Heat stroke is a life-threatening emergency characterized by the triad of altered mentation, generalized anhydrosis, and a core temperature >40.6°C (105.1°F). If not diagnosed and treated promptly, thermal injury results in worsening multi-organ dysfunction, culminating in outright organ failure and death.
There are two main variants of heat stroke: exertional heat stroke (EHS) and non-exertional (i.e., classical) heat stroke. EHS mostly occurs in young and healthy individuals who attempt to exercise in hot and humid conditions. Classical heat stroke occurs during heat waves, typically affecting the elderly and the very young.
In patients with heat stroke, the goals of management are to reduce the core temperature rapidly to <102˚F (39˚C), while supporting organ system function.
Immersion in an ice-water bath is the most effective way to rapidly cool the patient. However, this is often intolerable to conscious individuals and may also interfere with monitoring and access. Augmented evaporative cooling is an alternative that is better tolerated and does not interfere with monitoring; in this, the patient is sprayed with water and ambient air passed across the body with a large fan, promoting evaporative heat loss.
Heat stroke: hyponatremia
Hyponatremia (i.e., a sodium level <135mmol/L) may occur in heat stroke, secondary to salt loss. This is often a hypovolemic hyponatremia, as some degree of dehydration is also present. Unless severe or symptomatic, specific treatment is typically unnecessary.
Heat stroke is often complicated by rhabdomyolysis (i.e., breakdown of skeletal striated muscle). The contents of the damaged myocytes are released into the bloodstream, potentially causing electrolyte imbalances and acute kidney injury (AKI).
Myglobin is one such myocitic compound. Myoglobinuria occurs when serum myoglobin levels exceed ~0.5 - 1.5 mg/dL. Unbound myoglobin reacts with Tamm-Horsfall proteins in nephrons, promoting cast formation, preventing filtration, and leading to acute tubular necrosis and AKI.
Treatment is by the induction of diuresis with normal saline. While some authorities advocate the use of mannitol or furosemide as well clinical trials using these agents have been inconclusive.
Malignant hyperthermia is an inherited disorder in which affected individuals develop hyperthermia and generalized muscle rigidity following exposure to certain agents used in general anesthesia. The pathophysiology involves uncontrolled sarcoplasmic calcium release from skeletal muscles, resulting in a hypermetabolic syndrome. The anesthetic agents implicated include the volatile anesthetics sevoflurane, halothane, desflurane, and enflurane; as well as the depolarizing neuromuscular blockers succinylcholine, suxamethonium, and decamethonium.
The clinical presentation of malignant hyperthermia is highly variable; aside from hyperpyrexia and generalized muscle rigidity, tachycardia is often seen. Hypoxemia, hypercapnia, hyperkalemia, and acidosis may also occur. Survival depends largely on the early recognition of the characteristic symptoms and on immediate action on the part of the attending anesthetist.
Dantrolene is a skeletal muscle relaxant that inhibits calcium release from the sarcoplasmic reticulum of skeletal muscles; it acts on the ryanodine receptor, which is known to be dysfunctional in malignant hyperthermia.
In patients with malignant hyperthermia a dose of 2.5 mg/kg should be given stat and then repeated every 5 minutes until reversal of the reaction occurs or a maximum dose of 10 mg/kg is reached. Prompt use reduces mortality from 70-80% to a mere 5%.