Elsevier

Critical Care Clinics

Volume 28, Issue 4, October 2012, Pages 537-548
Critical Care Clinics

Carbon Monoxide Poisoning

https://doi.org/10.1016/j.ccc.2012.07.007Get rights and content

Introduction

Carbon monoxide (CO) poisoning is common. Unintentional, non–fire-related CO poisoning is responsible for approximately 15,000 emergency department (ED) visits and nearly 500 deaths annually in the United States.1, 2 CO is frequently unrecognized because the signs and symptoms are relatively nonspecific; consequently, the true incidence of CO poisoning remains unknown. Mortality rates range between 1% and 31%.3

Section snippets

Epidemiology

CO is an odorless, colorless gas that usually remains undetectable until exposure results in injury or death. CO poisoning occurs both as the result of routine domestic, occupational, and recreational activities and in the wake of large-scale disasters such as those caused by hurricanes,4 floods,5 and winter storms.6, 7

Sources of CO include faulty furnaces, inadequate ventilation of flame-based heating sources, exposure to internal combustion engine exhaust (bus exhaust from attached garages,

Mechanisms of toxicity/pathophysiology

CO toxicity is the result of a combination of tissue hypoxia-ischemia secondary to carboxyhemoglobin (COHb) formation and direct CO-mediated damage at a cellular level (Fig. 1).

CO binds hemoglobin (Hb) to form COHb with an affinity that is more than 200 times greater than that of oxygen.13, 14 The amount of COHb formed depends on the duration of the exposure to CO, the concentration of CO in the inspired air, and alveolar ventilation. Additionally, bound CO ligand at any of the 4 oxygen-binding

Clinical presentation

The spectrum of symptoms depends on the duration of the exposure and the levels of CO. The clinical effects of CO are diverse and symptoms are nonspecific and can be easily confused with other illnesses; therefore, a high index of suspicion is crucial for an appropriate and early diagnosis.9, 20 The severity ranges from mild flulike symptoms to coma and death. Because of their higher metabolic rate, the brain and the heart are most susceptible to CO toxicity.21 Common CO-induced manifestations

Diagnosis

Timely diagnosis of CO poisoning is critical, albeit challenging, because the clinical presentation is nonspecific and can mimic that of influenza or other viral illnesses. A high index of suspicion and consideration of the circumstances and environmental factors suggestive of exposure are therefore of paramount importance.2, 9, 20, 21 Source identification is important in cases of nonintentional poisoning to limit the risk to others. In the absence of exposure history, CO poisoning must be

Treatment

Field treatment of the CO-poisoned patient consists of removal of the patient from the source of exposure, immediate administration of 100% high-flow supplemental oxygen, and transport to a hospital, where aggressive supportive measures, including airway and cardiovascular support, can be provided.9, 20, 21 The administration of oxygen speeds the elimination of CO from the body. Without oxygen therapy, the elimination half-life of CO is 4 to 5 hours.47, 63 Supplementation with 100% oxygen via a

Disposition/prevention

No definitive guideline exists on how to triage patients with CO poisoning, although most patients can be managed in the ED because most symptoms improve with NBO. As a general approach, patients with minor symptoms should receive NBO in the ED until their COHb levels decrease to less than 10% and symptoms resolve. Patients with more severe or nonresolving symptoms, higher COHb levels, and major comorbidities should be hospitalized. Because many hospitals lack the ability to measure COHb,51

Summary

CO poisoning is common, potentially fatal, and frequently underdiagnosed because of its nonspecific clinical presentation. Immediate NBO with the highest possible fraction of inspired oxygen should be administered to patients with suspected poisoning, and aggressive supportive treatment should be promptly instituted. Diagnosis of CO exposure should be made by COHb measurement using multiwavelength spectrophotometry (CO-oximetry). The use of HBO is controversial and, if used, should be relegated

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      Intravascularly, CO induces leukocyte sequestration, platelet-neutrophil aggregation, and neutrophil degranulation. Therefore, CO causes free radical generation, apoptosis, and lipid peroxidation, resulting in endothelial dysfunction [6]. When ROS are overproduced and antioxidants are not sufficiently effective, cell redox balance is disrupted [7].

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