Toxidrome Identifier
Toxidrome Identifier
Map pupils, skin, bowel sounds, temperature, mental state, heart rate and the neuromuscular findings onto the classic toxidromes — built around the one discriminator that does the most work at the bedside, which is whether the skin is dry or wet.
Toxidrome pattern
Six signs → toxidromeDilated pupils, dry skin, absent bowel sounds, agitated and delirious, respiration normal, no clonus or hyperreflexia, temperature 38.4 °C, heart rate 124
How the pattern is resolved, and in what order
Miosis + respiratory depression → opioid
Clonus or hyperreflexia + wet skin → serotonergic
Mydriasis + dry skin → anticholinergic
Mydriasis + wet skin → sympathomimetic
CNS depression + nothing else abnormal → sedative-hypnotic
- dry against wet
- the one discriminator this page is built around. The last two lines above differ by a single selector value and by nothing else, and no rule below them can override either — so the page cannot name anticholinergic or sympathomimetic without the reader having committed to the skin. StatPearls: “The absence of sweating indicates anticholinergic toxicity”
- why cholinergic is tested first
- cholinergic and opioid poisoning both give miosis and both compromise breathing, so an order that tested opioid first would call a patient drowning in secretions an opioid overdose. Diaphoresis and diarrhoea are what separate them, and they are tested before respiratory depression is
- clonus
- the serotonergic and sympathomimetic pictures overlap almost entirely — mydriasis, diaphoresis, agitation, tachycardia, hyperthermia. Neuromuscular hyperreactivity is the difference, which is why it is a separate input and why it is tested before the mydriasis pair
- bowel sounds
- decreased in anticholinergic and opioid poisoning, increased in cholinergic and serotonergic. Useful confirmation, and load-bearing only in the cholinergic and anticholinergic rules, because it is the least reproducible finding of the set
- what has no toxidrome
- carbon monoxide, cyanide and methaemoglobinaemia produce cellular hypoxia rather than an autonomic pattern, and the CDC’s chart files them separately for that reason. They are not resolvable from pupils, skin and bowel sounds — see the carbon monoxide poisoning interpreter and the methaemoglobin interpreter
Worked example
Dilated pupils, dry skin, absent bowel sounds, agitated and delirious, respiration normal, no clonus or hyperreflexia, temperature 38.4 °C, heart rate 124
Pupils dilated, so the two miosis rules — cholinergic and opioid — are not reached
No clonus or hyperreflexia, so the serotonergic rule is not reached
Mydriasis with dry skin → anticholinergic toxidrome
Everything else agrees: absent bowel sounds, hyperthermia at 38.4, tachycardia at 124, and delirium. Red as a beet, dry as a bone, blind as a bat, mad as a hatter, hot as a hare, full as a flask
Now change one selector. Set the skin to diaphoretic and leave all seven other inputs exactly as they are — same dilated pupils, same delirium, same 38.4 °C, same heart rate of 124 — and the answer becomes sympathomimetic toxidrome
That is the whole argument for why this page is built the way it is. Hyperthermia, tachycardia, mydriasis and agitated delirium are common to both and discriminate nothing. The skin is what tells them apart, and the rules are arranged so that no other finding can override it
The clinical stakes of that one selector: the sympathomimetic patient wants benzodiazepines, fluid and cooling; the anticholinergic patient wants the same plus an ECG for QRS and QT prolongation and a bladder scan, and is the one in whom physostigmine might be considered by a specialist — and in whom it is contraindicated if a tricyclic is in the mix
And if clonus were present with wet skin instead, the answer would be serotonergic, which has its own validated rule rather than a toxidrome
The six toxidromes, feature by feature
| Pupils | Skin | Bowel sounds | Temperature | Mental state | Heart rate | |
|---|---|---|---|---|---|---|
| Anticholinergic | Mydriasis | Dry, flushed; dry mucous membranes | Decreased | Raised | Delirium, hallucination, picking, staccato speech | Tachycardia |
| Sympathomimetic | Mydriasis | Diaphoretic | Normal or increased | Raised | Anxiety, agitation, seizures | Tachycardia |
| Serotonergic | Mydriasis | Diaphoretic | Increased, diarrhoea | Raised | Agitation | Tachycardia — with clonus and hyperreflexia |
| Cholinergic | Miosis | Diaphoretic, lacrimation, salivation | Increased, diarrhoea | Normal | Altered, seizures | Bradycardia or tachycardia |
| Opioid | Miosis | Normal | Decreased | Normal or low | Lethargy then coma | Bradycardia |
