Eduovisual
Emergency & Toxicology
Heat stroke and heat exhaustion: management
— Heat exhaustion: core temp <40°C (104°F), intact mentation, volume/electrolyte depletion, profuse sweating, headache, nausea, myalgia.
— Heat stroke: core temp ≥40°C plus CNS dysfunction (confusion, ataxia, seizure, coma) — a true medical emergency with mortality 10–50% if cooling delayed.
— Classic (non-exertional): elderly, chronically ill, on anticholinergics/diuretics/antipsychotics, during heat waves; anhidrotic, slow onset over days.
— Exertional: young athletes, military recruits, laborers; often still sweating; rapid onset; high risk of rhabdomyolysis, DIC, AKI.
— Heat-wave vignette in an elderly nursing-home patient on a TCA or diuretic with altered mentation.
— High-school football player in August collapsing during practice with seizure.
— Marathon runner with tachycardia, confusion, T 41°C at mile 20.
Board pearl: The defining feature separating heat stroke from heat exhaustion is CNS dysfunction, not the presence or absence of sweating — exertional heat stroke patients are often still diaphoretic. Any altered mental status with hyperthermia in a hot environment = heat stroke until proven otherwise, and cooling must begin before the workup is complete.
— Elderly patient, urban heat wave, no air conditioning, found by family obtunded.
— Medications: thiazide, anticholinergic, antipsychotic, anti-Parkinsonian agent.
— Skin is hot and dry (anhidrosis), tachycardic, hypotensive, T 40.5–42°C.
— Onset over hours to days; often with concurrent dehydration and electrolyte derangement.
— Young athlete, military recruit, or laborer during prolonged exertion in heat/humidity.
— Wet bulb globe temperature (WBGT) typically high; protective gear (football pads, body armor) compounds heat retention.
— Often still sweating; sudden collapse, seizure, or "running through the wall."
— Rhabdomyolysis, DIC, hepatic injury, AKI develop rapidly.
— Headache, dizziness, nausea/vomiting, weakness, myalgia, orthostatic symptoms.
— Core temp 37–40°C with preserved mentation (may be irritable but oriented).
— Heavy sweating, tachycardia, orthostatic hypotension; resolves with rest, cooling, oral/IV fluids.
— Duration and intensity of heat exposure; access to AC/hydration.
— Medications (especially anticholinergics, diuretics, stimulants, SSRIs, MAOIs).
— Substance use (cocaine, methamphetamine, MDMA, alcohol).
— Prior heat illness (huge recurrence risk).
— Comorbidities: cardiac disease, diabetes, thyroid disease, skin disorders limiting sweating (scleroderma, cystic fibrosis, ectodermal dysplasia).
Key distinction: Anhidrosis is classic for non-exertional heat stroke but is not required — exertional heat stroke patients often present drenched in sweat. Do not let preserved sweating falsely reassure you when mental status is abnormal and core temperature is ≥40°C.
— Core temperature must be measured rectally (or esophageal/bladder probe) — oral, tympanic, axillary, and temporal readings are unreliable and falsely low in heat stroke.
— Tachycardia (often 130–160), tachypnea, hypotension (vasodilation + volume depletion), widened pulse pressure early; narrow pulse pressure and shock late.
— SpO₂ may be low from ARDS or aspiration.
— Spectrum: irritability → confusion → delirium → ataxia (cerebellum is exquisitely heat-sensitive) → seizure → coma.
— Pupillary changes, posturing, focal deficits possible — mimics stroke; do not skip glucose and consider CT head if focal findings.
— Persistent cerebellar dysfunction is a recognized long-term sequela.
— Classic: hot, dry, flushed, anhidrotic.
— Exertional: hot, diaphoretic.
— Look for needle marks (sympathomimetics), rashes (miliaria/heat rash), bullae over pressure points (suggest prolonged immobility).
— Hyperdynamic state initially; high cardiac output, low SVR — mimics distributive/septic shock.
