Neuro-Ophthalmology & Neuro-Otology
Third nerve palsy
Jul. 25, 2022
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Heat stroke is characterized by hyperpyrexia with core body temperature greater than 40°C (104°F) and neurologic dysfunction. Heat stroke is usually due to prolonged exposure to excessive atmospheric temperature but can also occur following prolonged exertion in athletes. It is distinct from fever due to disease. This article describes the pathophysiology, prevention, and management of heat stroke.
• Neurologic manifestations such as seizures and impairment of consciousness are the most prominent features of heat stroke when core body temperature exceeds 41°C.
• Apart from exposure to excessive heat, several diseases and drugs predispose to heat stroke.
• Rapid cooling by various measures is the most important part of management if temperature goes above 40°C.
Heat stroke, also termed "sun stroke," is characterized by hyperpyrexia with core body temperature greater than 40°C (104°F) and neurologic dysfunction. Heat stroke is the only condition that is a true heat illness as there is clear evidence for a pathological elevation of the core body temperature, and it is recommended that terms such as “heat fatigue”, “heat exhaustion,” and “heat syncope” should be removed from the modern lexicon (31). As an environmental hyperthermia, heat stroke is distinct from fever due to disease. Heat stroke is a total breakdown of thermoregulation, and 2 classical forms have been described: (1) nonexertional, which occurs during heat waves without physical exertion, and (2) exertional heat stroke, which typically follows strenuous sports.
Heat stroke has been mentioned in the older medical literature under one name or another. Most of the studies of thermoregulation were conducted following introduction into the clinical practice of thermometry in the 19th century. Historical perspectives on thermoregulation have been reviewed elsewhere (07).
A notable victim of this condition was Sir Victor Horsley, the British pioneer of neurologic surgery, who met an untimely death during World War I from heat stroke at the age of 59 years (37).
• Neurologic manifestations are the most prominent features of heat stroke at temperatures higher than 41°C (105.8°F).
• Heat stroke is associated with lack of sweating (anhidrosis) but presence of sweating does not rule out the diagnosis of heat stroke.
• Survival and sequela from exertional heat stroke depend on the duration of hyperthermia.
At temperatures higher than 41°C (105.8°F), neurologic manifestations are the most prominent features and include delirium, hallucinations, seizures, and impairment of consciousness. Ataxia is an early sign, but other neurologic finding may be present including decorticate or decerebrate posturing, hemiplegia, status epilepticus, and coma. Cerebral edema is a common finding.
Classically, heat stroke is associated with lack of sweating (anhidrosis), but presence of sweating does not rule out the diagnosis of heat stroke. In later stages, anhidrosis develops due to body fluid depletion and loss of sweat gland function. Cardiovascular manifestations include tachycardia, tachypnea, and hypotension due to vasodilatation. As internal body temperature rises, myocardial contractility begins to decrease and is manifested by bradycardia.
Heat stroke may present with signs of ischemic stroke. There are rare cases of isolated trochlear nerve palsy due to lacunar midbrain infarction caused by heat stroke (13).
Survival and sequela from exertional heat stroke depend on the duration of hyperthermia. Whole-body cooling until 39°C within the first 30 minutes of collapse is the critical requirement for favorable patient outcome. The prognosis is optimal if heat stroke is diagnosed early and management with cooling measures and fluid resuscitation are instituted immediately. The prognosis is poorest when treatment is delayed for more than 2 hours. With prompt recognition and appropriate treatment, the survival rate in heat stroke is 90% to 100%, but in some occupations (eg, firefighter) the mortality rate may approach 80%. Fever of 41°C (105.8°F) at admission for heatstroke is a poor prognostic factor (23). High serum level of procalcitonin, observed in heatstroke without any concomitant bacterial infection, is not a valid mortality predictor. Elevation of plasma high mobility group box-1 protein on admission is an indicator of the severity of illness and a useful predictor of mortality in exertional heatstroke (38). An increase in S100B protein level on admission is an independent biomarker of poor prognosis in patients with heat stroke and requires prompt treatment (06). Early complications of heat stroke include the following:
• Overshoot hypothermia or rebound hyperthermia
Delayed complications of heat stroke include the following:
• Persisting neurologic deficits occur in approximately 20% of patients
Even in a moderate exercise activity such as mountaineering, the possibility of development of rhabdomyolysis, though rare, should be considered for all cases of heat stroke, especially those with a history of antipsychotic neuroleptics.
