Acute carbon monoxide exposure: Diagnosis, evaluation, treatment

Carbon monoxide—odorless, colorless, tasteless . . . and deadly. What can you do about this poison? How can you identify and treat the victims?

Dawn Colomb-Lippa, PA-C, MHS

Ms. Colomb-Lippa is Assistant Professor of Physician Assistant Studies at Quinnipiac University, Hamden, Conn, and an emergency medicine PA at Charlotte Hungerford Hospital, Torrington, Conn. The author has indicated no relationships to disclose relating to the content of this article.

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Exposure to carbon monoxide (CO) can cause significant morbidity, including cardiac complications, neurologic disorders, and, in some cases, death. When patients present with acute CO poisoning, they are often unaware that such exposure is the cause of their symptoms, and the indistinct clinical signs further complicate the work-up and treatment. It is therefore imperative that all clinicians become familiar with the signs and symptoms of CO poisoning so that intervention strategies can begin early in order to reduce negative outcomes.

CO exposure continues to be the leading cause of accidental poisoning deaths in the United States and is responsible for more worldwide deaths by poisoning than any other substance.^1,2 CO is an odorless, colorless, tasteless by-product of incomplete combustion of fossil fuel, and people who are exposed to it generally have no sense of the danger they are in. Those with acute CO toxicity usually present to emergency departments or urgent care centers after failed suicide attempts, as a result of occupational exposure, or, most commonly, after unintentional residential exposures.³ Although numbers vary regionally, CO exposure is estimated to account for 3,000 to 5,000 visits to health care facilities each year.^4,5 Furthermore, evidence indicates that significant numbers of people who are exposed to levels of CO are exposed at levels that are insufficient to cause acute symptoms but are noxious enough to produce more insidious, vague symptoms.⁶ These chronically exposed patients may present to their primary clinician, or they may never seek a diagnosis at all.

Epidemiology

Although sources differ, an estimated 500 to 2,100 people die accidentally each year in the United States secondary to CO poisoning.^7,8 Since the symptoms associated with CO exposure may be mild or incorrectly attributed to other disease processes, the true incidence of CO poisoning is unknown.³ The most conclusive epidemiologic evaluations of CO toxicity have been completed with regards to ambient CO levels in air pollution. A number of authors have clearly demonstrated a rise in daily mortality rates as ambient CO concentrations increase.^9-12 In their review of Medicare hospital admissions data, Morris and colleagues demonstrated a consistent association between increasing levels of ambient CO and hospital admissions for treatment of heart failure among elderly patients.¹¹

Certain groups of patients may be more at risk for the ill effects of CO exposure secondary to underlying diseases, including those with cardiac disease, sickle cell anemia, thalassemia, and pulmonary disease.^11,13-15 In addition, several retrospective and animal-model studies have proven a strong correlation between fetal CO exposure and birth defects as well as low birth weight, suggesting that pregnant women should be aware of potential exposures.^16,17

Pathophysiology

The exact mechanism by which CO causes injury is still largely unknown, although several theories have been explored. In the mid 1800s, Claude Bernard hypothesized that the deleterious effects of CO exposure were due to the poison’s great affinity for hemoglobin; this view has been largely accepted as the primary mechanism by which CO causes hypoxia.⁵ Hemoglobin is well known to have a more than 200-fold greater affinity for binding CO over oxygen, the end product of which is the formation of carboxyhemoglobin (COhg). This binding causes a leftward shift of the oxygen hemoglobin saturation curve, making less oxygen available for the tissues and resulting in hypoxia. The hypoxia is further amplified by decreased cardiac function, which in turn leads to increasingly poor perfusion.

As less oxygen is available to the tissues, more hypoxia results and, therefore, more grave symptoms and outcomes of CO exposure might be expected. The problem is that serum COhg levels do not directly correlate with severity of symptoms, particularly neurologic injuries.^18,19 The exact reason why COhg levels cannot predict outcomes in patients who may have been exposed to CO is unknown, but this phenomenon may be related to a time lag between the person’s exposure and subsequent admission to a medical facility for evaluation.

Given these findings, scientists have conducted numerous studies in search of a secondary means of cellular injury due to CO exposure. While no clear consensus has been reached thus far, several theories have been investigated, including impairment of cellular respiration, free radical formation (peroxidation), and initiation of inflammatory cascade.^20,21

Sources of exposure

Environmental exposure Although normally present in ambient air in nontoxic concentrations, CO may be present in higher levels as a result of incomplete fossil fuel combustion from multiple sources. Automobile exhaust had been a great contributor to CO-related mortality until the introduction of catalytic converters in 1975. This safeguard modification is estimated to have decreased automobile CO emissions by roughly 77% and unintentional death from automobile CO emission by 81%.²² Despite these changes, CO poisonings may occur while automobiles are being warmed up in attached garages and when vehicle exhaust systems are either intentionally or accidentally obstructed.²³

