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Prosedurnya adalah:
  1. Memastikan korban mengalami heat stroke
  2. Memindahkan korban ke tempat sejuk dan berventilasi baik
  3. Mengguyur penderita dengan air dingin
  4. Massage kulit untuk mengatasi efek vasokontriksi dari air dingin dan mempercepat aliran darah
  5. Memeriksa suhu rektal tiap 10 menit jangan sampai kurang dari 38,5 0 C, (pertimbangan etis bisa dilakukan sublingual)
  6. Mempertahankan penderita jangan sampai relaps
  7. Pemberian obat jika perlu :
    • Infus cairan
    • Sedatif bila kejang terus menerus
Heat Stroke

The most serious type of heat related illness is heat stroke. Variably defined, heat stroke usually includes; (1) A core body temperature of more than 105°F (40.5°C), though the temperature may be lower (2) Central nervous system dysfunction, (3) Exposure to heat stress, endogenous or exogenous, and (4) Exclusions to include CNS infection, sepsis, neuroleptic malignant syndrome or malignant hyperthermia secondary to anesthetic agents. (Table 2) Some sources include a marked elevation of hepatic transaminases, however this is not universal. 1, 2 An alternate definition based on pathophysiology is as follows: a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multiorgan dysfunction in which encephalopathy predominates.4 The mortality in heat stroke patients is commonly cited as high as 10 percent, but may vary widely.16

Heat stroke in its severe form can lead to multiorgan dysfunction with a clearly increased mortality rate. Common complications include acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), shock, rhabdomyolysis, renal failure, cerebral edema, seizures, and hepatic dysfunction.2 In a retrospective chart study of patients with near fatal classic heatstroke that were admitted to an ICU in Chicago during the 1995 heat wave all had multi-organ dysfunction with neurologic impairment, 45% developed moderate to severe renal insufficiency; 10% developed ARDS; 57% had evidence of infection on admission. The inpatient mortality was 21%. In those discharged, a moderate to severe functional impairment existed in one third with no significant improvement at 1 year and an additional 28% of the patients had died.28

Several studies have attempted to characterize predictors of the development of multi-organ dysfunction in heat stroke. One of the most recent, a retrospective chart review of heatstroke patients admitted to teaching hospitals from 1998-2001 in India found the presence of metabolic acidosis, elevated creatinine kinase (CK) (>1000 IU/L), and elevated liver enzymes at initial presentation to be associated with the development of multi-organ dysfunction. Not surprisingly, those that progressed to multiorgan dysfunction presented for medical care later (4.1 vs. 2.3 mean days of hyperthermia prior to overall case fatality rate of 71.4%, increasing to 85% with concomitant multi-organ dysfunction. Delayed presentation, tertiary care facility with a possibly increased disease severity, and a delay in the initiation of treatment were all proposed factors contributing to the high mortality rate.2

Though the final common pathway of heat stroke is similar, there exist two distinct forms, classic (epidemic) and exertional heatstroke. Each has unique etiologies, risk factors, populations and presentations. Also known as epidemic heatstroke from its relation to heat waves, classic heat stroke typically is seen in the elderly and debilitated. Classic heatstroke primarily develops secondary to an external thermal insult. Exertion is not required or common in the development of classic heat stroke, with its development over days rather than minutes or hours. Several risk factors include lower socioeconomic status, alcoholism, and psychiatric medications. A case-control study revealed that those at greatest risk had pre-existing medical conditions, were socially isolated, confined to bed, lived on the top floor, or did not have access to air conditioning.29

Classical heat stroke victims often present anhidrotic secondary to the duration over which the condition develops, though this is not a diagnostic requirement. It is thought that failure of, or loss of sweating may play a more important role in the development of classical heat stroke than exertional.22 Hyperventilation, resulting in respiratory alkalosis with concomitant metabolic acidosis, is common in classical heat stroke with a pure lactic acidosis more typically seen in exertional heat stroke.1, 12, 14 Exertional heat stroke typically occurs in previously healthy young adults exercising or working in a hot and humid environment without prior acclimation, and is primarily due to internal heat production.30 It is typically reported in athletes, miners, foundry workers, firefighters and military recruits. Risk factors predisposing to the development of exertional heat stroke are similar to  classical heat stroke, see Table 3. Women have been cited to be relatively protected from exertional heat stroke as the body temperature at which thermoregulatory reflexes are activated are lower in women than men, and women appear to store less heat than men for a given workload. Proposed etiologies include lager muscle mass in men.22 This does not seem to be a universal finding however as a study of US Army soldiers revealed greater rates of hospitalizations and heat strokes among women than men.10 Patients usually present still sweating, tachycardic and hypotensive. Exertional heat stroke victims more commonly develop disseminated intravascular coagulation, acute renal failure, lactic acidosis, hypokalemia, and rhabdomyolysis when compared to classical heat stroke.16

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