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Year : 2020  |  Volume : 18  |  Issue : 2  |  Page : 87-93


Department of Emergency Medicine, Christian Medical College, Vellore, Tamil Nadu, India

Date of Submission03-Jan-2020
Date of Decision27-Jan-2020
Date of Acceptance06-Feb-2020
Date of Web Publication17-Apr-2020

Correspondence Address:
Dr. Abhijit Goyal-Honavar
Department of Emergency Medicine, Christian Medical College, Vellore, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cmi.cmi_4_20

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Heat-related illnesses are a common cause of morbidity and mortality in tropical climates; they range from innocuous heat cramps to life-threatening heat strokes, and yet, the data regarding their evaluation and management are far from definitive. It is a condition with an evolving definition, the most recent by the Japanese Association for Acute Medicine eschewing the use of specific temperature cutoffs. Cooling measures such as evaporative cooling are of utmost importance in bringing about a rapid decrease in core body temperature, with evidence showing the effectiveness of invasive measures and other techniques to reduce organ dysfunction unsatisfactory. High-quality prospective studies comparing various modalities of treatment is the need of the hour, and the implementation of preventive measures must be more widely undertaken.

Keywords: Definition, evaluation prognosis, heat stroke, heat-related illness, management

How to cite this article:
Goyal-Honavar A, Markose AP, Abhilash KP. Heatstroke. Curr Med Issues 2020;18:87-93

How to cite this URL:
Goyal-Honavar A, Markose AP, Abhilash KP. Heatstroke. Curr Med Issues [serial online] 2020 [cited 2023 Feb 3];18:87-93. Available from: https://www.cmijournal.org/text.asp?2020/18/2/87/282780

  Introduction Top

Heat-related illnesses: A spectrum of severity

Heat-related illnesses are a collection of disorders resulting from a mismatch between the metabolic production of heat and physiological measures to ensure heat loss.[1] They present with a constellation of symptoms and signs consequent to failure of thermoregulation and are characterized by hyperthermia, defined as the elevation of core body temperature above the normal range of 36°C–37.5°C. It is important to differentiate this elevation of core body temperature from fever, which is induced by cytokine activation during inflammation and is regulated at the level of the hypothalamus. They have a spectrum of severity, ranging from heat cramps to heatstroke (HS).

Heat cramps are the most innocuous of the heat-related illnesses, manifesting as brief cramps following periods of exertion. Despite core body temperatures between 37°C and 39°C, mental function is unaltered in such patients. The painful, involuntary muscle spasms that characterize heat cramps are caused by fluid and electrolyte loss following excessive exertion in hot environments.

Further along the spectrum of heat-related illnesses lies heat exhaustion, wherein generalized weakness, fatigue, nausea, headache, vertigo, and syncope predominate. Much like heat cramps, mental status is not disturbed despite a core body temperature of 37°C–40°C.

Heat cramps and heat exhaustion respond well to conservative measures, such as rest in a cool area and replenishing fluids and nutritional needs of the body.

Heatstroke: A paradigm shift

Farthest along the spectrum of severity lies HS, which is characterized by much higher morbidity and mortality than the other heat-related illnesses, with some estimates of mortality ranging from 10% to 50%.[2] Despite its well-recognized severity, even at the turn of this decade, it has not received the level of attention that it warrants. The definition of a HS is an evolving one, while authors such as Bouchama and Knochel[3] once described it as a condition characterized by core body temperature greater than 40°C and altered mental status following exposure to severe environmental heat, more recent attention cast on the subject by the Japanese Association for Acute Medicine (JAAM)[4] in 2014 led to a focus on organ dysfunction involving the central nervous system (CNS), coagulation cascades, liver, and kidney irrespective of temperature. The 2016 revision of the JAAM criteria by the HS Working Group[5] simplified the criteria to patients exposed to high environmental temperature and met at least one of the following:

  1. Glasgow Coma Scale (GCS) score ≤14
  2. Creatinine or total bilirubin levels of ≥1.2 mg/dL
  3. JAAM disseminated intravascular coagulation (DIC) score ≥4 [Table 1].
Table 1: Definition of heat stroke

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Despite its reliance on core body temperature, which has been shown to be an inconsistent feature of HS, Bouchama's definition remains the most commonly used worldwide to diagnose HSs.

Two forms of HS are recognized.[3] Exertional HS primarily affects young, healthy, and athletic individuals exercising vigorously in hot and humid climates until the body's normal thermoregulatory mechanisms are overwhelmed. Exertional HS is characterized by a rapid onset and is frequently associated with a high core temperature.

Classic (passive or nonexertional) HS is caused by environmental exposure and occurs in young children, in elderly patients, or in patients with underlying chronic illnesses, who are exposed to extreme environmental conditions. Classic HS can develop slowly over several days.

