Heat Stroke Clinical Presentation

Updated: May 18, 2017
  • Author: Robert S Helman, MD; Chief Editor: Joe Alcock, MD, MS  more...
  • Print
Presentation

History

Heat stroke is defined as hyperthermia exceeding 41°C associated with an altered sensorium. However, when a patient is allowed to cool down prior to measurement of the temperature (as may occur during transportation in a cool ambulance or evaluation in an emergency department), the measured temperature may be lower than 41°C, making the temperature criterion relative. Anhidrosis, or lack of sweating, has been cited as a feature of heat stroke, but some patients with heat stroke present with profuse sweating. Because of variable presentations, a high index of suspicion is needed to avoid delays in diagnosis and treatment.

Clinically, two forms of heat stroke are differentiated: classic, or nonexertional, heat stroke (NEHS) and exertional heat stroke (EHS). NEHS, which occurs during environmental heat waves, is more common in the very young and the elderly and should be suspected in children, elderly persons, and chronically ill individuals who present with an altered sensorium. NEHS occurs because of failure of the body's heat dissipating mechanisms.

On the other hand, EHS affects young, healthy individuals who engage in strenuous physical activity, and EHS should be suspected in all such individuals who exhibit bizarre, irrational behavior or experience syncope. EHS results from increased heat production, which overwhelms the body's ability to dissipate heat.

Exertional heat stroke

EHS is characterized by hyperthermia, diaphoresis, and an altered sensorium, which may manifest suddenly during extreme physical exertion in a hot environment.

A number of symptoms (eg, abdominal and muscular cramping, nausea, vomiting, diarrhea, headache, dizziness, dyspnea, weakness) commonly precede the heat stroke and may remain unrecognized. Syncope and loss of consciousness also are observed commonly before the development of EHS.

EHS commonly is observed in young, healthy individuals (eg, athletes, firefighters, military personnel) who, while engaging in strenuous physical activity, overwhelm their thermoregulatory system and become hyperthermic. Because their ability to sweat remains intact, patients with EHS are able to cool down after cessation of physical activity and may present for medical attention with temperatures well below 41°C. Despite education and preventive measures, EHS is still a leading cause of disability and death in high school athletes, particularly football players. [5]

Risk factors that increase the likelihood of heat-related illnesses include a preceding viral infection, dehydration, fatigue, obesity, lack of sleep, poor physical fitness, and lack of acclimatization. Although lack of acclimatization is a risk factor for heat stroke, EHS also can occur in acclimatized individuals who are subjected to moderately intense exercise. EHS also may occur because of increased motor activity due to drug use, such as cocaine and amphetamines, and as a complication of status epilepticus.

Nonexertional heat stroke

NEHS is characterized by hyperthermia, anhidrosis, and an altered sensorium, which develop suddenly after a period of prolonged elevations in ambient temperatures (ie, heat waves). Core body temperatures greater than 41°C are diagnostic, although heat stroke may occur with lower core body temperatures.

Numerous central nervous system (CNS) symptoms, ranging from minor irritability to delusions, irrational behavior, hallucinations, and coma have been described. Other possible CNS symptoms include seizures, cranial nerve abnormalities, cerebellar dysfunction, and opisthotonos.

Anhidrosis due to cessation of sweating is a late occurrence in heat stroke and may not be present when patients are examined.

Patients with NEHS initially may exhibit a hyperdynamic circulatory state, but, in severe cases, hypodynamic states may be noted.

Classic heat stroke most commonly occurs during episodes of prolonged elevations in ambient temperatures. It affects people who are unable to control their environment and water intake (eg, infants, elderly persons, individuals who are chronically ill), people with reduced cardiovascular reserve (eg, elderly persons, patients with chronic cardiovascular illnesses), and people with impaired sweating (eg, from skin disease or ingestion of anticholinergic or psychiatric drugs). In addition, infants have an immature thermoregulatory system, and elderly persons have impaired perception of changes in body and ambient temperatures and a decreased capacity to sweat.

