Letters to the Editor Carbon Monoxide
Poisoning
in Smoke Inhalation
To the Editor: We read the article by Young and Moss’ with interest. The authors point out the importance of carbon monoxide (CO) poisoning in the pathogenesis of clinical illness after smoke inhalation. Some of their statements, however, require clarification. In Table 1 of that article, the authors described the effects of CO poisoning at various carboxyhemoglobin (COHb) saturations. While this correlation may be approximately correct for acute exposure, in the practical clinical situation, the relationship between symptoms and COHb is quite poor. Frequently, by the time these patients are evaluated, a long period of time has elapsed since the CO exposure. They also have usually received therapeutic oxygen (0,). As a result of these two factors, blood COHb levels are usually low, but the patient may still be symptomatic. Piantadosi’ discussed the discrepancy between COHb levels and clinical symptoms. Young and Moss’s discussion’ of delayed neurologic sequelae noted that some clinicians recommend that the patient be kept on bed rest for 2 to 4 weeks to avoid the late syndrome. This recommendation is out of date and not followed in modern clinical practice. The authors also stated that the use of hyperbaric oxygen (HBO) has not been conclusively proven to be effective and that it is not clear that it offers a therapeutic advantage over 100% 0, administration at 1 atmosphere (ATA). In fact, there are several good reasons to recommend the use of HBO for symptoms of CO poisoning. CO binding to intracellular hemoproteins such as myoglobin and cytochrome oxidase has been demonstrated2 and is almost certainly a factor in the pathogenesis of CO poisoning. Cellular effects may explain the poor correlation between clinical symptoms and COHb levels. The rate of dissociation of CO from intracellular binding sites increases markedly at a higher partial pressure of oxygen (PO,). If mitochondrial PO, is on the order of 1 or 2 mmHg, the dissociation of CO from intracellular binding sites will be much slower than its dissociation from hemoglobin. Studies in rats in which blood was replaced by fluorocarbon also have shown that CO may produce tissue injury directly. HBO is likely to hasten the elimination of CO from cytochrome oxidase by raising intracellular PO,.
288
J. Clin. Anesth.,
vol. 2, July/August
1990
Furthermore, a review of CO poisoning by C;oulon et al.:’showed that the probability of late deterioration was significantly diminished in patients treated promptly with HBO compared to those treated with 0, at one atmosphere. Krantz rt al.’ presented a series of 79 patients treated with 100% 0, at 1 ATA. Norkool and Kirkpatrick” described a comparable group of 115 patients who were all treated with HBO. Mortality in the group receiving HBO was substantially lower than in the patients treated with 0, at one atmosphere. Clinical experience with patients treated with HBO usually indicates dramatic and almost immediate clinical improvement. The weight of evidence therefore supports the use of HBO in patients with smoke inhalation when complicated by CO poisoning. This point is not only a medicolegal issue, as suggested by the authors, but also a clinical one. We recommend the use of HBO in patients who have had a COHb level greater than 25%; have any history of neurologic impairment, ineluding unconsciousness; or have persistent symptoms or evidence of cardiac abnormalities. Richard
E. Moon, MD
Associate Professor of Anesthesiology Assistant Professor of Pulmonary Medicine Duke University School of Medicine Medical Director Duke Hyperbaric Center Claude A. Piantadosi,
MD
Associate Professor of Pulmonary Medicine Department of Medicine Duke University School of Medicine Scientific Director Duke Hyperbaric Center Durham, NC 27710
References 1. Young CJ, Moss J: Smoke inhalation: diagnosis and treatment. J C/in Anesth 1989; 1:377-86. 2. Piantadosi CA: Carbon monoxide, oxygen transport and oxygen metabolism. J Hyperbaric Med 1987;2:27-44. 3. Goulon M, Barois A. Rapin M, et al: Carbon monoxide
Letters to the Editor poisoning and acute anoxia due to breathing coal gas and hydrocarbons. J Hyperbaric Med 1986; 1:23-4 1. 4. Krantz T, Thisted B, Strom J, Sorensen MB: Acute carActa Anaesthesiol Stand bon monoxide poisoning. 1988;32:278-82.
5. Norkool DM, Kirkpatrick JN: Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: a review of 115 cases. Ann EmergMed 1985;14:1168-71.
