Heatstroke

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- core temperature > 41° C OR
- core temp > 40.5 ° C with anhidrosis, altered mental status or both

- exertional: typically seen in healthy young adults who overexert themselves in high ambient temperatures or in a hot environment to which they are not acclimatized. Patients sweat normally.
- non-exertional (classic): usually affects elderly and debilitated patients with chronic underlying disease. Result of impaired thermoregulation combined with high ambient temperatures. Often due to impaired sweating

- substantial fluid shift from central compartment to periphery. Reversible on cooling
- cardiac output increased +++ (3 l/min per ° C increase in rectal temperature). May fail in patients with limited cardiac reserve
- mediators such as endotoxin and cytokines are implicated in the pathogenesis of organ damage in heat stroke
- intractable DIC is usual mode of death in fatal cases

- hyperthyroidism
- exercise
- sepsis

• Drugs
  - anticholinergics, anti-Parkinsonian drugs, anti-histamines, butyrophenones, phenothiazines, tricyclics
• Abnormal sweat glands
  - sweat gland injury following acute heat stroke, barbiturate poisoning
  - cystic fibrosis
  - healed thermal burn
• salt and water depletion
  - diuretic induced
• hypokalaemia

• coma
• physical disability
• mental illness

• cardiovascular disease
• hypokalaemia (decreased muscle blood flow)
• dehydration

- elderly
- high ambient temperature and humidity, poor ventilation
- lack of acclimatization
- obesity
- fatigue
- DM
- malnutrition
- alcoholism

- often little in the way of warning prodrome prior to development of non-exertional heat stroke (classic heat stroke). As thermoregulatory mechanisms fail body temperature rises rapidly and patient can deteriorate rapidly from apparent baseline health to coma or an obtunded state
- 3 cardinal signs are:

• CNS dysfunction
• hyperpyrexia (core temperature >40° C)
• hot dry skin. Pink or ashen depending on circulatory state. However may be clammy and sweaty

- direct thermal toxicity causes cell death, cerebral oedema and local haemorrhage
- irritability or irrational behaviour may precede the development of either form of heatstroke
- confusion, aggressive behaviour, delirium, convulsions and pupillary abnormalities may progress rapidly to coma
- ± decorticate posturing, faecal incontinence, flaccidity or hemiplegia (however focal signs are unusual)
- cerebellar signs, including ataxia and dysarthria may be permanent in a few patients. Cerebellum particularly sensitive to heat
- hypothalamic damage may exacerbate heat stroke by further impairing sweating and heat loss
- LP may show increased protein, xanthochromia and slight increase in lymphocytes

- tachycardia
- hypotension or normotension with wide pulse pressure
- hyperdynamic haemodynamic profile
- myocardial pump failure. Myocardial damage and frank infarction frequent even in patients with normal coronaries due to the effect of heat on myocytes and coronary hypoperfusion secondary to hypovolaemia

ECG of a patient with a core temperature of 40°C

Same patient after cooling

- dysrhythmias

- extreme tachypnoea with RR up to 60/min
- crackles and cyanosis late signs of pulmonary oedema
- direct thermal injury to pulmonary vascular endothelium may lead to cor pulmonale or ARDS

- dehydration leading to raised urea and creatinine, and haemoconcentration
- sweating leading to low levels of Na, Mg, K, early in the illness. Hypokalaemia decreases sweat secretion and therefore exacerbates the condition
- rhabdomyolysis resulting in hyperkalaemia, hypocalcaemia and renal failure
- metabolic acidosis and respiratory alkalosis common. Hyperthermia alone can cause primary hyperventilation and respiratory alkalosis, while hypoperfusion, tissue hypoxia, and anaerobic metabolism may lead to lactic acidosis with respiratory compensation. Former less common.
- some biochemical differences between classic and exertional heat stroke:

• some renal damage occurs in nearly all patients as a direct result of heat
• potentiated by dehydration and rhabdomyolysis
• acute renal failure 5-6 times more common in patients with exertional heat stroke in whom it occurs in 30-35%

• ischaemic intestinal ulceration common. May lead to frank haemorrhage
• hepatic damage common. In 5-10% hepatic necrosis may be severe enough to cause death

• direct inactivation of platelets and clotting factors by heat
• liver failure
• unexplained decrease in platelets and megakaryocytes
• platelet aggregation due to heat
• DIC. Due to activation of clotting cascade by damaged vascular endothelium. Latter may be damaged as a direct result of heat

- temperature
- electrolytes, urea, creatinine, calcium
- LFTs
- CPK
- ABG: note that Paco2 and Pao2 will be falsely low and pH falsely elevated if results are not corrected for temperature
- ECG and ECG monitoring
- urine output
- FBC, clotting, fibrinogen, FDP, D-dimer. Anaemia frequent. Platelets low/normal. Lymphocytosis
- test urine for myoglobin

- anterior compartment syndrome of distal lower limbs may occur in patients with rhabdomyolysis
- pancreatitis

- tepid sponging combined with fan is usually all that is required
- aim for skin temperature of 30-33° C
- gastric or peritoneal lavage with iced saline only rarely required in refractory cases and when thermogenesis is on-going (eg malignant hyperthermia)
- when temperature approaches 39° active cooling should be terminated as the body temperature will continue to fall 1-2° C
- chlorpromazine 10-50 mg IV 6hrly may be useful in preventing shivering
- use of dantrolene controversial. Probably should not be used routinely at present.

- IV volume replacement. Note that many of these patients only require 1-1.2 l of replacement fluid
- if inotrope required dobutamine probably drug of choice
- urgent treatment of hyperkalaemia
- do not treat hypocalcaemia per se; only give calcium if ECG changes of severe hyperkalaemia occur as calcium may exacerbate rhabdomyolysis
- small dose of mannitol may benefit patients with rhabdomyolysis

- mortality 5-50%
- incidence of neurological damage: 7-14%
- prognostic factors: age, severity, neurological deficits, concentrations of liver and muscle enzymes, lactic acidosis

• cerebral malaria
• encephalitis
• meningitis
• stroke, especially brainstem haemorrhage
• thyroid storm, delirium tremens, anticholinergic poisoning, systemic sepsis

© Charles Gomersall December 1999

©Charles Gomersall, September, 2008 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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