Pediatric emergency medicine trisk 487

PT, prothrombin time; PTT, partial thromboplastin time; BUN, blood urea nitrogen; CPK, creatine
phosphokinase.

The severity of the patient’s presentation determines the degree of
cardiovascular support. If the skin is flushed and BP adequate, lowering body
temperature with close attention to heart rate and BP may be sufficient. Although
severe dehydration and electrolyte disturbances are uncommon, these should be
assessed and corrected if necessary. Fluids cooled to 4°C (39.2°F) hasten
temperature correction but may precipitate arrhythmias on contact with an already
stressed myocardium. Adult patients rarely have required more than 20 mL/kg
over the first 4 hours, but determinations of electrolytes, hematocrit, and urine
output, and clinical assessment of central vascular volume should guide precise
titration of fluids and electrolytes.
Inotropic support may be required after a fluid challenge (see Chapter 10
Shock ). Dobutamine is probably most appropriate as its β-agonist properties
increase myocardial contractility and maintain peripheral vasodilation.
Isoproterenol has been used successfully in the past but may cause myocardial
oxygen consumption to exceed oxygen delivery and thus may precipitate
myocardial ischemia. Additional fluid resuscitation may be necessary with the
initiation of either dobutamine or isoproterenol to fill the effectively increased
vascular space. Normal saline should be given to maintain the arterial BP in the
normal range. Dopamine may also be effective, infused at rates compatible with
inotropic support without vasoconstriction (i.e., 5 to 15 mcg/kg/min). In cases of
extreme hemodynamic instability, extracorporeal circulation may provide both
circulatory support and a means of rapid temperature correction. Agents with αagonist characteristics (epinephrine and norepinephrine) are not recommended for
initial management as they cause peripheral vasoconstriction, interfere with heat
dissipation, and may compromise hepatic and renal flow further. Atropine and
other anticholinergic drugs that inhibit sweating should be avoided.
Renal function should be monitored carefully, especially in patients who have
been hypotensive or in whom vigorous exercise precipitated heat stroke. BUN,
creatinine, electrolytes, calcium, and urinalysis for protein and myoglobin should

be obtained. Once the patient’s vascular volume has been restored and arterial
pressure normalized, hourly urine output should be monitored. If urine output is
inadequate (less than 0.5 mL/kg/hr) in the face of normovolemia and adequate
cardiac output, furosemide (0.5 to 1 mg/kg by IV) and/or mannitol (0.25 to 1 g/kg
by IV) should be given. If the response is poor, acute renal failure should be
suspected, and fluids should be restricted accordingly. Rapidly rising BUN or
potassium should prompt consideration of early dialysis.


Indications for Admission and Discharge
Patients with heat cramps can generally be discharged from the ED after
resolution of symptoms. Children with heat exhaustion may require admission for
ongoing fluid and electrolyte replacement and serial testing. Children with heat
stroke require admission to the ICU. Patients with ashen skin, tachycardia, and
hypotension demonstrate cardiac output insufficient to meet circulatory demand
and are in imminent danger of death. Monitoring of the electrocardiogram (ECG)
and arterial BP (with an indwelling arterial line) should determine support.

ACCIDENTAL HYPOTHERMIA
Goals of Treatment
The goals of treatment include general supportive measures, cardiopulmonary
resuscitation, and rewarming.
CLINICAL PEARLS AND PITFALLS
A high index of suspicion is needed to recognize hypothermia.
Hypothermia can mimic death; hence rewarming must be done before
pronouncing death.

Current Evidence
Hypothermia is defined as a core temperature below 35°C (95°F) and can be
classified by temperature into mild (32° to 35°C), moderate (28° to 32°C), severe

