Last reviewed: March 2026
Contents
MDM Templates
Heat Stroke
Patient presents with elevated core temperature and CNS dysfunction (altered mental status, confusion, seizure, or coma) in the setting of environmental heat exposure or exertional activity. Tachycardic, diaphoretic or anhidrotic, hemodynamically unstable.
Presentation consistent with heat stroke — core temperature >40°C with CNS dysfunction. This is a true medical emergency with mortality approaching 10-50% if cooling is delayed. Not consistent with primary CNS event (stroke, meningitis) as the precipitant given clinical context, though these must remain on the differential. Not consistent with endocrine emergency (thyroid storm, adrenal crisis) or toxicologic hyperthermia (NMS, serotonin syndrome, sympathomimetic toxicity) based on history and medication review.[1]
Plan: Aggressive cooling with goal temperature <38°C within 30-60 minutes. Refrigerated crystalloid resuscitation, evaporative cooling (mist with lukewarm water plus fans). Benzodiazepines for shivering or seizure. No antipyretics (hyperthermia is not hypothalamus-mediated). Admit to ICU. Monitor for rhabdomyolysis, DIC, hepatic failure, and renal failure.
If refractory to standard cooling after 45-60 minutes: Consider ECMO for temperature management. Intubation with removal of heat-moisture exchanger and disabling gas warming. Avoid vasopressors if possible (peripheral vasoconstriction impairs heat dissipation).
Heat Exhaustion / Minor Heat Illness
Patient presents with symptoms of heat-related illness after environmental exposure or exertion — nausea, headache, dizziness, muscle cramps, fatigue, diaphoresis. Core temperature elevated but <40°C. No CNS dysfunction, no altered mental status.
Presentation consistent with heat exhaustion from volume and salt depletion. The critical distinction from heat stroke is preserved mental status — any CNS dysfunction (confusion, ataxia, seizure) upgrades the diagnosis to heat stroke regardless of temperature. Not consistent with heat stroke (intact mentation), cardiac event, or metabolic derangement.[1]
Plan: Remove from heat, passive cooling, oral or IV rehydration with normal saline. Rest and observation. Once symptoms resolve and tolerating oral intake, discharge with heat avoidance counseling. Return for confusion, persistent vomiting, syncope, or recurrent symptoms.
Environmental Hypothermia
Patient presents with decreased core temperature after environmental cold exposure. Core temperature ***°C. Mental status ranges from alert (mild) to confused/obtunded (moderate-severe). No obvious non-environmental cause identified.
Presentation consistent with environmental hypothermia. Severity classification: mild (32-35°C, shivering, tachycardic), moderate (28-32°C, confusion, loss of shivering, bradycardia), severe (<28°C, obtunded, arrhythmia risk, cardiac arrest). Must also consider non-environmental causes if temperature is >32°C and patient fails to passively rewarm at ≥1°C/hour: hypoglycemia, hypothyroidism, adrenal insufficiency, sepsis, alcohol intoxication, or malnutrition.[2]
Plan: Active rewarming appropriate to severity. Warm IV crystalloid. Continuous cardiac monitoring (arrhythmia risk increases below 32°C). Admit for moderate-severe hypothermia. Discharge mild hypothermia if rewarming to normothermia and no underlying precipitant identified.
Hypothermic Cardiac Arrest
Patient in cardiac arrest with core temperature ***°C. Resuscitation initiated with attention to the physiology of hypothermic arrest.
Hypothermic cardiac arrest requires aggressive rewarming concurrent with ACLS. Defibrillation and medications are less effective below 30°C. Cannot prognosticate until the patient has been rewarmed — “not dead until warm and dead.” Potassium >10 mEq/L is the only reliable marker of non-survivability in hypothermic arrest.[2]
Plan: Standard ACLS with concurrent active rewarming. Limit defibrillation attempts to 3 until core temp >30°C. Warm IV fluids, heated humidified oxygen, consider thoracic lavage or ECMO (fastest rewarming at 9-18°C/hr). Continue resuscitation until rewarmed to ≥32°C. If potassium >10, termination of resuscitation is reasonable.
Clinical Education
Heat Illness Spectrum
| Syndrome | Features | Treatment |
| Heat cramps | Painful muscle spasms from salt depletion, normal temp | Oral salt replacement, rest |
| Heat syncope | Syncope from peripheral vasodilation and decreased venous return | Supine positioning, rehydration |
| Heat exhaustion | Volume/salt depletion, temp <40°C, intact mentation | Cooling, IV/PO rehydration |
| Heat stroke | Temp >40°C + CNS dysfunction (AMS, seizure, coma) | Aggressive cooling, ICU |
The defining feature of heat stroke is CNS dysfunction, not a specific temperature threshold. A confused patient at 39.5°C is more concerning than an alert patient at 40.5°C. Any altered mental status in the setting of heat exposure should be treated as heat stroke.[1]
Cooling Methods
Goal: core temperature <38°C within 30-60 minutes. Every minute of delay in cooling increases mortality. Cooling is the single most important intervention in heat stroke — it takes priority over everything except airway management.[1]
Refrigerated crystalloid: 1 L of cold IV fluid drops core temperature approximately 1°C. Rapid, effective, and simultaneously treats volume depletion.