While not usually the cause for accidental poisoning, tobacco smoke is another common generator of carbon monoxide. Smokers, as well as persons exposed to smoke, may have an increased tolerance for CO because of this ongoing exposure. Despite this presumed increase in tolerance, some have suggested that smokers’ self-imposed exposure may put them at increased risk for the negative sequelae of CO exposure, likely due to underlying lung dysfunction.²⁴

Household exposure Any fuel-burning appliance that is not vented properly can be a potential source of CO within the home. Among the possible culprits are malfunctioning furnaces, water heaters, gas ovens, fireplaces, and wood-burning stoves. The use of barbeque grills, lawnmowers, and other gas-powered tools in poorly ventilated spaces has also been linked to CO poisonings.^25,26

Recreation/hobby exposure There have been several reports of exposure to CO during recreational boating resulting in significant illness or death, including exposure with prolonged swimming near houseboats and poisoning from ski-boat exhaust.^27,28 The use of propane lanterns and grills in relatively enclosed spaces while camping has also been associated with CO-related illness.²⁹   

Occupational exposure Valent and colleagues conducted a retrospective analysis of workplace fatalities related to inhalation of toxic substances and found CO to be most frequently implicated in such deaths. Industries whose employees were considered to be more at risk for such fatal inhalations were construction, followed by agriculture, forestry, and fishing.³⁰ The occupational use of gas-powered equipment including concrete saws, pressure washers, forklifts, tractors, and floor burnishers has been linked to serious CO poisoning and death.^31-37 In addition, hepatic metabolism of methylene chloride results in the production of CO; therefore, CO toxicity may occur as a result of exposure to this chemical, which is found in many paint and varnish removers.³⁸

Clinical presentation

Given the many possible sources of this toxic gas, CO-related illness can occur at any time of the year from the use of seasonal equipment such as barbeques, lanterns, and grills or as a result of CO exposure during outdoor recreational activities. The incidence of exposure may be slightly higher during cooler months when more people are likely to be using alternative heating sources and exposure to exhaust fumes may be greater.³⁹ Medical providers must have a high index of suspicion for CO poisoning when evaluating patients who present with an indistinct cluster of complaints ranging from flulike symptoms to frank coma. The clinician should carefully question such patients regarding possible CO exposure, particularly when symptoms develop in the workplace or when other members of the household have similar complaints. It is useful to take a complete exposure history using a survey format that includes questions about possible community, home-hobby, and occupational vulnerability to CO (see Table 1).

One of the most common manifestations of both acute and chronic CO exposure is headache, although no typical characteristic or location of headache associated with CO exposure has been identified.^39,40 Other symptoms are vague and varied and may include dizziness, fatigue, visual changes, memory and concentration deficits, and shortness of breath (see Table 2). Less frequently, patients may present with pulmonary, cardiovascular, or GI complaints.

A prospective analysis of data from seven major metropolitan regions demonstrated a correlation between increases in ambient CO exposure and admissions to local hospitals for treatment of heart failure (HF). This suggests that HF may be a presenting diagnosis for people who are exposed to high levels of CO.¹¹ In addition to heart failure, arrhythmias and ischemic changes in the myocardium have been seen in both animal models and in humans exposed to high levels of CO.^13,39-43 Adults with underlying illness and children may be at increased risk for these cardiopulmonary toxic effects of CO exposure.^11,15,44

Some patients who have an acute exposure will develop a delayed neurologic condition characterized by a variety of symptoms. No consistent criteria predict who these patients will be, but the literature suggests that initial presentation of coma and a delay in hyperbaric oxygen therapy may be associated with belated neurologic deterioration.^45,46 These patients will appear to recover initially from anoxic insult, but after a latent period of from 2 days to 2 weeks they begin to experience a decline in neurologic function, including manifesting features that may appear parkinsonian or psychiatric in nature (see Table 3).⁴⁷

Physical examination of patients with possible CO toxicity should include a full evaluation of systems with particular attention to the cardiovascular and neurologic exams. A comprehensive neurologic examination should include neuropsychological testing such as the Mini-Mental Status Examination, in which the patient’s general orientation, memory, recall, and judgment are assessed. The clinician should also use Romberg’s test, heel-to-shin, and rapid alternating movements to evaluate cerebellar functioning. These tests are not only helpful during the initial evaluation, but may also serve as baseline studies for those patients who require follow-up after treatment for CO poisoning.