— Crackles if developing ARDS or pulmonary edema from aggressive fluids.
— Tender hepatomegaly (heat hepatitis); dark "tea-colored" urine suggests rhabdomyolysis/myoglobinuria.
— Rigidity raises concern for NMS or serotonin syndrome (mimics).
— Muscle tenderness suggests rhabdomyolysis.
Step 3 management: In the ED, the first three actions in suspected heat stroke before any imaging or extensive labs: (1) rectal temperature, (2) ABCs with airway protection if GCS ≤8, (3) initiate active cooling immediately — the diagnostic workup runs in parallel, never before. Every minute above 40°C increases mortality; "cool first, transport/work up second" is the mantra.
— Rectal core temperature (continuous probe ideal).
— Fingerstick glucose (hypoglycemia mimics AMS).
— ECG: sinus tachycardia universal; look for QT prolongation, conduction abnormalities, ischemic changes, hyperkalemia peaked T waves (rhabdo).
— CBC — leukocytosis common; thrombocytopenia suggests DIC.
— BMP — hyperkalemia, hyponatremia/hypernatremia, AKI (elevated Cr/BUN).
— CK — often markedly elevated in exertional heat stroke; rhabdomyolysis risk.
— LFTs — AST/ALT often in the thousands within 24–48 h; severe transaminitis is a hallmark of heat stroke and a prognostic marker.
— Coags (PT/INR, aPTT, fibrinogen, D-dimer) — DIC is common and a leading cause of death.
— Lactate, ABG — metabolic acidosis (lactic + AKI); respiratory alkalosis early from hyperventilation.
— UA — myoglobinuria (dipstick heme-positive without RBCs on micro).
— Troponin — demand ischemia, myocardial injury possible.
— Calcium, phosphate, magnesium — derangements from rhabdo and AKI.
— CXR — baseline, evaluate for ARDS, aspiration.
— CT head — if focal deficits, persistent coma after cooling, or trauma suspected; usually normal initially.
— Continuous telemetry; arterial line if shock or repeated ABGs needed.
— Foley catheter for urine output and core temperature monitoring.
Board pearl: A heat-stroke patient with AST/ALT >1000, CK >10,000, INR >1.5, and platelets <100K within 24 hours has classic multi-organ heat injury and a substantially elevated mortality. The transaminitis peaks at 24–72 hours, so a "normal" initial LFT does not rule out hepatic injury — repeat at 24 h.
— Indicated when meningitis/encephalitis cannot be excluded (fever + AMS + nuchal rigidity or persistent AMS after cooling to <39°C).
— Empiric ceftriaxone + vancomycin + acyclovir should not be delayed if LP cannot be performed promptly.
— Urine drug screen (cocaine, amphetamines, MDMA, PCP).
— Acetaminophen, salicylate (salicylism causes hyperthermia + AMS + tachypnea).
— Consider serotonin syndrome (recent SSRI/MAOI/tramadol/linezolid) and NMS (antipsychotic exposure) — both can present with hyperthermia >40°C and AMS.
— CK every 6–12 h until trending down.
— LFTs, coags, BMP every 12–24 h for 2–3 days; hepatic failure may peak day 2–3.
Key distinction: NMS has rigidity + recent antipsychotic exposure and develops over days; serotonin syndrome has clonus, hyperreflexia, and recent serotonergic drug change over hours; malignant hyperthermia follows anesthesia (succinylcholine/volatile); heat stroke has environmental exposure and no rigidity. Drug history and timeline distinguish them — temperature alone cannot.
— (1) ABCs + IV access × 2 large bore.
— (2) Rapid active cooling to target <39°C (102°F) within 30 minutes — this is the single most important intervention.
— (3) Stop cooling at 38.5–39°C to avoid overshoot hypothermia.
— (4) Volume resuscitation, electrolyte correction, organ support.
— Cold water immersion (CWI) is gold standard — ice water tub (2–14°C), patient seated upright with head/neck out, cools at ~0.15–0.35°C/min. Mortality near zero if cooling-to-target <30 min.
