Eduovisual
Emergency & Toxicology
Sympathomimetic toxidrome: cocaine and amphetamines
— Cocaine: blocks presynaptic reuptake of norepinephrine, dopamine, serotonin; also Na⁺-channel blockade (local anesthetic effect → wide QRS, Brugada-like ECG).
— Amphetamines/methamphetamine/MDMA: drive presynaptic release of monoamines via reverse transport (DAT/NET/SERT); longer half-life (8–12 h) than cocaine (~1 h) → prolonged agitation.
— Cathinones/synthetics: unpredictable potency, often undetected on standard tox screens, prolonged psychosis.
— Young or middle-aged patient with hyperthermia, tachycardia, hypertension, mydriasis, diaphoresis, agitation, psychosis.
— Chest pain in a patient under 50 with no traditional risk factors.
— New seizure in an adult without epilepsy history.
— Unexplained ICH, aortic dissection, or STEMI in a young patient.
— Severe agitation requiring restraints; "excited delirium" picture.
— Wide-complex tachycardia after recreational drug use.
Board pearl: The defining feature distinguishing sympathomimetic from anticholinergic toxidrome (both have tachycardia, hypertension, mydriasis, agitation, hyperthermia) is diaphoresis and bowel sounds present in sympathomimetic vs dry skin and absent bowel sounds in anticholinergic. This single physical-exam pivot is one of the most tested points across Step 2 and Step 3 toxicology questions, so anchor your differential on the skin and gut, not the vitals.
— Chest pain (cocaine-associated chest pain is the single most common ED stimulant complaint; ~6% have true MI).
— Severe agitation, paranoia, hallucinations — methamphetamine-induced psychosis can be indistinguishable from schizophrenia acutely.
— Seizure — usually single, generalized, within hours of use; recurrent seizures suggest body packing/stuffing or cathinones.
— Headache, focal deficits → consider hemorrhagic or ischemic stroke (cocaine ↑ risk of both).
— Hyperthermia + altered mental status — life-threatening; consider concurrent serotonin syndrome with MDMA + SSRI.
— Dyspnea — pulmonary edema (cocaine), "crack lung" (alveolar hemorrhage, eosinophilic infiltrate after inhaled crack).
— Route and timing: IV/smoked → minutes to peak; oral → 30–60 min; transdermal patches misused.
— Substance specifics: "ice," "crystal," "speed," "molly," "Adderall," "bath salts," "flakka."
— Co-ingestion: alcohol + cocaine → cocaethylene (longer half-life, more cardiotoxic); opioids + stimulants ("speedball") → mixed toxidrome.
— Body packing vs stuffing: Packers swallow well-wrapped packets for smuggling (large amount, delayed rupture); stuffers hastily swallow loose drug to evade police (smaller, faster onset).
— Medications: SSRIs, MAOIs, linezolid → serotonin syndrome risk with MDMA.
— Prior episodes: recurrent stimulant chest pain, prior MI, dilated cardiomyopathy.
Step 3 management: When a patient with stimulant chest pain arrives, your first three orders are simultaneous: 12-lead ECG within 10 minutes, IV benzodiazepine (lorazepam 2 mg or diazepam 5–10 mg), and cardiac monitor with troponin. Benzos before nitrates — they treat the upstream sympathetic drive that's causing the ischemia, anxiety, hypertension, and tachycardia all at once, often eliminating the need for additional antihypertensives.
— Temperature: often >38.5°C; >40°C is a toxicologic emergency demanding active cooling.
— Heart rate: sinus tachycardia 110–160; wide-complex tachycardia raises cocaine Na-channel toxicity.
— Blood pressure: SBP often 180–220; sustained severe HTN risks ICH, aortic dissection.
— Respiratory rate: elevated; hypoventilation suggests co-ingested opioid.
— Mydriasis with preserved light reflex.
— Hyperalert, pressured speech, paranoia, choreoathetoid movements ("meth dancing," "punding" — repetitive purposeless behavior).
— Hyperreflexia, clonus (especially if serotonergic co-ingestion).
— Focal deficit → stroke workup immediately.
— Diaphoresis (key differentiator from anticholinergic).
— Excoriations, "meth mites" (formication-driven picking).
— Nasal septal perforation (chronic cocaine snorting).
— "Meth mouth": rampant caries, xerostomia.