Cognitive functioning is affected, and the severity of impairment resulting from heat stroke can vary from mild deficits in attention and memory to severe global dementia. There can also be changes in affect and personality that are equally debilitating. Presenting temperature of 42°C (107.6°F) or higher, coma lasting more than 8 hours, and cardiovascular complications (hypotension and decreased cardiac output) indicate a poor prognosis.
Death is usually due to multiorgan failure, which is secondary to intravascular coagulation, acute renal failure due to rhabdomyolysis, liver failure, or adult respiratory distress syndrome.
In a retrospective cohort study on patients hospitalized with exertional heat illness, duration of recurrent hyperthermia, duration of CNS injury, and low Glasgow Coma Scale score in the first 24 hours following admission were independent risk factors of neurologic sequelae, which occurred in 24.4% of cases (41). The 90-day mortality rate varied according to the extent of CNS injury in these patients.
• Cause of heat stroke is loss of thermoregulation with hyperpyrexia.
• Several risk factors increase the susceptibility to heat stroke.
• As an environmental hyperthermia, heat stroke is distinct from fever due to disease.
• Heat stroke is a total breakdown of thermoregulation, and 2 classical forms are nonexertional heat stroke and exertional heat stroke, which typically follows strenuous sports.
Cause of heat stroke is loss of thermoregulation with hyperpyrexia. Risk factors for heat stroke are shown in Table 1.
• Extremes of age: infants and the elderly
- Involving genes that encode cytokines and heat-shock proteins
- Mutations altering channel properties of the TRPV1 gene
• Prolonged physical exertion in hot weather: athletes, soldiers, and miners
- Cardiovascular disorders
• Drug abuse
• Adverse effect of medications
- Alpha adrenergics
Heat waves are defined as 3 or more consecutive days during which the environmental temperature exceeds 32.2°C. Climate change may increase the risk of heat exhaustion around the world because it contributes to an increase in the frequency and severity of extreme weather events, including heat waves.
Heat stroke may manifest as “classic” or “exertional” depending on the etiology of the condition. Classic heat stroke occurs mostly in sick and immunocompromised individuals, with high morbidity and mortality during annual summer heat waves. Classic heat stroke is usually associated with exposure to hot environments in the absence of strenuous physical activity, and a common finding is hot, dry skin due to anhidrosis (20).
A series of cases has been described in which heat stroke resulted from a combination of factors: extreme weather conditions (external heat), exertion due to nonstop outdoor dancing to music, and use of recreational drugs (26).
Temperature balance. Body temperature is maintained as a balance between heat production from metabolism and heat loss or gain from the environment. Heat exchange at the body surface involves 4 mechanisms: (1) radiation, (2) convection, (3) conduction, and (4) evaporation. The first 3 mechanisms can be involved in both loss and gain of heat from the environment, with radiation being the most prominent.
Brain centers that control yawning are involved in thermoregulation, and yawning can be a symptom of loss of thermoregulation. According to the thermoregulatory theory of yawning, its function is to cool the brain in part by countercurrent heat exchange with the deep inhalation of ambient air (24). Several studies have confirmed and replicated the specific brain cooling and thermal window predictions derived from the thermoregulatory theory of yawning, and no evidence has been presented contrary to these findings.
Evaporation can only result in heat loss and is mainly a result of sweating. Evaporation of 1 L of sweat consumes 600 kcal of heat. Conditions that reduce sweating prevent loss of heat. Peripheral vascular diseases that impair vasodilatation also impair ability to tolerate heat stress. Thoracic sympathectomy can reduce sweating and disturb peripheral vascular and heart rate responses, which may play a role in the development of exertional heat stroke. Dehydration, by reducing sweating, predisposes to heat stroke.
Even with sweating, evaporation must occur for heat loss, and this is reduced in presence of high humidity. A combination of high temperature and high humidity is a strong risk factor for heat stroke.
Duration of physical exertion. Postmortem examinations of fatal exertional heat stroke cases reveal a possible association between the duration of exercise prior to the occurrence of exertional heat stroke and the extent of pathologic findings. In a retrospective study of athletes participating in endurance sports, for every serious cardiac adverse event, there were 10 serious events related to heat stroke (43).
