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Carbon Monoxide Toxicity Workup

  • Author: Guy N Shochat, MD; Chief Editor: Asim Tarabar, MD  more...
Updated: May 06, 2016

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.[2]

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.[20]

Elevated CO levels of at least 3–4% in nonsmokers and at least 10% in smokers are significant.[2] 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.[2] Presence of fetal hemoglobin, as high as 30% at 3 months, may be read as an elevation of HbCO level to 7%.[21] Symptoms may not correlate well with HbCO levels.

Findings on arterial blood gas measurement include the following:

  • Partial pressure of oxygen (PaO 2) levels should remain normal; oxygen saturation is accurate only if directly measured but not if calculated from PaO 2, which is common in many blood gas analyzers.
  • As with pulse oximetry, estimate PCO 2 levels by subtracting the carboxyhemoglobin (HbCO) level from the calculated saturation. PCO 2 level may be normal or slightly decreased. Metabolic acidosis occurs secondary to lactic acidosis from ischemia.

Cardiac marker results include the following:

  • Elevated high-sensitive troponin I levels often indicate cardiomyopathy, including reversible global dysfunction and a Takotsubo-like pattern [22]
  • Myocardial ischemia is common in patients hospitalized for moderate-to-severe CO exposure and is a predictor of mortality. [23]
  • 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:

  • Creatinine kinase, urine myoglobin - Nontraumatic rhabdomyolysis can result from severe CO toxicity and can lead to acute renal failure
  • Complete blood count - Mild leukocytosis may be present; disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura (TTP) require further hematologic studies
  • Electrolytes and glucose level - Hypokalemia and hyperglycemia occur with severe intoxication
  • Blood lactate level - Elevation is an indication of severity [2, 24] ; if the source of the CO was a house fire and the lactate level is 10 mmol/L or higher, the patient may have concomitant cyanide poisoning [2]
  • BUN and creatinine levels - Acute renal failure secondary to myoglobinuria
  • Liver function tests - Mild elevation in fulminant hepatic failure
  • Urinalysis - Positive for albumin and glucose in chronic intoxication
  • Methemoglobin level - Included in the differential diagnosis of cyanosis with low oxygen saturation but normal PaO 2
  • Toxicology screen - For instances of suicide attempt
  • Ethanol level - A confounding factor of both intentional and unintentional poisonings
  • 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:

  • Ground-glass appearance
  • Perihilar haze
  • Peribronchial cuffing
  • 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.

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.

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.[25]

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. 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.[7]


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.

Contributor Information and Disclosures

Guy N Shochat, MD Associate Clinical Professor of Emergency Medicine, University of California, San Francisco, School of Medicine

Guy N Shochat, MD is a member of the following medical societies: Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Michael Lucchesi, MD Chair, Associate Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center

Michael Lucchesi, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Peter MC DeBlieux, MD Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.
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