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* Levels of oxygen available for tissue use are decreased. This situation is described as CO shifting the [[oxygen-hemoglobin dissociation curve|oxygen dissociation curve]] to the left. Blood oxygen content is actually increased in the case of carbon monoxide poisoning; because all the oxygen is in the blood, none is being given to the tissues, and this causes tissue hypoxic injury.
* Levels of oxygen available for tissue use are decreased. This situation is described as CO shifting the [[oxygen-hemoglobin dissociation curve|oxygen dissociation curve]] to the left. Blood oxygen content is actually increased in the case of carbon monoxide poisoning; because all the oxygen is in the blood, none is being given to the tissues, and this causes tissue hypoxic injury.
[[File:Hemoglobin saturation curve.svg.png|thumb|left|369x369px|CO dissociation curve [https://commons.wikimedia.org/wiki/File:Hemoglobin_saturation_curve.svg Source:Case courtesy of By Hazmat2, via Wikimedia Commons]]]
[[File:Hemoglobin saturation curve.svg.png|thumb|right|369x369px|CO dissociation curve [https://commons.wikimedia.org/wiki/File:Hemoglobin_saturation_curve.svg Source:Case courtesy of By Hazmat2, via Wikimedia Commons]]]
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=== 2) CO and Myoglobin ===
=== 2) CO and Myoglobin ===

Revision as of 17:20, 22 February 2018

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Resident
Survival
Guide
Carbon monoxide poisoning
Spacefilling model of Carbon monoxide.
ICD-10 T58
ICD-9 986
DiseasesDB 2020
MedlinePlus 002804
eMedicine emerg/817 
MeSH C21.613.455.245

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [5] Fatima Shaukat, MD [6]

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Overview

Carbon monoxide poisoning occurs after the inhalation of carbon monoxide gas. Carbon monoxide (CO) is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Carbon monoxide is colorless, odorless, tasteless, and non-irritating, making it difficult for people to detect.

Carbon monoxide is a significantly toxic gas with poisoning being the most common type of fatal poisoning in many countries.[1] Symptoms of mild poisoning include headaches and flu-like effects; larger exposures can lead to significant toxicity of the central nervous system and heart. Following poisoning, long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of a pregnant woman.

The mechanisms by which carbon monoxide produces toxic effects are not yet fully understood, but hemoglobin, myoglobin, and mitochondrial cytochrome oxidase are thought to be compromised. Treatment largely consists of administering 100% oxygen or hyperbaric oxygen therapy, although the optimum treatment remains controversial.[2] Domestic carbon monoxide poisoning can be prevented by the use of household carbon monoxide detectors.

Historical perspective

  • Carbon monoxide poisoning may manifests as lethargy, fatigue and tiredness, depression, memory loss, emotional disturbance and visual/auditory hallucinations.
  • In a few cases, it was associated with 'haunted houses' where the residents experienced strange sounds and visions, feelings of dread, sudden onset illness and death of all the members in the house.
  • In 1921, Dr. William Wilmer, an ophthalmologist published a case in American journal of ophthalmology in which he described the experiences of a family with similar symptoms as mentioned above. [3]
  • In 2005, a report was published describing a young female of age 23, found delirious and hyperventilating, as a result of leakage and accumulation of gas from the heater . She believed to have seen a 'ghost' in the shower. [4]

Sources

  • Main sources of CO that are responsible for environmental pollution are house hold fires, heaters, furnaces, motor vehicle exhaust, propane fueled equipment i.e.ice resurfacers,[5] forklifts,[6] and engine-driven generators and wood burning stove.
  • CO poisoning can also occur in scuba diving due to malfunctioning diving air compressors.
  • Another source is exposure to the organic solvent methylene chloride, which is metabolized to CO by the body.[7]
  • Polluted air often contains unhealthy levels of carbon monoxide. Many areas of the US have struggled to achieve legislated limits. Significant advances have been made since the implementation by 1990 of a vehicle emissions limit of 3.4 gpm (grams per mile), a large reduction from the previous limit of 87 gpm. [7] [8] [9] [10]

Pathophysiology

The precise mechanisms by which toxic effects are induced by CO are not fully understood. It may damage the body in one of the following ways:[8]

  • Binds to hemoglobin thus reducing oxygen transportation in blood[9]
  • Binds with myoglobin to decrease its oxygen storage capacity[10]
  • Reacts with mitochondrial cytochrome oxidase (specifically cytochrome C) hence inhibiting cellular respiration.[11]