  Epidemiology Top

The National Crime Records Bureau reports that the annual mortality due to HS has been on the rise over the past several years, a trend which is expected to continue and attributable to climate change.[6] These deaths are most numerous in the states of Andhra Pradesh, Uttar Pradesh, and Punjab. They are also much more common among males, although the number of female deaths due to HS has risen steeply since 2014.

A study in our own center noted that 72 patients presented with heat-related illness between the predominant summer months of April and May 2016. Almost two-third of them were found to have HS, with near equal distribution between exertional and classical varieties. More than half the patients were male, although the disparity between genders was not as wide as reported elsewhere. Notably, the highest mortality was attributed to classical HS (23.8%), followed closely by exertional HS (20%) and heat exhaustion (15.4%).

Another study in Chennai, Tamil Nadu,[7] also found a slight male predominance, with a mean age of 53 years. A fifth of those patients had premorbid conditions, the most widely prevalent being diabetes and hypertension.

While heat-related illnesses are classically a problem of Southeast and East Asian countries, changing global climate and increased occurrence of heat waves in temperate regions is resulting in the appearance of this illness in previously unaffected countries, often leading to a diagnostic dilemma among physicians inexperienced with the condition.[8]

Extensive research and evaluation is the need of the hour to cope with the expected rise in HS deaths, which are expected to rise to two and a half times their current mortality by the 2050s.[9]

  Pathophysiology Top

Regulation of normal body temperature is a function of the anterior hypothalamus. As body temperature increases, active sympathetic cutaneous vasodilatation increases blood flow to the skin and initiates sweating.[10] Further exposure to heat leads to a reduction in intravascular volume, which may lead to heat syncope. Loss of water and salt depletion through this process leads to heat exhaustion and cramps.[11] These can be easily corrected by replenishing the lost fluids and electrolytes.

The pathophysiology of heatstroke, however, is a complicated cascade of acute physiological alterations. The cytotoxicity of heat, combined with systemic inflammatory response, oxidative damage, and attenuated heat shock responses lead to a state of multi-organ dysfunction.[12]

The physiological alterations implicated include arterial hypotension, intracranial hypertension, cerebral hypoperfusion, and increased metabolic rate.

Further, these inflammatory and procoagulant responses, together with direct cytotoxic effects of heat, cause vascular endothelial injury.[3] This leads to microthromboses and a consequent consumption of platelets. Clinically, the HS-induced coagulation and fibrin formation leads to a state of DIC.

The circulatory shock and cerebral ischemia closely correlate to the release of certain endotoxins and cytokines, implying that despite their core differences in the initiation, the propagation of the HS response and sepsis bear certain similarities.

The presence of comorbid conditions adds to the temperature dysregulation that causes HS. For example, diabetes mellitus causes decreased sweat gland innervation and cutaneous vasodilatation via its effect on the autonomic nervous system. Some therapeutic measures may negatively impact the temperature balance, such as the advent of SGLT2 inhibitors, which may themselves predispose to HS.

Another example of a drug that increases susceptibility to HS is topiramate, which finds utility in the treatment of migraine and epilepsy. Up to 10% of pediatric patients may develop oligohydrosis, and in combination with environmental factors or other medication it precipitates HS.

Heat shock response; the role of heat shock proteins

Heat shock proteins (HSPs) are a group of molecules that play a critical role in achieving thermotolerance and protect from stress-induced cellular damage induced by heat, cold, and ultraviolet radiation.[3],[8] Advanced age, preexisting illnesses, dehydration, insomnia, and poor physical fitness are associated with low levels of expression of HSPs such as HSP70, and these factors thus predispose to developing classical HSs.

Genetic factors in heatstroke

Recent evidence points to the role of genetic factors in the predisposition to HS, such as the calsequestrin 1 gene on chromosome 1.[16] This gene is known to modulate skeletal muscle contraction by regulating the release of calcium stored in the sarcoplasmic reticulum. Differential capacities of muscles among individuals to modulate and release heat may play a part in causing thermal dysregulation.

  Differential Diagnosis Top

The most important differentials considered in a patient with severe hyperthermia include neuroleptic malignant syndrome and malignant hyperthermia.

As previously mentioned, HS is characterized by the preceding history of exercise and/or exposure to high ambient temperature. This typical history can help differentiate it from other causes of hyperthermia.

Neuroleptic malignant syndrome

Neuroleptic malignant syndrome is an idiosyncratic reaction associated with the consumption of first-generation, and less commonly, second-generation antipsychotics. It is recognized by the presence of “lead pipe” muscle rigidity, altered mental status, choreoathetosis, tremors, and evidence of autonomic dysfunction such as dysrhythmias, diaphoresis, and labile blood pressures.