— If CWI unavailable: tarp-assisted cooling, ice packs to neck/axillae/groin, cold IV saline (limited effect), wet sheets + fans.
— Evaporative cooling preferred (tepid water mist + high-velocity fans) — better tolerated; CWI can precipitate arrhythmia or shivering in frail elderly.
— Ice packs to neck, axillae, groin as adjunct.
— Antipyretics (acetaminophen, NSAIDs, aspirin) — ineffective in heat stroke (hypothalamic set point is not elevated) and may worsen hepatotoxicity, AKI, coagulopathy.
— Alcohol baths (toxicity).
— Increases heat production; treat with benzodiazepines (lorazepam, midazolam) or low-dose meperidine; avoid phenothiazines (lower seizure threshold, anticholinergic).
— Crystalloid (NS or LR) 1–2 L bolus, then titrate to urine output 1–2 mL/kg/h; avoid overload — heat stroke patients are often less volume-depleted than they appear and develop ARDS easily.
CCS pearl: Order "ice water immersion" or "evaporative cooling with mist and fans" as the first intervention after IV access — before labs result. On CCS, advancing the clock without active cooling in a heat-stroke case is the classic dock-points trap.
— Acetaminophen: ineffective (no hypothalamic set point elevation), worsens hepatotoxicity.
— NSAIDs/aspirin: worsen AKI, GI bleeding, platelet dysfunction in setting of DIC.
— Benzodiazepines — lorazepam 1–2 mg IV or midazolam 2–5 mg IV; first-line, also treats agitation and seizures.
— Meperidine 25–50 mg IV — effective antishivering but accumulates with renal dysfunction; use cautiously.
— Lorazepam 2–4 mg IV, repeat as needed; load levetiracetam or fosphenytoin if status.
— Cool aggressively — most seizures resolve with temperature reduction.
— Benzodiazepines preferred.
— Avoid antipsychotics (haloperidol, olanzapine) — anticholinergic, impair sweating, lower seizure threshold, prolong QT.
— Crystalloid resuscitation first; if persistent after 30 mL/kg and core temp <39°C, start norepinephrine.
— Avoid pure α-agonists (phenylephrine) — vasoconstriction impairs cutaneous heat dissipation.
— Aggressive IV crystalloid to target urine output 200–300 mL/h.
— Monitor K+, Ca²⁺, phosphate; treat hyperkalemia (calcium gluconate, insulin/dextrose, kayexalate/lokelma).
— Urinary alkalinization with bicarbonate is not routinely recommended (no mortality benefit; data weak).
— Transfuse FFP, platelets, cryoprecipitate for active bleeding or invasive procedures.
— Vitamin K if INR elevated and hepatic synthetic dysfunction.
— Effective in malignant hyperthermia but not recommended in heat stroke (no benefit in trials).
Board pearl: If a vignette offers acetaminophen, ibuprofen, or dantrolene for heat stroke — all wrong. The right answer is cooling, and the right "drug" is a benzodiazepine for shivering/seizures.
— Tub of 2–14°C water; patient submerged to neck.
— Continuous rectal temperature monitoring; stop at 38.5–39°C.
— Cooling rate ~0.15–0.35°C/min; can normalize a 41°C patient in <15 min.
— On-site cooling at sporting events before transport ("cool first, transport second") improves survival.
— Strip patient, spray tepid (not cold) water on skin, direct high-velocity fans across body.
— Place ice packs at neck, axillae, groin.
— Cooling rate slower (~0.05–0.1°C/min) but better tolerated; less shivering and arrhythmia risk.
— Cold (4°C) IV crystalloid — modest effect, useful adjunct.
— Cooling blankets — slow alone; useful for maintenance after primary cooling.
— Wet sheets + fans — field-expedient when CWI unavailable.
— Endovascular cooling catheters (e.g., femoral cooling catheter) — ICU setting.
