Heat Illness in Hawai‘i

Abstract

Heat illness is a commonly encountered health problem in the Hawaiian Islands. Year round warm temperatures, proximity to the equator, and high humidity combined with a plethora of opportunities for outdoor activities put many individuals at risk. This paper will focus on the physiology, identification, and treatment of varying forms of heat illness. Severe heat illness can be life threatening. All outdoor enthusiasts should have a basic understanding of how to recognize this potentially life-threatening condition and employ preventive measures. We will discuss appropriate management in pre-hospital and hospital settings. Early recognition and cooling are the most crucial aspects of the management of heat illness.

Background

The human body's temperature is regulated in the pre-optic nucleus of the anterior hypothalamus, which in normal physiology is set at a core temperature of 98.6° F ± 2 degrees (37 C ± 1 degree). Outside of this range, the human body has the ability to tolerate significantly colder temperatures, but at warmer temperatures, particularly above 105° F, physiologic dysfunction occurs.

There are a variety of changes that occur on a cellular level in extreme heat. Elevated temperatures affect the exchange of ions across transport membranes in all cells. This process, coupled with alterations in renal blood flow, and changes in plasma volume, can lead to a variety of electrolyte derangements. Hyperthermia causes changes in the structure of cellular organelles including disruption of microfilaments and swelling of the mitochondria and the endoplasmic reticulum, leading to collapse of the cytoskeleton and deformation of the plasma membrane.¹ Reaction kinetics dictate that rate increases with heat, however, above a certain temperature reactions are unable to occur since the responsible enzyme begins to denature.²

To prevent heat illness, the body has cooling mechanisms to remove heat. Evaporation, radiation, convection, and conduction are the four main processes which reduce heat energy. Evaporation occurs when water vaporizes from the skin and respiratory tract. This is the body's most effective mechanism for getting rid of heat (an example would be an athlete sweating in the hot sun). Radiation occurs when heat is directly emitted into the environment. Convection is the transfer of heat to a liquid overlying the body (eg, a swimmer cooling off in the water). Conduction is direct transfer of heat to a cooler object (eg, application of an ice pack).¹

These processes all require a cardiovascular system that is able to increase blood flow to the distal vasculature to facilitate transfer of heat from the body core to the skin, where the four mechanisms for dissipating heat can take effect. During high heat loads, blood flow to the skin increases drastically to enable these processes. However, when the ambient temperature is higher than the body's core temperature, convection, conduction, and radiation are no longer effective. Environmental conditions also affect evaporative cooling. A water vapor pressure gradient must exist for sweat to evaporate and release energy into the environment. In high humidity evaporation becomes ineffective for transferring heat (typically around relative humidity >75%). Intrinsic factors that decrease ability to compensate for generation of heat energy include age (both very young and very old individuals), stimulants, poor cardiovascular fitness, and possibly the most modifiable risk factor, dehydration. Studies suggest that during intense exercise in the heat for every one percent of body mass lost from dehydration there is a concomitant increase in core body temperature of 0.22° C.³

The human body also has significant adaptive cellular mechanisms in place to counteract heat illness. A highly conserved response to physiologic stress including hyperthermia and hypoxia exists in nearly all prokaryotic and eukaryotic cells. This process is largely mediated by heat shock proteins. These are transcriptionally inducible molecular chaperones. They work to prevent the formation of damaged protein aggregates and assist proteins in the acquisition of their native structures. It is theorized that they are a physiologic response to cellular stress, rather than a prophylactic process already in place. Studies have shown those with high basal levels of heat shock proteins are more likely to experience acute heat induced illness.² These proteins may represent a biomarker to assess susceptibility to heat stress. When these defenses are overwhelmed by either passive heat accumulation (classic heat stroke) or by generation of excessive heat energy via activity (exertional heat stroke), heat illness occurs.

