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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



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