Pediatric emergency medicine trisk 484

FIGURE 90.4 Carbon monoxide shifts the oxyhemoglobin dissociation curve to the left and
changes its shape, making the unloading of oxygen in the tissues more difficult and provides an
inadequate diffusion gradient. (Left curve, P 50 >12 mm; right curve, P 50 >28 mm.)

Carbon monoxide interacts with several other cellular proteins, including
cytochrome oxidase. It appears to interfere with oxidative energy production and
may generate free radicals, which exacerbate CNS damage. Neuronal necrosis, as
well as apoptosis, is seen in animal models in the frontal cortex, globus pallidus,
and cerebellum, likely contributing to delayed cognitive effects such as deficits in
learning, memory, and dementia. Carbon monoxide also binds to myoglobin,
which may cause cardiac ischemia and/or dysrhythmias, particularly in
individuals with pre-existing coronary disease.

Clinical Recognition
History provides the most valuable clue to diagnosis. Symptoms of acute carbon
monoxide poisoning include dull headache, weakness, dizziness, dyspnea, nausea
or vomiting, confusion, blurred vision, or loss of consciousness. If exposure was
overnight at home, then numerous family members may awaken with headache
and vomiting, possibly leading to erroneous evaluation for increased intracranial
pressure. Carbon monoxide poisoning should also be suspected in all fire victims.


Presence or absence of the classically described cherry red skin color is of little
diagnostic value. In fact, patients with thermal injury may appear red, whereas
those with vasoconstriction may be quite pale. Both color and respiratory rate
may be deceptive and may lead the physician away from recognition of severe
tissue hypoxia. PaO2 and arterial saturation as determined by pulse oximetry
(SaO2 ) are likely to be normal in carbon monoxide intoxication; low values
reflect coexistent pulmonary dysfunction.

Triage Considerations

Most important is removal of the victim from the contaminated environment.
Resuscitation should proceed according to general principles. As soon as
possible, the patient suspected of suffering carbon monoxide poisoning should be
provided 100% oxygen to hasten elimination.

Clinical Assessment
Determination of blood levels of carboxyhemoglobin may help aid in diagnosis
and prognosis. Venous blood may be used because of the high affinity of carbon
monoxide for hemoglobin, but an arterial sample provides more precise
information about acid–base balance and adequacy of ventilation. The level of
hemoglobin should also be determined. Levels of carboxyhemoglobin as low as
5% in nonsmokers may impair judgment and fine motor skills. Mild intoxication
(20% carboxyhemoglobin) produces headache, mild dyspnea, visual changes, and
confusion. Moderate poisoning (20% to 40%) produces drowsiness, faintness,
nausea and vomiting, tachycardia, dulled sensation, and decreased awareness of
danger. At lower levels, these symptoms are noted only with exertion, but as the
fraction approaches 40%, they are present at rest. Between 40% and 60%,
weakness, incoordination, and loss of recent memory occur, and cardiovascular
and neurologic collapse is imminent. Above 60%, coma, convulsions, and death
are almost certain. Although carboxyhemoglobin levels and symptoms tend to
follow the pattern just described, individual patients may be more or less
symptomatic than predicted. An important caveat is that blood
carboxyhemoglobin levels will fall rapidly with time and may not reflect cellular
dysfunction, especially in high-demand tissues of the heart and CNS. COoximeters that measure the saturation of blood with carbon monoxide (SpCO) are
widely available for use in the ED. Their use should only assist in the diagnosis
and not direct triage or management due to lack of accuracy. A negative SpCO
level in patients with clinical suspicion of carbon monoxide poisoning requires
confirmation by carboxyhemoglobin levels.

Patients with severe poisoning are vulnerable to pressure trauma to skin,
subcutaneous tissue, and muscle, especially at sites that support body weight or
that are pinned under fallen objects. The history may suggest which sites are most
vulnerable, and pain is an early symptom. Muscle breakdown and myoglobin
deposition in renal tubular cells may precipitate acute renal failure. ECG obtained
in patients with carbon monoxide poisoning may show nonspecific cardiac
repolarization changes and arrhythmias.
Two long-term neurologic syndromes have been described with carbon
monoxide poisoning: permanent neurologic sequelae (PNS) and delayed
neurologic sequelae (DNS). PNS is defined by central nervous system symptoms
such as headache, mood disorders, personality changes and memory loss that
persist for more than 3 months. Patients with DNS appear to recover with
treatment and then exhibit a broad spectrum of neurologic and psychiatric
abnormalities days to weeks after the exposure. Studies of DNS, many of which
are methodologically flawed, have elucidated neither an exact mechanism nor a
consensus on prevention and treatment.

Management and Diagnostic Studies
After removal from the contaminated environment, 100% oxygen should be
administered ( Table 90.2 ). If the patient is breathing spontaneously, this can be
accomplished with a nonrebreather face mask. The half-life of
carboxyhemoglobin is approximately 4 hours in a patient breathing room air at
sea level and approximately 1 hour if pure oxygen is inspired. The half-life is
further reduced to less than 30 minutes if the patient has access to hyperbaric
oxygen (HBO) at 2 to 3 atmospheres of pressure. There is no widespread
agreement on indications for HBO, and transfer to a hyperbaric chamber should
not jeopardize cardiopulmonary stabilization. However, HBO administration may
have effects beyond the mere reduction in carboxyhemoglobin half-life. Some
studies in adults suggest a role for HBO in reducing the incidence of mortality
and DNS, but there are no studies in children addressing its effectiveness. Early

consultation with a poison control center or an HBO facility should be considered
( Table 90.3 ).


TABLE 90.2
MANAGEMENT OF CARBON MONOXIDE POISONING
Initial management
Remove from contaminated environment
Cardiopulmonary resuscitation as needed
Provide 100% supplemental oxygen
Laboratory determinations
Arterial blood gas analysis
Carboxyhemoglobin level, troponin
Complete blood cell count, electrolytes
Urinalysis for myoglobin
Monitoring
Heart rate, electrocardiogram, respiratory rate, blood pressure
Treatment
Correct anemia Hgb <10 g/dL
Continue supplemental oxygen until carboxyhemoglobin ≤5%
Decrease oxygen consumption with bed rest, avoid producing anxiety
Maintain urine output >1 mL/kg/hr
Consider hyperbaric oxygen
Severe metabolic acidosis in the context of normal carboxyhemoglobin and
methemoglobin should suggest the possibility of coexistent cyanide poisoning in
patients involved in closed-space fires (especially where nitrogen-containing
materials have burned such as plastic, vinyl, wool, or silk). Cyanide has high
mortality but a short half-life (approximately 1 hour), so empiric cyanide levels
on patients who have survived the scene are not recommended generally unless
confirmation is needed. If cyanide poisoning is strongly suspected in an early

presenting patient, hydroxocobalamin (Cyanokit) or the cyanide antidote kit
(formerly known as the Lilly kit) may be considered. The two-step cyanide
antidote kit must be used with caution because the nitrite-containing first step
induces methemoglobinemia. In case of doubt, the thiosulfate-containing second
step, which is able to scavenge cyanide without significant additional toxicity,
may be given alone. Hydroxocobalamin (a synthetic form of vitamin B12 ) was