Recommendations
Key Recommendations
Diagnosis of CO poisoning rests on a high index of clinical suspicion, as symptoms vary and can be nonspecific.[1] Diagnosis consists of a "clinical triad": a recent history of CO exposure, the presence of symptoms consistent with CO poisoning, and elevated arterial or venous blood carboxyhemoglobin (CO-Hb) levels.[2] Symptoms of acute poisoning do not necessarily correlate with the CO-Hb level, particularly with time after removal from the source or oxygen therapy.[26] It is important to be aware of the common sources of CO poisoning, seasonal and regional variations, and risks for exposure to CO.
History
When taking the history, common sources of exposure should be sought:
House fires
Exposure to internal combustion engine exhaust from a vehicle or generator (accidental or intentional act of self harm)
Use of improperly vented indoor heaters and stoves
Malfunctioning furnaces
Exposure to propane-operated heavy equipment in factory workers
For children: riding in the back of a pickup truck, particularly those with a closed canopy on the rear of the truck.
Symptoms in multiple household members should raise the possibility of unintentional exposure to a single source of CO.
The signs and symptoms of CO poisoning can be acute or chronic, depending on dose and duration of the exposure. Acute CO poisoning should be suspected in patients with: headache (often tension-type), nausea, vomiting, vertigo, drowsiness, dizziness, dyspnea, tachypnea, chest pain, confusion, syncope, irritability, diarrhea, and abdominal pain.[1][27] Chronic CO poisoning may occur over weeks to months. It is frequently misdiagnosed because the clinical features are nonspecific. These clinical features include: headache, lethargy/mild tiredness, nausea, memory problems, sleep changes, flu-like symptoms, confusion, stomach pains/nonspecific pain, and shortness of breath.[27] Symptoms and signs may be similar to those of acute poisoning, but with a more gradual and insidious onset.
Examination
Findings on presentation can range from mild symptoms with no clinical signs to severe cardiovascular and neurologic impairment.
Signs are usually a consequence of hypoxia, and patients may present with tachycardia, hypotension, cardiac ischemia, arrhythmias, cutaneous blisters, and pulmonary edema which may be of noncardiac etiology. Other clinical manifestations include neurologic signs ranging from confusion to coma, seizures, or stroke-like syndromes. The classically described cherry-red skin resulting from very high CO-Hb levels is very rarely seen in practice.[28]
Truncal ataxia is a common physical sign in those who are conscious. It can be assessed by examining gait, tandem gait (heel-toe walking forward and backwards with eyes open and closed), and sharpened Romberg. This test should be performed on a hard floor, preferably with bare feet. The patient is asked to place one foot in front of the other and place arms crossed on the chest with closed eyes.[29] A normal exam consists of maintaining an upright stance for at least 20 seconds.
Tests
Patients with suspected exposure to CO should have their CO-Hb level measured by laboratory blood gas CO-oximetry (drawn from venous or arterial blood). The result is generally reported as a CO-Hb level. It is important to note how much time has elapsed since the patient has left the site of CO exposure, as CO-Hb levels may decrease with time and treatment, and may not reflect the true severity of the exposure.[27] However, CO-Hb is extremely stable so if CO-oximetry cannot be immediately obtained, anticoagulated blood samples obtained at the time of presentation can be analyzed later if necessary.
Recommendations from national poison centers or local government agencies should be followed regarding CO-Hb levels. In the US, the Centers for Disease Control and Prevention (CDC) suggests that an elevated CO-Hb level of 2% in people who do not smoke, and >9% for those who smoke, strongly supports a diagnosis of CO poisoning.[27] The CDC further states that CO-Hb levels do not correlate well with severity of illness, outcomes or response to therapy; therefore, to determine type and intensity of treatment, clinical symptoms should always be carefully assessed and a detailed history of exposure taken.[27]
Noninvasive CO-oximetry using a specific fingertip CO pulse oximeter can differentiate between CO-Hb and oxyhemoglobin. Conventional pulse oximetry does not differentiate the oxyhemoglobin and CO-Hb complex and should not be used as a measure of oxygen saturation.[4][27] Several studies show relative agreement between noninvasive CO-oximetry and blood gas CO-oximetry; however, based on a lack of studies with high enough CO poisoning prevalence in the populations, American College of Emergency Physicians (ACEP) guidelines recommend that noninvasive CO-oximetry is not used to make a definitive diagnosis of CO poisoning.[4][30][31][32] Nonetheless, the pulse CO-oximeter can serve as a helpful early screening tool until definitive measurement of a blood sample is available.
The following additional investigations may be helpful in reaching a diagnosis and identifying complications and should be carried out in all patients:
Electrocardiography
Cardiac monitoring for dysrhythmias
Blood glucose (neurologic outcomes following CO poisoning are worse in patients with hyperglycemia)[33]
Complete blood count; may show leukocytosis
Urea and electrolytes; may show results outside of normal range
Creatinine; acute kidney injury is a feature of CO poisoning
Lactate levels (elevated in severe poisoning)
pH level (may be low in severe poisoning)
Cardiac biomarkers (e.g., cardiac-specific troponins)
Creatine kinase levels (for evidence of skeletal muscle damage).
The following should be carried out in some patients:
Bedside neuropsychometric tests (to assess cognitive function in CO poisoning and the patient's response to treatment)
Liver function tests; should be considered in patients with severe poisoning
A pregnancy test should be ordered for all women of childbearing age with suspected CO poisoning.[27] Exposure to CO during pregnancy can cause harm to the fetus.
Imaging
As altered mental status and neurologic deficits are common symptoms of CO poisoning, head computed tomography or magnetic resonance imaging (MRI) are often performed in patients presenting with CO poisoning. The most common findings on MRI are white matter hyperintensities and hippocampal atrophy.[4][34] Delayed posthypoxic leukoencephalopathy can develop in patients after CO poisoning. This syndrome can be associated with diffuse cerebral white matter hyperintensities.[35][36][37] Cardiac echocardiography or MRI may reveal significant abnormal ventricular function.[38] A chest x-ray may be performed in patients with severe CO poisoning to screen for noncardiogenic pulmonary edema.
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