difficult]
lsquoACUTE KIDNEY INJURYrsquo
Abrupt reduction [lt48 hrs] in kidney function defined as an absolute increase in S creatinine of ge03 mgdLA percentage increase in S creatinine of ge 50 [15 fold from baseline] or a reduction in urine output-- documented oliguria of lt 05 mlkghr for more than six hours
STAGING SYSTEM FOR AKISTAGE SCREATININE
CRITERIAURINE OUTPUT CRITERIA
1 INCREASE IN SCREATININE ge03mgdL OR INCREASE TO ge 150-200 FROM BASELINE
lt05 mlkghr FOR gt6HRS
2 INCREASE IN SCREATININE TO gt200-300[2-3 FOLD] FROM BASELINE
lt05 mlkghr FOR gt12 HRS
3 INCREASE IN S CREATININE TO gt300[gt3 FOLD] FROM BASELINE OR SCREATININE OF ge4mgdL WITH AN ACUTE INCREASE OF ATLEAST 05 mgdL
lt03mlkghr FOR 24 HRS OR ANURIA FOR 12 HRS
RIFLE criteria
CLASSIFICATION
PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
lsquoACUTE KIDNEY INJURYrsquo
Abrupt reduction [lt48 hrs] in kidney function defined as an absolute increase in S creatinine of ge03 mgdLA percentage increase in S creatinine of ge 50 [15 fold from baseline] or a reduction in urine output-- documented oliguria of lt 05 mlkghr for more than six hours
STAGING SYSTEM FOR AKISTAGE SCREATININE
CRITERIAURINE OUTPUT CRITERIA
1 INCREASE IN SCREATININE ge03mgdL OR INCREASE TO ge 150-200 FROM BASELINE
lt05 mlkghr FOR gt6HRS
2 INCREASE IN SCREATININE TO gt200-300[2-3 FOLD] FROM BASELINE
lt05 mlkghr FOR gt12 HRS
3 INCREASE IN S CREATININE TO gt300[gt3 FOLD] FROM BASELINE OR SCREATININE OF ge4mgdL WITH AN ACUTE INCREASE OF ATLEAST 05 mgdL
lt03mlkghr FOR 24 HRS OR ANURIA FOR 12 HRS
RIFLE criteria
CLASSIFICATION
PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
STAGING SYSTEM FOR AKISTAGE SCREATININE
CRITERIAURINE OUTPUT CRITERIA
1 INCREASE IN SCREATININE ge03mgdL OR INCREASE TO ge 150-200 FROM BASELINE
lt05 mlkghr FOR gt6HRS
2 INCREASE IN SCREATININE TO gt200-300[2-3 FOLD] FROM BASELINE
lt05 mlkghr FOR gt12 HRS
3 INCREASE IN S CREATININE TO gt300[gt3 FOLD] FROM BASELINE OR SCREATININE OF ge4mgdL WITH AN ACUTE INCREASE OF ATLEAST 05 mgdL
lt03mlkghr FOR 24 HRS OR ANURIA FOR 12 HRS
RIFLE criteria
CLASSIFICATION
PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
RIFLE criteria
CLASSIFICATION
PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
CLASSIFICATION
PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
PRERENAL ARF
Most common
Renal hypo perfusion
Important form in perioperative period
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
CAUSES-PRERENAL ARF
HYPOVOLEMIAgtHEMORRHAGEgtG-I LOSSESgtDECREASED INTAKEgtURINARY LOSSESgtSKIN LOSSESgtOTHERSBURNSPANCREATITISSEVERE HYPOALBUMINEMIA
ALTERED RENAL HEMODYNAMICS
LOW CARDIAC OUTPUT STATESgtCHF gtVALVULAR HEART DISEASE gtPPV gt REDUCED VENOUS RETURN
SYSTEMIC VASODILATIONgtSEPSIS gtANTIHYPERTENSIVES gtVASODILATORS gtANAPHYLAXIS
RENAL VASOCONSTRICTIONgtCATECHOLAMINES gtHYPERCALCEMIA
IMPAIREMENT OF RENAL AUTOREGULATIONgtNSAIDs gtACE-I gtARBs
HEPATORENAL SYNDROME
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
HYPOVOLEMIA- extrinsic
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
HYPOVOLEMIA- intrinsic
Tubuloglomerular feedback
Afferent arteriolar vasodilatation
Preferential efferent arteriolar vasoconstriction
Aim is to utilize the existing filtration reserve
maximally
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
In shorthellip
EXTRINSIC INCREASE MAP IMPROVE INTRAVASCULAR VOLUME
INTRINSIC IMPROVE RENAL PLASMA FLOW GFR amp GLOMERULAR PRESSURE
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
When the insult cross the limitshellip
Compensatory mechanisms overwhelmed renal perfusion decrease GFR fall
Decreased O2 delivery needs to decrease its work decrease filtration oliguria
Increased Na reabsorption = more work by medulla blood flow towards medulla ie away from cortex GFR decrease oliguria
ldquoacute renal successrdquo Increase perfusion pressure If we wait hellipATN
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
INTRINSIC ARFCAUSES
RENOVASCULARRENOVASCULARgtATHEROEMBOLISM gtMALIGNANT HTN gt gtHUS gt DIC gtPREECLAMPSIA
GLOMERULARGLOMERULARgtAGN
TUBULESTUBULES-ATN
ISCHEMIAISCHEMIAgtMAJOR CARDIOVASCULAR Sx gtTRAUMA gtHEMORRHAGE gtHYPOVOLEMIA
TOXINSTOXINSExogenous Radiocontrast dyeAntibiotics-AminoglycosidesChemotherapeutic agents-Cisplatin Amphotericin-B Ethylene glycolEndogenous myoglobinhemoglobincalciumbilirubinSEPSISSEPSIS
INTERSTITIUMINTERSTITIUMAllergic Antibiotics b-lactam quinolone rifampin NSAIDs BL pyelonephritis
INTRATUBULAR OBSTRUCTIONINTRATUBULAR OBSTRUCTION acyclovir methotrexate indinavir myeloma proteins
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Ischemic ATN
4 PHASES
INITIATIONGFR DECREASE OBSTRUCTION BY DEBRIS BACKLEAK
EXTENSION CONTINUEDhellip
MAINTENANCE GFR LOWEST URINE OP LOWEST UREMIC COMPLICATIONS MAY OCCUR
RECOVERY EPITHELIAL CELL REGENERATION GFR RETURNS
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
