Delayed Carbon Monoxide Poisoning
Identifying and treating delayed carbon monoxide poisoning is often hidden in plain sight and not recognized by many in the medical profession. This problem is often “occult” (hidden) and is common but not recognized.
“Misdiagnosing CO poisoning is common in the initial evaluation and management of the CO. Other diagnostic considerations include psychiatric illness, migraine headaches, stroke, acute alcohol intoxication, heart disease, flu, or even food poisoning. Chronic symptoms may present as flu-like illness, headaches, tearfulness, depression, agitation, anxiety, decreased memory, attentional and concentration skills, reduced coordination, poor reasoning skills, irritability, euphoria, and overall personality changes. Fatigue, headaches and dizziness are the three most common symptoms.” (1)
If you or your loved one have any of these symptoms, even months after “smoke inhalation,” then you must consult a specialist physician. The diagnosis is complex but the treatment is simple – HBOT. To assist you and your physician, please download the excellent four page medical descriptions of this confusing ailment click here to download.
(1) “Carbon Monoxide: Identification of Delayed Sequelae and Occult Exposure” — J. Thomas Millington, M.D. Joel Ellenswig, M.D. Karen L Shiltz, PHD
Identifying and treating delayed carbon monoxide poisoning is often hidden in plain sight and not recognized by many in the medical profession. This problem is often “occult” (hidden) and is common but not recognized.
“Misdiagnosing CO poisoning is common in the initial evaluation and management of the CO. Other diagnostic considerations include psychiatric illness, migraine headaches, stroke, acute alcohol intoxication, heart disease, flu, or even food poisoning. Chronic symptoms may present as flu-like illness, headaches, tearfulness, depression, agitation, anxiety, decreased memory, attentional and concentration skills, reduced coordination, poor reasoning skills, irritability, euphoria, and overall personality changes. Fatigue, headaches and dizziness are the three most common symptoms.” (1)
If you or your loved one have any of these symptoms, even months after “smoke inhalation,” then you must consult a specialist physician. The diagnosis is complex but the treatment is simple – HBOT. To assist you and your physician, please download the excellent four page medical descriptions of this confusing ailment click here to download.
(1) “Carbon Monoxide: Identification of Delayed Sequelae and Occult Exposure” — J. Thomas Millington, M.D. Joel Ellenswig, M.D. Karen L Shiltz, PHD
Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen - Thom SR; Taber RL; Mendiguren II; Clark JM; Hardy KR; Fisher AB
University of Pennsylvania Medical Center, Institute for Environmental Medicine, Philadelphia.
Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen.Ann Emerg Med. 1995; 25(4):474-80 (ISSN: 0196-0644)Thom SR; Taber RL; Mendiguren II; Clark JM; Hardy KR; Fisher AB
University of Pennsylvania Medical Center, Institute for Environmental Medicine, Philadelphia.
STUDY OBJECTIVE: Carbon monoxide (CO) poisoning is a major clinical problem. The risk of morbidity and the most effective treatment have not been clearly established. We measured the incidence of delayed neurologic sequelae (DNS) in a group of patients acutely poisoned with CO and tested the null hypothesis that the incidence would not be affected by treatment with hyperbaric oxygen (HBO). DESIGN: We conducted a prospective, randomized study in patients with mild to moderate CO poisoning who presented within 6 hours. Patients had no history of loss of consciousness or cardiac instability. INTERVENTIONS: The incidence of DNS was compared between groups treated with ambient pressure 100% oxygen or HBO (2.8 ATA for 30 minutes followed by 2.0 ATA oxygen for 90 minutes). DNS were defined as development of new symptoms after oxygen treatment plus deterioration on one or more subtests of a standardized neuropsychologic screening battery. RESULTS: In 7 of 30 patients (23%), DNS developed after treatment with ambient-pressure oxygen, whereas no sequelae developed in 30 patients after HBO treatment (P < .05). DNS occurred 6 +/- 1 (mean +/- SE) days after poisoning and persisted 41 +/- 8 days. At follow-up 4 weeks after poisoning, patients who had been treated with ambient pressure oxygen and had not sustained DNS exhibited a worse mean score on one subtest, Trail Making, compared with the group treated with HBO and with a control group matched according to age and education level. There were no differences in scores between the control group and the hyperbaric oxygen group. CONCLUSION: DNS after CO poisoning cannot be predicted on the basis of a patient's clinical history or CO level. HBO treatment decreased the incidence of DNS after CO poisoning.
University of Pennsylvania Medical Center, Institute for Environmental Medicine, Philadelphia.
