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 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 hours in a patient breathing room air at sea level and approximately 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 to 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 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 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