The so called diuretic phasehellip
bull Recovery phasebull Filtration recovers earlybull Recovery of epithelial function lags behind
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Nephrotoxic ATN
RISK FACTORSRISK FACTORS
Advanced agePreexisting kidney diseaseHypovolemiaCCFMultiple myeloma
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Toxinshellip
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Contrast nephropathy
FEATURES
REVERSIBLE
ACUTE ONSET [24-48 HRS]
PEAK 3-5 DAYS
RESOLUTION IN ONE WEEK
B UREA amp S CREATININE INCREASE
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
POSTRENAL ARF
Obstruction is always the most likely cause when there is anuriaBL uretericUL ureteric if single functioning kidneyBladder neck obstructionUrethral
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Perioperative oliguria - pathophysiology
bull Anesthetic agents no renal vasodilation per se effects by reducing CO amp BP
bull EDB amp high spinal anesthesia reduce sympathetic tone
bull PPV decrease renal blood flowbull ACE-I cause significant reduction in perfusion
pressure during anesthesiabull Narcotics can increase ADH response
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Clinical features
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Pre renal
vomiting diarrhoea Intestinal obstructionhellipCarry over casesNPOOOOOOO
Look forThirstReduced JVPDecreased skin turgorDry mucus membrane
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Intrinsic renal
oliguriaedemahypertension AGNIntake of nephrotoxic drugsho atrial fibrillation renal artery thrombusho vascular surgeries atheroembolic ARFMuscle trauma rhabdomyolysis
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Post renal
AnuriaFlank painho prostatic disease
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
INVESTIGATIONS
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
URINE MICROSCOPY
CONDITION FINDINGS
PRERENAL TRANSPARENT HYALINE CAST
POSTRENAL HYALINE CASTPUS CELLSHEMATURIA
ATN MUDDY BROWN GRANULAREPITHELIAL CAST
INTERSTITIAL NEPHRITIS WBCs RBC CASTS NON-PIGMENTED GRANULAR CASTEOSINOPHILS LYMPHOCYTES
AGN RBC CASTS
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Assessment of GFR
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Blood urea
15-40mgdL
Increased in dehydration post G-I bleed
May be a better guide in timing dialysis to avoid uremic complications
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Serum creatinineNormal lt15 mgdLOverestimate GFRLags behind renal injury amp recoveryRise by 1-2 mgdL in ARFgt2mgdL in rhabdomyolysisCritically ill patient a ldquonormalrdquo value may not be normal
condition creatinine
prerenal fluctuate
ATN Peak by 7-10 days
Contrast nephropathyIschemic ATN
Rise within 24-48hrs peak in 3-5 days reach baseline in 7-10 days
AMINOGLYCOSIDE Rise delayed till 2nd week
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Creatinine clearance
Volume of plasma cleared off creatinine per unit timeEarlier warnings 2hr samples[140-age] x body wt SCreatinine x 7291-130 ml min CrCl = U Creatinine [mgdL] x volume [mLmin] P Creatinine[mgdL]S cystatin C
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Assessment of tubular function
bull Renal Failure IndicesPRERENAL INTRINSIC
FENa lt1 gt1
URINARY Na lt20 gt40
URINE OSM gt400 250-300
URINEPLASMA OSMOLALITY
141 11
UrCr P Cr gt501 lt201
BUNCr gt20 lt10
SPECIFIC GRAVITY
gt1018 lt1015
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Assessment of tubular function
Differentiate pre renal from intrinsic renal failureFeNa is the most usefulRatio of Na clearance to Creatinine clearancePrerenal intact tubules Na reabsorption avidly takes place Cr Cl high FENa lt1ATNNa absorption impaired FENa gt 1CKD amp diuretics also FENa gt1Metabolic alkalosis FECl better
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Radiology
Abdominal USGSmall Htve Nephrosclerosis CRFNormal large DM AmyloidosisLarge kidneys with large dilated pelvis and uretersPyelography localizationMRA Doppler US arterial venous obstruction
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Others
renal biopsy Increased potassium phosphorus CK-MM Uric Acid decreased Calcium rhabdomyolysis
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Complications
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Complications
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Complications
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Alsohellip
hyperphosphatemiaInfectionUremic syndromeHypovolemia due to vigorous diuresis in recovery
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Prevention of ARF- in perioperative period
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Avoid nephrotoxinsbull ACE-I amp ARBbull NSAIDsbull AMINOGLYCOSIDESbull AMPHOTERICIN-Bbull CISPLATINbull ASPIRINbull CYCLOSPORINbull LMW-DEXTRANbull ACYCLOVIRINDINAVIRbull METHOTREXATE
