What is more severe than heat cramps and results from a loss of water and salt in the body?

Principles

Heat cramps are brief, intermittent, and often severe muscle cramps occurring typically in muscles that are fatigued by heavy work. Heat cramps appear to be related to a salt deficiency. They usually occur during the first days of work in a hot environment and develop in persons who produce large amounts of thermal sweat and subsequently drink copious amounts of hypotonic fluid.

Clinical Features

Athletes, roofers, steelworkers, coal miners, field workers, and boiler operators are among the most common victims of heat cramps. Heat cramps tend to occur after exercise, when the victim stops working and is relaxing (Box 133.2). In this respect, they differ from the cramps experienced by athletes during exercise, which tend to last for several minutes, are relieved by massage, and resolve spontaneously.

Differential Diagnosis

Heat cramps are occasionally confused with hyperventilation tetany, which can occur during heat exhaustion. Hyperventilation tetany can be distinguished by the presence of carpopedal spasm and paresthesias in the distal extremities and perioral area.

Diagnostic Testing

Heat cramps accompanied by systemic symptoms may be part of salt depletion heat exhaustion. Heat cramp victims exhibit hyponatremia and hypochloremia, so serum electrolyte levels should be measured. Rhabdomyolysis or resultant renal damage is not present with isolated heat cramps.

Management and Disposition

Heat cramps are usually rapidly relieved by salt solutions. Commercially available flavored electrolyte solutions are commonly ingested. Mild cases without concurrent dehydration are treated orally with a 0.1% or 0.2% salt solution (two to four 10-grain salt tablets [56–112 mEq] or

Heat Cramps

Heat cramps are usually rapidly relieved by salt solutions. Mild cases without concurrent dehydration may be treated with oral 0.1%–0.2% salt solution. Severe cases respond rapidly to intravenous isotonic saline.

Heat Edema

Heat edema is treated with simple leg elevation or thigh‐high support hose. In most persons, the problem resolves through adequate acclimatization.

Heat Syncope

Heat syncope is self‐limited because assumption of a horizontal position is the cure. Persons at risk for heat syncope should be warned to move often, flex leg muscles when stationary, avoid protracted periods of standing when in hot environments, and assume a sitting, horizontal position when prodromal warning signs occur.

Prickly Heat

Prickly heat can be prevented if the patient wears clean, light, and loose‐fitting clothes and avoids situations producing profuse sweating. Chlorhexidine in a light cream is the treatment of choice in the acute phase. Salicylic acid, 1%, can be applied to localized affected areas to assist in desquamation. The application of salicylic acid over large areas may cause salicylic toxicity. For diffuse or pustular rashes, erythromycin or dicloxacillin can be administered orally.

Heat Exhaustion

Heat exhaustion is primarily a volume‐depletion problem, and therefore fluid administration leads to rapid recovery. Decisions regarding the types of fluid and electrolyte replacements to be administered should be based on electrolyte measurements and hydration status. In mild cases, rest in a cool environment and hydration with an oral electrolyte solution may be sufficient. Patients with significant volume depletion or electrolyte abnormalities require intravenous hydration. Young, otherwise healthy patients with no significant electrolyte abnormalities who are responsive to treatment do not require hospitalization. Older patients, especially those with cardiovascular disease, will require a more cautious fluid and electrolyte replacement and are best managed as inpatients.

Heat Stroke

Heat stroke requires a rapid reduction of core temperature to 40 °C (104 °F), which is accomplished by physical cooling techniques. Immersion and evaporative (e.g., spray bottle and a standing fan) cooling are the most widely used cooling methods. When the body temperature reaches 40 °C, cooling measures should be discontinued to avoid hypothermic overshoot. Other adjunctive cooling methods include cooling blankets, cardiopulmonary bypass, peritoneal dialysis, and gastric/bladder lavage. Hypotension, caused by peripheral vasodilation, is common in heat stroke. Blood pressure usually rises with cooling and intravenous fluid administration. Airway management is critical in the resuscitation of any critically ill patients. Common early complications of heat stroke include seizures, rhabdomyolysis, hypokalemia, hypocalcemia, and shivering. All patients with heat stroke should be admitted for close observation and management.

