Pediatric emergency medicine trisk 485

approved by the FDA in 2006 for use in cyanide poisoning. Its mechanism of
action is that the hydroxyl group of the vitamin binds to free cyanide, forming the
nontoxic cyanocobalamin. The dose is 70 mg/kg (max 5 g) given over 15
minutes, with a repeat dose if necessary. The minimal side effects of
hydroxocobalamin make this an attractive alternative to the traditional nitrite
therapy.
TABLE 90.3
Considerations for Hyperbaric Oxygen Therapy a
Neurologic symptoms or signs (syncope, seizure, coma) either on presentation
or that persist despite normobaric oxygen
Signs of cardiac ischemia or metabolic acidosis
Pregnancy
a Consider

early consultation with a poison control center or HBO facility.

Anemia (hemoglobin less than 10 g/100 mL) must also be corrected to
maximize oxygen-carrying capacity. If myoglobinemia or myoglobinuria is
present, vigorous hydration and diuresis with furosemide (1 mg/kg intravenously)
and/or mannitol (0.25 to 1 g/kg intravenously) with close attention to urine output
may preserve renal function. If hydration and diuresis are ineffective, renal failure
should be considered and fluids restricted accordingly (see Chapter 100 Renal
and Electrolyte Emergencies ).

Indications for Discharge or Admission
Determination of disposition from the ED will depend on the history and clinical
status. Patients with significant respiratory distress or decreased neurologic status
should be admitted to an ICU. Patients who appear well on presentation to the ED
but have a significant history (loss of consciousness at the scene) or elevated CO
levels should be admitted for monitoring for other sequelae of smoke inhalation.
Severe disease course has been associated with low Glasgow Coma Scale score,

high leukocyte count, and high troponin T levels at presentation.

ENVIRONMENTAL AND EXERTIONAL HEAT ILLNESS
Goals of Treatment
Treatment of heat stroke involves rapid reversal of hyperpyrexia, cardiovascular
support, and correction of electrolyte imbalances.


CLINICAL PEARLS AND PITFALLS
Heat cramps involving the abdominal musculature may mimic an acute
abdomen.
Heat stroke is differentiated from heat exhaustion by the presence of
hyperpyrexia and anhidrosis with circulatory failure and/or severe CNS
dysfunction.
Active cooling may be achieved effectively using evaporation with fans
after spraying with cool water.

Current Evidence
In the United States alone, heat injury is responsible for approximately 650
preventable deaths every year. Heat stroke remains the third most common cause
(after head injury and cardiac disorders) of exercise-related mortality among U.S.
high school athletes, despite the fact that survival following acute heat stroke has
improved over the last century from an estimated 20% to more than 90%.
Although athletes are at risk for heat illnesses, children and especially those with
chronic conditions are generally more vulnerable because they produce more
metabolic heat, their core temperature rises faster during dehydration, and their
small organs are less efficient at heat dissipation. Environmental and exertional
heat illness occurs with excessive heat generation and storage. These conditions
arise when high ambient temperature prevents heat dissipation by radiation or
convection, and humidity limits cooling by sweat evaporation. The spectrum of

illness is broad, including heat cramps, heat exhaustion, and heat stroke. Heat
stroke is an acute medical emergency with significant associated morbidity and
mortality. Children with increased risk include those with cystic fibrosis or
congenital absence of sweat glands, children receiving medications that cause
oligohidrosis, those with eating disorders, diabetes insipidus, obesity, or
uncontrolled diabetes mellitus, infants left in automobiles on hot days, and young
athletes.
Heat-sensitive centers of the posterior hypothalamus control sympathetic tone.
This tone regulates vasoconstriction of arterioles and subcutaneous arteriovenous
anastomoses, which, in turn, controls heat conduction from the body core to the
skin. Flow through these areas may represent up to 30% of total cardiac output.
High flow provides efficient heat transfer from the body core to the skin, which is
an effective radiator. Low flow to the skin prevents radiation and allows only
inefficient diffusion through the insulating skin and subcutaneous tissues. When
body temperature rises, blood in the preoptic area of the anterior hypothalamus is


warmer than optimal. Impulses from this area increase and are conducted through
autonomic pathways to the spinal cord and then, through cholinergic fibers to the
sweat glands, where sweat is released. Exercise and certain emotional states
release circulating epinephrine and norepinephrine to increase sweat production.
A 0.6°C increase in core temperature causes a 10% elevation in basal metabolic
rate. There are four different ways for the body to reduce excess heat: convection,
conduction, radiation, and evaporation, with the latter being the most important
thermoregulatory mechanism.

