Handbook of Clinical Neurology, Vol. 131 (3rd series) Occupational Neurology M. Lotti and M.L. Bleecker, Editors © 2015 Elsevier B.V. All rights reserved
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]
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).
REFERENCES Amitai Y, Zlotogorski Z, Golan-Katzav V et al. (1998). Neuropsychological impairment from acute low-level exposure to carbon monoxide. Arch Neurol 55: 845–848. Anderson EW, Andelman RJ, Strauch JM (1973). Effect of low-level carbon monoxide exposure on onset and duration of angina pectoris. A study in ten patients with ischemic heart disease. Ann Intern Med 79: 46–50. Annane D, Chevret S, Jars-Guincestre MC et al. (2001). Prognostic factors in unintentional mild carbon monoxide poisoning. Intensive Care Med 27: 1776–1781. Aronow WS (1981). Aggravation of angina pectoris by two percent carboxyhemoglobin. Am Heart J 101: 154. Aronow WS, Issell MW (1973). Carbon monoxide effects on exercise-induced angina pectoris. Ann Intern Med 79: 392–395. Beard RR, Grandstaff N (1970). Carbon monoxide exposure and cerebral function. Ann N Y Acad Sci 174: 385–395.
Beard RR, Wertheim GA (1967). Behavioral impairment associated with small doses of carbon monoxide. Am J Public Health 57 (11): 2012–2022, Nov. Benignus VA (1994). Behavioral effects of carbon monoxide: meta analyses and extrapolations. J Appl Physiol 76 (3): 1310–1316. Benignus VA, Otto DA, Prah JD et al. (1977). Lack of effects of carbon monoxide on human vigilance. Percept Mot Skills 45: 1007–1014. Benignus VA, Muller KE, Barton CN et al. (1987a). Effect of low level carbon monoxide on compensatory tracking and event monitoring. Neurotoxicol Teratol 9: 227–234. Benignus VA, Kafer ER, Muller KE et al. (1987b). Absence of symptoms with carboxyhemoglobin levels of 16–23%. Neurotoxicol Teratol 9: 345–348. Benignus VA, Muller KE, Malott CM (1990). Dose-effects functions for carboxyhemoglobin and behavior. Neurotoxicol Teratol 12: 111–118. Benignus VA, Hazucha MJ, Smith MV et al. (1994). Prediction of carboxyhemoglobin formation due to transient exposure to carbon monoxide. J Appl Physiol 76 (4): 1739–1745. Beppu T (2014). The role of MR imaging in assessment of brain damage from carbon monoxide poisoning: a review of the literature. AJNR Am J Neuroradiol 35: 625–631. Beppu T, Nishimoto H, Ishigaki D et al. (2010). Assessment of damage to cerebral white matter fiber in the subacute phase after carbon monoxide poisoning using fractional anisotropy in diffusion tensor imaging. Neuroradiology 52: 735–743. Beppu T, Nishimoto H, Fujiwara S et al. (2011). 1H-magnetic resonance spectroscopy indicates damage to cerebral white matter in the subacute phase after CO poisoning. J Neurol Neurosurg Psychiatry 82: 869–875. Beppu T, Fujiwara S, Nishimoto H et al. (2012). Fractional anisotropy in the centrum semiovale as a quantitative indicator of cerebral white matter damage in the subacute phase in patients with carbon monoxide poisoning: correlation with the concentration of myelin basic protein in cerebrospinal fluid. J Neurol 259: 1689–1705. Bleecker ML, Lindgren KN (1999). The mere presence of low levels of carboxy- hemoglobin is not causal proof for altered neuropsychological performance. Arch Neurol 56: 1299. Bokonjic N, Buchthal F (1961). Postanoxic unconsciousness as related to clinical and EEG recovery in stagnant anoxia and carbon monoxide poisoning. In: H Gastaut, JS Meyer (Eds.), Cerebral anoxia and the electroencephalogram, pp. 118–127, Springfield, Ill, Charles C Thomas. Bruno A, Wagner W, Orrison WW (1993). Clinical outcome and brain MRI four years after carbon monoxide intoxication. Acta Neurol Scand 87: 205–209. Buckley NA, Juurlink D, Isbister G et al. (2011). Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev 4, CD002041. CDC (1993). Unintentional carbon monoxide poisoning from indoor use of pressure washers – Iowa, January 1992 – January 1993. MMWR Morb Mortal Wkly Rep 42 (40): 777–779, 785.
