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Heat Related Illnesses

Heat Stroke

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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

• Alcoholism

• Obesity

• Labours

• Medications

• Athletes, Military

• Medications

• Lack of acclimatisation

Drug Type MechanismAntiadrenergics and β-Blockers(e.g. Atenolol, Metoprolol)

Can decrease cardiac output, and therefore shunt warm blood from the body core to the periphery, limiting cooling.

Anticholinergics (e.g. Scopolamine)

Can prevent sweat glands from functioning properly (i.e. inhibits the rate of sweating and therefore the rate of cooling).

Antidepressants (e.g. Prozac, Zoloft, other SSRIs)

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.

Antihistamines (e.g. Brompheniramine)

Can inhibit the sweating mechanism.

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

Can inhibit the sweating mechanism.

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)

Can prevent dilation of the blood vessels in the skin of the periphery (hands, feet, face) reducing the ability to dissipate heat by convection.

Diuretics (e.g. Lasix) Can lead to dehydration. Hyponatremia is a common side effect.

Several drug classes (e.g. cholinesterase inhibitors, antiarrhythmics, calcium blockers)

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 40°c– 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-α, interferon γ, 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

Wet the body and clothes-spray

Evaporative

2) Ice water Immersion- immersing the patient in an ice water bath • Position the patient in tub of water (0-15°C)

with patient’s chest and extremities completely immersed with the head supported outside of the tub

• Remove the patient once core temperature reaches 39°C to avoid overshoot hypothermia

3) Ice packing

- has the advantage of not requiring constant supervision

Remove all of the patient’s clothing. Position the patient on plastic sheets or ina child’s plastic pool. Cover the patient’s chest and extremitieswith crushed ice. Remove the patient once core temperaturereaches 39°C.

Prevention

• Avoid strenuous out door activity during heat stress periods

• Light colored, loose clothingHYDRATE, HYDRATE, HYDRATEAvoid AlcoholAvoid 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 41°C. His blood pressure was 140/80 mmHg, pulse rate was 100 beats/min on admission and capillary blood sugar was 10 mmol/l