CARBON MONOXIDE POISONING
The injuries caused by
carbon monoxide (CO) traditionally have been viewed as due to a hypoxic stress
mediated by an elevated carboxyhemoglobin (COHb) level. While hypoxic stress is
clearly an element of poisoning, some injuries appear to be mediated by
systemic oxidative stress. Perivascular
and neuronal injuries arise by mechanisms other than hypoxia.(1,2) Neuropathology is due to a complex cascade of
biochemical events involving several pathophysiologic processes,(3-10) some independent of pure hypoxic stress(11-13).
Furthermore, the COHb level does not correlate with the development of
neurological or cognitive sequelae.(14-18)
The two organ systems most
susceptible to injury from CO are the cardiovascular and central nervous
systems. Human and animal data indicate that major cardiac injury at the time
of poisoning is due primarily to CO-induced hypoxic stress.(19-21) In addition,
the risk for cardiovascular-related death in patients with initial CO-induced
cardiac injury appears to be increased over the 10 years following injury.(22) Many
neurological problems can follow CO poisoning and include motor weakness,
peripheral neuropathies, hearing loss, and Parkinsonian-like syndrome. Cognitive sequelae following CO poisoning are
common. Also, the incidence of anxiety
and depression is high following acute CO poisoning and may not be influenced
by hyperbaric oxygen therapy (HBO2).(23)
Administration of
supplemental oxygen is the cornerstone of treatment of CO poisoning, although
there are no clinical trials demonstrating improved outcomes using oxygen
therapy administered at atmospheric pressure.
Nevertheless, supplemental oxygen inhalation will hasten dissociation of
CO from hemoglobin and provide enhanced tissue oxygenation. HBO2
hastens COHb dissociation compared to breathing pure oxygen at sea-level
pressure.(24-27) Additionally, HBO2,
but not ambient pressure oxygen treatment, has several actions, which have been
demonstrated in animal models to be beneficial in ameliorating central nervous
system (CNS) injuries. These include an improvement in mitochondrial oxidative
processes,(28,29) inhibition of lipid
peroxidation,(30) and impairment of leukocyte
adhesion to injured microvasculature.(31) Animals poisoned with CO
and treated with HBO2 have been found to have more rapid improvement
in cardiovascular status,(24) lower mortality,(32) and lower incidence of neurological sequelae.(33,34)
Since 1960, the clinical use
of HBO2 for CO poisoning has occurred with increasing frequency.
Over 1,500 CO-intoxicated patients were treated in North American hyperbaric
chambers from 1992 – 2002.(35) However, this number
represents only a small fraction of those poisoned with CO. Extrapolation of
data from a 1994 survey across three western states(36) and from Utah for 1996 and 1997,(37) gives an estimate that over 40,000 CO-poisoned
patients are evaluated in emergency departments annually in the United
States. Among patients treated with HBO2,
both mortality and neurocognitive morbidity are improved beyond that expected
with ambient pressure supplemental oxygen therapy.(38-43) The optimal benefit from HBO2 occurs in
those treated with the least delay after exposure.(39) In selected
patients, repeated treatments may yield a better outcome than a single
treatment.(43)
_________________________
More Information and References can be found
in the 12th Edition of the Hyperbaric Oxygen Therapy Indications
Book. For Sale on
the UHMS
Publications page.