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NUR CHAYATI
Dept. Gawat Darurat
PSIK FKIK UMY
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Old term: acute renal failure (ARF)
Traditionally defined as the abrupt decrease of
renal function sufficient to result in retention of
nitrogenous waste products, as well as loss ofregulation of extracellular volume and electrolytes
While consensus historically exists in this
definition, none exists regarding the quantificationof this decline in function to fully denote as ARF
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Anatomi ginjal
BEAN SHAPE
RETROPERITO
NEALLOWER THAN
THE LEFT
NEPHRON AS
UNIT
FUNCTIONAL
20-25% CO
1200 ml/mnt
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NEPHRONA.aFFEREN
A.eFFEREN
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Kidney function
Regulation of body fluid
Regulation of electrolyte balance
Regulation of acid base balance
Regulation of blood pressure
Excretion of nitrogenous waste product
Regulation of erytropoiesis
Metabolism of vitamin D
Synthesis of prostaglandin
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Kosinski (2009), acute renal failure is asudden decline in both glomerular andtubular function, resulting in the failure of thekidneys to excrete nitrogen and waste
products with a corresponding failure tomaintain fluid, electrolyte and acid-basebalance
ARF may be associated with decreasedurinary output of less than 30 ml/h.
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ARF: the sudden decline in GFR, resulting in
retention of nitrogenous waste products
(azotemia). Usually accompanied by oliguria
(uop < 400mL/24 hr)non oliguric (>
400mL/24hr)
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AKI
Decrease in renal function not limited to ARF,but broad clinical syndrome encompassingvarious etiologies: including specific kidney
disease (ex acute interstitial nephritis, acuteglomerular, and vasculitic renal diseases),non specific conditions (ischemia, toxic
injury), and extrarenal pathology.
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AKI
An abrupt (within 48hr) reduction in kidney function
currently defined as an absolute increase in serum
creatinine of either >0.3 mg/dL or a percentage
increase of >50% or a reduction in urin out put(documented as oliguria of 6hr)
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Definition and classification/staging system for acute
kidney injury (AKI)AKI stage Creatinine criteria Urine output criteria
AKI stage I Increase of serum creatinine by
0.3 mg/dl ( 26.4 mol/L)
or
increase to 150% 200% from baseline < 0.5 ml/kg/hour for > 6 hours
-------------------------------------------------------------------------------------------------------------------
AKI stage II Increase of serum creatinine to
> 200% 300% from baseline < 0.5 ml/kg/hour for > 12 hours
-------------------------------------------------------------------------------------------------------------------
AKI stage III increase of serum creatinine to
> 300% from baseline < 0.3 ml/kg/hour for > 24 hoursor or anuria for 12 hours
serum creatinine 4.0 mg/dl
354 mol/L) after a rise of at least 44 mol/L
ortreatment with renal replacement therapy
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Epidemiology
Prevalence 1% all patients admitted to hospital
10-30% patients admitted to ICU
Etiology
Hemodynamic 30% Parenchymal 65%
Acute tubular necrosis 55%
Acute glomerulonephritis 5%
Vasculopathy 3% Acute interstitial nephritis 2%
Obstruction 5%
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Mortality
Dialysis requiring 40-90%
Increased mortality even in patients not requiring dialysis
25% increase in creatinine associated with a
mortality rate of 31% compared with 8% for matched
patients without renal failure
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Etiology of Acute Renal FailurePRE RENAL
1. VOLUME DEPLETION1) Hemorrhage
2) Trauma
3) Surgery
4) Diarrhea
5) Vomitting
6) Diuretics
7) Osmotic diuresis
8) Diabetes incipidus
9) Burns
10) Hipoalbuminemia
2. VASODILATION
11) Sepsis
12) Anaphylaxis
13) Medication
(antihipertensive)
14) Anasthesia
3. IMPAIRED CARDIAC
PERFORMANCE
15) Heart failure
16) IMA
17) Cardiogenic shock
18) Pulmonary embolism19) Pulmonary
hypertension
4. MISCELLANEOUS
Renal
vasoconstriction
Hypercalcemia
Norepinephrine
NSAIDs
GFR
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Conditions that Lead to Intra-renal Acute Renal Failure
