The limits of body temperature for efficient thermoregulation are 35-40 C
Within certain body temp limits, normal thermoregulatory mechanisms can restore core temp to 37 C. Past 42 C metabolic pathways can be so altered that inappropriate physiologic responses occur leading to vascular collapse, shock and death.
Heat Exhaustion: Heat illness occurring in individuals who sweat profusely while engaging in exercise. It is a manifestation of cardiovascular strain resulting from maintaining normothermia.
The boundary between heat exhaustion and heatstroke is usually defined as 39.4 C to 40.0 C. Primarily a diagnosis of exclusion.
Signs and Symptoms: headache, confusion, fatigue, drowsiness, hyperirritability, anxiety, euphoria, nausea, vomiting, visual disturbances, dizziness, syncope, chilling, pilorection, sweating, moderately elevated temperatures, altered mental status, ataxia.
Also heat cramps, and heats sensations in the head and upper torso, tachycardia, hyperventilation, hypotension, syncope
Treatment:
Lower body temperature:
Rehydration:
Avoid returning to physical activity on the same day
FYI: Gastric emptying can provide 1.8L/hour under optimal conditions and the intestine can usually absorb 1.4-2.2 L/hour
Heat stroke: A maladaptive state whereby the body temp exceeds 40.5 C as a result of the mismatch between heat production and heat dissipation.
Classic Heat Stroke – poor dissipation of environmental heat.
Definition: Heat illness caused by high environmental heat loads resulting in collapse. Rectal temp usually greater than 40.4 C. Medical emergency.
Pathophysiologically: swelling and degeneration of tissue and cell structures, and widespread microscopic to massive hemorrhages.
Almost always accompanied by dehydration
Usually occurs over days (can be rapid in enclosed environments such as closed vehicles)
Risk populations: the elderly, malnutrition, chronic disease, and substance abuse
Risk factors: 1) those that effect thermoregulation: lack of acclimatization, fatigue, loss of sleep, dehydration, skin disorders
2) Those that increase heat production: obesity, lack of physical fitness, dehydration, febrile illness, sustained exercise.
Exertional Heat Stroke—excessive endogenous heat production and overwhelming of heat loss mechanisms
Definition: Heat illness caused by strenuous physical exercise in the heat resulting in collapse. Rectal temp usually greater than 40.5 C. Medical emergency
Heat susceptible persons include:
Obese, unfit, dehydrated, unacclimated, previous history of heat stroke, acute febrile illness, diarrhea, chronic disturbances of sweating mechanisms
Risk populations: sports participants, military, miners, heavy industry workers, and pilgrims to Mecca
Risk factors:
1) functional-physiologic: dehydration, poor physical fitness, lack of acclimatization, heat illness history, obesity, illness, fatigue, pregnancy
2) conditional circumstances: hot climate, external load, inadequate rest periods, impermeable clothing insulated materials, missed meals
3) Concurrent diseases and congenital abnormalities: CNS lesions, sweat gland dysfunction, infectious diseases, diabetes, skin disorders, diarrhea
4) Drugs: Drug abuse, medications alcohol, caffeine
5) Psychologic stress: over motivation, peers pressure.
Potentially harmful drugs include: Diuretics, anticholinergics, vasodilators, antihistamines, CNS inhibitors, muscle relaxants, tranquilizers and sedatives, B blockers, amphetamines and tricyclic antidepressants.
1) Acute Phase – CNS disturbances. Prodromal symptoms – minutes to hours
Dizziness, weakness, nausea, confusion, disorientation, drowsiness, irrational behavior.
2) Hematologic and enzymatic phase— alterations of physiologic parameters
3) Late phase – hepatic and renal failure
4) Recovery phase +/- chronic disability
Treatment:
With rapid reduction of temp, control of seizures, proper rehydration, and prompt evacuation to medical facility – 90% survival rate.
Full recovery without evidence of neurologic impairment has been achieved even after 24 hours in coma. . In some, neurologic impairments may persist but usually not for more than 12-24 months.
