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By Richard J. Hamilton, MD, FAAEM, ABMT
Everyone enjoys the winter for the fun indoor and outdoor activities that are part of the season. However, the season also brings an increased risk of carbon monoxide (CO) poisoning from the combination of cold weather, closed spaces, and fossil fuel heating. When seeing patients in the emergency department (ED), try to remember to put CO poisoning in the differential diagnosis of the many presenting complaints during the winter. While it is easy to set that as a goal during cold weather clinical practice, the protean nature of the symptoms of CO poisoning and the relatively small numbers of patients who suffer from it may make emergency physicians feel that they are chasing at shadows. Rather than review the complex pathophysiology of CO or delve into the controversies regarding treatment, this discussion will focus on the epidemiology and diagnosis of this disease to help emergency physicians identify an easily overlooked problem.
In emergency medicine, all things start with the chief complaint. When the chief complaint is "I smelled gas and I have a headache," clinicians need little convincing to consider CO. Although CO in and of itself is odorless and colorless, odors are associated with CO exposure. Natural gas is naturally odorless, but sulfur-containing compounds known as mercaptans are added to the gas line as an olfactory warning. Improperly maintained or blocked heaters may develop a leak or a faulty pilot light and allow natural gas into the environment. Although this does not cause CO toxicity, it is a condition associated with the partial combustion of fossil fuels that could signal CO exposure.
What if the chief complaint is simply, "I have a headache," or "I feel tired?" While this is certainly a clinical presentation for CO poisoning, it is a relatively common complaint. One strategy could be to measure carboxyhemoglobin (COHb) levels of all patients in the ED in the wintertime, but research indicates this would only identify an elevated COHb in 1% of patients.1 This strategy can be selectively applied to patients complaining of more typical CO complaints—headache, nausea, and dizziness—to increase the yield to about 10%.2
More importantly, asking specific questions can have a high predictive value. For example, two important studies examined the predictive value of asking patients whether they used gas ovens to heat their homes or whether they had cohabitants with similar symptoms. The authors noted an association for each of these two issues with CO toxicity in a series of patients.3 Then they validated this model by asking everyone who came to the ED with headache or dizziness whether they used gas stoves for heating purposes and whether there were similarly affected cohabitants.
To test the validity of this retrospectively derived rule, 65 patients were studied who were unaware of any CO exposure and who presented during the winter of 1986-1987 with headache or dizziness. The algorithm correctly identified three of four patients with COHb levels greater than 10% (75% sensitivity) and correctly excluded 45 of 61 patients with lower levels (74% specificity). The presence of symptomatic cohabitants alone was an equally sensitive (75%) but more specific (90%) marker for elevated COHb levels.4 Although not perfect, it helps the clinician more confidently sort through the nonspecific complaints that could be related to CO toxicity, and be a bit more parsimonious with testing.
Ultimately, there is no substitute for an inquisitive clinician with an awareness of the literature. Asking questions about the home or work environment, the health of co-workers or other family members, use of alternative heating methods, or activities at the onset of illness can be very illustrative.
Motor vehicles are a particular concern, and patients have been poisoned from a variety of activities associated with them—repairs, sleeping in vehicles, or occupying rooms adjacent to garages. Simply reading through Morbidity and Mortality Weekly Reports from the Centers for Disease Control and Prevention reveals a sampling of CO sources to consider other than heating systems or fires. Sources of CO poisoning reported within the last 10 years (fatal and nonfatal) include propane-powered forklifts, saws, gas grills, ice skating, driving an ice resurfacing machine, attending indoor tractor pulls, camping, playing bingo above an ice rink, cleaning with power washers, and shoveling snow from around idling motor vehicles. These sorts of activities generally are not part of the standard social history; thus, it is paramount to have an appropriate threshold of suspicion when it comes to CO.
Lest emergency physicians presume that an enclosed environment is a prerequisite for CO poisoning, there are a number of case reports of patients developing CO toxicity despite apparent ventilation. Pick-up trucks with campers can create a suction effect when the back window is opened and no front intake of air is present. This relative vacuum in the passenger compartment pulls exhaust into the passenger compartment.5 One case report of the operator and occupants of an open-air tractor who developed CO toxicity while operating the vehicle at a slow rate of speed in relatively still air highlights the insidious nature of this poison.6
In addition, methylene chloride is an overlooked source of CO toxicity. It is a one carbon molecule that is used as a paint stripper and solvent. Dermal or inhalational exposure, followed by absorption and metabolism, can lead to elevated CO levels. These types of exposures have caused the entire spectrum of neurologic and cardiovascular complications seen with CO poisoning.7,8
Once suspicion for acute CO poisoning has been triggered, making the diagnosis is as simple as knowing which test to order and understanding possible confounders. The standard of care is to obtain a venous blood sample for co-oximetry to determine the COHb level. This is reported as a percentage, along with oxyhemoglobin, deoxyhemoglobin, and methemoglobin, when a four wavelength co-oximeter is used. There is no need to perform arterial blood sampling, as CO is so avidly bound to hemoglobin that little CO exchange occurs in the lungs relative to the venous circulation. Remember that pulse oximeters generally mistake COHb for oxyhemoglobin and report falsely elevated saturations.
If the prevalence of CO poisoning is increased due to occupational or household exposures (e.g., firefighters who are seen for smoke inhalation or people who are from communities with older housing and outdated heating systems), investing in and maintaining any of the portable devices that measure exhaled CO may be an efficient approach, especially for identifying COHb levels above 10%.
COHb elevations are considered diagnostic for exposure with certain caveats. Cigarette smoking will elevate COHb levels to a range of 2-10%. Pregnant women and patients who have hemolytic anemia will demonstrate COHb elevations from the breakdown of heme proteins and endogenous CO production, but these are usually less than 10%. Fetal hemoglobin also causes false COHb elevations as a result of the partial absorption of fetal hemoglobin at light wavelengths that are used to detect COHb, but these generally are less than 5%.
CO toxicity, while often occult, is not always subtle in presentation. Patients with syncope, seizures, coma, acute myocardial infarction, arrhythmias, or cerebrovascular accident also could be suffering from CO poisoning. A specific associated sign, such as cutaneous bullae, should prompt consideration of CO toxicity in the differential diagnosis.8 Another telling finding is bilateral hypodensities in the globus pallidus on head CT. Although not pathognomonic, these appear to correlate with neurologic injury and have a poor prognosis.9
Clinicians who have a heightened suspicion for this disease and who are vigilant for an occult presentation as a simple viral syndrome or complete coma will be rewarded with a diagnostic save when they make the diagnosis of CO poisoning. Besides, it gives you something to explore the next time you go to the chart rack and see that the next three patients are from the same house with fatigue, nausea, and headache . . . sure it could be influenza, but with CO you just never know.
1. Turnbull TL, et al. Emergency department screening for unsuspected carbon monoxide exposure. Ann Emerg Med 1988;17:478-483.
2. Dolan MC, et al. Carboxyhemoglobin levels in patients with flu-like symptoms. Ann Emerg Med 1987;16: 782-786.
3. Heckerling PS, et al. Predictors of occult carbon monoxide poisoning in patients with headache and dizziness. Ann Intern Med 1987;107:174-176.
4. Heckerling PS, et al. Occult carbon monoxide poisoning: Validation of a prediction model. Am J Med 1988;84:251-256.
5. Struttmann TV, et al. Outdoor carbon monoxide poisoning attributed to tractor exhaust—Kentucky, 1997. MMWR Morb Mortal Wkly Rep 1997;46:1224-1227.
6. Myers R, et al. Cutaneous blisters and CO poisoning. Ann Emerg Med 1985;14:603-606.
7. Langehennig PL, et al. Paint removers and carboxy-hemoglobin. N Engl J Med 1976;295:1137.
8. Hampson NB, Norkool DM. Carbon monoxide poisoning in children riding in the back of pickup trucks. JAMA 1992;267:538-540.
9. Nardizzi LR. Computerized tomographic correlate of carbon monoxide poisoning. Arch Neurol 1979;36: 38-39.