| Sedative-hypnotic | Normal | Normal | Normal | Normal or low | Drowsy but arousable, then coma | Normal |
What each toxidrome is caused by, and what to do first
| Toxidrome | Typical agents | First moves |
|---|---|---|
| Anticholinergic | Diphenhydramine and other antihistamines, tricyclics, atropine, hyoscine, Datura and Brugmansia, belladonna alkaloids, quetiapine, benzatropine | Benzodiazepines, cooling, bladder scan, and an ECG for QRS and QT prolongation. Physothigmine is specialist-only and contraindicated where a tricyclic or sodium-channel blocker may be co-ingested |
| Sympathomimetic | Cocaine, amphetamines, MDMA, methamphetamine, ephedrine and pseudoephedrine, khat, synthetic cathinones | Generous benzodiazepines — they treat the agitation, tachycardia, hypertension and hyperthermia through one mechanism. Active cooling, fluids, creatine kinase, potassium, sodium, and an ECG. Avoid an unopposed beta blocker where cocaine is possible |
| Serotonergic | SSRIs and SNRIs with a second serotonergic drug — tramadol, pethidine, linezolid, methylene blue, an MAO inhibitor, lithium, triptans | Stop all serotonergic agents, benzodiazepines, active cooling. Apply the Hunter criteria rather than stopping at the toxidrome |
| Cholinergic | Organophosphate and carbamate insecticides, nerve agents, physostigmine, nicotine, some mushrooms | Atropine titrated against secretions, not heart rate, in large cumulative doses; pralidoxime for organophosphates. Decontaminate in personal protective equipment — staff get contaminated |
| Opioid | Heroin, morphine, oxycodone, fentanyl and analogues, methadone, codeine, tramadol, buprenorphine | Support ventilation; naloxone titrated to respiratory rate, not to consciousness. Extended observation for long-acting agents, and watch for non-cardiogenic pulmonary oedema |
| Sedative-hypnotic | Benzodiazepines, Z-drugs, barbiturates, gamma-hydroxybutyrate, alcohol | Airway, breathing, circulation. Flumazenil is controversial and risks withdrawal seizures. Look hard for a co-ingestion — paracetamol, salicylate, glucose, ECG |
Why a toxidrome is a starting point and not a diagnosis
| Limitation | Why | What to do about it |
|---|---|---|
| Mixed ingestions do not produce clean toxidromes | Most deliberate self-poisoning involves more than one agent, and the features do not average — an anticholinergic with a stimulant, or an opioid with a benzodiazepine, gives a picture matching no single column | Accept the “no single toxidrome fits” answer when it comes, treat the physiology, and get a paracetamol and salicylate concentration regardless of the story |
| A toxidrome does not replace a concentration | Where a level exists and changes management — paracetamol, salicylate, iron, lithium, digoxin, carboxyhaemoglobin, methaemoglobin — the level is the better test and the toxidrome is only the trigger for taking it | Send the assay. The toxidrome guides supportive care in the meantime; it does not substitute for a number that has a treatment threshold attached |
| They evolve | A toxidrome is a snapshot. Anticholinergic delirium can appear hours after the tachycardia; opioid poisoning can recur as naloxone wears off; serotonin toxicity escalates over hours | Re-examine rather than documenting once. The finding that was absent an hour ago is the one that completes the pattern |
| Non-toxicological illness imitates them | Hypoglycaemia, sepsis, head injury, intracranial haemorrhage, hypoxia, hypercapnia, a postictal state, thyroid storm and meningitis each reproduce parts of several toxidromes | Glucose, blood gas with co-oximetry, ECG and temperature in everybody. A toxidrome that fits is not evidence that the diagnosis is poisoning |
| Some poisons have no toxidrome | Carbon monoxide, cyanide, methaemoglobin-forming agents, toxic alcohols, salicylate and paracetamol produce metabolic or cellular effects rather than an autonomic pattern | These are diagnosed by the metabolic picture and by assay. See the osmolal gap calculator, the salicylate severity interpreter and the carbon monoxide interpreter |
Dry skin or wet skin: the one finding that carries the most weight
A toxidrome is a constellation of physical signs that points at a mechanism of poisoning rather than at a drug. It is worth having because it can be assembled in under a minute from an examination, with no history and no laboratory, in a patient who cannot say what they took — which is the situation in which poisoning is most dangerous. Six features do nearly all of the work: the pupils, the skin, the bowel sounds, the temperature, the mental state and the heart rate, with the respiratory pattern and the neuromuscular findings added for the two pairs that the first six cannot separate.
