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Presented by: Vikas Naik
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INTRODUCTIONINTRODUCTIONBody Fluid Compartments:Body Fluid Compartments:
ICF:ICF:55%~75%55%~75%
2/3
Male (60%) > female (50%) Most concentrated in skeletal muscle TBW=0.6xBW ICF=0.4xBW ECF=0.2xBW
IntravascularIntravascular
plasmaplasma
X 50~70%X 50~70%lean body weightlean body weight
ExtravascularExtravascular
InterstitialInterstitialfluidfluid
TBWTBW
ECFECF
3/4
1/4
1/3
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Introduction
Total body water 94% weight in early
gestation
Decreases to 78% at term
eac es a u t eve s o y mont s
23/03/2012
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INTRODUCTIONINTRODUCTIONComposition of Body Fluids:Composition of Body Fluids:
Na+
Cl-
HCO3-0
50
100
150Cations Anions
ECF
Ca +
Mg 2+
K+
PO43-
Organicanion
Protein
50
100
150
ICF
Osmolarity = solute/(solute+solvent)Osmolarity = solute/(solute+solvent)
Osmolality = solute/solvent (290~310mOsm/L)Osmolality = solute/solvent (290~310mOsm/L)
Tonicity = effective osmolalityTonicity = effective osmolality
Plasma osmolility = 2 x (Na) + (Glucose/18) + (Urea/2.8)Plasma osmolility = 2 x (Na) + (Glucose/18) + (Urea/2.8)
Plasma tonicity = 2 x (Na) + (Glucose/18)Plasma tonicity = 2 x (Na) + (Glucose/18)
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Objectives of IV Therapy
Maintain daily body fluid requirements
Restore previous body fluid losses
Replace present body fluid losses
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Average daily water balance of ahealthy adult (70 kg)
Intake output
Beverage 1200ml urine -1500mlsolid food 1000ml insens.loss- 900ml
Oxidation 300ml faces -100ml
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Fever Pyrexia increases insensible lossby about 20% for each C rise in bodytemperature
Ventilator
GI losses Equivalent volume of normalsaline added with potassium chloride use tocover the gastrointestinal fluid loss and fluidsequestrated in the bowel.
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Normal volume and composition ofbody fluids
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Clinical parameters for evaluation of water balance
CVP
Pulse Peripheral Veins Wei ht
Thirst Intake and Output Skin Edema Lab Values
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Maintenance dose
For 24hrs
100ml/kg for 1-10kg
50ml/kg for 11-20
- v
or 4ml/kg/hr for 1-10kg
2ml/kg/hr for 11-201ml/kg/hr for 21-above
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Pediatric neurosurgical patients over24hrs
premature 90-100ml/kgat term 80-90ml/kg
3m-1 r 70-80ml/k
>1yr 70ml/kg
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Effect on cerebral oedema formation
Effect on CPP
Effect on glucose
Effect on electrolytes
23/03/2012
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IV fluids divided into crystalloid and colloidde endin on molecular wei ht of solutes
crystalloids 30,000mmol
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Crystalloids:Crystalloids:
Isotonic crystalloids
- Lactated Ringers, 0.9% NaCl- only 25% remain intravascularly
- 3% NaCl
Hypotonic solutions
- D5W, 0.45% NaCl- less than 10% remain intra-
vascularly, inadequate for fluid
resuscitation
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Colloid Solutions:Colloid Solutions:
Contain high molecular weight
substancesdo not readily migrate across
capillary walls
repara onsPlasma protein fractions
Gelatins
Dextrans
Starches
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Plasma Derived Colloids
Plasma (FFP, cryoprecipitate)- Coagulation problems only
Plasma protein fraction/SHS
- Very expensive
- No proven benefit- ? harmful
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Colloids
GELATINS DEXTRANS HES
Molecular weight 28-35 kda 40-70 kda 70-450 kda
Advantages Improvescirculation
Improvescirculation
Improvescirculation,
endothelialunc on
Anaphylaxsis High small minimal
VOLUMEEFFECT
SHORT MEDIUM LONGTERM
COAGULATION +/- ++ +
DOSE
LIMITATION
NO 15ml/kg/24hr 33ml/kg/24hr
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Which Fluids ? Depends on Nature of Loss!
Balanced approach for resuscitation:
2-3 crystalloid then colloid
? 0.9% saline or HS for head injuries Ringers for other fluid resuscitation
Colloids included for major resuscitation
Blood as needed for Hct = 30
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Crystalloid
Extracellar expander
Limited volume expansion
Maintain urine output
Reduce plasma oncotic pressure Variable electrolyte content
Cheap!
