Carbon monoxide (CO) poisoning may be the most common cause of fatal poisonings worldwide. 1 The majority of poisonings occur in the Fall and Winter. It is that time of year when heaters that have lain dormant all summer are flicked on, sometimes in enclosed areas, introducing CO fumes into homes. The pathophysiology is complex, and not fully understood, but all ED physicians should be aware of the signs and symptoms of CO toxicity, and know how to treat it.

Pathophysiology

CO affects oxygen delivery through various mechanisms. The most obvious is through formation of carboxyhemoglobin (COHb). Hb binds CO 200 times more tightly than oxygen. About 85% of the CO binds to Hb to form COHb. COHb induces a left shift in the HbO2 dissociation curve, so O2 is not released to the tissues. The remainder of the CO is either dissolved in plasma, or bound to proteins, and wreaks havoc in a myriad of other ways. From the plasma, it can diffuse into cells where, like cyanide, it inhibits cytochrome oxidase, thereby interfering with cellular metabolism and ATP production. CO also causes endothelial damage which then triggers an inflammatory state. CO can also initiate a cascade of events that leads to NO release and vasodilation, causing hypotension. The intracellular toxicity along with hypoxia and hypotension can lead to myocardial infarction, neuron death, and rhabdomyolysis.

Symptoms and History

The diagnosis is challenging, particularly in more mild cases and in cases of chronic CO poisoning. Symptoms can range from flu-like illnesses (which also conveniently start to crop up around the same time of year), headache, vomiting, confusion, dyspnea, and chest pain, to focal neurologic deficits, seizures, ataxia, syncope, visual changes, and coma.

Obtaining a history, where possible, is key to the diagnosis. Ask about exposure to heaters, fires, or gas or propane-powered motors, particularly in close spaces. If the patient presented from a house fire, it is easy to focus on their burns or trauma, and forget the possibility of CO poisoning. If the exposure occurred at home, then multiple family members may be symptomatic though the symptoms may differ based on their age and underlying health status. Physical findings can also vary. The patient may be tachycardic, dyspneic, and hypotensive due to the physiologic changes described above. In severe cases, they may have cardiac or respiratory failure and arrest.

Diagnosis

The first key to diagnosis is to consider CO poisoning in your differential! The next step is to check a COHb level if your ABG/VBG machine has co-oximetry capability or if you have a non-invasive COHb monitor (although these are still under investigation). Routine ABG/VBG machines that lack co-oximetry may give a falsely high O2 sat reading. 2 In addition, you cannot trust your usual O2 sat probe! 3 COHb absorbs at around the same wavelength as HbO2, so the patient may be dyspneic, with very little tissue oxygen delivery, and yet have a very high O2 saturation reading on their finger probe.

The next challenge is in interpreting the co-oximetry result. You have to take into account:

The chronicity or duration of exposure

The time from exposure to measurement

Any intervening treatment (such as supplemental oxygen)

The underlying health of the patient

For all these reasons, the percentage of COHb does not always correlate with the patient’s symptoms or their prognosis. A patient may be severely neurologically damaged and have a lower COHb than a less symptomatic patient. This could be because the symptomatic patient had higher levels previously, but did not reach an ED and have a co-oximetry measured until later. Or it may be due to age or co-morbidities. For example, patients with underlying CAD may develop ischemia due to decreased oxygen delivery, have angina, exhibit an elevated troponin, or demonstrate ECG changes at COHb levels as low as 4-6%. 4

Meanwhile, smokers without any additional exposure can have baseline COHb levels as high as 10%. 2 However, as long as physicians take into account duration of exposure, time of measurement, and any intervening treatment (such as supplemental oxygen), the degree of COHb formation is a reasonable marker of the severity of the exposure.

Other lab values that can give a clue to CO poisoning are from the inhibition of intracellular metabolism, which leads to a metabolic, anion gap, lactic acidosis. In addition, an oxygen saturation gap of greater than 5% difference between O2 sat measured from a finger probe and measured on a blood gas sample can give a clue to the presence of aberrant hemoglobin forms. 5

Treatment

The treatment is oxygen, and lots of it.

On room air, the half-life of COHb is about 200 minutes. If a patient is put on 100% FiO2, that half-life drips to around 80 minutes. The route of administration will depend on the patient’s symptoms and severity. If the symptoms are mild to moderate, then they can be treated with 100% O2 on a facemask. If severe, they may require intubation, and in the most severe cases, hyperbaric oxygen. The indications for hyperbaric oxygen are still under debate. However, it should be considered in patients with “ataxia, seizure, syncope, chest pain, focal neurologic deficits, dyspnea, or EKG changes” or a COHb level over 25%. 2 Some studies recommend hyperbaric oxygen be considered for any acutely symptomatic patient. 6 However, the decision to transfer for hyperbaric oxygen (since most EDs will lack this capability) will also depend on the stability of the patient, and the distance to transfer. For more information about the hyperbaric oxygen therapy debate, read Dr. Repplinger’s nice ALiEM review, which is accompanied by Dr. David Juurlink’s expert peer review comments.

Patients with mild to moderate symptoms, who do not require hospitalization for any other reason, can usually be observed for 4 hours, treated with non-invasive oxygen, counseled regarding exposure and use of CO detectors, and discharged if they have a safe place to go. If there is a concern about home exposure, the fire department can also do a home assessment and check for CO leaks if there are no CO detectors.

Fetal Hb binds even more tightly to CO, 7 making CO poisoning even more dangerous for pregnant women. It is therefore recommended that pregnant women be referred for hyperbaric oxygen if there is a COHb level of 15% or higher. 4

Special case: Methylene chloride exposure

A special case is that of COHb formed due to methylene chloride exposure. 8 Methylene chloride is a component in some paint strippers and varnishes. Exposure can occur through ingestion or inhalation. The methylene chloride metabolism forms CO. Therefore, with an ongoing source of CO formation, the half-life can increase to 13 hours.

Summary

Consider CO poisoning in patients with non-specific symptoms such as headaches and nausea, as well as in those with focal neurologic deficits, syncope, or otherwise unexplained respiratory distress.

Ask about CO detectors in people’s homes.

Do not trust a finger pulse-oximetry measure in CO poisoning. It will be falsely elevated.

Check a VBG or ABG with co-oximetry if concerned.

Treat with oxygen, and in severe cases, consider transfer to a hyperbaric oxygen center, particularly in patients with more severe symptoms, higher COHb levels, or in pregnancy.

Image credit [1 and 2]

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