RATIONALE FOR THE TREATMENT OF SPECIFIC SYNDROMES
Carbon Monoxide Poisoning
Hemoglobin (Hb) binds CO with an affinity much higher (by a factor
of about 200) than that for O2
. Binding of CO with Hb to form carboxyhemoglobin
(COHb) has two major effects. First, the proportion of Hb that is occupied by CO
molecules is unavailable for O2
transport, which results in a functional
anemia. Second, the avidity with which the remaining Hb binds O2
is increased
(shift to the left of the Hb-O2
dissociation curve). The result is a
decreased ability to unload O2
from blood to tissue at the capillary.
Previously, it was believed that these effects were totally responsible for the
toxicity of CO. However, evidence has since been presented to show that binding
of CO to intracellular pigments (e.g., cytochrome aa3
,
myoglobin) and oxidative stress may contribute significantly to the toxicity of CO.
[19]
[76]
[91]
[92]
[93]
[94]
[95]
These mechanisms result in toxicity to multiple
organ systems, including the brain and heart.[96]
Late neurologic sequelae remain an important secondary toxic effect, often after
a clear window of lucidity.[97]
High PaO2
hastens the
removal of CO from blood such that the half-life of COHb is greatly reduced by HBO
therapy ( Table 70-6
). Additionally,
the increased dissolved
*Mean
values from data of Pace N, Strajman E, Walker E: Acceleration of carbon monoxide
elimination in man by high pressure oxygen. Science 111:652, 1950.
O2
in plasma may support tissue oxygenation pending removal of CO from
Hb and other proteins important for O2
transport. Evidence is steadily
mounting that for poisoning in which neurologic symptoms occur, HBO treatment may
decrease both early and late morbidity from this condition. The results of one randomized
prospective trial of hyperbaric versus normobaric oxygen revealed no apparent benefit
of HBO[98]
; however, in four trials HBO treatment
resulted in improved outcomes.[15]
[16]
[99]
[100]
The diagnosis of CO poisoning is made by a history of exposure
(internal combustion engine exhaust, fire, improperly adjusted gas or oil heating,
charcoal or gas grills, or exposure to paint stripper containing methylene chloride,
which is metabolized by the liver to CO). Confirmation of the diagnosis is made
by finding elevated COHb in either arterial or venous blood. The COHb concentration
in anticoagulated blood samples is stable for several days. Therefore, if COHb determination
is not available at a referring facility, the diagnosis can be confirmed with a blood
sample obtained at the time of initial evaluation and transported with the patient.
Fetal hemoglobin (hemoglobin F) can produce a falsely elevated reading for COHb
on certain four-wavelength laboratory co-oximeters.[101]
In the first few weeks of life, blood from normal infants may therefore falsely
indicate 7% to 8% COHb.
Actual COHb levels measured on arrival at the emergency department
correlate poorly with clinical status and should not be used as the sole criterion
to determine the need for treatment. Because of the lower intracellular PO2
,
elimination of CO from intracellular binding sites occurs more slowly. Significant
mental obtundation, vomiting, and headache may remain even in the face of a normal
COHb level.
Brain imaging may reveal a variety of abnormalities in patients
with CO poisoning, including hypodensities in the globus pallidus and subcortical
white matter, cerebral cortical lesions, cerebral edema, hippocampal lesions, loss
of gray-white differentiation, and white matter hyperintensities.[102]
[103]
[104]
Except
to exclude other pathologies, brain imaging is not useful for determining who should
receive HBO, but it may provide prognostic information. Computed tomography (CT)
scans in a group of 40 patients who received HBO for CO poisoning were systematically
reviewed by Pracyk and coworkers.[102]
Twenty of
23 patients (87%) with a normal CT scan had
a favorable clinical outcome, in contrast to only 6 of 17 patients (35%) with an
abnormal scan.
Supportable guidelines for the application of HBO therapy in CO
poisoning include the following:
- A history of neurologic impairment (including loss of consciousness)
- Symptoms or evidence of cardiac abnormalities (ischemia, arrhythmias, ventricular
failure)
- A COHb level that has been greater than 25%
Fetuses are particularly susceptible to CO toxicity. Accordingly,
HBO therapy is indicated for pregnant women who fulfill the aforementioned criteria
or for pregnancies with fetal distress. Case reports,[105]
[106]
[107]
published
series,[108]
[109]
and a critical review[110]
support the concepts
that inadequately treated CO poisoning is a serious risk to the mother and fetus
and that the benefits of HBO outweight the theoretical risk of HBO treatment to the
fetus. The potential adverse effects of currently implemented HBO treatment protocols
have not been confirmed in clinical practice.