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Colloid
Advantages:Intravascular expanders
Disadvantages:Coagulation problems
Variable electrol te
Rapid resuscitation
Maintain oncotic pressure
Less tissue oedemaLess pulmonary oedema
contentVariable half-life
Adverse reactions
EXPENSIVE!
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The Influence of Colloid & Crystalloid on BloodThe Influence of Colloid & Crystalloid on BloodVolume:Volume:
1000cc
200 600 1000
Lactated Ringers
Blood volume
Infusionvolume
500cc
500cc
500cc
5% Albumin
6% Hetastarch
Whole blood
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1.Should not be used except fortreatment
.
2.Solution of 5% dextrose ishypoosmolar
3.RL is also slightly hypoosmolar,administration of >3 litres canreduce
plasma osmolality.23/03/2012
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osmolality approximately that of plasma. , , . Hyperchloremic metabolic acidosis may
result with NS
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Usually Ringers lactate and/or NormalSaline
- vo ex rose u s Infusion rate should be to replace urineoutput and insensible losses ml. for ml.
Replace blood loss at 3:1 ratiocrystalloids or 1:1 of colloids downto
haematocrit of 25-30%23/03/2012
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Permissible blood loss
EBV x (HIHd ) /HI
EBV=weight x avg blood volume
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Increases plasma- cerebral parenchymaosmolality gradientdose -0.5-2.0 gm/kg
arge ose en ances cere ra ooflow and free radicalscavenging
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Mechanism of action is similar to mannitol Strengths of HS 3, 5 7.5%
causes less diuresis
23/03/2012
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Transfusion of blood in the form of packed cell if Hb< 8
Dilutional clinical coagulopathy when blood lossexceeds more than one blood volume
Fresh frozen plasma to be administered if prothrombintime> 1.5 time normal
Dose of FFP: 10- 15 ml/ k to obtain 30% of lasma
factor concentration) Prophylactic administration contraindicated
Platelet deficiency occurs if blood loss exceeds > 1.5times EBV (14)
Transfusion indicated if counts less than 50,000/ cmmor if higher counts with bleeding
Dose of platelet concentrate- one platelet concentrateper 10 kg body weight
Use of antithrombin III controversial
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Dual set of problems
Hypovolemia
Hyponatremia- CSW and SIADH
Avoid dehydration
ere ra vasospasm y
hypervolemia by CVP of 8- 10
hemodilution by PCV around 30- 35
hypertension Avoid dextrose containing solutions
Prefer colloids for volume expansion
23/03/2012
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ElectrolytesNormal values
Na+ - 130-149meq/l
K+ - 3.5-5meq/l
Cl- 95-110 meq/lCa- 8.1-10.4mg%
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Daily recommended amountElectrolyte Parenteral Equivalent of RDA Usual Intake
Sodium 12 meq/kg +
replacement, but
can be as low as
540 meq/d
Potassium 40100 meq/d +
replacement of
unusual lossesChloride As needed for acid-base
balance, but usually 2:1 to
1:1 with acetate
Acetate As needed for acid-base
balance
Calcium 10 meq 1020 meq/d
Magnesium 10 meq 816 meq/d
Phosphorus 30 mmol
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Factors controlling sodium Reabsorption
in Perioperative Period
RAS:- Renin secretion increases formation ofAngiotensin IIAldosterone Na reabsorption in
Distal tubule
Sympathetic nervous system- Increased
proximal tubule
ADH- it has little action on sodium excretion.,itmostly maintains extracellular fluid volume
ANP- it is released from atrial cells & causesafferent arteriolar dilation & efferent arteriolar
constriction thus increasing GFR & natriuresis
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HYPONATREMIA
Hypovolumic Hypervolumic EuvolumicCCF
NEPHROTIC SYNDROME
RENAL FAILURECIRRHOSIS
Extra renal sodium loss
diarrhea
VomitingBlood loss
Excessive sweating
Renal sodium loss
SIADHCNS
SOLTrauma
HemorrhageStrokeInflammatory
disordersdemyelination
Diuretics
Osmotic diuresis
Adrenal insufficiency
ketonuria
CarbamazepineChlorpropramidePhenothiazinesSRITCA
Pulmonary
conditionsInfectionsALINeoplasia
THIAZIDE DIURETICSHYPOTHYROIDISMADRENAL
INSUFFICIENCY
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Assesment of Pt with Hyponatremia
Clinical-
Skin turgor & mucous membranesJVP
.
daily wt.