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Management of AKI
1 Prevention
bull Because there are no specific therapies for ischemic or nephrotoxic AKI
Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients such as the elderly and those with preexisting renal insufficiency
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
bull Indeed aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma burns or cholera prevention is of paramount importance
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR for example reducing the dose or frequency of administration of drugs in patients with preexisting renal impairment
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Preliminary measures
bull Exclusion of reversible causes Obstruction should be relived infection should be treated
bull Correction of prerenal factors intravascular volume and cardiac performance should be optimized
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Maintenance of urine output Loop diuretics may be usefully to convert the oliguric form of ATN to the nonoliguric form
High doses of loop diuretics such as Furosemide (up to 200 to 400 mg intravenously) may promote diuresis in patients who fail to respond to conventional doses
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Specific Therapies bull To date there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity bull Management of these disorders should focus on
elimination of the causative hemodynamic abnormality or toxin avoidance of additional insults and prevention and treatment of complications
bull Specific treatment of other causes of intrinsic renal ARF depends on the underlying pathology
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Prerenal ARF
bull The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid
bull Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (eg burns pancreatitis)
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic Hypotonic solutions (eg 045 saline) are usually recommended as initial replacement in patients with prerenal ARF due to increased urinary or gastrointestinal fluid losses although isotonic saline may be more appropriate in severe cases
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Subsequent therapy should be based on measurements of the volume and ionic content of excreted or drained fluids Serum potassium and acid-base status should be monitored carefully
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Postrenal ARF
Management of postrenal ARF requires close collaboration between nephrologist urologist and radiologist
bull Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter which provides temporary relief while the obstructing lesion is identified and treated definitively Similarly ureteric obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
4 Supportive Measures (Conservative therapy )bull Dietary management
Generally sufficient calorie reflects a diet that provides 40-60 gm of protein and 35-50 kcalkg lean body weight
In some patients severe catabolism occurs and protein supplementation to achieve 125 gm of protein kg body weight is required to maintain nitrogen balance
Restricting dietary protein to approximately 06 gkg per day of protein of high biologic value (ie rich in essential amino acids) may be recommended in sever azotemia
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Fluid and electrolyte management
Following correction of hypovolemia total oral and intravenous fluid administration should be equal to daily sensible losses (via urine stool and NG tune o surgical drainage ) plus estimated insensible ( ie respiratory and derma ) losses which usually equals 400 ndash 500 mlday Strict input output monitoring is important
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Hypervolemia can usually be managed by restriction of salt and water intake and diuretics
Metabolic acidosis is not treated unless serum bicarbonate concentration falls below 15 mmolL or arterial pH falls below 72
More severe acidosis is corrected by oral or intravenous sodium bicarbonate
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted thereafter according to serum levelsPatients are monitored for complications of bicarbonate administration such as hypervolemia metabolic alkalosis hypocalcemia and hypokalemia From a practical point of view most patients requiring sodium bicarbonate need emergency dialysis within days
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Hyperkalemia cardiac and neurologic complications may occur if serum K+ level is gt 65 mEqL
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10 solution over 5
minutes
o Glucose solution 50 ml of 50 glucose plus Insulin
10 units IV
o Give potassium ndashbinding ion exchange resin