— Track marks, abscesses (IV use).
— Rales suggest pulmonary edema; murmurs raise endocarditis concern in IVDU.
— Pulse differential or interscapular tearing pain → aortic dissection.
— Active or hyperactive bowel sounds (vs anticholinergic ileus).
— Tenderness with rigid abdomen in body packer → consider rupture, ischemic bowel from mesenteric vasospasm.
— Rigidity, muscle tenderness → rhabdomyolysis.
— Compartment syndrome from prolonged immobility while intoxicated.
Key distinction: Sympathomimetic vs anticholinergic — both give tachycardia, hypertension, hyperthermia, mydriasis, and agitation. The sympathomimetic patient is wet (diaphoretic) with active bowel sounds; the anticholinergic patient is "dry as a bone, red as a beet, blind as a bat, mad as a hatter, hot as a hare" with absent bowel sounds and urinary retention. Serotonin syndrome adds clonus and hyperreflexia (lower-extremity predominant); neuroleptic malignant syndrome gives lead-pipe rigidity and develops over days.
— 12-lead ECG within 10 min for any chest pain or wide complex.
— CBC, BMP, magnesium, calcium, phosphorus.
— Troponin (high-sensitivity, serial at 0 and 3 h).
— CK and CK-MB; urinalysis with myoglobin — assess rhabdomyolysis.
— LFTs (ischemic hepatitis, MDMA hepatotoxicity).
— Coags (PT/INR, aPTT) if planning lumbar puncture or anticipating bleed/dissection.
— Lactate, ABG/VBG in severe toxicity or hyperthermia.
— Urine drug screen (UDS): detects cocaine metabolite (benzoylecgonine) up to 72 h; amphetamine class detected, but methamphetamine, MDMA, and especially cathinones often missed or cause false negatives/positives.
— Acetaminophen, salicylate, ethanol levels if any AMS or suicide concern.
— β-hCG in all women of reproductive age.
— Blood cultures × 2 if febrile IVDU (endocarditis screen).
— Sinus tachycardia (most common).
— Wide QRS >100 ms from cocaine Na-channel blockade → treat with sodium bicarbonate.
— QTc prolongation (methadone co-use, methamphetamine).
— Brugada pattern can be unmasked.
— ST elevation/depression — true ACS possible.
— CXR: pulmonary edema, "crack lung," widened mediastinum (dissection), pneumothorax (Valsalva from crack inhalation).
— CT head non-contrast for any focal deficit, severe headache, seizure, or persistent AMS.
— CTA chest if dissection suspected (tearing chest/back pain, BP differential).
— CT abdomen for suspected body packer (radiopaque packets, "double condom" sign).
Board pearl: A positive UDS does not confirm acute intoxication — benzoylecgonine persists 2–3 days (longer in heavy users, up to a week). Conversely, a negative UDS does not exclude stimulant toxicity: synthetic cathinones, novel phenethylamines, and methylphenidate often go undetected. Treat the clinical toxidrome, not the lab. This testing-limitations theme is heavily favored on Step 3 in tandem with biostatistics framing (sensitivity/specificity of bedside assays).
— TTE in all patients with stimulant-related chest pain, dyspnea, or murmur — evaluates regional wall motion abnormality, EF (stimulant cardiomyopathy is common in chronic methamphetamine users — often <30%), pericardial effusion, and valvular vegetations.
— TEE if endocarditis suspected and TTE non-diagnostic, or for aortic dissection when CTA contraindicated.
— CT coronary angiography or invasive cath if troponin positive and concern for type 1 MI; many cocaine MIs are demand ischemia or vasospasm, but plaque rupture in young users is documented and prematurely accelerates atherosclerosis.
— MRI brain if initial CT negative but persistent deficit — detects watershed infarcts, posterior reversible encephalopathy syndrome (PRES), early ischemic stroke.
— CTA/MRA head and neck for stroke workup; cocaine is associated with both ischemic stroke (vasospasm, accelerated atherosclerosis) and hemorrhagic stroke (HTN surge unmasking aneurysm/AVM).
— GC-MS or LC-MS/MS confirms specific agent; useful in forensic, occupational, or custody cases.
— Hair testing for chronic use patterns in custody/child-welfare contexts.
— EEG for persistent altered mental status without structural lesion or recurrent seizures.
