What is the role of oral N-acetylcysteine (NAC) in treating paracetamol (acetaminophen) toxicity?

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Last updated: November 11, 2025View editorial policy

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Role of Oral N-Acetylcysteine in Paracetamol Toxicity

Oral N-acetylcysteine (NAC) is a highly effective antidote for paracetamol overdose that should be administered at 140 mg/kg loading dose followed by 70 mg/kg every 4 hours for 17 doses (72-hour protocol), with treatment initiated as soon as possible and ideally within 8-10 hours of ingestion. 1, 2

Primary Indications for Oral NAC

  • Administer oral NAC when serum paracetamol levels plot in the possible or probable risk zones on the Rumack-Matthew nomogram (for patients presenting 4-24 hours post-ingestion). 1

  • Start NAC immediately for any patient presenting >24 hours after ingestion when the nomogram cannot be used, particularly if acetaminophen levels are detectable or liver transaminases are elevated. 1

  • Give NAC in acute liver failure cases where paracetamol ingestion is suspected or possible, even without confirmatory history, especially when very high aminotransferases (>3,500 IU/L) suggest paracetamol poisoning. 1

Oral vs Intravenous NAC: Route Selection

  • Both oral and intravenous NAC have equivalent efficacy in preventing hepatotoxicity, with meta-analysis showing similar rates of liver injury whether treated within 10 hours (3% vs 6%), late presentations 10-24 hours (30% vs 26%), or overall (16% vs 19%). 3

  • Oral NAC may preserve more hepatocytes than the 21-hour intravenous protocol according to mechanistic modeling, suggesting the oral 72-hour regimen provides superior hepatoprotection. 4

  • Intravenous NAC is preferred when oral administration is contraindicated: patients with coma, active vomiting, or when activated charcoal has been given (which may reduce oral NAC bioavailability). 5

  • Oral NAC has no absolute contraindications for treating paracetamol overdose per FDA labeling. 2

Critical Timing Considerations

  • The 0-8 hour window is critical: NAC initiated within 8 hours results in only 2.9% risk of severe hepatotoxicity. 6

  • Efficacy decreases progressively with delay: 6.1% hepatotoxicity risk when started within 10 hours, versus 26.4% when started 10-24 hours post-ingestion. 1, 6

  • NAC remains beneficial even after 24 hours: Among high-risk patients treated 16-24 hours post-ingestion, hepatotoxicity occurs in 41%—still lower than untreated controls (58%). 6

  • Treatment must be initiated within 24 hours of ingestion per FDA labeling, though benefit persists beyond this timeframe in established hepatotoxicity. 2

Oral NAC Dosing Protocol

  • Loading dose: 140 mg/kg orally or via nasogastric tube, diluted to 5% solution in juice or soft drink to mask the sulfur taste. 1, 6

  • Maintenance dosing: 70 mg/kg every 4 hours for 17 additional doses, totaling 72 hours of treatment. 1, 6

  • The full 72-hour oral course may be unnecessary in many cases, but provides superior protection compared to shorter intravenous protocols, particularly for delayed presentations or extended-release formulations. 4

Special Clinical Scenarios

  • High-risk patients require treatment at lower thresholds: Chronic alcohol users, fasting patients, or those on enzyme-inducing medications may develop toxicity at lower paracetamol levels and should receive NAC even below typical treatment thresholds. 1, 6

  • Repeated supratherapeutic ingestions (>4g per 24 hours): Treat with the standard 72-hour oral protocol if serum paracetamol ≥10 mg/mL or if AST/ALT >50 IU/L. 6

  • Extended-release paracetamol preparations: Use standard oral dosing but extend monitoring beyond 24 hours due to prolonged absorption. 1

  • Unknown time of ingestion with detectable paracetamol levels: Initiate oral NAC immediately without waiting for nomogram placement. 6

Activated Charcoal Considerations

  • Give activated charcoal (1 g/kg) just prior to starting NAC if patient presents within 4 hours of ingestion. 1, 6

  • Do not delay NAC administration even if activated charcoal has been given, though this creates a theoretical concern about reduced oral NAC bioavailability (favoring intravenous route in this scenario). 1, 5

Adverse Effects of Oral NAC

  • Nausea, vomiting, and diarrhea are the primary adverse effects of oral NAC administration. 5

  • Oral NAC avoids the anaphylactoid reactions (angioedema, bronchospasm, flushing, hypotension, rash) that occur in up to 10% of patients receiving intravenous NAC. 5

Treatment Discontinuation Criteria

  • Stop oral NAC when paracetamol level is undetectable AND liver function tests remain completely normal (no elevation in AST or ALT above normal range). 6

  • Continue or restart NAC immediately if: any transaminase elevation develops, rising AST/ALT trends, any coagulopathy appears, or detectable paracetamol persists. 6

  • For established hepatotoxicity (AST/ALT >1000 IU/L): Continue NAC until transaminases are declining and INR normalizes, as this reduces mortality from 80% to 52% regardless of time since ingestion. 6

Critical Pitfalls to Avoid

  • Never delay NAC while awaiting confirmatory paracetamol levels if there is strong clinical suspicion of significant overdose. 1

  • Do not rely on the Rumack-Matthew nomogram for presentations >24 hours post-ingestion—base treatment decisions on paracetamol levels, liver function tests, and clinical presentation. 6

  • Low or absent paracetamol levels do not rule out poisoning if ingestion was remote or occurred over several days. 6

  • Patients may develop hepatotoxicity despite "no risk" nomogram placement due to inaccurate history or increased susceptibility—maintain high clinical suspicion. 6

References

Guideline

N-Acetylcysteine Administration in Acetaminophen Overdose

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Use of N-acetylcysteine in clinical toxicology.

The American journal of medicine, 1991

Guideline

Acetaminophen Overdose Treatment Guidelines

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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