The single most useful of those is the skin, and it is worth being explicit about why. The anticholinergic and sympathomimetic toxidromes are the two most easily confused, and they overlap almost completely: both give dilated pupils, both give hyperthermia, both give tachycardia and hypertension, both give agitation or frank delirium, and both can end in seizures. Pupils, temperature, heart rate and mental state — four of the six features — discriminate nothing between them. What discriminates is sweating. Anticholinergic poisoning blocks muscarinic receptors at the sweat glands, so the skin is dry and hot and flushed; sympathomimetic poisoning drives them, so the skin is wet. The CDC’s own toxidrome chart lists dry skin under anticholinergic and diaphoresis under sympathomimetic, and StatPearls states it as a rule: the absence of sweating indicates anticholinergic toxicity. This page’s rules are arranged so that this is structural rather than advisory — the two verdicts are produced by conditions that differ in exactly one selector, nothing below them can override the result, and the page therefore cannot name either toxidrome without the reader having committed to dry or wet skin.
The same logic applies twice more. Cholinergic and opioid poisoning both produce constricted pupils and both compromise breathing, so the cholinergic pattern is tested first, on its diaphoresis and its active bowels: a patient drowning in secretions from an organophosphate must not be labelled an opioid overdose because the pupils were small. And the serotonergic pattern is almost indistinguishable from the sympathomimetic one — mydriasis, diaphoresis, agitation, tachycardia, hyperthermia in both — except in the neuromuscular findings, so clonus and hyperreflexia are a separate input tested before the pair. Where they are present the right next step is not this page at all but the Hunter criteria, which are a validated decision rule rather than a pattern.
What has to be said just as plainly is how often this does not work. Most deliberate self-poisoning involves more than one agent, and the features of two toxidromes do not average into something recognisable — they produce a picture that matches no column in any table. Partial treatment does the same, and so does the passage of time, because toxidromes evolve: anticholinergic delirium can appear hours after the tachycardia, and opioid poisoning recurs as naloxone wears off. Non-toxicological illness imitates them freely, which is why a glucose, a blood gas with co-oximetry, an ECG and a temperature belong in every such patient before the toxidrome is trusted. And a substantial part of clinical toxicology has no toxidrome at all: carbon monoxide, cyanide and methaemoglobinaemia cause cellular hypoxia rather than an autonomic pattern, and salicylate, paracetamol and the toxic alcohols declare themselves in the metabolic picture. So this record has an honest “no single toxidrome fits” outcome, and it is not a failure state — it is the correct answer in a mixed overdose.
Finally, the relationship between a toxidrome and a laboratory result. A toxidrome guides supportive care: it tells you to give benzodiazepines and cool the patient, or to support ventilation and titrate naloxone, or to give atropine against secretions, and it tells you that now rather than in two hours. It does not replace a concentration where one exists and changes management — paracetamol, salicylate, iron, lithium, digoxin, carboxyhaemoglobin, methaemoglobin — and in those poisonings the toxidrome’s job is to prompt the assay rather than to stand in for it. Poisoning management is time-critical and belongs with a poisons centre or clinical toxicology service; everything here exists to make that call better informed and earlier.
Frequently asked questions
How do you tell anticholinergic from sympathomimetic toxicity?
By the skin. Both cause dilated pupils, hyperthermia, tachycardia, hypertension, agitation or delirium and seizures, so four of the six classic toxidrome features discriminate nothing between them. Anticholinergic poisoning blocks muscarinic receptors at the sweat glands, so the skin is dry, hot and flushed with dry mucous membranes; sympathomimetic poisoning drives them, so the skin is wet. StatPearls puts it as a rule — the absence of sweating indicates anticholinergic toxicity — and the CDC’s toxidrome chart lists dry skin under one and diaphoresis under the other. Bowel sounds support the distinction, decreased in anticholinergic and preserved or increased in sympathomimetic, but the skin is the reproducible finding.
Why does a toxidrome matter if we can just measure drug levels?
Because for most poisons there is no level, and where there is one it usually arrives too late to guide the first hour. A toxidrome is assembled from an examination in under a minute, with no history, in a patient who cannot tell you what they took — and it tells you which supportive treatment to start now. Where a concentration exists and has a treatment threshold attached, though, the concentration is the better test: paracetamol, salicylate, iron, lithium, digoxin, carboxyhaemoglobin and methaemoglobin all fall into that group, and there the toxidrome’s job is to prompt the assay rather than to substitute for it.
What if the findings do not fit any toxidrome?
That is a common and legitimate result. Most deliberate self-poisoning involves more than one agent, and the features of two toxidromes do not blend into a recognisable third — an anticholinergic with a stimulant, or an opioid with a benzodiazepine, produces a picture that matches nothing. Partial treatment, a long transport and the simple passage of time do the same, because toxidromes evolve. And non-toxicological illness imitates them: hypoglycaemia, sepsis, head injury, intracranial haemorrhage, hypoxia, hypercapnia, a postictal state, thyroid storm and meningitis each reproduce parts of several. Check a glucose, a blood gas with co-oximetry, an ECG, a temperature, and a paracetamol and salicylate concentration, treat the physiology in front of you, and call a poisons centre.
