Heat stroke is a medical emergency and remains one of the leading preventable causes of death in sport.Rapid reduction of core body temperature is the cornerstone of treatment because the duration of hyperthermia is the main determinant of outcome. Patients diagnosed with exertional heatstroke (EHS) or non-exertional heatstroke (NEHS) should be admitted to the hospital for at least 48 hours to manage complications.
When heat stroke is suspected, cooling should begin immediately and should be continued while resuscitating the patient. The American College of Sports Medicine recommends that cooling be initiated on the spot before transporting the patient to an emergency department for further evaluation and treatment.Despite extensive education and training, delays are still reported due to athletic trainers' concern to accurately diagnose and promptly initiate treatment for EHS.
There is still controversy about which therapeutic modality is most effective in the treatment of heat stroke. However, the basic premise of rapidly reducing core temperature to around 39°C (to avoid overeating and rebound hyperthermia) remains the main goal. Rehydration therapy alone is insufficient for patients with heat stroke and must be combined with active cooling.[sixteen]
According to 1 study, oral temperature assessments consistently reflected inaccurate core body temperatures, delaying diagnosis and eventual treatment of patients with heat stroke. Rectal temperature remains the preferred method of accurately obtaining core body temperature.
Some studies have shown that rapidly reducing exposure to excessive heat can dramatically improve long-term results and reduce irreversible damage. If treatment is started within this so-called golden hour and is aggressive enough to rapidly reduce core body temperature, complications (including multi-organ failure) can be avoided and the patient can have a much better prognosis.
In a review of 19 clinical trials and observational studies involving 556 patients, the conduction cooling method was found to be most effective in active young adults with EHS. Unfortunately, this review did not identify a preferred treatment found for NEHS or a temperature endpoint to prevent overcooling.
Removing restrictive clothing and spraying the body with water, covering the patient with sheets soaked in ice water, or placing ice packs on the armpits and groin can significantly reduce the patient's temperature. Patients who are unable to secure their airway should be intubated. Patients who are awake and responsive should receive supplemental oxygen.
Intravenous lines may be placed prior to fluid resuscitation and for dextrose and thiamine infusion if indicated. Hypoglycemia is a common occurrence in patients with EHS and may be a manifestation of liver failure; therefore, infusion of 50% dextrose in aqueous solution (D50W) should be considered in all patients with heat stroke.
Critical care providers must pay close attention to the airway, reduce temperature, limit heat production, optimize circulation, and monitor and treat complications. Interventions to enable monitoring include the following:
Insert a thermistor probe or Foley catheter with temperature sensor to continuously monitor temperature
Insert a nasogastric tube to control gastrointestinal bleeding and fluid losses
Place a Foley catheter to monitor urine output and/or monitor body temperature
The goal of treatment is to reduce the temperature by at least 0.2°C/min to approximately 39°C. A flexible internal thermistor can be placed rectally or an esophageal probe to monitor core body temperature during treatment; Alternatively, a more modern method is to use a temperature-sensitive Foley catheter. As thermal instability can persist for a few days after the onset of heat stroke, the temperature must be continuously monitored until it stabilizes.
Antipyretics (eg, acetaminophen, aspirin, and other nonsteroidal anti-inflammatory drugs) have no role in the treatment of heat stroke because antipyretics interrupt the change in the hypothalamic set point caused by pyrogens; they are not expected to act on a healthy hypothalamus that has been overworked, as in the case of heatstroke. In this situation, antipyretics can actually be harmful in patients who develop liver, blood and kidney complications, as they can aggravate bleeding tendencies.
Dantrolene has been studied as a possible pharmacological option in the treatment of hyperthermia and heatstroke. However, so far, it has not been shown to be effective in clinical trials.
Immediate administration of benzodiazepines is indicated in patients with agitation and shivering to stop excessive heat production. Furthermore, benzodiazepines are the sedatives of choice in patients with sympathomimetic-induced delirium, as well as alcohol and sedative drug withdrawal.
Neuroleptics (eg, chlorpromazine), which have been mainstays of therapy in the past, should be avoided because of their deleterious adverse effects, including decreased seizure threshold, interference with thermoregulation, anticholinergic properties, hypotension, hepatotoxicity, and other adverse effects.
Benzodiazepines and, if necessary, barbiturates are the recommended agents for treating patients with seizures. Barbiturates can be used regardless of their theoretical sweat production impedance.
Phenytoin is not effective in controlling seizures in this situation. Patients whose seizures are refractory to benzodiazepines and barbiturates should be paralyzed and mechanically ventilated. Electroencephalographic monitoring is recommended in all these patients, and anticonvulsant medications should be adjusted accordingly.
Recommendations regarding administration of intravenous fluids for circulatory support differ among patient populations and depend on the presence of hypovolemia, pre-existing medical conditions, and pre-existing cardiovascular disease.
Although patients with heat stroke are invariably volume depleted, cooling can only improve hypotension and cardiac function by allowing blood to be redistributed centrally. Aggressive fluid resuscitation is generally not recommended because it can cause pulmonary edema. Cor pulmonale is also a common finding in patients with heat stroke.
