Nursing Spectrum Nurseweek
» Subscribe «

Nurse.com

Search Courses
User Login
Username or Email:
Password:
keep me logged in?
Login Help Create New Account
CE Tools
Recommendations
CE Resources
CE Home > Emergency Nursing > CE449 Too Hot to Handle: Heat-Related Injuries in the ED

CE449 · 1.0 hr
Too Hot to Handle: Heat-Related Injuries in the ED
Author: Jeff Solheim, RN

Course Objectives
Course Tools Sidebars | References | Authors | Print Course | Start Test
 

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, age 34, presents to triage stating that she collapsed while working outside in the yard. Near the end of your shift, Maureen, age 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. Nurses must be familiar with the signs and symptoms for hyperthermic conditions, as well as treatment modalities and preventive strategies.

Background

The human body is designed to function most effectively at a temperature of 98.6 F (37 C). Heat input in the body is a result of two factors: metabolism and the environment.1 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 potentially 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, norepinephrine).2

If the production of heat through cellular metabolism exceeds a person’s optimum temperature, the body is designed to dissipate the excess heat through the following mechanisms:

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 both 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. Convection accounts for an average of 10% to 15% of heat loss within the body.1

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. As much as 20% to 25% of heat loss occurs through the process of evaporation.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 the process of 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 20%, this is equivalent to an apparent temperature of 87 F (30 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 two to three liters of sweat per hour compared to nonacclimated people, who may produce only one liter.2 Exposure to a warm environment for one to two weeks is required for the body to acclimate and reduces the risk and potential severity of heat-related injuries.1

Heat regulation is dependent on a functioning 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 these people more susceptible to heat-related injuries.2

When core temperatures rise above 98.6F (37 C), the potential for heat-related injuries exists. The most common heat-related injuries include heat cramps, heat exhaustion, and heatstroke. Although each of these injuries may be potentially serious, heatstroke carries a mortality rate as high as 70%.4

Between 1999 and 2003, 3,442 people in the United States were reported to have died from exposure to extreme heat. This equates to an average of 688 deaths per year. Of these decedents for whom age information was available, 228 (7%) were people younger than 15, 1,810 (53%) were between ages 15 and 64, and the remaining 1,363 (40%) were 65 or older. 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 

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 the person quenches his or her thirst by consuming water and does 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.1

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 heatstroke. Because of their poor compensatory mechanisms, the very young and the elderly are at increased risk for this syndrome.2

When heatstroke 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).1 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 (MODS), in which entire organ systems fail.2

Diagnosis

Diagnosis of heat cramps is based heavily on the patient’s presentation and chief complaint.  Patients often admit to recent exposure to heat extremes with significant sweating. They may complain of intermittent muscle cramps that tend to affect large muscle groups such as the shoulders, lower extremities, and abdominal wall muscles.7 Such cramps usually occur after the person has stopped the physical activity or exercise and is resting.4 Additional symptoms that may accompany cramping include weakness, thirst, nausea, tachycardia, profuse diaphoresis, and pale, cool, moist skin. These symptoms suggest severe dehydration as well as electrolyte imbalances, specifically sodium imbalances from excessive sweating. Lab results may reveal an elevated hematocrit secondary to dehydration and hyponatremia, because salt loss usually exceeds water loss, and sodium levels may be further reduced from rehydration attempts using drinks that do not contain electrolytes.2

Heat exhaustion may accompany heat cramps or it may occur in isolation. Signs and symptoms leading to diagnosis of this syndrome may include fatigue, diaphoresis, dizziness, lightheadedness, nausea and vomiting, orthostatic hypotension, thirst, anxiety, malaise, headache, tachycardia, and syncope. The core body temperature on arrival may be normal if the patient has retained his ability to vasodilate and sweat, or it may be slightly elevated if heat gain exceeds the body’s attempt at heat loss www.medicalnewstoday.com/medicalnews.php?newsid=75919.