— Cold gastric/bladder/rectal/peritoneal lavage — used when external methods fail.
— ECMO/CRRT with cooled dialysate — last resort in refractory hyperthermia with multi-organ failure.
— Intubate for GCS ≤8, status epilepticus, ARDS, or aspiration.
— Lung-protective ventilation if ARDS develops.
— Indicated for refractory hyperkalemia, severe acidosis, oliguric AKI with volume overload, or uremia.
CCS pearl: On a CCS case of exertional heat stroke at a football game, the highest-value early order is "ice water immersion on site" rather than immediate ambulance transport — survival data favor on-field cooling to <39°C before evacuation. Document the rectal temperature before and after cooling.
— Impaired thermoregulation: reduced sweat response, blunted thirst, decreased cardiovascular reserve.
— Polypharmacy: diuretics (volume depletion), anticholinergics (impair sweating), β-blockers (blunt cardiac response), antipsychotics, TCAs.
— Comorbidities: CHF, COPD, dementia (can't escape hot environment), Parkinson disease.
— Higher mortality (up to 50% in heat waves); presents with stroke-mimic picture.
— Cooling: evaporative method preferred — CWI may precipitate arrhythmia, MI, or shock in frail elderly.
— Fluid resuscitation: more conservative; CHF patients tolerate <30 mL/kg poorly — give 250–500 mL aliquots, reassess.
— Baseline reduced ability to excrete potassium and handle volume swings.
— Higher risk of severe hyperkalemia with rhabdomyolysis.
— NSAIDs and contrast contraindicated; minimize nephrotoxins.
— Earlier nephrology consultation and lower threshold for RRT.
— Dose-adjust meperidine (avoid if GFR <30), avoid magnesium in severe CKD.
— Heat stroke causes hepatocellular injury (AST/ALT in thousands); pre-existing cirrhosis amplifies risk of fulminant failure.
— Coagulopathy worsens DIC risk.
— Avoid acetaminophen entirely; lactulose if encephalopathy.
— Hepatology consult; transplant evaluation if INR >6.5 or grade III/IV encephalopathy (King's College–style criteria for acute liver failure).
— Heat stress + aggressive fluids → pulmonary edema.
— Use bedside ultrasound (IVC, B-lines) and continuous SpO₂; consider invasive monitoring.
Step 3 management: In an elderly heat-wave patient on a thiazide and donepezil, the highest-yield interventions are (1) evaporative cooling, (2) cautious crystalloid 250–500 mL aliquots with reassessment, (3) hold the offending medications, (4) admit for telemetry — these patients deteriorate after the ED.
— Maternal hyperthermia >39°C in first trimester associated with neural tube defects, fetal demise.
— Heat stroke causes uteroplacental insufficiency, fetal distress, placental abruption, preterm labor.
— Management: same cooling principles; left lateral tilt to relieve IVC compression; continuous fetal monitoring if viable gestation.
— Avoid NSAIDs (always), and acetaminophen is still ineffective for heat stroke.
— OB and NICU on standby.
— Infants and young children: high surface-area-to-mass ratio, immature sweating, dependence on caregivers.
— Vehicular hyperthermia — car interiors reach >50°C in minutes; mandatory reporting in many states; child welfare consultation.
— Cooling: evaporative + ice packs; immersion in cold water acceptable if size permits; weight-based fluid resuscitation (20 mL/kg boluses).
— Watch for hypoglycemia (limited glycogen stores).
— Exertional heat stroke peaks August practices in football, military basic training.
— Sickle cell trait — increased risk of exertional rhabdomyolysis, sudden death; NCAA mandates screening.
— Acclimatization protocols (gradual exposure over 10–14 days) prevent most cases.
— Return to play requires medical clearance, asymptomatic exertional heat tolerance test; typically 7+ days minimum; some never return safely.
— Hydration, shade, rest cycles per WBGT; mandatory reporting of serious occupational illness.