— LP if febrile AMS to exclude meningitis when toxidrome resolves but mental status doesn't.
— Compartment pressures if rhabdomyolysis with focal limb pain or tense compartments.
— TSH in agitation differential when picture is atypical (thyroid storm mimic).
CCS pearl: On a CCS case of stimulant-related chest pain with positive troponin, after acute stabilization with benzodiazepines, aspirin, nitroglycerin, and heparin, advance the clock and order TTE within 24 hours and cardiology consult. Do not advance to discharge until echo is documented and a substance-use counseling consult is placed — both are scored as appropriate care steps and address the secondary-prevention dimension Step 3 weights heavily.
— Mild: mild tachycardia/HTN, anxiety, no end-organ injury → observation + oral benzodiazepine, hydration, discharge after 4–6 h sober.
— Moderate: persistent HTN >180/110, HR >130, agitation requiring parenteral sedation, mild rhabdo (CK <5,000), troponin negative → ED observation/short stay.
— Severe: hyperthermia >40°C, seizures, chest pain with troponin elevation, wide QRS, arrhythmia, stroke, dissection, MAP-threatening HTN, severe rhabdo, organ failure → ICU.
— Agitation: benzodiazepines, titrate aggressively.
— Body temperature: active external cooling (mist + fan, ice packs to groin/axillae, cold IV fluids) for T >40°C; target <38.5°C within 30 min.
— Cardiovascular: benzos first; address HTN/tachycardia after sedation if persistent.
— Decontamination: rarely useful — activated charcoal only for recent oral ingestion (body stuffer) and intact airway; whole-bowel irrigation with polyethylene glycol for confirmed body packers.
— Electrolytes/metabolic: correct hyperK, acidosis, hypoNa (MDMA-related SIADH).
— Fluids: liberal IV crystalloid for rhabdomyolysis (target urine output 1–2 mL/kg/h).
— Pure β-blockers (propranolol, metoprolol) classically taught to cause "unopposed α" → worsened HTN/coronary vasospasm. Recent literature is mixed, but boards still expect you to avoid β-blockade alone in acute cocaine toxicity.
— Haloperidol/typical antipsychotics: lower seizure threshold, worsen hyperthermia and QT.
— Succinylcholine: caution with hyperkalemic rhabdo — use rocuronium.
Step 3 management: Anchor every stimulant toxidrome plan on benzodiazepines as the universal first-line agent — they treat agitation, tachycardia, hypertension, hyperthermia (by reducing motor activity), seizure prophylaxis, and indirectly myocardial oxygen demand. Lorazepam 2 mg IV q5–10 min or diazepam 5–10 mg IV q5–10 min, titrated to calm, awake, and HR <120.
— Diazepam 5–10 mg IV q5–10 min (long half-life, rapid onset).
— Lorazepam 2–4 mg IV q10–15 min (good if hepatic dysfunction).
— Midazolam 2–5 mg IV/IM q5 min (fast onset, useful pre-IV access).
— Endpoint: calm but arousable, HR <120, SBP <160.
— No ceiling dose; very large totals (>100 mg diazepam-equivalents) sometimes required.
— Phentolamine 1–5 mg IV q5–10 min — α-blocker, ideal in cocaine-induced HTN/coronary vasospasm.
— Nitroglycerin IV infusion or SL — first-line for chest pain with HTN; relieves vasospasm.
— Nicardipine or clevidipine infusion — calcium-channel blockers, titratable.
— Avoid pure β-blockers; labetalol is debated — mixed α/β with α:β ~1:7 IV, so theoretically acceptable but not preferred; many tox sources still discourage it.
— Sodium bicarbonate 1–2 mEq/kg IV bolus, repeat to narrow QRS and target serum pH 7.45–7.55.
— Lidocaine is controversial (also a Na-channel blocker) but often used when bicarbonate fails.
— Avoid class IA/IC antiarrhythmics.
— Benzodiazepines first; if refractory, levetiracetam or phenobarbital (avoid phenytoin — Na-channel blocker, worsens cocaine cardiotoxicity).
— Aggressive external cooling + benzos ± non-depolarizing neuromuscular blockade (rocuronium) with intubation if refractory. Dantrolene is not indicated (no role outside malignant hyperthermia/NMS).
— Aspirin 325 mg, nitroglycerin, heparin, benzodiazepine; cath lab for STEMI.
