# Analgesic Poisoning > Analgesic poisoning in MBBS Forensic Medicine: paracetamol hepatotoxicity, NAC antidote, Rumack nomogram, salicylate acidosis, treatment lines. - Canonical URL: https://prepelephant.com/topics/mbbs/forensic-medicine/analgesic-poisoning - Exam / course: MBBS · Subject: Forensic Medicine - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Analgesic Poisoning", PrepElephant, https://prepelephant.com/topics/mbbs/forensic-medicine/analgesic-poisoning ## Direct answer Paracetamol heads nearly every Indian household's medicine shelf and heads the analgesic poisoning list with it: above roughly 150 milligrams per kilogram taken acutely (lower with alcoholism, malnutrition or enzyme-inducing drugs), the drug saturates glucuronidation and sulphonation, shunting metabolism to cytochrome P450 and generating N-acetyl-p-benzoquinone imine (NAPQI), which exhausts glutathione and necroses the liver in a centrilobular pattern over two to four days. Salicylate poisoning runs the other course — tinnitus, hyperventilation, early respiratory alkalosis, then a high anion gap metabolic acidosis, dehydration and hyperpyrexia — and threatens children dosed repeatedly for fever. The two antidote lines decide everything: N-acetylcysteine replenishes glutathione for paracetamol (guided by the Rumack-Matthew nomogram treatment line), and sodium bicarbonate alkalinises urine and tissue for salicylates, with haemodialysis reserved for the severe and deteriorating. ## What you must remember - **Paracetamol toxicity threshold:** acute ingestion around 150 milligrams per kilogram or 7.5-10 grams in adults; chronic or co-ingested alcohol lowers it substantially. - **Mechanism in one line:** overload of conjugation routes drives cytochrome P450-mediated NAPQI formation, glutathione depletion, and centrilobular hepatic necrosis. - **Clinical course:** 24 hours of nausea or silence, then rising aminotransferases peaking at 72-96 hours, coagulopathy and encephalopathy — the quiet first day is the trap. - **Antidote:** N-acetylcysteine, most effective within 8-10 hours, still beneficial later; oral loading 140 milligrams per kilogram followed by 70 milligrams per kilogram every four hours (intravenous protocols are standard in Indian hospitals). - **Nomogram:** the Rumack-Matthew treatment line beginning at 150 micrograms per millilitre at four hours separates patients needing the antidote — plot only single acute ingestions with known timing. - **Salicylate syndrome:** tinnitus, deafness, hyperventilation, sweating, hyperpyrexia; mixed acid-base disorder with respiratory alkalosis followed by high anion gap metabolic acidosis. - **Salicylate treatment:** activated charcoal early, sodium bicarbonate to alkalinise urine (targeting urinary pH around 7.5-8) trapping salicylate as its ion, and haemodialysis for severe intoxication, seizures or falling pH. - **Reye syndrome:** aspirin in children with viral illness is linked to this hepatic encephalopathy — the reason paediatric aspirin use collapsed. ## Working through an overdose timeline A 22-year-old woman swallows thirty 500-milligram paracetamol tablets at midnight after an exam result and reaches hospital at eight in the morning with only vomiting. The timing is gold: a four-hour-post-ingestion level is already behind, so treatment starts on exposure history alone — fifteen grams in a 50-kilogram adult is double the toxic threshold. N-acetylcysteine begins immediately while a level is awaited, and the level, when plotted on the Rumack-Matthew nomogram, sits well above the treatment line. The first twenty-four hours she looks insultingly well; on day two the ALT climbs into the thousands, the prothrombin time stretches, and on day three early encephalopathy appears with hypoglycaemia — the centrilobular necrosis declared on standard kinetics. Because the antidote was given inside ten hours, recovery is the expected outcome; had she presented on day three, the same units would be discussing transplantation criteria. Salicylate cases write a different file: the child dosed hourly for two days arrives already hyperventilating and acidotic, and the treatment is alkalinisation with bicarbonate while monitoring urine pH, potassium (alkalinisation wastes it) and clinical sedation — dialysis stands ready if the level, the mental state or the acidosis deteriorates. ## Where the viva probes The classic probe is why the paracetamol patient looks well on day one while the salicylate patient looks ill from the first hours — the expected answer contrasts direct pharmacological stimulation by salicylate with delayed toxic metabolite injury by NAPQI. The second favourite is the nomogram's limits: it cannot be used for staggered ingestions, chronic toxicity or unknown times — in those, treat on history and follow transaminases. Examiners also expect the alcoholism question (induced P450 plus depleted glutathione lower the threshold dangerously) and the forensic angle: paracetamol is a common co-ingestant in impulsive self-poisoning in India, and the doctor's duty includes psychiatric referral once the liver is safe, since repeatability is the real risk. ## Frequently asked questions ### What is the toxic dose of paracetamol in acute overdose? Approximately 150 milligrams per kilogram or 7.5-10 grams in adults, with a lower effective threshold in alcoholics, malnourished patients or those on enzyme inducers. ### How does N-acetylcysteine work as an antidote? It replenishes glutathione stores, detoxifying NAPQI before it binds hepatocytes; it is most effective within 8-10 hours but still helps later. ### What acid-base disturbance characterises salicylate poisoning? Early respiratory alkalosis from direct stimulation of the respiratory centre, followed by a high anion gap metabolic acidosis — the classic mixed picture. ### When is haemodialysis indicated in salicylate poisoning? Severe or symptomatic intoxication with high levels, refractory acidosis, seizures, encephalopathy or renal failure despite bicarbonate therapy. ### What is the medicolegal significance of analgesic overdose? Paracetamol dominates impulsive self-poisoning in India, so every case is an intentional-overdose assessment until proven otherwise, with documentation, psychiatric evaluation and poisoning reporting.