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INTRODUCTION

Acute Renal Failure accurs in less than 2% of all acetaminophen poisonings and
10% of severely poisoned patients
At therapeuthic dosages, acetaminophen can be toxic to the kidneys in patients
who are gluthathione depleted (chronic alcohol ingestion, starvation, or fasting)
Acute renal failure due to acetaminophen manifest as acute tubular necrosis
(ATN)
OVERVIEW
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
a sudden episode of kidney failure or kidney damage that happens within a few hours
or a few days. AKI causes a build-up of waste products in your blood and makes it
hard for your kidneys to keep the right balance of fluid in your body. AKI can also
effect other organs such as the brain, heart and lungs. Acute kidney injury is a
common in patients who are in th e hospital, in intensive care units and especially in
older adults.

* Acute Renal Failure is a complex disorder that occure in a variety of settings with clinical
manifestations ranging from a minimal elevation in serum creatinine to anuric renal
failure. It is often under-recognized and is associated with severe consequences
DEFINITION OF AKI AS ANY OF THE FOLLOWING :
Increase in SCr by > 0.3 mg/dl (X26.5 lmol/l) within 48 hours; or
Increase in SCr to > 1.5 times baseline, which is known or presumed to have
occurred within the prior 7 days; or
Urine volume <0.5 ml/kg/h for 6 hours.
FAKTOR RESIKO DAN ETIOLOGI AKI
CAUSES
Decreased blood flow
Direct damage to the kidneys
Blockage of the urinary tract
SIGNS AND SYMPTOMS
Too little urine leaving the body
Swelling in legs, ankles and around the eyes
Fatigue or tiredness
Shortness of breath
Confussion
Nausea
Seizures or coma in severe cases
Chest pain or pressure
Algoritma diagnosis AKI
RIFLE CRITERIA
R = risk for renal injury
I = injury to the kidney
F = failure of kidney function
L = loss of kidney function
E = end-stage renal disease
ACUTE RENAL FAILURE E.C ACETAMINOPHEN
INGESTION
In toxic amounts, acetaminophen can result in hepatic necrosis and acute tubular
necrosis.
At therapeutic dosage, acetaminophen can be toxic in patients who consume
alcohol or who take drugs that stimulate the P-450 microsomal oxidase enzymes.
CASE REPORT
IDENTITY: A 39 year old white woman
S : - nausea
- vomitting
- diarrhea
- abdominal pain
- decrease in urinal output
- 4 days before admission, consume
Nyquil and Tylenol for sore throat &
cough
O: : - BP 150/98
- HR 107x/menit
- oral temperature: 37,4
- periorbital edema, ecchymosis,
scleral icterus, and an enlarged,
tender liver.
REVIEW OF PATHOPHYSIOLOGY

Hepatotoxic
Vomitting (after 4-6 days) Liver enlarged
Toxic dose of
appear 12 to 24 and necrosis rise level of
acetaminophen
hours later around the SGOT and SGPT
central vein

*The azotemia of acetaminophen


toxicity may increase progressively
for 7 to 10 days before the
recovery of renal function occurs
DIAGNOSIS
- A single toxic dose of acetaminophen that will result in adverse effects usually
exceeds 15 g in 80% of cases
- Alcoholics have a predisposition to both the hepatotoxic and nephrotoxic effects
of acetaminophen
- An acetaminophen level should be determined 4 to 12 hours after ingestion.
Levels obtained before 4 hours may not represent peak levels in plasma, and
those drawn days after the poisoning may not detect acetaminophen.
- A renal biopsy may be indicated in patients with an unobtainable history or
atypical presentation.
TERIMA KASIH

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