Heat cramps

Heat cramps result from loss of salt and water through sweating. They are characterized by cramps in voluntary muscles, especially in connection with exercise. Removing the patient from the hot environment and giving fluid is usually enough to resolve the situation.

Heat exhaustion

Heat exhaustion is a form of heat illness that is characterized by headache, nausea, and vomiting. Heat cramps and profuse sweating are present. There is usually an intact mental function, but there may be poor judgment and irritability. The patient usually recovers rapidly if removed from the hot environment and given fluids. If untreated, the condition may progress to heatstroke.

Heatstroke

Heatstroke is a severe condition in which temperature regulation collapses. There is a dramatic sudden onset and heatstroke is accompanied by a core temperature that often exceeds 42 °C. There is typically photophobia, delirium, seizures and progressive vasodilatation, tachycardia, and tachypnea. As core temperature rises there is decreasing myocardial contractility with ensuing bradycardia and myocardial irritability. Mortality is approximately 30%.

There are two types of heatstroke: exertional and classic. Exertional heatstroke mostly occurs in athletes, military personnel, or other persons working hard in a hot environment. The heat gain is thus greater and accumulates faster than the body can cope. Persistent sweating as a result of increased catecholamine production can be seen in about 50% of individuals suffering from exertional heatstroke, while sweating is usually absent in the classic form.

Classic heatstroke usually occurs in periods of sustained high temperatures and humidity, such as during heat waves. Elderly persons, especially those with a preexisting disease, are particularly at risk. However, only a small proportion of these deaths fulfill the strict clinical criteria of hyperthermia – documented antemortem temperature above 40.6 °C. From a forensic point of view it is therefore advised that other criteria are used to decide whether death is heat-related. A recent publication recommends that elderly, frail individuals with or without known preexisting illness and younger persons with evidence of acute or chronic illness should be considered the victims of heat-related deaths when there is substantial environmental or circumstantial evidence of heat as a contributing factor. For instance, that the deceased was found in a hot room with the windows closed and without cooling devices. Furthermore, obesity seems to constitute an additional risk factor. Medication such as diuretics and major tranquilizers, anticholinergic, or antiparkinsonian drugs may also add to the risk.

Saunas may likewise precipitate heat illness, exposing individuals to high temperatures and humidity, and thus making it difficult to get rid of heat through sweating and evaporation.

As in hypothermia, babies and small children are also at risk of succumbing to hyperthermia. Heatstroke can be caused by too much clothing or placing the baby or child in a hot environment such as an unventilated car, or too close to a heating device (Figure 5). From a forensic point of view it should also be mentioned that hyperthermia is a well-known risk factor for sudden infant death syndrome (SIDS).

Malignant hyperthermia

Malignant hyperthermia is an inherited disorder of skeletal muscles that causes a rapid increase in intracellular calcium in response to commonly used inhalational anesthetics and depolarizing muscle relaxants of the succinylcholine type. There is a variable clinical expression: tachycardia and arrhythmia are the earliest and most frequent symptoms. These and other symptoms, such as raised temperature, muscular rigidity, rhabdomyolysis, and acidosis may develop rapidly, and the incidence of fulminant crisis is 6.5% of cases. The literature indicates that this figure may be too high as milder forms are prone to be overlooked.

Family members of a patient who has suffered from malignant hyperthermia should be tested for this condition in order to avoid a similar incident. The only way to do this – as there is no specific mutation occurring in all potential patients – is to take an open biopsy from the thigh muscle (quadriceps femoris). The diagnosis of malignant hyperthermia is established if a pathological muscle contracture occurs after administration of the anesthestic.

Although there is no specific mutation in malignant hyperthermia, more than 20 different point mutations in the calcium release channel of the sarcoplasmic reticulum (ryanodine receptor) on chromosome 19 have been identified. The incidence of such mutations in families with malignant hypertension is 2–10%. In addition mutations have been identified in loci on chromosomes 1, 3, 5, 7, and 17.