1) CO and Hemoglobin

  • Carbon monoxide has a significant affinity to the iron sites in hemoglobin, the principal oxygen-carrying compound in blood. The affinity between carbon monoxide and hemoglobin is 240 times stronger than the affinity between hemoglobin and oxygen.
  • CO binds to hemoglobin, producing carboxyhemoglobin (COHb) - the traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen-carrying capacity of the blood. This inhibits the transport, delivery, and utilization of oxygen.[12]
  • Because hemoglobin is a tetramer with four oxygen binding sites, binding of CO at one of these sites also increases the oxygen affinity of the remaining 3 sites, which interferes with normal release of oxygen. This causes hemoglobin to retain oxygen that would otherwise be delivered to the tissue.[13]
  • Levels of oxygen available for tissue use are decreased. This situation is described as CO shifting the oxygen dissociation curve to the left. Blood oxygen content is actually increased in the case of carbon monoxide poisoning; because all the oxygen is in the blood, none is being given to the tissues, and this causes tissue hypoxic injury.
CO dissociation curve Source:Case courtesy of By Hazmat2, via Wikimedia Commons


2) CO and Myoglobin

  • CO has 60 times greater affinity to myoglobin as compared to oxygen. It can bind readily to myoglobin, which is another heme containing protein, abundantly present in the muscles of body.
  • Binding of CO to myoglobin markedly reduces its oxygen carrying capacity, leading to decrease in cardiac output, hypotension which ultimately caused brain ischemia
  • CO bound to myolobin is later released in the body, which subsequently binds with the hemoglobin. This phenomenon is responsible for delayed return of symptoms in CO poisoning. [14]

3) CO and Mitochondrial Cytochrome oxidase C

  • CO has lesser affinity with cytochrome oxidase C in mitochondria than oxygen so the damage occurs only in the setting of significant hypoxia.
  • CO damages the cell by interfering with aerobic metabolism and synthesis of ATP, which leads to shifting of metabolism to anaerobic and accumulation of lactic acid intracellularly with significant anoxia. This ultimately leads to cell death and necrosis.
  • Once CO is bound to cytochrome oxidase C, the rate of dissociation is very slow. Hence causing prolonged damage to oxidaive metabolism in the cell.[15]

Epidemiology & Demographics

  • Carbon monoxide poisoning is the most common type of fatal poisoning in France and the United States. It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States.[16]
  • In many industrialized countries, carbon monoxide may be the cause of greater than 50% of fatal poisonings.
  • In the U.S., about 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment. The CDC reports, "Each year, more than 500 Americans die from unintentional CO poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves."[17]

CO and Suicide

  • Carbon monoxide in town gas emerged as a common mean of suicide by poisoning, since the placement of strict legal restrictions on poisons like Cyanide and arsenic.
  • Suicide was also often committed by inhaling exhaust fumes of running car engines. In the past, motor car exhaust may have contained up to 25% carbon monoxide. However, newer cars have catalytic converters, which can eliminate over 99% of carbon monoxide produced.[18] However, even cars with catalytic converters can produce substantial carbon monoxide if an idling car is left in an enclosed space. This is due to reduced oxygen availability, and therefore, less efficient combustion.
  • As carbon monoxide poisoning via car exhaust has become less of a suicide option, there has been an increase in new methods of carbon monoxide poisoning such as burning charcoal or other fossil fuels within a confined space, such as a small room, tent, or car.[19]

Toxicity

Carbon monoxide is a significantly toxic gas, although patients may demonstrate varied clinical manifestations with different outcomes, even under similar exposure conditions.[20] Toxicity is also increased by several factors, including: increased activity and rate of ventilation, pre-existing cerebral or cardiovascular disease, reduced cardiac output, anemia or other hematological disorders, decreased barometric pressure, and high metabolic rate.

Under ordinary conditions, it is less dense than air, but during fires, it accumulates on the ground, so that if poisoning causes loss of consciousness, the amount of carbon monoxide inhaled increases and the possibility of fatality is radically increased.

Carbon monoxide is life-threatening to humans and other forms of air-breathing life, as inhaling even relatively small amounts of it can lead to hypoxic injury, neurological damage, and possibly death. A concentration of as little as 0.04% (400 parts per million) carbon monoxide in the air can be fatal. The gas is especially dangerous because it is not easily detected by human senses. Early symptoms of carbon monoxide poisoning include drowsiness and headache, followed by unconsciousness, respiratory failure, and death. First aid for a victim of carbon monoxide poisoning requires access to fresh air; administration of artificial respiration and, if available, oxygen; and, as soon as possible, medical attention.