— Workers' compensation implications.
Board pearl: A football player with sickle cell trait collapsing in early-season practice with hyperthermia, dark urine, and severe muscle pain has exertional rhabdomyolysis — aggressive cooling, IV fluids to UOP 200–300 mL/h, electrolyte monitoring, and ICU admission. Sickle trait + exertion + heat = high mortality.
— Seizures, coma, cerebellar dysfunction (ataxia, dysarthria — often persistent), cerebral edema.
— Long-term cognitive impairment in 20–30% of survivors of severe heat stroke.
— High-output state → distributive shock → cardiogenic shock if myocardial injury.
— Arrhythmias (AF, VT), demand ischemia, troponin elevation.
— Stress cardiomyopathy.
— AKI in 25–30% of heat stroke patients — multifactorial: prerenal, ATN from rhabdomyolysis, direct heat injury.
— Hyperkalemia, hyperphosphatemia, hypocalcemia (rhabdo).
— Hepatocellular injury universal in severe heat stroke; transaminases peak 24–72 h.
— Acute liver failure (5–10% of severe cases) — coagulopathy, encephalopathy, hyperammonemia; some require transplant.
— DIC — major cause of mortality; thrombocytopenia, prolonged PT/PTT, elevated D-dimer, low fibrinogen.
— Petechiae, GI bleeding, oozing from venipuncture sites.
— ARDS, aspiration pneumonia (post-seizure or coma), pulmonary edema (fluid overload).
— Rhabdomyolysis (especially exertional) — CK often >50,000 in severe cases.
— Compartment syndrome if prolonged immobility.
— Endotoxin translocation across heat-injured gut → SIRS amplification.
— Mesenteric ischemia, stress ulcers, hepatic injury.
— SIADH or DI; hypoglycemia (hepatic failure); adrenal stress response.
— Peak temperature ≥42°C; duration of hyperthermia >2 h before cooling; coma on arrival; AST >1000 at 24 h; AKI requiring RRT; DIC; advanced age.
Key distinction: AKI in classic heat stroke is usually prerenal/ischemic; AKI in exertional heat stroke is dominated by myoglobinuric ATN from rhabdomyolysis. Both require aggressive fluids, but the latter mandates serial CK and urine output targets of 200–300 mL/h.
— Core temp ≥40°C with CNS dysfunction — admit to ICU regardless of apparent improvement after cooling.
— Hemodynamic instability requiring vasopressors.
— Respiratory failure, ARDS, intubation.
— Seizures, coma, persistent AMS.
— Severe rhabdomyolysis (CK >5,000–10,000), AKI, hyperkalemia.
— DIC or significant coagulopathy.
— Transaminases >3× ULN (rising).
— Nephrology — AKI, rhabdomyolysis, RRT planning.
— Hepatology — transaminases >1000 or coagulopathy; transplant center referral if INR rising or encephalopathy.
— Hematology — DIC management.
— Neurology — persistent AMS, seizures, suspected non-convulsive status.
— Cardiology — troponin elevation, arrhythmia, stress cardiomyopathy.
— OB/GYN — pregnant patients.
— Toxicology / Poison Control — if mimic (NMS, serotonin syndrome, stimulants) cannot be excluded.
— Observation 2–4 h with oral or IV fluids; discharge when symptoms resolve, orthostatic VS normalized, electrolytes corrected.
— Discharge education: hydration, environment modification, return precautions.
— Reliable transport home, AC access, social support assessment.
— Tertiary care center for liver transplant evaluation, ECMO, advanced cooling.
— Stabilize and cool before transport — never transport a hyperthermic patient without active cooling en route.
CCS pearl: Even if the patient's temperature normalizes and mental status clears in the ED, admit heat stroke to the ICU for at least 24–48 h — DIC, hepatic failure, and AKI peak after initial recovery. Discharging from the ED is a CCS error.
— Recent antipsychotic exposure (haloperidol, risperidone, olanzapine) or dopamine withdrawal (Parkinson meds stopped).