STUDY OBJECTIVE: Carbon monoxide (CO) poisoning is a major clinical problem. The risk of morbidity and the most effective treatment have not been clearly established. We measured the incidence of delayed neurologic sequelae (DNS) in a group of patients acutely poisoned with CO and tested the null hypothesis that the incidence would not be affected by treatment with hyperbaric oxygen (HBO). DESIGN: We conducted a prospective, randomized study in patients with mild to moderate CO poisoning who presented within 6 hours. Patients had no history of loss of consciousness or cardiac instability. INTERVENTIONS: The incidence of DNS was compared between groups treated with ambient pressure 100% oxygen or HBO (2.8 ATA for 30 minutes followed by 2.0 ATA oxygen for 90 minutes). DNS were defined as development of new symptoms after oxygen treatment plus deterioration on one or more subtests of a standardized neuropsychologic screening battery. RESULTS: In 7 of 30 patients (23%), DNS developed after treatment with ambient-pressure oxygen, whereas no sequelae developed in 30 patients after HBO treatment (P < .05). DNS occurred 6 +/- 1 (mean +/- SE) days after poisoning and persisted 41 +/- 8 days. At follow-up 4 weeks after poisoning, patients who had been treated with ambient pressure oxygen and had not sustained DNS exhibited a worse mean score on one subtest, Trail Making, compared with the group treated with HBO and with a control group matched according to age and education level. There were no differences in scores between the control group and the hyperbaric oxygen group. CONCLUSION: DNS after CO poisoning cannot be predicted on the basis of a patient's clinical history or CO level. HBO treatment decreased the incidence of DNS after CO poisoning.
Brief Narrative Summary of Key Indication-Specific Literature - ACUTE CARBON MONOXIDE INTOXICATION
Prepared for the Health Care Financing Administration (Medicare)
~ Medicare Coverage Issues Manual 35-10
Dick Clarke, CHT
Program Director, Hyperbaric Medicine Service
Palmetto Richland Memorial Hospital
Columbia, South Carolina
ACUTE CARBON MONOXIDE INTOXICATION
Bartlett, R: Carbon monoxide poisoning. Clinical management of poisoning and drug overdose. WB Saunders, Lester M Haddad, James F Winchester editors; 3rd edition; 1997
General review article, emphasizing both the modern appreciation of the complex pathophysiology involved, and the multifactorial benefits of HBO therapy.
Thom, SR: Carbon monoxide-mediated brain lipid peroxidation in the rat. J. Appl. Physiol. 1990;68(3): 997-1003
A publication that advanced the pathophysiology of CO poisoning from the simple concept of inhibition of hemoglobin function. This data indicates that critical cellular toxicity occurs.
Thom, SR: Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen. Toxicol. Appl. Pharmacol. 1990; 105: 340-344
In reference to the above elucidation of a cellular poisoning, this companion study demonstrates the ability of HBO therapy to inhibit the toxic process.
Thom, SR: Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol. Appl. Pharmacol. 1993; 123: 243-247
Recent evidence of complex tissue injury, here involving a leukocyte -mediated brain injury as a result of acute CO poisoning.
Thom, SR: Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon- monoxide-mediated brain injury in rats. Toxicol. Appl. Pharmacol. 1993; 123: 248-256
A companion article to that pathophysiology noted in the previous article. This research demonstrates the functional inhibition of leukocytes by HBO therapy, thereby antagonizing CO medicated oxidative brain injury. Clearly, CO poisoning involves multiple and complex pathologies. Hyperbaric oxygen has been consistently demonstrated as antagonistic to these processes: something no other intervention, including oxygen delivered without a hyperbaric chamber, has demonstrated.
Myers RAM, Snyder SK, Emhoff TA: Subacute sequelae of carbon monoxide poisoning. Ann Emerg Med. December 1985; 14: 1163-1167
A large case series that reports the ability of HBO therapy to minimize/eliminate post exposure relapse, which occurred in 12% of CO poisoned patients not treated hyperbarically. The reader is asked to consider the morbidity and cost (work-related absence, etc.) associated with such sequelae.
Norkool DM, Kirkpatrick JN: Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: A review of 115 cases. Ann Emerg Med. December 1985; 14: 1168-1171
Further evidence of the significant (43%) relapse/ late complications that characterize CO poisoned patients who do not receive hyperbaric oxygenation.
Van Hoesen KB, Camporesi EM, Moon RE, Hage ML, Piantadosi CA: Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning? A case report and literature review. JAMA 1989; 261: 1039-1043
A report of the heightened risk/morbidity/mortality to the fetus in maternal CO poisoning. The authors provide a recommended management protocol that centers around HBO therapy.
McNulty JA, Maher BA, Chu M, ET AL.: Relationship of short-term verbal memory to the need for hyperbaric oxygen treatment after carbon monoxide poisoning. Neuropsychiatry, Neuropsychology and Behavioral Neurology 1997;10: 174-179
A case controlled study demonstrating the benefit of HBO therapy in improving short-term memory following CO exposure.
Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB: Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Annuals of Emergency Medicine. April 1995; 25:4: 474-480
Prospective randomized clinical trial that confirms the findings of above noted and non-controlled reports: namely: HBO therapy "decreased the incidence of delayed neurological sequelae after CO poisoning."