Progression from heat stress to heat stroke. As a response to heat stress, the thermoregulatory center in the anterior hypothalamus stimulates the autonomic nervous system. An increase in cutaneous blood flow and stimulation of sweating via parasympathetic fibers occurs, resulting in loss of water and salt. The blood is shunted to the periphery, and the visceral perfusion is reduced, particularly to the intestines and the kidneys. Dehydration and salt depletion impair temperature regulation.
Several cytokines are produced in response to acute heat stress. These mediate an inflammatory response with fever, leukocytosis, muscle catabolism, and stimulation of the hypothalamic-pituitary-adrenal axis. Expression of heat-shock proteins also occurs due to binding of the heat-shock transcription factors to the heat-shock elements. Increased level of heat-shock proteins serves a protective function against a subsequent heat stress. Conditions associated with low levels of expression of heat-shock proteins such as aging, lack of acclimatization, and genetic polymorphisms, may facilitate the progression from heat stress to heat stroke. Long-term consequences of heat stroke are due to a systemic inflammatory response syndrome that may lead to multi-organ dysfunction and death. In those who survive, the inflammatory response diminishes in magnitude and eventually subsides to allow return-to-normal homeostasis (14).
Contribution of drugs to heat stroke. Several medications impair the body's ability to disperse heat. For example, anticholinergic drugs impair sweating and diuretics cause volume depletion. Phenothiazines deplete the central stores of dopamine and interfere with the thermoregulatory center of the hypothalamus.
Neuroleptics deregulate mechanisms of temperature regulation and can predispose to heat stroke. During a heat wave in Brazil in 2014, with environmental temperatures ranging between 350°C to 420°C, an elderly schizophrenic patient on long-term clozapine therapy presented with heat stroke and axillary temperature of 41.90°C, but recovered with cooling measures without discontinuation of clozapine (16).
Inflammatory disorders as predisposing factors. Nonfebrile infections and other inflammatory disorders can aggravate the hyperthermia of exercise and possibly increase susceptibility to heat stroke.
Gene mutations. A genetic form of anhidrosis has been reported in members of a family in the presence of structurally normal eccrine sweat glands, but a homozygous missense mutation in the gene ITPR2, which encodes the type 2 inositol 1,4,5-trisphosphate receptor, and loss of this receptor-mediated Ca2+ release causes isolated anhidrosis (19).
Whole exome sequencing has enabled identification of mutations altering channel properties of the TRPV1 gene, which is involved in thermoregulation and nociception, and is linked to exertional heat stroke -- 1 of the top 3 causes of sudden death in athletes (02). This finding provides the basis to explore genetic causes and molecular mechanisms governing pathophysiology of exertional heat stroke.
Pathomechanism of heat cytotoxicity and its prevention. An animal experimental study has demonstrated increasing SO2 values in lysosomes during heat shock, which protects against damage induced by heat shock through regulating oxidative stress (44).
Pathophysiology of multiorgan dysfunction. This results from interplay of circulatory failure resulting from hyperthermia, the direct cytotoxicity of heat, and the inflammatory and coagulation responses of the host. There are alterations of flow in the microcirculation and injury to the vascular endothelium.
Pathophysiology of CNS changes in heat stroke. The central nervous system is particularly vulnerable to heat stroke. Cerebellum is the first part to be affected as manifested by ataxia and the last to recover. Downbeat nystagmus was described in a patient following classical heat stroke with vestibulocerebellar injury, but the patient made a full recovery without any neurologic sequelae, and a follow-up CT scan showed no cerebellar atrophy (08). Heat stroke is associated with cerebral ischemia as well as increased levels of interleukin-1beta, dopamine, and glutamate in the brain. These factors are known to increase free radical production.
Normal EEG tracing and reversibility of the unresponsive pupils were observed. In heat stroke patients with coma with convulsions who recovered after 2 weeks of successful treatments, MRI showed hyperintense signals on the right temporoparietooccipital cortex, which disappeared within 1 week (10). The cause of death in heat stroke is probably not CNS damage but systemic hemodynamic deterioration.
• Mortality rates for heat stroke range from 10% to 75%.
• Heat stroke is the third leading cause of death among American athletes.
• With global warming and increasing occurrence of heat waves, an increase in the incidence of heatstroke is expected in the future.
