Heat Illness - Permian Basin STEPS

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Transcript Heat Illness - Permian Basin STEPS

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
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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
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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
 100-250 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 temperatureinsulator 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 0.10.3 degrees C (0.18-0.54 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
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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 2000- 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
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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:
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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
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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
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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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