HEAT INJURIES
Heat injuries is a collective term to denote quot;many illnesses associated with acute or prolonged exposure to excessive heatquot;, due to—(a) high environmental temperature in tropical countries during summer season, (b) endogenous heat over-production during strenuous exercise/sport activities, (c) defective dissipation of body heat by radiation (excessive clothing) or evaporation (impaired sweating), or (d) impairment of thermoregulatory mechanisms.
Only 25% of energy produced during by muscular contraction is utilized for actual work, while rest is converted into heat. Body dissipates this heat by radiation (60%), evaporation (25%) and convection.
Children are more susceptible for heat injuries due to—(a) immature heat-elimination mechanisms, e.g. poor sweating, and (b) excessive endogenous heat generation due to sports/outdoor activities. However, children have adequate capability to acclimatize after prolonged heat exposure.
Clinical manifestations of heat injuries depend on the severity, duration and individual cooling mechanisms. Important heat injuries include:
• Heat cramps in calf and hamstring muscles, are most common manifestations of minor heat injuries, usually seen after strenuous exercise due to electrolyte imbalance following sweating and ingestion of hypotonic fluids, e.g. water. These cramps respond well to oral rehydration with electrolyte solutions (1 tsf salt/500 ml water) and gentle stretching of muscles.
• Heat syncope, i.e. fainting after prolonged standing/ exercise in hot and humid environment, e.g. school assemblies, is attributed to depleted intravascular volume and peripheral pooling of blood after cutaneous vasodilatation. Placing the child in supine position under cool-shade is usually enough to recover from these attacks, which may be prevented by consuming plenty of fluids.
• Heat edema over hands/feet during initial exposure in hot environment is more common in adults than in children and usually subsides spontaneously after some time.
• Heat tetany, i.e. carpopedal tingling or spasm, is related to heat-related hyperventilation with subsequent alkalosis, which responds to shifting the child in cooler environment and re-breathing into a paper-bag.
• Heat exhaustion is usually seen after prolonged exposure to moderately hot and humid weather, due to progressive fluid and salt depletion.
• Heat-stroke, a potentially life-threatening heat injury, which may be fatal in ~50% cases unless recognized and treated promptly, discussed later.
Clinically, these cases present with headache, fatigue, nausea/vomiting, vertigo, dehydration and postural hypotension. Fever, though common, is not a must for diagnosis of heat exhaustion and CNS signs are characteristically absent (d/d heat stroke).
Treatment includes shifting the case to cooler environment, cold-sponging and administration of adequate fluids and electrolytes via PO/IV route.
Heat stroke (hyperpyrexia) is of two types—(a) classic heat stroke, which is mainly seen in elderly and chronic debilitated patients, exposed to summer heat wave, and (b) exertional heat stroke, which is usually seen in children/ adolescents after unacclimatized exercise.
In India, heat stroke is common in hot and humid months of April to July, with preceding history of prolonged outdoor activity/sport participation.
Pathophysiology of heat stroke relates to unexplained failure of thermoregulatory mechanisms and elevation of hypothalamic thermostat, which prevents activation of heat-dissipation mechanisms, e.g. sweating. Although the exact mechanism for this failure is unknown, an energydepletion model has been suggested (excessive heat production gt; over-activation of Na+/K+ ATPase pump gt; excessive sodium efflux from the cells gt; depletion of cellular energy, essential for thermoregulation).
Clinically, heat stroke may be sudden or preceded by a brief prodrome of headache, nausea/vomiting and dizziness, characterized by a triad of:
• Hyperpyrexia with core-temperature gt; 40°C,
• Neurological dysfunction with delirium, coma, tremors, seizures, muscular rigidity, etc.,
• Dry, flushed skin with absence of sweating.
However, sweating may be present in exertional stroke in young children.Other important and late manifestations include: (a) cardiovascular manifestations, e.g. tachycardia, shock or CCF due to myocardial injury, (b) hepatic manifestations, e.g. jaundice or elevated transaminase levels, (c) coagulopathies, e.g. purpura, conjunctival hemorrhage, orificial bleeds, (d) acute renal failure,
(e) lactic acidosis with respiratory alkalosis, and
(f) metabolic/electrolyte disturbances, e.g. hypoglycemia, hypokalemia, hypernatremia and hypocalcemia.
Diagnosis depends on: (a) history of heat exposure, (b) clinical triad, as above, (c) exclusion of other causes for hyperpyrexia with CNS signs, e.g. cerebral malaria, CNS infections and dhatura or atropine poisoning.
Management: Heat stroke is a medical emergency that needs immediate hospitalization and intensive care. Primary aim of the management in these cases is the rapid body cooling, followed by hemodynamic and metabolic stabilization and treatment of complications. Important steps include:
• External body cooling by: (a) shifting the patient in cooler environment with removal of cloths, (b) whole body immersion in ice-cool water except the head, (c) evaporative cooling by placing large fans near the patient's body. Many PICUs in hot-humid regions, where heat stroke is common in summers, have specially designed body-cooling units for this purpose.
Other cooling methods, e.g. gastric/rectal lavage with cool water, application of ice-packs, etc. may be used. Vigorous shivering during rapid cooling may be controlled by chlorpromazine, if necessary.
Antipyretics are contraindicated in heat stroke, which may worsen hepatic and hematological injury.
• Hemodynamic support: Hypotension is common due to peripheral vasodilatation, which usually improves with peripheral cooling. However, persistent hypotension/shock need appropriate fluid replacement and inotropic support under hemodynamic supervision, e.g. CVP monitoring.
#945;-adrenergic drugs, e.g. noradrenaline, should not be used, which may cause cutaneous vasoconstriction and reduce heat loss.
• Treatment of complications, e.g. seizures (diazepam), coagulopathy (transfusions), acute renal failure and metabolic disturbances, depending on the laboratory values.
• Post-recovery monitoring: All patients should be closely monitored for 24-48 hours for temperature, vital signs, urinary output, biochemical parameters, e.g. attacks, which may be prevented by consuming plenty of glucose, liver transaminases, urea/creati- nine, serum electrolytes, and ABG, to detect late complications, e.g. coagulopathy or liver damage.