Too Hot to Handle - PT449

Too Hot to Handle

Heat-Related Injuries in the ED

by Jeff Solheim, MSN, RN-BC, CEN, CFRN, FAEN
PT449
(4.4 / 66 ratings )

This course is credentialed for:
Physical Therapy (1.00 Hour(s))


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The doors to the ambulance bay open and a gust of hot, humid air from outside the department blasts into the nursing station where you are charting. As the day progresses, you realize that even though you are enjoying the air-conditioned environment of your workplace, you are suffering the consequences of the current heat wave. Four hours into your shift, Carl, age 22, presents to triage with road rash to his face, right arm and right leg. He states he “wiped out” while riding his bike after suffering severe lower leg cramps. An hour later, Amy, 34, presents to triage stating that she collapsed while working outside in the yard. Near the end of your shift, Maureen, 71, is brought by ambulance after being found in an unresponsive state in her overheated apartment.
 
While each of these patients exhibits unique and varying signs and symptoms, they are all suffering a heat-related injury. Healthcare providers as a team must be familiar with the signs and symptoms for hyperthermic conditions, as well as treatment modalities and preventive strategies.
 
Human beings are able to maintain a body temperature between 95 F and 105.8 F (35 C to 41 C) regardless of the ambient temperature around the body.1 The ability to generate heat in the body in order to maintain this ideal temperature is a result of two factors: metabolism and the environment. Cellular metabolism creates heat within the body. At rest, cells produce 100 kilocalories of heat per hour, which can raise the core temperature by 1.8 F (1.1 C) per hour. Strenuous exercise can increase heat production to 10 times this amount.2 Other factors known to increase heat production include shivering, tremors, seizures, fever and sympathomimetic drugs (e.g., epinephrine and norepinephrine).2
 
The body is designed to dissipate excess heat through the following mechanisms if the production of heat through cellular metabolism (the main driver of endogenous heat production) exceeds a person’s optimum temperature:
 
Radiation: Heat transfers from areas of higher temperature to areas of lower temperature through the process of radiation. The body facilitates this process through the constriction and dilation of blood vessels. When blood vessels dilate, they are in closer proximity to the surface of the body, resulting in radiation of heat through the skin to the external environment. Radiation may account for as much as 65% of heat loss in temperate climates.2
 
Convection: The loss of internal heat to air and water is referred to as convection. Beads of sweat that form under the skin carry heat. These droplets of sweat then relocate to the skin’s surface, transferring that heat externally.
 
Evaporation: When sweat is converted from a liquid to a gas on the surface of the skin, heat is allowed to evaporate from the body with the sweat. About 580 kcal of heat is lost for each liter of evaporated sweat.1
 
The environment plays another significant role in heat regulation. If the ambient environmental temperature is less than body temperature, heat radiates from the core of the body to the outside. As ambient temperatures approach or surpass body temperature, heat may no longer radiate away from the body. In extremely hot and humid climates, reverse radiation of heat from the environment into the body may actually elevate the core temperature.3
 
Various other environmental factors further influence heat regulation. Moisture in the air (humidity) impedes convection and radiation, as sweat is less likely to change from a liquid to a gas and evaporate in humid conditions. For example, if the outside temperature is 90 F (32 C) and the humidity level is 40%, this is equivalent to an apparent temperature of 91 F (33 C). However, if the humidity climbs to 80% and the ambient temperature remains at 90 F (32 C), the apparent temperature is 113 F (45 C).3 Evaporation no longer occurs when humidity levels reach 75%.2 Direct exposure to sunlight further increases absorption of heat from the environment to the core of the body by increasing the apparent temperature by up to 15 F.3
 
In addition to environmental influences, specific individual traits, such as body fat and acclimation, increase the risk for heat-related injuries. People with a higher body mass index and increased fat layers retain additional heat. Acclimated people may produce 2 to 3 liters of sweat per hour, compared to nonacclimated people, who may produce only 1 liter.2 Exposure to a warm environment for six to 14 days is required for the body to acclimate; such exposure reduces the risk and potential severity of heat-related injuries.1
 
Heat regulation depends on the hypothalamus. The hypothalamus acts as the body’s thermostat and is responsible for the radiation of heat through vasoconstriction and vasodilation, as well as stimulating or preventing sweat, key factors in convection and radiation. Therefore, an adequately functioning hypothalamus is essential for proper temperature regulation. The hypothalamus of children and older adults may exhibit lower functioning, resulting in less effective thermoregulation and making such people more susceptible to heat-related injuries.2
 
When core temperatures rise above 98.6 F (37 C), the potential for heat-related injuries exists. The most common heat-related injuries are heat cramps, exhaustion and stroke. Although each of these injuries may be serious, heat stroke carries a mortality rate as high as 50%.4
 
Between 1999 and 2010, 7,415 people in the U.S. died of exposure to extreme heat. This equates to an average of 618 deaths per year. Males accounted for 68% of those deaths. Those who do survive heat-related injuries may experience increased morbidity. For example, 33% of patients who survived the 1995 Chicago heat wave had severe neurological damage that resulted in death within one year.5,6(Level B)
 
Pathophysiology
 
As the core body temperature begins to climb, the initial reaction of the body is to increase heat dissipation efforts via increased production of sweat. This in turn leads to the depletion of both body fluid and sodium, contributing to the sensation of thirst. If people quench their thirst by consuming water but do not replace sodium losses, a dilutional hyponatremia may develop. This can contribute to the muscle cramps that are sometimes associated with exposure to heat; in severe cases, seizure and death can ensue.
 
Prolonged periods of exposure to elevated temperatures may result in the heat-dissipating mechanisms of the body fatiguing. If the patient continues to experience excessive perspiration, which contributes to worsening fluid losses and electrolyte depletion, a syndrome known as heat exhaustion may result. In addition, the elevation of core body temperature may exceed the body’s abilities for dissipation, further increasing the core temperature. The diagnosis of heat exhaustion is elusive because of vague clinical manifestations; however, if untreated, heat exhaustion may progress to heat stroke. Because of their poor compensatory mechanisms, the very young and the elderly are at increased risk for this syndrome.2
 
When heat stroke occurs, the existing heat-dissipating mechanisms become overwhelmed, and heat stress destroys the thermoregulatory system of the body. At this point, the hypothalamus fails to control vasodilation, vasoconstriction and sweat production. Core temperature climbs rapidly and unabated to above 104 F (40 C).7 These extreme temperatures begin denaturing body proteins and destroying cellular membranes, initiating the body’s inflammatory cascade. Cellular death results, followed by tissue death, ultimately leading to multiple organ dysfunction syndrome, in which entire organ systems fail.2

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