Medicine — Poisoning and Toxicology, NMC MBBS licence examination syllabus (Nepal Medical Council).
Poisoning: the patient who looks well is the dangerous one
Most poisons have no antidote. Almost all of them have a treatable airway.
Toxicology attracts a particular kind of attention — the exotic antidote, the obscure toxin, the dramatic reversal. That emphasis is almost exactly backwards. The overwhelming majority of poisoned patients recover with good supportive care and no antidote at all, and the ones who die usually die of something ordinary: an obstructed airway, an arrhythmia, aspiration, or a missed hypoglycaemia.
So this chapter is organised around what actually changes outcomes. Resuscitate first. Recognise the pattern when the history is missing or false. Know the handful of poisons where a specific action genuinely matters — and know that paracetamol is dangerous precisely because the patient feels fine.
🩺 Where this lives: In Nepal and much of South Asia, organophosphate poisoning is not a textbook curiosity — agricultural pesticides are widely available and deliberate self-poisoning with them is a major cause of death. These patients arrive drowning in their own secretions, and the treatment is large, repeated doses of atropine titrated to drying of the chest, not a single standard dose. Recognising the cholinergic toxidrome quickly is a genuinely life-saving skill in this setting in a way it may not be elsewhere.
💡 A note on doses. This chapter deliberately gives none. Poisoning management is dose-critical and protocol-driven, antidote regimens differ between national guidelines, and a half-remembered figure from a revision note is a dangerous thing to carry into a resuscitation room. Learn the mechanism and the sequence here; take the numbers from your local protocol or poisons information service at the bedside.
The general approach
The single most useful habit in toxicology is to stop asking "what did they take?" until the patient is safe. Airway, breathing, circulation, glucose and temperature come first — and in a patient with reduced consciousness and pinpoint pupils, opioid reversal is part of resuscitation rather than a separate diagnostic step.
HOW MUCH DOES THE HISTORY HELP?
Frequently not much.
Patients under-report and over-report.
Consciousness may be impaired.
CO-INGESTION is the rule, not the exception —
alcohol and paracetamol accompany a great deal.
So:
ALWAYS check paracetamol levels in deliberate
self-poisoning, whatever the patient says they took.
Look at what was brought in — packets, bottles,
the ambulance report, the scene.
Ask family and check the medication list, including
what is prescribed to other people in the house.
DECONTAMINATION — a smaller role than expected
Activated charcoal may bind some poisons if given early,
and only when the airway is protected. It is useless for
metals, alcohols and corrosives.
Gastric lavage and forced emesis have largely been
abandoned — the risks outweigh the benefit.
Reading the poison off the patient
💡 Exam angle: the sweaty versus dry distinction is the highest-yield discriminator here. Sympathomimetic and anticholinergic toxidromes both produce dilated pupils, agitation, tachycardia and hyperthermia — but sympathomimetic patients are drenched in sweat and anticholinergic patients have bone-dry skin, because sweat glands are cholinergically innervated. One examination finding separates two syndromes that otherwise look identical.
Paracetamol
WHY IT MATTERS SO MUCH IN EXAMS AND IN PRACTICE
It is COMMON, it is available everywhere, and its early
course is SILENT — the three properties that produce
preventable deaths.
KEY PRINCIPLES
A level taken TOO EARLY is uninterpretable — timing of
ingestion determines when the level means anything.
STAGGERED overdose (taken over hours) and overdose at
an UNKNOWN time cannot be assessed on a single level
against a nomogram. These patients are generally
treated.
Treatment thresholds are read from a nomogram plotting
level against time since ingestion. Know that the tool
exists and how to use it locally rather than
memorising values.
Certain patients are at higher risk from a given dose —
chronic alcohol use, malnutrition, enzyme-inducing
drugs — because glutathione reserves are lower.
ALT, INR, creatinine and pH determine severity and
prognosis. A RISING INR is the marker that matters most.
Criteria exist for referral to a liver unit and for
transplantation. Recognise a deteriorating patient and
escalate rather than waiting.
If a chapter on poisoning teaches one thing, it should be this: do not be reassured by a well patient after a paracetamol overdose. The first 24 hours are supposed to look fine. By the time jaundice and confusion appear, the window in which treatment is most effective has closed.
