Last reviewed: March 2026
Contents
MDM Templates
Sympathomimetic Toxicity — Mild
Patient presents with agitation, diaphoresis, mydriasis, and tachycardia consistent with sympathomimetic toxicity. Alert, oriented, cooperative after initial assessment. No chest pain, no seizure, no hyperthermia.
Presentation consistent with sympathomimetic intoxication. Not consistent with thyroid storm, anticholinergic toxidrome (would expect dry, not diaphoretic), serotonin syndrome (no clonus), NMS (no rigidity), sepsis, or intracranial pathology.[1]
Plan: Benzodiazepines for agitation and sympatholysis. Observation with serial reassessments. If improving mental status, no dysrhythmias, and tolerating oral intake after 4-6 hours, discharge with return precautions. Return for chest pain, confusion, seizure, or fever.
Sympathomimetic Toxicity — Severe
Patient presents with severe sympathomimetic toxicity — significant agitation, hyperthermia, tachycardia, hypertension, and altered mental status. Not controlled with initial benzodiazepine dosing.
Severe sympathomimetic intoxication carries risk of hyperthermia, rhabdomyolysis, seizures, intracranial hemorrhage, aortic dissection, and cardiac dysrhythmias. Agitation itself generates heat and worsens the cascade. Must also consider co-ingestion and body packing/stuffing in the appropriate clinical context.[1]
Plan: Aggressive benzodiazepine dosing. Active cooling if hyperthermic (goal <38°C). IV crystalloid resuscitation. If agitation refractory to benzodiazepines, consider ketamine 4 mg/kg IM or phenobarbital loading. Avoid antipsychotics (lower seizure threshold, impair heat dissipation). If intubation needed, rocuronium preferred over succinylcholine (rhabdomyolysis risk). Admit to ICU.
Cocaine-Associated Chest Pain
Patient presents with chest pain in the setting of recent cocaine use. Hemodynamically stable. No signs of heart failure or acute hemodynamic compromise.
Approximately 6% of cocaine-associated chest pain presentations are acute MI. Cocaine causes coronary ischemia through coronary vasoconstriction, in situ thrombus formation, platelet activation, and demand ischemia from tachycardia and hypertension. Not consistent with aortic dissection, tension pneumothorax, or pulmonary embolism based on current evaluation.[2]
Plan: Aspirin, nitroglycerin, benzodiazepines (reduce cardiac demand and reverse vasoconstriction). Heparin if concern for ACS. Avoid beta-blockers (unopposed alpha stimulation can worsen coronary vasoconstriction and hypertension). PCI preferred over fibrinolysis if STEMI (vasospasm does not respond to thrombolytics). Serial troponins, observation, and cardiology consultation as indicated.
Body Packer / Body Stuffer
Patient presents with concern for body packing (ingested drug-filled containers for transport) or body stuffing (hastily swallowed loose drug containers to avoid law enforcement).
Body packers carry large quantities of well-packaged drug containers and are at risk for massive toxicity if a package ruptures. Body stuffers typically ingest smaller, poorly packaged amounts with lower risk. Packet rupture can cause sudden cardiovascular collapse, seizures, and death from massive drug exposure.[1]
Plan: Abdominal imaging to identify and count packets. Whole-bowel irrigation with polyethylene glycol until packets pass and radiologic clearance confirmed. If symptomatic from packet rupture, emergent surgical consultation for operative removal. Benzodiazepines for any sympathomimetic symptoms. Asymptomatic body stuffers may be observed for 4-6 hours and discharged if remaining asymptomatic.
Clinical Education
Sympathomimetic Toxidrome
Classic findings: agitation, diaphoresis, mydriasis, tachycardia, hypertension, hyperthermia. The key distinguishing feature from anticholinergic toxidrome is diaphoresis — sympathomimetics are wet (diaphoretic), anticholinergics are dry. Both cause mydriasis, tachycardia, and agitation.[1]
Common agents: cocaine, methamphetamine, MDMA, amphetamines (Adderall), synthetic cathinones (“bath salts”), pseudoephedrine in massive doses.
Life-threatening complications: hyperthermia (the primary killer), rhabdomyolysis, seizures, intracranial hemorrhage, aortic dissection, coronary vasospasm/MI, and cardiac dysrhythmias.
