|
|
|
|
|
IN THIS ARTICLE
OTHER TOPICS   The End of Stress, now available at amazon.com
|
Carbon Monoxide Poisoning Stephen R. Thom, M.D., Ph.D. Dr. Thom is Professor of Emergency Medicine and Chief, Hyperbaric Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA. Within the past 12 months, Dr. Thom reports no commercial conflicts of interest. It's a deadly, odorless, colorless and tasteless gas we live with every day. You could be dying from it and never know something was wrong. Carbon monoxide is a by-product of the combustion from wood stoves, heaters, automobiles. It kills tens of thousands of people every year and is misdiagnosed and mistreated in thousands of others. Much more common than most people believe, carbon monoxide poisoning occurs when carbon monoxide (CO) gas is inhaled in unventilated conditions. Many poisonings could be prevented if people better understood the dangers of CO. Worldwide, CO may be responsible for over half of all fatal poisonings.1,2,3 Often it occurs from cooking or operating combustion engines indoors or leaking heating systems. It is estimated that CO poisoning is the third leading cause of unintentional deaths in the United States and that the incidence of nonfatal poisonings varies from 15,000 to 40,000 cases per year.4,5,6,7 Because misdiagnosis of CO poisoning is common, however, the real incidence is probably much higher.8,9 How CO Damages the Body When you inhale CO, it enters the bloodstream and takes the place of oxygen by binding with hemoglobin, turning this life-sustaining molecule into a killer: a compound called carboxyhemoglobin (COHb). Hemoglobin's normal role is to bind with oxygen and carry it to all parts of the body. Unfortunately CO binds to hemoglobin several hundred times more strongly than oxygen does; this means that carboxyhemoglobin tends to remain in the body for a long time, where it leads to oxygen starvation. The only way to clear it from the blood is lengthy exposure to fresh air or pure oxygen. Even worse, because the brain regulates breathing based on the levels of carbon dioxide in the blood rather than on the amount of oxygen in the blood, a CO poisoning victim can easily lose consciousness without realizing that anything is wrong because the brain just doesn't register that oxygen levels in the blood and in the body are falling to dangerous levels. Five basic processes occur simultaneously within the body that contribute to CO poisoning:
Impaired Delivery and Use of Oxygen As described above, CO binds to hemoglobin. The resulting formation of carboxyhemoglobin (COHb) is a well understood effect of CO exposure.10 CO binding with hemoglobin interferes with the delivery of oxygen to bodily tissues.11 Levels of carbon monoxide in the blood can be determined by a simple blood test to measure carboxyhemoglobin. Carbon monoxide is produced naturally in the body and also functions as a neurotransmitter. Normal carboxyhemoglobin levels in an average person are less than 5%; heavy cigarette smokers may have levels as high as 9%. Serious health problems tend to be seen when carboxyhemoglobin levels rise above 25%, and a serious risk of death with levels over 70%. Still, the relationship between carboxyhemoglobin levels and its toxic effects vary quite a bit from person to person. For this reason, carboxyhemoglobin levels tell us more about the degree of exposure than they do about how a poisoning victim will do in the short or long term.12,13,14,15,16,17,18,19,20,21 Disrupted O2-CO-Nitric Oxide Balance Our bodies normally use oxygen, carbon monoxide and nitric oxide. The body makes use of all three of these gases in a fixed relationship with each other. When there are elevated levels of CO, this equilibrium is disturbed and the extra nitric oxide that often results can cause further toxic effects.22,23,24 Damage to Blood Vessels CO poisoning also causes deposits along vascular walls, causing damage to the lining of the blood vessels.25,26,27,28,29,30,31,32 Damage to the Nervous System Elevations in neurotransmitters initiating nervous system activity occur in the brain during CO poisoning.33,34,35 This could be caused by any (or all) of the three components of CO poisoning listed above.36 This elevated activity can damage nerve cells and is the same sort of mechanism that is implicated in stroke, traumatic brain injury and diseases of the central nervous system (CNS) such as Lou Gehrig's Disease and amyotrophic lateral sclerosis (ALS). Immune System Responses During Recovery Other complications from CO poisoning can happen during treatment and recovery. The damage to blood vessels combined with the other components above damage myelin, an important protein coating neurons that helps transmit messages more quickly within the nervous system and brain. The damage to brain tissues arouses the immune system, which responds by causing brain inflammation, and which, in turn, causes