IM22.1-13 | Poisoning — Glossary

The enzyme responsible for hydrolysing acetylcholine at cholinergic synapses; inhibited by organophosphates (irreversibly via phosphorylation) and carbamates (reversibly via carbamylation); its inhibition causes accumulation of ACh and the cholinergic toxidrome.

The principal toxic alkaloid of Aconitum species (monkshood/vatsanabha); activates and permanently opens voltage-gated sodium channels (Nav), causing paraesthesiae, paralysis, and life-threatening ventricular arrhythmias.

A highly adsorptive substance that binds most organic toxins in the GI lumen, preventing systemic absorption; standard dose 50 g (1 g/kg in children) orally or via NGT within 1–2 hours of ingestion; contraindicated for corrosives, iron, lithium, and hydrocarbons.

Hepatic encephalopathy with coagulopathy (INR > 1.5) in a patient without pre-existing liver disease, occurring within 26 weeks of acute hepatic injury; paracetamol is the most common cause in developed countries; managed with intensive care support and liver transplant evaluation.

The time-dependent strengthening of the covalent bond between organophosphate and the AChE active site serine, making the phosphorylation irreversible; most agricultural OPs age within 24-48 hours; military nerve agents (soman) age within minutes; after ageing, pralidoxime is ineffective.

The hepatic enzyme responsible for metabolising methanol, ethylene glycol, and ethanol; the key therapeutic target in toxic alcohol poisoning — inhibiting ADH with fomepizole or ethanol prevents generation of toxic metabolites.

A fumigant and rodenticide (marketed as Celphos, Quickphos) that reacts with moisture to release phosphine gas; the most common cause of fatal pesticide poisoning in north India; no specific antidote.

A non-IgE-mediated reaction occurring during the loading dose of IV N-acetylcysteine infusion (flushing, urticaria, bronchospasm); managed by slowing/stopping the infusion and giving antihistamine; not a contraindication to NAC — restart at slower rate after symptoms resolve.

Na⁺ − (Cl⁻ + HCO₃⁻); normal 8–12 mEq/L; elevated in high anion gap metabolic acidosis (HAGMA), which in poisoning is caused by methanol, ethylene glycol, salicylates, cyanide, and iron.

Syndrome caused by muscarinic receptor blockade; characterised by hot-blind-dry-red-mad mnemonic (hyperthermia, mydriasis, dry flushed skin, delirium/agitation); caused by Datura, antihistamines, tricyclic antidepressants.

Acute respiratory distress syndrome caused by direct phosphine toxicity to pulmonary endothelium, leading to non-cardiogenic pulmonary oedema; a late and serious complication of severe AlP poisoning requiring mechanical ventilation with lung-protective strategy.

A competitive muscarinic receptor antagonist used as the primary antidote in cholinergic (organophosphate) poisoning; dose titrated to drying of secretions; no upper dose limit in cholinergic crisis.

A competitive muscarinic receptor antagonist that reverses the muscarinic features of cholinergic toxidrome (dries secretions, reverses bronchospasm and bradycardia); titrated to drying of bronchial secretions; no dose ceiling; does NOT reverse nicotinic (fasciculations, paralysis) or CNS features.

The clinical target for atropine titration in OP poisoning: drying of bronchial secretions and clearing of pulmonary wheeze — NOT pupil dilation and NOT heart rate normalisation; the most commonly misunderstood principle in OP poisoning management.

A wide-complex tachycardia with alternating QRS axis (beat-to-beat change in axis by 180 degrees); pathognomonic of cardiac glycoside toxicity (digoxin or plant glycoside poisoning).

Crystals formed from oxalic acid (ethylene glycol metabolite) combining with serum calcium; deposit in renal tubules causing AKI; appear in urine (monohydrate and dihydrate forms) at 4-8 hours post-ingestion; associated with hypocalcaemia.

Poisoning by carbamate insecticides (carbofuran, methomyl) that reversibly carbamylate AChE; clinically similar to OP poisoning but shorter duration; pralidoxime NOT required as carbamylation reverses spontaneously.

