Heat Related Illnesses

Heat related illnesses are not uncommon as Malaysia is a tropical country with a constantly hot weather
Heat related illness occurs commonly in Saudi Arabia during the Haj season whereby many Malaysian pilgrims are affected every year and some die

Recently, Malaysia was shocked by the news of three-year old girl who died from heat stroke after being left in a car for 5 hours
In child, it can take as little as 15 minutes in an overheated car for a child to suffer life-threatening brain and kidney injuries

Worldwide, heat stroke is uncommon in subtropical climates while residents of areas that experience heat waves are most at risk

In France in 2003, a 20-day heat wave resulted in >14,000 deaths while in Britian in 2003 was reported to have caused approximately 1000 deaths in 1 week
Heat stroke demands urgent attention because High mortality Can cause permanent neurological damage

Thermoregulation

Nov 2006

Heat Loss
Conduction
transfer of heat between two surfaces of differing temperatures through direct physical contact

Convection
transfer of heat through contact with air or water molecules across the skin

 Radiation
Transfer of infrared waves emitted from one object and absorbed by another

Evaporation
evaporation of water from the skin

Heat Injury Predisposition

3 Factors Influencing Heat Production 1. Increased Internal Heat Production.
Physical Activity Febrile illness Pharmacologic agents

2. Increased External Heat Gain

Exposure to high ambient temperature

3. Decreased Ability to Disperse Heat

Pharmacologic agents Humidity

Heat Injury Predisposition

Elderly Infants Malnutrition Chronic illness Dehydration Labours Medications Athletes, Military Medications Lack of acclimatisation

Alcoholism
Obesity

Drug Type Mechanism Antiadrenergics and -Blockers Can decrease cardiac output, and therefore shunt warm blood from the (e.g. Atenolol, Metoprolol) body core to the periphery, limiting cooling. Anticholinergics (e.g. Scopolamine) Antidepressants (e.g. Prozac, Zoloft, other SSRIs) Can prevent sweat glands from functioning properly (i.e. inhibits the rate of sweating and therefore the rate of cooling). Many have anticholinergic properties (see above) and some can raise the brain's thermal set-point decreasing centrally induced thermoregulation. SSRIs can increase the risk of hyponatremia. Can inhibit the sweating mechanism. Can inhibit the sweating mechanism.

Antihistamines (e.g. Brompheniramine) Anti-Parkinsonians (e.g. Benztropine, Levodopa, Trihexyphenidyl)

Antipsychotics (e.g. Olanzapine) Can inhibit the sweating mechanism. Can induce a hyperthermic syndrome (neuroleptic malignant syndrome) on their own, which would be compounded by the effects of heat. Sympathomimetics (e.g. Pseudoephedrine) Diuretics (e.g. Lasix) Several drug classes (e.g. cholinesterase inhibitors, antiarrhythmics, calcium blockers) Can prevent dilation of the blood vessels in the skin of the periphery (hands, feet, face) reducing the ability to dissipate heat by convection. Can lead to dehydration. Hyponatremia is a common side effect. Can provoke diarrhea and/or vomiting, leading to dehydration.

Spectrum of heat illnesses

Heat cramps

Heat syncope

Heat exhaustion

Heat stroke

Heat cramps
characterized by sharp, painful spasm of skeletal muscles present during or after intense prolonged exercise in the heat Cause is unknown
due to the loss of salt through the sweat postulated that intracellular calcium is increased by a reduction in the sodium gradient across the cell membrane stimulate actin-myosin interactions causing the muscle contraction

 Treatment :
Rest and cooling down Massage and stretching of affected muscles NS or oral salt water

Heat syncope
occurs during prolonged standing or abrupt standing following vigorous activity often associated with hot weather environments Pathophysiology :
The person is maximally vasodilated when activity is stopped pooling of blood in dilated vessels of the skin and the lower parts of body reduced venous return insufficient flow of blood to brain

 Treatment:
Rest in sitting, recumbent or supine position in a cool place with slightly elevated legs Drink cold water

Heat Exhaustion
most common form of heat related illness & not associated with evidence of organ damage occurs when the body cannot sustain the necessary level of cardiac output to meet the combined demands of skin blood flow blood flow for exercising skeletal muscle

 Predisposing factors:
Exposure to high heat and humidity Sustained exertion in heat Lack of acclimatization Low fluid intake Low dietary salt intake

 Symptoms & signs :

