Q1 LONG ANSWER 10M ★ High-yield

Describe the general principles of management of acute poisoning including decontamination, enhanced elimination, antidotes and toxidromes.

Pharmacology · 2nd Professional — Para-Clinical

General Principles

The management of acute poisoning follows five steps: (1) resuscitation and supportive care, (2) decontamination, (3) enhanced elimination, (4) specific antidote, (5) continuing supportive care.

Supportive care saves far more lives than any antidote — airway, breathing, circulation, glucose, temperature and seizure control. Most poisons have no antidote, and most patients recover if these are attended to
"Treat the patient, not the poison" — the identity of the agent is frequently unknown or wrong, and waiting for it delays the treatment that matters
Always check the blood glucose and give thiamine before glucose in a possible alcoholic

Decontamination

Method	Indication and technique	Limitations
Surface decontamination	Remove clothing, wash skin and eyes copiously — essential in organophosphate and corrosive exposure, with staff protection	Rescuers may be contaminated
Activated charcoal	1 g/kg orally; adsorbs most drugs. Most useful within 1 hour of ingestion	Does not bind — metals (iron, lithium), alcohols, acids and alkalis, hydrocarbons, pesticides in solvent. Contraindicated in an unprotected airway or ileus; risk of aspiration
Gastric lavage	Only within about 1 hour, for a potentially life-threatening ingestion, with a protected airway	Rarely justified now; contraindicated after corrosives (risk of perforation) and hydrocarbons (aspiration pneumonitis). Causes hypoxia, arrhythmia and oesophageal injury
Whole bowel irrigation	Polyethylene glycol; for sustained-release or enteric-coated preparations, iron, lithium, and body packers	Contraindicated in obstruction or ileus
Induced emesis (ipecac)	—	Abandoned — ineffective and dangerous

CLINICAL PEARL

Almost everything that used to be done to the stomach has been abandoned. Emesis, routine lavage and "wash out and admit" delayed resuscitation, caused aspiration and removed very little poison. What replaced them is unglamorous: secure the airway, support the circulation, correct the glucose, and give charcoal early if it will bind the agent. Recognising that doing less was better took decades.

Enhanced Elimination

Method	Basis	Poisons
Multiple-dose activated charcoal	Interrupts enterohepatic and enteroenteric recirculation — "gut dialysis"	Theophylline, carbamazepine, dapsone, phenobarbitone, quinine
Urinary alkalinisation	Sodium bicarbonate raises urine pH; weak acids become ionised and cannot be reabsorbed — ion trapping	Salicylates, phenobarbitone, methotrexate; potassium must be corrected first or the urine cannot be alkalinised
Haemodialysis	Requires a small volume of distribution, low protein binding, low molecular weight and water solubility	Salicylates, methanol, ethylene glycol, lithium, theophylline, phenobarbitone, metformin (lactic acidosis)
Haemoperfusion	Blood passed over charcoal	Theophylline, carbamazepine; largely superseded
Lipid emulsion	A "lipid sink" drawing lipophilic drug out of tissue	Local anaesthetic toxicity; possibly other lipophilic drugs

Dialysis is useless where the volume of distribution is large — digoxin, tricyclics, benzodiazepines and chloroquine are all in tissue rather than plasma, so removing plasma achieves nothing

Specific Antidotes

Poison	Antidote	Mechanism
Paracetamol	N-acetylcysteine	Replenishes glutathione to detoxify NAPQI
Opioids	Naloxone	Competitive antagonist; shorter-acting than most opioids
Organophosphates	Atropine + pralidoxime	Atropine blocks muscarinic effects; pralidoxime reactivates cholinesterase
Benzodiazepines	Flumazenil	Competitive antagonist; risks seizures in dependence and mixed overdose
Warfarin / heparin	Vitamin K + prothrombin complex / protamine	Restores or neutralises
Iron	Desferrioxamine	Chelation
Lead	Calcium disodium EDTA, DMSA (succimer), dimercaprol	Chelation
Mercury, arsenic, gold	Dimercaprol (BAL), DMSA, penicillamine	Chelation
Methanol / ethylene glycol	Fomepizole or ethanol	Compete for alcohol dehydrogenase, preventing formation of the toxic metabolite
Cyanide	Hydroxocobalamin; sodium thiosulphate; sodium nitrite; dicobalt edetate	Binds cyanide or provides sulphur for detoxification
Digoxin	Digoxin-specific Fab fragments	Antibody binding
Methaemoglobinaemia	Methylene blue	Reduces methaemoglobin
Beta-blocker	Glucagon	Raises cardiac cAMP bypassing the blocked receptor
Calcium channel blocker	Calcium; high-dose insulin with glucose	Inotropic support
Isoniazid	Pyridoxine, gram for gram	Restores GABA synthesis; conventional anticonvulsants fail
Snake envenomation	Polyvalent antivenom	Neutralises venom
Local anaesthetic	Intravenous lipid emulsion	Lipid sink

Toxidromes

Toxidrome	Features	Causes
Cholinergic	Salivation, lacrimation, urination, defecation, bronchorrhoea, miosis, bradycardia, fasciculation	Organophosphates, carbamates, physostigmine
Anticholinergic	"Mad as a hatter, hot as a hare, dry as a bone, red as a beet, blind as a bat" — delirium, hyperthermia, dry skin, flushing, mydriasis, retention, tachycardia	Atropine, antihistamines, tricyclics, datura
Opioid	Coma, pinpoint pupils, respiratory depression	Morphine, heroin
Sympathomimetic	Agitation, tachycardia, hypertension, hyperthermia, mydriasis, sweating (unlike anticholinergic, where the skin is dry)	Cocaine, amphetamines, theophylline
Sedative-hypnotic	Drowsiness, coma, normal pupils, respiratory depression	Benzodiazepines, barbiturates, alcohol
Serotonin syndrome	Altered mental state, autonomic instability, clonus and hyperreflexia; onset in hours	SSRIs with tramadol, MAO inhibitors, linezolid

Applied Aspects

The dry skin of anticholinergic poisoning distinguishes it from sympathomimetic poisoning, which otherwise looks similar; this single sign changes the diagnosis at the bedside
Take a careful history from relatives, ambulance staff and the container, and keep the container; in India, agricultural pesticide poisoning is common and the label identifies the compound
Contact a poisons information centre; the National Poisons Information Centre at AIIMS provides round-the-clock advice
Deliberate self-poisoning requires psychiatric assessment before discharge, and the risk of repetition is highest in the following weeks
Pesticide poisoning is a major cause of death in rural India, and restricting access to the most toxic compounds has reduced suicide rates more than any clinical intervention
Protect yourself and the department in organophosphate and corrosive poisoning; secondary contamination of staff is a documented hazard
Observe for a delayed peak with sustained-release preparations, anticholinergic drugs that slow gastric emptying, and paracetamol; a reassuring early assessment does not exclude serious poisoning

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