Clinical Recognition
Three types of heat illnesses are recognized and represent different physiologic
disturbances ( Table 90.4 ). Heat cramps refer to the sudden onset of brief,
intermittent, and excruciating cramps in muscles after they have been subjected to

severe work stress. Cramps tend to occur after the work is done, on relaxing, or
on taking a cool shower. Occasionally, abdominal muscle cramps may simulate
an acute abdomen. The usual victim is highly conditioned and acclimatized.
Typically, these individuals can produce sweat in large quantities and provide
themselves with adequate fluid replacement but inadequate salt replacement.
Electrolyte depletion is probably the cause of heat cramps.
Most spasms last less than a minute, but some persist for several minutes,
during which a rock-hard mass may be palpated in the affected muscle. Cramps
often occur in clusters. Rapid voluntary contraction of a muscle, contact with cold
air or water, or passive extension of a flexed limb may reproduce a cramp.
Laboratory investigation reveals hyponatremia and hypochloremia and virtually
absent urine sodium. The blood urea nitrogen (BUN) level is usually normal but
may be mildly elevated.
Heat exhaustion is less clearly demarcated from heat stroke than are heat
cramps. There are two types of heat exhaustion with significant overlap: water
depleted and sodium depleted. In most cases, water depletion predominates
because individuals who live and work in a hot environment do not always
voluntarily replace their total water deficit. Progressive lethargy, intense thirst,
and inability to work or play progress to headache, vomiting, CNS dysfunction
(including hyperventilation, paresthesias, agitation, incoordination, or actual
psychosis), hypotension, and tachycardia. Hemoconcentration, hypernatremia,
hyperchloremia, and urinary concentration are typical. Body temperature may rise
but rarely to higher than 39°C (102.2°F). If unattended, heat exhaustion may
progress to frank heat stroke.
Heat exhaustion may also occur because of predominant salt depletion. As in
heat cramps, water losses are replaced but without adequate electrolyte


supplementation. Symptoms include profound weakness and fatigue, frontal
headache, anorexia, nausea, vomiting, diarrhea, and severe muscle cramps.

Tachycardia and orthostatic hypotension may be noted. Hyponatremia,
hemoconcentration, and significantly diminished urine sodium are consistent
findings. Children with cystic fibrosis, particularly those who are young and
unable to meet increased salt requirements, are at risk for electrolyte depletion
because salt losses in their sweat apparently do not respond to acclimatization and
aldosterone stimulation of the sweat gland.
Heat stroke is a life-threatening emergency. Classic signs are hyperpyrexia
(41°C [105.8°F] or higher); hot, dry skin that is pink or ashen (anhidrosis)
depending on the circulatory state; and severe CNS dysfunction. Often sweating
ceases before the onset of heat stroke.
The onset of the CNS disturbance may be abrupt, with sudden loss of
consciousness. Often, however, premonitory signs and symptoms exist. These
include a sense of impending doom, headache, dizziness, weakness, confusion,
euphoria, gait disturbance, and combativeness. Posturing, incontinence, seizures,
hemiparesis, and pupillary changes may occur. Any level of coma may be noted.
Cerebrospinal fluid findings are usually normal. The extent of damage to the CNS
is related to the time and extent of hyperpyrexia and to the adequacy of
circulation. In severe cases, coma may persist even after the body temperature is
lowered.
Patients able to maintain cardiac output adequate to meet the enormously
elevated circulatory demand are most likely to survive. Initially, the pulse is rapid
and full, with an increased pulse pressure. Total peripheral vascular resistance
falls as a result of vasodilation in the skin and muscle beds, and splanchnic flow
diminishes. If hyperpyrexia is not corrected, ashen cyanosis and a thin, rapid
pulse herald a falling cardiac output. The cause may be either direct thermal
damage to the myocardium or significant pulmonary hypertension with secondary
right ventricular failure. Even after body temperature is returned to normal,
cardiac output remains elevated and peripheral vascular resistance remains low
for several hours, resembling the compensatory hyperemia after ischemia noted in
post-trauma, post-shock, and post-septic states. Persistently circulating vasoactive

substances probably account for this phenomenon.