When pulse rate, arterial pressure, and urine output do not provide adequate hemodynamic information, fluid administration should be guided by more invasive hemodynamic parameters such as central venous pressure (CVP), pulmonary capillary pressure, and systemic vascular resistance index (SVRI) . , and cardiac index (CI) measurements. Patients who exhibit a hyperdynamic state (ie, high CI, low SVRI) generally respond to cooling and do not require large amounts of intravenous crystalloid infusions.
Hypotensive patients who exhibit a hypodynamic response (ie, high CVP, low CI) have historically been treated with low doses of isoproterenol; however, its arrhythmogenicity has raised questions about its continued use. Dobutamine, which is less arrhythmogenic than isoproterenol and more cardioselective, may be the inotrope of choice in these patients. Alpha-adrenergic drugs are generally contraindicated because they cause vasoconstriction and may interfere with heat loss.
the occurrence ofrhabdomyolysisIt may be heralded by the development of dark, tea-colored urine and tender, edematous muscles. Rhabdomyolysis releases large amounts of myoglobin, which can precipitate in the kidneys and causeacute kidney injury(GO). Renal failure is especially common in patients who develop hypotension or shock during the course of their illness and may occur in up to 25-30% of patients with EHS.
Treatment of rhabdomyolysis involves infusion of large amounts of intravenous fluids (fluid requirements can be as high as 10 L), alkalinization of the urine, and infusion of mannitol. Fluid administration is best guided by invasive hemodynamic parameters, and urine output should be maintained at 3 mL/kg/hr to minimize the risk of renal failure.
Urine alkalinization (to a pH of 7.5 to 8.0) prevents myoglobin precipitation in the renal tubules and may control acidosis and hyperkalemia in acute massive muscle necrosis. Mannitol can improve renal blood flow and glomerular filtration rate, increase urine output, and prevent fluid accumulation in the interstitial compartment (through its osmotic action). Mannitol is also a free radical scavenger and therefore can reduce free radical damage. Once renal failure occurs, dialysis is the only effective therapeutic modality for rhabdomyolysis.
Muscle necrosis can occur so rapidly that hyperkalemia, hypocalcemia, and hyperphosphatemia become significant enough to cause cardiac arrhythmias and require immediate treatment. In the presence of renal failure, hemodialysis may be required.
Hypertonic dextrose and sodium bicarbonate can be used to displace potassium into the intracellular environment, depending on more definitive measures (eg, intestinal potassium binding, dialysis). The use of insulin may not be necessary in non-diabetic patients and may be harmful for patients with EHS and patients with hepatic impairment, who commonly develop hypoglycemia.
Calcium must be used wisely because it can precipitate and cause further muscle damage. The use of calcium is reserved for patients with ventricular ectopy, impending seizures, or electrocardiographic evidence of hyperkalemia.
Other electrolyte abnormalities have been reported in patients with heat stroke and should be closely monitored and treated with care. These abnormalities may be related to conditions that alter solutes, such as vomiting, diarrhea, and diuretic use. For example, hypokalemia, which is common in the early stages of heat stroke, can develop in response to respiratory alkalosis, diarrhea, and sweating. Likewise, hyponatremia may be due to sodium losses and/or rehydration with low-salt solutions (eg, water), and hypernatremia may be due to dehydration.
Heat stroke usually leads to severe but reversible liver damage. Liver injury is represented by elevations in transaminase and bilirubin levels. During this phase, hypoglycemia, abnormal clotting, cerebral edema and death can occur, although rarely.
Prolonged clotting times may also indicate the development ofdisseminated intravascular coagulation(CID), which, when present, carries a poor prognosis for the patient. Clinical manifestations can range from abnormal laboratory values to widespread bleeding that occurs approximately 48 hours after the initial insult. IHD can also predispose patients to the development of acute respiratory distress syndrome (ARDS), which also increases mortality.
Treatment of liver failure includes the following:
Infusion of dextrose solutions to correct hypoglycemia
Early recognition and treatment of DIC, with replacement of clotting factors, fresh frozen plasma, platelets and blood
meticulous respiratory support
Pulmonary edema is a common complication of heat stroke and can be caused by a number of factors, including fluid overload from aggressive rehydration, renal failure, congestive heart failure, and ARDS. The latter can develop due to multiple insults, including heat-induced lung injury, aspiration pneumonia, and as a complication of liver failure. ARDS must be treated aggressively, with early mechanical ventilation and positive end-expiratory pressure (PEEP).
Acute kidney injury (AKI) can occur due to direct thermal injury to the kidney, myoglobinuria, hypotension and/or shock.acute tubular necrosis). Early manifestations of AKI include oliguria, low-grade proteinuria, and granular casts.
AKI is initially treated with intravenous fluid therapy, diuretics, and correction of associated electrolyte and acid-base abnormalities. In the setting of rhabdomyolysis, mannitol may be the diuretic of choice because it does not interfere with the acid-base status of the urine and may have antioxidant activity. Furosemide can cause tubular acidosis and therefore promote myoglobin deposition in the renal tubules. Once kidney failure occurs, hemodialysis is the most effective therapy.