OVERVIEW: What every practitioner needs to know
Heat illness is caused by the inability to maintain normal body temperature because of excessive heat production or exposure, an inability to dissipate the heat, or a combination of both. Heat exhaustion and heat stroke will be addressed in this chapter.
Are you sure your patient has heat-related illness? What are the typical findings for this disease?
Heat exhaustion and heat stroke are on the same spectrum of disease, with heat stroke being the more severe form of heat-related illness.Table I lists the common symptoms of each and at what body temperature the diagnosis can be made.
|Heat Exhaustion||Heat Stroke|
|Core Body Temperature||38-40°C||>40°C|
|Primary Symptoms||Mild to moderate dehydration, profuse sweating||Anhidrosis, lack of sweating are common in classic heat stroke; in exertional heat stroke, the patient may be sweating, have altered mental status|
|Secondary Symptoms||Nausea and general malaise||Nausea, malaise, tachycardia with hypotension, mild to moderate dehyration|
What other disease/condition shares some of these symptoms?
There are some diseases that can mimic heat exhaustion or heat stroke. Most of these can be ruled out with an accurate history. The following lists some of these diseases.
Sepsis with high fever and altered mental status can mimic heat stroke. A focus of infection is often discovered but may not be immediately obvious.
Pathologic states of the central nervous system (CNS), such as status epilepticus or acute or chronic injury to the hypothalamus from infection, hemorrhage, or trauma, can cause neurogenic fever. In all of these cases there is a preceding neurologic injury.
Hemorrhagic shock and encephalopathy syndrome is a rare condition that includes fever, altered mental status, shock, disseminated intravascular coagulopathy, diarrhea, renal insufficiency, and liver failure. It occurs in infants less than 1 year of age and may be related to heat stroke.
Toxic overdose from drugs including cocaine, methamphetamine, amphetamine, MDMA (Ecstasy), salicylates, and anticholinergic agents (pesticides) can mimic heat-related illness.
Thyroid storm can present with hyperpyrexia, tachycardia, agitation, and delirium.
Malignant hyperthermia can mimic heat stroke but usually follows general anesthesia.
Serotonin syndrome is associated with increased serotonin activity in the brain causing mental status changes, autonomic hyperactivity, and neuromuscular abnormalities. There must be a history of exposure to a serotonergic drug.
Neuroleptic malignant syndrome is a severe reaction to antipsychotic medications leading to hyperthermia, muscle rigidity, altered mental status, choreoathetosis, trmeors, arrhythmias, sweating, and labile blood pressure.
What caused this disease to develop at this time?
Simple environmental conditions in which there is high temperature and high humidity impair the body’s ability to dissipate heat because the sweat cannot evaporate. This puts any patient at increased risk for a heat-related illness. Children, however, have certain attributes that increase their risk for heat exhaustion and heat stroke. First, they have a greater surface area to body mass ratio. They also produce more metabolic heat/kilogram body weight than adults, yet they have a slower rate of sweating than adults. They also do not begin sweating until the temperature is higher than that which typically triggers sweating in adults.
Children have a lower cardiac output at a given metabolic rate than do adults, which means they are not moving metabolites through their system at the same rate. Children have a slower acclimatization rate than do adults. Finally, because children have a blunted thirst response compared with adults, they often exist in a state of hypohydration. They do not cognitively recognize their signs of thirst as readily or as early as adults and, further, they may not know how or where to find hydration.
There are other predisposing conditions that may increase the risk of a child experiencing heat exhaustion or heat stroke. Any condition that causes excessive fluid loss or impaired sweating puts the child at increased risk for the development of heat exhaustion or heat stroke.
Examples of conditions in which there can be excessive fluid loss include diabetes insipidus, diabetes mellitus, gastroenteritis, and fever, as well as hyperthyroidism or congenital heart defects in which there is increased sweating. Conditions of impaired sweating include obesity, cystic fibrosis, and spina bifida. Finally, young children or developmentally delayed children may have a decreased thirst drive or may be unable to communicate their thirst effectively.
Obtaining an accurate history is imperative to understanding the cause of the problem. Important questions should include the following:
– Exposure history—what was the heat index at the time of injury and how long was the patient exposed to those conditions?
– What type of clothing was the patient wearing?
– Is the patient on any medications?
– Does the patient have any predisposing clinical conditions?
– Does the patient feel fatigued or confused?
– Did the patient take any illicit drugs?