Evaporative cooling: Mist or dampen the patient with lukewarm (not ice cold) water and direct fans over the body. Lukewarm water evaporates more effectively and avoids triggering shivering. Expected cooling rate ~0.1°C/min. This is the most accessible and effective surface cooling method.
Ice packs to groin, axillae, neck: Conductive cooling. Less effective than evaporative cooling and risks cold burns. Use as adjunct, not primary method.
No antipyretics. Hyperthermia is not mediated by the hypothalamic set point (unlike fever). Acetaminophen and NSAIDs are useless and potentially hepato/nephrotoxic in a patient already at risk for organ failure.
Anti-shivering: Shivering generates heat and counteracts cooling. Benzodiazepines first, then consider propofol or ketamine if intubated. Avoid meperidine (lowers seizure threshold).
Toxicologic Hyperthermia
Three toxicologic syndromes cause dangerous hyperthermia and must be distinguished from environmental heat stroke:
| Syndrome | Key Features | Treatment |
| NMS | Lead-pipe rigidity (generalized), bradykinesia, antipsychotic use, develops over days | Benzos aggressively, consider bromocriptine, dantrolene. Paralysis if refractory rigidity |
| Serotonin syndrome | Clonus (lower > upper), hyperreflexia, agitation, serotonergic drug, develops over hours | Benzos, cyproheptadine 12 mg PO/NG then 4 mg q4h |
| Malignant hyperthermia | Intraoperative, volatile anesthetics/succinylcholine, masseter rigidity | Dantrolene 2.5 mg/kg IV, stop triggering agent |
NMS vs serotonin syndrome: Both cause hyperthermia with rigidity. NMS has generalized lead-pipe rigidity with bradykinesia (slow onset over days). Serotonin syndrome has lower extremity clonus and hyperreflexia with preserved upper extremity tone (rapid onset over hours). NMS is from dopamine blockade (antipsychotics); serotonin syndrome is from serotonin excess (SSRIs, MAOIs, tramadol, linezolid).[3]
In NMS, the goal is breaking the rigidity cycle. Benzodiazepines aggressively. If refractory, consider high-dose phenobarbital load (10-20 mg/kg) or a single dose of a neuromuscular blocker (vecuronium) in consultation with toxicology and ICU.
Hypothermia Pearls
| Severity | Temp | Features |
| Mild | 32-35°C | Shivering, tachycardia, vasoconstriction, intact mentation |
| Moderate | 28-32°C | Loss of shivering, confusion, bradycardia, atrial fibrillation |
| Severe | <28°C | Obtunded, VF risk, fixed dilated pupils, appears dead |
If temperature is >32°C and the patient fails to passively rewarm at least 1°C/hour, suspect a non-environmental cause: hypoglycemia, hypothyroidism (myxedema coma), adrenal insufficiency, sepsis, alcohol intoxication, or malnutrition.[2]
Osborn (J) waves on ECG are characteristic of hypothermia — positive deflection at the J point, most prominent in inferior and lateral leads. They are a marker of severity but not specific to hypothermia.
Handle hypothermic patients gently. The cold myocardium is highly irritable. Rough handling, jostling, or central line placement can trigger ventricular fibrillation. Minimize unnecessary stimulation.
Rewarming Methods
| Method | Rate |
| Shivering (endogenous) | ~1.5°C/hr |
| Forced-air warming blanket (Bair Hugger) | ~2°C/hr |
| Heated humidified oxygen (mask) | ~1°C/hr |
| Heated humidified oxygen (ETT) | ~1.5°C/hr |
| Warm IV fluids (40-42°C) | Prevents further cooling, minimal active warming |
| ECMO | 9-18°C/hr |
ECMO is the gold standard for severe hypothermia and hypothermic cardiac arrest when available. It provides rapid rewarming and hemodynamic support simultaneously. Thoracic lavage (warm saline via bilateral chest tubes) is an alternative when ECMO is not available.[2]
Afterdrop: Core temperature may transiently decrease during rewarming as cold peripheral blood returns to the central circulation. This is expected and does not indicate treatment failure. It can trigger arrhythmias — monitor closely during initial rewarming.
Disposition
Hyperthermia — Discharge: Minor heat illness (cramps, syncope, mild exhaustion) that resolves with cooling and rehydration. Normal mental status throughout. No end-organ dysfunction. Return for confusion, persistent vomiting, dark urine, or recurrent symptoms.
Hyperthermia — Admit (ICU): Heat stroke (any CNS dysfunction). Rhabdomyolysis. DIC or hepatic failure. Refractory hyperthermia. NMS or serotonin syndrome with significant hyperthermia.
Hypothermia — Discharge: Mild hypothermia that rewarms to normothermia with passive measures. No underlying precipitant requiring admission. Safe discharge environment.
Hypothermia — Admit: Moderate or severe hypothermia. Failure to passively rewarm (concern for underlying cause). Arrhythmia. Cardiac arrest (ICU). Significant comorbidities or unsafe living situation.
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