o Dialysis it medial therapy fails or the patient is very
toxic
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral aluminum hydroxide or calcium carbonate which reduce gastrointestinal absorption of phosphate
Hypocalcemia does not usually require treatment
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
bull Anemia may necessitate blood transfusion if severe or if recovery is delayed
bull GI bleeding Regular doses of antacids appear to reduce the incidence of gastrointestinal hemorrhage significantly and may be more effective in this regard
than H2 antagonists or proton pump inhibitors
bull Meticulous care of intravenous cannulae bladder catheters and other invasive devices is mandatory to avoid infections
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Dialysis
Indications and Modalities of Dialysis - Dialysis replaces renal function until regeneration and repair restore renal function Hemodialysis and peritoneal dialysis appear equally effective for management of ARF Absolute indications for dialysis include
1048766 Symptoms or signs of the uremic syndrome
1048766 Refractory hypervolemia
1048766 Sever hyperkalemia
1048766 Metabolic acidosis
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Clinical course and prognosis
Stages acute renal failure due to ATN typically occurs in three stages Azotemic Diuretic and recovery phases The initial azotemic stage can be either oliguric or non oliguric type
bull Morbidity and mortality are affected by the presence of oliguria o GI bleeding septicemia metabolic acidosis and neurologic abnormalities are more common in oliguric patients than in nonoliguric patients
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
The mortality rate for oliguric patients is 50 where as that of nonoliguric patients is only 26
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Prognosis
The mortality rate among patients with ARF approximates 50 It should be stressed however that patients usually die from sequelae of the primary illness that induced ARF and not from ARF itself
Mortality is affected by both severity of the underlying diseases and the clinical setting in which acute renal failure occurs Eg the mortality of ATN is 60 when it results from surgery or trauma 30 when it occurs as a complication of medical illnesses and 10-15 when pregnancy is involved
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
bull Ischemia associated ATN has 2X the mortality risk of nephrotoxic ATN
bull In agreement with this interpretation mortality rates vary greatly depending on the cause of ARF ~15 in obstetric patients ~30 in toxin-related ARF and ~60 following trauma or major surgery
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Oliguria (lt400 mLd) at time of presentation and a rise in serum creatinine of gt3 mgdl are associated with a poor prognosis and probably reflect the severity of renal injury and of the primary illness
bull Mortality rates are higher in older debilitated patients
and in those with multiple organ failure
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
bull Patients with no complicating factors who survive an
episode of acute renal failure have a 90 chance of
complete recovery of kidney function
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Pharmacologic strategies
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Mannitol
Improve urinary flowPlasma expansionOsmotic hemodilutionFree radical scavengingVolume increase volume depletionIncrease O2 consumptionPulmonary edema intra renal vasoconstriction
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Mannitol
bull 625-125g is given 15 mins prior to the defined insult repeated 4-6 hrs
bull 24 hr cumulative dose not gt15 mgkgbull Aortic surgeriesbull Renal transplantationbull CABGbull rhabdomyolysis
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Frusemide
bull Inhibit Na-K ATPase in mTALbull Renal vasodilationbull Clear debris bull oliguric to non oliguric conversionbull segmental blockade with thiazide eg
metolazone 25-50mg pobull Ototoxicity interstitial nephritisbull Shouldnrsquot be given if pt is not adequately
fluid loaded
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Frusemide
bull Pigment nephropathy[ 2-3 times the normal dose with aggressive hydration]
bull Contrast nephropathy [with saline]bull May reverse medullary hypoxia induced by
toxinsbull 2-10 mgkg for converting oliguric to non
oliguric renal failurebull Continuous infusion 1-10mghr after a LD of
10-20mg
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Dopamine
bull Non specific DA1+DA2 agonistbull ldquosubpressor dopamine has proved
ineffective in clinical trials may trigger arrhythmias and should not be used as a renoprotective agent in this settingrdquo
bull SE increased myocardial O2 consumption decrease hypoxic drive intestinal ischemia