Do normal pupils exclude opioid poisoning?
No, and this page has a dedicated outcome for exactly that situation. StatPearls states it directly: normal pupil examination findings do not exclude opioid toxicity. Pupils can be normal or even dilated with pethidine and tramadol, in mixed overdose with an anticholinergic or a stimulant, and — importantly — where hypoxia or hypercapnia has supervened, since hypoxia itself dilates pupils. So the sickest opioid-poisoned patients can be the ones whose pupils look wrong. Central nervous system and respiratory depression with normal pupils should be treated as possible opioid toxicity, with ventilatory support and a naloxone trial titrated to respiratory rate, while the rest of the differential is worked through.
Which poisons have no toxidrome?
The ones that act metabolically or at the cellular level rather than on the autonomic nervous system. Carbon monoxide, cyanide and the methaemoglobin-forming agents cause cellular hypoxia — the CDC’s chart files them under that heading rather than as toxidromes, because they are not resolvable from pupils, skin and bowel sounds. Salicylate, paracetamol, iron and the toxic alcohols are the same: they declare themselves in the acid-base picture, the osmolal gap, the liver function or an assay, not in an examination. Carbon monoxide is the most important of these to remember, because pulse oximetry reads falsely normal in it and only a co-oximeter or blood gas will find it.
What separates the serotonergic toxidrome from the sympathomimetic one?
The neuromuscular findings, and essentially nothing else. Both produce mydriasis, diaphoresis, agitation, tachycardia and hyperthermia. Serotonin toxicity adds clonus — inducible, spontaneous or ocular — and hyperreflexia, which is why this page takes them as a separate input and tests them before the mydriasis pair. Increased bowel sounds and diarrhoea also favour the serotonergic pattern. Where clonus or hyperreflexia is present the right next step is the Hunter Serotonin Toxicity Criteria, which are a validated branching decision rule with 84% sensitivity and 97% specificity, rather than a pattern match.
Related calculators
References
- Centers for Disease Control and Prevention, National Center for Environmental Health. Toxidromes chart (Toxidromes_Chart-508). Anticholinergic: cutaneous flushing, hyperthermia, dry skin, mydriasis, dry mucous membranes, disorientation, hallucination, seizures, tachycardia, hypertension, urinary retention. Sympathomimetic: tachycardia, hypertension, hyperthermia, diaphoresis, mydriasis, hyperreflexia, anxiety, seizures. Cholinergic crisis: salivation, diarrhoea, lacrimation, bronchorrhoea, diaphoresis, urination, with miosis, fasciculations, weakness, bradycardia or tachycardia, hypotension or hypertension, altered mental status, seizures. Opioid: lethargy, miosis, respiratory depression, progressing to coma, pulmonary oedema, hypotension, bradycardia. Carbon monoxide and cyanide are filed under cellular hypoxia rather than as toxidromes.
- Anticholinergic Toxicity. StatPearls. NCBI Bookshelf. “The absence of sweating indicates anticholinergic toxicity” — the discriminator from sympathomimetic toxicity; decreased bowel sounds; the mnemonic “red as a beet, dry as a bone, blind as a bat, mad as a hatter, hot as a hare, full as a flask”; diphenhydramine associated with wide-complex dysrhythmias and QT prolongation.
- Anxiolytics and Sedative-Hypnotics Toxicity. StatPearls. NCBI Bookshelf. “The most common presentation of BZD toxicity is CNS depression with otherwise normal hemodynamics and examination findings”; opioid toxicity distinguished by depressed respiratory rate, decreased tidal volumes, decreased bowel sounds and gastrointestinal motility, and miotic pupils; “Normal pupil examination findings do not exclude opioid toxicity”; flumazenil controversial because of the risk of withdrawal seizures in chronic benzodiazepine use or coingestion of proconvulsant agents.
- Sympathomimetic Toxicity. StatPearls. NCBI Bookshelf. Tachycardia, hypertension, hyperthermia, diaphoresis and mydriasis, with benzodiazepines as first-line management of the agitation, hypertension and hyperthermia together.
- Dunkley EJC, Isbister GK, Sibbritt D, Dawson AH, Whyte IM. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM. 2003;96(9):635–642. The validated rule that replaces a pattern match once clonus or hyperreflexia is present; sensitivity 84%, specificity 97%.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.