Reply: We appreciate the constructive comments of Drs. Moon and Piantadosi regarding our article on smoke inhalation.’ We concur with their experience that carbon monoxide (CO) poisoning may often be overlooked and can be important in the pathophysiology of the smoke inhalation syndrome. Indeed, there is increasing evidence that even low levels of CO exposure can have adverse effects on compromised patients.2 While carboxyhemoglobin (COHb) levels at the time the patient presents for treatment may be misleading, the extrapolated COHb levels may be helpful in assessing the severity of the syndrome. As in many burn centers, our patients often are admitted 1 or more hours after the incident. Clearly, clinical signs and symptoms can be misleading; a high index of suspicion on the part of clinicians is necessary. The key issue relates to the proven effectiveness of hyperbaric oxygen (HBO) in the treatment of CO poisoning. This issue has been a subject of debate for some years. Drs. Moon and Piantadosi cite several series in which there appears to be a benefit. Nonetheless, the results of other series in the literature are equivocal. Because randomized double-blind studies are difficult to perform in the acute care setting, few are available which fail to rigorously meet the criteria for therapeutic effectiveness. The article by Krantz et al3 documents the effects of normoxic therapy in 79 patients over 15 years of clinical experience and specifically presents arguments for long-term neurologic follow-up. This work is compared to another study from Seattle,4 where emergency medicine is among the best in the world. In this latter study, all patients were treated with HBO, and the investigators achieved a superior outcome. While we can learn much from such one-legged clinical trials, we must evaluate the efficacy of HBO as carefully as we would evaluate the efficacy of any other drug or intervention. When a careful evaluation is performed, it is not clear that HBO has the same documented efficacy in CO poisoning as it demonstrates in wound healing, gas gangrene, or embolism. Indeed, a recent randomized study of 629 patients concluded that HBO was not
useful in patients who did not lose consciousness, irrespective of their COHb levels5 Because of the power of this trial (97%), the authors suggested that HBO is not indicated therapy in patients with no loss of consciousness.’ Although there may be some potential benefit to aggressive HBO treatment of patients who present with an initial loss of consciousness, the study design only compared patients who had received two treatments to those who had received a single treatment. No benefit was derived from this more aggressive therapy. A recent comprehensive review article on hyperbaric medicine concurs that the therapeutic efficacy of HBO in CO poisoning remains unproven.” We do use HBO but are cognizant of the fact that not every medical center will have access to a chamber. The real question is a practical one. Should the ambulance drive an extra 10, 15, or 60 minutes so that the patient with CO poisoning can receive the benefits of HBO? We think that rigorous studies demonstrating the effectiveness of HBO in CO poisoning have not been performed and thus such action is not supported at this time. The intent of our article, which we believe is reflected in the comments from Drs. Moon and Piantadosi, is to suggest that HBO may influence the course of recovery from CO poisoning. While we do not share their conviction as to its efficacy, we are in accord that clinicians should be aware of the significance of this syndrome and of available modes of therapy. Christopher Young, MD Resident Department of Anesthesia Brigham & Women’s Hospital Boston, MA 02 115 Jonathan Moss, MD, PhD Professor and Vice Chairman for Research Department of Anesthesia and Critical Care University of Chicago Chicago, IL 60637 J. Clin. Anesth., vol. 2, July/August
1990
289
Poisoning
in Smoke Inhalation
To the Editor: We read the article by Young and Moss’ with interest. The authors point out the importance of carbon monoxide (CO) poisoning in the pathogenesis of clinical illness after smoke inhalation. Some of their statements, however, require clarification. In Table 1 of that article, the authors described the effects of CO poisoning at various carboxyhemoglobin (COHb) saturations. While this correlation may be approximately correct for acute exposure, in the practical clinical situation, the relationship between symptoms and COHb is quite poor. Frequently, by the time these patients are evaluated, a long period of time has elapsed since the CO exposure. They also have usually received therapeutic oxygen (0,). As a result of these two factors, blood COHb levels are usually low, but the patient may still be symptomatic. Piantadosi’ discussed the discrepancy between COHb levels and clinical symptoms. Young and Moss’s discussion’ of delayed neurologic sequelae noted that some clinicians recommend that the patient be kept on bed rest for 2 to 4 weeks to avoid the late syndrome. This recommendation is out of date and not followed in modern clinical practice. The authors also stated that the use of hyperbaric oxygen (HBO) has not been conclusively proven to be effective and that it is not clear that it offers a therapeutic advantage over 100% 0, administration at 1 atmosphere (ATA). In fact, there are several good reasons to recommend the use of HBO for symptoms of CO poisoning. CO binding to intracellular hemoproteins such as myoglobin and cytochrome oxidase has been demonstrated2 and is almost certainly a factor in the pathogenesis of CO poisoning. Cellular effects may explain the poor correlation between clinical symptoms and COHb levels. The rate of dissociation of CO from intracellular binding sites increases markedly at a higher partial pressure of oxygen (PO,). If mitochondrial PO, is on the order of 1 or 2 mmHg, the dissociation of CO from intracellular binding sites will be much slower than its dissociation from hemoglobin. Studies in rats in which blood was replaced by fluorocarbon also have shown that CO may produce tissue injury directly. HBO is likely to hasten the elimination of CO from cytochrome oxidase by raising intracellular PO,.
