Rose JJ, Wang L, Xu Q, McTiernan CF, Shiva S, Tejero J, Gladwin MT.
Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy.
Am J Respir Crit Care Med. 2017 Mar 1;195(5):596-606. doi: 10.1164/rccm.201606-1275CI.
Abstract/Text
Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The clinical presentation runs a spectrum, ranging from headache and dizziness to coma and death, with a mortality rate ranging from 1 to 3%. A significant number of patients who survive CO poisoning suffer from long-term neurological and affective sequelae. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15-40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic leukoencephalopathy or diffuse brain atrophy. Management of these patients requires the identification of accompanying drug ingestions, especially in the setting of intentional poisoning, fire-related toxic gas exposures, and inhalational injuries. Conventional therapy is limited to normobaric and hyperbaric oxygen, with no available antidotal therapy. Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.
Harper A, Croft-Baker J.
Carbon monoxide poisoning: undetected by both patients and their doctors.
Age Ageing. 2004 Mar;33(2):105-9. doi: 10.1093/ageing/afh038.
Abstract/Text
Carbon monoxide poisoning represents a potentially preventable and reversible cause of mortality and morbidity if sources and cases can be identified. The elderly have been shown to be particularly at risk. Concerns continue to be raised about potential unrecognised cases of carbon monoxide poisoning. These concerns arise from difficulties in knowing who to suspect as a potential victim of poisoning as well as how, when and what to test. In general carbon monoxide has no helpful unique clinical presentation and is known to mimic common illnesses as well as exacerbate established diseases. As a gas it is undetectable by the human senses and is potentially present in most households. This paper reviews the issues associated with carbon monoxide poisoning including pointers to early diagnosis and discussion of pathophysiology and management.
Nañagas KA, Penfound SJ, Kao LW.
Carbon Monoxide Toxicity.
Emerg Med Clin North Am. 2022 May;40(2):283-312. doi: 10.1016/j.emc.2022.01.005. Epub 2022 Apr 5.
Abstract/Text
Carbon monoxide accounts for thousands of deaths worldwide each year. Clinical effects can be diverse and include headache, dizziness, nausea, vomiting, syncope, seizures, coma, dysrhythmias, and cardiac ischemia, and severe toxicity generally affects the nervous and cardiovascular systems. Because of its complex pathophysiology, effects of toxicity can be acute or delayed. The diagnosis can be elusive, as carboxyhemoglobin levels do not always correlate with the degree of poisoning. Even when the diagnosis is certain, appropriate therapy is widely debated. Normobaric oxygen is the standard therapy, and the efficacy of hyperbaric oxygen is unclear.
Copyright © 2022 Elsevier Inc. All rights reserved.
Tomaszewski C.
Carbon monoxide poisoning. Early awareness and intervention can save lives.
Postgrad Med. 1999 Jan;105(1):39-40, 43-8, 50. doi: 10.3810/pgm.1999.01.496.
Abstract/Text
Each year, particularly during the heating season, thousands of people are poisoned by carbon monoxide, with potentially devastating outcomes. Initial diagnosis can be difficult because symptoms closely resemble those of influenza and are often misinterpreted. Dr Tomaszewski discusses diagnosis and treatment, including the benefits and risks of hyperbaric oxygen therapy.
Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD.
Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning.
JAMA. 2006 Jan 25;295(4):398-402. doi: 10.1001/jama.295.4.398.
Abstract/Text
CONTEXT: Carbon monoxide (CO) poisoning is a common cause of toxicological morbidity and mortality. Myocardial injury is a frequent consequence of moderate to severe CO poisoning. While the in-hospital mortality for these patients is low, the long-term outcome of myocardial injury in this setting is unknown.
OBJECTIVE: To determine the association between myocardial injury and long-term mortality in patients following moderate to severe CO poisoning.
DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort study of 230 consecutive adult patients treated for moderate to severe CO poisoning with hyperbaric oxygen and admitted to the Hennepin County Medical Center, a regional center for treatment of CO poisoning, between January 1, 1994, and January 1, 2002. Follow-up was through November 11, 2005.
MAIN OUTCOME MEASURE: All-cause mortality.