Next:

Physical Examination

Vital signs

Temperature: Typically, the patient's temperature exceeds 41°C. However, in the presence of sweating, evaporating mechanisms, and the initiation of cooling methods, body temperatures lower than 41°C are common.

Pulse: Tachycardia to rates exceeding 130 beats per minute is common.

Blood pressure: Patients commonly are normotensive, with a wide pulse pressure; however, hypotension is common and may result from a number of factors, including vasodilation of the cutaneous vessels, pooling of the blood in the venous system, and dehydration. Hypotension also may be due to myocardial damage and may signal cardiovascular collapse. Blood pressure will usually correct with normalization of the body temperature.

Central nervous system

Symptoms of CNS dysfunction are present universally in persons with heat stroke. Symptoms may range from irritability to coma.

Patients may present with delirium, confusion, delusions, convulsions, hallucinations, ataxia, tremors, dysarthria, and other cerebellar findings, as well as cranial nerve abnormalities and tonic and dystonic contractions of the muscles. Seizures may occur. Patients also may exhibit decerebrate posturing, decorticate posturing, or they may be limp.

Coma also may be caused by electrolyte abnormalities, hypoglycemia, hepatic encephalopathy, uremic encephalopathy, and acute structural abnormalities, such as intracerebral hemorrhage due to trauma or coagulation disorders.

Cerebral edema and herniation also may occur during the course of heat stroke.

Eyes

Examination of the eyes may reveal nystagmus and oculogyric episodes due to cerebellar injury. The pupils may be fixed, dilated, pinpoint, or normal.

Cardiovascular

Heat stress places a tremendous burden on the heart. Patients with preexisting myocardial dysfunction do not tolerate heat stress for prolonged periods.

Patients commonly exhibit a hyperdynamic state, with tachycardia, low systemic vascular resistance, and a high cardiac index. However, a hypodynamic state, with a high systemic vascular resistance and a low cardiac index, may occur in patients with preexisting cardiovascular disease and low intravascular volume. A hypodynamic state also may signal cardiovascular collapse.

The central venous pressure generally is within the reference range or elevated unless the patient is severely volume depleted.

High-output cardiac failure and low-output cardiac failure may occur.

Pulmonary

Patients with heat stroke commonly exhibit tachypnea and hyperventilation caused by direct CNS stimulation, acidosis, or hypoxia.

Hypoxia and cyanosis may be due to a number of processes, including atelectasis, pulmonary infarction, aspiration pneumonia, and pulmonary edema.

Gastrointestinal

Gastrointestinal hemorrhage and intestinal infarction are complications that can occur in patients with heat stroke.

Hepatic

Patients commonly exhibit evidence of hepatic injury, including jaundice and elevated liver enzymes.

Rarely, fulminant hepatic failure occurs, accompanied by encephalopathy, hypoglycemia, and disseminated intravascular coagulation (DIC) and bleeding.

Musculoskeletal

Muscle tenderness and cramping are common; rhabdomyolysis is a common complication of EHS. The patient's muscles may be rigid or limp.

Renal

Acute kidney injury is a common complication of heat stroke and may be due to hypovolemia, low cardiac output, and myoglobinuria (from rhabdomyolysis). Patients may exhibit oliguria and a change in the color of urine.

Previous
Next:

Causes

The etiology of heat stroke may involve any of the following:

  • Increased heat production

  • Decreased heat loss

  • Reduced ability to acclimatize

  • Reduced behavioral responsiveness

Increased heat production

Increased metabolism can result from any of the following:

  • Infections

  • Sepsis

  • Encephalitis

  • Stimulant drugs

  • Drug withdrawal

Increased muscular activity may involve any of the following:

  • Exercise

  • Convulsions

  • Strychnine poisoning

  • Sympathomimetics

  • Drug withdrawal

  • Thyroid storm

Moderate physical exercise, convulsions, and shivering can double heat production and result in temperature elevations that generally are self-limited and resolve with discontinuation of the activity.