Malignant neuroleptic syndrome

This condition is induced by chronic abuse of psychoactive drugs, particularly phenothiazines, haloperidol, lithium, and monoamine oxidase inhibitors. It seems to be caused by inhibition of dopamine receptors in the hypothalamus, causing increased heat generation and decreased heat loss. Unlike malignant hypertension, malignant neuroleptic syndrome develops slowly, is not triggered by succinylcholine, and is not inherited.

Ecstasy

The ring-substituted amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA) or “ecstasy” is increasingly used by young people, especially those involved in rave dance culture. The symptoms of ecstasy intoxication are anxiety, agitation, mental confusion, tremors, muscle rigidity, tachycardia, hypertension, and hyperthermia. Of these, hyperthermia is the most life-threatening. Ecstasy induces release of serotonin in the brain. Animal experiments have shown that it also induces the release of catecholamines and, to a lesser extent, dopamine. There also is inhibition of the reuptake and metabolism of these substances. Serotonin stimulates the thermal control regions in the hypothalamus, possibly by increasing the temperature set point.

Heat Cramps

Heat cramps are painful muscle spasms that typically occur several hours after vigorous exertion. They are thought to be due to repletion of water without adequate salt intake. The voluntary muscles of the calves, thighs, and shoulders are most commonly affected. Symptoms typically last only a few minutes but may recur. The affected muscles feel hard to palpation. Laboratory abnormalities include hyponatremia with very low or undetectable urine sodium.

Heat Exhaustion

Heat exhaustion occurs secondary to water or salt depletion, or both. Affected patients experience systemic complaints, including fatigue, weakness, nausea, vomiting, diarrhea, and headache. Irritability may be a prominent sign in infants and nonverbal children. The core temperature is mildly elevated (<39°C), and the patient often experiences tachycardia, orthostatic hypotension, profuse sweating, and flushed skin. Laboratory abnormalities include hyponatremia or hypernatremia and hemo- and urinary concentration.

Heatstroke

Without adequate recognition and initiation of effective therapies, heat exhaustion can progress to life-threatening heatstroke. Classic heatstroke, also referred to as nonexertional heatstroke, typically occurs in children with predisposing factors that put them at increased risk. These factors include children's limited ability to increase their fluid intake (e.g., young infancy, nonverbal status), remove themselves from a hot environment (e.g., immobility), or dissipate heat (e.g., overdressing, obesity, underlying medical condition). Exertional heatstroke usually occurs in otherwise healthy individuals who participate in vigorous activities when it is hot and humid, often with inadequate efforts to maintain hydration.

Patients present with a significantly elevated core body temperature (>40°C) associated with central nervous system dysfunction. Anhidrosis is frequently but not universally observed. Neurologic symptoms include progressive lethargy, confusion, headache, delirium, seizures, and coma. On physical examination, patients are tachycardic, hypotensive, and tachypneic (hyperventilation causes a respiratory alkalosis). Laboratory abnormalities include hyponatremia or hypernatremia, hypokalemia, hemo- and urinary concentration, acute renal failure, and elevated liver function tests.

The extent and severity of the central effects depend on the extent of the hyperpyrexia. Rhabdomyolysis may occur as a result of thermal injury to myocytes. Circulating myoglobin as well as thermal and ischemic insults can result in acute renal compromise.

Malignant Hyperthermia

When a susceptible individual is exposed to a triggering agent, the uncontrolled influx of calcium into the muscle cell results in muscle contraction, accelerated metabolism, and resultant hyperthermia. Initially, end-tidal carbon dioxide increases and arterial oxygen decreases, with muscle rigidity and a rapid rise in body temperature.2,3

Laboratory evaluation reveals acidosis as well as hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobinuria from muscle breakdown. Although serum creatinine starts to rise almost immediately due to the rhabdomyolysis, peak levels are not seen until several days after the exposure.