Heat Illness LA Wilson MD, FACEP. Heat Illness- Topics  Epidemiology  Pathophysiology: heat transfer, response to heat stress, path to heat illnesses.

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Presentation transcript:

Heat Illness LA Wilson MD, FACEP

Heat Illness- Topics  Epidemiology  Pathophysiology: heat transfer, response to heat stress, path to heat illnesses.  Clinical features of heat illness  Treatment and Prevention

Heat Illness  Most common cause of environmentally related death in the U.S. during the past decade  More than floods, tornadoes, lightning, hurricane, cold, or winter related fatalities

Heat Illness  Annual heat related deaths 1 per million in ages 5-44 years  5 per million for the population over 85 years of age  400 heat related deaths per year in the US over the past 10 years

Risk Factors for Heat Illness  Hot, humid environmental conditions  Dehydration  Use of heavy equipment or clothing  (football or hockey uniform)  High-intensity exercise  Short-term illness or fever  Eating disorders  Obesity

Risk Factors for Heat Illness Risk Factors for Heat Illness  Deconditioning  Certain medications (e.g., diuretics)  Chronic or long-term diseases (e.g., diabetes)  Alcohol consumption  Other substance abuse (heroin, cocaine, Ecstasy)  Recent move to hot, humid environment  Elderly and very young  Acclimatization

Medication and Heat Illness  Medications that interfere with heat loss:  Antipsychotics, tranquilizers, anticholinergics, antiparkinsonian agents, cardiovascular meds (beta blockers, calcium channel blockers, vasodilators, diuretics), sleep aids, stimulants

Thermoregulation Metabolic Heat Environmental Heat Body Temperature ++

Heat Transfer  Radiation  Conduction; Convection  Evaporation

Radiation  Main heat loss at low temperature  In hot weather causes heat gain  ckal/hr heat burden from sun light possible

Conduction  Kinetic energy of warm surface (skin) transferred to less kinetically active molecules of a cool surface (solid objects, water or air)  Conduction normally accounts for less than 3% of the bodies heat loss  In still air, the air next to the skin will rapidly warm to the skin temperature- insulator zone

Convection  Allowing for air movement, and thus replacing the warm air with cooler air will result in a more rapid conductive heat loss  Conduction coupled with convection may account for 15% of heat loss  Heat loss by conduction in water is 32 times more efficient than in air at the same temperature

Evaporation  Primary heat loss in high temperatures  Basal levels: 600 ml of water loss through respiration and sweating daily  25% of heat loss in cooler temperatures  100% at higher temperatures  High humidity impairs heat loss by evaporation

Evaporation  Dependent on adequate hydration  1% dehydration impairs heat dissipation and the physiological responses  Each 1% body weight loss to dehydration results in a core temperature increase of degrees C ( deg F)  Well acclimatized and trained athletes will hypohydrate and produce sweat at a more rapid rate than can be absorbed through the GI tract.

Physiological Response to Heat Stress  Temperature regulation fails as temperature deviates from the normal  35 C (95 F) >core temperature > 40 C (104 F)  May sustain with body temperature as high as 42 C (107.6 F) for short times without ill effects  Highest core temperature of heat stroke survivor was 46.5 C (115.7 F)

Physiological Heat Response  Vasodilatation (mainly in skin)  Increased sweating  Decreased heat production  Behavioral heat control

Vasodilatation  Skin blood flow increase from 0.2L/min to max of 8L/min  Cardiac out put increase of 3L/min/1 degree C elevation

Sweat and Heat production  Cholinergic and catecholamine stimulation by elevated temperature increase sweating  Anterior hypothalamus signals the posterior hypothalamus to decrease body heat production primarily by inhibiting shivering

Behavioral Responses  Dressing appropriately  Finding cooler environments

Acclimatization  Maximized at 7-10 days  Primarily improved sweating, enhanced skin blood flow, improved cardiovascular function and reset the thermoregulatory set point

Heat Injury  Three processes  Increased heat production  Increased external heat gain  Decreased heat loss

Non-exertional (classic) heat injury  Periods of high environmental heat stress  Slow rise in heat burden allow volume and electrolyte abnormalities to develop  Elderly and the young at risk  Those with psychological, physiological, pharmacological impairment at risk

Confinement Hyperpyrexia  July June 2001:  1960 nonfatal and 78 fatal heat injuries to children left in closed vehicles on hot days  Many of the deaths related to confinement in cars or trucks

Exertional Heat injury  Physically fit participating in athletic events  Jobs performed in high heat stress conditions such as military or fire fighters  Basal heat production is 60 kcal/hr per square meter (100 kcal/hr for average 70 kg man).  With exertion the rate can increase by a factor of 20.