Board pearl: Phentolamine is the classically tested answer for cocaine-induced hypertension and coronary vasospasm that doesn't resolve with benzodiazepines alone. When the stem says "the patient remains hypertensive after lorazepam," reach for phentolamine or nitroglycerin, not metoprolol or labetalol.
— Whole-bowel irrigation with PEG-electrolyte solution 1–2 L/h via NG until clear effluent and imaging confirms passage.
— Activated charcoal 1 g/kg if recent ingestion and packet integrity uncertain.
— Surgical consultation for symptomatic toxicity (packet rupture) — emergent laparotomy; do not endoscope intact packets (rupture risk).
— Admit until all packets accounted for; serial KUB/CT.
— Single-dose activated charcoal if intact airway and recent (<1 h).
— Observe 6–8 h; most do well.
— Hyponatremia from SIADH + free-water intake at raves → seizures, cerebral edema.
— Treat symptomatic hyponatremia with hypertonic 3% saline 100 mL bolus, repeat to seizure resolution.
— Serotonin syndrome risk if patient on SSRI/MAOI → benzodiazepines, cyproheptadine 12 mg PO then 2 mg q2h, supportive cooling.
— Chronic users with reduced EF — standard HF guideline-directed therapy (ACEi/ARB/ARNI, β-blocker once abstinent, MRA, SGLT2i); abstinence can produce partial recovery.
— Same workup as standard ACS; cath if STEMI or refractory; continue benzodiazepines during workup.
— On discharge: aspirin, statin, ACEi if indicated; β-blockers historically avoided but increasingly accepted after abstinence is established — carvedilol the best-studied agent.
— Benzodiazepines first; if antipsychotic needed, prefer second-generation (olanzapine 5–10 mg IM, ziprasidone 10–20 mg IM) over haloperidol; monitor QT.
CCS pearl: For a body packer, the correct sequence is NPO, IV fluids, NG tube, whole-bowel irrigation with PEG, abdominal CT, surgery consult on standby, ICU/monitored bed. Discharge only after two consecutive negative imaging studies and packet-free stools documented by nursing. Skipping the imaging confirmation costs CCS points.
— Lower physiologic reserve → higher rates of MI, stroke, aortic dissection, type-A dissection in particular.
— Baseline polypharmacy: SSRIs, MAOIs (rasagiline/selegiline for Parkinson's) → serotonin syndrome risk.
— Pre-existing HTN, CAD, atrial fibrillation worsen presentations; AF rate control complicated by avoidance of β-blockers acutely.
— Reduce benzodiazepine doses by 25–50%: start lorazepam 0.5–1 mg IV; risk of delirium and respiratory depression.
— Lower threshold for CT head (subdural risk with falls), ECG, troponin, and admission for observation.
— Cocaine and amphetamines undergo hepatic metabolism primarily; metabolites renally excreted, may accumulate.
— Rhabdomyolysis with AKI is the dominant renal concern — aggressive IV fluids (isotonic saline; bicarbonate-containing fluids no longer routinely recommended) to target UOP 1–2 mL/kg/h.
— Dialysis indications: refractory hyperkalemia, severe acidosis, oligo/anuria with volume overload, uremia.
— Avoid nephrotoxic adjuncts (NSAIDs, contrast when feasible).
— MDMA can cause severe hepatotoxicity (acute hepatitis, fulminant failure).
— Cocaine + alcohol → cocaethylene → exaggerated hepatotoxicity and cardiotoxicity.
— Prefer lorazepam or oxazepam (glucuronidated, not CYP-dependent) over diazepam in cirrhosis.
— Monitor LFTs, INR, ammonia; consult hepatology/transplant if INR rising, encephalopathy.
Step 3 management: In an elderly patient on selegiline or rasagiline who presents after MDMA or methamphetamine use with hyperthermia and clonus, you are dealing with serotonin syndrome plus sympathomimetic overlap. First-line is benzodiazepines + aggressive cooling + cyproheptadine; avoid bromocriptine and dantrolene (those are for NMS and malignant hyperthermia respectively, and Step 3 loves to test this confusion).
— Cocaine: placental abruption (classic teaching: painful third-trimester bleeding), preterm labor, IUGR, preterm PROM, fetal stroke.
