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Ernst and Zibrak,
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Interim analysis of an ongoing randomized clinical trial5 and one completed randomized clinical trial6 of the role of hyperbaric oxygen therapy in acute carbon monoxide poisoning have failed to demonstrate differences in outcomes between patients treated with normobaric oxygen and those treated with hyperbaric oxygen. Both of these trials enrolled comatose patients with carbon monoxide poisoning. We acknowledge that some authorities recommend that such patients receive hyperbaric oxygen, but there is no compelling data from clinical trials indicating that they require hyperbaric oxygen. There are risks associated with hyperbaric oxygen, including those related to oxygen transport, barotrauma affecting the middle and inner ear, and in cases of carbon monoxide poisoning, a 1 to 3 percent probability of a seizure induced by hyperbaric oxygen.6,7
In an ongoing longitudinal follow-up study conducted at our institution, approximately 30 percent of the patients with acute carbon monoxide poisoning have neurocognitive problems one year after poisoning. Of these patients, approximately one third have the delayed neuropsychiatric syndrome and two thirds have persistent neurocognitive problems, primarily difficulties with memory and executive function.5,8 Unfortunately, the clinical and laboratory findings at presentation are not predictive of long-term outcome. The effect of hyperbaric oxygen on long-term outcome is still unknown. We agree that carbon monoxide poisoning is common and may be associated with substantial neurocognitive morbidity8 and that patients should be treated with 100 percent oxygen and possibly with hyperbaric oxygen.
Lindell K. Weaver, M.D.
Ramona O. Hopkins, Ph.D.
Gregory Elliott, M.D.
LDS Hospital
Salt Lake City, UT 84143
References
Contrary to what Ernst and Zibrak state, national and local standards do exist for electronic carbon monoxide detectors. Underwriters Laboratories has published standards used by manufacturers of carbon monoxide detectors since 1991.3 These detectors approved by Underwriters Laboratories are designed to sound an alarm when ambient carbon monoxide levels are reached that would cause a carboxyhemoglobin level of 10 percent or greater in a person engaged in work requiring heavy exertion. In 1994, Chicago became one of the first large metropolitan areas to require residential carbon monoxide detectors.4 St. Louis, Albany, New York, and Fort Lee, New Jersey, are among the other municipalities that have such ordinances. Also, the National Fire Protection Association has published recommended practices for the installation of household carbon monoxide–warning equipment.5 It is clear that electronic carbon monoxide detectors are effective tools for ameliorating the public health problem of carbon monoxide poisoning and that they can help unmask "the silent killer."
Jerrold B. Leikin, M.D.
Jack C. Clifton II, M.D.
Paul K. Hanashiro, M.D.
Rush–Presbyterian–St. Luke's Medical Center
Chicago, IL 60612
References
Improved care of anesthesia machines has been shown to reduce the incidence of carbon monoxide exposure from approximately 1 in 200 to 1 in 2000 first cases,3 but some remote or seldom-used facilities may be at particularly high risk. Exposure can be severe; carboxyhemoglobin concentrations over 30 percent have been documented in humans,4 and animals have been exposed to lethal concentrations of over 80 percent carboxyhemoglobin in clinical scenarios.5 It is possible that most exposure goes undetected because monitoring for carbon monoxide or carboxyhemoglobin is not routine in these circumstances, because the symptoms of carbon monoxide poisoning are masked by the effects of general anesthesia, and because, after the patient emerges from anesthesia, signs and symptoms remain nonspecific.
Harvey J. Woehlck, M.D.
Medical College of Wisconsin
Milwaukee, WI 53226
References
Several reports of such victims serving as successful donors of kidneys,2 livers,3 hearts,4 and even a lung5 indicate that careful evaluation of organ function in these victims can identify organs that are suitable for transplantation. All these reports came from outside the United States.
The waiting list of the United Network for Organ Sharing on October 31, 1998, had 62,994 registrants (including 41,544 waiting for kidneys, 11,601 waiting for livers, 4184 waiting for hearts, 3088 waiting for lungs, and 2235 waiting for pancreases or kidneys and pancreases). Many of these patients are in urgent need of transplants and are on life-support mechanisms. Therefore, the judicious evaluation of individual organ function of brain-dead victims of carbon monoxide poisoning could lead to a slight easing of the critical shortage of organ donors.
H. Myron Kauffman, M.D.
United Network for Organ Sharing
Richmond, VA 23225-8770
References
Donal P. Ryan, M.D.
Anthony M. Cosentino, M.D.
St. Mary's Medical Center
San Francisco, CA 94117
References
To the Editor: Our review of carbon monoxide poisoning concentrated on the more common sources of production that might be encountered by primary care and emergency medicine clinicians. Treatment is often based on recommendations, rather than evidence-based studies with conclusive results.
As pointed out by Dr. Woehlck, improperly maintained anesthesia circuits may be a cause of carbon monoxide poisoning. This, fortunately, is a rare circumstance not commonly encountered by practicing clinicians. Appropriate and diligent maintenance of anesthesia machines should alleviate this problem.
Carbon monoxide detectors are useful but have not been conclusively demonstrated to reduce morbidity and mortality. The cited study by Yoon et al.1 is a descriptive analysis that does not actually compare an intervention group with a nonintervention group. We agree with Leikin et al. that carbon monoxide detectors have the potential to decrease the incidence of carbon monoxide poisoning in residential settings, but they are a form of secondary prevention and not a substitute for proper maintenance and appropriate use of heating equipment.
We agree with Weaver et al. that "undisputed" may have been a poor choice of words for describing indications for hyperbaric-oxygen therapy in comatose patients. However, we continue to believe strongly that the weight of clinical empirical evidence supports this practice. Our review of the literature concerning neurologic dysfunction as a consequence of hyperbaric-oxygen therapy in patients with carbon monoxide poisoning fails to convince us of a uniform negative effect. In fact, hyperbaric oxygen appears to modify favorably the propensity of neurocognitive defects to develop and is considered the standard of care by most authorities.2,3 Only further research can answer these questions more definitively.
We agree with Dr. Kauffman that victims of carbon monoxide poisoning need to be considered as potential organ donors. Carbon monoxide poisoning may lead to cellular damage in a variety of organ systems, but such an effect should not be considered an absolute contraindication to organ transplantation. Several reports in the literature confirm the feasibility of this approach.4,5 This area also is in need of further research and protocols should be established to help alleviate the current shortage of organs.
Drs. Ryan and Cosentino correctly point out that the ordinate of Figure 1 of our article is mislabeled. This axis is intended to represent the relative oxygen saturation of the residual hemoglobin molecules not bound to carbon monoxide: 100–Z, where Z is the percent of total hemoglobin molecules bound to carbon monoxide. As suggested, the correct label is that used by Roughton: 100 (Hemoglobin O2)÷([Hemoglobin O2]+[Red Hemoglobin]). For a given percentage of carboxyhemoglobin, this yields the ratio of oxygen-bound hemoglobin to the sum of oxygen-bound hemoglobin and reduced (unbound) hemoglobin. Thus for a carboxyhemoglobin concentration of 60 percent (as depicted in the figure), when all the remaining hemoglobin is bound to oxygen, and red hemoglobin is therefore 0 percent, the expression yields: 100 x (40 ÷ [40 + 0]), or 100 percent.
Armin Ernst, M.D.
Joseph Zibrak, M.D.
Beth Israel Deaconess Medical Center
Boston, MA 02215
References
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