The physical examination will be very helpful in determining whether the patient has heat exhaustion, heat stroke, or a disease that mimics it. Some findings that are useful, but not specific, include the following:
– Normal blood pressure or hypotension
– Dry mucous membranes
– Sweating or anhidrosis
– Mental status that ranges from normal to that seen in encephalopathy
– Purpura, hemoptysis, hematemesis, melena, or hematochezia (can be seen in heat stroke)
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
For patients with suspected heat exhaustion, routine laboratory studies are not necessary. A basic metabolic panel may reveal slight abnormalities in serum sodium levels. Hyponatremia might result from the loss of hypotonic fluids or hypernatremia may result from excessive salt loss in sweat.
For patients with suspected heat stroke, there will be certain abnormal laboratory findings that would be consistent with the systemic inflammatory response and end organ damage that result from the heat stress. The following laboratory tests are indicated in any patient with heat stroke: – Blood glucose determination to assess for hypoglycemia
– Blood gas determination to evaluate the presence and severity of metabolic acidosis
– Complete blood count, prothrombin time, partial thromboplastin time, and international normalized ratio to detect anemia and disseminated intravascular coagulopathy
– Serum electrolyte determinations to look for hyperkalemia, hyponatremia or hypernatremia
– Liver enzyme determinations to assess for liver injury
– Blood urea nitrogen and creatinine determinations to assess for prerenal azotemia and kidney function relative to myoglobinuria
– Serum creatine kinase, ionized or total calcium, and phosphate determinations to look for rhabdomyolysis and associated hypocalcemia and hyperphosphatemia
– Drug screen to look for drugs with adverse effects that are similar to heat stroke
– Urinalysis to evaluate for hemoglobinuria and specific gravity
Certainly, as with any patient, the diagnostic evaluations are directed by the patient and how they are or are not responding to therapy. These initial laboratory data should help determine the degree to which the patient has been injured by their exposure to heat.
Would imaging studies be helpful? If so, which ones?
A patient diagnosed with heat exhaustion does not require any routine imaging studies.
In patients with suspected or known heat stroke, a chest radiograph may be useful if the patient is exhibiting signs of high-output cardiac failure. A 12-lead electrocardiogram may also be indicated if there are any electrolyte abnormalities. Finally, a computed tomographic scan of the brain should be considered if the patient’s mental status does not improve despite optimal therapy.
If you are able to confirm that the patient has heat-related illness, what treatment should be initiated?
Therapies to Institute Immediately
Prompt recognition and treatment of heat exhaustion is critical to prevent progression to heat stroke. If the patient already has heat stroke, the initial therapy or intervention is the same as it is for heat exhaustion.
The patient should immediately stop participating in the current activity and be moved to a cooler environment. Excess clothing should be removed to help with evaporative heat loss. In heat exhaustion, the patient should be given a chilled, salt containing liquid like Gatorade or Powerade.
For heat exhaustion, treatment beyond this is often unnecessary. Only patients who do not respond to this initial therapy need further management. If these patients arrive at the hospital, rectal temperature should be obtained and an intravenous line should be placed to give a normal saline bolus of 20 mL/kg of body weight. Children with heat exhaustion should begin to improve within 30 minutes of therapy.
In a patient with heat stroke, assessment of the airway, breathing, and circulation is also important because of the risk of seizures and hypotension. Rapid cooling should begin immediately and, in the field or before insertion of an intravenous line, ice packs can be applied to the axillae, the neck, and the groin. Again, removing excess clothing to increase evaporative heat loss is important.
Once the patient with heat stroke arrives at the hospital, or hopefully before, resuscitation with intravenous normal saline has begun. There are electrolyte abnormalities that can be common in heat stroke, such as hyponatremia and hypo- or hyperkalemia. Taking these abnormalities into consideration during fluid resuscitation is important. Cardiac function can also be decreased during heat stroke, so the patient should be observed for signs of congestive heart failure during fluid resuscitation.
Despite fluid resuscitation, some patients may require vasopressor therapy because of depressed cardiac function or decreased systemic resistance. Typically this is necessary for only 24-48 hours.
Treatment of the multisystem organ involvement in severe heat stroke is critical to the survival of the patient. The hematologic and coagulation studies should be followed daily in moderate heat stroke and more often in severe heat stroke. In rare cases, a transfusion with packed red blood cells may be needed to treat progressive anemia. Additionally, although active hemorrhage is rarely a common problem, occasionally bleeding occurs and may require fresh frozen plasma and platelets to control.
The neurologic sequelae of heat stroke are one of the hallmarks of this disease. Confusion, ataxia, coma, obtundation, and seizures may be the presenting signs. Seizures can typically be controlled with a single anticonvulsant. Phenytoin is the drug of choice because it can control seizures without depressing the CNS. Cerebral edema is thought to be common after heat stroke. The pathologic features of the edema are unclear but are thought to be due to thermal injury of the neurons.