Malignant hyperthermia

Malignant hyperthermia is an autosomal dominant disorder, caused by mutations in the Ryanodine calcium channel receptor. It manifests following treatment with anesthetic agents, most commonly succinylcholine and halothane. Clinical findings include muscle rigidity, especially masseter stiffness, sinus tachycardia, hypercarbia, and skin cyanosis with mottling.

Other differentials to consider are listed in [Table 2].
Table 2: Differential diagnoses of heat stroke

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  Prognostic Factors Top

A study performed in the medical intensive care unit (ICU) of our center[17] reports that more than three-quarter of patients admitted with HS developed multi-organ dysfunction. They noted respiratory failure to be the most common form of organ dysfunction.

Predictors of multi-organ dysfunction were recognized to be creatinine phosphokinase level >1000 U/L, metabolic acidosis, elevated liver enzymes, aspartate aminotransferase/alanine aminotransferase more than twice normal, lactate dehydrogenase >500 U/L, and leukocytosis defined as white blood cell count >11,000/cu mm.

A study from France by Argaud et al. among non-exertional HSs during the 2003 Paris heat wave considered all patients with core body temperature >40°C found much higher mortality among elderly patients with classical HS than younger patients with exertional HS (63% vs. 15%). They noted that the risk of mortality rose substantially in patients presenting with anuria, coma, or cardiovascular failure, as well as those who developed DIC during the course of treatment.[18]

Another study during the same period in France used a different cutoff for core body temperature (38.5°C) and identified previous treatment with diuretics, living in an institution, age >80 years, the presence of cardiac disease or cancer, core temperature >40°C, systolic arterial pressure <100 mmHg, GSC scale <12, and transportation to hospital in ambulance as prognostic factors associated with death in nonexertional HS.

A third French multicenter study examining patients affected by the same heat wave using Bouchama's original definition found high Simplified Acute Physiology Score II score, initial high body temperature, prolonged prothrombin time, and the use of vasoactive drugs in the 1st day of ICU admission to be predictors of hospital death.

Interestingly, Misset et al. also found that the risk of hospital death was almost twice as high among ICUs without air conditioning as compared to those equipped with air conditioning. There was no significant difference among ICUs with and without air conditioning in terms of beds, senior physicians, or the number of heatstroke patients admitted per ICU.[19] Hence, it is our unbridled recommendation that all critical care units anticipating management of cases of HS should be equipped with air-conditioning facilities, as a simple but effective means of lowering its mortality.

Hifumi et al.[20] from Japan, using the JAAM-HS criteria, noted that patients who developed DIC were more than twice as likely to suffer hospital mortality, with worsening mortality as the DIC score increased.

These factors are summarised in [Table 3]. Thus, it appears that the development of coagulopathy significantly worsens the outcome of HS. In our center, we recommend the use of DIC, core body temperature >40°C, and significant renal or hepatic dysfunction in determining the prognosis of HS patients.
Table 3: Prognostic factors among patients with heat stroke

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  Treatment Top

Patients with HS often present after a significant delay and with compromised airway, breathing, circulation, or a combination of these. Immediate recognition of this clinical syndrome will enable concurrent initiation of urgent stabilizing measures as well as definitive cooling methods.

Following this, the management of a case of HS involves preventing organ dysfunction and supporting organ systems [Figure 1].
Figure 1: Principles of management of heat stroke.

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Cooling the patient: How, how much, and how fast?

The former, i.e., cooling the victim, is the cornerstone of therapy and requires the creation of a gradient for heat loss between the skin and environment.

This may employ the four physical phenomena for heat transfer, namely radiation, conduction, convection, and evaporation. Several cooling methods have been described, ranging widely in cost, complexity, and mechanism, though most seem to be equally effective.

Noninvasive methods are simpler to implement and more widely used, including conductive whole-body immersion, limb immersion, and ice packs in the neck, axillae, and groin as well as evaporative wet sheets, water sprays, and fans.[21],[22],[23]

A prospective nonrandomized study showed that immersion in ice water between 1°C and 3°C of the torso and upper legs reduced the core body temperature at twice the rate of exposure to 24.4°C ambient air without any fans (0.2°C/min vs. 0.11°C/min) and reduced rectal temperature by 1°C within 5.6 ± 0.6 s. However, like other studies on the subject, it suffers many limitations that reduce the significance of these findings.[24]

Invasive methods described include the use of cold water bladder, gastric, peritoneal, and rectal lavage,[25] as well as hemodialysis and cardiopulmonary bypass. Novel intravascular cooling methods have been described, such as the use of intravascular balloon devices, and initial intravascular cooling has been shown to have good results.[26] Intravascular methods are particularly beneficial in effecting rapid cooling, with rates of up to 0.1°C/min. When compared to conventional cooling methods, intravascular methods achieved a significant reduction in the Sequential Organ Failure Assessment score in the first 24 h.