Toxicity from Na/K-ATPase inhibition by digoxin or plant glycosides (oleandrin, thevetin); manifests as nausea, bradyarrhythmias, AV block, ventricular arrhythmias, and hyperkalaemia; treated with digoxin-specific Fab fragments.

A syndrome caused by excess acetylcholine accumulation from acetylcholinesterase inhibition; characterised by SLUDGE (Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis), miosis, bradycardia, bronchospasm, and muscle fasciculations; classic cause is organophosphate poisoning.

An Indian plant (garari/oduvan) whose leaves contain diterpenoid toxins that inhibit oxidative phosphorylation; causes hypokalaemia, metabolic acidosis, ascending paralysis, and renal failure; no antidote.

Type of tissue injury caused by acid corrosives; proteins are denatured, forming a firm eschar that limits further penetration; predominantly affects the stomach.

Oral administration of 30-60 mL coconut oil as a harm-reduction measure in AlP ingestion; the hydrophobic lipid layer over the tablet may limit water contact needed for phosphine liberation; limited observational evidence, no RCT; safe, inexpensive.

Drugs or conditions that increase CYP2E1 activity, dramatically increasing NAPQI generation and lowering the toxic paracetamol threshold: chronic alcohol use, rifampicin, isoniazid, carbamazepine, phenytoin; the standard Rumack-Matthew nomogram treatment line should be lowered by 50% in these patients.

The terminal complex of the mitochondrial electron transport chain; binds oxygen and pumps protons; inhibited by phosphine (and cyanide); its inhibition causes complete cessation of aerobic ATP production.

A plant (jimsonweed/dhatura) containing belladonna alkaloids (atropine, scopolamine, hyoscyamine) that cause anticholinergic toxidrome; characterised by mydriasis, dry flushed skin, tachycardia, hyperthermia, delirium, and urinary retention.

Intentional self-injury or ingestion of a harmful substance with intent to harm oneself; all DSH cases require mandatory psychiatric consultation before discharge under the Mental Healthcare Act 2017.

An iron chelator that binds free ferric iron and excretes it as ferrioxamine in urine (vin rosé urine — a monitoring sign); indicated for serum iron > 500 mcg/dL or symptomatic iron poisoning.

Antibody fragments (Digibind/DigiFab) that bind and inactivate digoxin; each vial binds 0.5 mg digoxin; indicated for life-threatening digoxin-related arrhythmias, serum digoxin > 10 ng/mL, or severe hyperkalaemia in digitalis toxicity.

Competitive substrate for ADH used to block metabolism of methanol or ethylene glycol when fomepizole is unavailable; target blood ethanol 100-150 mg/dL; requires dose increase during haemodialysis (dialysis removes ethanol); risk of hypoglycaemia, especially in children.

A toxic alcohol found in automotive antifreeze; metabolised by ADH to glycolic acid and oxalic acid; causes AKI from calcium oxalate crystal deposition and hypocalcaemia; no visual toxicity; antidote is ADH inhibition (fomepizole or ethanol) + calcium + pyridoxine.

A competitive GABA-A receptor antagonist that reverses benzodiazepine sedation; dose 0.2 mg IV, repeatable; contraindicated in BZD-dependent patients and when TCAs are co-ingested (risks precipitating seizures).

Used in methanol poisoning to enhance the folate-dependent pathway that converts formate to CO₂ + H₂O; dose folic acid 50 mg IV every 4-6 hours; safe, inexpensive, and should be given to all methanol-poisoned patients.

An alcohol dehydrogenase inhibitor used as the preferred antidote for methanol and ethylene glycol poisoning; prevents conversion to toxic metabolites (formic acid and oxalic acid respectively); ethanol is the alternative when fomepizole is unavailable.