CDC (1996). Carbon monoxide poisoning at an indoor ice arena and bingo hall – Seattle 1996. MMWR Morb Mortal Wkly Rep 45 (13): 265–267. CDC (1998). Carbon monoxide poisoning and death after the use of explosives in a sewer construction project. DHHS (NIOSH) Publication number 98-122, National Institute for Occupational Safety and Health (NIOSH), Atlanta, GA. CDC (2005). Carbon monoxide poisoning after Hurricane Katrina – Alabama, Louisiana, and Mississippi, August– September 2005. MMWR Morb Mortal Wkly Rep 54 (39): 996–998. CDC (2006). Carbon monoxide poisoning after two major hurricanes – Alabama and Texas. August–October 2005. MMWR Morb Mortal Wkly Rep 55 (9): 236–239. CDC (2011). Carbon monoxide exposures – United States, 2000–2009. MMWR Morb Mortal Wkly Rep 60 (30): 1014–1017. Cervellin G, Comelli I, Rastelli G et al. (2014). Initial blood lactate correlates with carboxyhemoglobin and clinical severity in carbon monoxide poisoned patients. Clin Biochem 47 (18): 298–301. Chang KH, Han MH, Kin HS et al. (1992). Delayed encephalopathy after acute carbon monoxide intoxication: imaging features and distribution of cerebral white matter lesions. Radiology 184: 117–122. Chang CC, Chang WN, Lui CC et al. (2010). Longitudinal study of carbon monoxide intoxication by diffuse tensor imaging with neuropsychiatric correlation. J Psychiatry Neurosci 35: 115–125. Choi IS (1983). Delayed neurological sequelae in carbon monoxide intoxication. Arch Neurol 40: 433–435. Choi IS (2002). Parkinsonism after carbon monoxide poisoning. Eur Neurol 48: 30–33. Clower JH, Hampson NB, Iqbal S et al. (2012). Recipients of hyperbaric oxygen treatment for carbon monoxide poisoning and exposure circumstances. Am J Emerg Med 30: 846–851. Coburn RF, Forster RE, Kane PB (1965). Considerations of the psychological variables that determine the blood carboxyhemoglobin concentration in men. J Clin Invest 44: 1899–1910. Crystal HA, Ginsberg MD (2000). Carbon monoxide. In: PS Spencer, HH Schaumburg (Eds.), Experimental and clinical neurotoxicology, 2nd edn. Oxford University Press, New York, pp. 318–329. De Reuck J, Decoo D, Lemahieu I et al. (1993). A positron emission tomography study of patients with acute carbon monoxide poisoning treated by hyperbaric oxygen. J Neurol 240: 430–434. Department of the Environment (1994). Expert panel on air quality standards. Carbon Monoxide. HMSO, London. Deschamps D, Geraud C, Julien H et al. (2003). Memory one month after acute carbon monoxide intoxication: a prospective study. Occup Environ Med 60: 212–216. Durak AC, Coskun A, Yikilmaz A et al. (2005). Magnetic resonance imaging findings in chronic carbon monoxide intoxication. Acta Radiol 46: 322–327.
