Wet versus dry. Big pupils versus tiny. Name the pattern first, then pick the antidote that matches the mechanism.
A 58-year-old gardener is brought in confused after spraying crops. He is drenching wet with saliva and tears, his pupils are pinpoint, and you hear wheezing bilaterally. Heart rate is 46/min. His shirt smells like pesticide.
What toxidrome is this?
Anticholinergic
Cholinergic
Opioid
Sympathomimetic
Recognition
Five Toxidromes You Cannot Miss
Tap each card. Front = the one line pattern. Back = mechanism and board move.
Cholinergic
Wet & tight
tap
Board pattern
SLUDGE: salivation, lacrimation, urination, diarrhea, GI upset, emesis. Plus miosis, bronchospasm, bradycardia. Cause: organophosphates, nerve agents, carbamates.
Anticholinergic
Dry & mad
tap
Board pattern
Hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter, full as a flask. Mydriasis, urinary retention, ileus. Antidote: physostigmine if severe.
Opioid
Pinpoint & still
tap
Board pattern
Triad: miosis, respiratory depression, decreased mental status. Skin often cool. Antidote: naloxone after airway support.
CNS depression with normal or small pupils. Benzodiazepines, barbiturates, alcohol. Flumazenil only for isolated benzo overdose without mixed ingestion.
Chicago chain: wet versus dry decides the antidote class
Cholinergic: too much acetylcholine at muscarinic receptors → everything that should squeeze or secrete is overactive → atropine blocks the receptor, pralidoxime fixes the enzyme.
Anticholinergic: muscarinic receptors are blocked → patient is hot, dry, red, blind, mad, full → physostigmine raises acetylcholine if CNS toxicity is severe.
Opioid: mu receptor activation in the brainstem → breathing slows before everything else → ventilate, then naloxone.
Sympathomimetic: catecholamine surge → big pupils, fast heart, hot agitation → benzodiazepines first.
Sedative: global CNS depression → flumazenil only when benzo overdose is isolated and airway is safe.
⚠
Miosis lives in two toxidromes. Wetness tells them apart.
Opioids and cholinergic poisoning both shrink pupils. Opioids make the patient dry and still. Cholinergic patients are wet and wheezy. If you only memorize pinpoint pupils, you will pick naloxone for an organophosphate.
Path to treatment
Diagnose the Pattern, Then the Poison
Vitals and exam beat history when the bottles are missing.
1
Unresponsive overdose, no story. First move?
ABCs and dextrose, every time. Airway, breathing, circulation, glucose. Intubate before charcoal. Naloxone can go intranasally while you bag. Stabilize the patient before you try to name the poison.
2
Stable now. The bottles are missing. What names the toxidrome?
The exam beats the history. Pupils, skin moisture, bowel sounds, mental status, temperature, reflexes. Clonus points to serotonin syndrome. Lead-pipe rigidity after antipsychotics points to NMS.
3
Pattern in hand. Which test catches the silent killer after a pill ingestion?
Targeted labs, not a shotgun. Acetaminophen level, salicylate, osmolar gap, anion gap, COHb on co-oximetry, and an ECG for QRS and QT. Wide QRS after pills screams TCA until proven otherwise.
4
ECG shows a wide QRS after an overdose. Best antidote?
Match the mechanism, do not grab a reversal agent just because it exists. Naloxone for opioid, sodium bicarbonate for TCA wide QRS, NAC for acetaminophen, deferoxamine for iron.
Stabilize, pattern, targeted labs, mechanism-matched antidote. That is the order every time.
High yield poison antidotes
Acetaminophen
N-acetylcysteine
Iron
Deferoxamine
Digoxin
Fab fragments
Heparin
Protamine sulfate
Warfarin
Vitamin K / PCC
Methanol / ethylene glycol
Fomepizole
Cyanide
Hydroxocobalamin
Methemoglobin
Methylene blue
Lead
Succimer / EDTA
TCA wide QRS
Sodium bicarbonate
⚠
Never give physostigmine for TCA overdose
TCAs block fast sodium channels and have anticholinergic effects, but physostigmine can cause asystole. If QRS is wide, the move is sodium bicarbonate, not more cholinergic tone.
Mechanism drill
Build the Antidote Chain
Tap the correct sequence for organophosphate poisoning: stabilize breathing, block muscarinic receptors, then reactivate enzyme.
Organophosphate protocol
Put the steps in order. Wrong order costs lives in clinical practice and in the ED.
1
empty
2
empty
3
empty
Pattern to antidote
Toxidrome Identifier
Read the clue set. Tap the antidote. Each pattern has exactly one mechanism-matched answer.
Salivation, lacrimation, urination, diarrhea, emesis, and bronchorrhea. Pupils are pinpoint. Heart rate 42. Pesticide exposure. What is the antidote pair?
Cholinergic toxidrome. Organophosphates flood every muscarinic receptor with acetylcholine. Atropine blocks the receptor and dries the lungs. Pralidoxime reactivates acetylcholinesterase before the bond ages irreversibly. Wet + miosis + bradycardia = SLUDGE. Antidote: atropine first, then 2-PAM.