RESULTS: Myocardial injury (cardiac troponin I level > or =0.7 ng/mL or creatine kinase-MB level > or =5.0 ng/mL and/or diagnostic electrocardiogram changes) occurred in 85 (37%) of 230 patients. At a median follow-up of 7.6 years (range: in-hospital only to 11.8 years), there were 54 deaths (24%). Twelve of those deaths (5%) occurred in the hospital as a result of a combination of burn injury and anoxic brain injury (n = 8) or cardiac arrest and anoxic brain injury (n = 4). Among the 85 patients who sustained myocardial injury from CO poisoning, 32 (38%) eventually died compared with 22 (15%) of 145 patients who did not sustain myocardial injury (adjusted hazard ratio, 2.1; 95% confidence interval, 1.2-3.7; P = .009).
CONCLUSION: Myocardial injury occurs frequently in patients hospitalized for moderate to severe CO poisoning and is a significant predictor of mortality.
American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Carbon Monoxide Poisoning:; Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD.
Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning.
Ann Emerg Med. 2017 Jan;69(1):98-107.e6. doi: 10.1016/j.annemergmed.2016.11.003.
Abstract/Text
林寛之：火事場で発生するシアン（青酸）ガスもお忘れなく．Step Beyond Resident 5 外傷・外科診療のツボ編 Part 2：羊土社，2008年；191-196.
Hampson NB, Piantadosi CA, Thom SR, Weaver LK.
Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning.
Am J Respir Crit Care Med. 2012 Dec 1;186(11):1095-101. doi: 10.1164/rccm.201207-1284CI. Epub 2012 Oct 18.
Abstract/Text
Carbon monoxide (CO) poisoning is common in modern society, resulting in significant morbidity and mortality in the United States annually. Over the past two decades, sufficient information has been published about carbon monoxide poisoning in the medical literature to draw firm conclusions about many aspects of the pathophysiology, diagnosis, and clinical management of the syndrome, along with evidence-based recommendations for optimal clinical practice. This article provides clinical practice guidance to the pulmonary and critical care community regarding the diagnosis, management, and prevention of acute CO poisoning. The article represents the consensus opinion of four recognized content experts in the field. Supporting data were drawn from the published, peer-reviewed literature on CO poisoning, placing emphasis on selecting studies that most closely mirror clinical practice.
Hampson NB, Bodwin D.
Toxic CO-ingestions in intentional carbon monoxide poisoning.
J Emerg Med. 2013 Mar;44(3):625-30. doi: 10.1016/j.jemermed.2012.08.033. Epub 2012 Nov 5.
Abstract/Text
BACKGROUND: Intentional carbon monoxide (CO) poisoning is responsible for two-thirds of the deaths from CO poisoning in this country and an estimated 15,000 Emergency Department visits annually.
OBJECTIVES: In an attempt to optimize medical management of such patients, this study was conducted to examine the frequency and types of toxic co-ingestions that may accompany CO inhalation.
METHODS: Records of all patients treated with hyperbaric oxygen for acute, intentional CO poisoning at a regional referral center for hyperbaric medicine in Seattle from 1980 to 2005 were reviewed. For those where co-ingestions were identified, information about type of poison(s) and results of toxicology screens was recorded and analyzed.
RESULTS: Over the 25-year period examined, 433 patients were treated for intentional CO poisoning and records were available for 426. Of those, 188 (42%) had ingested one or more poisons in addition to CO. Ethanol was most common, but a wide variety of other drug classes were also identified. Toxicology screening studies of some type were performed in 49 patients.
CONCLUSIONS: Toxic co-ingestions seem to be relatively common in patients treated for intentional CO poisoning. For this reason, providers should be vigilant and open to clinical signs that can't be explained with CO exposure alone, and ready to treat clinical issues that arise from co-ingestions.
Copyright © 2013 Elsevier Inc. All rights reserved.
Touger M, Gallagher EJ, Tyrell J.
Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning.
Ann Emerg Med. 1995 Apr;25(4):481-3. doi: 10.1016/s0196-0644(95)70262-8.
Abstract/Text
STUDY OBJECTIVE: To test the hypothesis that venous carboxyhemoglobin (V-COHb) levels accurately predict arterial (A-COHb) levels.
DESIGN: Prospective comparison of A-COHb and V-COHb levels in patients with suspected carbon monoxide (CO) poisoning.
SETTING: Municipal hospital emergency department with contiguous multiplace hyperbaric chamber staffed 24 hours a day.
PARTICIPANTS: Unselected convenience sample of 61 adults with suspected CO toxicity.
INTERVENTION: Simultaneous sampling of arterial and venous blood.