Ducasse JL, Celsis P, Marc-Vergnes JP: Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea Hyperbaric Med 1995; 22(1): 9-15
Prospective and randomized blinded clinical trial. The authors conclude that HBO therapy "reduces the time of initial recovery and the number of delayed functional abnormalities…"
Jiang J, Tyssebotn I: Normobaric and hyperbaric oxygen treatment of acute carbon monoxide poisoning in rats. Undersea Hyperbaric Med 1997; 24(2): 107-116
A comparative trial of various groups; involving no treatment, pressurized air treatment and pressurized oxygen treatment, in a severe CO and cerebral ischemic model. "Compared to normoxic treatments, the HBO… significantly reduced the mortality and neurologic morbidity." HBO was also significantly better than ‘normal oxygen’ in increasing survival rate…"
~ Medicare Coverage Issues Manual 35-10
Dick Clarke, CHT
Program Director, Hyperbaric Medicine Service
Palmetto Richland Memorial Hospital
Columbia, South Carolina
ACUTE CARBON MONOXIDE INTOXICATION
Bartlett, R: Carbon monoxide poisoning. Clinical management of poisoning and drug overdose. WB Saunders, Lester M Haddad, James F Winchester editors; 3rd edition; 1997
General review article, emphasizing both the modern appreciation of the complex pathophysiology involved, and the multifactorial benefits of HBO therapy.
Thom, SR: Carbon monoxide-mediated brain lipid peroxidation in the rat. J. Appl. Physiol. 1990;68(3): 997-1003
A publication that advanced the pathophysiology of CO poisoning from the simple concept of inhibition of hemoglobin function. This data indicates that critical cellular toxicity occurs.
Thom, SR: Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen. Toxicol. Appl. Pharmacol. 1990; 105: 340-344
In reference to the above elucidation of a cellular poisoning, this companion study demonstrates the ability of HBO therapy to inhibit the toxic process.
Thom, SR: Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol. Appl. Pharmacol. 1993; 123: 243-247
Recent evidence of complex tissue injury, here involving a leukocyte -mediated brain injury as a result of acute CO poisoning.
Thom, SR: Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon- monoxide-mediated brain injury in rats. Toxicol. Appl. Pharmacol. 1993; 123: 248-256
A companion article to that pathophysiology noted in the previous article. This research demonstrates the functional inhibition of leukocytes by HBO therapy, thereby antagonizing CO medicated oxidative brain injury. Clearly, CO poisoning involves multiple and complex pathologies. Hyperbaric oxygen has been consistently demonstrated as antagonistic to these processes: something no other intervention, including oxygen delivered without a hyperbaric chamber, has demonstrated.
Myers RAM, Snyder SK, Emhoff TA: Subacute sequelae of carbon monoxide poisoning. Ann Emerg Med. December 1985; 14: 1163-1167
A large case series that reports the ability of HBO therapy to minimize/eliminate post exposure relapse, which occurred in 12% of CO poisoned patients not treated hyperbarically. The reader is asked to consider the morbidity and cost (work-related absence, etc.) associated with such sequelae.
Norkool DM, Kirkpatrick JN: Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: A review of 115 cases. Ann Emerg Med. December 1985; 14: 1168-1171
Further evidence of the significant (43%) relapse/ late complications that characterize CO poisoned patients who do not receive hyperbaric oxygenation.
Van Hoesen KB, Camporesi EM, Moon RE, Hage ML, Piantadosi CA: Should hyperbaric oxygen be used to treat the pregnant patient for acute carbon monoxide poisoning? A case report and literature review. JAMA 1989; 261: 1039-1043
A report of the heightened risk/morbidity/mortality to the fetus in maternal CO poisoning. The authors provide a recommended management protocol that centers around HBO therapy.
McNulty JA, Maher BA, Chu M, ET AL.: Relationship of short-term verbal memory to the need for hyperbaric oxygen treatment after carbon monoxide poisoning. Neuropsychiatry, Neuropsychology and Behavioral Neurology 1997;10: 174-179
A case controlled study demonstrating the benefit of HBO therapy in improving short-term memory following CO exposure.
Thom SR, Taber RL, Mendiguren II, Clark JM, Hardy KR, Fisher AB: Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Annuals of Emergency Medicine. April 1995; 25:4: 474-480
Prospective randomized clinical trial that confirms the findings of above noted and non-controlled reports: namely: HBO therapy "decreased the incidence of delayed neurological sequelae after CO poisoning."
Ducasse JL, Celsis P, Marc-Vergnes JP: Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea Hyperbaric Med 1995; 22(1): 9-15
Prospective and randomized blinded clinical trial. The authors conclude that HBO therapy "reduces the time of initial recovery and the number of delayed functional abnormalities…"
Jiang J, Tyssebotn I: Normobaric and hyperbaric oxygen treatment of acute carbon monoxide poisoning in rats. Undersea Hyperbaric Med 1997; 24(2): 107-116
A comparative trial of various groups; involving no treatment, pressurized air treatment and pressurized oxygen treatment, in a severe CO and cerebral ischemic model. "Compared to normoxic treatments, the HBO… significantly reduced the mortality and neurologic morbidity." HBO was also significantly better than ‘normal oxygen’ in increasing survival rate…"