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Management of Atropine Poisoning

Immediate Recognition and Clinical Presentation

Atropine poisoning presents with classic anticholinergic toxicity: delirium, hot and dry erythematous skin, mydriasis, tachycardia, hyperthermia, tachypnea, and absent bowel sounds. 1

• Excessive dosing causes palpitation, dilated pupils, difficulty swallowing, hot dry skin, thirst, dizziness, restlessness, tremor, fatigue, and ataxia 2
• Toxic doses progress to restlessness, excitement, hallucinations, delirium, and coma 2
• Severe intoxication leads to circulatory collapse, blood pressure decline, respiratory failure, paralysis, and death 2
• The fatal adult dose is unknown; in pediatric populations, 10 mg or less may be fatal 2

Primary Treatment Algorithm

First-Line Management

Discontinue atropine immediately and provide aggressive supportive care with IV fluids and benzodiazepines for agitation. 1

• Ensure airway, breathing, and circulation are secured 1
• Administer benzodiazepines (diazepam or lorazepam) for agitation and convulsions 1
• Avoid short-acting barbiturates for sedation, as central depressant action may worsen late-stage atropine poisoning depression 2
• Central stimulants are contraindicated 2

Physostigmine Administration

For severe anticholinergic toxicity with significant CNS effects or life-threatening peripheral manifestations, administer physostigmine 1-2 mg IV in adults or 0.02 mg/kg IV in pediatrics by slow intravenous injection. 1, 2

• Physostigmine rapidly abolishes delirium and coma caused by large atropine doses 2
• Because physostigmine is rapidly destroyed, patients may relapse into coma after 1-2 hours, requiring repeated doses 2
• Absolute contraindications to physostigmine include cardiovascular disease, asthma, gangrene, diabetes, or mechanical obstruction of the intestine or urinary tract 1

Management of Specific Complications

Hyperthermia Control

Use external cooling measures including ice bags and alcohol sponges, especially in pediatric populations. 2

• Hyperthermia is a critical feature distinguishing anticholinergic toxicity (hot, dry skin) from sympathomimetic toxicity (diaphoresis) 1

Cardiac Complications

For QRS prolongation or dysrhythmias, administer sodium bicarbonate. 1

• Monitor for cardiovascular effects including tachycardia and mild hypertension 1
• Consider cardiac biomarkers (troponin, CK-MB) if significant tachycardia, chest pain, or signs of myocardial ischemia occurred, as atropine increases myocardial oxygen consumption 3

Respiratory Support

Provide artificial respiration with oxygen as necessary for respiratory failure. 2

• Respiratory failure is the terminal event in severe atropine poisoning 2

Laboratory Monitoring

Obtain a complete metabolic panel, glucose, and potassium within the first few hours of presentation. 3

• Serial glucose and potassium monitoring every 4-6 hours is critical, particularly if high-dose insulin therapy was used concurrently (as in organophosphate cases) 3
• Standard electrolyte panel including sodium, chloride, and bicarbonate should assess overall metabolic status 3
• The primary clinical endpoints are resolution of delirium, normalization of vital signs (heart rate, temperature), and return of bowel sounds—not laboratory values 3

Observation Period

Monitor patients for at least 48-72 hours as delayed complications can occur, especially with continued absorption in ingestion cases. 3

Critical Pitfalls to Avoid

• Never delay supportive care for laboratory results—management is primarily clinical 3
• Avoid succinylcholine in patients with anticholinergic crisis as it may cause prolonged paralysis 1
• Do not use large sedative doses as they may coincide with late-stage depression in atropine poisoning 2
• Atropine is not removed by dialysis 2