A potent competitive inhibitor of alcohol dehydrogenase; the preferred antidote for methanol and ethylene glycol poisoning; dose 15 mg/kg IV loading then 10 mg/kg every 12 hours; does not cause CNS depression unlike ethanol; expensive and not available in most Indian hospitals.

Collection and labelling of clinical samples with potential evidential value — gastric aspirate, vomitus, blood, urine — in cases of suspected homicidal or assault-related poisoning; samples must be labelled with patient ID, date, time, and case number and sealed for police chain of custody.

The toxic metabolite of methanol; inhibits cytochrome c oxidase (Complex IV of the ETC) selectively in optic nerve and retinal cells, causing visual loss; also accumulates as an anion causing high anion gap metabolic acidosis.

Irrigation of the stomach via a large-bore orogastric tube to physically remove ingested toxin; rarely indicated, reserved for life-threatening ingestion of non-charcoal-adsorbed toxin within 1 hour with protected airway; largely replaced by activated charcoal.

A 15-point neurological assessment scale (Eye 4 + Verbal 5 + Motor 6) used to quantify level of consciousness in the poisoned patient; GCS ≤ 8 mandates airway protection and intubation.

Used in beta-blocker poisoning to restore cardiac rate and contractility by activating adenylyl cyclase via a non-adrenergic pathway, bypassing the blocked beta receptor; dose 3–5 mg IV bolus then infusion.

Indicated for salicylate level > 100 mg/dL, acute kidney injury, arterial pH < 7.2, CNS dysfunction, or pulmonary oedema in salicylate toxicity; removes water-soluble, low-protein-bound salicylate effectively; faster than urinary alkalinisation alone in severe cases.

Removes toxic alcohols and their metabolites directly from the blood; far faster than renal excretion; indicated for methanol with pH < 7.2, visual disturbance, or level > 50 mg/dL; and for ethylene glycol with AKI or pH < 7.25; must continue ADH inhibitor during dialysis at increased dose.

Illegally distilled or adulterated alcohol in India; a common cause of methanol poisoning outbreaks when ethanol has been adulterated or replaced with methanol; community outbreak pattern (multiple cases from same batch) is the clinical clue.

Legal doctrine allowing emergency medical treatment of an unconscious or incapacitated patient without explicit consent, on the presumption that a reasonable person would consent to life-saving treatment; documented in the clinical notes; does not remove the need to obtain consent from family or the patient when possible.

A complication of OP poisoning occurring 24-96 hours after the acute cholinergic crisis resolves; characterised by proximal limb weakness, neck flexor weakness, and respiratory muscle paralysis; caused by persistent NMJ dysfunction (depolarisation block); treated with mechanical ventilation.

A complication specific to organophosphate poisoning (NOT phosphide poisoning) — proximal muscle weakness and respiratory failure 24-96 hours after the acute cholinergic crisis; included here to contrast with AlP which has no such delayed NMJ-specific complication.

A mechanical circulatory support device inserted via the femoral artery into the descending aorta; inflates during diastole (augmenting coronary perfusion) and deflates during systole (reducing afterload); considered in refractory cardiogenic shock from AlP poisoning when available.

Attempt to suicide under the Indian Penal Code; largely decriminalised by the Mental Healthcare Act 2017 (Section 115), which states that persons who attempt suicide shall be presumed to be under severe stress; prosecution under this section is now rare.

Criteria for liver transplant referral in paracetamol-induced acute liver failure: pH < 7.3 after resuscitation, OR the simultaneous combination of INR > 6.5 + creatinine > 300 mcmol/L + Grade 3-4 hepatic encephalopathy.

High anion gap metabolic acidosis from accumulation of lactate produced by anaerobic glycolysis in tissues deprived of aerobic ATP generation; rising serum lactate despite resuscitation is the most reliable predictor of fatal outcome in AlP poisoning.

The interval between ingestion of methanol/ethylene glycol and onset of severe toxicity; 6-24 hours for methanol, 4-12 hours for ethylene glycol; prolonged by co-ingestion of ethanol (ADH competition); the window during which ADH inhibitor treatment is most effective.

