Chapter 222: Carbon Monoxide

INTRODUCTION AND EPIDEMIOLOGY

Carbon monoxide (CO) is one of the most common toxic exposures that emergency physicians will encounter. It is the second most common cause of fatal poisoning, either intentional (suicidal) or accidental, in the United States,¹ and is suspected to be the most common cause of fatal poisoning worldwide. Despite a great deal of clinical experience and several randomized trials, there is no clear consensus on the best approach to managing CO exposures.²

Exact statistics for CO poisoning are difficult to determine, mainly due to incomplete reporting. In 2016, the American Association of Poison Control Centers Toxic Exposure Surveillance System reported 13,620 exposures, with 48 deaths.³ Deaths in the United States from both intentional and accidental exposures are over 1200 per year.⁴ Decades ago, vehicular emissions were the major source of CO poisoning in U.S. adults. Currently, nonvehicular sources, such as heating systems, are more common, as modern exhaust systems reduce CO emissions.⁵ Table 222-1 lists the most common sources of CO exposures.^3,6-8

Peak incidence occurs in the fall and winter months, generally due to use of space heaters, wood-burning stoves, charcoal burning for heat, or portable generators without adequate ventilation.⁴ It is not uncommon for whole families to be affected. Exposures have been reported in persons riding in the back of pickup trucks, as well as persons riding in vehicles with exhaust pipes occluded by snow. It is believed that CO poisoning is probably the most pressing danger from smoke inhalation and is a major contributor to fire-related deaths.

An unusual source of CO is methylene chloride, which is found in varnishes and paint strippers and bubbling fluid in Christmas ornaments. Routes of exposure are inhalational or by ingestion. Methylene chloride is metabolized in the liver to CO. As a result of ongoing metabolism, persistent elevation of carboxyhemoglobin occurs despite oxygen therapy.⁹ Time to peak CO levels may be ≥8 hours.

PATHOPHYSIOLOGY

CO is typically described as a colorless, odorless gas. It is normally present in air at 10 ppm or less, perhaps higher in urban areas. CO is also an endogenous substance, with production occurring in the body during normal breakdown of heme. Normal physiologic CO levels (as carboxyhemoglobin) from this process are approximately 1% in healthy nonsmokers. Physiologic production can be increased in hemolysis or sepsis. CO toxicity causes profound tissue hypoxia and activation of inflammatory mediators that may lead to permanent injury of the heart, the CNS,^8,10-14 and less commonly, the peripheral nervous system.¹⁵