Approximately 390 deaths per year were reported in the United States between 1979 and 1995, with the highest incidence of 5 per million among those over 85 years compared to less than 1 per million in those ages 5 to 44 years (04). Current figures from the Centers for Disease Control and Prevention indicate that approximately 618 persons in the United States are killed by extreme heat every year. These figures are underreported, and other estimates range as high as 4000 deaths per year in the United States. Mortality rates for heat stroke range from 10% to 75%. Heat stroke is the third leading cause of death among American athletes. Since 1995, 39 football players have died in heat-related deaths in the United States. A study of heat illness hospitalizations for the United States Army from 1980 through 2002 shows a 5-fold increase in heat stroke hospitalization rates (1.8 per 100,000 in 1980 to 14.5 per 100,000 in 2001), although the hospitalizations from other heat-related illnesses declined during this period (03).
A Japanese study reported that deaths are more prevalent among males in the age groups of younger than 4 years, 15 to19 years, 50 to 54 years, and 80, whereas such deaths are rare among young females, although the number gradually increases with aging, peaking in the age group of 80 to 84 years (27).
Mortality rates are affected by improvement in preventive and intervention strategies. In Milwaukee, Wisconsin, heat-related deaths in 1999 were at least 49% lower than levels predicted by the 1995 relation between heat and heat-related deaths (39). Reductions in heat-related morbidity and mortality in 1999 were not attributable to differences in heat levels alone; rather, changes in public health preparedness and response may also have contributed to these reductions.
A heat wave in 2003 caused approximately 1000 deaths in 1 week alone in the United Kingdom and approximately 10,000 overall in France, where temperatures were higher (18). The heat wave resulted in an elevation of the death rates of patients admitted to the hospital and the intensive care unit in Paris. Despite adequate cooling and supportive therapies, the mortality rate for heat stroke remained elevated, and the neurologic after-effects were severe (25). Heat stroke was responsible for a 25% increase in hospital mortality in France during that summer in 2003, compared to the same period during 2002, and is regarded as a nosocomial disease (09). With global warming and increasing occurrence of heat waves, an increase in the incidence of heatstroke is expected in the future.
An analysis of data from heatstroke studies of 2006, 2008, and 2010 carried out by the Heatstroke Surveillance Committee of the Japanese Association for Acute Medicine, showed that incidence of neurologic sequelae in patients with heat-related illness was 2.2% (28). Another finding was that heatstroke patients who were admitted to the hospital with severe disturbance of consciousness, and a higher body temperature requiring a longer cooling time to achieve the target temperature, were more likely to experience neurologic sequelae.
• Heat stroke is predictable and preventable.
• The best prevention is to avoid hot environments, particularly those at risk.
Heat stroke is predictable and preventable. The incidence of heat stroke can be reduced by attention to environmental conditions and acclimatization of the athletes, soldiers, and miners. During the heat wave in summer of 1999 in Chicago, which resulted in 80 deaths, a working air conditioner was found to be the strongest protective factor against heat-related deaths (29). Preventive strategies in general have reduced the mortality from heat stroke.
The best prevention is to avoid hot environments. To assess the environmental danger, a Heat Index Chart produced by the United States National Weather Service may help to determine when outside activity should be avoided (Table 2). The heat index combines the effects of heat and humidity to arrive at an apparent temperature.
Possible heat disorders for people in higher risk groups
130°F or higher
Heat stroke and sunstroke highly likely with continued exposure
105°F to 130°F
Sunstroke, heat cramps, or heat exhaustion likely, and heat stroke possible with prolonged exposure or physical activity
90°F to 105°F
Sunstroke, heat cramps, and heat exhaustion possible with prolonged exposure or physical activity
Source: U.S. National Weather Service
Guidelines from the American College of Sports Medicine emphasize fluid replacement and acclimatization to the heat as well as practice uniforms and other modifications to reduce the risk for heat exhaustion and exertional heat stroke in young football players (01). If exertional heat stroke is suspected, players should be stripped of equipment and immediately cooled in a tub of ice water until emergency personnel can assume care and evacuate the athlete to the nearest emergency facility.
Prevention of heat stroke involves identification of persons at risk who should avoid exposure to extreme heat. This is important for soldiers wearing protective gear who may be exposed to extreme heat while on active duty in hot climates. Some soldiers may have a genetic predisposition to exertional heat illness that should be identified and should be grounds for nondeployment to active duty. Two measures are useful if exposure to extreme heat is unavoidable: refreshing oneself at least 2 hours per day in a cool place (less than 26°C or 78.8°F) and drinking before feeling thirsty.