Ernst A, Zibrak JD (1998). Carbon monoxide poisoning. N Engl J Med 339 (22): 1603–1608. Farrow JR, Davis GJ, Weaver LK et al. (1990). Fetal death due to nonlethal maternal carbon monoxide poisoning. J Forensic Sci 35 (6): 1448–1452. Fawcett TA, Moon RE, Fracica PJ et al. (1992). Warehouse workers’ headache, carbon monoxide poisoning from propane-fueled forklifts. J Occup Med 34 (1): 12–15. Forbes WH, Sargent F, Roughton FJW (1945). The rate of carbon monoxide uptake by normal men. Am J Physiol 143 (4): 594–608. Fujiwara S, Beppu T, Nishimoto H et al. (2012). Detecting damaged regions of cerebral white matter in the subacute phase after carbon monoxide poisoning using voxel-based analysis with diffusion tensor imaging. Neuroradiology 54: 681–689. Gale SD, Hopkins RO, Weaver LK et al. (1999). MRI, quantitative MRI, SPECT, and neuropsychological findings following carbon monoxide poisoning. Brain Inj 13 (4): 229–243. Gawlikowski T, Golasik M, Gomolka E et al. (2014). Proteins as biomarkers of carbon monoxide neurotoxicity. Inhal Toxicol 26: 885–890. Gilbert GJ, Glaser GH (1959). Neurologic manifestations of chronic carbon monoxide poisoning. N Engl J Med 10: 1217–1220. Gliner JA, Horvath SM, Mihevic PM (1983). Carbon monoxide and human performance in a single and dual task methodology. Aviat Space Environ Med 54 (8): 714–717, Aug. Grunnet ML, Petajan JH (1976). Carbon monoxide-induced neuropathy in the rat. Ultrastructural changes. Arch Neurol 33: 158–163. Guzman JA (2012). Carbon monoxide poisoning. Crit Care Clin 28: 537–548. Hampson NB, Hampson LA (2002). Characteristics of headache associated with acute carbon monoxide poisoning. Headache 42: 220–223. Hampson NB, Norkool DM (1992). Carbon monoxide poisoning in children riding in the back of pickup trucks. J Amer Med Assoc 267 (4): 538–540. Hampson NB, Kramer CC, Dunford RG et al. (1994). Norkool DM. Carbon monoxide poisoning from indoor burning of charcoal briquets. J Amer Med Assoc 271 (1): 52–53. Hanafy KA, Oh J, Otterbein LE (2013). Carbon monoxide and the brain: time to rethink the dogma. Curr Pharm Des 19: 2771–2775. Hara S, Mukai T, Kurosaki K et al. (2002). Modification of the striatal dopaminergic neuron system by carbon monoxide exposure in free-moving rats, as determined by in vivo brain microdialysis. Arch Toxicol 76: 596–605. Henke K, Kroll NE, Behniea H et al. (1999). Memory lost and regained following bilateral hippocampal damage. J Cogn Neurosci 11: 682–697. Henz S, Maeder M (2005). Prospective study of accidental carbon monoxide poisoning in 38 Swiss soldiers. Swiss Med Wkly 135: 398–406.
CARBON MONOXIDE INTOXICATION Holstege CP, Baer AB, Eldridge DL et al. (2004). Case series of elevated troponin I following carbon monoxide poisoning. J Toxicol Clin Toxicol 42 (5): 742–743. Hopkins RO, Fearing MS, Weaver LK et al. (2006). Basal ganglia lesions following carbon monoxide poisoning. Brain Inj 20 (3): 273–281. Ide T, Kamijo Y (2009). The early elevation of interleukin 6 concentration in cerebrospinal fluid and delayed encephalopathy of carbon monoxide poisoning. Am J Emerg Med 27: 992–996. Ide T, Kamijo Y, Ide A, Yoshimura K et al. (2012). Elevated S100B level in cerebrospinal fluid could predict poor outcome of carbon monoxide poisoning. Am J Emerg Med 30: 222–225. Jaeckle RS, Nasrallah HA (1985). Major depression and carbon monoxide-induced parkinsonism: diagnosis, computerized axial tomography, and response to L-dopa. J Nerve Ment Dis 173 (8): 503–508, Aug. Jasper BW, Hopkins RO, Van Duker H et al. (2005). Affective outcome following carbon monoxide poisoning a prospective longitudinal study. Cogn Behav Neurol 18 (2): 127–134, June. Juurlink DN, Buckley NA, Stanbrook MB et al. (2005). Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rrev 1, CD002041. Kao LW, Nanagas KA (2006). Toxicity associated with carbon monoxide. Clin Lab Med 26: 99–125. Kesler SR, Hopkins RO, Blatter DD et al. (2001). Verbal memory deficits associated with fornix atrophy in carbon monoxide poisoning. J Int Neuropsychol Soc 7: 640–646. Kim HY, Kim BJ, Moon SY et al. (2002). Serial diffusionweighted MR imaging in delayed postanoxic encephalopathy. A case study. J Neuroradiol 29 (3): 211–215, Sept. Kim JH, Chang KH, Song IC et al. (2003). Delayed encephalopathy of acute carbon monoxide intoxication: Diffusivity of cerebral white matter lesions. AJNR Am J Neuroradiol 24: 1592–1597. Klawans HL, Stein RW, Tanner CM et al. (1982). A pure parkinsonian syndrome follow acute carbon monoxide intoxication. Arch Neurol 39: 302. Koike A, Wasserman K, Armon Y et al. (1991). The work-rate dependent effect of carbon monoxide on ventilatory control during exercise. Respir Physiol 85: 169–183. Kondziella D, Danielsen ER, Hansen K et al. (2009). 1H MR spectroscopy of gray and white matter in carbon monoxide poisoning. J Neurol 256: 970–979. Lapresle J, Fardeau M (1967). The central nervous system and carbon monoxide poisoning. II. Anatomical study of brain lesions following intoxication with carbon monoxide (22 cases). Prog Brain Res 24: 31–74. Laties VG, Merigan WH (1979). Behavioral effects of carbon monoxide on animals and man. Annu Rev Pharmacol Toxicol 19: 357–392. Lee MH (1978). Clinical studies on delayed sequelae in carbon monoxide intoxication. J Korean Neuropsychiatr Assoc 17: 374–385. Li W, Zhang Y, Gu R et al. (2013). DNA pooling base genomewide association study identifies variants at NRXN3
associated with delayed encephalopathy after acute carbon monoxide poisoning. PLoS One 8 (11): e79159. Liang F, Li W, Zhang P et al. (2013). A PARK2 polymorphism associated with delayed neuropsychological sequelae after carbon monoxide poisoning. BMC Med Genet 14: 99. Lin WC, Lu CH, Lee YC et al. (2009). White matter damage in carbon monoxide intoxication assessed in vivo using diffusion tensor MR imaging. AJNR Am J Neuroradiol 30 (5): 1017–1021. Lo CP, Chen SY, Lee KW et al. (2007). Brain injury after acute carbon monoxide poisoning: early and late complications. AJR Am J Roentgenol 189 (4): W205–W211. Long LD, Hill EP (1977). Carbon monoxide uptake and elimination in fetal and maternal sheep. Am J Physiol 232: H324–H330. McDonald WL (1967). Structural and functional changes in human and experimental neuropathy. In: Modern trends in neurology, Vol. 4. Butterworth, London, p. 145. McFarland RA (1973). Low level exposure to carbon monoxide and driving performance. Arch Environ Health 27: 355–359, Dec. Messier LD, Myers RA (1991). A neuropsychological screening battery for emergency assessment of carbon-monoxidepoisoned patients. J Clin Psychol 47: 675–684. Mihevic PM, Gliner JA, Ho SM (1983). Carbon monoxide exposure and information processing during perceptualmotor performance. Int Arch Occup Environ Health 51: 355–363. Mikulka P, O’Donnell, Heinig P et al. (1970). The effect of carbon monoxide on human performance. Ann N Y Acad Sci 174: 409–420. Min SK (1986). A brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication. Acta Psychiatr Scand 73: 80–86. Murata T, Kimura H, Kado H et al. (2001). Neuronal damage in the interval form of CO poisoning determined by serial diffusion weighted magnetic resonance imaging plus 1 H-magnetic resonance spectroscopy. J Neurol Neurosurg Psychiatry 71: 250–253. Myers RAM, DeFazio A, Kelly