— Methamphetamine: IUGR, prematurity, neonatal abstinence/withdrawal-like state, cleft palate, cardiac defects (limited data).
— MDMA: limited human data, possible cardiac and musculoskeletal anomalies.
— Workup: continuous fetal monitoring if ≥23 weeks viable, OB consult, RhoGAM if Rh-negative with bleeding, abruption workup (fibrinogen, DIC labs).
— Treat mother first: benzodiazepines safe acutely; lorazepam preferred. Phentolamine, nitroglycerin, hydralazine, labetalol all acceptable for severe HTN in pregnancy (most prefer labetalol/hydralazine here despite the unopposed-α concern — maternal stabilization wins).
— Mandatory toxicology screening varies by state; many states require reporting positive maternal/neonatal toxicology to child protective services.
— Withdrawal from in-utero stimulant exposure is mild compared to opioids — irritability, poor feeding, tremor; rarely needs pharmacotherapy.
— Methamphetamine-exposed infants: lower birth weight, neurodevelopmental follow-up.
— Accidental: toddlers ingesting cocaine left out, prescription amphetamines from siblings — seizures, tachycardia, hyperthermia.
— Adolescent recreational use: MDMA at concerts, "study drugs" (Adderall, Vyvanse), vaping cathinones.
— Workup: same as adult, plus child-protection evaluation for accidental exposures (home safety assessment).
— Activated charcoal if recent oral ingestion and protected airway.
— Cocaine and amphetamines pass into breast milk → infant toxicity reported. Advise abstinence from breastfeeding while using.
Board pearl: Painful third-trimester vaginal bleeding + cocaine use = placental abruption until proven otherwise. Compare with painless bleeding = placenta previa. The cocaine-abruption association is one of the most frequently tested OB-tox overlaps on both Step 2 and Step 3.
— Acute MI (vasospasm + plaque rupture + thrombus); risk highest in first hour, persists 24 h.
— Aortic dissection — type A more common with cocaine; tearing chest/back pain, BP differential.
— Arrhythmias: SVT, wide-complex VT, Brugada unmasking, sudden cardiac death.
— Dilated cardiomyopathy — chronic methamphetamine.
— Endocarditis in IVDU (right-sided, S. aureus; left-sided MRSA increasing).
— Pulmonary edema — cardiogenic and non-cardiogenic.
— Accelerated atherosclerosis in chronic cocaine users.
— Ischemic stroke (vasospasm, accelerated atherosclerosis, embolic from endocarditis).
— Intracerebral hemorrhage — HTN surge + ruptured aneurysm/AVM.
— Subarachnoid hemorrhage — classic on boards.
— Seizures, status epilepticus.
— PRES, hypoxic-ischemic injury.
— Chronic cognitive impairment, Parkinsonism risk with methamphetamine (dopaminergic neurotoxicity).
— "Crack lung" — fever, hypoxia, diffuse infiltrates after crack inhalation.
— Pneumothorax/pneumomediastinum (Valsalva).
— Aspiration pneumonia post-seizure.
— Rhabdomyolysis with AKI — most common preventable complication.
— Hyperkalemia, lactic acidosis, hyperphosphatemia.
— Hyponatremia (MDMA + SIADH + free water).
— Mesenteric ischemia (vasospasm).
— Acute hepatitis, fulminant hepatic failure (MDMA).
Key distinction: "Crack lung" vs aspiration pneumonia vs cardiogenic pulmonary edema — crack lung shows diffuse alveolar hemorrhage and eosinophilia within hours of inhaled crack; aspiration shows focal infiltrate (often RLL or posterior segments) after seizure or AMS; cardiogenic edema shows cardiomegaly, Kerley B lines, and elevated BNP. Treatment of crack lung is supportive ± steroids; treatment of cardiogenic edema is diuresis and afterload reduction.
— Hyperthermia ≥40°C requiring active cooling.
— Refractory agitation requiring repeated parenteral sedation or intubation.
— Status epilepticus or recurrent seizures.
— Hemodynamic instability — shock, refractory HTN on infusion, arrhythmia.
— Wide-complex tachycardia or significant ECG abnormality (QRS >120, QTc >500).
— Acute MI with positive troponin or ongoing chest pain.
— Stroke (ischemic or hemorrhagic), SAH.
— Aortic dissection.
— Severe rhabdomyolysis (CK >20,000) or AKI requiring dialysis.