Type of tissue injury caused by alkali corrosives; lipid saponification and protein solubilisation cause penetrating, deep injury that does not self-limit; predominantly affects the oesophagus.

A proven suicide prevention strategy involving reducing access to methods of self-harm; in the clinical context, involves counselling families to lock medicines, remove agricultural chemicals from accessible storage, and manage prescription drugs for at-risk patients.

A critical distinction in MLR writing: a medical opinion states what the physician can conclude from clinical and investigative evidence ('findings are consistent with organophosphate poisoning'); a legal conclusion states guilt, intent, or criminal liability ('this was a homicidal poisoning') — the physician writes the former, the court determines the latter.

Any case where the injury or illness has potential legal consequences — includes all poisoning cases (accidental, suicidal, homicidal), assault, RTAs, and unnatural deaths; requires MLC registration, proper documentation, and police intimation as appropriate.

A formal medical document recording clinical findings, investigations, treatment, and medical opinion in a medico-legal case; structured in 7 sections; written in passive voice for history and precise clinical language for findings; medical opinion must never include legal conclusions.

Indian legislation governing mental health care; Section 115 decriminalises attempted suicide (person presumed to be under severe stress, not to be punished under IPC 309); mandates provision of mental health care for persons who attempt suicide; empowers patients with rights to advance directives and informed consent.

A toxic alcohol found in illicit hooch, solvents, and antifreeze; metabolised by ADH to formaldehyde then formic acid; causes visual loss and severe metabolic acidosis; antidote is ADH inhibition (fomepizole or ethanol) + folic acid.

Dissipation of the proton gradient across the inner mitochondrial membrane without generating ATP; heat is produced instead; caused by phosphine, salicylates, and dinitrophenol; results in hyperthermia and ATP depletion.

Characteristic of salicylate overdose: early respiratory alkalosis (from direct medullary respiratory centre stimulation) combined with high anion gap metabolic acidosis (from uncoupled oxidative phosphorylation generating organic acids); net pH depends on the relative magnitude of each component.

Repeated doses of activated charcoal given every 4 hours to enhance elimination of toxins with enterohepatic recirculation or slow GI absorption; useful in some OP poisoning cases where modified-release formulations prolong absorption.

Repeated doses of activated charcoal (25-50 g every 4 hours) used for toxins with enterohepatic recirculation (carbamazepine, quinine, thevetin/cardiac glycosides); the gut-dialysis mechanism removes already-absorbed toxin.

Clinical effects of excess ACh at muscarinic receptors: SLUDGE + miosis + bradycardia + bronchospasm + bronchorrhoea + hypotension; reversed by atropine (competitive muscarinic antagonist).

A glutathione precursor used as the antidote for paracetamol poisoning; replenishes hepatic glutathione to prevent accumulation of NAPQI; indicated when serum paracetamol falls above the Rumack-Matthew nomogram treatment line.

The sodium-potassium pump in cell membranes; inhibited by cardiac glycosides (digoxin, oleandrin, thevetin); inhibition causes increased intracellular sodium, increased intracellular calcium, triggered arrhythmias, and hyperkalaemia.

A pure competitive opioid receptor antagonist that reverses opioid toxidrome; dose 0.4–2 mg IV/IM/intranasal, repeatable every 2–3 minutes; shorter half-life than most opioids requires repeat dosing or infusion.

The hepatotoxic metabolite of paracetamol produced by CYP2E1; normally detoxified by glutathione; accumulates when glutathione is depleted in overdose, causing covalent binding to hepatocellular proteins and centrilobular necrosis.

Clinical effects of excess ACh at nicotinic receptors: fasciculations (NMJ stimulation, early), followed by flaccid muscle weakness and paralysis (NMJ depolarisation block, later); diaphragmatic paralysis is a major cause of respiratory failure; not reversed by atropine.