Experience with past heat waves, and the possibility of future heat waves associated with global warming, points out the importance of prevention of heat stroke as it carries significant mortality and morbidity despite aggressive treatment. Preventive measures include environmental heat stress reduction, air conditioning, increased fluid intake, heat emergency warning systems, and avoiding exposure of the elderly to heat. Commercially available sensors can be embedded into football helmets to monitor an athlete's temperature. The device alerts the coach when a player's temperature reaches over 39.2°C (102.5°F). In a study on Chinese military personnel, heat acclimatization training before strength training in a high temperature and humidity environment was shown to effectively reduce the degree of inflammation reaction of exertional heat syndrome, protect the physiological functions of various organs, and reduce the incidence of multiple organ dysfunction syndrome (22). Measurement of antibodies to heat-shock proteins may be useful in assessing how individuals are responding to abnormal heat stress within their living and working environment and may be used as a biomarker to evaluate their susceptibility to heat-induced diseases.
The diagnosis of heat stroke is based on the history of heat exposure or physical exertion, underlying medical problems, and use of drugs predisposing to this condition. It should be differentiated from another heat-related disorder, heat exhaustion, which is characterized by the following:
• Hyperpyrexia or normal temperature
Heat exhaustion may precede and partially overlap heat stroke. Heat exhaustion should be recognized and managed prior to progression to heat stroke. Other main conditions in differential diagnosis of heat stroke are malignant hyperthermia, neuroleptic malignant syndrome, and serotonin syndrome. Exercise-induced rhabdomyolysis can be considered in the differential diagnosis, as patients with this condition have mutations at the ryanodine receptor (RYR1) gene and are susceptible to malignant hyperthermia. A study found mutations in the RYR1 gene in 13% of patients with exertional heat stroke, which is higher than that expected in the general population (36). This finding, along with a positive response to the malignant hyperthermia in vitro contracture test, indicates an association between exertional heat stroke and malignant hyperthermia. High fever due to infections such as meningitis, brain abscess, typhoid, and cerebral malaria should be ruled out. Neurologic conditions in differential diagnosis include cerebellar disorders, status epilepticus, and cerebral hemorrhage.
Exertional heat stroke can occur in cool atmospheric conditions in marathon runners, and rectal temperature should be measured in collapsed long distance runners who do not show rapid recovery of vital signs and cognitive function.
• Vital signs and routine blood examination.
• Brain imaging if there are neurologic signs.
• Diffusion tensor tractography.
Vital signs to be recorded in victims of heat stroke include pulse and blood pressure measurement and rectal temperature recordings. An electrocardiogram and a chest x-ray should be taken. Laboratory evaluation should include arterial blood gas analysis, a complete blood count, toxicology screen, blood coagulation studies, and measurement of electrolytes, blood urea nitrogen, creatinine, glucose, creatine phosphokinase, and liver enzymes.
Brain imaging studies should be done in patients with neurologic signs. There may be loss of distinction between gray and white matter on CT scans. MRI is particularly useful. Cerebral edema and cerebellar damage can be detected. Symmetric lesions in the dentate nuclei and cerebellar peduncles have been reported in MRI of heat stroke patients (21). Lesions of the globus pallidus and hippocampal hyperintensities have also appeared on the MRI of a patient with heat stroke (15). Neurophysiological monitoring is indicated in the acute stages of hyperpyrexia to monitor the neurologic effects and to determine prognosis.
Diffusion tensor tractography is a useful tool for evaluating the status of white matter tracts across a wide range of conditions where CT and MRI may not show significant findings. In a patient with heat stroke, the corticospinal tract, the corticoreticular pathway, the cingulum, the fornix, the medial lemniscus, and the arcuate fasciculus were reconstructed using diffusion tensor tractography (05). A narrowing, discontinuation, and decreased fractional anisotropy and fiber volume of the examined neural tracts were correlated well with the symptoms and helped in planning appropriate rehabilitation strategies.
Race simulation testing on a treadmill should be considered in marathon runners with recurrent exertional heat stroke for decisions about return-to-activity and limits of performance. This test was used on a runner in an environmental chamber at 25°C and 60% relative humidity at a treadmill pace of 10.5 to 12.9 km/h (35). The test was stopped at 70 minutes when the rectal temperature rose to 39.5°C with weight loss due to profuse sweating, which led to the recommendation to limit runs to less than 1 hour, acclimatization to heat before racing, and adequate replacement of fluids as well as salt during activity.