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Others
bull Fenoldapambull Nor adrenalinebull Dopexaminebull CCBsbull PGE1bull ANPbull ADENOSINEbull AMINOSTEROIDS
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
ALSO NOTEhellip
FORCED ALKALINE DIURESIS IN RHABDOMYOLYSIS
N-ACETYL CYSTINE IN ACETAMINOPHEN INDUCED INJURY
CONTRAST NEPHROPATHYhydration n-acetyl cystiene theophyllineaminophyllin bicarbonate containing IVFs[rather than saline]
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Treatment of complications of ARF
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Hyperkalemia
bull regular insulin 10 u + glucose [50 mL 50 dextrose
bull Ca gluconate 105 10 mlivbull Inhaled salbutamol 5 mg nebulisedbull KayexelateNa polystyrene sulfonatebull NaHCO3 50-100 mEq ivbull dialysis
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
others
bull Metabolic acidosis NaHCO3 to keep its level gt15mmolL or pH gt72
bull Hyperphosphatemia Ca carbonate Al(OH)3bull Hypocalcemia Ca gluconate CaCl2bull Nutritionbull Anemiabull Rx of CHF
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Renal replacement therapy
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Criteria for initiation of RRT
Anuria Oliguria Pulmonary edemaHyperkalemia gt65mmolLSevere acidemia lt72Uremic encephalopathyUremic pericarditisDrug overdose with dialyzable toxins
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Dialysis
dialyserdialysateblood delivery systemVascular accessDiffusion technique
heparinized blood and dialysate flows in opp direction through a synthetic membrane down a conc gradientConvection technique
similar to what happens in glomeruli Blood passes across a filter which has pores of different sizes so as to filter various molecules
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
hemodialysis
ADVANTAGESEfficient solute removal in short period of timeLower costmore suitable in severe hyperkalemiamore effective than PD in ARF
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
hemodialysis
DISADVANTAGESNeed for large bore venous accessNeed for anticoagulationNo removal of cytokinesUnsuitable if hemodynamically unstable
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Complications Hypotension poor tolerance to fluid removal or due to acetate component Treatment decrease blood flow rate IVFsHypoxemia loss of CO2 via dialyzer bronchospasm TreatmentAdr b-agonist aminophyllineHemorrhage 1mg of protamine100iu of heparin Arrhythmias Dialysis disequilibrium syndrome headache nausea delirium seizures
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
hemodialysis
bull Intermittent HD 3-4hrs per day3-4 times per week
bull Slow Low Efficiency Dialysis ^-12 hrs per day
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Continuous RRT
When intermittent HD failsWhen patient is not tolerating intermittent HD due to hemodynamic instability
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Types
Arteriovenous
Venovenous
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Venovenous
Continuous venovenous hemodialysis
Continuous venovenous hemofiltration
Continuous venovenous hemodiafiltration
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Advantages
better hemodynamic stabilityLess arryhthmiasImproved nutritional supportBetter pulmonary gas exchangeBetter fluid control
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Disadvantages
High risk of bleedingImmobilization prolongedCostlyDifficult vascular accessFilter problems
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
peritoneal dialysis
Less effective than HDUseful if HD not availableBleeding diathesisImpossible to attain vascular accessHemodynamically unstableNo anticoagulation is needed
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
disadvantagesImpaired drainage
PeritonitisProtein lossCompromised lung functionAbnormal blood sugar amp electrolyte valuesVery slow and ineffective when rapid correction is needed
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
Peritoneal dialysis
Access via a peritoneal catheter15-3L of a dextrose containing solution infusedAllowed to dwell for a short period of time[2-4hrs]Convective + diffusive clearance
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
ldquoRecent evidence suggest that more intensive hemodialysis [eg daily rather than alternative day intermittent dialysis] may be clinically superior and confers improved survival in ARF once dialysis is requiredrdquo
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
References Harrisons principles of internal medicine17th eAcute kidney injury network akinetorgPrinciples of critical care2nd e Farokh Erach UdwadiaAcute renal failure Dr Rebecca Jacob IJA 200347(5)Anesthesia and coexisting disease4th eccmtutorialscomPerioperative acute renal failure and its management Dr D Mallikarjuna [isacon-2007
THANK YOU
THANK YOU