Fibrous narrowing of the oesophagus due to scarring after severe corrosive injury (more common with alkali); manifests as progressive dysphagia weeks to months after acute ingestion; treated with serial oesophageal dilatation.

Common name for Nerium oleander (containing oleandrin and neriine) and Thevetia peruviana/yellow oleander (containing thevetin and neriifolin); both contain cardiac glycosides that inhibit Na/K-ATPase, causing bradyarrhythmias and hyperkalaemia.

Classic triad of miosis (pinpoint pupils), respiratory depression, and decreased consciousness resulting from μ-opioid receptor stimulation; reversed by naloxone.

Poisoning by organophosphate compounds (chlorpyrifos, malathion, monocrotophos, etc.) that irreversibly phosphorylate AChE; the most common cause of acute cholinergic crisis in India; treated with atropine and pralidoxime.

A rare late complication of certain OP compounds (triorthocresyl phosphate) occurring 2-4 weeks post-exposure; caused by inhibition of neuropathy target esterase (NTE); manifests as distal axonal neuropathy with ascending weakness and sensory loss; no treatment.

The difference between measured serum osmolality and calculated osmolality (2×Na + glucose/18 + BUN/2.8); an osmolar gap > 10 mOsm/kg suggests presence of unmeasured osmoles, classically toxic alcohols (methanol, ethylene glycol, isopropanol).

In early toxic alcohol poisoning: elevated osmolar gap (parent alcohol present) with normal anion gap. In late poisoning: normal osmolar gap (parent metabolised) with elevated anion gap (metabolites accumulated). A normal osmolar gap at late presentation does NOT exclude toxic alcohol poisoning.

Supreme Court of India ruling that a physician must treat a medico-legal case patient first, regardless of police presence, documentation requirements, or payment — the duty to treat in emergencies takes precedence over all legal formalities.

The toxic gas liberated when aluminium or zinc phosphide reacts with water; potent inhibitor of cytochrome c oxidase (mitochondrial Complex IV) causing cellular ATP depletion; characteristic garlic or fish-like odour in vomitus.

A reversible anticholinesterase that crosses the blood-brain barrier; used to reverse severe anticholinergic delirium (e.g., Datura poisoning); dose 1-2 mg slow IV; contraindicated with TCA co-ingestion due to risk of seizures and arrhythmias.

Air in the mediastinum, visible on chest X-ray as radiolucency outlining mediastinal structures; in corrosive poisoning, indicates oesophageal or tracheal perforation — a surgical emergency.

A 24-hour toxicological advisory service staffed by trained toxicologists; provides toxin identification, management guidance, antidote dosing, and risk stratification; National Poison Control Helpline India: 1800-116-117.

Written notification to the nearest police station by the treating physician when circumstances of a medico-legal case suggest assault, homicide, or unknown circumstances; NOT required for all poisoning cases; required when there is reason to suspect the involvement of another person or when the patient is incapacitated and circumstances are unclear.

An oxime that reactivates acetylcholinesterase inhibited by organophosphates before irreversible ageing occurs; dose 1–2 g IV over 15–30 minutes; must be given within 6–8 hours of OP exposure for most compounds.

Parameters associated with high mortality: dose >1 tablet, early cardiovascular collapse (<4 hours), metabolic acidosis pH < 7.2, serum lactate > 8 mmol/L and rising, QRS widening or VT on ECG, rapidly worsening SpO₂ requirements.

A formal clinical communication to the psychiatry team requesting assessment; must include clinical summary, reason for referral (DSH/substance use/altered mental state), specific questions (is discharge safe? does patient need admission?), and urgency level; must be initiated early in the admission, not at discharge.

A characteristic MRI finding in severe methanol poisoning; bilateral necrosis and haemorrhage in the putamen and other basal ganglia; caused by formate-mediated Complex IV inhibition in these high-metabolic-demand structures; associated with poor neurological prognosis.

Fibrous narrowing of the pyloric channel due to acid corrosive injury of the gastric antrum and pylorus; a delayed complication (weeks to months); causes gastric outlet obstruction with vomiting, early satiety, and weight loss.

