Keywords: carbon monoxide (PubMed Search)
Posted: 10/20/2011 by Fermin Barrueto, MD
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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
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
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…)
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