125: Carbon Monoxide

HISTORY AND EPIDEMIOLOGY

Carbon monoxide (CO) is formed during the incomplete combustion of virtually any carbon-containing compound. Because it is an odorless, colorless, and tasteless gas, it is remarkably difficult to detect in the environment even when present at high ambient concentrations and is a leading cause of poisoning morbidity and mortality in the United States. Based on US national death certificate data, there were 439 annual deaths from unintentional non-fire exposure to CO from 1999 to 2004.^25,123 The groups with the highest risk were male gender and elderly age, possibly because of occupational exposure and inability to discern CO symptoms, respectively. CO related mortality remained essentially unchanged in 2002 despite increased CO detector use.^22,24,26 More than half of these cases (64%) occurred in homes with faulty furnaces, usually in the fall or winter months. Many clusters are associated with power failures during catastrophic weather, such as ice storms, blizzards, and hurricanes.^22,23 With improved data collection, the CDC WONDER database reported 1944 deaths in the United States in 2010 due to the toxic effects of CO.²⁷

Just as important as mortality, are the greater number of survivors from CO poisoning. Despite increased awareness for CO poisoning, in 2004 to 2006, there were still an average of 20,636 nonfatal, unintentional, non–fire-related CO exposures treated annually in the United States.²⁶ More than 40% of cases occurred in the winter, with almost 75% occurring in residences. However, exclusion of intentional and fire related cases severely underestimates the extent of the problem. Based on firsthand hospital data, a minimum of 50,000 CO cases present to US Emergency Departments (EDs) each year, up to half resulting in hospitalization.^80,91 More recent data using probable and suspected cases suggests that there were over 230,000 ED visits in 2007 alone that were unintentional and related to non-fire CO poisoning.⁹²

The bigger problem with CO poisoning may be the associated morbidity that survivors risk even after acute treatment. The most serious complication is persistent or delayed neurologic or neurocognitive sequelae, which occurs in up to 50% of patients with symptomatic acute poisonings.^68,144,196 There is still no highly reliable method of predicting who will have a poor outcome, requiring the threshold for HBO therapy for CO poisoning and follow-up be particularly low.

Potential sources of CO abound in our society, often resulting in unintentional poisoning²⁶ (Table 125–1). Although CO is found naturally in the body as a byproduct of hemoglobin degradation by heme oxygenase found in the liver and spleen,⁴⁰ it is readily available for inhalation from the incomplete combustion of virtually any carbonaceous fuel. Alternatively, absorption—dermal, ingestion, or inhalation—of methylene chloride may result in CO toxicity after hepatic metabolism¹²⁸ (Chap. 108). Despite catalytic converters and other emission controls, more than ...