— Develops over days; "lead-pipe" rigidity, hyperthermia, autonomic instability, AMS.
— Markedly elevated CK; treat with dantrolene, bromocriptine, supportive care.
— Recent serotonergic drug change (SSRI, SNRI, MAOI, tramadol, linezolid, MDMA, triptan).
— Onset within hours; clonus, hyperreflexia, tremor (lower extremities prominent), agitation, hyperthermia.
— Treat by stopping offending agent; cyproheptadine; benzodiazepines.
— Triggered by succinylcholine or volatile anesthetics (halothane, sevoflurane).
— Hyperthermia, masseter rigidity, hypercapnia, acidosis, hyperkalemia, rhabdomyolysis.
— Treat with dantrolene 2.5 mg/kg IV, stop trigger, cool aggressively.
— Hyperthermia, tachycardia, AMS, often with goiter or Graves disease history.
— Treat with propranolol, PTU/methimazole, iodine (Lugol/SSKI) after thionamide, hydrocortisone, cooling.
— "Hot as a hare, dry as a bone, red as a beet, mad as a hatter, blind as a bat."
— Mydriasis, urinary retention, tachycardia, AMS; antidote physostigmine in select cases.
— Cocaine, methamphetamine, MDMA — hyperthermia, hypertension, tachycardia, agitation, diaphoresis.
— Benzodiazepines first-line; avoid β-blockers (unopposed α).
— Hyperthermia, tachypnea, mixed acid-base (respiratory alkalosis + anion gap acidosis), tinnitus.
— Alkalinize urine; hemodialysis if severe.
Key distinction: Timeline and drug exposure history distinguish these syndromes — heat stroke has environmental exposure, no rigidity, no clonus, and no antipsychotic/serotonergic/anesthetic trigger. Ask about every medication change and substance in the last 72 hours.
— Fever, AMS, tachycardia, hypotension, leukocytosis — clinically near-identical early.
— Often coexists with heat stroke (gut translocation, aspiration pneumonia).
— Empiric broad-spectrum antibiotics if source uncertain or patient not improving with cooling alone.
— Lactate, blood cultures, procalcitonin (limited utility).
— Fever, AMS, headache, nuchal rigidity, photophobia.
— LP if meningismus or AMS persists after cooling; empiric ceftriaxone + vancomycin + acyclovir.
— Focal deficits, AMS — overlap with heat stroke (cerebellar findings).
— Non-contrast CT head if focal exam or trauma history.
— Hyperthermia from sustained motor activity; postictal AMS.
— EEG if subtle; benzodiazepines + antiepileptics.
— Dehydration, AMS, tachycardia — check glucose immediately; HHS especially in elderly heat-wave patients.
— Always check fingerstick glucose in any AMS patient.
— Hypotension, hyponatremia, hyperkalemia, fatigue; consider in known Addison or chronic steroid use.
— Episodic hypertension, headache, diaphoresis, tachycardia.
— Alcohol or benzodiazepine withdrawal — hyperthermia, AMS, autonomic hyperactivity, seizures.
— Benzodiazepines are first-line.
Board pearl: When a heat-wave vignette describes an elderly patient with hyperthermia + AMS, the test-writer almost always wants heat stroke, but simultaneously work up sepsis — empiric antibiotics are reasonable until cultures and clinical course clarify. Missing concurrent infection is a common real-world error.
— Verify resolution of symptoms, normal mental status, normal orthostatic vital signs, corrected electrolytes.
— Oral hydration with electrolyte solutions (sports drinks, oral rehydration salts) — not plain water alone (hyponatremia risk).
— 24–48 h rest in cool environment before resuming activity.
— Return precautions: fever, persistent vomiting, confusion, dark urine, decreased urination.
— Discharge typically after 3–7 days inpatient (depending on organ recovery).
— Medication reconciliation — discontinue or substitute anticholinergics, high-dose diuretics, antipsychotics where feasible; counsel on heat risk with remaining agents.
