ABSTRACT
Carbon monoxide (CO) poisoning is the leading cause of toxicologic death in the United States of America, with 5600 fatalities reported annually.1 Worldwide CO remains the most lethal toxin in every community in which it has been studied.2 While mortality rates associated with acute exposure to CO may have declined over the past two decades, the total public health burden has not decreased.3 Most notably, delayed neuropsychiatric sequelae in a significant percentage of CO-poisoning survivors continues to pose an enormous challenge.4−9
The following chapter will focus primarily on the various treatment aspects of acute CO poisoning. It should be kept in mind that our present knowledge regarding
8417: “8417_c016” — 2007/9/11 — 12:15 — page 342 — #2
several First, effective medical treatment is ideally guided by diagnosis of either positive or negative outcomes following exposure to toxic substances. For example, blood or urine levels of toxins, combined with characteristic signs or symptoms of toxicity often aid in the institution of appropriate therapy. Unfortunately, symptoms relating to CO exposure are notoriously vague, and some studies estimate that the diagnosis is missed in 30% of cases presenting to the emergency department.10 For instance, when all neurologic admissions over a 5-month period were screened, it was determined that three out of 29 patients admitted with impaired consciousness and no lateralizing neurological signs had serious CO intoxication.11 A further toxicological challenge is that carboxyhemoglobin (COHb) levels neither correlate with toxicity nor predict the risk for development of long-term effects.12,13 Although other predictors of long-term neuropsychiatric sequelae have been proposed (i.e., loss of consciousness,14 cerebral edema on brain computed tomography,15 elevated blood glucose16 or a history of a “soaking” type exposure,17)their sensitivity and specificity are largely unproven. As a result, how best to treat patients with these clinical warning signs and symptoms remains controversial. Second, appropriate therapy for poisoned patients is ideally guided by an understanding of the toxic mechanisms of that poison. Unfortunately, even though CO has most likely been present since the beginning of time, and has been studied clinically for over 100 years, an adequate understanding of its toxic mechanisms continues to elude us. Lastly, treatment guidelines should ideally be on the basis of prospective, well-controlled, peer-reviewed studies. There is a dearth of such studies relating to CO-poisoning treatment in the literature.