Unlike external cooling methods, these do not result in peripheral vasoconstriction but do necessitate the placement of an intravascular balloon catheter, which requires additional training and resources.

Extracorporeal circulation using hemodiafiltration circuits has also been employed with some benefit;[27] however, it is important to consider that no prospective, comparative studies have been performed confirming the superiority of any initial cooling method and conclusive data on the comparative efficacy of these are needed.

Also lacking is evidence to support a specific temperature end-point, though various studies have shown endpoints between 38°C and 39.6°C to be safe.[28] The largest of these case series concluded that a rectal temperature of 39.4°C is a safe and achievable endpoint.[3]

Since both the degree and the duration of hyperthermia contribute to the damage inflicted by exertional HS, many authors conclude that lowering the core body temperature within the “golden hour,” or the 1st h following HS is critical in mitigating the mortality and sequelae caused by the episode.[29],[30],[31]

In the experience of the authors of this review, evaporative and convectional cooling via application of sprayed water and forced air currents over the body work well to lower the core body temperature in HS and are easy to implement in most centers. We support rapid cooling of HS patients to a core body temperature of 101.2°F (38.4°C) in the 1st h with an ideal cooling rate between 0.1°C and 0.2°C/min.

Management of organ dysfunction

HS is associated with an inexorable progression to organ dysfunction; hence, managing the complications of HS is an important component of treating the patient.

A study in France[7] found that more than 40% of patients with HS had severe limitation of activity by Knaus et al. classification 1-year following HS. Nearly the same proportion of patients had a strong limitation of activity, while none had no limitation of activity at 1-year following the HS. It is to be noted, however, that the subjects of this study had several functional limitations to begin with, and only 1 of the subjects had no functional limitation prior to having the HS. Studies in younger subjects[32] found that prominent neurological or behavioral sequelae in HS victims were rare 6 months following hospitalization. Nakamura et al. observed that 1.5% of 1441 cases of HS exhibited CNS sequelae. Patients presenting with lower GCS scores and higher body temperatures at admission were more likely to experience these sequelae.

While case reports indicate the usefulness of continuous electroencephalogram monitoring in predicting CNS sequelae, there is no prospective, comparable study on adequate neuromonitoring and the effect of temperature control on the CNS.[33]

Attempts to address the disordered coagulation in HS appear promising, with measures including the use of antithrombin type III and thrombomodulin hastening recovery and lowering markers of inflammation in HS such as interleukin (IL)-1B, tumor necrosis factor-a, and IL-6 levels.[34],[35],[36],[37]

Multiple Japanese authors have reported the use of blood purification therapy to clear pro-inflammatory molecules from the circulation, namely continuous venovenous hemofiltration, plasma exchange, and continuous renal replacement therapy (CRRT) in HS, observing lower 30-day mortality in patients treated with CRRT.[18],[38]

Another recent case report described the use of a variant of plasma exchange called continuous plasma diafiltration, which uses smaller pore sizes and more efficiently removes low- and intermediate-molecular weight albumin-bound proteins.[30]

A consistent feature of the research studying these costly and often time-consuming methods is a lack of prospective, comparable studies, with a predominance of case reports or retrospective studies with low sample sizes that make it hard to draw conclusions that can be used in clinical practice.

Interventions to be avoided

Several measures in HS have been attempted in the past but must be avoided in practice, ranging from the ineffective, such as antipyretics and the use of dantrolene,[39],[40] to the inherently harmful, including the use of anti-cholinergic, alpha-adrenergic, salicylate, and nonsteroidal anti-inflammatory drug medication.

It is essential for the primary care physician to learn to differentiate a heat-related illness from several of its mimics. They must also inculcate simple measures to reduce core body temperature into their management of HS and watch out for the potential organ dysfunction, recognizing and referring cases which require higher care to facilities that can provide them.

  Conclusion Top

Heat-related illness is a widely prevalent disorder with a wide spectrum of severity an ever-rising burden. Its pathophysiology is complex and involves a systemic inflammatory response due to a mismatch between heat production and dissipation. While rapid cooling of patients has been shown to be effective, the evidence is unsatisfactory regarding the competence of various measures, as well as the methods to treat organ dysfunction in HS. Conducting high-quality prospective studies comparing various modalities of treatment is the need of the hour. Ultimately, it would seem that prevention is far better than cure.

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Conflicts of interest

There are no conflicts of interest.

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  [Figure 1]

  [Table 1], [Table 2], [Table 3]

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