brain damage. This kind of brain damage usually happens during the recovery period, causing memory and learning problems and movement disorders, and may not become apparent until days or weeks after the poisoning incident. What to Look For: Signs and Symptoms If you know what to look for, you can see early symptoms of CO poisoning. Headache, nausea and dizziness are early signs. Because these symptoms are shared by so many common conditions, the diagnosis and identification of CO poisoning is often overlooked by victims, who may take a pain killer rather than opening windows or going out into the fresh air.37,38,39,40,41,42,43,44,45 A tip-off that the headache you are having is related to CO exposure is that it subsides when you go outside. Often these headaches occur in the morning when people wake up from a night of sleeping in an over-insulated home (which has little fresh air) with woodstove or heater produced CO pollution. Victims commonly have increased heart rates and rapid breathing; blood pressure is variable.46 In some cases, heart attack and even cardiac arrest can occur.47,49,50,51,52,53,54,55,56,57,58 A rare symptom is red coloration and skin blisters, particularly when victims have been laying comatose for a period of time.59,60 Testing for CO Poisoning Doctors typically measure the patient's levels of carboxyhemoglobin (COHb) to confirm the diagnosis of CO exposure.61 EKGs and plasma screens are also done, both because of the risk of circulatory system damage from CO and in light of the fact that those who suffer an acute cardiac injury from CO poisoning have an increased risk for cardiovascular-related death in the following 10 years. A chest X-ray also should be part of the ER evaluation, especially in cases of smoke inhalation.62,63 Some studies have reported a correlation between blood COHb levels and symptoms of headache and dizziness among victims with relatively low COHb levels on the order of 2 to 10%. Unfortunately, no reliable correlation exists between COHb level and more severe symptoms. The lack of objective measures for establishing the severity of CO poisoning complicates diagnosis and treatment. While there is evidence showing brain abnormalities following CO poisoning, unless there is evidence of an intracranial bleed, neuroimaging is not likely to help with evaluation of the CO poisoning victim.64,65,66,67,68,69,70,71 Treating CO Poisoning Emergency Stabilization The first step in treating someone who is suffering from CO poisoning is to clear the victim's airway, get them breathing and give the person pure oxygen. Oxygen supplementation is the cornerstone of treatment for CO poisoning. Oxygen inhalation will hasten the separation of CO from hemoglobin, as well as bring vital oxygen to starving bodily tissues. There is a consensus among research studies that the average amount of time it takes a victim to rid their body of COHb while breathing air is around 320 minutes (5.5 hours), but measured times in individuals vary from 128 to 409 minutes.72,73,74,75,76,77 In victims breathing 100% high-flow oxygen through a mask, the average time is approximately two hours -- 113 minutes, with individual times ranging from 27 to 464 minutes. Hyperbaric oxygen therapy (HBOT) is the only treatment shown to improve outcome in severe CO poisoning. There are several mechanisms of action. It will speed up the replacement of COHb by oxygen. The time it takes to get rid of excess COHb decreases to approximately 23 minutes when breathing pure oxygen in a hyperbaric chamber. However, animal studies indicate that the benefits of HBOT are probably not based on quicker "flushing out" of COHb.78 Even without oxygen treatment, HBOT alone has been proven to counteract several of the damaging effects of CO poisoning.79,80,81 For example, animals poisoned with CO and treated with HBOT alone have been found to have more rapid cardiovascular recovery,82 lower mortality83 and lower chances of long-term immune-related neurological problems.84,85,86,87,88,89,90,91,92,93,94,95,96 Summary CO poisoning is only partly the result of oxygen starvation from the binding of CO and hemoglobin. CO has several other damaging effects on the body, and these other effects are even more important than oxygen deprivation because they cause most of the long-term health problems suffered by CO poisoning victims. CO threatens life by causing heart failure. Neurological injuries arise from an interplay of oxygen deprivation, vascular damage, and neurological injuries. The autoimmune events that evolve in the days and weeks following CO poisoning can be avoided by prompt intervention. There are a number of theoretical treatments that might benefit CO victims, but the only treatment known to be safe and effective right now is hyperbaric oxygen. It is also clear that the best intervention is education, in order to prevent CO poisoning before it occurs.