• Cooling by immersion in water, selective brain cooling, and endovascular cooling.
• Treatment of systemic effects of heat stroke.
A febrile illness should be ruled out as the treatment of fever differs from that of environmental hyperthermia. Attempts to cool a febrile patient rapidly may cause shivering, and the body may attempt to reset the thermostat to maintain the set point temperature. Antipyretic medications are used in fever, but they are not useful for environmental hyperthermia. Dantrolene is the drug of choice for the treatment of malignant hyperthermia, but it has not proven effective in the treatment of heat stroke.
Initial resuscitation following heat stroke involves establishment of intravenous access with normal saline or lactated ringer solution to replace fluid losses, insertion of an electronic thermistor rectal probe for monitoring core temperature, high flow supplemental oxygen, and pulse oximetry.
Cooling. If temperature is above 40°C (104°F), rapid cooling should be initiated. Cooling in the field immediately at time of collapse can be done with ice or tepid water (1°C to 16°C; 33.8°F to 60.8°F) and in the emergency department by immersion in ice water (1°C to 5°C; 33.8°F to 41°F) and evaporation. Evaporation cooling techniques are simple, noninvasive, and readily available everywhere and can be supplemented by ice packs. Ice water immersion is very effective in exertional heat stroke, with no fatality in a large case series of younger patients, whereas evaporative plus convective cooling is recommended for older patients with nonexertional heat stroke (11).
If simple measures are not adequate, immersion of the patient in water can be considered but it is cumbersome and not practical for comatose patients, particularly in those with various lines and monitoring equipment. Cold gastric or peritoneal lavage is an invasive procedure and is slower. A severe case of exertional heatstroke with multiple organ dysfunction has been successfully treated with induced therapeutic hypothermia (33°C) using a noninvasive external cooling system (17). Innovative methods of cooling include the following.
Selective brain cooling. This can be accomplished by using intranasal delivery of a mixture of high flow gas and cold liquid.
Endothermic cooling. A study has shown that CAERvest®, a chemically activated and unpowered cooling device, is effective for reducing body temperature in healthy normothermic individuals without presence of cold injury (40). Further investigation should be done in patients with heat stroke.
Endovascular cooling. Cool Line catheter and Cool Gard cooling device for intravascular application are highly efficacious for prophylactic control of body temperature in neurologic intensive care patients with severe intracranial disease and can be applied to heat stroke victims. Cooling is stopped when the temperature drops to 38.5°C to 39°C (101.3°F to 102.2°F) to avoid overshoot hypothermia.
Management of systemic manifestations. When multiple organs are affected, multidisciplinary management may be required in an intensive care unit. Other manifestations may be managed as required:
• Shivering can be treated with chlorpromazine.
• Seizures can be controlled with diazepam or phenobarbital.
• Mannitol and diuretics should be administered as needed to maintain urine output at 50 to 100 mL per hour.
• In patients with multiorgan failure, treatment with antithrombin and steroids may be useful. Heat stroke is a severe inflammatory response disease, and anticoagulants, such as antithrombin III, inhibit inflammation resulting from various causes. Correction of reduced antithrombin III levels to supranormal by therapeutic administration of antithrombin III concentrate in disseminated intravascular coagulation of heat stroke is not associated with any bleeding complications. Antithrombin III pretreatment was shown to improve survival in a rat model of heat stress-induced acute inflammation, and the improvement was possibly due to inhibition of secretion of cytokines (12). Therapeutic plasma exchange has been shown to be effective in reversal of the inflammatory process and recovery from multiorgan failure (33).
• Hyperbaric oxygen therapy has been successfully used for treatment of heat stroke with multiple organ dysfunction (30).
• In an animal experimental study, circulatory shock and cerebral ischemia injury in heat stroke was attenuated by combination treatment with dexamethasone and hydroxyethyl starch (42).
Rapidly worsening organ dysfunction in heat stroke may lead to death, even when cooling procedures and intensive care management are promptly started (32).
Only 1 report implicated heat stroke as a probable cause of multiple fetal anomalies (34). Since then, no definite studies are available on this topic.
K K Jain MD†
Dr. Jain was a consultant in neurology and had no relevant financial relationships to disclose.See Profile
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