Heat Stroke

GENERAL PRINCIPLES

• Heat stroke occurs in two varieties: classic and exertional. Both are present with high core temperatures that result in direct thermal tissue injury. Secondary effects include acute renal failure from rhabdomyolysis.

• The cardinal features of heat stroke are hyperthermia (gt;40°C [104°F]) and altered mental status. Although patients presenting with classic heat stroke may have anhidrosis, this is not considered a diagnostic criterion because 50% of patients are still diaphoretic at presentation.

• The CNS is very vulnerable to heat stroke with the cerebellum being highly sensitive. Ataxia may be an early sign. Seizures are common. Neurologic injury is a function of maximum temperature and duration of exposure.⁶

DIAGNOSIS

Diagnosis is based on the history of exposure or exercise, a core temperature usually of 40.6°C (105°F) or higher, and changes in mental status ranging from confusion to delirium and coma.

Differential Diagnosis

• Drug associated

î Toxicity

#9632; Anticholinergic

#9632; Stimulant toxicity

#9632; Salicylate toxicity

î Neuroleptic malignant syndrome (NMS) is associated with antipsychotic drugs. It is worth noting that NMS and malignant hyperthermia are both accompanied by severe muscle rigidity.

î Serotonin syndrome

î Malignant hyperthermia

î Drug withdrawal syndrome (ethanol withdrawal)

î Drug fever

• Infections

î Generalized infections (sepsis, malaria, etc.)

î CNS infections (meningitis, encephalitis, brain abscess)

• Endocrine

î Thyroid storm

î Pheochromocytoma

• Hypothalamic dysfunction due to stroke or hemorrhage

î Status epilepticus

î Cerebral hemorrhage⁷

Diagnostic Testing

LABORATORIES

• Laboratory studies should be directed toward identifying potential end organ damage or other underlying etiology and may include complete blood count (CBC); partial thromboplastin time; prothrombin time; electrolytes; blood urea nitrogen (BUN); creatinine, glucose, calcium, and creatine kinase levels; liver function tests (LFTs); and urinalysis.

• If an infectious etiology is suspected, obtain appropriate cultures.

• If there is a concern for cardiac ischemia, obtain an ECG and troponin.

IMAGING

If a CNS etiology is considered likely, CT imaging followed by spinal fluid examination is appropriate.

TREATMENT

• If the patient is obtunded or hemodynamically unstable, acute life support measures should be initiated, such as intubation or central venous access.

• Immediate cooling should be started within 30 minutes of illness recognition.⁷

î For most young, athletic, or otherwise healthy patients, cold water immersion therapy is considered the most efficient cooling method in both the field and hospital settings.⁸ Ideally, this consists of immersing the patient up to the neck in a slurry of ice and water but may be impractical in many settings and can interfere in other resuscitative efforts.

î Evaporative measures are also very effective and often more feasible. In this case, remove the patient's clothing to achieve maximum body surface exposure. Mist the patient continuously with tepid water (20-25°C [68-77°F]) and cool the patient with a large electric fan.

î Ice packs should be placed at points of major heat transfer, such as the groin, axillae, and chest, to further speed cooling, but there is no evidence to suggest they be used as a primary cooling method.

î Neither antipyretics nor dantrolene sodium are indicated.⁸

• Monitor core temperatures continuously by rectal probe or Foley catheter. Oral and tympanic membrane temperatures may be inaccurate.

• Discontinue cooling measures when the core temperature reaches 39°C (102.2°F), which should ideally be achieved within 30 minutes. A temperature rebound may occur in 3-6 hours and should be retreated.

• For hypotension, administer crystalloids: If refractory, treat with vasopressors and monitor hemodynamics. Avoid pure #945;-adrenergic agents because they cause vasoconstriction and impair cooling. Administer crystalloids cautiously to normotensive patients.