References 1. National Safety Council: How people died in home accidents, 1981. Accident Facts, ed. N.S. Council. 1982, Chicago. 80-84. return 2. Cobb N. and Etzel RA. Unintentional carbon monoxide-related deaths in the United States, 1979 through 1988. JAMA, 1991. 266: p. 659-663. return 3. MMathieu D, Mathieu-Nolf M and Wattel F. [Carbon monoxide poisoning: current aspects]. Bull Acad Natl Med, 1996. 180(5): p. 965-71; discussion 972-3. return 4. United States Department of Health and Human Services (US DHHS), Centers for Disease Control and Prevention (CDC), National Center for Health Statistics (NCHS), Compressed Mortality File (CMF) compiled from CMF 1999-2002, Series 20, No. 2H 2004 on CDC WONDER On-line Database. Available at: http://woonder.cdc.gov/mortSQL.html. return 5. Mott JA, et al. National vehicle emissions policies and practices and declining US carbon monoxide-related mortality. Jama, 2002. 288(8): p. 988-95. return 6. Unintentional non-fire-related carbon monoxide exposures--United States, 2001-2003. MMWR Morb Mortal Wkly Rep, 2005. 54(2): p. 36-9. return 7. Chen BH, et al. Indoor air pollution in developing countries. 1990. 43: p. 127-138. return 8. Litovitz, TL, et al. 1991 annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med, 1992. 10(5): p. 452-505. return 9. Barret L, Danel V and Faure J. Carbon monoxide poisoning, a diagnosis frequently overlooked. Clin.Toxicol., 1985. 23: p. 309-313. return 10. Douglas CG, Haldane JS and Haldane JB. The laws of combination of haemoglobin with carbon monoxide and oxygen. J Physiol, 1912. 44(4): p. 275-304. return 11. Tenney SM. A theoretical analysis of the relationship between venous blood and mean tissue oxygen pressures. Respir Physiol, 1974. 20(3): p. 283-96. return 12. Chance B and Williams GR. The respiratory chain and oxidative phosphorylation. Adv Enzymol Relat Subj Biochem, 1956. 17: p. 65-134. return 13. Chance B, Erecinska M and Wagner M. Mitochondrial responses to carbon monoxide toxicity. Ann.N.Y.Acad.Sci., 1970. 174: p. 193-204. return 14. Keilin D. and Hartree EF. Cytochrome and cytochrome oxidase. Proc.R.Soc.Lond.B.Biol.Sci., 1939. 127: p. 167- 191. return 15. Coburn RF and Forman HJ. Carbon monoxide toxicity, in Handbook of Physiology, A.P. Fishman, L.E. Farki, and S.R. Geiger, Editors. 1987, Williams & Wilkies: Baltimore. p. 439-456. return 16. Brown SD, Piantadosi CA and Volume RV. In vivo binding of carbon monoxide to cytochrome C oxidase in rat brain. J.Appl.Physiol., 1990. 68: p. 604-610. return 17. Piantadosi CA, Tatro L, and Zhang J. Hydroxyl radical production in the brain after CO hypoxia in rats. Free Rad.Biol.Med., 1995. 18: p. 603-609. return 18. Zhang J et al. Cerebral amino acid, norepinephrine and nitric oxide metabolism in CNS oxygen toxicity. Br.Res., 1993. 606: p. 56-62. return 19. Piantadosi CA et al. Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat. Expt.'l.Neurol., 1997. 147: p. 103-114. return 20. Gilmer B et al. Hyperbaric oxygen does not prevent neurologic sequelae after carbon monoxide poisoning. Acad Emerg Med, 2002. 9(1): p. 1-8. return 21. Okeda R et al. Comparative study pathogenesis of selective cerebral lesions in carbon monoxide poisoning and nitrogen hypoxia in cats. Acta Neuropathol., 1982. 56: p. 265-272. return 22. Thom SR, Ohnishi ST and Ischiropoulos H. Nitric oxide released by platelets inhibits neutrophil B2 integrin function following acute carbon monoxide poisoning. Toxicol Appl Pharmacol, 1994. 128(1): p. 105-10. return 23. Thom SR and Ischiropoulos H. Mechanism of oxidative stress from low levels of carbon monoxide. Res Rep Health Eff Inst, 1997(80): p. 1-19; discussion 21-7. return 24. Thom SR, Xu YA and Ischiropoulos H. Vascular endothelial cells generate peroxynitrite in response to carbon monoxide exposure. Chem Res Toxicol, 1997. 