Heat Stroke

HEAT STROKE

PATHOPHYSIOLOGY

Heat stroke is the most serious manifestation of heat related illness and is the extreme end of the heat related illness spectrum. Heat stroke is a true medical emergency and is imminently life threatening as it represents the complete breakdown of thermoregulatory processes resulting in rapid core body temperature elevation and cell death (Leon, 2015).

Heat stress results in the release of proinflammatory cytokines which act to promote vasodilatation and vascular permeability. These changes initially result in heat dissipation through radiation and of energy from the blood as it enters superficial cutaneous vascular beds where it is evaporatively cooled. If core temperatures continue to rise a systemic inflammatory response develops (Leon, 2015). This process is marked by diffuse vasodilatation resulting in a large relative decrease in effective circulating volume. If core temperatures are sustained at or above 42°C thermoregulatory mechanisms begin to fail, leading to an unchecked accumulation of heat energy and rapid core temperature elevation (Bouchama A, 2002). Beyond 42.5°C, cellular proteins begin to denature. As large numbers of cells die and release their intracellular contents, a massive cytokine surge pushes the vascular system into distributive shock. Surviving cells have massively increased metabolic demands to cope with the ongoing heat stress. This increased metabolic demand coupled with hypoperfusion due to widespread vasodilation results in neuronal cell death and encephalopathy. The eventual clinical manifestation is that of distributive shock, end organ ischemia, hypoxic brain injury, and cardiac collapse resulting in death (Toru Hifumi, 2018). Common risk factors for of heat stroke include:

• Advanced age
• Coronary artery disease
• Diabetes mellitus
• Poor mobility
• Dementia
• Cerebrovascular disease
• Extreme levels of exertion
• Renal impairment
• Lack of acclimatization

CLINICAL PRESENTATION & DIAGNOSIS

Heat stroke has been historically classified into two groups according to the presence or absence of exertion Exertional heat stroke develops in healthy individuals, such as athletes, soldiers, or workers engaging in rigorous physical activities in high ambient temperatures. Even with prompt treatment, the mortality rate for exertional heat stroke has been quoted to be between 5-15% (Leon, 2015). Conversely, non-exertional heat stroke develops typically in more elderly individuals with comorbidities including obesity, poor mobility, diabetes, peripheral vascular disease, heart disease, renal disease, and dementia. The mortality rate for non-exertional heat stroke approaches 65% with prompt treatment (Leon, 2015). This discrepancy in mortality rate is due, in part, to the higher burden of co-morbid conditions in the non-exertional heat stroke group. It should be noted that when environmental heat stress is maximal, exertion is not required to generate heat related illness in young healthy individuals (Toru Hifumi, 2018).

To date, no universally accepted definition of heat stroke exists. The most commonly utilized criteria for heat stroke worldwide are the Bouchama criteria. Bouchama  defined heat stroke as a core body temperature that rises above 40.5°C, accompanied by hot dry skin and central nervous system abnormalities, such as delirium, convulsions, or coma (Bouchama A, 2002). Bouchama’s definition:

• Alteration of mental status (coma, delirium, disorientation, or seizures)
• Core temperature greater than 40.5°C or documented evidence of cooling before the first record temperature
• Reliable history of environmental heat exposure
• Hot, dry, or flushed skin

Many subsequent guidelines have included hepatic and renal dysfunction, in addition to coagulopathy as part of their diagnostic criteria. Given that these investigations are not available to a covering sport medicine physician in the field they will not be discussed. It should be noted that several fatal cases have been reported in patients with core body temperatures below 40°C (Jean-Marie Robine, 2008). The presence of altered level of consciousness with a strong clinical suspicion for heat stroke should prompt immediate intervention and cooling.

DIFFERENTIAL

• Central nervous system hemorrhage
• Sepsis / Infection
• Thyroid storm
• Encephalitis
• Sympathomimetic ingestion
• Serotonin syndrome
• Seizure

TREATMENT

Immediate cooling is the most important aspect of heat stroke treatment. Evaporative cooling is the modality of choice. Cooling should begin immediately upon recognition of heat stroke while waiting transport to hospital. The patient should be moved to a shaded or air-conditioned area. All clothing and equipment should be removed from the patient’s body. The patient is then copiously sprayed with ice water and large fans or blankets are used to rapidly move air across the patient’s body. Ice packs to the head, neck, axilla, and groin may be used as effective adjuvants to evaporative cooling. The target core temperature while cooling a patient is 38°C to avoid hypothermic overshoot (Platt, 2014).

COOLING METHODS – LITERATURE REVIEW AND RECOMMENDATIONS

Rapid cooling is the single most important therapeutic objective in heat stroke. Each minute effective cooling is delayed the risk of death and long-term neurologic impairment increases. Several cooling methods are well described in the literature. However, consensus on the best cooling modality remains elusive. This is due largely in part to a lack of quality evidence and significant confounders related to comorbid conditions in non-exertional heat stroke patients. The most accepted and widespread cooling techniques include ice water immersion, evaporative cooling with cold water and fans, ice packing, and body cooling units (Hadad, 2004).