Temperatures often range between 98.6 F and 105 F (37 C to 40.5 C).7 Because of such vague signs and symptoms, the diagnosis of heat exhaustion is often made by that of exclusion. Lab results are similar to those listed for heat cramps although the dehydration-related hemoconcentration and hyponatremia may be more pronounced. Acute prerenal failure secondary to excess fluid depletion may contribute to elevated blood urea nitrogen and creatinine levels.2

It’s often easier to recognize and diagnose heatstroke than heat cramps or heat exhaustion because of the extreme presentation of these patients. Because the thermoregulatory system is failing, sweating slows and ultimately ceases, and the core temperature quickly climbs. The patient presents with a core temperature exceeding 104 F (40 C) and the skin is usually dry and hot to the touch.8 Level of consciousness is altered because of direct thermal damage to the brain. The patient may arrive with confusion, hallucinations, loss of muscle coordination, combativeness, abnormal posturing, dilated and unresponsive pupils, seizures, or coma. Some patients may proceed from heat cramps and heat exhaustion to heatstroke, and indications of dehydration, sodium imbalances, and pre-renal failure may also be present. Other patients may progress rapidly into heatstroke, bypassing both heat cramps and heat exhaustion and may not show any of these clinical manifestations.4

The nurse may also recognize early indications of MODS, including coagulopathies associated with elevated liver enzymes and hypotension secondary to cardiac failure, as well as indications of acute respiratory distress syndrome (ARDS) www.nurse.com/ce/CE345, including development of crackles, decreasing oxygen saturations, and symptoms of acidosis. Disseminated intravascular coagulation (DIC) — another illness associated with MODS — is marked by low clotting factors resulting in microvascular bleeding into the tissues manifested as petechiae.

Treatment

Treatment of heat-related injuries depends heavily on the patient’s initial presentation. In the case of heat cramps, oral replacement of fluids and electrolytes with a commercially prepared balanced electrolyte drink such as Gatorade or Powerade is usually sufficient.7 If lab values indicate that dehydration and electrolyte imbalances are severe, IV replacement with normal saline is initiated. The nurse should immediately move the patient to a cool location to prevent exacerbation of the condition and encourage the patient to rest while fluid replacement is initiated.7 

The patient who presents to the hospital with indications of heat exhaustion should receive similar treatment. Remove the patient’s unnecessary clothing and find a cool place within the department in which to deliver care. The nurse initiates either oral or intravenous replacement of fluids similar to those provided to the patient with heat cramps. If the patient’s temperature is above normal, consider placing cool cloths over the patient’s body to facilitate evaporation of heat away from the body. Potential heat-related muscle damage may result in the release of potassium, triggering hyperkalemia. The treatment plan for such patients also includes cardiac monitoring.4

Because of the life-threatening nature of heatstroke, as well as the potential for untoward sequelae, patients with this condition are always admitted, most often to the critical care unit, and treatment is rapid and aggressive (www.aafp.org/afp/20050601/2133.html). As with all resuscitative attempts, the patient’s airway is assessed because he or she may present with a decreased level of consciousness and inability to protect the airway. Nurses should begin immediate administration of supplemental oxygen appropriate for the patient’s level of consciousness.4 After gaining IV access, fluid resuscitation with normal saline begins with careful monitoring. Because of the rapid onset of many cases of heatstroke, the patient may not be as dehydrated as patients suffering from heat cramps or heat exhaustion. Vasodilation can contribute to early heart failure and fluid accumulation in the lungs secondary to early ARDS. Lactated Ringer’s solution is rarely used because the failing liver may be unable to metabolize the lactate.4 Vasopressors may be considered as an alternative for severe hypotension.1

After stabilizing the patient’s airway and breathing and circulation, the nurse should attend to aggressively reducing the core temperature. The earlier cooling is initiated, the better the odds are of the patient’s survival.8 The patient’s clothing is removed, and convection and evaporation are replicated by repeatedly spritzing the body with water or covering the body with water-soaked sheets and directing fans toward the patient. Ice packs are often placed in highly vascular areas such as the groin, axilla, and neck.6 Commercial cooling blankets are a less attractive alternative, as cooling from wet skin is 25 times more effective than cooling from dry skin.4 In severe cases of heatstroke or instances when the patient does not respond to these cooling methods, invasive methods of cooling such as iced peritoneal lavage, rectal lavage, continuous venous hemodialysis, or cardiopulmonary bypass are considered.

