Signs, Symptoms and Antidotes of Common Poisons

The bedside toxidrome examination is five lines long and runs in the same order every time. Pupils first (miosis, mydriasis, normal). Skin next (dry, sweaty, flushed, cyanosed). Pulmonary secretions and bowel sounds (wet versus dry). Vital signs (heart rate, blood pressure, respiratory rate, temperature). Mental status last (agitated, depressed, normal). The cluster, not any single finding, identifies the class.

Two pairs trip up new registrars. Anticholinergic and sympathomimetic both give mydriasis and tachycardia, but the anticholinergic patient is bone dry and the sympathomimetic patient is drenched in sweat. Cholinergic and opioid both give miosis and coma, but the cholinergic patient is wet (audible crackles across the chest, drooling, urine on the sheet) and the opioid patient is dry with a respiratory rate of four. Applying those two discriminators consistently gives correct class identification approximately 80 percent of the time, which is sufficient to select the antidote.

The cholinergic pattern is the highest-yield single toxidrome in Indian practice because organophosphate self-poisoning still dominates rural emergency presentations across Maharashtra, Andhra Pradesh, Telangana, Karnataka and West Bengal. The Indian Council of Medical Research Burden of Suicide study and successive NCRB Accidental Deaths and Suicides reports have placed pesticide ingestion among the top three suicide methods nationally for over a decade. The agents have shifted over the years (parathion and methyl parathion gave way to chlorpyrifos and monocrotophos as regulation tightened, and aluminium phosphide carved out its own large share in northern grain belts) but the toxidrome remains the same and the bedside drill remains the same.

The opioid toxidrome has changed shape too. Urban Indian emergency departments now see a steady trickle of tramadol overdose in young adults, often co-ingested with alprazolam, which complicates the classical triad because the benzodiazepine deepens respiratory depression but does not give miosis. Heroin and brown sugar overdose still appears in Mumbai, Delhi, Punjab and the northeast. Transdermal fentanyl misuse, common in Western emergency literature, is rare in Indian government hospitals but has been reported in metro private practice and is rising. Recognising the toxidrome in any of these patterns is the same: pinpoint pupils, depressed breathing, depressed mental status, dry skin.

The cholinergic toxidrome is produced by inhibition of acetylcholinesterase. Acetylcholine accumulates at muscarinic, nicotinic and central receptors. The muscarinic side gives DUMBBELS (Diarrhoea, Urination, Miosis, Bronchospasm and Bronchorrhoea, Bradycardia, Emesis, Lacrimation, Salivation). The nicotinic side gives fasciculations, muscle weakness and tachycardia (which can mask the muscarinic bradycardia). Central effects give seizures, coma and central respiratory failure.

1. Decontaminate and protect the airway
   Remove soaked clothes. Wash skin with soap and water (organophosphates are well absorbed through skin and the treating team can self-poison). Intubate early if secretions are unmanageable or GCS is falling. Pulmonary toilet is non-negotiable.
2. Atropine bolus and double-dose escalation
   Atropine sulphate 1.8 to 3 mg IV bolus (three to five ampoules of 0.6 mg). Reassess at five minutes. If chest is not drying and heart rate is below 80 or systolic BP below 80, double the dose. Repeat doubling every five minutes until atropinised. Indian protocols routinely use 50 to 200 mg of atropine in the first 24 hours; some severe cases need more.
3. Atropine infusion to hold the end point
   Once atropinised, run an infusion at 10 to 20 percent of the total loading dose per hour. Titrate to keep chest dry and heart rate above 80. Premature stopping is the commonest cause of rebound.
4. Pralidoxime within 36 hours
   Pralidoxime chloride (2-PAM) 30 mg/kg IV bolus over 30 minutes, then 8 to 10 mg/kg/hour infusion. Effective only before aging of the enzyme-OP bond, broadly within 24 to 36 hours of exposure. Standard at AIIMS Delhi, JIPMER Puducherry and the major medical college emergency rooms.
5. Treat the complications
   Intermediate syndrome on day two to four (neck flexor weakness, respiratory failure) needs ventilation. Delayed neuropathy weeks later needs physiotherapy. Aspiration pneumonia is the leading cause of death after the acute cholinergic crisis is over.

Carbamate poisoning (propoxur, carbaryl, the household cockroach gels) produces the same toxidrome but the inhibition is spontaneously reversible, so the course is shorter and pralidoxime is not routinely indicated. Amanita muscaria and a handful of other mushrooms produce a pure muscarinic picture treated with atropine alone. The same applies to a class of plants containing pilocarpine-like alkaloids, which Indian rural patients occasionally consume in home remedies; the picture is short, self-limiting and responds to small doses of atropine.