Prolongation of QRS duration beyond 100 ms due to tricyclic antidepressant-mediated fast sodium channel (Nav) blockade in ventricular myocardium; QRS > 100 ms predicts arrhythmia risk; QRS > 160 ms predicts ventricular fibrillation.

Prolongation of the corrected QT interval on ECG caused by direct organophosphate effects on cardiac ion channels; predisposes to torsades de pointes; requires continuous ECG monitoring and correction of hypokalaemia throughout the acute phase and intermediate syndrome period.

An ECG marker specific to TCA sodium channel toxicity; the terminal 40 ms QRS vector shifts rightward due to slowed right ventricular conduction, producing a positive R wave in lead aVR greater than 3 mm; indicates significant Na channel blockade.

Haemodynamic instability with low cardiac output and end-organ hypoperfusion not responding to fluid resuscitation and standard vasopressor therapy; occurs in severe AlP poisoning from combined mitochondrial cardiomyopathy and distributive vasodilation.

A graph plotting serum paracetamol concentration against time post-ingestion; values above the treatment line (approximately 150 mg/L at 4 hours) mandate N-acetylcysteine therapy to prevent hepatic necrosis.

CNS depression with near-normal pupils, respiratory depression, hypotension, and absence of secretions or fasciculations; caused by benzodiazepines, barbiturates, and ethanol; treated supportively with flumazenil for benzodiazepines.

RBC AChE and plasma pseudocholinesterase measured as a diagnostic and severity marker in OP/carbamate poisoning; normal RBC AChE 6.9-10.3 U/mL; < 50% confirms poisoning; < 25% indicates severe poisoning.

A bedside diagnostic test for phosphine: a strip of 10% silver nitrate paper placed over the patient's vomitus turns grey-black in the presence of phosphine gas; highly specific but not uniformly available.

Mnemonic for cholinergic muscarinic features: Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis — indicating excess acetylcholine at muscarinic receptors.

Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis — the hallmark muscarinic features of cholinergic toxidrome caused by excess acetylcholine at postganglionic parasympathetic nerve endings.

The primary treatment for TCA-induced QRS widening and arrhythmia; dose 1-2 mEq/kg IV bolus, target serum pH 7.45-7.55; alkalinisation increases ionised (charged) TCA fraction that cannot enter sodium channels; excess Na+ competes for channel binding.

Syndrome from excessive catecholamine stimulation causing tachycardia, hypertension, hyperthermia, diaphoresis, and mydriasis; caused by cocaine and amphetamines; diaphoresis distinguishes it from anticholinergic toxidrome.

A cluster of signs and symptoms reflecting the specific pharmacological mechanism of a class of toxin; the five major toxidromes are cholinergic, anticholinergic, sympathomimetic, opioid, and sedative-hypnotic.

Tramadol is a weak mu-opioid agonist that also inhibits serotonin and noradrenaline reuptake; in overdose it causes opioid toxidrome (respiratory depression, miosis) but additionally causes seizures (distinct from pure opioid overdose); naloxone reverses respiratory depression but may not fully prevent seizures.

Administration of IV sodium bicarbonate to raise urine pH > 7.5, enhancing renal clearance of weak acid drugs (salicylates, phenobarbital) by ion trapping in the tubular lumen.

Endoscopic grading system for corrosive injury: Grade 0 (normal) to Grade 3b (extensive necrosis); Grades 2b and above carry significant risk of stricture and perforation; used to guide management and predict prognosis.

Optimal timing for upper GI endoscopy after corrosive ingestion: 12-48 hours post-ingestion; too early (less than 12 hours) risks perforation through oedematous tissue; too late (after 5 days) also risks perforation as sloughing progresses.

A rodenticide (Zn₃P₂) that releases phosphine on contact with gastric acid; identical mechanism of toxicity to aluminium phosphide but lower potency per gram; somewhat better prognosis than AlP.