(25° to 28°C), and profound (<25°C). According to the 2012 Kids’ Inpatient
Database, accidental hypothermia has been associated with a mortality rate of
8.45%. It is more prevalent among infants and less frequent among 6- to 10-yearold children and adolescents.
Neonates, with large surface:volume ratios and small amounts of subcutaneous
fat, conserve heat poorly and are unable to produce heat by shivering. Therefore,
minor deviations in the thermal environment may produce hypothermia in
neonates. The capacity for nonshivering thermogenesis—primarily metabolism of
brown fat—is intact, but oxygen consumption is significantly increased. This may
result in metabolic acidosis, hypoglycemia, and hypocalcemia. Physical disability,
especially immobilizing conditions, and drug or alcohol ingestion increase risk at
any age. Healthy young people who work or play to exhaustion in a cold
environment are also at risk, as are those who fail to take preventative or


corrective measures. The rising popularity of cold weather sports is producing
more cases of accidental hypothermia. However, environmental conditions need
not be extreme, and the diagnosis should be considered even in temperate
climates. For example, cold-related deaths are twice as common as heat-related
deaths in the southern United States.
When core temperature begins to fall to less than 37°C (98.6°F), physiologic
mechanisms that produce and conserve heat are activated. Cooled blood
stimulates the hypothalamus to increase muscle tone and metabolism (oxidative
phosphorylation and high-energy phosphate production) and to augment heat
production by 50% during nonshivering thermogenesis. When muscle tone
reaches a critical level, shivering begins, and heat production increases two to
four times basal levels.
Although the surface temperature of the body, especially of the extremities,
may drop to nearly the environmental temperature, several mechanisms work to
conserve heat and to protect blood and core structures from ambient air
temperature, humidity, and wind. Sweating is abolished, decreasing heat loss by

evaporation (unless there is external moisture), and vasoconstriction of cutaneous
and subcutaneous vessels reduces losses further. Piloerection occurs, which in
many animal species traps an insulating layer of air next to the skin, but is
ineffective in humans.
Once homeostatic mechanisms fail and core temperature falls, predictable
physiologic changes take place. If shivering does not occur, basal metabolic rate
decreases steadily, reaching 50% of normal at 28°C (82.4°F). As a result, oxygen
consumption and carbon dioxide production decline. The oxygen–hemoglobin
dissociation curve shifts to the left.
Although respiratory depression occurs late, impaired mental status and coldinduced bronchorrhea predispose the patient to airway obstruction and aspiration.
Acid–base balance follows no predictable pattern. Respiratory acidosis occurs,
but tissue hypoxia, increased lactic acid production, and decreased lactate
clearance by the liver produce metabolic acidosis.
Decreased heart rate contributes primarily to a drop in cardiac output.
Peripheral vasoconstriction and an early increase in central vascular volume cause
a transient rise in BP, which later falls to become clinically significant at less than
25°C (77°F). A variety of cardiac conduction abnormalities arise, including
decreased sinus rate, T-wave inversion, prolongation of ECG intervals, and the
appearance of pathognomonic J waves ( Fig. 90.5 ), which may provide the first
clue to the diagnosis. Atrial fibrillation may occur at temperatures less than 33°C
(91.4°F) but is usually not hemodynamically significant. With severe


hypothermia at less than 28°C (82.4°F), myocardial irritability increases
dramatically, and ventricular fibrillation becomes more likely.
Cold-induced vasoconstriction and elevated central blood volume and pressure
contribute to a diuresis, which subsequently diminishes intravascular volume. At
lower temperatures, tubular dysfunction allows salt and water loss. Acidosis
causes potassium to shift from cells to the urine, where it is eliminated. Increased
capillary permeability results in loss of fluid into the extracellular space.

FIGURE 90.5 J wave (Osborn wave), pathognomonic of hypothermia. Rounded contour
distinguishes it from an RSR′. It may also be confused with a T wave with a short Q-T interval.
(Reprinted with permission from Welton D, Mattox K, Miller R, et al. Treatment of profound
hypothermia. JAMA 1978;240:2291–2292. Copyright © 1978 American Medical Association.
All rights reserved.)

Hematologic abnormalities may also occur. Plasma loss causes an increased
hematocrit level, whereas splenic sequestration may be responsible for a fall in
white blood cell and platelet counts. Disseminated intravascular coagulation is
sometimes seen.
CNS abnormalities are progressive. Each fall of 1°C produces a 6% to 7%
decline in cerebral blood flow. Plasma loss increases blood viscosity, which
further contributes to impaired cerebral microcirculation and mentation.
Peripheral nerve conduction slows, and deep tendon reflexes decrease. Pupils
dilate and react sluggishly, if at all, at less than 30°C (86°F). The
electroencephalogram deteriorates progressively with falling temperature, from
high-voltage slow waves, to burst suppression patterns, to electrical silence at
20°C (68°F).