Heat Stroke

Heat Stroke Definition and epidemiology

Heat stroke is defined as a failure to maintain body temperature, and is characterised by a core temperature of >40.6°C (>105°F), severe central nervous system dysfunction (psychosis, delirium, coma), and anhidrosis (hot, dry skin). These are the three defining criteria.

The two groups primarily affected are older adults who are chronically ill (classic or non-exertional heat stroke) and the young undergoing strenuous exercise (exertional heat stroke).

Mortality is as high as 80% once this syndrome is manifest.

Hypo- and hyperthermic states are predominantly disorders of older adults. Morbidity and mortality increase during particularly hot or cold periods, especially among the ill elderly, and much of this illness is caused by an increased incidence of cardiovascular disorders (myocardial infarction and stroke) or infectious disease (pneumonia) during these periods. Pathophysiology — why older people are vulnerable

The major pathophysiological mechanisms of temperature dysregulation in ageing are impaired temperature perception and diminished sweating in hyperthermia.

Dermal vascularisation and the number of sweat glands both decrease with age, along with sebum production. Since dermal vascularisation and sweating are the major mechanisms for balancing body temperature and losing heat from the skin, and both are impaired with age, elderly people tend to experience hyperthermia in hot weather.

There are multiple predisposing factors for heat stroke in older adults, but most often there is a prolonged heat wave. Others: cardiovascular disease, diabetes, dementia, immobility, social isolation, living alone without cooling, obesity, dehydration and blunted thirst.

Drugs: anticholinergics, antihistamines, tricyclic antidepressants and antipsychotics (impair sweating); diuretics (volume depletion); β-blockers (limit the cardiac output response); alcohol.

Mechanism of injury: heat produces direct cytotoxic injury plus a systemic inflammatory response with cytokine release, causing endothelial damage, coagulopathy and multi-organ failure — the syndrome behaves like sepsis.

The diagnosis requires a high level of suspicion, because the early manifestations are non-specific.

Early signs (Table 12-14): dizziness, weakness, sensation of warmth, anorexia, nausea, vomiting, headache and dyspnoea.

Later signs: central nervous system dysfunction, psychosis, delirium, coma, anhidrosis, and hot dry skin.

Differential diagnosis: sepsis, thyroid storm, neuroleptic malignant syndrome, serotonin syndrome, malignant hyperthermia, anticholinergic toxidrome, meningitis and status epilepticus. In older people the presentation overlaps heavily with delirium and infection.

Cardiac: myocardial damage, congestive heart failure, arrhythmias. Renal: renal failure in 20–25%.

Neurological: cerebral oedema, seizures, diffuse and focal findings. Hepatic: hepatocellular necrosis, jaundice, liver failure.

Muscle: rhabdomyolysis with myoglobinuria. Haematological: bleeding diathesis, disseminated intravascular coagulation.

Metabolic: electrolyte disturbance, acid–base disturbance (metabolic acidosis, respiratory alkalosis). Infective: aspiration pneumonia, sepsis. Circulatory: dehydration and shock.

Investigations: rectal core temperature (most accurate), full blood count, electrolytes, urea and creatinine, liver function, creatine kinase, coagulation screen, arterial blood gases, urinary myoglobin, ECG, chest radiograph, blood cultures, and CT head if there are focal signs.

Once the full syndrome has developed for any length of time the prognosis is very poor. Management at this stage requires intense multisystem care, but the key is rapid specific therapy consisting of cooling to 38.9°C (102°F) within the first hour.

Ice packs and ice-water immersion are superior to convection cooling with alcohol sponge baths or electric fans. This is the single most important therapeutic statement in the chapter.

ABC: airway protection if comatose, high-flow oxygen, large-bore intravenous access, continuous cardiac monitoring, and careful fluid resuscitation guided by haemodynamics — older patients are at risk of precipitating pulmonary oedema.

Adjunctive measures: remove clothing, cold intravenous fluids, cold gastric or bladder lavage, benzodiazepines to control shivering and seizures, fluids and urinary alkalinisation for rhabdomyolysis, and correction of electrolyte disturbance and coagulopathy.

Do not give antipyretics (paracetamol or NSAIDs) — the hypothalamic set point is normal, so they are ineffective and may worsen hepatic and renal injury. Do not give dantrolene — it has no role in heat stroke, unlike malignant hyperthermia.

In view of the poor survival, efforts must be directed toward prevention. Prevention appears to be the most appropriate approach to management of temperature dysregulation in older adults.

Older patients should be cautioned about the dangers of hot weather. For those at particularly high risk, temporary relocation to more protected environments should be considered.

Education of older adults about their susceptibility to hypo- and hyperthermia in extremes of environmental temperature, education as to appropriate behaviour in such conditions, and close monitoring of the most vulnerable older adults should help reduce morbidity and mortality.

Practical measures: remain indoors and in shade between noon and 3 pm; drink fluids on a schedule rather than waiting for thirst, since thirst is blunted with age; light, loose cotton clothing; cool showers; avoid alcohol, caffeine and heavy meals; pre-summer medication review; buddy or check-in systems for those living alone; and access to cooling centres.