When carbon monoxide is inhaled, it takes the place of oxygen in hemoglobin, the red blood pigment that normally carries oxygen to all parts of the body. Because carbon monoxide binds to hemoglobin several hundred times more strongly than oxygen, its effects are cumulative and long-lasting, causing oxygen starvation throughout the body. Prolonged exposure to fresh air (or pure oxygen) is required for the CO-tainted hemoglobin (carboxyhemoglobin) to clear.

The effects of carbon monoxide in parts per million are listed below:

  • 35 ppm (0.0035%) Headache and dizziness within six to eight hours of constant exposure
  • 100 ppm (0.01%) Slight headache in two to three hours
  • 200 ppm (0.02%) Slight headache within two to three hours
  • 400 ppm (0.04%) Frontal headache within one to two hours
  • 800 ppm (0.08%) Dizziness, nausea, and convulsions within 45 minutes. Insensible within two hours.
  • 1,600 ppm (0.16%) Headache, dizziness, and nausea within 20 minutes. Death in less than two hours.
  • 3,200 ppm (0.32%) Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes.
  • 6,400 ppm (0.64%) Headache and dizziness in one to two minutes. Death in less than 20 minutes.
  • 12,800 ppm (1.28%)Unconsciousness after 2-3 breaths. Death in less than three minutes.

In addition, a recent report concludes that carbon monoxide exposure can lead to significant loss of lifespan after exposure due to damage to the heart muscle. [21]

Carboxyhaemoglobin

Levels of carbon monoxide bound in the blood can be determined by measuring carboxyhaemoglobin, which is a stable complex of carbon monoxide and hemoglobin that forms in red blood cells. Carbon monoxide is produced normally in the body, establishing a low background carboxyhaemoglobin saturation. Carbon monoxide also functions as a neurotransmitter. Normal carboxyhemoglobin levels in an average person are less than 5%, whereas cigarette smokers (two packs/day) may have levels up to 9%.[22]

Serious toxicity is often associated with carboxyhemoglobin levels above 25%, and the risk of fatality is high with levels over 70%. Still, no consistent dose response relationship has been found between carboxyhemoglobin levels and clinical effects.[23] Therefore, carboxyhemoglobin levels are more guides to exposure levels than effects as they do not reliably predict clinical course or short- or long-term outcome.[24]


Symptoms

Acute

This often makes the diagnosis of carbon monoxide poisoning difficult. If suspected, the diagnosis can be confirmed by measurement of blood carboxyhemoglobin. The main manifestations of poisoning develop in the organ systems most dependent on oxygen use: the central nervous system and the heart. The clinical manifestations include :

  • Skin lesions
  • Visual and auditory problems

One of the major concerns following CO poisoning is the severe neurological manifestations that may occur days or even weeks after an acute poisoning. Common problems encountered are

  • Difficulty with higher intellectual functions and short-term memory
  • Irritability
  • Speech disturbances

Chronic

Long term, repeat exposures present a greater risk to persons with coronary heart disease and in pregnant patients.[28] Chronic exposure may increase the incidence of cardiovascular symptoms in some workers, such as motor vehicle examiners, firefighters, and welders. Patients often complain of persistent headaches, lightheadedness, depression, confusion, and nausea. Upon removal from exposure, the symptoms usually resolve themselves.[29]

Treatment

First aid for carbon monoxide poisoning is to immediately remove the victim from the exposure without endangering oneself, call for help, and apply CPR if needed. The main medical treatment for carbon monoxide poisoning is breathing 100% oxygen by a tight fitting oxygen mask. Oxygen hastens the dissociation of carbon monoxide from hemoglobin, improving tissue oxygenation by reducing its biological half-life. Hyperbaric oxygen is also used in the treatment of CO poisoning; hyperbaric oxygen also increases carboxyhemoglobin dissociation and does so to a greater extent than normal oxygen. Hyperbaric oxygen may also facilitate the dissociation of CO from cytochrome oxidase.

A significant controversy in the medical literature is whether or not hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen in terms of increased survival or improved long term outcomes. There have been clinical trials[24][30][31][32][33][34] in which the two treatment options have been compared; of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen. Some of these trials have been criticized for apparent flaws in their implementation.[35][36][37] A recent robust review of all the literature on carbon monoxide treatment concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a clinically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.[2]

Further specific treatment for other complications such as seizure, cardiac abnormalities, pulmonary edema, and acidosis may be required. The delayed development of neuropsychiatric impairment is one of the most serious complications of poisoning, with extensive follow up and treatment often being required.