Relevance to Hawai‘i and Asia-Pacific

Heat illness on a wide spectrum is a common threat to people who spend time outdoors in Hawai‘i. On all the islands, May through October is considered summer and winter the rest of the year. Honolulu is a well studied example of a sea level climate, where summer highs average 85° F while winter highs average 78° F. Due to proximity to the equator the UV index is almost always high, with an average index of 6–7 in the winter and 11–12 for summer months. Recent research suggests that temperatures will be increasing for the Hawaiian Islands in coming years. In Honolulu, Hawai‘i, the average temperature has increased 4.4° F over the last century and research suggests it will continue to increase, while precipitation has decreased approximately 20% over the last 90 years.^4,5

Due to year round warm temperatures and sunshine, Hawai‘i is a popular tourist destination. There are many outdoor activities which require exertion, including hiking and water sports, both of which result in prolonged sun exposure. Non-acclimatized or poorly conditioned individuals, as well as young children and the elderly are particularly at risk of experiencing heat illness under these conditions.

In addition, there are numerous organized sporting events. A glance at a calendar for one of Honolulu's sporting events organizations shows an average of eight organized races of various distances per month.⁶ The Big Island of Hawai‘i is home to the world championship ironman triathlon, the ultimate test of endurance. Participants in these events are typically well conditioned and acclimatized, yet a determined athlete may ignore warning signs.⁷

Finally, Hawai‘i has a large military population. The military has classically been a leading source of literature on the prevention and management of heat illnesses. A soldier's duties often require engaging in vigorous activity while wearing heavy gear, often under conditions which make adequate nutritional and hydration status difficult to maintain. While training exercises are meant to simulate the stress of combat, not all soldiers are able to stand these conditions for prolonged periods of time.⁸

Clinical Description

Heat illness occurs on a spectrum. The ICD 9 contains ten different diagnoses which categorize the physiologic manifestations of excess heat stress. The umbrella term for these illnesses is heat injury (evidence of both hyperthermia and end organ damage). We will discuss a few specific terms. The main distinction to note is the difference between intermediate and severe forms of heat illness. Intermediate illnesses have no neurologic impairment, while severe heat illness is a form of distributive shock in which patients have altered or depressed mentation as a consequence.

Heat rash, characterized by pruritic papules due to occluded sweat glands, and heat cramps, painful muscle spasms attributed to electrolyte abnormalities and dehydration, are both mild forms of heat illness.¹ Heat exhaustion presents with malaise, nausea and vomiting, headaches, and is classified as an intermediate severity form of heat illness. A patient's vital signs may demonstrate tachycardia and hypotension; however there is normal mentation and no central nervous system involvement. Heat syncope, also called exercise associated collapse, falls within the intermediate range of illness as well. Both syndromes are associated with slightly elevated core temperature.²

Heat shock is a multisystem illness, and is the most severe form of heat illness. The hallmark features are core temperature of 104° F or greater, encephalopathy, and additional evidence of end organ damage. Complications of heat shock are numerous and usually attributable to ischemia and oxidative damage. A systemic inflammatory response occurs as in other forms of distributive shock. Clinical findings include tachycardia, tachypnea, and hypotension, skin is warm and may be hyperhidrotic or dry, pupils are often dilated from activation of the sympathetic nervous system, patients may have altered sensorium or even be comatose, and seizures can occur. Heat shock can be a cause of non-cardiogenic pulmonary edema and crackles may be auscultated. From a cardiac standpoint, myocardial infarction is a potential concern, as are arrhythmias due to electrolyte derangements including massive potassium shifts. Other physiologic complications include rhabdomyolysis, acute kidney injury from either decreased renal perfusion in the setting of massive hemodynamic compromise and/or pigment nephropathy, gastrointestinal bleeding as a consequence of ischemic colitis, and ischemic hepatic injury. Interestingly heat shock can lead to sepsis; when the combination of high temperature and reduced intestinal blood flow injures the intestinal wall, translocation of lipopolysaccharide and other bacteria, toxins occurs through the portal vein and peritoneal space.^1,9