The lungs are typically relatively unaffected by heat stroke. In the event of aggressive fluid resuscitation in the presence of depressed cardiac function, pulmonary edema may result. If there is respiratory failure, it is typically secondary to CNS dysfunction rather than pulmonary disease.
Renal insufficiency or failure is secondary to the increased load of myoglobin to the kidneys in the face of hypotension. The treatment is aggressive hydration; however occasionally short-term, and less often long-term, dialysis may be needed in a patient who had preexisting kidney disease. Routine use of mannitol or bicarbonate to alkalinize the urine is controversial. There are no prospective, randomized controlled studies that have been able to prove that either mannitol or alkalinization are superior to vigorous hydration alone.
Generally, the insult to the kidneys is transient and the kidneys typically recover from this insult well.
Liver involvement in heat stroke is common. Hepatic enzyme elevation is so common that it is often used to help make the diagnosis of heat stroke. In severe heat stroke, transient liver failure with hepatic necrosis may occur. Management of coagulopathy and maintenance of blood pressure and hydration generally is sufficient for the liver to recover completely.
Rapid cooling and management of the consequences of heat stroke is the mainstay of treatment.
What are the adverse effects associated with each treatment option?
Adverse effects related to the treatment of heat exhaustion are most commonly associated with aggressive fluid resuscitation. Careful observation for signs of congestive heart failure is very important in both heat exhaustion and heat stroke. Additionally, electrolyte abnormalities are common and if not attended to, severe hyperkalemia, hypokalemia, hypernatremia, or hyponatremia can be exacerbated by fluid resuscitation that does not consider these electrolytes.
In heat stroke, there may be occasion to use blood products. Any time a patient receives blood products he/she is at risk for the development of an adverse reaction such as hives, hypotension, or anaphylaxis. Blood products must be carefully typed and screened to ensure the safest delivery of care.
What are the possible outcomes of heat-related illness?
Most children with heat exhaustion will not have any long-term sequelae. Rarely they will require hospitalization to correct an electrolyte disturbance, but otherwise the prognosis for these children is excellent, with return to normal activity in nearly all cases.
Patients with mild to moderate heat stroke typically recover completely. The renal and hepatic insufficiency that is seen during heat stroke is usually transient and there are generally no short- or long-term sequelae.
Those who survive moderate to severe heat stroke also have a significant chance of making a complete recovery, but the risk of long-term sequelae is higher. If the core temperature was greater than 107.6°F (42°C), patients have a poorer prognosis. Often the neurologic deficits persist in these patients. These neurologic changes may include behavioral changes, dysarthria, impaired memory, decreased visual acuity, poor coordination and ataxic gait.
In patients with severe heat stroke, up to one third have moderate to severe neurologic impairment. The mortality rate for severe heat stroke may be as high as 10%.
The family should recognize the risk of heat exhaustion porgressing to heat stroke if not caught and treated early. The only inherent risk to the treatment is development of hyper- or hyponatremia if the wrong type of fluid is used for rehydration.
For patients with heat stroke, the family should know that the risk of not treating heat stroke far outweighs the risks associated with the available treatments. Certainly aggressive fluid resuscitation carries the risk of causing pulmonary edema and worsening an electrolyte abnormality. Close monitoring of electrolytes and physical examination would decrease any real risk of this occurring.
In patients with progressive anemia and/or coagulopathy, treatment with blood products carries the inherent risk of infection, immunologic reaction, or anaphylaxis to the blood or blood product. Again, not treating progressive anemia or severe coagulopathy carries a greater risk to the patient than does the use of the blood products to treat it. Further, treatment of seizure activity or renal failure are well established treatments with inherent risks that should be discussed should the need arise. However, again, the risk of not treating these sequelae of heat stroke far outweighs the risk of using available treatments.
What causes this disease and how frequent is it?
Between 1997 and 2006, 26,171 children less than age 19 years were treated in North American emergency departments for heat-related injuries. There is clearly a peak during the summer months in all states. In southern states, heat-related illnesses are a possibility at any time of the year.
Most often, heat-related illnesses occur in male patients. The most commonly implicated activities are football, exercise, and mowing the lawn. Certainly a state of hypohydration, as is common in the pediatric population, can predispose a child to experience the signs and symptoms of heat stroke more quickly. There are other reasons that children are more susceptible to heat-related illnesses as well. They have a bigger body surface to body mass ratio, which results in a greater rate of heat absorption in a hot environment. Children also have a lower rate of sweating than do adults and slower acclimatization, leading to a slower rate of evaporation of heat from the body.
Aside from any predisposing medical conditions, there are no known genetic factors that contribute to heat exhaustion.
