Toxicology

A

• Acetaminophen (Paracetamol) Overdose — ED Management

  Acetaminophen overdose causes dose-dependent hepatic injury after toxic NAPQI metabolite formation exhausts glutathione stores. N-acetylcysteine replenishes glutathione and is highly effective when started early, but it also benefits patients who present after liver injury has begun. Management depends on whether ingestion is a single acute event with a reliable time, an extended-release or delayed-absorption exposure, a repeated supratherapeutic ingestion, or an unreliable history. The Rumack-Matthew nomog
• Acetaminophen Overdose — NAC Protocol

  Use timing and level on the Rumack Matthew nomogram for single acute ingestions; start N acetylcysteine immediately if timing unknown, delayed presentation, or high risk.
• Acetaminophen Overdose — NAC Protocols, Risk Nomogram, and Transplant Criteria

  For single acute ingestions, use the Rumack‑Matthew nomogram (≥4 h level) to guide treatment; for staggered or unknown ingestions, start NAC immediately. Prefer IV NAC for severe toxicity, late presenters, or vomiting; monitor LFTs/INR and apply transplant criteria when ALF develops.

B

• Beta Blocker and Calcium Channel Blocker Overdose — High-Dose Insulin

  Severe beta-blocker and calcium-channel-blocker poisoning can cause bradycardia, conduction delay, cardiogenic shock, and vasoplegia. Stabilize the airway and circulation, obtain continuous ECG and glucose monitoring, use vasopressors, give calcium for CCB toxicity, and institute high-dose regular insulin with dextrose and potassium surveillance for significant hypotension. Glucagon is an adjunct for beta-blocker poisoning, and VA-ECMO is appropriate for refractory reversible shock.
• Beta Blocker Overdose — Glucagon and High Dose Insulin

  Life-threatening beta-blocker overdose causes bradycardia, atrioventricular block, myocardial depression, hypotension, and shock, with agent-specific complications such as seizures from propranolol and QT prolongation from sotalol. Treat shock with vasopressors, glucagon, and high-dose insulin when hypotension is refractory, and escalate selected cases to dialysis or VA-ECMO.

C

• Calcium Channel Blocker Overdose — High Dose Insulin

  Severe calcium channel blocker poisoning causes vasodilatory and cardiogenic shock, bradycardia, conduction delay, hyperglycemia, and potentially cardiac arrest. Stabilize airway and circulation, give calcium and vasopressors, start high-dose insulin with glucose monitoring for significant hypotension, and escalate early to toxicology consultation and mechanical circulatory support when shock is refractory.
• Calcium Channel Blocker Overdose — High‑Dose Insulin Euglycemia and Adjuncts

  Severe hypotension/bradycardia from CCB toxicity requires airway protection, calcium salts, vasopressors, and **high‑dose insulin euglycemia therapy (HIE)** with dextrose and electrolyte monitoring; add lipid emulsion for lipophilic agents and consider ECMO for refractory shock.
• Carbon Monoxide Poisoning — 100% Oxygen, HBOT Criteria, and Disposition

  CO binds hemoglobin and impairs cellular respiration. Treat immediately with 100% oxygen; consider hyperbaric oxygen for severe poisoning (neurologic symptoms, COHb ≥25%—lower thresholds in pregnancy—or cardiac ischemia). Monitor for delayed neurocognitive sequelae.
• Carbon Monoxide Poisoning — 100% Oxygen, Indications for HBOT, and Neuro Follow‑Up

  Headache, dizziness, and flu‑like illness in winter or from fires suggest CO poisoning. Give 100% oxygen immediately and consider hyperbaric oxygen for severe poisoning (e.g., COHb ≥25%, loss of consciousness, pregnancy, neurologic deficits, or cardiac ischemia). Observe for delayed neurologic sequelae.
• Cyanide Poisoning — Hydroxocobalamin Protocol

  Cyanide poisoning causes cellular hypoxia by inhibiting mitochondrial cytochrome oxidase and can produce abrupt cardiovascular collapse, severe lactic acidosis, coma, and seizure despite adequate oxygen delivery. Diagnosis is clinical because cyanide concentrations are rarely available fast enough to guide emergency care. Remove ongoing exposure, provide high-flow oxygen and full resuscitation, and give hydroxocobalamin promptly when severe cyanide poisoning is strongly suspected, particularly after enclose

M

• Methanol Ethylene Glycol Poisoning — Fomepizole and Dialysis

  Suspect in high anion gap metabolic acidosis with osm gap; give fomepizole promptly, correct acidosis, and arrange hemodialysis for standard indications.
• Methemoglobinemia — Methylene Blue

  Suspect with hypoxia unresponsive to oxygen and chocolate colored blood; confirm with co oximetry; treat with methylene blue when symptomatic or levels elevated.
• Methemoglobinemia — Recognition and Treatment

  Methemoglobinemia occurs when hemoglobin iron is oxidized to the ferric state and cannot carry oxygen effectively. Suspect it when cyanosis and hypoxic symptoms persist despite oxygen, especially with an exposure to oxidizing drugs or chemicals and a saturation gap. Confirm by co-oximetry, remove the trigger, give oxygen, and treat significant symptomatic acquired methemoglobinemia with methylene blue unless contraindications require an alternative strategy.

