14.2 Toxicology, Anaphylaxis & Temperature Emergencies

The General Approach to the Poisoned Patient

Toxicology emergencies are managed with a disciplined sequence: stabilize, decontaminate, give a specific antidote if one exists, and enhance elimination — always starting with airway, breathing, and circulation. Most poisoned patients die from a preventable ABC problem (airway loss, hypoventilation, arrhythmia, or hypotension), not from the lack of an exotic antidote, so supportive care is the foundation.

Recognize the toxidrome. A cluster of vital signs and exam findings often reveals the class of agent: the cholinergic toxidrome (salivation, lacrimation, urination, defecation, bronchorrhea, bradycardia — organophosphates), the anticholinergic toxidrome ('hot as a hare, dry as a bone, red as a beet, mad as a hatter'), the sympathomimetic toxidrome (tachycardia, hypertension, hyperthermia, diaphoresis — cocaine/amphetamines), and the opioid toxidrome (miosis, respiratory depression, coma). Recognizing the pattern narrows the antidote choice quickly.

Decontamination and Elimination

Activated charcoal (typically 1 g/kg) adsorbs many toxins if given within about 1-2 hours of ingestion, but is withheld when the airway is unprotected (risk of aspiration) or for agents it does not bind — lithium, iron, alcohols, potassium, and hydrocarbons. Enhanced elimination includes urinary alkalinization (for salicylates) and hemodialysis for dialyzable toxins remembered by the mnemonic I-STUMBLE / 'ISTUMBLE': Isopropanol (though usually supportive), Salicylates, Theophylline, Uremia, Methanol, Barbiturates, Lithium, and Ethylene glycol.

Key Antidotes

The CCRN tests a compact list of poison-antidote pairs. Memorize the table below; note the traps in the explanations that follow.

Antidote Traps to Remember

Acetaminophen (paracetamol) toxicity is silent early — the patient looks well for 24 hours before hepatic failure. N-acetylcysteine (NAC) replenishes glutathione and is most effective within 8 hours; the Rumack-Matthew nomogram plots the 4-hour level to decide treatment after an acute single ingestion. Naloxone reverses opioid respiratory depression but has a shorter half-life than many opioids, so recurrent depression demands redosing or an infusion. Flumazenil reverses benzodiazepines but is dangerous in chronic users or mixed (especially TCA) overdoses because it can precipitate refractory seizures — hence 'caution.' Tricyclic antidepressant toxicity causes a wide QRS and ventricular arrhythmia; sodium bicarbonate is the treatment. For beta-blocker overdose, glucagon bypasses the blocked beta-receptor to raise intracellular cAMP; calcium-channel-blocker overdose responds to IV calcium and high-dose insulin-euglycemia therapy. Digoxin-specific Fab fragments are indicated for life-threatening dysrhythmias or hyperkalemia in acute digoxin poisoning.

Anaphylaxis

Anaphylaxis is a rapid, IgE-mediated distributive shock with airway, breathing, circulation, and skin involvement — stridor, wheeze, angioedema, hypotension, and urticaria after an exposure. The single most important, life-saving intervention is intramuscular epinephrine, 0.3-0.5 mg of the 1 mg/mL (1:1000) concentration, into the mid-outer thigh (vastus lateralis), repeated every 5-15 minutes as needed. Epinephrine is first-line and time-critical — antihistamines and corticosteroids are adjuncts that treat the rash and may reduce biphasic reactions but do not reverse airway edema or shock, so they must never delay epinephrine. Add large-volume IV crystalloid for the distributive shock and airway management for laryngeal edema. Refractory anaphylaxis (persisting after repeated IM doses) escalates to an IV epinephrine infusion with aggressive fluids; patients on beta-blockers who fail to respond may need glucagon.

Temperature Emergencies

Heat Stroke

Heat stroke is a core temperature above 40 C (often >40.5 C) with central nervous system dysfunction — altered mentation, seizures, coma. The priority is immediate, aggressive active cooling (evaporative cooling, ice-water immersion, cooling blankets) to lower the core temperature rapidly, targeting roughly 38-39 C before stopping to avoid overshoot. Antipyretics such as acetaminophen are ineffective because the hypothalamic set point is normal — this is a failure of heat dissipation, not a resetting of the thermostat. Monitor for rhabdomyolysis, disseminated intravascular coagulation, and multi-organ failure.

Malignant Hyperthermia

Malignant hyperthermia (MH) is a genetic, hypermetabolic crisis triggered by volatile anesthetics or succinylcholine. The earliest sign is often a rising end-tidal CO2 unresponsive to increased ventilation, followed by masseter/generalized rigidity, tachycardia, and a late, steep temperature rise. Treatment is to stop the trigger, hyperventilate with 100% oxygen, give dantrolene (the specific antidote, which blocks calcium release from the sarcoplasmic reticulum), actively cool, and treat hyperkalemia and acidosis.

Hypothermia

Hypothermia (core <35 C) is staged mild (32-35 C), moderate (28-32 C), and severe (<28 C). Rewarming is matched to severity: passive external rewarming (warm blankets) for mild; active external (forced-air warmers) for moderate; and active internal/core rewarming (warmed IV fluids, warmed humidified oxygen, and — in cardiac arrest or severe cases — extracorporeal warming) for severe. Handle the patient gently, because a cold, irritable myocardium can fibrillate. The maxim 'not dead until warm and dead' reflects that resuscitation continues during rewarming, since profound hypothermia can be neuroprotective.