288
J. Clin. Anesth.,
vol. 2, July/August
1990
Furthermore, a review of CO poisoning by C;oulon et al.:’showed that the probability of late deterioration was significantly diminished in patients treated promptly with HBO compared to those treated with 0, at one atmosphere. Krantz rt al.’ presented a series of 79 patients treated with 100% 0, at 1 ATA. Norkool and Kirkpatrick” described a comparable group of 115 patients who were all treated with HBO. Mortality in the group receiving HBO was substantially lower than in the patients treated with 0, at one atmosphere. Clinical experience with patients treated with HBO usually indicates dramatic and almost immediate clinical improvement. The weight of evidence therefore supports the use of HBO in patients with smoke inhalation when complicated by CO poisoning. This point is not only a medicolegal issue, as suggested by the authors, but also a clinical one. We recommend the use of HBO in patients who have had a COHb level greater than 25%; have any history of neurologic impairment, ineluding unconsciousness; or have persistent symptoms or evidence of cardiac abnormalities. Richard
E. Moon, MD
Associate Professor of Anesthesiology Assistant Professor of Pulmonary Medicine Duke University School of Medicine Medical Director Duke Hyperbaric Center Claude A. Piantadosi,
MD
Associate Professor of Pulmonary Medicine Department of Medicine Duke University School of Medicine Scientific Director Duke Hyperbaric Center Durham, NC 27710
References 1. Young CJ, Moss J: Smoke inhalation: diagnosis and treatment. J C/in Anesth 1989; 1:377-86. 2. Piantadosi CA: Carbon monoxide, oxygen transport and oxygen metabolism. J Hyperbaric Med 1987;2:27-44. 3. Goulon M, Barois A. Rapin M, et al: Carbon monoxide
Letters to the Editor poisoning and acute anoxia due to breathing coal gas and hydrocarbons. J Hyperbaric Med 1986; 1:23-4 1. 4. Krantz T, Thisted B, Strom J, Sorensen MB: Acute carActa Anaesthesiol Stand bon monoxide poisoning. 1988;32:278-82.
5. Norkool DM, Kirkpatrick JN: Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: a review of 115 cases. Ann EmergMed 1985;14:1168-71.
Reply: We appreciate the constructive comments of Drs. Moon and Piantadosi regarding our article on smoke inhalation.’ We concur with their experience that carbon monoxide (CO) poisoning may often be overlooked and can be important in the pathophysiology of the smoke inhalation syndrome. Indeed, there is increasing evidence that even low levels of CO exposure can have adverse effects on compromised patients.2 While carboxyhemoglobin (COHb) levels at the time the patient presents for treatment may be misleading, the extrapolated COHb levels may be helpful in assessing the severity of the syndrome. As in many burn centers, our patients often are admitted 1 or more hours after the incident. Clearly, clinical signs and symptoms can be misleading; a high index of suspicion on the part of clinicians is necessary. The key issue relates to the proven effectiveness of hyperbaric oxygen (HBO) in the treatment of CO poisoning. This issue has been a subject of debate for some years. Drs. Moon and Piantadosi cite several series in which there appears to be a benefit. Nonetheless, the results of other series in the literature are equivocal. Because randomized double-blind studies are difficult to perform in the acute care setting, few are available which fail to rigorously meet the criteria for therapeutic effectiveness. The article by Krantz et al3 documents the effects of normoxic therapy in 79 patients over 15 years of clinical experience and specifically presents arguments for long-term neurologic follow-up. This work is compared to another study from Seattle,4 where emergency medicine is among the best in the world. In this latter study, all patients were treated with HBO, and the investigators achieved a superior outcome. While we can learn much from such one-legged clinical trials, we must evaluate the efficacy of HBO as carefully as we would evaluate the efficacy of any other drug or intervention. When a careful evaluation is performed, it is not clear that HBO has the same documented efficacy in CO poisoning as it demonstrates in wound healing, gas gangrene, or embolism. Indeed, a recent randomized study of 629 patients concluded that HBO was not
useful in patients who did not lose consciousness, irrespective of their COHb levels5 Because of the power of this trial (97%), the authors suggested that HBO is not indicated therapy in patients with no loss of consciousness.’ Although there may be some potential benefit to aggressive HBO treatment of patients who present with an initial loss of consciousness, the study design only compared patients who had received two treatments to those who had received a single treatment. No benefit was derived from this more aggressive therapy. A recent comprehensive review article on hyperbaric medicine concurs that the therapeutic efficacy of HBO in CO poisoning remains unproven.” We do use HBO but are cognizant of the fact that not every medical center will have access to a chamber. The real question is a practical one. Should the ambulance drive an extra 10, 15, or 60 minutes so that the patient with CO poisoning can receive the benefits of HBO? We think that rigorous studies demonstrating the effectiveness of HBO in CO poisoning have not been performed and thus such action is not supported at this time. The intent of our article, which we believe is reflected in the comments from Drs. Moon and Piantadosi, is to suggest that HBO may influence the course of recovery from CO poisoning. While we do not share their conviction as to its efficacy, we are in accord that clinicians should be aware of the significance of this syndrome and of available modes of therapy. Christopher Young, MD Resident Department of Anesthesia Brigham & Women’s Hospital Boston, MA 02 115 Jonathan Moss, MD, PhD Professor and Vice Chairman for Research Department of Anesthesia and Critical Care University of Chicago Chicago, IL 60637 J. Clin. Anesth., vol. 2, July/August
1990
289