1. GLOMERULAR,
VASCULAR/
HEMATOLOGICAL
PROBLEM
Glomerulonephritis
(post streptococcal)
Vasculitis
Malignant
hypertension
SLE
DIC
Hemolytic uremic
syndrome Scleroderma
Hypertension og
pregnancy
Thrombosis
a/v.renalis
2. TUBULAR PROBLEM
(ACUTE TUBULAR
NECROSIS/ ACUTE
INTERSTITIAL
NEPHRITIS)
Ischemia
Causes of prerenal azotemia
Hypotension from
any cause
Hypovolemia from
any cause
Medication Radiocontrast
DM
Advanced age
Transfussion
reacting causing
hemoglobinuria
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Common Nephrotoxic Medications
NSAIDS ACE inhibitors
Angiotensin receptor blockers
Antibiotics
Penicillins methacillin
Ampicillin, amoxacillin, carbenacillin, oxacillin
Cephalosporins
Quinolones (ciprofloxacin)
Anti-tuberculous medications (rifampin, INH, ethambutol)
Sulfonamides (TMP-SMX, furosemide, thiazides)
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COMMON NEPHROTOXIC AGENTS
Antimicrobial agents
Aminoglycosides
Amphotericin B
Acyclovir
Foscarnet Pentamidine
Chemotherapy drugs: Cisplatin, 5-FU, mitomycin C,
streptozocin
Antiviral: Acyclovir, indinavir, Ritonavir, Adenovir
Radiocontrast agents
Miscellaneous
Allopurinol, cimetidine,
dilantin
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Radiocontrast-Induced
Acute Renal Failure
Induces renal vasoconstriction and direct cytotoxicity via
oxygen free radical formation
Risk factors:
Renal insufficiency - Diabetes
Advanced age - > 125 ml contrast
Hypotension
Usually non-oliguric ARF; irreversible ARF rare
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Contrast Induced Nephropathy
Assess CIN risk eGFR 60, Discontinue metformin
Optimal Volume Status
Low-osmolality contrast media
Evaluate Creatinine 24 72hr after contrast exposure
Adequate IV volume expansion with isotonic crystalloid for 3 12hr before
the procedure and continue for 6 24hr afterward. Oral fluid data is
insufficient No adjunctive medical or mechanical treatment has been proved to be
efficacious
Prophylactic hemodialysis and hemofiltration not validated
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Conditions that Lead to Post-renal Acute Renal Failure
1.BPH
2. Blood clots
3. Renal stones or crystals
4. Tumors
5. Post operative edema6. Drugs
Tricyclic antidepressants
Ganglionic blocking agents
7. Foley cathether obstruction
8. Ligation of ureter duringsurgery
5 K St i E l ti A t R l
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5 Key Steps in Evaluating Acute Renal
Failure
1) Obtain a thorough history and physical;
review the chart in detail
2) Do everything you can to accurately assess
volume status
3) Always order a renal ultrasound
4) Look at the urine5) Review urinary indices
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Symptoms:
Fever, rash, joint pains, myalgias
Concern for SLE, vasculitis, acute interstitial nephritis.
Dyspnea heart failure. Hemoptysis
Preceding bloody diarrhea
Preceding pharyngitis post-Strep, post-infectious
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3 phases of the disease process
INITIATION
(ONSET) PHASE
MAINTENANCE
(OLIGURIC/ANURIC) PHASE
RECOVERY
(DIURETIC )PHASE
From the occurrence of the
precipitating event to thebeginning of the change in
urine output.
1. Several hours-2 days
2. Normal renal process
begin to deteriorate
3. INTRINSIC RENAL
DAMAGE IS NOT YET
ESTABLISHED
Potentially reversible
- Intrinsic renal damage iswell established
- GFR 5-10 mL/mnt
- Last 8-14 days 1-11
months
- Anuric Condition
oliguric (uop > 400mL/mnt)
- Complication:
hyperkalemia, infection
- Renal tissue recovers and
repairs itself (4-6 months)
- Gradual increase in uop
& improvement in
laboratory value
- Diuresis happen caused
of:
1. salt and water
accumulation in ECF
2. osmotic diuresis from
retained waste
product
3. Diuretic agents
DANGER????
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Nursing care plan
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Assessment
Physical Exam.
Skin new rashes.
Petechiae
Malar rash
Eye
Papilledema
Cardio
Rub
Gallop
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Assessing volume status.
Is the patient intravascularly volume depleted?
Neck veins JVP
Peripheral edema or lack of.
Orthostatic vitals.
Pt. may be edematous (low albumin) or have
significant right sided heart disease.
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BUN/Creatinine ratio. > 20:1 suggest prerenal or obstruction.
Can be elevated by anything leading to increased ureaproduction/absorption.