— Counseling on lifelong increased susceptibility to recurrent heat illness in many patients.
— Asymptomatic for 7+ days minimum.
— Normal labs (CK, LFTs, renal function).
— Gradual reintroduction of exercise in cool environment over 1–2 weeks, then heat reacclimatization over additional 2 weeks.
— Some authorities recommend heat tolerance testing before unrestricted return.
— Document clearance from sports medicine specialist.
— Hydration before/during/after heat exposure; pre-hydration with cool fluids.
— Acclimatization (10–14 days of gradually increasing heat exposure).
— Avoid alcohol and stimulants in heat.
— Light, loose, light-colored clothing; wide-brimmed hats.
— Schedule outdoor activities for early morning/evening.
— Air conditioning access (cooling centers in heat waves) — public health intervention.
— Heat-wave check-ins for elderly, homeless, mentally ill.
— Medication review at annual visits in summer months.
Step 3 management: At the post-discharge follow-up after heat stroke (within 1–2 weeks), perform a complete medication review, recheck LFTs/BMP/CK, screen for cognitive sequelae, and provide written heat-avoidance counseling — this is the ambulatory transition-of-care visit Step 3 loves to test.
— Continuous core temperature for first 24 h.
— Serial CK every 6–12 h until clearly downtrending.
— Daily BMP, LFTs, coags for 3–5 days; LFTs peak at 48–72 h.
— Urine output 1–2 mL/kg/h goal (200–300 mL/h in rhabdomyolysis).
— Daily weights, fluid balance.
— Neuro checks every 2–4 h.
— BMP, LFTs, CK, CBC, coags.
— Most resolve within 2–4 weeks; persistent elevation warrants subspecialty referral.
— Primary care visit at 1–2 weeks.
— Repeat labs at 2 weeks and 4 weeks if abnormal at discharge.
— Neuropsychiatric evaluation if cognitive concerns persist beyond 4 weeks.
— Cardiology follow-up if troponin elevation or stress cardiomyopathy.
— Hepatology if persistent transaminitis.
— Physical therapy for deconditioning, especially after prolonged ICU stay.
— Speech and cognitive rehabilitation for cerebellar or cortical dysfunction.
— Occupational therapy if ADL impairment.
— Cerebellar ataxia, cognitive dysfunction, peripheral neuropathy.
— CKD progression after AKI.
— Recurrent heat intolerance — counsel on lifestyle modification.
— Risk of recurrence is elevated; some patients permanently lose thermoregulatory reserve.
— Avoid concomitant nephrotoxins, anticholinergics if possible.
— Identify cooling centers, hotline numbers, and family check-in plans before next heat season.
— Heat-related deaths reportable to local health departments in many jurisdictions; vehicular hyperthermia in children mandatorily reported to child protective services.
Board pearl: Persistent cerebellar ataxia at the 1-month follow-up after heat stroke is a recognized permanent sequela — refer to neurology, document baseline cognition, and counsel the patient and family on driving and occupational implications.
— Mandatory reporting to child protective services in essentially all US states when a child is left in a hot vehicle, regardless of caregiver intent.
— Document objective findings, exposure timeline, caregiver statements verbatim; involve social work early.
— Coroner notification required for fatal cases.
— Heat-wave deaths in elderly often reflect social isolation, inadequate caregiving, or inability to access cooling.
— Adult Protective Services referral if neglect suspected (mandatory reporters in most states: physicians, nurses, social workers).
— OSHA-reportable for hospitalization or death; workers' compensation coverage.
— Employer obligation to provide water, rest, shade per OSHA recommendations.
— Document occupational exposure history carefully.
— Pre-participation screening including sickle cell trait, prior heat illness.
— Mandated cooling resources (immersion tub) at high-risk practices in many state high school athletic associations.
— Documentation of WBGT and modifications.