Poor prognosis: Core temp greater than 41 C, prolonged duration of hyperthermia, hyperkalemia, acute renal failure, and increased LFTs, and persistence of coma after return to normothermia
Prevention:
Sunburn – cutaneous inflammatory response to acute overexposure to UVA and UVB sunrays
An exaggerated sunburn response can occur in those taking phototoxic drugs including: sulfonamides, tetracyclines, chlorothiazides, doxycycline, phenothiazines, furosemide, nalidixic acid, amiodarone and psoralens
Treatment:
Prevention:
Photo protection
1) Sunscreen
With UVA and UVB protection
2 mg/ square cm
SPF is primarily a measure of UBV protection
|
SPF |
UVB Absorption (%) |
|
2 |
50 |
|
4 |
75 |
|
8 |
87.5 |
|
15 |
93.3 |
|
30 |
96.7 |
|
50 |
98 |
2) Clothing protection: dry dark fabrics have a higher SPF than wet and white fabrics. A typical dry white cotton t-shirt has an SPF of 5-9.
3) Sun avoidance
4 phases:
1) Prefreeze: secondary to chilling and before ice crystal formation. Tissue temps range from 3-10 C. Sensation usually disappears at 10C
2) Freeze-thaw: ice crystal formation in the tissues. Tissue temps drop below 0 C. Ambient temps drop below –15 - -6 C
3) Vascular stasis: spasticity and dilation of vessels, plasma leakage, stasis coagulation and shunting
4) Late ischemia: thrombosis and arteriovenous shunting, ischemia, gangrene, and autonomic dysfunction.
Degrees:
First degree: numbness and erythema, a white or yellowish firm plaque in the area of injury, edema present but no tissue loss.
Second degree: superficial skin blisters filled with a clear or milky fluid, surrounded by erythema and edema.
Third degree: deeper blisters filed with a purple bloody fluid with injury into the reticular dermis and beneath the dermal vascular plexus.
Fourth degree: injury completely through the dermis, involving the subcuticular tissues including muscle and/or bone.
Coldness, numbness and clumsy feeling in affected body part.
Throbbing pain 2-3 days after rewarming lasting for a variable duration
Residual tingling sensation usually after about 1 week
Without tissue loss symptoms usually subside within 1 month
With tissue loss disablement may exceed 6 months
Spontaneous burning, subsides within 2-3 weeks
Spontaneous electric current like shock: in 97% of those with tissue loss, usually begins 2 days after injury, lasts approx. 6 weeks, worse at night
All frostbite victims experience some degree of sensory loss for at least 4 years after injury.
Clinical appearance:
Yellowish white or mottled blue,
Insensate
Could be frozen solid
Hyperemia with rewarming
Sensation returns after thawing and persists until blebs appear
Edema with rewarming, lasts for 5 days or longer
Blisters form 6-24 hours after rewarming
Within the first 9-15 days severe frostbite results in a black, hard and dry eschar.
Mummification occurs within 22-45 days
Good prognosis: sensation to pin prick, normal colour, warmth and large clear blebs that appear early and extend to the tips of the digits
Poor prognosis: small dark blebs that occur late and do not extend to the tips, absence of edema, presence of cyanosis that does bot blanch with pressure.
Treatment:
If nearby to a medical facility (within 2 hours):
If not nearby:
In ER:
Prevention:
Core body temp of <35 C, measured rectally or by an esophageal temperature probe
Mild 35-32.2 C
At 32 C
Moderate 32.2-28 C
Severe <27.7
18 C
Risks: prolonged exposure to cold temperatures, immersion in cold water, impaired sensation, extremes of age, poor health, poor nutrition, alcohol or drug use, certain meds which impair thermoregulation like phenothiazines and barbiturates.
Treatment:
Active rewarming . If defibrillation fails continue active rewarming until core temp is above 30 C and then try defibrillation again.
Active rewarming techniques:
Core:
Active rewarming may precipitate cardiac arrythmias such as V-fib or asystole
A-fib usually spontaneously converts to sinus rhythm upon rewarming and does not respond to medications
Ventricular arrythmias may also be resistant to standard antiarrythmics but should respond to some of them
Prevention:
Many victims of hypothermia especially children have been resuscitated after prolonged hypothermic events due to a lowered metabolic rate and slowed CNS changes.
No patient is dead until warm and dead.
Submitted by Carrie Beallor