— Body packer with symptoms or imaging concern for rupture.
— Severe MDMA hyponatremia (Na <125 with neuro symptoms).
— Fulminant hepatic failure.
— Persistent tachycardia HR >120 after 4–6 h of treatment.
— Chest pain ruled out for MI but with risk factors.
— Mild–moderate rhabdomyolysis on IV fluids.
— Resolving agitation but still requiring observation.
— Cardiology — ACS, arrhythmia, new cardiomyopathy.
— Neurology/neurosurgery — stroke, ICH, SAH.
— Vascular/CT surgery — dissection.
— Toxicology / Poison Control (1-800-222-1222) — for any severe or atypical case; document the consult.
— Psychiatry — psychosis, suicidality, agitation needing chronic management.
— Addiction medicine / social work — every patient before discharge.
— OB — pregnant patients.
— Child protective services / adult protective services — when dependent harm suspected.
— Vitals normalized x ≥2 h, mental status at baseline, ambulating, tolerating PO, no end-organ injury, safe disposition.
CCS pearl: Always call Poison Control on CCS cases involving significant toxic exposure and document it — the simulator credits the consult, and in real practice this is the standard of care. Pair it with addiction medicine or social work referral before discharge — both are scored as appropriate longitudinal care.
— Shares tachycardia, HTN, hyperthermia, mydriasis, agitation.
— Differs by: dry flushed skin, urinary retention, absent bowel sounds, mumbling speech.
— Treat with physostigmine in pure anticholinergic delirium (contraindicated with TCA overdose — risk of asystole).
— Triad: autonomic instability + mental status change + neuromuscular hyperactivity (clonus, hyperreflexia, lower-extremity predominant).
— Treat: stop offending agent, benzodiazepines, cyproheptadine, cooling.
— Slow onset (days), lead-pipe rigidity, hyporeflexia, very high CK, hyperthermia.
— Treat: stop antipsychotic, supportive, bromocriptine, dantrolene.
— Intra/post-op masseter rigidity, hypercarbia, hyperthermia, rhabdo.
— Treat: dantrolene, cooling, stop trigger.
— PCP/ketamine: vertical/horizontal nystagmus, dissociation, violent behavior; mild sympathomimetic features.
— Treat: benzodiazepines, low-stimulation environment.
— Variable; can mimic sympathomimetic with severe agitation; treat supportively.
— Alcohol/benzodiazepine withdrawal mimics sympathomimetic (tachycardia, tremor, diaphoresis, HTN) — distinguished by history and benzodiazepine response is therapeutic and definitive.
— Opioid withdrawal: mydriasis + GI distress + yawning + piloerection; usually less severe HTN.
Key distinction: Use the skin (wet vs dry), reflexes (hyperreflexia/clonus vs lead-pipe rigidity), and onset (minutes vs days) to triangulate among sympathomimetic, anticholinergic, serotonin syndrome, and NMS. Memorize this 2×2×2 grid — it's recycled across virtually every tox shelf and Step 3 toxidrome question.
— Thyroid storm: tachycardia, hyperthermia, tremor, AMS — but goiter, exophthalmos, history of Graves; TSH suppressed, free T4 high. Treat with PTU/methimazole, propranolol (yes, β-blockade indicated here), iodine, steroids.
— Pheochromocytoma: episodic HTN, headache, palpitations, diaphoresis — 24-h urine metanephrines or plasma metanephrines; treat with α-blockade first (phenoxybenzamine), then β-blockade.
— Hypoglycemia: tachycardia, diaphoresis, tremor, AMS — check fingerstick on EVERY altered patient.
— Adrenal crisis (paradoxical, but considered in shock).
— Sepsis: fever, tachycardia, AMS — distinguished by source, lactate, leukocytosis; remember stimulant users often have concurrent infection (endocarditis, abscess, pneumonia).
— Meningitis/encephalitis: fever + AMS + headache ± neck stiffness; LP if any uncertainty.
— CNS abscess in IVDU.
— Status epilepticus: post-ictal AMS, tachycardia, hyperthermia.
— Stroke / SAH: distinguished by focal deficits and imaging.
— Hypertensive emergency from other causes: renovascular HTN, cocaine just being one trigger.
— Acute MI without stimulant use in a young patient — consider familial hyperlipidemia, SCAD (especially in postpartum women), Kawasaki sequelae.
