The diagnosis is best made by measuring carboxyhemoglobin levels. Although carboxyhemoglobin in and of itself may not be the most significant factor in carbon monoxide–mediated injury, obtaining free plasma carbon monoxide is rarely feasible. Thus, carboxyhemoglobin serves as a marker of severity of exposure and can help to stratify patients at risk for delayed sequelae. Co-oximetry, which measures total hemoglobin as well as oxyhemoglobin, methemoglobin, and carboxyhemoglobin saturation, is the only accurate measurement tool. Routine arterial blood gas analyzers without co-oximetry calculate, rather than measure, saturation, and will not differentiate the contribution of dyshemoglobinemias to total saturation. As a result, the oxygen saturation may appear artificially high. There is excellent correlation between arterial and venous carboxyhemoglobin levels, and thus, a venous blood gas with co-oximetry is sufficient in most cases.12
Interpreting carboxyhemoglobin levels can be challenging and needs to take into consideration time and duration of exposure, time from exposure to presentation, treatment (such as high-flow oxygen) rendered en route, and clinical symptoms. Although a markedly elevated level, such as 50%, is a clear indicator of severe intoxication, a level of 10% in a patient who experienced serious symptoms a few hours earlier presents a dilemma in terms of diagnosis and appropriate disposition. Symptomatology and carboxyhemoglobin levels do not always correlate well: levels as high as 47% have been reported in minimally symptomatic patients, whereas levels as low as 10% have been reported in comatose patients in whom the diagnosis of carbon monoxide poisoning was ultimately confirmed.13
Standard pulse oximetry is unreliable in the diagnosis of carbon monoxide poisoning. The wavelengths for carboxyhemoglobin fall into the same range of those for oxyhemoglobin, and standard pulse oximetry does not differentiate the two. As a result, the oxyhemoglobin saturation by pulse oximetry reading will appear artificially high14 (Figure 222-1). The pulse oximetry gap is a measure of this discordance. When the pulse oximetry values are compared to the oxygen saturation on an arterial blood gas, the oxygen saturation on the pulse oximeter will be higher than the saturation on the arterial blood gas.
Carboxyhemoglobin "shift to the left" reshaping of the oxyhemoglobin (HbO2) dissociation curve. (A) Carbon monoxide (CO)–affected HbO2 dissociation curve (asymptotic) and (B) normal HbO2 dissociation curve (sigmoid).
Data on currently available pulse co-oximeters are mixed. Until a large, randomized, and well-designed study looking at the accuracy of these devices in an ED setting can be performed, it is not recommended to rely solely on pulse co-oximeters to exclude carbon monoxide poisoning.15,16,17
Other laboratory and diagnostic testing can be also be informative. Elevated lactate from the interference in the electron transport chain, an unexplained elevated anion gap metabolic acidosis, elevated creatine phosphokinase, or elevated troponin may trigger an investigation for carbon monoxide poisoning. Concomitant cyanide poisoning may be seen in patients rescued from structure fires. Neuron-specific enolase or S100B,18 CNS proteins that are released in greater quantities into the plasma when neuronal injury has occurred, and cerebrospinal fluid myelin basic protein are markers for carbon monoxide neurotoxicity. However, these tests may be more useful in determining prognosis than diagnosis and are rarely available for use in ED clinical decision making.
Electrocardiographic findings may range from entirely normal to acute injury patterns, such as ST elevation myocardial infarction. There does not appear to be any classic carbon Monoxide ECG pattern. Few patients with acute myocardial infarction due to carbon monoxide poisoning have occlusive lesions identified at cardiac catheterization.19
Radiographic imaging is generally of limited utility and is usually more helpful in establishing an alternative diagnosis. There is, however, one radiographic finding that has been specifically associated with carbon monoxide poisoning, and that is lesions in the globus pallidus. Lesions are generally bilateral and symmetric and are usually noted in severely poisoned patients.7