Cocaine Pearls
Cocaine half-life is 0.5-1.5 hours, but active metabolites persist 4-8 hours. Clinical effects may outlast the expected duration based on the parent compound alone. Benzoylecgonine (primary metabolite) is detectable in urine for days.[2]
Cocaine washout syndrome: Persistent lethargy after sympathomimetic phase resolves. Caused by neurotransmitter depletion after excessive sympathomimetic stimulation. Lasts 12-24 hours. Must rule out ICH before attributing AMS to washout — obtain CT head.
Cocaine and abdominal pain: Consider mesenteric ischemia (associated with all routes of administration), renal infarction, and aortic dissection. Cocaine-induced vasospasm can affect any vascular bed.
Cocaine-related seizures: CT head to rule out ICH. If patient returns to baseline, can be discharged. For refractory seizures, benzodiazepines and phenobarbital are first- and second-line. Phenytoin is not recommended (does not address the underlying mechanism and may worsen cardiac conduction).
Methamphetamine Pearls
Methamphetamine has a much longer half-life than cocaine (10-12 hours), leading to prolonged agitation, prolonged ED stays, and higher risk of hyperthermia and rhabdomyolysis from sustained sympathomimetic stimulation.[1]
Chronic methamphetamine use causes dilated cardiomyopathy. Consider heart failure in any chronic meth user presenting with dyspnea or edema. Echocardiogram if suspected. Some degree of reversibility with abstinence.
Methamphetamine-associated dental disease (“meth mouth”) increases risk of dental abscess and Ludwig’s angina. Examine the floor of mouth in any meth user with facial pain or swelling.
Agitation Management
Benzodiazepines are first-line for sympathomimetic agitation. They address the agitation, reduce cardiac demand, lower seizure threshold concerns, and allow the body to dissipate heat. There is no maximum dose — titrate to effect.[1]
Avoid antipsychotics, especially haloperidol. They lower the seizure threshold, impair thermoregulation (anticholinergic effects reduce sweating), and can cause QT prolongation. This is the opposite of what you want in sympathomimetic toxicity.
Ketamine 4 mg/kg IM is effective for refractory agitation when benzodiazepines are inadequate. Rapid onset, reliable absorption. Prepare for airway management.
Hypertension management: Benzodiazepines first. If refractory, nitroprusside (0.5 mcg/kg/min, titrate) or phentolamine (1 mg IV, then infusion titrated to effect) for pure alpha antagonism. Avoid beta-blockers — unopposed alpha stimulation worsens hypertension and coronary vasoconstriction. Nicardipine is a reasonable alternative (used for cocaine-associated ICH).
Intubation considerations: Rocuronium preferred over succinylcholine. Succinylcholine can worsen hyperkalemia in the setting of rhabdomyolysis.
Cocaine Cardiac Complications
Cocaine-associated MI: Aspirin, nitroglycerin, benzodiazepines, and heparin are the initial therapies. PCI is preferred over fibrinolysis because the mechanism is often vasospasm rather than thrombotic occlusion — thrombolytics do not address vasospasm. Avoid beta-blockers in the acute setting.[2]
Cocaine dysrhythmias — supraventricular: Adenosine can be tried but SVT often recurs while cocaine is still active. Diltiazem is a reasonable second-line agent.
Cocaine dysrhythmias — ventricular: Caused by sodium channel blockade (similar to TCA toxicity) and increased adrenergic tone. Treat with benzodiazepines, sodium bicarbonate (for wide QRS), and lidocaine. Avoid procainamide and other class IA/IC antiarrhythmics.
Disposition
Discharge: Mild toxicity with improving mental status. No dysrhythmias over 4-6 hours of observation. No chest pain, no hyperthermia, no seizure. Tolerating oral intake and ambulating. Return for chest pain, confusion, seizure, fever, dark urine, or abdominal pain.
Admit: Persistent agitation requiring ongoing benzodiazepine dosing. Hyperthermia. Rhabdomyolysis. Chest pain with troponin elevation or ECG changes. Seizure. Dysrhythmia. Body packer with retained packets. ICU for severe toxicity, refractory agitation, or hemodynamic instability.
References
- Richards JR, Albertson TE, Derlet RW, et al. Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review. Drug Alcohol Depend. 2015;150:1-13. PubMed
- McCord J, Jneid H, Hollander JE, et al. Management of cocaine-associated chest pain and myocardial infarction: AHA scientific statement. Circulation. 2008;117(14):1897-1907. PubMed
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