RESULTS: Correlation between V-COHb and A-COHb showed an r value of .99 (95%CI, .99 to .99), and an r2 value of .98. Agreement between V-COHb and A-COHb levels was examined by use of a plot of arteriovenous differences against the mean of the two measurements. The mean arteriovenous difference was .15% COHb (95%CI, .13% to .45%), with 95% of the differences ranging from 2.4% COHb to -2.1% COHb.
CONCLUSION: Venous COHb levels predict arterial levels with a high degree of accuracy. Patients with suspected CO poisoning can be screened with the use of venous blood, without the need for arterial puncture.
Hampson NB, Hauff NM.
Risk factors for short-term mortality from carbon monoxide poisoning treated with hyperbaric oxygen.
Crit Care Med. 2008 Sep;36(9):2523-7. doi: 10.1097/CCM.0b013e31818419d8.
Abstract/Text
OBJECTIVE: Carbon monoxide (CO) poisoning is common in the United States, accounting for approximately 2,700 deaths annually. Few publications have described the mortality rate of CO-poisoned patients who survive to reach a hospital and die despite maximal medical care. Further, while risk factors for cognitive sequelae in survivors of CO poisoning have become clearer recently, factors associated with death are less well defined. This study was conducted to 1) determine the short-term mortality risk for patients treated with hyperbaric oxygen for CO poisoning, and 2) determine whether any factors related to the poisoning episode are predictive of mortality.
DESIGN/SETTING/PATIENTS: A departmental database and medical records of 1,505 consecutive patients treated with hyperbaric oxygen at a single institution from 1978 to 2005 were reviewed.
MEASUREMENTS: Demographic and clinical data were extracted for analysis. Mortality data, including cause of death, were obtained through a search of the National Death Index of the National Center for Health Statistics.
MAIN RESULTS: A total of 38 patients experienced short-term mortality from their episode of CO poisoning, yielding a death rate of 2.6% in medically treated patients. Characteristics significantly associated with mortality included fire as a source of CO, loss of consciousness, carboxyhemoglobin level, arterial pH, and presence of endotracheal intubation during hyperbaric treatment.
CONCLUSIONS: The mortality rate for medically treated CO-poisoned patients in this series was 2.6%, similar to the limited combined experience previously reported in the literature. Factors most strongly associated with mortality were severe metabolic acidosis and need for endotracheal intubation.
Gerald M.: Carbon monoxide. Tintinalli, J.E. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill, 2011; 1410-1413.
Kim YM, Shin HJ, Choi DW, Kim JM, Lee SW, Jeong SH, Kim H.
Comparison of high-flow nasal cannula oxygen therapy and conventional reserve-bag oxygen therapy in carbon monoxide intoxication: A pilot study.
Am J Emerg Med. 2020 Aug;38(8):1621-1626. doi: 10.1016/j.ajem.2019.158451. Epub 2019 Nov 6.
Abstract/Text
BACKGROUND: High-flow nasal cannula oxygen (HFNC) creates a positive pressure effect through high-flow rates compared to conventional oxygen therapy. The purpose of this human pilot study is to compare the effects of HFNC and conventional oxygen therapy on the rate of carbon monoxide (CO) clearance from the blood in patients with mild to moderate CO poisoning.
METHODS: CO-poisoned Patients randomly received 100% oxygen from a rebreathing reserve mask (NBO2, flow of 15 L/min) or HFNC (flow of 60 L/min). The fraction of COHb value (fCOHb) was measured in 30-min intervals until it fell to under 10%. We determined the Half-life time of fCOHb (fCOHb t1/2).
RESULTS: A total of 22 patients had fCOHb levels ≥ 10% at the time of ED arrival, with 9 of them having fCOHb level ranging between 25% and 50%. There was no significant difference in the fCOHbt1/2 between the HFNC group and NBO2 group. However, the mean fCOHbt1/2 in the HFNC group (48.5 ± 12.4 min) has a smaller standard deviation than that in the NBO2 group (99.3 ± 93.38 min). There were significant between-group differences in the mean COHbt1/2 among the patients with fCOHb levels less than 25% (HFNC 43.6 ± 10.6 vs. NBO2 134.2 ± 111.3).
CONCLUSIONS: In this pilot randomized controlled trial study, HFNC therapy did not reduce fCOHbt1/2 compared to NBO2 therapy but could be beneficial in maintaining a constant fCOHbt1/2 as well as in reducing fCOHbt1/2 in mild CO poisoning patients compared to conventional NBO2 therapy. However, further studies with a larger number of patients are needed to establish HFNC therapy as an alternative therapy for CO poisoning patients.