Other important poisons
🔍 The ones that come up repeatedly
OpioidsReduced consciousness, pinpoint pupils, low respiratory rate. Naloxone reverses it — but its half-life is shorter than most opioids, so the patient can re-sedate after an apparently successful reversal. They need observation, not discharge.
OrganophosphatesThe cholinergic toxidrome: pinpoint pupils, bradycardia, and secretions everywhere. Death is usually from bronchorrhoea and respiratory failure. Atropine is titrated to drying of the chest — often needing far more than a conventional dose — with pralidoxime alongside. Wear protection: rescuers can be contaminated.
Tricyclic antidepressantsAnticholinergic features plus cardiac sodium channel blockade — a widening QRS, arrhythmia and seizures. Sodium bicarbonate is the specific measure for a widened QRS. A common and lethal overdose.
BenzodiazepinesUsually a good outcome with supportive care. Flumazenil exists but is rarely used, because it can precipitate seizures — particularly with co-ingested tricyclics or in dependence.
Carbon monoxideHeadache, nausea and confusion in several people from the same building — often over a cooking or heating source. Pulse oximetry reads falsely normal; it cannot distinguish carboxyhaemoglobin. Give high-flow oxygen.
Alcohols and glycolsMethanol and ethylene glycol cause a raised-anion-gap metabolic acidosis with an osmolar gap. They need specialist treatment — the acid–base chapter's MUDPILES mnemonic includes them for this reason.
IronVomiting, abdominal pain and gastrointestinal bleeding, then apparent recovery before shock and liver failure. Another poison with a deceptive quiet phase.
💡 Exam angle: naloxone's short half-life is asked repeatedly. A patient who wakes fully after reversal can slip back into respiratory depression once it wears off, especially with long-acting opioids. The correct answer is admission and observation, sometimes with an infusion — never discharge on the basis of a good initial response. The same "improved then relapsed" structure appears with iron and paracetamol, and it is worth recognising as a pattern.
After the acute episode
THE OVERDOSE HAS A REASON
Every deliberate self-poisoning needs:
RISK ASSESSMENT for further self-harm and suicide,
including intent, planning, and whether the patient
expected to be found
MENTAL HEALTH ASSESSMENT before discharge — the medical
recovery is not the end of the episode
SAFEGUARDING considerations — children in the home,
vulnerable adults, domestic circumstances
PRACTICAL prevention — reducing access to the agent
used, and to others in the house
In accidental poisoning, particularly in children, the
question shifts to storage, labelling and supervision.
Treating the toxin and discharging without any of this
addresses the least important part of the presentation.
Clinical reasoning: four presentations
🔍 Case 1 — the well patient
PresentationA 19-year-old took a large quantity of paracetamol six hours ago after an argument. She now feels completely well, has normal observations, and wants to go home.
TrapFeeling well is taken as evidence of a minor overdose.
ReasoningThe first 24 hours of paracetamol poisoning are characteristically asymptomatic. Hepatic injury develops afterwards, and the effectiveness of treatment declines with time — so this is precisely the window in which acting matters most.
AnswerTake a timed paracetamol level, baseline bloods including INR, and treat according to the nomogram and local protocol. She also needs a mental health assessment before any discharge. Wellness now predicts nothing.
🔍 Case 2 — the farmer
PresentationA 34-year-old farmer is brought in drowsy, with pinpoint pupils, profuse salivation, vomiting, incontinence and loud wet crackles throughout both lungs. Pulse 48. A pesticide container was found beside him.
Key cluesPinpoint pupils with wet everything and bradycardia — the cholinergic toxidrome.
ReasoningOrganophosphate poisoning. Death comes from bronchorrhoea and respiratory failure rather than from the pupils or the pulse, so the airway and secretions are the priority.
AnswerPersonal protective equipment, decontaminate, secure the airway, and give atropine titrated to drying of the chest — often far beyond a conventional dose — with pralidoxime and specialist advice. Do not treat the bradycardia in isolation.
🔍 Case 3 — the premature discharge
PresentationA patient with heroin overdose, respiratory rate 5, receives naloxone and wakes fully within minutes. He is alert, wants to leave, and the department is busy.
TrapA dramatic reversal reading as a resolved problem.
ReasoningNaloxone has a shorter duration of action than most opioids. As it wears off, respiratory depression can return — occasionally fatally, and often after the patient has left.
AnswerObserve for a period appropriate to the opioid involved, with repeated doses or an infusion if sedation recurs. Also offer harm reduction and follow-up. The reversal buys time; it does not remove the drug.