Heat Related Illnesses  Heat Edema  Prickly Heat  Heat Cramps  Heat Tetany  Heat Syncope  Heat Exhaustion  Heat Stroke

Heat Cramps  Involuntary spasmodic muscle contractions, commonly of the calves, but other muscles possible.  Occurs most commonly several hours after vigorous physical activity but may occur with or without exercise.  Related to relative deficit in fluids, sodium and potassium  Treatment is fluid and electrolyte replacement  Two salt tabs (650 mg each) in a quart of water delivers 0.1% saline solution.

Heat Tetany  Carpal Pedal spasm resulting from hyperventilation- common result from short exposures to extreme heat stress

Heat Syncope  Orthostatic hypotension due to vasodilatation, decreased motor tone and perhaps fluid loss.  Common in non-acclimatized persons in heat stress environments

Heat Exhaustion  Nonspecific symptoms resulting from volume depletion and sometimes salt depletion  Weakness, Malaise, Nausea, vomiting, headache and myalgias  Hypotension, tachycardia, tachypnea, diaphoresis and syncope  Temp range from normal to 40 C (104 F)

Heat Exhaustion  Treatment:  Fluid resuscitation, electrolyte replacement  Careful hydration when co-morbidities exist such as CHF

Heat Exhaustion vs. Heat Stroke  Classical differentiation includes:  Anhidrosis  CNS changes  Core temp > 40 C (104 F)

Heat Exhaustion vs. Heat Stroke  Exertional heat stroke victims may perspire  Defining CNS changes is subjective  There is no temperature threshold for heat stroke

Heat Stroke  End organ damage- hepatic enzyme elevation may be used to define heat stroke  Hepatic enzyme elevation may be delayed

Heat Stroke  Hyperpyrexia and CNS dysfunction should have heat stroke in the differential.

Heat Stroke Dif DX:  Drug toxicity  Drug or Alcohol withdrawal syndromes  Serotonin Syndrome  Neuroleptic Malignant Syndrome

Heat Stroke Dif DX  Infections- Sepsis, other systemic infections, Meningitis  Endocrinopathies (DKA, Thyroid Storm)  Neurologic: Status epilepticus, brain hemorrhage

Heat Stroke and the CNS  Cerebellum susceptible: Ataxia may be seen early  Virtually any neurological signs are possible: + Babinski, posturing, hemiplegia, seizure, coma  Cerebral edema is common  Lower temperature for longer do more poorly than higher temperature for short periods

Heat Stroke Diagnosis  Diagnosis of exclusion  Evaluate all the possible causes, and treat as appropriate

Resuscitation  ABCD, E  Fluid resuscitation is paramount  Assess for end organ damage: CBC, CMP, UA, myoglobin,  Cooling

Cooling  Evaporative  Immersion  Ice packing- hypothermia blanket  Cold gastric lavage  Cold peritoneal lavage

Morbidity and Mortality  End organ damage  Muscular: rhabdomyolysis, shivering  Neurological: delirium, seizures, coma: cerebral edema and death  Cardiac: heart failure  Pulmonary: edema, ARDS  Renal: oliguria: ARF  GI: diarrhea; hepatic failure, GI hemorrhage

Morbidity and Mortality  End organ damage  Metabolic: hypokalemia, hypernatremia; Hyperuricemia, hyperkalemia, hypocalcemia; lactic acidosis highly correlated with morbidity and mortality  Hematologic: thrombocytopenia, DIC

Prevention  Avoid strenuous out door activity during heat stress periods  Light colored, loose clothing  Increase carbohydrate and decrease protein  HYDRATE, HYDRATE, HYDRATE  Avoid Alcohol

Prevention  Do not take salt tablets  Avoid direct sun exposure  Use the shade

Public Prevention  Pay attention to environmental conditions  Air conditioning and heat breaks  Emphasize hydration  Social services to the home bound and chronically ill  Acclimatization  Educate parents, coaches, teachers

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