Copyright © 2019 Elsevier Inc. All rights reserved.
Er B, Esquinas AM.
Comparison of non-invasive CPAP with mask use in carbon monoxide poisoning: Some concerns about methodology.
Am J Emerg Med. 2021 Jan;39:240. doi: 10.1016/j.ajem.2020.05.036. Epub 2020 May 21.
Abstract/Text
Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ.
Hyperbaric oxygen for carbon monoxide poisoning.
Cochrane Database Syst Rev. 2011 Apr 13;2011(4):CD002041. doi: 10.1002/14651858.CD002041.pub3. Epub 2011 Apr 13.
Abstract/Text
BACKGROUND: Poisoning with carbon monoxide (CO) remains an important cause of accidental and intentional injury worldwide. Several unblinded non-randomized trials have suggested that the use of hyperbaric oxygen (HBO) prevents the development of neurological sequelae. This has led to the widespread use of HBO in the management of patients with carbon monoxide poisoning.
OBJECTIVES: To examine randomised trials of the efficacy of hyperbaric oxygen (HBO) compared to normobaric oxygen (NBO) for the prevention of neurologic sequelae in patients with acute carbon monoxide poisoning.
SEARCH STRATEGY: We searched the following electronic databases; Cochrane Injuries Group Specialised Register (searched June 2010), Cochrane Central Register of Controlled Trials (The Cochrane Library 2010, Issue 2), MEDLINE (Ovid SP) 1950 to June 2010, EMBASE (Ovid SP) 1980 to June 2010, ISI Web of Science: Science Citation Index Expanded (SCI-EXPANDED) 1970 to June 2010, ISI Web of Science: Conference Proceedings Citation Index-Science (CPCI-S) 1990 to June 2010.
SELECTION CRITERIA: All randomised controlled trials of HBO compared to NBO, involving non-pregnant adults who are acutely poisoned with carbon monoxide (regardless of severity).
DATA COLLECTION AND ANALYSIS: Two authors independently extracted from each trial information on: the number of randomised patients, types of participants, the dose and duration of the intervention, and the prevalence of neurologic symptoms at follow-up.
MAIN RESULTS: Seven randomised controlled trials of varying quality were identified; one was excluded because it did not evaluate clinical outcomes. Of the six remaining trials involving 1361 participants, two found a beneficial effect of HBO for the reduction of neurologic sequelae at one month, while four others did not. One of these is an incomplete publication (an abstract of an interim analysis). Although pooled random effects meta-analysis does not suggest a significant benefit from HBOT (OR for neurological deficits 0.78, 95%CI 0.54 to 1.12), significant methodologic and statistical heterogeneity was apparent among the trials, and this result should be interpreted cautiously. Moreover, design or analysis flaws were evident in all trials. Importantly, the conclusions of one positive trial may have been influenced by failure to adjust for multiple hypothesis testing, while interpretation of the other positive trial is hampered by a high risk of bias introduced during the analysis including an apparent change in the primary outcome. Both were also stopped early 'for benefit', which is likely to have inflated the observed effect. In contrast three negative trials had low power to detect a benefit of HBO due to exclusion of severely poisoned patients in two and very poor follow-up in the other. One trial that was said to be finished around eight years ago has not reported the final analysis in any forum.
AUTHORS' CONCLUSIONS: Existing randomised trials do not establish whether the administration of HBO to patients with carbon monoxide poisoning reduces the incidence of adverse neurologic outcomes. Additional research is needed to better define the role, if any, of HBO in the treatment of patients with carbon monoxide poisoning. This research question is ideally suited to a multi-center randomised controlled trial.
Silver DA, Cross M, Fox B, Paxton RM.
Computed tomography of the brain in acute carbon monoxide poisoning.
Clin Radiol. 1996 Jul;51(7):480-3. doi: 10.1016/s0009-9260(96)80186-3.
Abstract/Text
Of 107 patients admitted to the South Western Hyperbaric Medical Centre with acute carbon monoxide poisoning for hyperbaric oxygen therapy 19 had cerebral imaging performed: 17 patients had CT, one patient had MRI and CT and one patient MRI alone. The role of brain CT is established in determining the prognosis from acute carbon monoxide poisoning. Brain imaging was indicated because of unconsciousness on admission and failure or delayed improvement in neurological status after initiation of hyperbaric oxygen therapy. Of the 18 patients who underwent brain CT, seven were found to have the characteristic changes of bilateral low attenuation areas within the globus pallidus and six had low attenuation changes within cerebral white matter. In two patients there were both globus pallidus and cerebral white matter changes. Out of the total of the 19 patients who were studied, four patients died, 10 recovered fully and five had variable disabilities ranging from short term memory loss to more severe cognitive impairment and physical disability. The role of CT and the practicalities of hyperbaric oxygen therapy for acute carbon monoxide poisoning are discussed in the light of the experience from a regional dedicated medical diving centre.