MP (1998). Chronic carbon monoxide exposure: a clinical syndrome detected by neuropsychological tests. J Clin Psychol 54: 555–567. Neufeld MY, Swanson JW, Klass DW (1981). Localized EEG abnormalities in acute carbon monoxide poisoning. Arch Neurol 38: 524–527. O’Donnell P, Buxton PJ, Pitkin A et al. (2000). The magnetic resonance imaging appearances of the brain in acute carbon monoxide poisoning. Clin Radiol 55: 273–280. O’Donoghue JL (1985). Carbon monoxide, inorganic nitrogenous compounds, and phosphorus. In: JL O’Donoghue (Ed.), Neurotoxicity of industrial and commercial chemicals, 1. CRC Press, Florida, pp. 193–200. Ogawa M, Minami T, Katsurada K et al. (1973). Early electroencephalographic change following acute carbon monoxide poisoning in relation to cerebral metabolism. Med J Osaka Univ 24: 85–90. Okeda R, Funata N, Takano T et al. (1981). The pathogenesis of carbon monoxide encephalopathy in the acute
phase – physiological and morphological correlation. Acta Neuropathol (Berl) 54: 1–10. Park S, Choi IS (2004). Chorea following acute carbon monoxide poisoning. Yonsei Med J 45: 363–366. Park E, Ahn J, Min YG et al. (2012). The usefulness of the serum s100b protein for predicting delayed neurological sequelae in acute carbon monoxide poisoning. Clin Toxicol (Phila) 50: 183–188. Park EJ, Min YG, Kim GW et al. (2014). Pathophysiology of brain injuries in acute carbon monoxide poisoning: a novel hypothesis. Med Hypotheses 83: 186–189. Parkinson RB, Hopkins RO, Cleavinger HB et al. (2002). White matter hyperintensities and neuropsychological outcome following carbon monoxide poisoning. Neurology 58: 1525–1532. Petajan JH, Packham SC, Frens DB et al. (1976). Sequelae of carbon monoxide- induced hypoxia in the rat. Arch Neurol 33: 152–157. Peterson JE, Stewart RD (1970). Absorption and elimination of carbon monoxide by inactive young men. Arch Environ Health 21: 165–171. Peterson JE, Stewart RD (1975). Predicting the carboxyhemoglobin levels resulting from carbon monoxide exposures. J Appl Physiol 39: 633–638. Porter SS, Hopkins RO, Weaver LK et al. (2002). Corpus callosum atrophy and neuropsychological outcome following carbon monoxide poisoning. Arch Clin Neuropsychol 17: 195–204. Prockop LD (2005). Carbon monoxide brain toxicity: clinical, magnetic resonance imaging, magnetic resonance spectroscopy, and neuropsychological effects in 9 people. J Neuroimaging 15 (2): 144–149, Apr. Pulst SM, Walshe TM, Romero JA (1983). Carbon monoxide poisoning with features of Gilles de la Tourette’s syndrome. Arch Neurol 40: 443–444. Putz VR (1979). The effects of carbon monoxide on dual-task performance. Hum Factors 21 (1): 13–24. Raphael JC, Elkharrat D, Jars-Guincestre MC et al. (1989). Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet 334: 414–419. Rasmussen LS, Poulsen M, Christiansen M et al. (2004). Biochemical markers for brain damage after carbon monoxide poisoning. Acta Anaesthesiol Scand 48: 469–473. Raub JA, Benignus VA (2002). Carbon monoxide and the nervous system. Neurosci Biobehav Rev 26: 925–940. Raub J, Mathieu-Nolf M, Hampson N et al. (2000). Carbon monoxide poisoning – a public health perspective. Toxicology 145: 1–14. Rottman SJ, Kaser-Boyd N, Cannis T et al. (1995). Low-level carbon-monoxide poisoning: inability of neuropsychological testing to identify patients who benefit from hyperbaric oxygen therapy. Prehosp Disaster Med 10: 276–282. Schulte JH (1963). Effects of mild carbon monoxide intoxication. Arch Environ Health 7: 524–530. Schwartz A, Hennerici M, Wegener OH (1985). Delayed choreoathetosis following acute carbon monoxide poisoning. Neurology 35: 98–99.