Not naloxone. Opioids also cause miosis, but opioid patients are dry. This patient is drenched in secretions. Wet miosis = cholinergic crisis. Dry miosis = opioid. Naloxone does nothing here. Correct antidote: atropine + pralidoxime.
Dry flushed skin, temperature 39.8, mydriasis, urinary retention, confusion, and ileus. No diaphoresis. No clonus. CNS toxicity is severe. Which antidote applies?
Anticholinergic toxidrome. Hot, dry, red, blind, mad, full = muscarinic blockade everywhere. Physostigmine crosses the blood-brain barrier and raises acetylcholine by inhibiting acetylcholinesterase, competing at blocked receptors. Use only when CNS toxicity is severe and QRS is narrow. Never with TCA co-ingestion.
Atropine would worsen this. Atropine is itself an anticholinergic. Giving it to an anticholinergic poisoning pours gasoline on the fire. The correct antidote for severe anticholinergic toxicity is physostigmine, the pro-cholinergic agent that rebuilds the deficient acetylcholine tone.
Respiratory rate 5. Pinpoint pupils. Cool dry skin. Decreased mental status. Pill bottles at bedside. No bronchorrhea. What is the antidote?
Opioid toxidrome. Mu receptor activation in the brainstem suppresses respiratory drive. Naloxone is a competitive mu antagonist that reverses this within minutes. Ventilate first if needed, then naloxone. Triad: miosis + respiratory depression + depressed mental status. Skin is dry and cool, not wet. That is the key split from cholinergic.
Wrong toxidrome. Atropine and pralidoxime treat organophosphate-induced cholinergic crisis, which is wet: bronchorrhea, salivation, lacrimation, diarrhea. This patient is dry. Dry miosis with bradypnea = opioid. The antidote is naloxone.
Mydriasis, heart rate 148, BP 192/112, temperature 38.9, agitation, and diaphoresis. Found at a party. No pill bottles. No clonus. Best initial treatment?
Sympathomimetic toxidrome. Cocaine, amphetamines, and bath salts flood catecholamine receptors. Everything fires: big pupils, fast heart, high pressure, hot, agitated, diaphoretic. Benzodiazepines dampen the catecholamine storm and lower BP without exposing the heart to unopposed alpha. Never use beta-blockers alone in cocaine toxicity.
Naloxone is for opioids. Opioids cause miosis, bradypnea, and CNS depression, not tachycardia with hypertension and agitation. This patient has a catecholamine surge, the opposite of opioid toxicity. Correct treatment: benzodiazepines to dampen the storm.
CNS depression, normal pupils, no bronchorrhea, no clonus. Known benzodiazepine prescription, no history of TCA use, no chronic daily benzo use. You want to reverse the sedation.
Benzodiazepine toxidrome. Flumazenil competitively blocks the benzodiazepine site on GABA-A receptors and reverses sedation within 1 to 2 minutes. Critical caveat: avoid if chronic benzo use (precipitates withdrawal seizures) or if TCA co-ingestion is possible (removes the only seizure brake). This case is isolated benzo overdose, so flumazenil is appropriate.
Physostigmine treats anticholinergic toxicity. It raises acetylcholine to compete at blocked muscarinic receptors. This patient has sedative CNS depression, not a dry-hot-red-mad-full anticholinergic pattern. The antidote for isolated benzo overdose is flumazenil.
8 grams of acetaminophen ingested 6 hours ago. Nausea only so far. Liver function tests rising. Serum level plots above the Rumack-Matthew treatment line.
Acetaminophen toxicity. NAPQI, the toxic metabolite, depletes glutathione and alkylates hepatocytes. N-acetylcysteine replenishes glutathione and allows safe conjugation of NAPQI before necrosis sets in. Most effective within 8 hours but given even late in overdose. The nomogram tells you who needs treatment based on timed serum level.
Sodium bicarbonate is the TCA antidote. It restores sodium channel conductance in tricyclic poisoning. Acetaminophen toxicity does not involve sodium channels. The hepatotoxic mechanism is glutathione depletion by NAPQI, which requires N-acetylcysteine to reverse.
QRS 144 ms after an ingestion. Terminal R wave in aVR. Hypotension. Altered mental status. No clonus. Patient takes amitriptyline at home.
TCA overdose. Tricyclics block fast sodium channels in the myocardium, widening QRS and destabilizing the membrane. Sodium bicarbonate overloads the channel with extracellular sodium and alkalinizes tissue, stabilizing conduction. Wide QRS after TCA = sodium bicarbonate. Do not give physostigmine here, it causes asystole in this setting.
Flumazenil is contraindicated here. TCAs lower the seizure threshold. Flumazenil removes benzodiazepine GABA inhibition and can precipitate a seizure in a patient who is already at high risk from TCA toxicity. This is one of the most important TCA board traps. Correct antidote: sodium bicarbonate for the wide QRS.
Prove It
Board Walkthrough
9 vignette bank, 5 dealt per round, answer choices shuffled, never-repeat within a round.
Medically reviewed by Kaitlyn Cocuzzo, MD and Fatima Ali, DO · Last reviewed June 2026
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