especially in those with risk for CO exposure.

Inquire about the location of presumed exposure and

whether or not anyone else in the vicinity has developed

symptoms. Ask about the presence of regularly maintained

CO detectors in the house. High-risk scenarios for CO exposure include fire victims, patients in older houses with faulty

furnaces during the winter time and/or those using alternative forms of combustion to heat their homes, and patients

in enclosed spaces with running automobiles. Finally, ask

about the recent use of any paint stripper or solvents, as

these compounds may contain methylene chloride.

� Physical Examination

As with other poisonings, rapidly assess the patient's airway,

breathing, and circulation. Take careful note of a full set of

vital signs, keeping in mind that standard pulse oximetry is

of minimal utility in this setting. Tachypneic patients may

be attempting to compensate for an underlying metabolic

acidosis. Although patients with acute CO poisoning are

classically described as having a "cherry red" appearance to

their skin due to the bright red color of carboxyhemoglo ­

bin, this finding is absent far more often than present.

Perform a detailed neurologic exam, looking for signs

of altered mental status and loss of coordination, as neurologic findings often dictate final care. Perform an ocular

exam, looking for signs of retinal flame hemorrhages. The

cardiovascular exam should focus on signs of hemodynamic instability and dysrhythmia, which might indicate

underlying myocardial ischemia.

Carefully auscultate the lungs, noting any inspiratory

crackles, which may be indicative of chemical injury to the

lung parenchyma with secondary acute respiratory distress

syndrome. Finally, check the skin for any signs of thermal

injury in fire victims. Rarely, CO poisoning has been

known to cause diffuse bullous lesion in the absence of

thermal burns.

DIAGNOSTIC STUDIES

� Laboratory

Order an immediate COHb level on all patients to help

confirm the diagnosis and estimate the severity of the

exposure. COHb analysis requires co-oximetry of the

blood sample and can be done on either a venous or arte ­

rial specimen. Of note, COHb levels correlate poorly with

patient symptoms and should not be used in isolation to

guide management. Check a metabolic panel looking for

electrolyte abnormalities and to calculate the anion gap, as

significant CO poisoning will result in an anion gap metabolic acidosis. Use the anion gap calculation along with a

blood gas analysis to determine the severity of the acidbase derangement.

Obtain a urine pregnancy on all females of childbearing

age, as a positive pregnancy test will markedly impact management. Check a serum lactate level. Significantly high

levels (> 10 mmol!L) indicate severe cellular toxicity or

concurrent cyanide poisoning. Order serum cardiac

markers in all patients complaining of chest pain or with

electrocardiogram (ECG) abnormalities, as myocardial

ischemia has been reported, especially in patients with

underlying coronary artery disease (CAD). Finally, check a

creatine phosphokinase level in patients with unknown

downtimes, as rhabdomyolysis is a serious concern.

� Electrocardiogram

Obtain an ECG looking for signs of ischemia in patients

complaining of chest pain, shortness of breath, and those

with underlying CAD.

� Imaging

Check a chest x-ray in patients with shortness of breath

or a history of smoke inhalation, as chemical injury to the

lungs with secondary pulmonary edema is common.

Order a computed tomography ( CT) of the brain in

patients with altered mental status or focal neurologic

deficits to rule out alternative etiologies. Low-density

lesions of the bilateral globus pallidi have been reported

CARBON MONOXIDE POISONING

with CO poisoning, and patients with abnormalities on

CT imaging are more likely to exhibit chronic neurologic

sequelae.