Sener RD (2003). Acute carbon monoxide poisoning: diffusion MR imaging findings. AJNR Am J Neuroradiol 24: 1475–1477. Singhal AB, Topcuoglu MA, Koroshetz WJ (2002). Diffusion MRI in three types of anoxic encephalopathy. J Neurol Sci 196: 37–40. Snyder RD (1970). Carbon monoxide intoxication with peripheral neuropathy. Neurology 20: 177–180. Stewart RD (1975). The effect of carbon monoxide on humans. Annu Rev Pharmacol 15: 409–423. Stewart RD, Peterson JE, Baretta ED et al. (1970). Experimental human exposure to carbon monoxide. Arch Environ Health 21: 154–164. Stewart RD, Newton PE, Hosko M et al. (1973). Effects of carbon monoxide on time perception. Arch Environ Health 27: 155–160. Teksam M, Casey SO, Michel E et al. (2002). Diffusionweighted MR imaging findings in carbon monoxide poisoning. Neuroradiology 44: 109–113. Terajima K, Igarashi H, Hirose M et al. (2008). Serial assessments of delayed encephalopathy after carbon monoxide poisoning using magnetic resonance spectroscopy and diffusion tensor imaging on 3.0 T system. Eur Neurol 59: 55–61. Thom SR, Taber RL, Mendiguren II et al. (1995). Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann Emerg Med 25: 474–480. Thom SR, Bhopale VM, Fisher D et al. (2004). Delayed neuropathy after carbon monoxide poisoning is immunemediated. Proc Natl Acad Sci U S A 101: 13660–13665. Thom S, Bhopale V, Milovanova T et al. (2010). Plasma biomarkers in carbon monoxide poisoning. Clin Toxicol (Phila) 48 (1): 47–56. Townsend CL, Maynard RL (2002). Effects on health of prolonged exposure to low concentrations of carbon monoxide. Occup Environ Med 59: 708–711. Verma A, Hirsch DJ, Glatt CE et al. (1993). Carbon monoxide: a putative neural messenger. Science 259: 381–384. von Rappard J, Sch€ onenberger M, Ba¨rlocher L (2014). Case report: carbon monoxide poisoning following use of a water pipe/hookah. Dtsch Arztebl Int 111: 674–679. Wang B, Cao W, Biswal S (2011). Carbon monoxide-activated Nrf2 pathway leads to protection against permanent focal cerebral ischemia. Stroke 42: 2605–2610. Weaver LK (2008). Carbon monoxide poisoning. In: LB Gesell (Ed.), Hyperbaric oxygen therapy indications, 12th edn. Undersea and Hyperbaric Medical Society, Durham, NC, pp. 19–28. Weaver LK (2009). Carbon monoxide poisoning. N Engl J Med 360 (12): 1217–1225. Weaver LK, Hopkins RO, Larson-Lohr V (1996). Neuropsychologic and functional recovery from severe carbon monoxide poisoning without hyperbaric oxygen therapy. Ann Emerg Med 27 (6), June. Weaver LK, Hopkins RO, Chan KJ et al. (2002). Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 347: 1057–1067.
CARBON MONOXIDE INTOXICATION Weaver LK, Valentine KJ, Hopkins RO (2007). Carbon monoxide poisoning risk factors for cognitive sequelae and the role of hyperbaric oxygen. Am J Respir Crit Care Med 176: 491–497. WHO (1999). Environmental health criteria 213: Carbon monoxide. 2nd edn. World Health Organization, Finland. Widdop B (2002). Analysis of carbon monoxide. Ann Clin Biochem 39: 378–391. Wilson G, Winkleman NW (1924). Multiple neuritis following carbon monoxide poisoning. J Amer Med Assoc 82: 1407. Wolf SJ, Lavonas EJ, Sloan EP et al. (2008). Clinical policy: critical issue in the management of adult patients present-
ing to the emergency department with acute carbon monoxide poisoning. Ann Emerg Med 51 (2): 138–152. Yabluchanskiy A, Sawle P, Homer-Vanniasinkam S (2012). CORM-3, a carbon monoxide- releasing molecule, alters the inflammatory response and reduces brain damage in a rat model of hemorrhagic stroke. Crit Care Med 42: 544–552. Yardan T, Cervik Y, Donderici O et al. (2009). Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning. Am J Emerg Med 27: 838–842. Yoshii F, Kozuma R, Takahashi W et al. (1998). Magnetic resonance imaging and 11C-N-methylsiperone/positron emission tomography studies in a patient with the interval form of carbon monoxide poisoning. J Neurol Sci 160: 87–91.