GI bleed TPN
Steroids
Drugs Tigecycline.
Creatinine in anephric state typically only rises1mg/dl/day. If greater should be concerned for rhabdomyolysis
Serum Cr. Dipengaruhi oleh massa otot tiap individu
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Nursing Dx
1. Excess fluid volume related to sodium and
water retention and excess intake
2. Risk for infection r.t depressed immune
response secondary to uremia and impaired
skin integrity
3. Imbalanced nutrition: less than body
requirements related to uremia, altered oral
mucous membranes, and dietary restriction
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Nursing Dx
4. Anxiety r.t diagnosis, treatmen plan,
prognosis, and unfamiliar environment
5. Deficient knowledge r.t disease process and
theraeutic regimen
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NOC, NIC
Its for your home work
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Nurse competencies
AACN Synergy Model. The eight nursing
competencies of the Synergy Model are as
follows: clinical judgment, advocacy and moral
agency, caring practice, collaboration, systemsthinking, response to diversity, facilitator of
learning, and clinical inquiry.
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Nutrition
- low in protein and sodium and
- high in fats and carbohydrates to prevent theprotein burden on the patients kidneys
(Campbell, 2003).- Fluids are generally restricted to the amount
of the patients urine output plus 500 to 700
ml.- Parental nutrition is recommended if thegastrointestinal tract is not functional.
i i f i l d
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Provision of emotional support and
teaching
Acute renal failure is often very sudden andunexpected for both the patient and the family
members.Thorough patient teaching about nutritionalneeds, fluid restrictions, medications, and therole of dialysis is essential in providing
emotional support patients and familymembers.
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Complication
1. Renal
1. The primary effect of ARF is a decrease inurinary output that leads to fluid retention and
edema.2. The decrease in filtration leads to BUN and
creatinin build up in the blood as the kidney losesits ability to remove waste products.
3. metabolic acidosis, hypercalemia, hyponatremia,hyperphosphatemia, hypocalcemia, andhypermagnesemia.
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3. Cardiovascular
- In general, the fluid volume overload experienced inARF may lead to hypertension, pulmonary edema,
peripheral edema, and arrhythmias.
- The kidneys fail to excrete excess potassium which maylead to the following: muscle weakness, neuromuscular
irritability, bradycardia, heart block, asystole, or otherarrhythmias (Campbell, 2003).
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4. Respiratory
Dyspnea may result from the decrease in
oxygenation either from associated
anemia or from fluid volume overload andpulmonary edema associated with ARF.
Auscultation of lung field may revealcrackles.
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5. Hematologic
Anemic secondary to the impaired RBC production,hemolysis, bleeding, hemodilution, and decreaseRBC survival.
Damaged kidneys produce less erythropoietin tostimulate RBC production and the damaged redblood cells are not replaced.
The decrease in hemoglobin leads to insufficientoxygenation manifested by dyspnea.
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6. Gastrointestinal
Uremia may cause nausea, vomiting, anorexia,
gastric ulcers and colitis which places the
patient at risk for GI bleeding.
The increase in urea may also cause the
patients breath to smell like foul urine.
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Diagnostic Tools
Conventional Biomarkers
1. urine output
2. creatinin
3. urea.
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New Biomarkers
Cystatin C,
Interlukin 18 (IL 18),
Neutrophil Gelatinas-Associated Lipocalin
(NGAL), and
Kidney injury Molecule (KIM-1).
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Diagnostic Imaging
1. X rays,
2. computed tomography scan (CT),
3. magnetic resonance imaging (MRI),
ultrasound,
4. arteriogram,
5. renal biopsy.
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Evidence Based Practice
Contrast induced nephropathyHow is this
happen? What should the nurses do?
Canadian Association of Radiologist
(Consensus Guidelines for The Prevention of
Contrast Induced Nephropathy)*
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Refferences
1. KDIGO Clinical prctice guideline for acute kidneyinjury. 2012. 2 (1).http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf
2. So Yoon Jang, S.Y. Renal Fellow. UNC Kidney Center Atthe Courtesy of Dr. Hladik and Dr. Derebail.
3. Sole, Klein & Moseley. 2009. Introduction to Criticalcare Nursing. Fifth Edition. Saunders. Elsevier.
4. Stroud, B. 2013. Acute Renal Failure.
http://rnjournal.com/journal-of-nursing/acute-renal-failure
http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdfhttp://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdfhttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://rnjournal.com/journal-of-nursing/acute-renal-failurehttp://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdfhttp://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf