Laboratory Studies
The clinical diagnosis of acute carbon monoxide (CO) poisoning should be confirmed by demonstrating an elevated level of carboxyhemoglobin (HbCO). Either arterial or venous blood can be used for testing. [3]
Analysis of HbCO requires direct spectrophotometric measurement in specific blood gas analyzers. Bedside pulse carbon monoxide (CO)-oximetry is now available but requires a special unit and is not a component of routine pulse oximetry. A 2012 study showed that noninvasive pulse CO-oximetry correlates with more rapid diagnosis and initiation of hyperbaric oxygen therapy than laboratory CO-oximetry. However, the impact on clinical outcome is still not proven. [25] A 2017 clinical policy statement from the American College of Emergency Physicians (ACEP) recommends against using pulse CO-oximetry to diagnose CO toxicity in patients with suspected acute CO poisoning (level B recommendation). [26]
Elevated CO levels of at least 3–4% in nonsmokers and at least 10% in smokers are significant. [3] However, low levels do not rule out exposure, especially if the patient already has received 100% oxygen or if significant time has elapsed since exposure. HbCO levels in cigarette smokers typically range from 3-5%, but may be as high as 10% in some heavy smokers. [3] Presence of fetal hemoglobin, as high as 30% at 3 months, may be read as an elevation of HbCO level to 7%. [27] Symptoms may not correlate well with HbCO levels.
Findings on arterial blood gas measurement include the following:
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Partial pressure of oxygen (PaO2) levels should remain normal; oxygen saturation is accurate only if directly measured but not if calculated from PaO2, which is common in many blood gas analyzers.
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As with pulse oximetry, estimate PCO2 levels by subtracting the HbCO level from the calculated saturation. PCO2 level may be normal or slightly decreased. Metabolic acidosis occurs secondary to lactic acidosis from ischemia.
The ACEP recommends obtaining an electrocardiogram and cardiac biomarker levels in emergency department patients with moderate to severe CO poisoning (level B recommendation). [26] Cardiac marker results include the following:
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Elevated high-sensitive troponin I levels often indicate cardiomyopathy, including reversible global dysfunction and a Takotsubo-like pattern [28]
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Myocardial ischemia is common in patients hospitalized for moderate-to-severe CO exposure and is a predictor of mortality. [29]
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Patients with preexisting cardiovascular disease can experience increased exertional angina with HbCO levels of just 5-10%; at high HbCO levels, even young healthy patients develop myocardial depression
Other test results include the following:
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Creatinine kinase, urine myoglobin - Nontraumatic rhabdomyolysis can result from severe CO toxicity and can lead to acute renal failure.
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Complete blood count - Mild leukocytosis may be present; disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura (TTP) require further hematologic studies.
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Electrolytes and glucose level - Hypokalemia and hyperglycemia occur with severe intoxication.
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Blood urea nitrogen (BUN) and creatinine levels - Acute kidney failure may result from myoglobinuria.
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Liver function tests - Mild elevation in fulminant hepatic failure
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Urinalysis - Positive for albumin and glucose in chronic intoxication
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Methemoglobin level - Included in the differential diagnosis of cyanosis with low oxygen saturation but normal PaO2
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Toxicology screen - For instances of suicide attempt
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Ethanol level - A confounding factor of both intentional and unintentional poisonings
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Cyanide level - If cyanide toxicity also is suspected (eg, industrial fire); cyanide exposure is suggested by an unexplained metabolic acidosis; rapid determinations rarely are available. Smoke inhalation is the most common cause of acute cyanide poisoning.
Imaging Studies
Obtain a chest radiograph in patients with significant intoxications, pulmonary symptoms, evidence of hypoxia, or if hyperbaric oxygen is to be used. Findings usually are normal. Changes such as the following imply a worse prognosis than normal findings:
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Ground-glass appearance
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Perihilar haze
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Peribronchial cuffing
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Intra-alveolar edema
Computed tomography
Obtain a CT scan of the head with severe intoxication or change in mental status that does not resolve rapidly. Assess cerebral edema and focal lesions; most are typically low-density lesions of the basal ganglia. [33]
Positive CT scan findings generally predict neurologic complications. In one study, 53% of patients hospitalized for acute CO intoxication had abnormal CT scan findings; all of these patients had neurologic sequelae. Of those patients with negative scan results, only 11% had neurologic sequelae. [33]
Serial CT scans may be necessary, especially with mental status deterioration. One report describes the evolution of acute hydrocephalus in a child poisoned with CO, documented by serial CT scans. [34]
Magnetic resonance imaging
MRI is more accurate than CT scans for detection of focal lesions and white matter demyelination and is often used for follow-up care. [35] The progression from conventional MRI to diffusion-weighted imaging (DWI) and then diffusion tensor imaging (DTI) has enabled increasingly sensive evaluation of damage from CO poisoning. DTI can visualize progressive pathologic changes in the early stage of CO toxicity, allowing prediction of chronic conditions. [8]
Other Tests
On electrocardiography, sinus tachycardia is the most common abnormality. Arrhythmias may be secondary to hypoxia, ischemia, or infarction. Even low HbCO levels can have a severe impact on patients with cardiovascular disease.
Neuropsychologic testing
Formal neuropsychologic testing of concentration, fine motor function, and problem solving consistently reveal subtle deficits in even mildly poisoned patients.
Abridged versions of these tests are available that can be performed in about 30 minutes by a well-trained examiner. These are more applicable to the emergency department (ED) setting. These tests have been developed as possible means to assess the risk of delayed neurologic sequelae, to assess the need for hyperbaric oxygen therapy, and to determine the success of hyperbaric therapy in preventing delayed sequelae. The tests are used in some institutions, but studies prospectively confirming the conclusions are lacking.
Research indicates a specific link to deficits in context-aided memory in CO poisoing.Use of such specific testing in the ED has been proposed, as a tool for measuring the severity of neurologic involvement.
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Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.