The Indian organophosphate casebook has a few specific patterns worth noting. Chlorpyrifos (sold as Sumithion and a long list of generic formulations) is a slowly hydrolysed thiophosphate that produces a long, drawn-out clinical course with high pralidoxime requirements. Monocrotophos (Nuvacron, Azodrin) is fast acting and high mortality. Methyl parathion (Folidol-M), still in some informal supply chains, is among the most lethal agents per millilitre swallowed. Dichlorvos (Nuvan) is volatile and produces both ingestional and inhalational poisoning, the latter sometimes seen in workers cleaning empty containers without ventilation. Each of these responds to the same atropine plus pralidoxime backbone, but the dose, duration and ICU stay vary widely.

The anticholinergic patient is hot, dry, red, blind and mad: hyperthermic, anhydrotic, flushed, with fixed dilated pupils and an agitated delirium. In India the commonest agent is Datura stramonium (dhatura), ingested deliberately as an intoxicant or accidentally as a roadside criminal sedative used to rob travellers. Tricyclic antidepressant overdose (amitriptyline, imipramine) and first-generation antihistamines (chlorpheniramine, diphenhydramine) follow.

Treatment of anticholinergic poisoning is mostly supportive: benzodiazepines for agitation, active cooling for hyperthermia, urinary catheterisation, and cardiac monitoring (tricyclics widen the QRS and can produce ventricular arrhythmias treated with sodium bicarbonate). Physostigmine, the specific antidote, is rarely available in Indian hospitals and is reserved for severe central toxicity without QRS widening; the seizure and asystole risk has kept it off most state formularies.

The opioid toxidrome is among the most reliably reversible presentations in emergency toxicology. The triad of pinpoint pupils, respiratory depression and depressed mental status is pathognomonic. Naloxone (sold in India as Nalox, Naltima and as generic ampoules of 0.4 mg/ml) reverses the picture within 60 to 90 seconds.

Sympathomimetic toxidrome (amphetamine, methamphetamine, MDMA, cocaine, synthetic cathinones) shares mydriasis and tachycardia with the anticholinergic pattern but the patient is diaphoretic and has active bowel sounds. Treatment is benzodiazepines in escalating doses for agitation, hypertension and tachycardia; active cooling for hyperthermia (mortality climbs steeply above 40 degrees Celsius); and avoidance of beta-blockers as a single agent because unopposed alpha stimulation can worsen coronary spasm in cocaine toxicity.

Sedative-hypnotic toxidrome is the most familiar urban presentation: alprazolam, diazepam, clonazepam, alone or with alcohol. Supportive care covers most cases. Flumazenil (the specific benzodiazepine antagonist, 0.2 mg IV every minute up to 1 mg) reverses pure benzodiazepine overdose but is rarely used in Indian practice. The reason is straightforward: most Indian benzodiazepine overdoses are mixed (typically with tricyclics, sedating antipsychotics or ethanol) and flumazenil can unmask seizures or arrhythmias from the co-ingestant. The risk-benefit calculation has pushed Indian protocols toward airway support and observation rather than reversal.

Ethanol deserves a separate paragraph because it sits inside the sedative-hypnotic toxidrome but with extra dimensions. The hypoglycaemia that accompanies acute alcohol intoxication, particularly in malnourished or chronic users, has to be ruled out at the door with a point-of-care glucose. Wernicke encephalopathy in a chronic user can be precipitated by a glucose bolus given before thiamine; the Indian default is to give 100 mg IV or IM thiamine before any glucose load in a comatose patient with a history of alcohol use. Methanol contamination of country liquor is the other concern. Any cluster of patients arriving from the same village or the same hooch source with sedation, blurred vision, metabolic acidosis or breathlessness is treated as methanol until proven otherwise, and the working antidote is intravenous ethanol with haemodialysis as covered in Section 4.

Beyond the five toxidromes, several poisons have specific antidotes that change outcome decisively. The shelf reality in India splits these into three tiers: routinely stocked across district hospitals, stocked at tertiary centres only, and effectively unavailable outside a handful of metros.

The National Poisons Control Centre at AIIMS Delhi publishes the recommended antidote list for state and district pharmacies. The WHO essential medicines list defines a minimum stocking floor (atropine, naloxone, NAC, methylene blue, ASV, calcium gluconate for hydrofluoric acid). Implementation varies by state. Punjab and Kerala stock close to the recommended list at district hospitals; several northeastern states and parts of Bihar and Madhya Pradesh fall short, particularly on pralidoxime continuity.

The reasons for these gaps are operational rather than scientific. Pralidoxime ampoules have a short shelf life relative to atropine and need cold storage. Polyvalent ASV needs strict cold chain. Hydroxocobalamin in the Cyanokit format is expensive and is ordered only against forecasted demand, which is low in most district hospitals. Digoxin-Fab fragments are imported and priced beyond the reach of most public formularies. The result is a patchy national antidote map where the toxidrome can be recognised correctly and the antidote still be unavailable. The NPCC at AIIMS Delhi, and to a lesser extent the NPIC at Madras Medical College, do informal redistribution and referral coordination across this map; the helpline numbers are worth keeping in every emergency department contacts file.

