2-3 million years ago, our human ancestors evolved to be without fur because it gave them one great evolutionary advantage - the newly evolved device of total body perspiration (humans perspire far more than any other animal) becomes much more effective when there is no hair, and a perspiring naked skin can more rapidly lose body heat than any other animal - a great evolutionary advantage in the hot African plains where the human ancestors had evolved to walk upright and walk and run long distances hunting for food. In addition, this added ability to lose heat was essential to ensuring heat protection for the growth in the size of the brain - the human brain gives off ~20W of heat inside an enclosed skull and this needs to be dissipated to prevent brain dysfunction as occurs in heat stroke.
logically, scalp hair was the only body hair retained en masse as it served to protect the scalp of the erect hominid from the radiant heat of the midday sun, and reduce the brain from over-heating.
as an aside, from studies on the 3 types of human lice, it appears that after losing their body fur, our ancestors evolved gorilla-hair-like sparse, thick shafted pubic hair not suitable for the grips and limb length of the head louse, and thus the gorilla louse evolved to become human pubic lice, and when we started wearing clothing some 650,000 years ago, the head louse evolved to become a 3rd human louse parasite - the body louse which primarily resides in clothing.
dehydration and heat stress:
it is possible to sweat up to 15 litres per day
thirst does not match all fluids lost by sweating, even if fluids are freely taken
mild to moderate dehydration increases cardiac work and reduces fluid available for sweating
even mild dehydration is associated with increased risk of injury, heat stress illness and poorer performance of complex tasks.
factors impairing the ability of the body to cope with heat stress:
high ambient temperatures
inability to control environment - clothing, cooling systems, access to water, confined to bed
defined as a body temperature higher than 41.1°C (106°F) associated with neurologic dysfunction
HOWEVER, the diagnosis of heatstroke should be considered for patients with altered mental status during environmental heat waves, even in the absence of severe hyperthermia.
two forms of heat stroke:
exertional heat stroke (EHS)
generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment
tend to have hyperthemia with diaphoresis (ie. sweating)
because their ability to sweat remains intact, this group of patients are able to cool down after cessation of physical activity and may present for medical attention with temperatures well below 41°C.
tend to have hyperthermia with anhidrosis (ie. dry skin), although anhidrosis is late occurrence and may not be present
occurs in individuals who lack the capacity to modulate the environment and those at highest risk are infants and elderly persons and patients with diminished cardiovascular reserves are unable to generate and cope with the physiologic responses to heat stress
the redistribution of blood flow to the periphery, coupled with the loss of fluids and electrolytes in sweat, place a tremendous burden on the heart, which ultimately may fail to maintain an adequate cardiac output
patients with skin diseases and those taking medications that interfere with sweating also are at increased risk for heatstroke because they are unable to dissipate heat adequately
occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years.
when therapy is delayed, the mortality rate may be as high as 80%; however, with early diagnosis and immediate cooling, the mortality rate can be reduced to 10%.
full recovery has been observed in patients with temperatures as high as 46°C, and death has occurred in patients with much lower temperatures.
body temperatures exceeding 106°F or 41.1°C generally are catastrophic and require immediate aggressive therapy.
potential complications
hypoxia and cyanosis may be due to a number of processes, including atelectasis, pulmonary infarction, aspiration pneumonia, Acute Respiratory Distress Syndrome (ARDS) and pulmonary edema
GIT hemorrhage occurs frequently in patients with heatstroke.
patients commonly exhibit evidence of hepatic injury, including jaundice and elevated liver enzymes and hypoglycaemia
acute liver failure due to centrilobular hepatic necrosis and cholestasis generally occurs in the first 48 hours, but it can peak as long as 2 weeks after the onset of heatstroke.
rhabdomyolysis occurs in nearly all patients with heat stroke, but particularly those with EHS.
although most are dehydrated, aggressive fluid resuscitation generally is not recommended because it may lead to pulmonary edema, and Rx of the hyperthermia may improve hypotension and cardiac function
rehydration will depend on pre-existing medical conditions, presence of hypovolaemia, etc.
critical patients will generally need a CVP line to assist in determining appropriate fluid replacement
hypotensive patients with high CVP may require inotropes, and it seems dobutamine may be the best in this situation as one wishes to avoid cutaneous vasoconstriction of alpha-adrenergic agents.
aim for urine output > 3ml/kg/hr to minimise rhabdomyolysis-induced renal failure
rapid reduction of the core body temperature to 39deg C at a rate of at least 0.2°C/mins the cornerstone of treatment because the duration of hyperthermia is the primary determinant of outcome.
insert temperature probe eg. rectal probe for continuous temperature monitoring
a thermal instability may persist for a few days, the temperature must be monitored continuously until it is stable.
remove clothing
spray water on body and use a fan - more comfortable and practical than submersion in ice-water
cover the patient with ice water–soaked sheets
place ice packs in the axillae and groin
cease active external cooling when temp falls to 39deg C to avoid overshooting & iatrogenic hypothermia
NB. antipyretics (eg. paracetamol) have no role in heat stroke and may be harmful, exacerbating liver damage
NB. dantrolene has not been proven efficacious in Rx of heat stroke
nil orally
may resume oral feeding when mental status, swallowing, and GIT function are normal
nasogastric tube to monitor for GIT bleed and fluid losses as well as to rest the GIT