**6. Prognostic factors**

**Table 1** shows prognostic factors in patients with heat stroke. These factors increase mortality and morbidity.

### **7. Risk factors for heat stroke**

The factors that increase the chances of a classic heat stroke are age, obesity, poor physical condition, lack of acclimatization, no air conditioning, and social isolation. Other risk factors are the use of illicit drugs, recreational drugs, and comorbidities such as cardiovascular disease and diabetes mellitus.

The factors associated with increased mortality and morbidity in heat-exertion patients are the degree of temperature elevation and the number of organ dysfunction [1, 5].

### **8. Clinical presentation**

Elevated core body temperature and central nervous system disorder are diagnostic presentations of heat stroke.

With increased body temperature or hyperthermia, there will be tachycardia, tachypnea, wide pulse pressure, and hypotension mostly due to dehydration. Organ dysfunction can manifest as noncardiogenic pulmonary edema with crepitation and desaturation.

If coagulopathy is severe will be skin rashes, petechiae, and ecchymosis, the neurological dysfunction will be manifested by an altered level of consciousness, speech distortion, agitation and irritability, seizure, or coma [6].

## **9. Diagnosis**

A missed diagnosis of heat stroke increases mortality and morbidity. Accurate measurement of core body temperature is essential in these patients. The X-ray chest may show diffuse infiltrates and signs of pulmonary edema. ECG may show different changes, from dysrhythmias to ST segment changes [1, 4].

CBC (complete blood count), renal function, coagulation parameters, and serum urinary electrolytes may be deranged. Usually, liver function takes a day or two to be deranged.

### **10. Management**

Early diagnosis, quicker cooling, correction of electrolyte abnormalities, and supportive care are essential for a better patient outcome.

Depending on the patient's level of consciousness, if the patient is still able to obey commands, oxygen supplementation via face mask or nasal cannula should be enough. If the patient has lower GCS and cannot protect the airway, intubation, and mechanical ventilation are mandatory.

Hypotension or shock management should be guided in critically ill patients with the use of novel tools for hemodynamic monitoring and the use of point-of-care ultrasound technologies.

These patients, if still hypotensive after resuscitation, may require vasopressors and inotropes. Cooling with temperature monitoring. Rapid cooling with accurate core body temperature monitoring is essential for patients with heat stroke.

Evaporative and connective cooling are found to have a better outcome, as they are effective maneuver and easy to perform.

Evaporative and connective cooling are performed with a spray of a moist tube of warm water and using fans to blow air over the moist skin of a naked patient.

The technique may require sedation with shorter-acting agents, particularly if patients are irritable or have altered mental status.

Immersing these patients in ice water is also a rapid, noninvasive method of cooling patients. Those patients are immersed, and it is difficult to have a venous cannula. Another alternative is to place the patient on a porous stretcher positioned on top of a tub of ice water and have paramedical staff continuously pour ice water from the bath onto to patient and manage the major muscular area [7]. Here, we can better monitor patients and have intravascular accesses.

Otherwise continuously applying ice to the axilla, neck, and groin will also help in cooling.

More invasive is peritoneal and pleural cold water. Continuous lavage is an alternative but is invasive, and one has to be careful in patients with coagulopathy. More recently, intranasal cooling was also used in those patients [7].

Pharmacological therapy and alcohol sponges should be avoided. Alcohol may get absorbed by dilated skin vessels and may cause toxicity, whereas those anti pyritic medications, aspirin, and paracetamol are not useful in heat stroke patients as the mechanism does not involve a change in the hypothalamic set point. These may cause adverse effects on the liver [5, 7, 8].

All these patients' temperatures should be monitored continuously and accurately, either by rectal or oropharyngeal temperature monitoring.

Cooling measures should be stopped once a temperature of 38 or 39C is achieved in order to reduce the iatrogenic hypothermia [8].