Biochemical-
Serum Na+ & osmolarityUrine vol,S.G, Na+ & Osmolarity
BUN ,Cr,K+, Uric acid, Albumin,Cortisol
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HYPONATREMIA Contd ECG features-
Mostly non specific Appears when Na+< 115mmol/l
, ,
Bradycardia, Ventricular ectopics alsopossible
At values< 110mmol/l cardiac arrest mayoccur.
Algorithm for assesment of Hyponatremia
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Serum
Na
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Dose of Na+(meq)=wt(Kg)(140-Na+)
0.63%NS
- . -
Na=125meq/l
Half the deficit can be administered over 1st 8hrs, rest over 1-3 days
Correct underlying disorder
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Hypertonic saline - symptomatic
Fluid restriction /Normal saline -asymptomatic patients
a t rep acement
23/03/2012
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Complication of Treatment
Pontine Myelinolysis - quadriparesis ,ataxia,abnormal extraocular movements. can occur withra id correction
Renal Failure, Peripheral edema, pulmedema, heart failure
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SIADHDiagnostic Criteria of SIADH:-summarised by
Harrigan 1996 Serum sodium serum osmolality
Normal thyroid, adrenal, renal function
Absence of peripheral edema ordehydration
Clinical features are same of hyponatremia
Specific Treatment of SIADH
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Specific Treatment of SIADH
Fluid restriction- 1 l/day. (0.9% saline is usualchoice)
Furosemide
- -,
on renal tubule
Demeclocycline -900-1200 mg in divided doses,takes 3wks for maximal effect, Induces nephrogenicDI.
Fludrocortisone -requires 1-2 wks &,retains
sodium, inhibits thirst.
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Cerebral salt wasting
syndrome
Renal loss of sodium due to intracranial
disease, leading to hyponatremia &hypovolemia
Causes: Head injury Brain tumor
Stroke Intracerebral hemorrhage Tuberculous meningitis
Craniosynostosis repair
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Cerebral salt wasting syndrome (
CSWS ) Pathophysiology not fully understood-
hypothesis
natriuretic response due to SNS overactivityand DA release causes urinary sodium loss
release - brain natriuretic peptide, C-typenatriuretic peptide or an oubain like peptide,by the injured brain
CSWS usually appears in the first week afterbrain injury and spontaneously resolves in 2-
4 weeks
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Specific Treatment of CSWS
Fluid & Sodium Resuscitation -0.9%saline used
acute s m tomatic -h onatremia 3%
NS Oral fludrocortisone - 0.1mg-0.4mg to
limit ve sodium balance in ptsrefractory to salt & fluid therapy
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Aneurysmal SAH Abnormal sodium levels seen in acute
period(4-10days) Incidence is 29%-43% Sayamaet alNeurolog res2000; 22:151-55, found
. om- -a w ypona rem aMCA-18% - a/w hyponatremia
Moringaet al -84% with hyponatremia hadsymptomatic vasospasm
Hasan et al Ann neurol 1990;27:106-180didnt finddifference in mortality rates
Possible cause of hyponatremia is release of
BNP
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Transsphenoidal surgery for Pituitary Tumors
DI is Common
CSW may commonly co-existAlbanese et al ,andrews et al Neurosurg1986;18:469-471
CSW is thou ht to occur secondaril to
release of BNP. After pituitary adenomaresection.
Triple response
-initial 4-8 day period of DI-excessive release of ADH for 14
days
-Permanent DI
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23/03/2012
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Surgery for Craniosynostosis
Frequently occurs, but usually
asymptomatic & transient
Etiology not conclusive-could be SIADH a/w large fluid shifts
CSWS has also been reported by
KappyPlastic reconstr surgery 2001;108:1501-1508
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Defined as serum Na >145mmol/l Clinical variables:
Hypernatremia
1. Body weight2. Peripheral oedema
3. CVP
4. Serum sodium/ Urine spot sodium
23/03/2012
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Major causes of hypernatremia
CAUSES
Impaired Thirst
MECHANISMS
Coma,Essential Hypernatremia
Excessive water loss Renal
Extrarenal
Combined disorders
Mannitol, DKA, Non ketotichyperosmolar coma
Pituitary DI,Nephrogenic DI
Sweating
Coma + Hypertonic nasogastricfeeding
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Most s/s of hypernatrmia are
neurological
Altered mental status
Hypernatremia
Weakness Neuromuscular irritability
Focal neurological deficit Occasional coma/seizures
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Algorithim for assessment of Hypernatremia
Serum Na
> 145 mmol/L
Urine
Inappropriately
Urine
Appropriately
Assess urine
osmolality
Dilute concentrated
HypovolemicEuvolemic
Hypervolemic
Hypovolemic Euvolemic
Hypervolemic
Diabets Insipidus
Renal Disease
Mineralocorticoid
Excess
Extrarenal
Water loss
Iatrogenic Na
Administration
Assess volume
status
Assess volume
status
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Management of Hypernatremia Goals
Stop loss of water by T/t of cause Correct water deficit
Water deficit can be calculated as
(S Na+
-140/140)x TBW.If serum glucose is elevated, then thecorrected formula is
S Na+=S Na+
+( S glu-90)/36As in hyponatremia, rapid correction ofhypernatremia is also dangerous
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Water deficit to be corrected over 48-72 hrs No more than 0.5mmol/l/hr &12mmol/l/day
Management of Hypernatremia
u
Safest method of correction is water by
mouth or NG tube.