Prevention

Prevention remains a vital public health issue, requiring public education on the safe operation of appliances, heaters, fireplaces, and internal-combustion engines, as well as increased emphasis on the installation of carbon monoxide detectors. Carbon monoxide alarms are usually installed in homes around heaters and other equipment. If a high level of CO is detected, the device sounds an alarm, giving people in the area a chance to ventilate the area or safely leave the building. Unlike smoke detectors, they do not need to be placed near ceiling level. The Consumer Product Safety Commission says that "carbon monoxide detectors are as important to home safety as smoke detectors are," and recommends that each home should have at least one carbon monoxide detector.[38]

The devices, which retail for USD $20-$60 and are widely available, can either be battery-operated or AC powered (with or without a battery backup). Since CO is colorless and odorless (unlike smoke from a fire), detection in a home environment is impossible without such a warning device. Some state and municipal governments, including those of Ontario, Canada, and New York City, require installation of CO detectors in new units. Massachusetts and Illinois began to require a detector in all residences on January 1, 2007.[39][40] The carbon monoxide can be easily detected by the filtering paper impregnated by the solution of the palladium chloride. Carbon monoxide reduces the palladium monoxide to the black metallic palladium. This reaction is very sensitive.

See also

Resources

Template:Poisoning and toxicity

References

  1. ↑ Omaye ST. (2002). "Metabolic modulation of carbon monoxide toxicity". Toxicology. 180 (2): 139–50. PMID 12324190.
  2. ↑ 2.0 2.1 Buckley NA, Isbister GK, Stokes B, Juurlink DN. (2005). "Hyperbaric oxygen for carbon monoxide poisoning : a systematic review and critical analysis of the evidence". Toxicol Rev. 24 (2): 75–92. PMID 16180928.
  3. ↑ [1]
  4. ↑ Jiann-Ruey Ong, Sheng-Wen Hou, Hsien-Tsung Shu, Huei-Tsair Chen, and Chee-Fah Chong. Diagnostic pitfall: carbon monoxide poisoning mimicking hyperventilation syndrome. The American Journal of Emergency Medicine Volume 23, Issue 7 , November 2005, Pages 903-904
  5. ↑ Johnson C, Moran J, Paine S, Anderson H, Breysse P (1975). "Abatement of toxic levels of carbon monoxide in Seattle ice-skating rinks". Am J Public Health. 65 (10): 1087–90. PMID 1163706.
  6. ↑ Fawcett T, Moon R, Fracica P, Mebane G, Theil D, Piantadosi C (1992). "Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts". J Occup Med. 34 (1): 12–5. PMID 1552375.
  7. ↑ Kubic VL, Anders MW. (1975). "Metabolism of dihalomethanes to carbon monoxide. II. In vitro studies". Drug Metab Dispos. 3 (2): 104–12. PMID 236156.
  8. ↑ Brunori M, Bonaventura J, Bonaventura C, Antonini E, Wyman J (1972). "Carbon monoxide binding by hemoglobin and myoglobin under photodissociating conditions". Proc Natl Acad Sci U S A. 69 (4): 868–71. PMC 426583. PMID 4502938.
  9. ↑ Culnan DM, Craft-Coffman B, Bitz GH, Capek KD, Tu Y, Lineaweaver WC; et al. (2018). "Carbon Monoxide and Cyanide Poisoning in the Burned Pregnant Patient: An Indication for Hyperbaric Oxygen Therapy". Ann Plast Surg. doi:10.1097/SAP.0000000000001351. PMID 29461288.
  10. ↑ Lim M, Jackson TA, Anfinrud PA (1995). "Binding of CO to myoglobin from a heme pocket docking site to form nearly linear Fe-C-O". Science. 269 (5226): 962–6. PMID 7638619.
  11. ↑ Alonso JR, Cardellach F, López S, Casademont J, Miró O (2003). "Carbon monoxide specifically inhibits cytochrome c oxidase of human mitochondrial respiratory chain". Pharmacol Toxicol. 93 (3): 142–6. PMID 12969439.
  12. ↑ Haldane J. (1895). "The action of carbonic oxide on man". J Physiol. 18: 430–62.
  13. ↑ Gorman D, Drewry A, Huang YL, Sames C. (2003). "The clinical toxicology of carbon monoxide". Toxicology. 187 (1): 25–38. PMID 12679050.
  14. ↑ Omaye ST (2002). "Metabolic modulation of carbon monoxide toxicity". Toxicology. 180 (2): 139–50. PMID 12324190.