(Gaudio, 2016). BCU = body cooling unit, ED = Emergency Department, TTC = time to cooling target of 38°C

The heterogeneity of the available evidence makes comparison between study groups difficult given the lack of control with respect to variables such as etiology of heat stroke, comorbidities, and post cooling intensive care. However, a clear trend is visible with respect to increased risk of death and neurologic dysfunction if cooling is delayed or is insufficiently rapid once initiated.

Ice water immersion results in rapid reduction of core temperatures, typically yielding a cooling rate of 0.22-0.25°C / min (Gaudio, 2016). This corresponds to a core temperature drop of 3°C in as little as 10 minutes. While highly effective, this cooling modality is cumbersome, interferes with patient care, lacks widespread availability, and is technically challenging. Moreover, ice water immersion is rarely possible on site while provided medical coverage for an athletic event. As a result, ice water immersion should be reserved for use in hospitals with the necessary equipment and expertise (Platt, 2014).

Evaporative cooling is the modality of choice to initiate for exertional heat stroke patients while on the sidelines awaiting transport to hospital. Evaporative cooling involves extrication of the patient to a cooler environment away from direct sunlight and the removal of all clothing and equipment from the patient’s body. The patient is then copiously sprayed with ice water and large fans or blankets are used to rapidly move air across the patient’s body. This modality employs evaporative, radiative, and convective heat exchange strategies to lower core body temperature. Evaporative cooling is effective, yielding a cooling rate of 0.14±0.11°C/min in a 2004 study of 52 Israeli soldiers afflicted with exertional heat stroke (Gaudio, 2016). This cooling rate corresponds to a core temperature drop of 3°C in as little as 20 minutes when properly utilized. Evaporative cooling is effective, readily available, requires minimal equipment, and is technically simple to perform. Ice packs to the head, neck, axilla, and groin may be used as effective adjuvants to evaporative cooling.

Regardless of cooling strategy, the target core temperature should be 38°C to avoid hypothermic overshoot. Core temperatures should be continuously monitored and maintained between 37-38 °C. Cooling should be restarted if core temperature rises above 39°C (Platt, 2014).

PEDIATRIC CONSIDERATIONS

            Children are at increased risk for the development of heat related illness, particularly heat stroke as a direct result of their pediatric physiology (Bytomski, 2003).

Metabolism

• Children have higher basal metabolic rates producing more heat energy per kilogram of body weight over a given time. In the setting of impaired thermoregulation or excess environmental heat, children will accrue excess heat energy rapidly.

Anatomy

• Children have higher surface area to body weight ratios which results in a higher rate of environmental heat absorption. This is true for both high ambient air temperatures and thermal heating from direct sunlight.
• Children begin sweating at higher core body temperatures than adults. Additionally, pediatric sweat glands produce less sweat over a given period of time. Therefore, evaporative cooling is less efficient in children.
• Children have lower rates of expression of heat shock proteins which act to stabilize cellular structures during periods of thermal stress. As a result, children have a lower threshold for cellular dysfunction in the setting of elevated core body temperatures.
• Children have lower rates of melanin production, making them more likely to sustain sunburns which limit evaporative cooling.
• Acclimatization is known to be less efficient and occur more slowly in children.

Hematology

• Smaller blood volumes limit the rate at which heat energy can be transported from the core to the cutaneous vessels of the skin for dissipation.

Cardiovascular

• Children have smaller cardiac outputs per kilogram of body weight than adults at baseline. Additionally, children are less able to augment their stroke volume, relying on heart rate to increase cardiac output. Further limiting blood supply to cutaneous vessels.
• Children, especially the very young, have immature vascular control and are less able to vasodilate and shunt blood peripherally.

Behavioural

• Children may be unable to remove themselves from environmental heat stress depending on their age. Moreover, they may be unable to express thirst or seek water themselves.
• Children are less likely to replace volume losses even with readily available water.

Dr. Erik Leci and Dr. Graham Briscoe (May 10, 2020 – PR ND)

References:

Leon, B. (2015). Heat Stroke. Comprehensive Physiology , Vol.5 (2) 611 – 647.

Bouchama A, K. J. (2002). Heat stroke. New England Jounral of Medicine , 346:1978–88.

Toru Hifumi, Y. K. (2018). Heat stroke. Journal of Intensive Care , 320-328.

Jean-Marie Robine, S. L.-P. (2008). Death toll exceeded 70,000 in Europe during the summer of 2003. Comptes Rendus Biologies, 171-178.

Platt, a. P. (2014). Heat Illness . In H. W. Marx, Rosen’s emergency medicine: Concepts and clinical practice (8th ed.) (pp. 1896 – 1905). Philadelphia, PA: Elsevier/Saunders.

Hadad, E. M. (2004). Cooling heat stroke patients by available field measures. Intensive Care Medicine , 338-340.

Gaudio, a. G. (2016). Cooling Methods in Heat Stroke. The Journal of Emergency Medicine, Vol. 50, No. 4, pp. 607–616.

Bytomski, a. S. (2003). Heat illness in children. Current Sports Medicine, 2003;2(6):320.

Drezner, C. R. (2007). Inter-Association Task Force on emergency preparedness and management of sudden cardiac arrest in high school and college atheletics. Journal of Athletic Training , 143-158.