10(9): p. 1023-31. return 25. Thom SR et al. Intravascular neutrophil activation due to carbon monoxide poisoning. Am J Respir Crit Care Med, 2006. 174: p. 1239-1248. return 26. Hirayama A et al. S-nitrosothiols are stored by platelets and released during platelet-neutrophil interactions. Nitric Oxide, 1999. 3(2): p. 95-104. return 27. Brennan ML et al. A tale of two controversies: defining both the role of peroxidases in nitrotyrosine formation in vivo using eosinophil peroxidase and myeloperoxidase-deficient mice, and the nature of peroxidase-generated reactive nitrogen species. J Biol Chem, 2002. 277(20): p. 17415-27. return 28. Baldus S et al. Spatial mapping of pulmonary and vascular nitrotyrosine reveals the pivotal role of myeloperoxidase as a catalyst for tyrosine nitration in inflammatory diseases. Free Radic Biol Med, 2002. 33(7): p. 1010. return 29. Marletta MA et al. Macrophage oxidation of L-arginine to nitrite and nitrate: nitric oxide is an intermediate. Biochem., 1988. 27: p. 8706-8711 return 30. Sohn HY et al. Crucial role of local peroxynitrite formation in neutrophil-induced endothelial cell activation. Cardiovasc Res, 2003. 57(3): p. 804-15. return 31. Zouki C et al. Peroxynitrite induces integrin-dependent adhesion of human neutrophils to endothelial cells via activation of the Raf-1/MEK/Erk pathway. Faseb J, 2001. 15(1): p. 25-27. return 32. Thom SR et al. Delayed neuropathology after carbon monoxide poisoning is immune-mediated. Proc Natl Acad Sci U S A, 2004. 101(37): p. 13660-5. return 33. Hara S et al. Characterization of hydroxyl radical generation in the striatum of free-moving rats due to carbon monoxide poisoning, as determined by in vivo microdialysis. Brain Res, 2004. 1016(2): p. 281-4. return 34. Hiramatsu M et al. Changes in concentrations of dopamine, serotonin, and their metabolites induced by carbon monoxide (CO) in the rat striatum as determined by in vivo microdialysis. Pharm.Biochem.Behavior., 1994. 48: p. 9- 15. return 35. Newby MB, Roberts RJ and Bhatnagar RK. Carbon monoxide- and hypoxia-induced effects on catecholamines in the mature and developing rat brain. J.Pharmacol.Expt.Therap., 1978. 206: p. 61-68. return 36. Thom SR et al. Neuronal nitric oxide synthase and N-methyl-D-aspartate neurons in experimental carbon monoxide poisoning. Toxicol Appl Pharmacol, 2004. 194(3): p. 280-95. return 37. Burney RE, Wu SC and Nemiroff MJ. Mass carbon monoxide poisoning: clinical effects and results of treatment in 184 victims. Ann.Emerg.Med., 1982. 11: p. 394-399. return 38. Dolan MC et al. Carboxyhemoglobin levels in patients with flu-like symptoms. Ann.Emerg.Med., 1986. 15: p. 653. return 39. Fisher J and Rubin KP. Occult carbon monoxide poisoning. Arch.Intern.Med., 1982. 142: p. 1270-1271. return 40. Grace TW and Platt FW. Subacute carbon monoxide poisoning. JAMA, 1981. 246: p. 1698-1700. return 41. Heckerling PS, et al. Predictors of occult carbon monoxide poisoning in patients with headache and dizziness. Ann.Internal.Med., 1987. 107: p. 174-176 return 42. Heckerling PS, Leikin JB and Maturen A. Occult carbon monoxide poisoning: validation of a prediction model. Am.J.Med., 1988. 84: p. 251-256. return 43. Heckerling PS, et al. Occult carbon monoxide poisoning in patients with neurologic illness. J Toxicol Clin Toxicol, 1990. 28(1): p. 29-44. return 44. Kirkpatrick JN. Occult carbon monoxide poisoning. West.J.Med., 1987. 146: p. 52-56. return 45. Crocker PJ and Walker JS. Pediatric carbon monoxide toxicity. J.Emerg.Med., 1985. 3: p. 443-448. return 46. Choi S. Delayed neurologic sequelae in carbon monoxide intoxication. Arch.Neurol., 1983. 40: p. 433-435. return 47. Scharf SM, Thames MD and Sargent RK. Transmural myocardial infarction after exposure to carbon monoxide in coronary-artery disease. Report of a case. N Engl J Med, 1974. 