72.1Heat Stroke

It was the month of July; a 55-year-old male laborer became unconscious at work. On examination, he was found to be obtunded with minimal response to painful stimulus. His skin was hot and flushed. He was tachypneic, tachycardiac, hypotensive, and hyperthermic (core temperature 107°F).

Normal temperature is a balance between heat production and dissipation. High fever can have serious consequences such as renal failure, disseminated intravascular coagulation, and death. Prompt and appropriate management can improve the outcome in these patients.

Step 1: Initiate resuscitation

•These patients should be resuscitated as mentioned in Chap. 78.

•Administer IV fluids promptly as these patients are dehydrated. The type and amount of fluid should be guided by volume status, electrolytes, and cardiac functions.

Step 2: Assess the type of hyperthermia by history and examination

•Hyperthermia is a core temperature greater than 104°F. The most common causes are heat stroke and adverse reactions to drugs.

J. Dureja, M.D., F.N.B. (*)

Department of Anaesthesia, BPS Mahilla Medical College, Khanpur, Sonipat, India e-mail: drdureja@gmail.com

H. Singh, M.D.

Department of Medicine, Pt. B.D. Sharma Post Graduate Institute of Medical Sciences, Rohtak, India

Heat stroke is caused commonly by prolonged exposure to excessive heat:

•Exertional heat stroke occurs in young, healthy individuals engaged in heavy exercise during periods of high ambient temperature and humidity.

•Nonexertional heat stroke is precipitated by various conditions. Vasodilation, sweating, and other heat-loss mechanisms are reduced by medications, such as anticholinergic drugs, antihistaminics, and diuretics, antipsychotics (e.g., MAO inhibitors and tricyclic antidepressants), neuroleptic agents, and illicit drugs (amphetamines, cocaine, LSD, MDMA), brain hemorrhage, status epilepticus, and damage to the hypothalamus can also cause hyperthermia. Thyrotoxicosis and pheochromocytoma cause hyperthermia by increased heat production. Malignant hyperthermia is a rare complication of general anesthetics such as succinylcholine and halothane.

•A patient with heat stroke usually has a body temperature above 104°F.

•A high core temperature with appropriate history (e.g., environmental heat exposure, anticholinergics, neuroleptics, tricyclic antidepressants, succinylcholine, and halothane) is needed to diagnose heat stroke.

•Signs and symptoms include altered mentation or seizures, possible hallucinations, delirium, dry skin, rapid pulse, tachypnea, rales due to noncardiogenic pulmonary edema, pupil dilation, muscle rigidity, hypotension, arrhythmias, rhabdomyolysis, dyselectrolytemia, and coma. Disseminated intravascular coagulation and mixed acidosis can accompany the elevated temperature.

•Malignant hyperthermia: This should be suspected if there is sudden rise of EtCo2 in a patient undergoing surgery under general anesthesia.

Step 3: Send investigations

•Hemogram

•Creatine phosphokinase—elevated levels suggest hyperthermia.

•Renal functions

•Urine for myoglobin

•When indicated, coagulation studies, toxicologic screening, CT head, and lumbar puncture should be carried out.

•Diagnosis of malignant hyperthermia is confirmed by in vitro muscle contracture test.

Step 4: General management

•Ask the patient to rest, preferably in a cool place.

•If the patient is conscious, offer fluids but avoid alcohol and caffeine.

•Confirm the diagnosis with a calibrated thermometer to measure high temperature (40–47°C).

•Encourage him/her to shower and bath, or sponge off with cool water.

•There is no role of antipyretics (acetaminophen/acetylsalicylic acid).

•Monitor core temperature continuously with a rectal or esophageal probe.

•In order to avoid iatrogenic hypothermia, stop cooling at 39.5°C (103°F).

•Cooling measures: The biggest predictor of outcome is the degree and duration of hyperthermia.

External cooling techniques are easier to implement and are effective, welltolerated, and include the following:

–Conductive cooling—direct application of sources such as hypothermic blanket, ice bath, or ice packs to neck, axillae, and groins. Ice packs are effective but poorly tolerated by the awake patient. Avoid vasoconstriction and shivering as vasoconstriction impedes the heat loss and shivering creates heat.

–Convective techniques include removal of clothing and use of fans and air conditioners.

–Evaporative cooling can be accelerated by removing clothing and using a fan in conjunction with misting the skin with tepid water or applying a singlelayer wet sheet to bare skin. Shivering may be suppressed with IV benzodiazepines such as diazepam (5 mg) or lorazepam (1–2 mg).

•Immersing the patient in ice water is the most effective method of rapid cooling but complicates monitoring and access to the patient.

•Internal cooling techniques such as ice water gastric or rectal lavage, thoracic lavage, and extracorporeal blood cooling are effective, but they are difficult to manage and are associated with complications. Cold peritoneal lavage results in rapid cooling but is an invasive technique contraindicated in pregnant patients or those with previous abdominal surgery.

•Cold O2 and cold IV fluids are useful adjuncts.

Step 5: Specific management: Malignant hyperthermia and neuroleptic malignant syndrome

•Dantrolene, a nonspecific skeletal muscle relaxant, is the mainstay of treatment. It acts by blocking the release of calcium from the sarcoplasmic reticulum, thereby decreasing the myoplasmic concentration of free calcium, and diminishes the myocyte hypermetabolism that causes the symptoms.

•It is most effective if given early in the illness, when maximal calcium can be retained within the sarcoplasmic reticulum.

•There is associated risk of hepatotoxicity with dantrolene, so it should be avoided if liver function tests are abnormal (see Fig. 72.1 for detail).

Step 6: Manage complications

•Rhabdomyolysis

–Expand the intravascular volume with normal saline and administer mannitol and sodium bicarbonate.

–Alkalinization of urine prevents the precipitation of myoglobin in the renal tubules.

–The goal is to prevent myoglobin-induced renal injury by promoting renal blood flow, diuresis, and urinary alkalinization. Monitor serum electrolytes to prevent life-threatening arrhythmias.