Strenuous exercise and status epilepticus can increase heat production 10-fold and, when uninterrupted, can overwhelm the body's heat-dissipating mechanisms, leading to dangerous rises in body temperature.

Stimulant drugs, including cocaine and amphetamines, can generate excessive amounts of heat by increasing metabolism and motor activity through the stimulatory effects of dopamine, serotonin, and norepinephrine. The development of heat stroke in individuals intoxicated with stimulants is multifactorial and may involve a complex interaction between dopamine and serotonin in the hypothalamus and the brainstem.

Neuroleptic agents also may elevate body temperature by increasing muscle activity, but, occasionally, these agents may cause neuroleptic malignant syndrome (NMS). NMS is an idiosyncratic reaction characterized by hyperthermia, altered mental status, muscle rigidity, and autonomic instability and appears to be due to excessive contraction of muscles.

Certain drugs, such as inhaled volatile anesthetics and succinylcholine, may result in malignant hyperthermia. In contrast to heat stroke, malignant hyperthermia is believed to be induced by a decreased ability of the sarcoplasmic reticulum to retain calcium, resulting in sustained muscle contraction.

Decreased heat loss

Reduced sweating can result from any of the following:

  • Dermatologic diseases

  • Drugs

  • Burns

Reduced central nervous system (CNS) responses may result from the following:

  • Advanced age

  • Young age (toddlers and infants)

  • Alcohol

  • Barbiturates

  • Other sedatives

Reduced cardiovascular reserve may result from the following:

  • Advanced age

  • Beta-blockers

  • Calcium channel blockers

  • Diuretics

  • Cardiovascular drugs - Interfere with the cardiovascular responses to heat and, therefore, can interfere with heat loss

Drugs that can result in decreased heat loss include the following:

  • Anticholinergics

  • Neuroleptics

  • Antihistamines

Exogenous factors that can decrease heat loss include the following:

  • High ambient temperatures

  • High ambient humidity

Reduced ability to acclimatize

Persons at the extremes of age (ie, toddlers and young children, the elderly) may be less able to generate adequate physiologic responses to heat stress. Diuretic use and hypokalemia can also impair accommodation to heat stress.

Reduced behavioral responsiveness

Infants, patients who are bedridden, and patients who are chronically ill are at risk for heat stroke because they are unable to control their environment and water intake. To compound matters, comorbidities and polypharmacy in the elderly can compromise their recovery.

Previous
Next:

Complications

Heat stroke is a multisystem insult that potentially can affect almost every organ system.

The central nervous system (CNS) is especially sensitive to the damaging effects of hyperthermia. Widespread cell death occurs but is more evident in the region of the cerebellum (Purkinje cells). Heat stroke–related long-term CNS sequelae include cerebellar deficits, dementia, hemiplegia, quadriparesis, and personality changes.

In one study, rhabdomyolysis was observed in almost all patients with EHS and in as many as 86% of patients with NEHS. Compartment syndrome is observed most commonly in patients with severe rhabdomyolysis and in patients who are immobilized.

Acute kidney injury may occur in as many as 25-30% of patients who have heat stroke (especially EHS).

Acute liver failure due to centrilobular hepatic necrosis and cholestasis generally occurs in the first 48 hours, but it can peak as long as 2 weeks after the onset of heat stroke. In rare instances, liver failure may be complicated by a fulminant course requiring liver transplantation. Patients who survive generally have a complete return of hepatic function.

DIC is a rare complication and caries a poor prognosis when it occurs. Electron microscopy studies have shown that direct thermal injury to the vascular endothelium is the primary trigger of platelet aggregation and, possibly, DIC.

ARDS may be due to direct thermal injury to the lung, or it may complicate liver failure, infection, or aspiration. When associated with liver failure, the patient's prognosis is much worse.

Previous