🔍 Case 4 — the falsely normal saturation
PresentationIn winter, three members of one household present with headache, nausea and confusion. They cook indoors over a charcoal stove. Oxygen saturation reads 98% on air in each of them.
Key clueSeveral people, one building, one heat source — and symptoms that improved when they were outside.
ReasoningCarbon monoxide poisoning. Pulse oximetry cannot distinguish carboxyhaemoglobin from oxyhaemoglobin, so the saturation reads normal while oxygen delivery is severely impaired.
AnswerHigh-flow oxygen immediately, measure carboxyhaemoglobin on a blood gas co-oximeter, and treat all exposed occupants. Make the source safe — this is a public health problem as much as a clinical one.
Commonly confused
Confusion
The distinction
Why it matters
Well patient vs minor overdose
Paracetamol is silent for the first day
The asymptomatic phase is the treatable one.
Sympathomimetic vs anticholinergic
Sweaty versus bone-dry skin
Both have dilated pupils; one sign separates them.
Opioid vs cholinergic
Both pinpoint; cholinergic patients are WET
Entirely different antidotes.
Naloxone response vs cure
Naloxone is shorter-acting than the opioid
Patients re-sedate after discharge.
Normal SpO₂ vs normal oxygenation
Oximetry misreads carboxyhaemoglobin
CO poisoning hides behind a reassuring number.
Single vs staggered overdose
A nomogram needs a single known time
Staggered or unknown timing is assessed differently.
Medical clearance vs discharge
Mental health assessment comes first
The overdose has a cause that remains untreated.
Rapid revision
MUST-KNOW FACTS
1. Resuscitate first — most poisoned patients die of airway or arrhythmia.
2. Check GLUCOSE and temperature in every reduced consciousness.
3. Assume CO-INGESTION; always check paracetamol in deliberate self-poisoning.
4. Gastric lavage and forced emesis are obsolete.
5. Charcoal only early, only for some poisons, only with a protected airway.
6. Paracetamol is ASYMPTOMATIC for the first 24 hours.
7. Mechanism: saturated conjugation → NAPQI accumulates → glutathione exhausted.
8. NAC replenishes glutathione; give it early, and still give it late.
9. A level taken too early is uninterpretable — timing matters.
10. Staggered or unknown-time overdoses cannot be read off a nomogram.
11. A rising INR is the key marker of paracetamol severity.
12. Opioid toxidrome: pinpoint pupils, low respiratory rate, low GCS.
13. NALOXONE is shorter-acting than most opioids — observe, do not discharge.
14. Cholinergic toxidrome: pinpoint pupils and WET everything.
15. Organophosphates kill by bronchorrhoea — atropine to a DRY chest.
16. Protect yourself: organophosphate patients can contaminate rescuers.
17. Anticholinergic: dilated pupils, DRY hot skin, delirium, retention.
18. Sympathomimetic: dilated pupils, SWEATY skin — benzodiazepines first.
19. Tricyclics: widened QRS → sodium bicarbonate.
20. Flumazenil is rarely used — it can precipitate seizures.
21. Carbon monoxide: oximetry reads FALSELY NORMAL; give high-flow oxygen.
22. Methanol and ethylene glycol: raised anion gap with an osmolar gap.
23. Iron and paracetamol both have a deceptive quiet phase.
24. Every deliberate overdose needs a mental health assessment before discharge.
25. Take doses from your local protocol or poisons service, not from memory.
💡 Exam angle: the reliable threads are (a) the asymptomatic paracetamol patient, (b) sweaty versus dry separating two big-pupil toxidromes, (c) naloxone wearing off before the opioid, (d) the falsely normal saturation in carbon monoxide, and (e) atropine titrated to secretions rather than to pulse. Every one of them is a situation where a normal or improving observation is the trap — the pattern this whole stream keeps circling back to.
Syllabus points
Resuscitation before identification
History, co-ingestion and the limits of decontamination
The four toxidromes and how to tell them apart
Paracetamol: the asymptomatic phase and its timeline
The NAPQI mechanism and how NAC works
Timing, staggered overdose and severity markers
Opioids and the naloxone half-life problem
Organophosphates and atropine titration
Tricyclics, benzodiazepines and carbon monoxide
Antidotes worth knowing
Risk assessment, mental health and safeguarding
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