Emergency Medicine · Toxicology
The facts most likely to be tested
The primary clinical presentation of stimulant toxicity includes sympathomimetic toxidrome characterized by tachycardia, hypertension, hyperthermia, and mydriasis.
Benzodiazepines are the first-line pharmacologic treatment for agitation, hypertension, and tachycardia to reduce sympathetic outflow.
Beta-blockers are strictly contraindicated in acute cocaine toxicity due to the risk of unopposed alpha-adrenergic stimulation, which can precipitate coronary vasospasm and severe hypertension.
Cocaine-induced myocardial infarction is managed with benzodiazepines, aspirin, nitroglycerin, and calcium channel blockers if symptoms persist.
Patients presenting with agitated delirium and hyperthermia are at high risk for rhabdomyolysis, requiring aggressive intravenous fluid resuscitation and monitoring of creatine kinase levels.
Amphetamine toxicity is frequently associated with seizures and hypertensive emergency, necessitating rapid stabilization with benzodiazepines.
Urine toxicology screens detect cocaine metabolites (e.g., benzoylecgonine) but are not required for diagnosis, as the clinical presentation is sufficient for management.
Vignette unlocked
A 28-year-old male is brought to the emergency department by police after being found combative in a public park. On examination, the patient is diaphoretic and agitated with a heart rate of 145 bpm, blood pressure of 180/105 mmHg, and a temperature of 102.4°F. Physical exam reveals dilated pupils and tremulousness. An ECG shows sinus tachycardia without ischemic changes. The patient denies any medical history.
Which of the following is the most appropriate initial pharmacologic intervention?
Intravenous lorazepam
The patient exhibits a classic sympathomimetic toxidrome; benzodiazepines are the first-line treatment to control agitation and autonomic hyperactivity while avoiding the risks associated with beta-blockers.
Full handout
High yield triage
Etiology / Epidemiology
Excessive sympathomimetic stimulation via catecholamine surge. Common in young adults and recreational users.
Clinical Manifestations
Mydriasis, diaphoresis, and hypertension. Look for psychomotor agitation and tachycardia.
Diagnosis
Clinical diagnosis. Urine toxicology screen for detection; ECG to rule out ischemia.
Treatment
Benzodiazepines are first-line. Avoid beta-blockers due to risk of unopposed alpha-adrenergic stimulation.
Prognosis
Risk of myocardial infarction and rhabdomyolysis. Monitor for hyperthermia and end-organ failure.
Full handout
Epidemiology & Etiology
Prevalent in emergency settings involving polysubstance abuse. Cocaine acts as a potent reuptake inhibitor of dopamine, norepinephrine, and serotonin. Amphetamines trigger massive presynaptic release of these same neurotransmitters.
Pertinent Anatomy
Systemic effects target the cardiovascular system (myocardial oxygen demand) and the central nervous system (limbic system). Peripheral vasoconstriction leads to ischemic end-organ damage.
Pathophysiology
Cocaine blocks the sodium channel (local anesthetic effect) and inhibits catecholamine reuptake. Amphetamines enter the neuron via transporters to displace catecholamines from storage vesicles. The resulting sympathetic storm causes profound vasoconstriction and hypermetabolism.
Clinical Manifestations
Patients present with tachycardia, hypertension, and mydriasis. Watch for seizures, chest pain, and hyperthermia. Agitated delirium is a hallmark of severe toxicity.
Diagnosis
Diagnosis is primarily clinical. ECG is mandatory to evaluate for ST-segment elevation or arrhythmias. Urine toxicology confirms exposure but does not correlate with severity. Creatine kinase levels are indicated if rhabdomyolysis is suspected.
Treatment
Administer benzodiazepines (e.g., lorazepam) to control agitation and sympathetic outflow. Beta-blockers are strictly contraindicated as they cause unopposed alpha-adrenergic vasoconstriction. Use phentolamine or nitroprusside for refractory hypertension.
Prognosis
Major complications include myocardial infarction, aortic dissection, and intracranial hemorrhage. Monitor urine output closely to assess for acute kidney injury secondary to rhabdomyolysis.
Differential Diagnosis
Anticholinergic toxicity: dry skin vs. diaphoresis in stimulants
Serotonin syndrome: presence of clonus and hyperreflexia
Thyroid storm: history of goiter or Graves disease
Pheochromocytoma: episodic hypertension with headache and palpitations
Alcohol withdrawal: presence of tremor and history of chronic use