291(2): p. 85-6. return 48. Anderson EW, et al. Effects of low-level carbon monoxide exposure on onset and duration of angina pectoris. Ann.Intern.Med., 1973. 79: p. 46-50. return 49. Marek Z and Piejko M. Circulatory failure in acute carbon monoxide poisoning. Forensic Sci, 1972. 1(4): p. 419- 25. return 50. Hubalewska A., et al. Clinical status of carbon-monoxide- poisoned patients and the results of rest 99mTc-MIBI and 99mTc-Amiscan heart scintigraphy performed in the acute phase of intoxication and stress-rest 99mTc-MIBI scintigraphy six month later. Przegl Lek, 2004. 61(4): p. 213-6. return 51. Allred FN, et al. Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease. N.Eng.J.Med., 1989. 321: p. 1426-1432. return 52. Cramlet SH, Erickson HH and Gorman HA. Ventricular function following acute carbon monoxide exposure. J.Appl.Physiol., 1975. 39: p. 482-486. return 53. Favory R, et al. Myocardial dysfunction and potential cardiac hypoxia in rats induced by carbon monoxide inhalation. Am J Respir Crit Care Med, 2006. 174(3): p. 320-5 return 54. Satran D, et al. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Coll Cardiol, 2005. 45(9): p. 1513-6. return 55. Henry CR, et al. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. Jama, 2006. 295(4): p. 398-402. return 56. Biasucci LM, et al. Intracellular neutrophil myeloperoxidase is reduced in unstable angina and acute myocardial infarction, but its reduction is not related to ischemia. J Am Coll Cardiol, 1996. 27(3): p. 611-6. return 57. Furman MI, et al. Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease. J Am Coll Cardiol, 1998. 31(2): p. 352-8. return 58. Ott I, et al. Increased neutrophil-platelet adhesion in patients with unstable angina. Circulation, 1996. 94(6): p. 1239-46. return 59. Myers R, Snyder S and Emhoff T, Subacute sequelae of carbon monoxide poisoning. Ann.Emerg.Med., 1985. 14: p. 1163-1167. return 60. Torne R, et al. Skin lesions in carbon monoxide intoxication. Dermatologica, 1991. 183(3): p. 212-5. return 61. Perrone J and Hoffman RS. Falsely elevated carboxyhemoglobin levels secondary to fetal hemoglobin. Acad Emerg Med, 1996. 3(3): p. 287-9. return 62. Swank G, et al. Carbon monoxide poisoning: a case report of reversible cardiormyopathy. W V Med J, 2004. 100(6): p. 228-31. return 63. Johnson CD. Carbon monoxide toxicity with neurological and cardiac complications. Bol Asoc Med P R, 2005. 97(4): p. 315-22.return return 64. Pach D, et al. B-type natriuretic peptide plasma concentration in acutely poisoned patients. Przegl Lek, 2005. 62(6): p. 465-7. return 65. Ferrier D, et al. Magnetic resonance features in carbon monoxide poisoning. Can Assoc Radiol J, 1994. 45(6): p. 466-8. return 66. Tuchman RF, Moser FG and Moshe SL. Carbon monoxide poisoning: bilateral lesions in the thalamus on MR imaging of the brain. Pediatr.Radiol., 1990. 20: p. 478-479. return 67. Kawanami T, et al. The pallidoreticular pattern of brain damage on MRI in a patient with carbon monoxide poisoning. J Neurol Neurosurg Psychiatry, 1998. 64(2): p. 282. return 68. Porter SS, et al. Corpus callosum atrophy and neuropsychological outcome following carbon monoxide poisoning. Arch Clin Neuropsychol, 2002. 17(2): p. 195-204. return 69. Kesler SR, et al. Verbal memory deficits associated with fornix atrophy in carbon monoxide poisoning. J Int Neuropsychol Soc, 2001. 7(5): p. 640-6. return 70. Gale S, et al. MRI,quantitative MRI, SPECT, and neuropsychological findings following carbon monoxide poisoning. Brain Injury, 1999. 13(4): p. 229-243. return 71. Parkinson R, et al. White matter hyperintensities and neuropsychological outcome following carbon monoxide poisoning. Neurology, 2002. 58: p. 1525-1532. return 72. Pace N, Strajman E and Walker EL. Acceleration of carbon monoxide elimination in man by high pressure oxygen. Science, 1950. 