Oh No, CO! (Re-post)

Tis the season for flu-like symptoms. Many of you will see multiple members of the same family with the flu. But what if it isn’t the flu? When should one be worried about carbon monoxide poisoning? Let’s take a look at this colorless, odorless, potentially deadly gas.

What exactly is CO poisoning?

CO is a byproduct of the combustion of organic matter – often gasoline powered tools and machinery like older motor vehicles, heaters, generators and cooking equipment and residential fires. CO has a higher diffusion coefficient than oxygen. When it binds to hemoglobin carboxyhemoglobin is formed, thus shifting the oxygen-dissociation curve to the left. Hemoglobin’s affinity for CO is 230 times that of oxygen. The molecular end result is displaced oxygen, and hemoglobin that will not dissociate from CO under atmospheric oxygen partial pressures.

Mild acute poisoning manifests as headache, lightheadedness, confusion and general flu-like symptoms. Greater exposures lead to CNS toxicity, myocardial dysfunction and death. CO readily binds myoglobin which depresses cardiac function and therefore cardiac output. This along with the promotion of free radical formation are responsible for the deleterious CNS effects. Chronic low-level exposure may lead to subacute onset of depressed mood, memory loss and confusion.

When should I obtain co-oximetry? What levels are dangerous?

First of all, a standard pulse oximeter is not an effective diagnostic tool. Carboxyhemoglobin is similar enough to oxyhemoglobin such that a pulse ox can’t tell the difference. Measurement of carboxyhemoglobin levels therefore has utility. Traditionally this is obtained from blood samples, but finger pulse oximeters and breath monitors are available. The breath monitors are not a viable option in obtunded patients, or children, since they require cooperation and deep inhalation with breath holding in order to register. Peripheral pulse-oximeters however are becoming more widespread.

Carboxyhemoglobin levels do not correlate directly with symptoms. However, the higher the level, the worse the symptoms. Headaches can be seen at levels >10%, with 50-75% resulting in seizures, coma and death. It is important to note that some people (smokers) have higher baseline levels of carboxyhemoglobin (two pack/per/day smokers can reach almost 10%).

In the Peds ED it is more difficult to get an arterial sample – especially with the risk of hematoma and other complications increased because of the more compact anatomy. Cannon et al. in the Annals of Emergency Medicine  noted that in general the correlation between venous and arterial samples is excellent. Given that the correlation between level and symptoms is not ironclad I suggest that a venous sample is more than acceptable, especially in kids.

How do I manage patients? What if I don’t have access to hyperbaric therapy?

Start with the ABCs naturally, and consider endotracheal intubation early on. Cardiac monitoring and pulse oximetry are appropriate to start early. Try to get a co-ox as soon as possible. Try to get CO measurements from the local fire or EMS agency if applicable. In general it is a really good idea to continue 100% O2 until patients are asymptomatic. The half life of CO is 30-90 minutes at 100% O2, so one can estimate length of therapy based on initial levels. If you choose to follow serial carboxyhemoglobin levels some authorities recommend discontinuing 100% O2 if the level is <10% in the asymptomatic patient. In patients with cardiopulmonary compromise hedge your bets and treat until the level is <2%.

If you have a local hyperbaric option consider immediate transfer at levels >40%, or if you are seeing cardiac or neurologic dysfunction. Hyperbaric chambers deliver O2 at higher partial pressures than the atmosphere. This further decreases the half life of CO. Admission is warranted for patients with levels >30-40% or >25% if severely symptomatic. However, research has failed to conclusive show that hyperbaric therapy is mandatory – so don’t bend over backwards trying to transport a patient to a chamber out of your facility especially if there is inclement weather.

Even without  the option to dive, management should also include serial neuro exams and CT/MRI in comatose patients to assess for cerebral edema. Do not freak out if your patient is acidotic unless the pH is <7.15. Remember that an acidotic state shifts the oxygen dissociation curve to the right – which we want. Acidosis will get better on its own in most cases with oxygen therapy. In patients exposed to a house fire you may also want to treat with a cyanide kit – which consists of sodium thiosulfate 12.5g IV – which ameliorates a further leftward shift of the dissociation curve.

What about pregnant women? Aren’t they better off? I remember seeing that on an episode of ER.

Mom’s are protected, but at the expense of the fetus. Fetal hemoglobin has an even higher affinity (10-15% greater) for CO than grown up hemoglobin. The fetus cannot efficiently eliminate CO and even in the face of mild maternal symptoms loss of pregnancy may occur. Pregnant patients with levels in excess of 15% are also potential candidates for hyperbaric therapy.

The post Oh No, CO! (Re-post) appeared first on FOAM EM RSS.

Source: http://www.foamem.com/

Leave a Reply