  15. ↑ Blumenthal I (2001). "Carbon monoxide poisoning". J R Soc Med. 94 (6): 270–2. PMC 1281520. PMID 11387414.
  16. ↑ Hampson NB. (1998). "Emergency department visits for carbon monoxide poisoning in the Pacific Northwest". J Emerg Med. 16 (5): 695–8. PMID 9752939.
  17. ↑ [2]
  18. ↑ Vossberg B, Skolnick J. (1999). "The role of catalytic converters in automobile carbon monoxide poisoning: a case report". Chest. 115 (2): 580–1. PMID 10027464.
  19. ↑ Chung WS, Leung CM. (2001). "Carbon monoxide poisoning as a new method of suicide in Hong Kong". Psychiatr Serv. 52 (6): 836–7. PMID 11376237.
  20. ↑ Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. (2000). "Carbon monoxide poisoning-a public health perspective". Toxicology. 145 (1): 1–14. PMID 10771127.
  21. ↑ Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD, MD (2006). "Myocardial Injury and Long-term Mortality Following Moderate to Severe Carbon Monoxide Poisoning". JAMA. 295: 398–402. Abstract
  22. ↑ Ford MD, Delaney KA, Ling LJ, Erickson T., ed. (2001). Clinical toxicology. WB Saunders Company. ISBN 0-7216-5485-1.
  23. ↑ Hardy KR, Thom SR. (1994). "Pathophysiology and treatment of carbon monoxide poisoning". J Toxicol Clin Toxicol. 32 (6): 613–29. PMID 7966524.
  24. ↑ 24.0 24.1 Scheinkestel CD, Bailey M, Myles PS, Jones K, Cooper DJ, Millar IL, Tuxen DV. (1999). "Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial". Med J Aust. 170 (5): 203–10. PMID 10092916.
  25. ↑ Ilano AL, Raffin TA. (1990). "Management of carbon monoxide poisoning". Chest. 97 (1): 165–9. PMID 2403894.
  26. ↑ Choi IS. (2001). "Carbon monoxide poisoning: systemic manifestations and complications". J Korean Med Sci. 16 (3): 253–61. PMID 11410684.
  27. ↑ Roohi F, Kula RW, Mehta N. (2001). "Twenty-nine years after carbon monoxide intoxication". Clin Neurol Neurosurg. 103 (2): 92–5. PMID 11516551.
  28. ↑ Allred EN, Bleecker ER, Chaitman BR, Dahms TE, Gottlieb SO, Hackney JD, Pagano M, Selvester RH, Walden SM, Warren J. (1989). "Short-term effects of carbon monoxide exposure on the exercise performance of subjects with coronary artery disease". N Engl J Med. 321 (21): 1426–32. PMID 2682242.
  29. ↑ Fawcett TA, Moon RE, Fracica PJ, Mebane GY, Theil DR, Piantadosi CA. (1992). "Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts". J Occup Med. 34 (1): 12–5. PMID 1552375.
  30. ↑ Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB. (1995). "Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen". Ann Emerg Med. 25 (4): 474–80. PMID 7710151.
  31. ↑ Raphael JC, Elkharrat D, Jars-Guincestre MC, Chastang C, Chasles V, Vercken JB, Gajdos P. (1989). "Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication". Lancet. 2 (8660): 414–9. PMID 2569600.
  32. ↑ Ducasse JL, Celsis P, Marc-Vergnes JP. (1995). "Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation?". Undersea Hyperb Med. 22 (1): 9–15. PMID 7742714. Text " pdf" ignored (help)
  33. ↑ Mathieu D, Mathieu-Nolf M, Durak C, Wattel F, Tempe JP, Bouachour G, Sainty JM. (1996). "Randomized prospective study comparing the effect of HBO vs 12 hours NBO in non-comatose CO-poisoned patients: results of the preliminary analysis". Undersea Hyperb Med. 23: 7.
  34. ↑ Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH. (2002). "Hyperbaric oxygen for acute carbon monoxide poisoning". N Engl J Med. 347 (14): 1057–67. PMID 12362006.
  35. ↑ Gorman DF. (1999). "Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Unfortunate methodological flaws". Med J Aust. 170 (11): 563. PMID 10397050.
  36. ↑ Scheinkestel CD, Jones K, Myles PS, Cooper DJ, Millar IL, Tuxen DV. (2004). "Where to now with carbon monoxide poisoning?". Emerg Med Australas. 16 (2): 151–4. PMID 15239731.
  37. ↑ Isbister GK, McGettigan P, Harris I. (2003). "Hyperbaric oxygen for acute carbon monoxide poisoning". N Engl J Med. 348 (6): 557–60. PMID 12572577.
  38. ↑ [3]
  39. ↑ Massachusetts General Laws, Chapter 148, Section 26F 1/2. Also known as "Nicole's Bill". Enacted November 4, 2005.
  40. ↑ Illinois Public Act 094-0741. Effective 01/01/2007.

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