How do these exposures cause the disease?
Exposure to a high heat index predisposes children to heat-related illnesses. Evaporation is the principal mechanism of heat loss in a hot environment, but if the humidity is greater than 75%, it becomes ineffective. Children sustain a heat-related illness such as heat stroke when the critical thermal maximum (CTM) is exceeded. The CTM is defined as the degree of elevated body temperature and duration of heat exposure that can be tolerated before cell damage occurs. This generally occurs at a temperature of 42°C.
Heat stress can cause cell injury through a variety of proposed mechanisms. First, through the production of acute-phase reactants, such as cytokines, which initiate an inflammatory cascade. These acute-phase reactants are countered to some degree by heat shock proteins, which attempt to protect the cells by preventing the unfolding of denatured proteins and by stopping cytokine production. Second, cell injury can occur through a direct route because of denaturation of the cell proteins. Third, heat stress can cause direct injury to the vascular endothelium, resulting in impaired microcirculation and disseminated intravascular coagulation. Finally, it can cause intestinal ischemia, which leads to increased permeability of the gut followed by endotoxemia. All of these physiologic changes lead to a systemic inflammatory response that causes multisystem organ failure.
What complications might you expect from the disease or treatment of the disease?
As has already been discussed, multisystem organ failure, neurologic complications, and death may result from heat stroke. Long-term complications of this disease could include kidney and liver failure, as well as neurologic complications such as pancerebellar syndrome, spasticity, speech impairment, memory loss, gait abnormalities, and discoordination. In most cases of mild to moderate heat stroke, the patient makes a complete recovery. The complications that you might expect are typically only seen if the patient experienced severe heat stroke.
How can heat-related illness be prevented?
Heat exhaustion can develop into heat stroke, which is a potentially devastating disease for which there is no cure, only supportive care. Therefore, prevention is critically important. Reducing the known and modifiable risks for heat stroke is the key for prevention.
Environmental conditions are an important consideration when planning outside activities. Avoiding strenuous or outside activities during the hottest part of the day is very important. Allowing for frequent breaks in a cooler area, increased player substitutions, and improved and recurrent hydration breaks, even if the child is not thirsty, is important.
Reducing modifiable risks is the key for prevention. On average, a 40-kg child should drink 150 mL every 20 minutes and a 60-kg child should drink 250 mL every 20 minutes during outside activities. Additionally, allowing for a gradual progression of intensity during hotter months can help children avoid heat-related illnesses. Children generally acclimatize more slowly than do adults and that should be considered when participating in outside activities. Wearing appropriate clothing when playing or participating in outdoor activities can help with the evaporation of heat. Lightweight, light-colored clothing with only one layer of absorbent material can help with the evaporation of sweat.
What is the evidence?
Bytomski, JR, Squire, DL. “Heat illness in children”. Curr Sports Med Rep. vol. 2. 2003. pp. 320-4.
Jardine, DS. “Heat illness and heat stroke”. Pediatr Rev. vol. 28. 2007. pp. 249-58.
Nelson, NG, Collins, CL, Comstock, RD. “Exertional heat-related injuries treated in emergency departments in the U.S., 1997-2006”. Am J Prev Med. vol. 40. 2011. pp. 54-60.
Wexler, RK. “Evaluation and treatment of heat-related illnesses”. Am Fam Physician. vol. 65. 2002. pp. 2307-14.
Ongoing controversies regarding etiology, diagnosis, treatment
There is some ongoing controversy regarding the most appropriate method for rapid cooling during the treatment of heat stroke. Please refer to the following article for further information about this controversy.
Bouchama, A, Dehbi, M, Chaves-Carballo, E. “Cooling and hemodynamic management in heatstroke: practical recommendations”. Crit Care. vol. 11. 2007. pp. R54
Huerta-Alardin, AL, Varon, J, Marik, PE. “Bench-to-bedside review: rhabdomyolysis—an overview for clinicians”. Crit Care. vol. 9. 2005. pp. 158-69.
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- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has heat-related illness? What are the typical findings for this disease?
- What other disease/condition shares some of these symptoms?
- What caused this disease to develop at this time?
- What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
- Would imaging studies be helpful? If so, which ones?
- If you are able to confirm that the patient has heat-related illness, what treatment should be initiated?
- What are the adverse effects associated with each treatment option?
- What are the possible outcomes of heat-related illness?
- What causes this disease and how frequent is it?
- How do these exposures cause the disease?
- What complications might you expect from the disease or treatment of the disease?
- How can heat-related illness be prevented?
- What is the evidence?
- Ongoing controversies regarding etiology, diagnosis, treatment