Heat Illness and Cold Exposure
HEAT ILLNESS
Heat illness represents a spectrum of disorders, including mild and moderate forms in which the thermoregulatory mechanisms of the body remain intact (heat cramps, heat exhaustion) to life-threatening heat stroke, in which the body’s thermoregulatory mechanisms fail. The factors that predispose patients to develop heat illness include:
An increased wet-bulb globe temperature (WBGT) found when there is a high ambient heat and humidity
Lack of acclimatization or physical conditioning
Obesity
Strenuous exertion and fatigue
Cardiovascular disease
Alcohol consumption
Anticholinergic drug ingestion
Old age
A history of heat illness.
Environmental factors play an extremely important role in the development of heat illness; the WBGT is the most accurate measure of the environmental heat load and reflects the impact of humidity and radiant heat on dry air temperature. It has been estimated that 90% of cases of heat stroke occur when the WBGT is 30°C (85°F) or more.
Heat Cramps
Heat cramps typically occur in hot weather when heavily exercising muscles (most often the legs) contract without reflex inhibition from antagonist muscles. The shoulders may also be affected. Cramping may occur during exercise or may be delayed by several hours. Although the cause of heat cramps is poorly understood, loss of salt during exertion and replacement with free water seem implicated. Patients usually have a history of profuse sweating during strenuous exertion with inadequate or inappropriate fluid replacement. Treatment consists of rest in a cool environment and water and salt replacement either orally with a 0.1% salt solution (made by adding one-quarter teaspoon of salt to each quart of water) or intravenously with normal saline, 1 L intravenously over 1 to 3 hours. A variety of commercially available replacement drinks can also be used. Plain salt tablets are not recommended, because their dissolution in the stomach produces a hypertonic solution often causing gastric irritation, nausea, and vomiting. Enteric-coated salt tablets are poorly absorbed and not recommended.
Heat Exhaustion
Heat exhaustion is also caused by salt and water loss; heat exhaustion caused by predominant water loss typically develops rapidly over a few hours, whereas that caused by predominant salt loss may have a more insidious onset over several days.
Diagnosis
Symptoms include headache, light-headedness, giddiness, anorexia, nausea, vomiting, malaise, excessive thirst, and muscle cramping.
The examination usually reveals the patient to be flushed and sweating profusely; the rectal temperature is usually less than 38°C to 39°C (102°F) but can be as high as 40°C (104°F); evidence of dehydration, including tachycardia and orthostatic hypotension, is often noted as well. The mental status examination, except as noted, should be normal; patients with abnormalities of mental status should be considered to have heat stroke (see “Heat Stroke”).
Laboratory data may reveal evidence of dehydration (a mildly elevated BUN and concentrated urine and hematocrit); the serum sodium may be mildly elevated (if no rehydration has occurred) or normal (if fluids have been ingested). Mild to moderate rises in creatinine kinase and hepatic enzymes may be found as well; hypoglycemia is also occasionally noted.
Treatment
Treatment includes rest in a cool environment and intravenous replacement of salt and water initially with 5% dextrose in normal saline, adjusted subsequently based on the patient’s electrolytes. Patients with significant hyperthermia should be treated with cooling in the usual manner. Young, physically fit patients may require up to 3 to 4 L of fluid over 4 to 8 hours and generally become completely asymptomatic and well within approximately 6 to 12 hours. Patients with little improvement after 6 to 8 hours of treatment in the emergency department (ED) should be admitted to the hospital for further therapy; similarly, patients with persisting orthostatic hypotension or cardiovascular compromise, as well as elderly patients, require admission for more gradual intravenous fluid replacement.
Heat Stroke
Heat stroke develops when the body’s thermoregulatory mechanisms fail or are overwhelmed; the body temperature then rises to levels that produce widespread cellular damage. The diagnosis is based on a core temperature above 40.5°C (104.9°F) and evidence of CNS dysfunction; anhidrosis (lack of sweating) may or may not be present (see later).
History
Although temperatures above 42°C (107.6°F) are universally associated with heat stroke, symptoms may occur at lower temperatures, but always, however, above 40.5°C (104.9°F). Two types of heat stroke have been described: nonexertional (or classic) and exertional.
Nonexertional or classic heat stroke occurs in infants and ill or elderly patients and usually develops over a period of several days, often during a period of excessive ambient temperatures. Patients with classic heat stroke may be severely dehydrated; therefore, sweating may not be seen.