Jones JS, Lagasse J, Zimmerman G.
Computed tomographic findings after acute carbon monoxide poisoning.
Am J Emerg Med. 1994 Jul;12(4):448-51. doi: 10.1016/0735-6757(94)90059-0.
Abstract/Text
Selective necrosis and degeneration of the globus pallidus are characteristic autopsy findings in patients with severe carbon monoxide (CO) poisoning. The objective of this study was to show that computed tomography (CT) may demonstrate these morphological changes in the brain during life, and provide a clue to prognosis. The authors reviewed the medical records of 19 consecutive patients with acute CO poisoning who underwent CT examination during hospitalization. Abnormal CT findings were found in 10 of the 19 patients (53%). The most common abnormal findings were low-density areas in the basal ganglia. These lesions were found in 7 of the 10 cases, and varied from small (limited to the globus pallidus) to large (extending to the internal capsule). Of the 10 patients with abnormal CT scans, 9 survived to hospital discharge but all had some degree of functional neurological impairment. Eighty-nine percent (8 of 9) of the patients with normal CT scans were discharged neurologically intact. Awareness of the potential for basal ganglia lesions in CO poisoning should lead to more accurate CT interpretation and may have significant prognostic implications.
J.Stephen H.: Altered mental status and coma. Tintinalli, J.E. Tintinalli’s Emergency Medicine: A Comprehensive Studi Guide. 7th ed. New York: McGraw-Hill, 2011;1135-1142.
Weaver LK, Valentine KJ, Hopkins RO.
Carbon monoxide poisoning: risk factors for cognitive sequelae and the role of hyperbaric oxygen.
Am J Respir Crit Care Med. 2007 Sep 1;176(5):491-7. doi: 10.1164/rccm.200701-026OC. Epub 2007 May 11.
Abstract/Text
RATIONALE: Carbon monoxide poisoning is common and causes cognitive sequelae. Hyperbaric oxygen (HBO(2)) reduces cognitive sequelae incidence, but which patients may benefit from HBO(2) is unclear.
OBJECTIVES: Risk factor determination for 6-wk cognitive sequelae from CO poisoning and risk modification with HBO(2).
METHODS: Patients were from a randomized controlled trial, enrolling acutely CO-poisoned patients more than 15 years of age. Patients eligible but not enrolled in the randomized trial, and not receiving HBO(2), were followed during the study interval. In patients not receiving HBO(2), we performed univariate analyses including risk factors identified by randomized trial subgroup analyses. A multivariable analysis was performed using univariate results with and without HBO(2).
MEASUREMENTS AND MAIN RESULTS: In 163 patients not receiving HBO(2), 68 (42%) manifested sequelae. Risk factors for sequelae from subgroup analyses were loss of consciousness, age of 36 years or more, and carboxyhemoglobin levels greater than or equal to 25%. By univariate analyses, risks for sequelae were age of 36 years or more (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.3-4.9; P = 0.005), and exposure intervals greater than or equal to 24 hours (OR, 2.4; 95% CI, 1.2-4.8; P = 0.019). Including 75 patients receiving HBO(2), cognitive sequelae was reduced in patients age of 36 years or more (OR, 0.3; 95% CI, 0.2-0.6; P < 0.001). Exposure intervals greater than or equal to 24 hours are an independent risk factor for sequelae (OR, 2.0; 95% CI, 1.0-3.8; P = 0.046).
CONCLUSIONS: HBO(2) oxygen is indicated for patients with acute CO poisoning who are 36 years or older or have exposure intervals greater than or equal to 24 hours. In addition, subgroup analyses support that patients with loss of consciousness or higher carboxyhemoglobin levels warrant HBO(2).
Jeon SB, Sohn CH, Seo DW, Oh BJ, Lim KS, Kang DW, Kim WY.
Acute Brain Lesions on Magnetic Resonance Imaging and Delayed Neurological Sequelae in Carbon Monoxide Poisoning.
JAMA Neurol. 2018 Apr 1;75(4):436-443. doi: 10.1001/jamaneurol.2017.4618.
