Handbook of Clinical Neurology, Vol. 131 (3rd series) Occupational Neurology M. Lotti and M.L. Bleecker, Editors © 2015 Elsevier B.V. All rights reserved
Chapter 12
Carbon monoxide intoxication MARGIT L. BLEECKER* Center for Occupational and Environmental Neurology, Baltimore, MD, USA
INTRODUCTION Carbon monoxide (CO) is a colorless, odorless, nonirritant gas absorbed through the lungs. The rate of CO uptake depends upon duration of exposure, concentration of CO in the environment, and minute ventilation (Forbes et al., 1945). Carboxyhemoglobin (COHb) is formed when CO binds with hemoglobin with an affinity 200 times greater than oxygen, thereby decreasing oxygen-carrying capacity and the release of oxygen to tissues, leading to tissue hypoxia. Since CO causes the remaining oxyhemoglobin to hold the oxygen more strongly, the oxygen dissociation curve is shifted to the left, making it more difficult to release the remaining oxygen in the blood to the tissues. At low COHb levels (1–5%) intrinsic compensatory physiologic mechanisms prevent CO hypoxia through increased blood flow and increased oxygen extraction. At a COHb below 20% changes in oxygen consumption in the brain are negligible and therefore brain function should not be affected (Benignus et al., 1990). A 10% decrement in brain oxygen consumption does not occur until a COHb level of 27% is reached (Raub and Benignus, 2002). See Table 12.1 for progression of effects in humans as COHb levels increase. Once loss of consciousness accompanied by hypotension occurs with CO poisoning there is the possibility for the development of delayed neurologic sequelae (DNS). DNS may present after recovery with a lucid interval of 2–40 days during which diffuse demyelination develops in the brain with a constellation of signs and symptoms that is reversible in the majority of patients (Lee, 1978; Choi, 1983; Min, 1986; Crystal and Ginsberg, 2000; Lin et al., 2009).
SOURCES OF CO EXPOSURE CO is a product of incomplete combustion of hydrocarbons, leading to elevated air levels, in poorly functioning
heating systems and inadequate ventilation of flamebased heating sources. CO poisoning has occurred when gasoline-powered pressure washers were used indoors to clean livestock (CDC, 1993); in warehouses where propane-powered forklifts are needed (Fawcett et al., 1992; Wesley et al., 1995); with indoor burning of charcoal briquettes (Hampson et al., 1994); riding in the back of pick-up trucks (Hampson and Norkool, 1992); or in ice skating rinks using propane-powered resurfacing machines (CDC, 1996). Data from the US National Poison Data System during 2000–2009 showed 68 316 CO exposures, with 45.1% managed on site and 53.7% treated at a healthcare facility. Most occur during the winter months and are primarily located in the Midwest and Northeast, with 77.6% at residence site and 12% at the workplace. The most common clinical symptoms with CO exposure are headache, nausea, and dizziness (CDC, 2011). From 2008 to 2010, 87 hyperbaric facilities reported information on 864 patients who received treatment for CO poisoning (Clower et al., 2012). The most common CO sources were furnace or boiler 32%, generator 20%, motor vehicle 13%, grill 6%, and space heater 5%, with 75% of the patients treated in the fall and winter. The most common fuel involved was gasoline 48%, natural gas/propane 36%, and diesel 2%. CO poisoning occurs following hurricanes due to the use of portable generators and gasoline-powered appliances that are used improperly by inappropriate placement and ventilation. Following Hurricane Katrina during August 29 to September 24, 2005, 51 cases of CO poisoning were treated at hyperbaric facilities in Alabama, Louisiana, and Mississippi (CDC, 2005). Investigations in Alabama and Texas after hurricanes found nearly all were due to gasoline-powered generators that, even when outside, were placed close to window air conditioners and few homes had CO detectors (CDC, 2006).