If patient cannot take orally, 5% Dextrose canbe given intravenously
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23/03/2012
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CENTRAL DI:-
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CENTRAL DI:
It is a failure of release of ADH fromHypothalamo-pituitary axisCharacterised by inability to concentrate
urine ,thus passage of large amount of
dilute urineRise in Plasma osmolality & progressive
dehydration
Particularly seen after pituitarysurgery,TBI, A Com Art aneurysmalSAH, & in brain death patients
*Compromise of Hypothalamic centers or the supra
optic tract above the median eminence:-permanentDI
Damage below median eminence or removal ofposterior lobe of pituitary:- transient DI
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Etiology of Central DI
Acquired Head trauma
Post-pituitary surgery
Congenital Midline craniofacial
anomalies
Holo rosence hal
Granulomas Infections
Inflammations
Chemical toxins Tetrodoxins,Snake
venoms
Vascular
Idiopathic
Ectopia of Pituitary Genetic
Autosomal dominant
Autosomal Recessive
X-linked recessive
Deletionchromosome7q
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ETIOLOGY OF NEPHROGENIC DI
Acquired
Drugs Lithium Demeclocycline
Vascular
SCD ATN
Granulomas
Amphotericin B Aminoglycoside Cisplatin Rifampicin Foscarnet
Metabolic Hypercalcemia Hypokalemia
Obstruction
Infiltrations Pregnancy IdiopathicGeneticX-linked recessive(ADH
receptor V2).Autosomal Recessive
(Aquaporin-2 gene)
Diagnosis of postoperative
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g p p
diabetes insipidus
Rule out osmotic diuresis or fluid overload
Clinical signs and symptoms
Polyuria, abrupt high volumes (4 L/day18 L/day)( within 2448 hours postoperatively)
Polydipsia, with craving for cold fluids
With/without hypovolemia
Diagnosis of postoperative
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Laboratory data
Dilute urine (specific gravity 50ml/kg+
urine osmol
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ALGORITHM FOR DIAGNOSIS OF DI
urine osmol 300mosmol/kg
Urine osmol50% Small/no increase Plasma AVP same
Severe Pituitary DI Severe nephrogenic DI Partial Nephrogenic DIPartial pituitary DI
/Primary polydipsia
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Maintenance
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Maintenance
drink according to thirst
Supplement hypotonic (D5W to D51/2NSS)
Monitor for resolution of transient DI or triphasic response
Positive daily fluid > 2 L suggests SIADH
Withhold -Antidiuretic hormone therapy
Manage anterior pituitary insufficiencystress dose -hydrocortisone 100 mg TDS
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Chlorpropramide It acts by potentiating the action of AVP or activation
of V2 raceptors Dose is 125-500mg OD
nset slow efficac less efficac can be increasedby simultaneous use of Thizides.Hypoglycemia is asignificant side effect
Clofibrate & Carbamazepine is also helpful infew patients
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Nephrogenic DI:-
T/t of cause & omitting the culprit druggenerally cures the disease
Amiloride (esp in pts. On lithium) Indomethacin
Low sodium diet
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FLUID DEPRIVATION TEST
Indication Evaluation of Diabetes InsipidusPrecautions: Requires close
monitoring
Monitor urine output Monitor vital signs
Monitor weight Do not allow weight loss to exceed
>3-5%
CONTD..