O

• Opioid Overdose — ED Management

  Opioid overdose is a time-critical toxicologic emergency defined primarily by respiratory depression, not by altered mental status alone. Immediate care centers on airway opening, oxygenation, ventilation, and naloxone titrated to restore effective spontaneous breathing and protective airway reflexes. Patients require observation for recurrent toxicity, evaluation for coingestants and complications, and overdose prevention and opioid use disorder treatment before discharge when appropriate.
• Opioid Overdose — Naloxone and Supportive Care

  Respiratory depression and pinpoint pupils suggest opioid toxicity; support airway and ventilation and give titrated naloxone; monitor for recurrence from long acting opioids.
• Organophosphate Poisoning — Atropine and Pralidoxime

  Organophosphate poisoning produces an acute cholinergic syndrome from acetylcholinesterase inhibition, with life-threatening bronchorrhea, bronchospasm, bradycardia, seizures, and neuromuscular weakness. Decontaminate safely, secure oxygenation and ventilation, give rapidly escalating atropine until pulmonary secretions and bronchospasm improve, add pralidoxime early for clinically important poisoning, and treat seizures with benzodiazepines.

S

• Salicylate Poisoning — Alkalinization and Dialysis

  Salicylate poisoning produces respiratory stimulation, metabolic acidosis, neurologic toxicity, pulmonary edema, and cellular energy failure. Diagnose with serial salicylate levels interpreted alongside pH and clinical status. Correct volume and potassium deficits, administer IV sodium bicarbonate to alkalinize serum and urine, avoid preventable acidemia, and initiate early hemodialysis for severe neurologic, pulmonary, renal, acid-base, or concentration-based toxicity.
• Salicylate Toxicity — Alkalinization and Dialysis

  Assess acid base status and symptoms; start sodium bicarbonate infusion for alkalinization and consider hemodialysis for severe toxicity.
• Serotonin Syndrome — Cyproheptadine and Support

  Triad of mental status change, autonomic instability, and neuromuscular hyperactivity after serotonergic drug exposure; stop offending agents, provide supportive care, benzodiazepines, and cyproheptadine for moderate to severe cases.
• Serotonin Syndrome — Recognition and Treatment

  Serotonin syndrome is a rapidly developing toxidrome caused by excessive serotonergic activity, characterized by neuromuscular hyperactivity, autonomic excitation, and altered mental status. Diagnosis is clinical, with clonus and hyperreflexia especially useful. Stop serotonergic drugs, provide benzodiazepines and supportive care, use aggressive external cooling for hyperthermia, and consider oral or enteral cyproheptadine for persistent moderate toxicity.
• Serotonin Syndrome — Recognition, Benzodiazepines, Cooling, and Cyproheptadine

  Triad of mental status changes, autonomic hyperactivity, and neuromuscular abnormalities (clonus, hyperreflexia). Stop serotonergic agents, give benzodiazepines for agitation, aggressive cooling for hyperthermia, and cyproheptadine for moderate–severe cases. Avoid antipyretics and succinylcholine.

T

• Toxic Alcohol Ingestion — Fomepizole, Adjuncts, and Dialysis Triggers

  Methanol/ethylene glycol ingestions cause high anion gap metabolic acidosis and osmolal gap. Start fomepizole immediately, give cofactors (folinic acid/pyridoxine/thiamine), correct acidosis, and consult poison control; initiate hemodialysis for severe toxicity.
• Toxic Alcohols — Fomepizole and Dialysis

  Methanol and ethylene glycol poisoning are metabolic emergencies in which toxic metabolites cause severe acidosis and organ injury. Suspect exposure with an unexplained high-anion-gap acidosis, osmolar-gap abnormalities, visual symptoms, renal injury, or suggestive history. Give fomepizole promptly when indicated, correct severe acidosis, administer toxin-specific cofactors, and arrange hemodialysis for severe poisoning using toxicology and EXTRIP criteria.
• Tricyclic Antidepressant Overdose — Sodium Bicarbonate Protocol

  Tricyclic antidepressant overdose can rapidly cause seizures, coma, hypotension, and malignant dysrhythmias through sodium-channel blockade and other receptor effects. Obtain an immediate ECG, support ventilation and circulation, give hypertonic sodium bicarbonate for QRS widening, hypotension, or ventricular dysrhythmia, use benzodiazepines for seizures, and escalate to vasopressors or extracorporeal support when cardiotoxicity remains refractory.