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Dr. Andrew Rynne
MD
Dr. Andrew Rynne

Family Physician

Exp 50 years

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Article Home First Aid and Emergency Acetaminophen poisoning

Acetaminophen poisoning

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Acetaminophen is the most common over the counter mediation available for pain and fever. It can be incidental or accidental poisoning. Acetaminophen poisoning seriously damages the liver, and in severe cases liver transplantation is life saving.

 

Causes

  • Acetaminophen is primarily metabolized by the liver. Overdose acetaminophen can overwhelm the liver normally functions.
  • Production of acetaminophen's toxic metabolite- NAPQI, causes liver damage, necrosis, and failure.
  • If the liver is already damaged because of viral or bacterial infection, alcohol abuse, or other illness, there is increased susceptibility of damage from acetaminophen overdose.

Signs and symptoms

End-organ (liver and kidney) toxicity is often delayed 24-48 hours postingestion.

Patients with malnutrition, AIDS, chronic alcohol abuse, are at increased risk for morbidity because of deficient glutathione stores and inadequate detoxification of NAPQI.

Phase 1- (0 – 24 hrs)

  • Asymptomatic
  • Anorexia/ Malaise
  • Nausea/Vomiting
  • Pallor
  • Diaphoresis/Increased sweating
  • Subclinical rise in LFT (serum transaminases levels) begins at about 12 hours of ingestion

Phase 2- (24 – 72 hrs)

  • Right upper quadrant abdominal pain
  • Anorexia
  • Nausea/vomiting
  • Right upper quadrant abdominal tenderness
  • Tachycardia
  • Hypotension
  • Continued rise in LFT (serum transaminases) levels

Phase 3 (72- 96 hrs)

  • With centrilobular liver necrosis- the intensity and severity abdominal pain increases
  • Jaundice
  • Increased bleeding manifestation
  • Hepatic encephalopathy
  • Renal failure
  • Fatality
  • Tenderness in liver edge
  • Gastrointestinal (GI) bleeding

Phase 4 (4 days – 3 wk)

Complete resolution of symptoms and organ failure

Tests and diagnosis

Serum acetaminophen concentration

Serum APAP concentration (N-acetyl-p-aminophenol)

Liver function test

  • Transaminases levels- SGOT and SGPT, toxicity is defined as serum SGOT or SGPT levels greater than 1000 IU/L.
  • Direct and indirect bilirubin levels
  • Serum albumin and total proteins
  • Prothrombin time, Bleeding time and Clotting time

Serum electrolytes

Renal function test- blood urea and creatinine

Human chorionic gonadotropin (HCG levels) in females of childbearing age

Urinalysis- proteinuria and hematuria in acute tubular necrosis

Arterial blood gas analysis

Treatment

Emergency care

  • Supportive therapy with IV fluids, Oxygen and Cardiac monitoring

Gastric decontamination

  • Activated charcoal is the drug of choice for patients presenting within 1-2 hrs of ingestion
  • Activated charcoal avidly adsorbs acetaminophen and should be administered if the patient presents within 1 hour of ingestion
  • 1 g/kg orally or 10 times the amount of drug ingested

Antidote- N-acetyl-cysteine

  • Early administration of N-acetyl-cysteine, within 8 hours of ingestion, is nearly 100% hepato protective. 
  • It’s the drug of choice for prevention and treatment of acetaminophen-induced hepatotoxicity.
  • It can be administered orally after diluting with chilled juice or cola to a 5% solution.
  • Can also be given by nasogastric tube, if nausea and vomiting is severe
  • When administered IV, dilute in 5% dextrose solution.

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