*Correspondence to: Margit L. Bleecker, MD, PhD, Director, Center for Occupational and Environmental Neurology, 2 Hamill Road, Suite 225, Baltimore MD 21210, USA. Tel: +1-410-433-2077, Fax: +1-410-433-0622, E-mail: [email protected]
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Table 12.1 Human response with varying levels of carboxyhemoglobin (COHb) COHb (%)
Findings in humans
6 hours to treat hypoxia, for blood pressure support, and to address any cardiac issues if present. From 2008 to 2010, 87 hyperbaric facilities reported information on 864 patients who received treatment for CO poisoning (Clower et al., 2012), of which 353 required hospitalization (median COHb 25%, range 1–77%) and 475 were discharged after treatment (median COHb 21%, range 0.1–46%). The most common symptoms were headache (66%), dizziness (51%), nausea/vomiting (46%), loss of consciousness (44%), and confusion
(30%). Twenty-one patients reported no symptoms. Thirty-eight percent had loss of consciousness for 10 minutes, while for 49% the duration was unknown. Since the indications of when to use HBO therapy for CO poisoning have remained controversial (Raphael et al., 1989; Weaver et al., 1996), Ernst and Zibrak (1998) published guidelines in 1998. These included: (1) coma; (2) any period of unconsciousness; (3) any abnormal score on the CO Neuropsychological Screening Battery; (4) COHb > 40%; (5) pregnancy and COHb level > 15%; (6) signs of cardiac ischemia or arrhythmia; (7) history of ischemic heart disease and COHb level > 20%; (8) recurrent symptoms for up to 3 weeks; and (9) symptoms that do not resolve with normobaric oxygen after 4–6 hours. As discussed in the section on neuropsychologic effects, above, if the only finding was an abnormal score on one of the tests in the CO Neuropsychological Screening Battery, this should not warrant treatment with HBO. The Undersea and Hyperbaric Medical Society recommends HBO treatment for CO-poisoned patients regardless of COHb levels when there is transient or prolonged unconsciousness, neurologic signs, cardiovascular dysfunction, or severe acidosis, or if their age is 36 years, or if the CO exposure duration interval is 24 hours. They agree that the role of neuropsychologic testing to determine need for HBO therapy is not clear. The optimal protocol for HBO treatment with CO poisoning has not been determined and whether clinical improvement or reduced rate of neurocognitive sequelae occurs when HBO is administered beyond 6 hours from poisoning is unknown (Weaver, 2008). These recommendations are made in the absence of well-designed randomized control studies or appropriate study design to allow for meaningful interpretation of the results. The controversy over HBO treatment for CO poisoning continues as the American College of Emergency Physicians subcommittee could not reach a consensus on any variable for which HBO was indicated with CO poisoning (Wolf et al., 2008). Two Cochrane reviews critiqued multiple randomized controlled trials and concluded that the evidence did not support that HBO therapy for CO poisoning reduced the persistence of adverse neurologic outcomes (Juurlink et al., 2005; Buckley et al., 2011). In light of marked variability in patient selection and CO poisoning in these studies, a more conservative recommendation suggested one HBO treatment at 2 atmosphere within 12 hours of CO exposure for comatose patients with acute nonsuicidal CO poisoning and COHb greater than 25%. Any pregnant woman with CO poisoning should receive HBO therapy (Guzman, 2012) because CO
CARBON MONOXIDE INTOXICATION exposure in pregnant women is dangerous, as there may be a lag time for CO uptake, but eventually the COHb level in the fetus is higher than in the mother (Long and Hill, 1977). The fetal hemoglobin releases less oxygen to the tissues, resulting in significant hypoxia (Farrow et al., 1990). To test the hypothesis that HBO therapy is needed to prevent the development of DNS, Thom et al. (1995) treated patients with CO poisoning with HBO: none developed DNS while 23% developed DNS after treatment with ambient-pressure oxygen. There was a problem with case definition for DNS. None of these patients had loss of consciousness and their level of function (going to work) with persistent symptoms of headache, dizziness, and difficulty concentrating is not commonly used to define DNS. In this study differences in performance on the neuropsychologic battery between the two treatment groups could be attributed to premorbid abilities as the ambient pressure oxygen group had fewer years of education and this was not taken into account in the analyses (Thom et al., 1995). There is concern that advocates for HBO treatment are located at facilities that offer this treatment. Some believe further randomized controlled trials are unnecessary, as withholding HBO treatment in CO-poisoned patient is unethical, while others feel further trials are unethical given the absence of data showing the effectiveness of HBO treatment and the expense of transferring patients to such facilities (Kao and Nanagas, 2006). HBO is not free of side-effects; some include painful barotrauma, decompression sickness, pulmonary edema and hemorrhage, seizures, and oxygen toxicity. The presence of a pneumothorax is an absolute contraindication for HBO treatment (Kao and Nanagas, 2006).