Example Cases

Case 1

A four-year-old child on vacation from Michigan spends the day on the beach. His parents remind him to drink water and he finishes one water bottle over the course of the day. As the family packs up to leave, the boy's parents notice he is less interactive than usual. He sits still and appears flushed. Thirty minutes later he is unresponsive and an ambulance is called. His vital signs are as follows: blood pressure, 80/50; heart rate, 130; respiratory rate, 24; oxygen saturation, 98% on room air; and a rectal temperature is measured at 105° F. Before the initial assessment is complete, the patient suffers a five minute generalized tonic clonic seizure which spontaneously abates. His pupils are reactive but dilated. This patient has classic (non-exertional) heat stroke, in which the environment overwhelms the patient's ability to dissipate heat.

Case 2

A thirty-year-old schoolteacher who lives in Kaneohe has recently decided to get in shape. At the urging of a few of her friends, she signs up for a fifteen mile trail run. She trains for only a week beforehand by running a few miles after work in the evenings. The race starts at 1000. It is a hot and humid day. Two miles from the finish line, she collapses. On assessment by the medical staff present, her rectal temperature is 104° F, she is profusely sweating and disoriented when questioned. This patient has exertional heat stroke, in which intrinsic heat production is the primary cause for hyperthermia.

Case 3

A 19-year-old military recruit is hospitalized after competing in the expert field medical badge. Following completion of the course, he collapses and is brought to the emergency room. He recovers consciousness and on initial assessment there is notable hypotension, temperature of 105° F, diffuse myalgias, elevated CK, acute renal failure with a Cr of 2.5, potassium of 6.0, electrocardiogram showed peaked T waves, and elevated liver associated enzymes. He is immediately given fluids for his rhabdomyolysis, calcium chloride, albuterol, and insulin with dextrose for his hyperkalemia. A few hours after presentation, he goes into hypoxic respiratory failure and is emergently intubated. The patient spends the next three days in the intensive care unit requiring mechanical ventilation, vasopressor support, and renal replacement therapy. This case highlights the potential multi organ system involvement of heat shock and associated disorders.

Treatment in Resource-Constrained Environments

Providing care for a patient with heat stroke involves three main concepts: stabilization of airway and circulation, rapid cooling, and finally transport to advanced care with monitoring for potential complications of heat illness. Sources agree that if the patient is otherwise stable, cooling should be addressed first and transport second. Morbidity and mortality are directly related to the duration of core temperature elevation, and therefore rapid cooling is strongly stressed.³

In an austere environment, materials to initiate cooling may not be readily available. All equipment and excess clothing should be immediately removed. The patient should be moved to a shaded area. Immersion in ice water is highly effective for rapid cooling. The water should be stirred frequently during cooling to ensure continual contact with cool fluid. If ice water is not available, any cool water source will suffice. A nearby stream or pool of water can be used if no other options exist. If ice is available but no tub, the patient can be placed in a tarp or sheet, covered with a large amount of ice, and then the tarp or sheet can be wrapped around them.

Alternatively, if immersion in water is not possible, application of cool wet cloths can be used, with frequent re-application as soon as the material warms. As much body surface area as possible should be covered when using this method. Spraying cool water over the patient is also an alternative method if available. Fanning may be helpful, however never allow a conscious patient to fan themselves as this will only generate more heat via skeletal muscle contraction.³

Cooling via ice water immersion is estimated to occur at a rate of approximately 1°C for every five minutes (1°F every three minutes).³ If temperature monitoring is not possible, we suggest cooling the patient for fifteen to twenty minutes, or until the patient begins to shiver. This allows for a reduction to a safe temperature without risking over cooling. Other general interventions which should be performed in the field include intravenous access if possible followed by fluid administration, or oral rehydration if the patient is able to tolerate oral intake.