Diagnostic studies

COhg levels may be useful in confirming a diagnosis in a patient with a significant exposure history and presentation consistent with CO toxicity. Although the point was heavily debated in the past, now there seems to be a consensus regarding the accuracy of venous blood evaluation for predicting arterial COhg levels, and arterial blood draws are no longer considered necessary.⁴⁸

The normal CO level is 1% to 3%, with smokers’ levels rising to the 10% range without subjective complaints—although some patients with this minimal exposure may complain of headache and shortness of breath.^24,38 Symptoms are usually present when COhg levels are 10% to 30% and may include headache, dizziness, weakness, dyspnea, irritability, nausea, and vomiting. At COhg levels of 30% and higher, the risk of toxic effects is serious and the patient may present with coma, seizures, and cardiovascular compromise.^24,38,49,50 COhg levels above 25% appear to correlate with an increased risk of long-term cognitive impairment.⁴⁵ A normal COhg level does not definitively rule out CO poisoning. In the absence of diagnostic evidence, the clinician may have to correlate significant information gathered in the history and relevant characteristics noted in the physical examination and make a presumptive diagnosis of CO toxicity.

All patients presenting with acute confusion should have a blood glucose finger-stick test in order to rule out hypoglycemia. To determine concomitant rhabdomyolysis, creatine kinase levels should be considered for patients who present in frank coma. A chemistry panel or an arterial blood gas analysis will help to identify patients with metabolic acidosis, who may benefit from early hyperbaric oxygen therapy.⁵¹ The clinician should order a 12-lead ECG on patients with cardiac complaints in order to rule out ischemia or infarction.

A handheld breath analysis device has been tested for use in detecting abnormal end expiratory CO levels, but the accuracy of such a device in determining toxic CO levels is still unclear. This breath analyzer may be useful in the initial triage of patients suspected of having CO poisoning, particularly in women who are nonsmokers. The normal expected breath CO measurement in this group of patients is 0 to 6 ppm.⁵²

Although specific brain abnormalities on MRI and CT have been described in people with known CO poisoning, the extent of diagnostic damage is not clearly correlated to prognosis.⁵³ Pulse oximetry has no value in the diagnosis of CO toxicity.⁵⁴

Treatment

All patients with suspected CO exposure should be placed on high-flow oxygen by non-rebreather mask during the initial history, physical examination, and diagnostic evaluation, as this is the primary treatment for CO toxicity. Those with significant neurologic deficits or those in respiratory distress should be evaluated for possible endotracheal intubation.

Although initial studies did not show improvement in outcome, evidence now supports the use of hyperbaric oxygen therapy for patients with a history of obvious CO exposure and/or moderate to severe symptoms of CO toxicity (see “CO exposure treatment algorithm”).⁵⁵ A prospective, double-blind study demonstrated a reduced frequency of negative cognitive sequelae from 46% in patients treated with normobaric-oxygen to 25% in those treated with hyperbaric oxygen. The authors found that CO-toxic patients who underwent three sequential hyperbaric oxygen therapy sessions were less likely to have neurologic deficits at 6 weeks posttreatment and also in a 12-month follow-up after acute CO poisoning.⁵¹ Based on the results of this study, practitioners should consider the use of hyperbaric oxygen therapy in patients with documented CO exposure who present with significant signs and symptoms of CO toxicity—particularly confusion, loss of consciousness, myocardial ischemia, or metabolic acidosis.

Because fetal hemoglobin has a high affinity for CO, a fetus should be presumed at great risk of very serious neurologic impairment and possible demise when a pregnant woman presents with symptoms of CO exposure.⁵⁶ While results of animal studies indicate that hyperbaric oxygen may be a teratogen, a prospective study of the use of hyperbaric oxygen in pregnant women who presented with mild to severe symptoms of CO toxicity at various gestational stages suggested an improvement in fetal outcome with this treatment modality.⁵⁷ Findings of this study support the use of one 2-hour hyperbaric oxygen session at 2 ATA (atmosphere absolute) in pregnant women presenting with a supportive history and features suggestive of CO poisoning.

A retrospective study on the use of hyperbaric oxygen therapy in children suggested that mortality resulting from CO poisoning may be decreased in children who undergo hyperbaric oxygen treatment. However, further prospective studies would be helpful in clarifying the benefit.⁵⁸

Supportive measures such as aggressive IV hydration in patients with rhabdomyolysis, benzodiazepine administration for patients with seizures, and the use of nitroglycerine and thrombolytics in patients with myocardial ischemia are important in treating the complications of CO toxicity.    

Conclusion

Exposure to CO can cause significant morbidity and mortality. Because the signs and symptoms of exposure are so vague, practitioners in urgent care, primary care, and emergency medicine should have a heightened awareness of the possibility of CO poisoning during the cooler months of the year, in certain warm weather circumstances, and when clusters of family members or coworkers present with similar symptoms. The difficulty in treating patients with CO poisoning is in determining who these patients are. When treating uncomplicated CO toxicity characterized by mild symptoms, the mainstay is high-flow oxygen therapy. Patients with more severe poisoning should undergo hyperbaric oxygen therapy, which has been proven to significantly reduce long-term morbidity. Practitioners should counsel patients about the installation and proper use of carbon monoxide detectors in their homes in order to encourage prevention of this potentially lethal exposure. 

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