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Chapter 12
Carbon monoxide intoxication MARGIT L. BLEECKER* Center for Occupational and Environmental Neurology, Baltimore, MD, USA
INTRODUCTION Carbon monoxide (CO) is a colorless, odorless, nonirritant gas absorbed through the lungs. The rate of CO uptake depends upon duration of exposure, concentration of CO in the environment, and minute ventilation (Forbes et al., 1945). Carboxyhemoglobin (COHb) is formed when CO binds with hemoglobin with an affinity 200 times greater than oxygen, thereby decreasing oxygen-carrying capacity and the release of oxygen to tissues, leading to tissue hypoxia. Since CO causes the remaining oxyhemoglobin to hold the oxygen more strongly, the oxygen dissociation curve is shifted to the left, making it more difficult to release the remaining oxygen in the blood to the tissues. At low COHb levels (1–5%) intrinsic compensatory physiologic mechanisms prevent CO hypoxia through increased blood flow and increased oxygen extraction. At a COHb below 20% changes in oxygen consumption in the brain are negligible and therefore brain function should not be affected (Benignus et al., 1990). A 10% decrement in brain oxygen consumption does not occur until a COHb level of 27% is reached (Raub and Benignus, 2002). See Table 12.1 for progression of effects in humans as COHb levels increase. Once loss of consciousness accompanied by hypotension occurs with CO poisoning there is the possibility for the development of delayed neurologic sequelae (DNS). DNS may present after recovery with a lucid interval of 2–40 days during which diffuse demyelination develops in the brain with a constellation of signs and symptoms that is reversible in the majority of patients (Lee, 1978; Choi, 1983; Min, 1986; Crystal and Ginsberg, 2000; Lin et al., 2009).
SOURCES OF CO EXPOSURE CO is a product of incomplete combustion of hydrocarbons, leading to elevated air levels, in poorly functioning
heating systems and inadequate ventilation of flamebased heating sources. CO poisoning has occurred when gasoline-powered pressure washers were used indoors to clean livestock (CDC, 1993); in warehouses where propane-powered forklifts are needed (Fawcett et al., 1992; Wesley et al., 1995); with indoor burning of charcoal briquettes (Hampson et al., 1994); riding in the back of pick-up trucks (Hampson and Norkool, 1992); or in ice skating rinks using propane-powered resurfacing machines (CDC, 1996). Data from the US National Poison Data System during 2000–2009 showed 68 316 CO exposures, with 45.1% managed on site and 53.7% treated at a healthcare facility. Most occur during the winter months and are primarily located in the Midwest and Northeast, with 77.6% at residence site and 12% at the workplace. The most common clinical symptoms with CO exposure are headache, nausea, and dizziness (CDC, 2011). From 2008 to 2010, 87 hyperbaric facilities reported information on 864 patients who received treatment for CO poisoning (Clower et al., 2012). The most common CO sources were furnace or boiler 32%, generator 20%, motor vehicle 13%, grill 6%, and space heater 5%, with 75% of the patients treated in the fall and winter. The most common fuel involved was gasoline 48%, natural gas/propane 36%, and diesel 2%. CO poisoning occurs following hurricanes due to the use of portable generators and gasoline-powered appliances that are used improperly by inappropriate placement and ventilation. Following Hurricane Katrina during August 29 to September 24, 2005, 51 cases of CO poisoning were treated at hyperbaric facilities in Alabama, Louisiana, and Mississippi (CDC, 2005). Investigations in Alabama and Texas after hurricanes found nearly all were due to gasoline-powered generators that, even when outside, were placed close to window air conditioners and few homes had CO detectors (CDC, 2006).