Heavy sweating Fatigue, weakness Dizziness, giddiness, headache Diarrhea, nausea, and sometimes vomiting Mental status is typically normal Body core temperature is usually normal / does not exceed 40c Inability to continue work or exercise in heat is typical

 Treatment :
rest, cooling, and rehydration with oral/IV fluids heavy clothing should be removed gentle cooling (time in a cool environment, cold compresses and fanning)

Heat stroke
Is a Medical Emergency Classical triad : - Rectal temperature > 41C - Altered mental state - Hot dry skin

 Predisposing factor:
sustained physical exertion in high heat with minimum rest and rehydration breaks dehydration chronic cardiovascular disease

 Signs/Symptoms
Headache, dizziness, irritability Decreased LOC, seizures Examination Bounding pulse progressing to rapid, weak pulse Hypotension secondary to vasodilation Altered mental status Any neurological sign is possible e.g. ataxia, ophistotonus, +ve Babinski sign

Altered LOC + Hot Environment = THINK - Heat Stroke

How does heat stress cause damage to cells?

3 mechanisms:
1) heat directly denatures cellular proteins, interrupt cellular enzymatic processes and results in cell swelling as well as apoptosis 2) heat stress results in increased expression of cytokines (eg. tumor necrosis factor-, interferon , interleukin-6) hypoperfusion in certain areas especially in the splanchnic bed
endotoxinemia and production of reactive oxygen and nitrogen species thermoregulatory failure and shock

1) heat stress results in vascular endothelial injury, increased

vascular permeability, activation of the coagulation cascade and disseminated intravascular coagulation

Complications
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

 End organ damage

Metabolic: hypokalemia, hypernatremia; hyperuricemia, hyperkalemia, hypocalcemia; lactic acidosis Hematologic: thrombocytopenia, DIC

Differential diagnosis
CNS Infection Meningitis/Encephalitis Cerebral malaria Severe sepsis Neuroleptic malignant syndrome Malignant hyperthermia Thyroid storm

Drug toxicity

Stimulants Serotonin Syndrome

Alcohol withdrawal syndrome Status epilepticus CVA, ICB

Investigations
FBC PT, aPTT BUSE/Creat, LFT, CK ABG, Chest X-Ray, ECG CT brain

Management
rapid reduction of body core temperature duration of heat stress is the determining factor in survival and delayed cooling increases mortality

Resuscitation
A,B,C Fluid resuscitation Cooling : - Remove all clothing - Apply cooling method - Close monitoring of rectal temperature (aim temperature 38.5c)

Cooling Method
Evaporative Cooling Ice water Immersion Ice packing

1) Evaporative Cooling - fastest and most efficient noninvasive technique Mist over patient constantly, using spray bottles Place large fans to circulate warm room air directed at the patient

Evaporative

Wet the body and clothes-spray

2) Ice water Immersion - immersing the patient in an ice water bath Position the patient in tub of water (0-15C) with patients chest and extremities completely immersed with the head supported outside of the tub Remove the patient once core temperature reaches 39C to avoid overshoot hypothermia

3) Ice packing

- has the advantage of not requiring constant

supervision Remove all of the patients clothing. Position the patient on plastic sheets or in a childs plastic pool. Cover the patients chest and extremities with crushed ice. Remove the patient once core temperature reaches 39C.

Prevention
Avoid strenuous out door activity during heat stress periods Light colored, loose clothing HYDRATE, HYDRATE, HYDRATE Avoid Alcohol Avoid direct sun exposure

Supportive treatment
Fluid resuscitation followed by inotrope and vasopressor therapy Ventilation for ARDS Platelet, FFP and cryoprecipitate support as indicated Dialysis for ARF

Antipyretics (eg, acetaminophen, aspirin) have no role because antipyretics interrupt the change in the hypothalamic set point caused by pyrogens. Antipyretics actually may be harmful in patients who develop hepatic, hematologic, and renal complications because they may aggravate bleeding tendencies.

A 70 year-old Malay man, was found unconscious by the passer-by inside his car parked under the scorching heat of the hot sun This man had just come out from his cardiac clinic follow-up visit and continuation of his medications. He had trouble looking for his car. After about 15 minutes of walking under the hot sun, he finally found his car. When he got into his car, he felt dizzy and fainted. On arrival to the emergency department, he was still drowsy and unresponsive to call. His core temperature was noted to be 41C. His blood pressure was 140/80 mmHg, pulse rate was 100 beats/min on admission and capillary blood sugar was 10 mmol/l