In contrast, the patient with exertional heat stroke may be a healthy young person, often unacclimatized, with symptoms that develop in a matter of hours and that
are most often caused by an unusually heavy heat load associated with exercise or exertion. The patient with exertional heat stroke may not be severely dehydrated and is most often sweating. Symptoms may include chills, headache, nausea, unsteadiness, light-headedness, piloerection involving the arms and chest, paresthesias of the hands and feet, bizarre behavior, syncope, seizures, and coma.
The Physical Examination
The physical examination in patients with heat stroke reveals the rectal temperature to be above 40.5°C (104.9°F), although it may be lower if prehospital treatment has been initiated. The skin may be red and flushed, or ashen gray and dry, or patients may be sweating profusely. The respiratory and heart rates are usually elevated; hypotension may occur as a result of high-output or low-output cardiac failure as well as severe dehydration. Seizures and coma are the most frequent serious central nervous system findings in the ED, although a wide variety of other disturbances are described. These include oculogyric crises, tremors, dystonia, muscle rigidity, decerebrate or transient hemiplegia, dilated and fixed pupils, and a flatline electroencephalogram (EEG).
Diagnostic Tests
A variety of abnormal laboratory studies are noted.
ABG: Arterial blood gases usually reveal an acidosis, particularly in exertional heat stroke, caused by elevated lactate levels.
Complete blood count (CBC): A leukocytosis is common and may be as high as 30,000 to 50,000.
LFTs: The AST, ALT, and lactate dehydrogenase enzymes are markedly elevated. The AST levels in the first 24 hours are said to be prognostic. If the level is less than 1,000 IU/L, the prognosis is generally good with serious injury to the brain, liver, and kidneys unlikely; if levels are above 1,000 IU/L, the prognosis is generally poor, with damage to all three organs likely.
CPK: Creatinine kinase levels are markedly elevated because of muscle fiber damage. Rhabdomyolysis is especially common in exertional heat stroke, and myoglobinuria, hyperuricemia, and a creatinine elevated out of proportion to the BUN are seen.
BMP/electrolytes: The sodium, BUN, and osmolality will vary depending on the state of hydration. Hyperkalemia caused by muscle cell damage may be noted after 12 to 24 hours, in addition to hypocalcemia as a result of its deposition in injured muscle. Serum glucose levels may be normal or low; the latter is common in the hypotensive, preterminal state. Hypophosphatemia as low as 1 mg/dL has been described.
Coagulation studies: Evidence of coagulopathy is common, with disseminated intravascular coagulopathy seen in severe cases.
ECG: The electrocardiogram (ECG) may show nonspecific ST-segment and T-wave abnormalities, evidence of injury, and a variety of arrhythmias and bundle branch blocks; most of these are reversible with cooling.
A toxic screen should be ordered as well.
Treatment
Treatment of this lethal disease must be prompt and aggressive.
Cooling. The first priority is immediate cooling of the patient. The means by which this is undertaken is controversial, and no controlled studies comparing one method with another exist at this time. Antipyretics are ineffective.
The evaporative technique is simple to implement and unlike immersion, minimally impairs the ability of the staff to monitor and/or treat the patient. The evaporative
technique results in cooling rates of up to 0.33°C/min and is undertaken by removing all of the patient’s clothing, wetting the skin with a spray of lukewarm water, and circulating cool, dry air rapidly over the patient’s body with fans; the patient is kept wet with the use of a tepid or lukewarm water spray bottle. Cold water should not be used because shivering, which is counterproductive, may be provoked.
Ice packs can be used as well; they should be placed in areas of maximal heat transfer: the groin, axillae, and neck. Cooling rates of 0.1°C/min have been reported with this technique.
Ice-water immersion requires that patients be placed in a container of ice water, sufficiently deep to cover the abdomen and chest and the proximal extremities; ice-water immersion results in a cooling rate of 0.11°C/min but is technically difficult when patients are ill, is not feasible in most EDs, and probably should not be used.
Ice-water gastric lavage may be useful in refractory cases; however, the patient must be intubated.
Ice-water peritoneal lavage can also be used in refractory cases but is recommended neither in pregnant patients nor in patients with previous abdominal surgery.Related posts:
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