Treatment in Non-Austere Environments

Research has shown mortality correlates with the degree of temperature elevation, time to initiation of cooling, and number of organ systems involved. Management in the hospital setting should focus on modifying these factors. Continuous temperature monitoring should be initiated. External temperature is not reliable. Instead a bladder catheter with temperature probe, flexible rectal thermistor, or esophageal temperature monitoring should be used.¹⁰

A detailed history regarding precipitation of the event, medications, drugs of abuse, and medical history looking in particular for predisposing processes like sickle cell disease and heart disease, should be obtained.

If the cooling process initiated in the field has not lowered temperature to normal limits, it should be continued with ice water immersion or cutaneous application of ice packs in the hospital setting. Some studies show systemic cooling with a central venous catheter is also effective; however the potential complications from the procedure outweigh any benefit over using conventional methods of cooling. Multiple studies have shown pharmacologic treatment, including non-steroidal anti-inflammatories, acetaminophen, and dantrolene, have no outcome improvement, but may worsen complications. Therefore pharmacologic adjuncts to cooling are not generally recommended.¹⁰

Laboratory studies should be obtained including a complete blood count, electrolyte panel, creatine kinase level, urinalysis, lactate, blood gas, hepatic function tests, and coagulation studies. An electrocardiogram and chest X-ray should also be obtained. These studies are adequate to assess for the potential complications of heat stroke discussed above. During assessment, continuous vital signs monitoring and telemetry should be initiated.

Resuscitation with crystalloids should be aggressive and titrated to improvement in vital signs and laboratory parameters. Delirium and seizures are both treated with intravenous benzodiazepines. Electrolyte abnormalities should be corrected appropriately with removal or repletion. Many affected patients may need to be hospitalized for a period of observation and monitoring for complications. Hypotension after fluid resuscitation, seizure, encephalopathy that is not rapidly resolving, persistent oliguria, rhabdomyolysis, and evidence of gastrointestinal bleeding, are all examples. Patients with signs of multi organ dysfunction or evidence of disseminated intravascular coagulation are admitted to an intensive care setting.⁹

The importance of preventive measures should be stressed. Proper education regarding hydration, warning signs, and risk factors is crucial in preventing heat illness. Acclimatization by gradually increasing exertion in heat and maintenance of cardiovascular fitness are also important. The physiologic adjustments that occur are expansion of the plasma volume, earlier and increased sweating, lower salt concentration in sweat, and lower skin and core temperatures for a given amount of exercise. Wet bulb globe temperature (WBGT) should be used to predict environmental risk instead of ambient temperature alone. WBGT is a composite temperature used to estimate the effect of temperature, humidity, and wind speed on overall heat burden.⁷ Patients with risk factors for heat related illness should be aware of their predilection. A variety of medications increase risk, including diuretics, antihistamines, and sympathomimetics.¹

Though an individual presenting with heat illness may appear to have a straightforward etiology of their illness, a differential diagnosis should still be considered. Clinical entities that could present with decreased consciousness, autonomic dysfunction, and hyperthermia include pontine or midbrain infarct, meningitis, drug induced toxidrome, and parasitic infections such as malaria.

Conclusion

Heat stroke continues to be a common and potentially lethal event. The method used for cooling is not crucial, instead the speed of cooling and transport to advanced medical care is more important prognostically. The recognized complications of heat stroke are numerous and in the worst case scenario it can result in multiorgan failure. Thorough laboratory assessment as well as electrocardiogram and chest X-ray should be performed upon arrival to a higher level of care to avoid missing complications. Medical care is largely aimed at supportive therapy with cooling and intravenous crystalloids, with the goal of maintaining normal vital signs and preventing end organ damage.

Disclosures

The author reported no conflicts of interest.

Disclaimer

The views expressed in this manuscript are those of the author and do not reflect the official policy or position of the Department of the Army, Department of Defense, or the US Government.