Carbon monoxide is one of the most common causes of fatal poisoning in
the U.S., by either intentional (suicidal) or accidental exposure,
and may be the most common worldwide cause of fatal poisoning.1 Despite a
great deal of clinical experience and randomized trials, there remains
a great deal of controversy about the ideal approach to managing
carbon monoxide exposures.
Exact statistics for carbon monoxide poisoning are difficult
to ascertain, mainly due to incomplete reporting and misdiagnosis. Data
from the American Association of Poison Control Centers Toxic Exposure
Surveillance System in 20052 reported 16,449 exposures,
with 66 deaths. However, this information is limited, as many exposures
and some deaths are not reported to the local poison control center.
It is also unclear how often patients with milder carbon monoxide
poisoning are misdiagnosed and thus are not included in the database.
Data from the Centers for Disease Control and Prevention paint a
much broader picture of exposures than the Toxic Exposure Surveillance
System database. The most recent large epidemiologic report from
the center on the subject, the 2001–2003 data on non–fire-related
carbon monoxide exposures, revealed 480 deaths and 15,200 exposures.3 The
incidence of carbon monoxide exposure has not decreased despite
more widespread use of carbon monoxide detectors.3,4
In the past, vehicular emissions were the major source of carbon
monoxide poisoning in adults. In recent years, nonvehicular sources
have become more common as use of catalytic converters has reduced
carbon monoxide in vehicular exhaust emissions5 (Table 217-0.1).
Table 217-0.1 Sources of Carbon Monoxide
| Save Table
Table 217-0.1 Sources of Carbon Monoxide
|Wood- or coal-burning stoves or heaters|
|Gasoline-powered generators or motors|
|Natural gas–powered heaters/furnaces/generators|
Peak incidence occurs in the fall and winter months, generally
due to increased use of space heaters, wood-burning stoves, charcoal
burning for heat, or portable generators without adequate ventilation.3 Whole
families may be affected in such exposures. Additional sources of
carbon monoxide exposure include air conditioners, portable generators
in camping tents, exhausts on motorboats, and from Zamboni® machines used
in ice rinks.6–8 Exposures have been reported
in persons riding in the back of a pickup truck and riding in a
vehicle whose exhaust pipe was occluded by snow.
Carbon monoxide poisoning is probably the most toxic component
in smoke inhalation and is a major contributor to fire-related deaths.
One other source for carbon monoxide poisoning is methylene chloride, which
is found in varnishes and paint strippers, and is the bubbling fluid in
Christmas lights. Routes of exposure are inhalational or by ingestion. Methylene
chloride is metabolized in the liver to carbon monoxide. As a result
of ongoing methylene chloride metabolism, persistent elevation of serum carboxyhemoglobin (COHb)
occurs despite oxygen therapy.9 Time to peak carbon
monoxide levels may be 8 hours or longer.
Carbon monoxide is a colorless, odorless gas. It is normally
present in air at 10 parts per million (ppm) or less, perhaps higher
in urban areas. There are multiple industries in which there may
be occupational exposure to carbon monoxide. The U.S. Occupational
Health and Safety Administration set a permissible exposure level
of carbon monoxide of 50 ppm averaged over an 8-hour shift (http://www.osha.gov/SLTC/healthguidelines/carbonmonoxide/recognition.html).
Toxicity generally begins at ambient levels of 100 ppm.
Carbon monoxide is also an endogenous substance, with production
occurring in the body during normal breakdown of heme. Normal physiologic
blood carbon monoxide levels from this process are ~1% in
healthy nonsmokers but can be higher in conditions of hemolysis
or sepsis. In smokers, baseline blood levels in smokers of up to
10% have been reported.
The binding affinity of normal adult hemoglobin for carbon monoxide is
about 200 times that of oxygen. Fetal hemoglobin has an even higher binding
affinity, which may account for potentially more severe fetal toxicity.10 Approximately
85% of carbon monoxide is bound to hemoglobin to form COHb,
and the rest is dissolved in plasma or bound intracellularly, often
to myoglobin. There are mathematical models for predicting the half-life
of COHb; these have been evaluated in both volunteer human models
and actual carbon-monoxide poisoned patients. Half-lives of
COHb on room air at normal atmospheric pressure range from 249 to
320 minutes.8 On 100% oxygen
at atmospheric pressure, this is reduced to an average of 74 to
80 minutes.11 The exception
to this is COHb generated by methylene chloride exposure, which
can have a half-life of up to 13 hours due to ongoing metabolism.9
COHb does not provide oxygen delivery to the cells, and as COHb levels
increase, relative anemia and hypoxia occur. Furthermore, carbon monoxide
shifts the oxyhemoglobin dissociation curve to the left (Figure 217-1), impairing oxygen release to
the tissues. However, this alone does not fully explain the acute
physiologic effects of carbon monoxide or its neurologic sequelae.
Patients with corresponding levels of hypoxia or anemia, who are
not carbon monoxide poisoned, do not have similar short- and long-term
effects seen with carbon monoxide poisoning. This indicates that
there is a separate toxicity to carbon monoxide irrespective of
the level of COHb. COHb appears to be more a marker for the degree of
poisoning than the primary cause of injury itself. The best experimental evidence
of this involved dogs that were given carbon monoxide by inhalation
to produce COHb levels of 80%.12 Exchange
transfusion of COHb-saturated blood into healthy dogs produced no
symptoms, suggesting that something other than simply the COHb level
is at play in explaining the full range of toxic effects.
Carboxyhemoglobin “shift to the left” reshaping
of the oxyhemoglobin (HbO2) dissociation curve. (a...
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