*Correspondence to: Margit L. Bleecker, MD, PhD, Director, Center for Occupational and Environmental Neurology, 2 Hamill Road, Suite 225, Baltimore MD 21210, USA. Tel: +1-410-433-2077, Fax: +1-410-433-0622, E-mail: [email protected]
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Table 12.1 Human response with varying levels of carboxyhemoglobin (COHb) COHb (%)
Findings in humans
6 hours to treat hypoxia, for blood pressure support, and to address any cardiac issues if present. From 2008 to 2010, 87 hyperbaric facilities reported information on 864 patients who received treatment for CO poisoning (Clower et al., 2012), of which 353 required hospitalization (median COHb 25%, range 1–77%) and 475 were discharged after treatment (median COHb 21%, range 0.1–46%). The most common symptoms were headache (66%), dizziness (51%), nausea/vomiting (46%), loss of consciousness (44%), and confusion
(30%). Twenty-one patients reported no symptoms. Thirty-eight percent had loss of consciousness for 10 minutes, while for 49% the duration was unknown. Since the indications of when to use HBO therapy for CO poisoning have remained controversial (Raphael et al., 1989; Weaver et al., 1996), Ernst and Zibrak (1998) published guidelines in 1998. These included: (1) coma; (2) any period of unconsciousness; (3) any abnormal score on the CO Neuropsychological Screening Battery; (4) COHb > 40%; (5) pregnancy and COHb level > 15%; (6) signs of cardiac ischemia or arrhythmia; (7) history of ischemic heart disease and COHb level > 20%; (8) recurrent symptoms for up to 3 weeks; and (9) symptoms that do not resolve with normobaric oxygen after 4–6 hours. As discussed in the section on neuropsychologic effects, above, if the only finding was an abnormal score on one of the tests in the CO Neuropsychological Screening Battery, this should not warrant treatment with HBO. The Undersea and Hyperbaric Medical Society recommends HBO treatment for CO-poisoned patients regardless of COHb levels when there is transient or prolonged unconsciousness, neurologic signs, cardiovascular dysfunction, or severe acidosis, or if their age is 36 years, or if the CO exposure duration interval is 24 hours. They agree that the role of neuropsychologic testing to determine need for HBO therapy is not clear. The optimal protocol for HBO treatment with CO poisoning has not been determined and whether clinical improvement or reduced rate of neurocognitive sequelae occurs when HBO is administered beyond 6 hours from poisoning is unknown (Weaver, 2008). These recommendations are made in the absence of well-designed randomized control studies or appropriate study design to allow for meaningful interpretation of the results. The controversy over HBO treatment for CO poisoning continues as the American College of Emergency Physicians subcommittee could not reach a consensus on any variable for which HBO was indicated with CO poisoning (Wolf et al., 2008). Two Cochrane reviews critiqued multiple randomized controlled trials and concluded that the evidence did not support that HBO therapy for CO poisoning reduced the persistence of adverse neurologic outcomes (Juurlink et al., 2005; Buckley et al., 2011). In light of marked variability in patient selection and CO poisoning in these studies, a more conservative recommendation suggested one HBO treatment at 2 atmosphere within 12 hours of CO exposure for comatose patients with acute nonsuicidal CO poisoning and COHb greater than 25%. Any pregnant woman with CO poisoning should receive HBO therapy (Guzman, 2012) because CO
CARBON MONOXIDE INTOXICATION exposure in pregnant women is dangerous, as there may be a lag time for CO uptake, but eventually the COHb level in the fetus is higher than in the mother (Long and Hill, 1977). The fetal hemoglobin releases less oxygen to the tissues, resulting in significant hypoxia (Farrow et al., 1990). To test the hypothesis that HBO therapy is needed to prevent the development of DNS, Thom et al. (1995) treated patients with CO poisoning with HBO: none developed DNS while 23% developed DNS after treatment with ambient-pressure oxygen. There was a problem with case definition for DNS. None of these patients had loss of consciousness and their level of function (going to work) with persistent symptoms of headache, dizziness, and difficulty concentrating is not commonly used to define DNS. In this study differences in performance on the neuropsychologic battery between the two treatment groups could be attributed to premorbid abilities as the ambient pressure oxygen group had fewer years of education and this was not taken into account in the analyses (Thom et al., 1995). There is concern that advocates for HBO treatment are located at facilities that offer this treatment. Some believe further randomized controlled trials are unnecessary, as withholding HBO treatment in CO-poisoned patient is unethical, while others feel further trials are unethical given the absence of data showing the effectiveness of HBO treatment and the expense of transferring patients to such facilities (Kao and Nanagas, 2006). HBO is not free of side-effects; some include painful barotrauma, decompression sickness, pulmonary edema and hemorrhage, seizures, and oxygen toxicity. The presence of a pneumothorax is an absolute contraindication for HBO treatment (Kao and Nanagas, 2006).
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