Technique
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Technique Fluid restrict patient
Mild polyuria (10 L/day) Start fluid restriction 2 hours before test
Follow Serum Osmolality to steady state
water Measure Serum Osmolality hourly until endpoint: Two values are within 30 mOsm of each other Weight loss exceeds 3-5%
Administer endogenous ADH Vasopressin 5 units Sc Intranasal DDAVP 10 ug
Measure Serum Osmolality 1 hour after ADH
administered
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Hypokalemia
Normal requirement 1meq/kg/day
Serum otassium < 3.5 mE / liter
Causes: intracellular shiftpotassium depletion
23/03/2012
Hypokalemia
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Transcellular shift:
beta agonists
diuretics
alkalosis
hypothermiainsulin
Potassium depletion:renal losses: diuresis/ failure
Extra renal losses: diarrhea/ NG drainage
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Clinical features hypokalemia
Muscle weakness and mental status
ECG changes prominent U waves,flattening and inversion of T waves,prolonged QT interval
Does not cause arrhythmias on its ownbut definitely is proarrythmic
23/03/2012
Hypokalemia
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Hypokalemia
23/03/2012
DiarrhoeaUrine chloride
< 15 mEq/ ltr
Urine chloride
> 15 mEq/ ltr
NG drainage
Alkalosis
Diuresis
Mg depletion
Management of hypokalemia
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Correct the primary cause
Potassium deficits in hypokalemia for 70Kg male
Serum potassium Potassium Deficit in %
3.0 175 52.5 350 10
2.0 470 15
1.5 700 201.0 875 25
23/03/2012
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Serum potassium > 5.5 mEq/ liter
Most common cause is traumatichemolysis during venipuncture
20% blood sample incidence withelevated potassium
Source: transcellular shift ( urinary
K>30)renal cause ( urinary K< 30)
23/03/2012
Trans cellular shift:
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Acidosis
Rhabdomyolysis
Drugs: digitalis/ beta antagonists Renal causes:
Adrenal insufficiencyDrugs: ACE inhibitors/ B-
blockers/ cyclosporine/ digitalis/ diuretics/
heparin/ NSAIDS/ septran/ muscle relaxants Blood transfusions
23/03/2012
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Management
Guided by serum potassium and ECGmanifestation
. evere cases - ve m - ca c um
gluconate over 5 minutes
Repeat second dose if necessary
No role for third doseAction lasts for 20 minutes
23/03/2012
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2. Insulin dextrose: 10 U regular insulin in500 ml 20% dextrose to infuse over 1 hour-
decreases K by an average of 1 mEq/ L
3.Loop diuretics
4.Exchange resins
5.If refractory - hemodialysis
23/03/2012
Metabolic acidosis
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High Anion Gap
Renal failure
toxins ketoacidosis
orma an on gap
(hyperchloremic) Hyperkalemia obstructive uropathy diarrhea renal tubular acidosis
Some medications23/03/2012
Clinical features
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Headache
Drowsiness
Nausea/ vomiting/ diarrhea Kussmauls respirations
-
Hyperkalemia Hypotension
Bradycardia
GI distention
pH low (< 7.35)
HCO3 low (< 22)23/03/2012
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Management:
Fluid resuscitation
Correct underlying disorder Sodium bicarbonate only if pH< 7.20
Method: 0.5 x body weight x base deficit
correct half as slow infusion over few
minutes
other half to be repeated over 8 hours
repeat ABG values
stop when ph 7.2023/03/2012
M b li lk l i
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Metabolic alkalosis Etiology:
1.Vomiting2.Diuretics
3.Volume depletion
4.Hypokalemia
5.Organic anions like lactate
6.Chronic CO2 retention
23/03/2012
Metabolic alkalosis
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Clinical features
Shallow breathing Nausea/vomiting/diarrhea
on us on
Numbness / tingling
Hypocalcemia
Hypokalemia pH high (> 7.45)
HCO3 high (>26) cal features:23/03/2012
M t b li lk l i
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Metabolic alkalosis Management: saline infusion (0.2*body
weight* chloride deficit) In resistant cases give 0.1N HCl (0.5*
body weight* base excess)
Acetazolamide
23/03/2012
M t b li lk l i
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Management: saline infusion (0.2*body
weight* chloride deficit) In resistant cases give 0.1N HCl (0.5*
Metabolic alkalosis
body weight* base excess)
Acetazolamide
23/03/2012
R i t id i d lk l i
7/28/2019 Fluid and Electrolyte Balance in Neurosurgery
91/92
Respiratory acidosis and alkalosis
Treatment of underlying cause
Correction of oxygenation Sedation, reassurance and CO2
rebreathing for alkalosis
Ventilatory support and chestphysiotherapy
23/03/2012
7/28/2019 Fluid and Electrolyte Balance in Neurosurgery
92/92
THANK YOU