— Aortic dissection from Marfan, bicuspid valve.
— Acute mania — pressured speech, agitation, decreased sleep — but lacks hyperthermia and mydriasis severity; lithium/valproate use.
— Acute psychosis from schizophrenia — chronic course; harder to distinguish acutely from meth psychosis.
Board pearl: Pheochromocytoma vs cocaine intoxication — both present with paroxysmal HTN, headache, diaphoresis, palpitations. Cocaine is acute, witnessed, drug-screen positive, resolves within hours; pheochromocytoma is episodic over weeks–months, plasma/urine metanephrines elevated, MIBG or CT/MRI shows adrenal mass. Treatment of both initially overlaps — α-blockade first, never β-blockade alone.
— Brief motivational intervention in the ED — SBIRT (Screening, Brief Intervention, Referral to Treatment) has Level-A evidence.
— No FDA-approved pharmacotherapy for cocaine or methamphetamine use disorder.
— Evidence-supported behavioral interventions: contingency management (highest-evidence intervention for stimulant use disorder), cognitive behavioral therapy, matrix model, mutual-help groups (Cocaine Anonymous, Crystal Meth Anonymous).
— Investigational/off-label: bupropion + naltrexone combo, mirtazapine, topiramate — discuss with addiction medicine.
— Aspirin 81 mg daily indefinitely.
— High-intensity statin (atorvastatin 40–80 mg or rosuvastatin 20–40 mg).
— ACEi/ARB if reduced EF or HTN.
— β-blocker: avoid in active users; carvedilol is the preferred agent once abstinence is achieved (also some α-blockade).
— Dual antiplatelet for ACS/PCI per standard guidelines.
— Nitrates for ongoing angina from vasospasm.
— Counsel: continued cocaine use after MI confers >5× higher recurrent MI risk.
— Screen and treat HIV, HCV, HBV, syphilis in IVDU.
— Vaccinate: HBV, HAV, pneumococcal, influenza, COVID, Tdap.
— Naloxone prescription if opioid co-use.
— Sterile-injection supplies/needle exchange referral (harm reduction).
— Treat depression, anxiety, ADHD (cautiously — non-stimulant agents like atomoxetine preferred).
— Housing referral, food security, transportation.
— Legal/employment support; reentry programs.
— Family/partner counseling and child protective screening when indicated.
Step 3 management: Every stimulant-toxidrome patient gets SBIRT in the ED, referral to outpatient addiction services, harm-reduction counseling (including naloxone if any opioid contact), and screening for HIV/HCV/HBV/STI. Don't discharge without addressing all five — Step 3 explicitly tests the ambulatory transition piece.
— Within 24–72 hours: primary care or addiction-medicine visit; bridge benzodiazepine taper if alcohol co-use; review labs (rhabdo trend, troponin, LFTs).
— Within 1 week: cardiology if stimulant-associated MI or cardiomyopathy; repeat ECG and consider outpatient stress imaging.
— Within 2–4 weeks: outpatient echocardiogram if cardiomyopathy; comprehensive metabolic and renal panel if AKI.
— Within 1 month: psychiatry/addiction follow-up; behavioral therapy initiation.
— Cardiac: repeat TTE at 3–6 months if cardiomyopathy — abstinence often produces measurable EF improvement.
— Renal: serial creatinine and UA after rhabdomyolysis-AKI.
— Hepatic: LFTs at 1–2 weeks post-MDMA hepatitis.
— Mental health: PHQ-9, GAD-7, suicide risk reassessment at each visit; withdrawal "crash" peaks days 1–3, depression can persist weeks.
— Urine drug screens as part of contingency-management program (rewarding negative tests is the active therapeutic mechanism).
— Cardiovascular risk: cocaine increases MI risk 24×fold in first hour after use; abstinence drops risk.
— Drug interactions: avoid mixing with alcohol (cocaethylene), serotonergics (MDMA), opioids.
— Pregnancy planning and contraception.
— Driving safety, occupational safety.
— Recognize withdrawal symptoms: dysphoria, hypersomnia, hyperphagia, anhedonia, intense cravings; suicide risk elevated.
— Naloxone training if opioid co-use.
— Recognizing relapse, when to call 911.
— Al-Anon/Nar-Anon for family support.