The first sixty minutes after a poisoned patient arrives at an Indian district emergency room follows a stable sequence. The team has limited investigation back-up (often no immediate toxicology screen, no ABG machine outside the ICU, point-of-care glucose and not much else), so the toxidrome and the history carry most of the diagnostic weight.

1. Airway, breathing, circulation
   Intubate if GCS is below 8 or airway reflexes are gone. Oxygen for everyone. IV access, fluid bolus if hypotensive. Cardiac monitor. Point-of-care glucose (thiamine before glucose in alcohol-suspected coma). Naloxone trial if opioid is plausible.
2. Quick toxidrome examination
   Pupils, skin, secretions, bowel sounds, vitals, mental status. Five lines, one minute. Match to the toxidrome table.
3. Decontamination, narrowed indications
   Activated charcoal 1 g/kg orally or via NG tube within one hour of ingestion, useful only if the agent binds charcoal (not iron, lithium, alcohols, heavy metals, hydrocarbons). Gastric lavage is no longer routine; it is reserved for life-threatening ingestion within an hour, with a protected airway. Skin decontamination for organophosphates and corrosives.
4. Specific antidote if indicated
   Atropine and pralidoxime for cholinergic. Naloxone for opioid. NAC for paracetamol within eight hours of ingestion. Methylene blue for cyanosis with normal PaO2. ASV for snakebite with 20-minute WBCT positive or local progression.
5. Sample collection for toxicology
   Gastric aspirate before charcoal, urine 100 ml, blood (plain tube 10 ml for chemistry, EDTA 5 ml for metals), preserved with sodium fluoride if alcohol is suspected. Chain of custody under BNSS 2023 Section 105 and BSA Section 63.
6. Disposition
   Most pesticide and AlP ingestions need ICU. Most opioid overdoses need 6 to 12 hours of observation after the last naloxone dose. Most benzodiazepine overdoses need an observation bed. The threshold to call the NPCC AIIMS Delhi helpline on 011-26593677 should be low for any unusual agent or any case with an inconsistent toxidrome.

The 20-minute whole blood clotting time (WBCT) deserves a separate mention. A clean glass test tube, 2 ml of venous blood, left undisturbed for 20 minutes and then tilted. If it has not clotted, the patient has consumption coagulopathy from a viper bite and ASV is indicated even without obvious local signs. The test costs nothing, needs no laboratory, and is the workhorse triage tool in rural Indian snakebite care.

The literature on Indian poisoning outcomes consistently identifies a handful of avoidable errors. Understanding these failure modes directly improves outcomes.

Under-atropinisation is the commonest. Doctors stop atropine because the pupils have dilated or the heart rate is 110. Both are wrong end points. The patient must have a dry chest and clear lungs. A heart rate of 110 in an organophosphate case is the goal, not a problem. Audit data from medical college emergency departments in Maharashtra and Karnataka have repeatedly shown that adequate atropinisation reduces mortality from around 25 percent to under 10 percent in moderate-severity organophosphate poisoning.

Late pralidoxime is the second. The 36-hour window is shorter than most people remember. Once the enzyme-OP bond ages, no oxime will reactivate it and the patient is committed to a long course of intermediate syndrome and neuropathy.

Inappropriate gastric lavage is the third. Lavage after one hour, lavage without a protected airway in a drowsy patient, lavage with cold water in a patient with corrosive ingestion. The procedure is no longer routine; the indications have narrowed. Aspiration pneumonia from a botched lavage often kills more patients than the original poison.

Empirical flumazenil in mixed overdose is the fourth. Flumazenil in a patient who has co-ingested a tricyclic can precipitate ventricular tachycardia. Flumazenil in a chronic benzodiazepine user can precipitate seizures. The Indian default is to support the airway and skip the antagonist.

Failure to repeat ASV is the fifth. After the initial 10 vials, the WBCT should be rechecked at six hours. If it is still positive, give another 10 vials. Several rural Indian deaths from Russell's viper envenomation have been traced back to a single round of ASV followed by no clinical reassessment.

A sixth error, less often discussed but routine in audits, is reliance on the prescription found on the patient. A bottle of organophosphate next to an unconscious patient does not rule out a paracetamol co-ingestion, an alcohol level that needs separate treatment, or a separate undisclosed antidepressant ingestion. The clinical pattern, the toxidrome and the timeline matter at least as much as the bottle. Patients and families sometimes hand over the wrong bottle, and substance availability at the scene reflects what was easily reachable rather than what was actually swallowed. Treat the patient, not the bottle, and keep the toxicology screen in mind for the cases that do not fit.

A short note on paediatric poisoning closes this section. Children present with a narrower set of agents (paraffin and kerosene ingestion, household cleaners, iron tablets, accidental adult medication exposure, agricultural products in farming households) and a wider therapeutic margin of error. Indian paediatric protocols (Indian Academy of Paediatrics) keep iron poisoning, hydrocarbon aspiration and accidental alprazolam ingestion at the top of the differential. The toxidrome examination is the same; the doses scale by weight; the threshold to admit and observe is lower.