111: p. 652-654. return 73. Peterson JE and Stewart RD. Absorption and elimination of carbon monoxide by inactive young men. Arch Environ Health, 1970. 21(2): p. 165-71. return 74. Rood W. Carbon Monoxide. Handbook of Physiology, ed. W. Fenn and H. Rahn. Vol. II, Sect. 3. 1965, Washington DC: American Physiological Society. return 75. Weaver L, et al. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest, 2000. 117: p. 801-808. return 76. Jay GD, et al. Portable hyperbaric oxygen therapy in the emergency department with the modified Gamow bag. Ann Emerg Med, 1995. 26(6): p. 707-11. return 77. Myers R, Jones D and Britten J. Carbon monoxide half-life study. Proceedings of the Eighth International Congress on Hyperbaric Medicine, ed. E. Kindwall. 1987, Flagstaff, AZ: Best Publishing. 263-266. return 78. Dolinay T, et al. Inhaled carbon monoxide confers antiinflammatory effects against ventilator-induced lung injury. Am J Respir Crit Care Med, 2004. 170(6): p. 613-20. return 79. Brown SD and Piantadosi CA. Recovery of energy metabolism in rat brain after carbon monoxide hypoxia. J.Clin.Invest., 1991. 89: p. 666-672. return 80. Thom SR. Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen. Toxicol Appl Pharmacol, 1990. 105(2): p. 340-4. return 81. Thom SR. Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. Toxicol Appl Pharmacol, 1993. 123(2): p. 248-56. return 82. End E and Long CW. Oxygen under pressure in carbon monoxide poisoning. J.Ind.Hyg.Toxicol., 1942. 24: p. 302- 306. return 83. Peirce EC 2nd, et al. Carbon monoxide poisoning: experimental hypothermic and hyperbaric studies. Surgery, 1972. 72(2): p. 229-37. return 84. Thom SR, Bhopale VM and Fisher D. Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity. Toxicol Appl Pharmacol, 2006. 213(2): p. 152-9. return 85. Logue C. Hyperbaric Oxygen for Carbon Monoxide Poisoning, in Letter to the Editor, C. Review, Editor. 2006. return 86. Ducasse JL, Celsis P and Marc-Vergnes JP. Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea.and.Hyperbaric.Med., 1995. 22: p. 9-15. return 87. Scheinkestel C, et al., Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. MJA, 1999. 170: p. 203-209. return 88. Raphael JC, et al. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet, 1989: p. 414-419. return 89. Thom SR, et al. Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann Emerg Med, 1995. 25(4): p. 474-80. return 90. TWeaver LK, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med, 2002. 347(14): p. 1057-67. return 91. Junker C, et al. The CONSORT statement. JAMA, 1996. 276(23): p. 1876-7; author reply 1877. return 92. JSchiltz KL. Failure to assess motivation, need to consider psychiatric variables, and absence of comprehensive examination: a skeptical review of neuropsychologic assessment in carbon monoxide research. Undersea Hyperb Med, 2000. 27(1): p. 48-50. return 93. Raphael J, et al. Managing carbon monoxide poisoning with hyperbaric oxygen. J. Toxicol. Clin. Toxicol., 2004. 42: p. 455-456.return 94. Brown SD and Piantadosi CA. Hyperbaric oxygen for carbon monoxide poisoning. The.Lancet, 1989: p. 1032-1033. return 95. JGorman D, Gilligan J and Clayton D. Hyperbaric oxygen for carbon monoxide poisoning (letter). Lancet, 1989. 2: p. 1032. return 96. Goulon M, et al. Intoxication oxycarbonee et anoxie aigue par 7inhalation de gaz de charbon et d'hydrocarbures. Ann.Med.Interne.(Paris.), 1969. 120: p. 335-349. return |
|||||
|
Download printer friendly version --> |
 |
||||
|
NEWS SEARCH CONTENTS MEDITORIAL ASK DISCUSS REGISTER HELP HOME |
||||||
© 2008 interMDnet Corporation. All Rights Reserved. PRIVACY POLICY |
||||||
Dark patches of skin above the temples may be a sign of Giant Cell
Arteritis, a serious, though treatable, condition. 