During the cooling process, the nurse monitors the patient closely for shivering, which may actually elevate the core temperature. Shivering is often controlled with 10 mg to 25 mg of chlorpromazine (Thorazine) IV.4

The nurse must also carefully monitor the patient’s core temperature to ensure that when the core temperature reaches 102 F (39 C), cooling methods are reduced to prevent inadvertent hypothermia.4 Continuous temperature monitoring via the use of a rectal probe, esophageal probe, or Swan-Ganz catheter is preferred.

Laboratory studies should be carefully evaluated for the evolution of clotting abnormalities marked by prolonged prothrombin or partial thromboplastin times, as well as decreased platelet or fibrinogen levels. Urinary output is monitored, as reductions may herald the onset of renal failure. The color of the urine is observed for a reddish or dark brown color, which may indicate possible rhabdomyolysis, a condition characterized by the spilling of myoglobin into the urine secondary to muscle damage.9

Nursing implications

Since heat-related injuries are considered preventable illnesses, nurses are encouraged to deliver preventive education to patients and the community. Teaching focuses on clients with higher risks for heat-related injuries, such as the very young and the elderly.  People with preexisting conditions such as obesity, hypertension, diabetes, heart disease, scleroderma, and dermatitis also pose a greater risk.1 Medications that may contribute to heat-related illnesses include anticholinergics, phenothiazines, butyrophenones, tricyclic antidepressants, antihistamines, antispasmodics, diuretics, antiparkinsonian drugs, beta-blockers, and many illicit drugs (www.bhchp.org/BHCHP%20manual/pdf_files/Part2_PDF/Hyperthermia.pdf).4  Finally, people who participate in activities, such as exercising or working, that require exertion in elevated ambient temperatures are also at greater risk for heat-related injuries. 

The most obvious message to include in teaching is to avoid exposure or exertion in elevated ambient temperatures. Children must not be left in unventilated cars, and the elderly should be moved to air-conditioned spaces in extreme heat. If working in hot, humid climates cannot be helped, people are encouraged to avoid insulated clothing and opt for open-mesh clothing. Educate those who are exposed to extreme temperatures to regularly monitor their weight. People who lose 2% to 3% of their body weight during time of exposure need to drink additional fluids and should be within one kilogram of starting weight before the next day’s exposure. Loss of more than 4% of body weight should result in limited activity for the next 24 hours.10

Nurses should encourage the consumption of electrolyte-containing drinks in hot climates; cooler liquids are absorbed more readily in the digestive tract. An option for maintaining sodium levels is to add one rounded tablespoon of table salt to five gallons of any sweetened drink.9 Teach patients to avoid drinks containing caffeine or alcohol.

Finally, nurses should remind people who must work in increased ambient temperatures about the importance of acclimation. It takes 10 days to 14 days for the body to adjust its ability to withstand higher temperatures. Sweat production generally increases with exposure to heat over this time, providing increased protection secondary to evaporation. Teach people to limit their exposure to extreme heat to 15 minutes initially, with slow increases to 90 minutes after acclimation occurs.9

Nurses must be prepared to recognize and treat the heat-related injuries they encounter. Nurses may care for a patient like Carl, the 22-year-old who experienced heat cramps while bicycling in a heat wave. The nurse must not only recognize the nature of Carl’s illness, but also assist him in replacing the fluids and electrolytes that have become depleted. Or, nurses may care for a patient like Amy, the 34-year-old who collapsed with heat exhaustion while working in her garden under high ambient temperatures and who requires not only fluid and electrolyte replacement, but also cooling measures to prevent her from progressing to heatstroke. And nurses must also be prepared to intervene in the life-threatening situation that 71-year-old Maureen found herself in when she developed heatstroke in her non-air-conditioned apartment. Immediate lifesaving interventions coupled with aggressive cooling measures and careful monitoring of sequelae by the nurse may mean the difference between life and death for this patient. 

Finally, nurses must adhere to their role of patient advocacy by teaching preventive measures, thereby helping the public avoid these potentially life-threatening illnesses.

 
Page 1