15 year old male with no past medical history brought in by EMS after being found unresponsive at home by his father. His mother reports that he had called her at work prior to his father coming home and was complaining of a headache. His parents deny any previous history of drug or alcohol use. They also deny any use of medications by anyone in the household. Initial vital signs were: BP 106/64 RR 16 HR 68 O2 98% on NRB and Temp of 98.4 F. Physical exam reveals a well developed well nourished adolescent male, obtunded with a GCS of 6, but no obvious signs of trauma. His initial ABG revealed: H pH 7.3, PaCO2 31.8, PaO2 40.9 mmHg, HCO3 16, SaO2 72%, and SBE -8.5. What does this patient have?
Carbon monoxide is a product of incomplete combustion or organic matter due to insufficient oxygen supply to enable complete oxidation of carbon dioxide. CO is often produced by older motor vehicles and other gasoline powered tools, heaters, and cooking equipment. Carbon monoxide causes adverse effects in humans by combining with hemoglobin to form carboxyhemoglobin. CO has approximately a 250 times stronger affinity for hemoglobin than oxygen, thereby reducing the oxygen carrying capacity, delivery, and utilization of oxygen by the body thus causing tissue hypoxia. Since hemoglobin is a tetramer there are four possible locations for oxygen to bind. The binding of CO at one of these sites increases the oxygen affinity at the remaining sites causing the hemoglobin molecule to retain oxygen molecules that would otherwise be release to the tissues. This causes the oxygen dissociation curve to shift to the left. Fetal hemoglobin has an even higher affinity for CO than maternal hemoglobin and so maternal carboxyhemoglobin does not accurately reflect the level of hypoxia in the fetus.
Symptoms of CO poisoning include lightheadedness, confusion, headache, blurry vision, exertional dyspnea, vertigo, nausea, vomiting, fatigue, and flu like symptoms. A cherry red color has typically been described as a classic finding in CO poisoning- however, this is typically a post mortem finding. More significant exposures can lead to significant toxicity of the CNS and heart and even death. The carbon monoxide tolerance level for any person is altered by several factors including activity level, pre existing cerebral or cardiovascular disease, cardiac output, anemia, sickle cell disease, hematologic disorders, barometric pressure, and metabolic rate.
In the ED having a high level of suspicion is most important. Pulse oximetry is not a reliable source for evaluating patients with suspected Co poisoning. Peripheral cooximetry is available to assess Co levels. The best way to detect CO is via a blood gas. VBG is sufficient for checking level of carboxyhemoglobin. Normal carboxyhemoglobin levels in the body range from 1-2% in non smokers and 5-10% in smokers. At levels of 10-20% patients typically have flu like symptoms, nausea, fatigue, and headaches. At 30% severe headache and impaired judgment are typical. By the time levels of 40 -50% are reached patients suffer from confusion, and loss of consciousness. This is the considered the minimum level for lethality. 60-70% cause seizures and cardiovascular collapse.
Management of carbon monoxide poisoning begins with removal from the source. 100% oxygen administered by face mask should be started as soon as the diagnosis is suspected. Hyperbaric oxygen as a treatment for CO toxicity has been controversial among the community of toxicologists but is largely recommended is several specific situations. Any evidence of end organ damage (i.e LOC, seizures, AMS, visual changes, myocardial ischemia and dysrthymias, and persistent symptoms after treatment) are considered indications for hyperbaric oxygen treatment. CO levels greater than 25% or greater than 15% in pregnant women or children are also indications for hyperbaric treatment. HBO is initiated primarily to decrease delayed neurologic sequelae. It displaces CO from myoglobin and cytochrome oxidase in tissues more rapidly than oxygen alone. This therefore improves oxygen delivery to tissues. Patients who receive HBO within the first six hours after exposure do better than those who receive it later.