Carbon Monoxide Toxicity and Hyperbaric Oxygen Treatment
CO disrupts cellular function by several mechanisms at a cellular/mitochondrial level. Ultimately, these disruptions are manifested as tissue hypoxia and hypoperfusion. Initial symptoms may be subtle and nonspecific. Be sure to ask about CO exposure when evaluating “viral syndrome” or patients that present with non-specific neurological complaints especially during fall and winter months, when people first start using their heating, or after power outages and generator use. Dysrhythmias, cardiomopathy, MI and sudden cardiac arrest are reported in severe CO poisoning.
Lab studies- COHb, base excess, lactate and any other studies based on presentation.
Supplemental oxygen is the cornerstone of treatment. Oxygen delivered at hyperbaric pressure (as opposed to sea-level) will increase the rate of CO dissociation from hemoglobin, and mitigate damage to cellular and mitochondrial function.
Definite Indications for HBOT: Current evidence supports the use for HBOT to reduce cognitive sequelae in CO poisoned patients who have: LOC , seizure, exposure >23 hours, COHb of 25% or more, and age >36. Relative Indications: persistent symptoms after 100% O2 or change in mental status, pregnancy, persistent cardiac ischemia, increased COHb levels.
Disposition: Clinical judgment should guide your decision. Most patients with mild symptoms can be discharged after treatment. If patient has a more concerning presentation with several risk factors (extremes of age, CAD, unconscious at arrival in the ED, etc…) consider admission.