— Heat stroke patients are typically encephalopathic and cannot consent — proceed under emergency doctrine (implied consent) for life-saving cooling and resuscitation.
— Identify surrogate decision-maker as soon as practicable.
— For invasive procedures (intubation, central line, RRT initiation), document surrogate consent or emergency exception.
— Heat stroke patients deteriorate 24–72 h after initial cooling (DIC, hepatic failure, AKI).
— ED-to-ICU handoff: communicate cooling timeline, peak temp, organ injury trajectory, hold list.
— ICU-to-floor handoff: ensure recurrent lab monitoring continues; deterioration after step-down is a recognized safety event.
— Heat mortality disproportionately affects low-income, elderly, urban-heat-island, and homeless populations — connect to cooling centers and social work.
Step 3 management: On a vignette of a toddler found unresponsive in a parked car at 105°F, the answer set includes (1) immediate cooling and resuscitation, (2) mandatory CPS report, (3) social work consult, and (4) coroner notification if death — all four are expected, not just the medical management.
— Heat exhaustion: <40°C with intact mentation.
— Heat stroke: ≥40°C with CNS dysfunction.
— Cooling target: <39°C within 30 min.
— Stop cooling at 38.5–39°C to avoid overshoot.
— AST/ALT often >1000; peak at 24–72 h.
— CK >10,000 in exertional rhabdo.
— DIC: ↓ platelets, ↑ INR/PTT, ↓ fibrinogen, ↑ D-dimer.
— AKI in 25–30%.
— Hours after serotonergic drug → serotonin syndrome.
— Days after antipsychotic → NMS.
— Minutes after anesthesia → malignant hyperthermia.
— Environmental exposure → heat stroke.
Board pearl: When in doubt, the right answer is "cool now, work up in parallel" — every Step 3 heat-stroke question rewards the management option that starts cooling before completing the diagnostic workup.
— 17-year-old football player collapses at August practice, rectal T 41.2°C, GCS 10, still sweating. Best next step?
— Answer: Cold water immersion immediately.
— Distractor traps: CT head first, acetaminophen, ceftriaxone, dantrolene.
— 82-year-old found in non-AC apartment during heat wave, T 40.8°C, confused, hot dry skin, on HCTZ and oxybutynin. Best next step?
— Answer: Evaporative cooling with mist and fans + ice packs.
— Distractor: cold water immersion (riskier in frail elderly).
— Patient on fluoxetine started on tramadol 6 hours ago, now agitated with clonus, hyperreflexia, T 39.8°C.
— Answer: Serotonin syndrome — stop drugs, benzodiazepines, cyproheptadine.
— Distractor: heat stroke (no environmental exposure, no rigidity, recent serotonergic drug = serotonin syndrome).
— Marathon runner with T 41°C, dark urine, CK 45,000. Best next step?
— Answer: Cooling + aggressive IV crystalloid to urine output 200–300 mL/h.
— Distractor: urinary alkalinization with bicarbonate (not routinely indicated).
— Heat exhaustion patient improved after 2 L NS. Best discharge advice?
— Answer: Oral electrolyte solution, cool environment, 24–48 h rest, return precautions.
— Distractor: plain water only (risks hyponatremia).
— Toddler found in car, T 42°C, unresponsive. Required actions?
— Answer: Cooling + resuscitation + CPS report + social work.
— Football player 5 days post heat stroke wants to return.
— Answer: Defer ≥7 days asymptomatic + normal labs + graded reintroduction + sports medicine clearance.
— Heat stroke patient — acetaminophen vs cooling?
— Answer: Cooling. Acetaminophen is ineffective.
Key distinction: The recurring Step 3 pattern is management sequencing: cooling before workup, fluids before vasopressors, benzodiazepines before antipsychotics, and admission to ICU even when the patient looks better in the ED.
Heat stroke is hyperthermia ≥40°C with CNS dysfunction in the setting of heat exposure, and the only intervention that changes mortality is rapid active cooling to <39°C within 30 minutes — every other action is supportive.