|

Carbon Dioxide Poisoning
By Lewis Nelson, MD
A 50-year-old medical researcher was discovered unconscious in
a large walk-in refrigerator containing 15 large blocks of dry ice.
The dry ice had been stored in the 39.2° F refrigerator at
approximately 9:00 A.M. that day, and the researcher had last been
seen at around noon; at least three hours, therefore, had elapsed
between storage and exposure. There were no signs of struggle, and
the victim had no history of psychiatric disorders, recent personal
crises, or medical illnesses. At investigation of the scene, the
blocks of dry ice appeared grossly intact, but the external ventilation
system was nonfunctional. Additional investigation confirmed that
ambient carbon dioxide (CO2) was at a life-threatening concentration.
MECHANISMS OF TOXICITY
Dry ice is frozen CO2. Under normal ambient conditions, CO2 is a
colorless, odorless, nonexplosive gas. At high concentrations, it
imparts an acidic taste in the mouth as it dissolves in mucosal
water to form carbonic acid. Carbon dioxide dissolved in the plasma
(PCO2) is primarily responsible for our respiratory drive. The central
nervous system tightly controls PCO2 through its regulation of breathing.
In fact, physicians have used exogenous CO2, in combination with
oxygen, as a respiratory stimulant in neonates.
Dry ice is extremely cold: less than -109° F, as opposed
to 32° F for water ice. Rather than melting, it undergoes sublimation--conversion
directly from solid to gas without liquefaction. In the case presented
here, the dry ice was stored in the freezer to slow sublimation.
Apparently, however, even at the cold temperatures of a refrigerated
room, sublimation progresses rapidly.
Carbon dioxide intoxication may be acute or subacute. Subacute
toxicity may be caused by the body's failure to eliminate endogenous
CO2, as occurs in hypoventilation resulting from chronic obstructive
pulmonary disease, opioid poisoning, or other causes of respiratory
failure. Medical interventions such as permissive hypercapnea can
also cause subacute CO2 toxicity, which typically manifests itself
as gradual somnolence.
Patients exposed to high levels of CO2 in the environment, on
the other hand, may experience immediate hypoxia or anoxia in response
to the displacement of ambient oxygen. At any given temperature
and pressure, a liter of air can contain only a certain number of
particles. In this case, the sublimation of dry ice to CO2 gas displaced
the other components of ambient air, the most important of which
was oxygen.
The displacement of breathable oxygen by another gas produces
asphyxiation, impaired pulmonary gas exchange culminating in hypoxemia.
Asphyxiation may be caused by a physical mechanism, such as choking,
or by the reduction of the oxygen content in breathable air. A person
who has suffocated in a plastic bag, for example, has actually asphyxiated
from the selective depletion of oxygen caused by rebreathing into
the bag. Fire may deplete ambient oxygen and produce asphyxiation
independently of the effects of smoke inhalation or carbon monoxide
poisoning.
Asphyxiation can also occur at high altitudes, where reduced atmospheric
pressures lead to reduced partial pressures of oxygen. Although
the percentage of oxygen in air remains normal, fewer molecules
of oxygen are inspired with each breath, resulting in hypoxia.
Unfortunately, this mechanism is assuming increased clinical importance
with the resurgence of volatile hydrocarbon abuse. Users inhale
concentrated hydrocarbon vapors from butane lighters, for example,
or breathe in the propellant from spray paint cans, and the reduced
partial pressure of the inhaled oxygen leads to hypoxemia. Hypoxemia,
in turn, exacerbates the prodysrhythmic effects of inhaled halogenated
hydrocarbons, such as trichloroethane.
In contrast to simple gaseous asphyxiants, chemical asphyxiants
are able to induce tissue hypoxia without producing hypoxemia. One
such compound is cyanide, which inhibits mitochondrial oxidative
phosphorylation and thereby prevents the cells from using oxygen.
As a result, the tissue asphyxiates, despite adequate oxygenation
of the blood.
The "toxicity" of simple asphyxiants does not involve any deleterious
effect from the gases themselves; rather, the clinical findings
are largely proportional to the reduction in the fraction of inspired
oxygen (FIO2). In experimental models of acute CO2 poisoning, however,
central nervous system and respiratory status deteriorated within
seconds when FIO2 was maintained at normal levels, which suggests
that CO2 is not just a simple asphyxiant but also has acute systemic
effects. In 1986, Lake Nyos, a carbonated lake in Cameroon, released
a massive cloud of CO2 gas into the local community, killing thousands
of people.
Like the victims of the Lake Nyos disaster, the patient in this
report appeared to have succumbed rapidly, which is characteristic
of acute massive CO2 exposure and probably reflects the effects
of hypercapnea as well as hypoxemia. Because there was no indication
that the patient was trapped in the cooler or that a myocardial
infarction, seizure, or similar event prevented him from fleeing,
the most likely explanation is that he was incapacitated by the
massive exposure and subsequently asphyxiated.
OTHER SOURCES OF CO2 EXPOSURE
Occupational exposure to CO2 is widespread. The gas is used in carbonation
of soft drinks and as a shielding gas for welding. Carbon dioxide
is produced when organic material decomposes or ferments, and asphyxiation
from CO2 exposure has occurred in workers entering grain elevators,
the holds of cargo ships, and brewery vats. In the past, miners
would lower candles or mice into caves before entering, to guard
against the "black damp"--oxidation of carbonaceous material to
CO2, a process that both requires and depletes environmental oxygen.
Compressed CO2 gas is widely used as a fire extinguisher because
of its ability to safely displace oxygen from the atmosphere surrounding
a fire. When the gas is used in a closed space such as an airplane,
however, that property may prove lethal. Dry ice is often used to
generate artificial smoke for stage productions and is widely used
in the biomedical and transportation industries. Storage of dry
ice in closed spaces, such as submarines and automobiles, has proved
hazardous in the past, although the patient in this case may not
have known that the walk-in refrigerator did not have a functioning
ventilation system.
TREATMENT
Removal from the exposure and oxygenation are the only specific
therapies needed to treat CO2 poisoning. Emergency supportive care,
such as endotracheal intubation and hemodynamic support, should
be used as clinically indicated. Central nervous system impairment
is probably the most common adverse effect and may occur in isolation
or as a component of multisystem organ failure. Complications notwithstanding,
the long-term outcome for patients with mild to moderate CO2 poisoning
is excellent.
The patient in this report could not be resuscitated, however.
Results of a postmortem examination were unrevealing, as would be
expected with an exposure of this type, and the results of toxicologic
studies also were negative. Because a rapid increase in PCO2 can
be anticipated after death, assessment of the PCO2 level was not
performed in this patient.
Dr. Nelson is director of the medical toxicology fellowship and associate
director of the New York City Poison Control Center. He is also an
assistant professor in the department of surgery/emergency medicine
at New York University School of Medicine.
Emerg Med 32(05):36-38, 2000
|