CCS pearl: On a discharge CCS case, order PCP follow-up within 1 week, addiction-medicine follow-up within 2 weeks, cardiology follow-up within 1 week if MI, and a repeat TTE in 3–6 months for new cardiomyopathy. Add PHQ-9, naloxone Rx if any opioid risk, and HIV/HCV/HBV screening — these longitudinal orders consistently score.
— Acutely intoxicated patients lack capacity for refusal of life-saving care; document the specific capacity assessment (understanding, appreciation, reasoning, choice) and proceed under emergency doctrine if needed.
— Once sober, revisit consent for any non-emergent procedures and for substance-use treatment referral.
— Surrogate decision-makers if persistent incapacity.
— Suspected child abuse/neglect with stimulant use in a caregiver — mandated reporter in all 50 states.
— Elder/dependent-adult abuse: most states mandate reporting.
— Intimate partner violence: variable by state; document and offer resources regardless.
— Impaired driving: state-specific physician reporting laws — know your jurisdiction; some states require reporting to DMV.
— Pregnancy + substance use: some states classify as child abuse or require reporting; document and follow local law.
— Federal 42 CFR Part 2 protects substance-use treatment records — requires specific patient consent beyond standard HIPAA for disclosure.
— Workplace and law-enforcement requests for tox results require subpoena or written consent.
— High risk of relapse and overdose within 7 days of ED discharge.
— Always provide written discharge instructions, naloxone if any opioid risk, warm handoff to outpatient services, and a 24/7 crisis line.
— Do not discharge to an unsafe environment without social work involvement.
— Use least restrictive option; document indication, time-limited orders, monitoring.
— Avoid prone restraint (asphyxia deaths).
— "Excited delirium" diagnosis is increasingly controversial — focus on objective findings (hyperthermia, agitation, rhabdo) rather than the label.
Board pearl: A patient who refuses care while acutely intoxicated does not have decision-making capacity for that refusal. Treat under the emergency exception, document the capacity assessment, and revisit when sober. This is the single most testable ethics scenario in toxicology on Step 3.
Key distinction: β-blockers in stimulant cardiac disease — avoid acutely; consider carvedilol once abstinent for HF or post-MI. This nuance distinguishes the high-performer answer from the trap on Step 3.
— Best initial step: IV lorazepam + aspirin + nitroglycerin.
— Trap answer: IV metoprolol.
— Best step: Sodium bicarbonate 1–2 mEq/kg IV.
— Trap: amiodarone or procainamide.
— Best step: 3% hypertonic saline 100 mL bolus.
— Trap: normal saline alone or fluid restriction without correction.
— Answer: anticholinergic (consider TCA, antihistamine, jimsonweed).
— Trap: cocaine.
— Answer: placental abruption → continuous fetal monitoring, type and screen, OB consult.
— Answer: Whole-bowel irrigation with PEG; admit; surgery on standby.
— Trap: induce emesis or endoscopic retrieval.
— Answer: standard GDMT (ACEi, MRA, SGLT2i); carvedilol after abstinence; counsel that abstinence may reverse disease.
— Answer: stop SSRI, benzodiazepines, cyproheptadine, cooling.
— Trap: dantrolene or bromocriptine.
— Answer: benzodiazepines + active external cooling + IVF + intubation if refractory; not dantrolene.
— Answer: Lacks capacity; treat under emergency doctrine; document capacity assessment.
Step 3 management: When a stem hands you a stimulant-toxidrome vignette, always start with benzodiazepines, always avoid pure β-blockers acutely, and always add SBIRT/addiction referral and harm-reduction to the disposition plan. These three reflexes solve 80% of stem variations.
Sympathomimetic toxidrome from cocaine or amphetamines presents as a hot, fast, hypertensive, dilated, sweaty, agitated patient whose first-line treatment is aggressive benzodiazepines plus active cooling, with phentolamine/nitrates (not β-blockers) for persistent hypertension, sodium bicarbonate for cocaine-induced wide QRS, and mandatory SBIRT plus harm-reduction at discharge.
Board pearl: If a Step 3 stem hands you a young patient who is hot, fast, hypertensive, mydriatic, and wet, your first answer is almost always IV benzodiazepine, your second is active cooling and supportive care, and your disposition always includes addiction-medicine referral and harm-reduction counseling — get those three reflexes right and you will reliably score on this topic.