Newsletters

POSTED: December 7th, 2017
POSTED IN: EM Pulse - The Official Newsletter of MOCEP, November/December 2017, Toxicology,

So it’s finally that time of year. The leaves are falling, the thermometers are dropping, and the heaters are being turned on. Unfortunately, this also means toxicity or fires from either faulty heaters or using inappropriate heat sources. What does this mean for the emergency physician? It means you need to worry about carbon monoxide (CO) and cyanide toxicity.

CO is the great imitator. Toxicity can present in a variety of ways with anything from flu like symptoms to headaches to neurologic deficits, syncope, or arrhythmias. The common dreaded scenario is the patient that presents with fatigue, myalgias, headaches and improves while sitting in the waiting room for a few hours.  The patient either then leaves without being seen or looks well upon finally getting back for evaluation and is rapidly discharged home where they are re-exposed. Standard pulse oximeters are not helpful in making the diagnosis; they cannot tell the difference between oxyhemoglobin and carboxyhemoglobin. Newer handheld detectors, commonly used by pre-hospital personnel, designed to detect CO have rapidly gotten better and are fairly reliable. The gold standard is still co-oximetry. Importantly, this can be run on venous samples so an arterial stick solely to get a CO level is not necessary. A lactate is also helpful to evaluate signs of cellular toxicity that might not otherwise be apparent. Once the diagnosis is suspected, patients should be placed on a nonrebreather as this dramatically decreases the half-life of CO from room air. If the diagnosis is confirmed, then the decision needs to be made about hyperbaric oxygen (HBO). While the correct answer on most test questions, HBO is actually rather controversial as the literature showing that it prevents delayed neurologic sequelae (DNS) is mixed. DNS is basically a syndrome of delayed or persistent neurologic sequelae occurring after toxic exposures to CO. Some potential indications are syncope, levels > 25, pregnancy (possibly with a level >15 or if there are signs of fetal distress), neurologic deficits, metabolic acidosis, and cardiac arrhythmias.

Cyanide toxicity is not going to occur from a faulty heater; it is going to occur in a house fire. This diagnosis can also be difficult to make as time is spent treating burns and CO poisoning and cyanide concentrations won’t return for days. Also, the classic finding of cherry red skin is generally a post mortem or late finding and lack of this is not reliable enough to exclude this diagnosis. Luckily, other laboratory tests can be helpful. Comparing a venous and arterial blood gas is helpful. Cyanide will poison the mitochondria, not allowing the body to efficiently use oxygen. Therefore the pO₂ on the venous and arterial blood gas will be similar as the venous pO₂ is a lot higher than it should be. Additionally a lactate concentration greater than 8 mmol/L is concerning for cyanide toxicity, even with co-occurring CO toxicity. Historically, treatment consisted of sodium nitrite and sodium thiosulfate. The problem with sodium nitrite is it creates methemoglobin (particularly concerning if the patient also has CO toxicity) and can cause hypotension. Sodium thiosulfate takes time to begin to work. The preferred treatment is hydroxocobalamin which combines with cyanide to form cyanocobalamin, or vitamin B-12. While very safe, it does turn things such as urine red. It also can interfere with your pulse oximeter and with certain laboratory tests. If the patient presents in extremis, consideration for empiric treatment prior to labs returning can be considered.