Abstract/Text
IMPORTANCE: Preventing delayed neurological sequelae is a major goal of treating acute carbon monoxide poisoning, but to our knowledge there are no reliable tools for assessing the probability of these sequelae.
OBJECTIVES: To determine whether acute brain lesions on diffusion-weighted imaging are related to subsequent development of delayed neurological sequelae after acute carbon monoxide poisoning.
DESIGN, SETTING, AND PARTICIPANTS: This registry-based observational study was conducted at a university hospital in Seoul, Korea, between April 1, 2011, and December 31, 2015. Of 700 patients (aged ≥18 years) with acute carbon monoxide poisoning, 433 patients (61.9%) who underwent diffusion-weighted imaging at an emergency department were considered for the study. Patients who developed cardiac arrest before diffusion-weighted imaging (n = 3), had persistent neurological symptoms at discharge (n = 8), committed suicide soon after discharge (n = 1), and were lost to follow-up (n = 34) were excluded.
EXPOSURE: The presence of unambiguous, high-signal-intensity, acute brain lesions on diffusion-weighted imaging (b = 1000 s/mm2).
MAIN OUTCOMES AND MEASURES: Development of delayed neurological sequelae defined as any neurological symptoms or signs that newly developed within 6 weeks of discharge.
RESULTS: Of the 387 included patients (143 women [37.0%]; median age, 42.0 years [interquartile range, 32.0-56.0 years]), acute brain lesions on diffusion-weighted imaging were observed in 104 patients (26.9%). Among these, 77 patients (19.9%) had globus pallidus lesions, 13 (3.4%) had diffuse lesions, and 57 (14.7%) had focal lesions (37 patients [9.6%] had >1 pattern concurrently). Lesions were supratentorial and infratentorial in 101 and 23 patients, respectively. Delayed neurological sequelae occurred in 101 patients (26.1%). Multivariable logistic regression analysis indicated that the presence of acute brain lesions was independently associated with development of delayed neurological sequelae (adjusted odds ratio, 13.93; 95% CI, 7.16-27.11; P < .001). The sensitivity and specificity of acute brain lesions to assess the probability of delayed neurological sequelae were 75.2% (95% CI, 66.8%-83.7%) and 90.2% (95% CI, 86.8%-93.7%), respectively. In addition, the positive and negative predictive values were 73.1% (95% CI, 64.6%-81.6%) and 91.2% (95% CI, 87.9%-94.5%), respectively.
CONCLUSIONS AND RELEVANCE: The presence of acute brain lesions was significantly associated with the development of delayed neurological sequelae. Diffusion-weighted imaging during the acute phase of carbon monoxide poisoning may therefore help identify patients at risk of developing these debilitating sequelae.
Yang S, Liu H, Peng Q, Li J, Liu Q.
Predicting scale of delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning: A retrospective study.
Am J Emerg Med. 2022 Feb;52:114-118. doi: 10.1016/j.ajem.2021.10.056. Epub 2021 Nov 3.
Abstract/Text
OBJECTIVE: To establish and validate a predictive formula for calculating the possibility of developing delayed neurological sequelae (DNS) after acute carbon monoxide (CO) poisoning to facilitate better decision-making about treatment strategies.
METHODS: This study retrospectively enrolled 605 consecutive patients who had been newly diagnosed with CO poisoning from the Central Hospital of Enshi Prefecture between January 1, 2015 and December 31, 2020. The cohort was randomly divided into two subgroups: the development cohort (n = 104) and validation cohort (n = 44). Univariate analysis and backward elimination of multivariate logistic regression were used to identify predictive factors, and a predictive formula was established. The performance was assessed using the area under the curve (AUC), the mean AUC of five-fold cross-validation, and calibration plots.
RESULTS: The formula included four commonly available predictors: initial GCS score, duration of exposure, CK, and abnormal findings on MRI. We next created a formula to calculate the risk score for developing DNS: Risk score = -4.54 + 3.35 * (Abnormal findings on MRI = yes) - 0.51 * (Initial GCS score) + 0.65 * (Duration of exposure) + 0.01 * (CK). Then, the probability of developing DNS could be calculated: Probability of DNS = 1/(1 + e Risk score). The model revealed good discrimination with AUC, and mean AUC of fivefold cross-validation in two cohort, and the calibration plots showed good calibration.
CONCLUSIONS: This study established a prediction predictive formula for predicting developing of DNS, which could facilitate better decision-making about treatment strategies.
Copyright © 2021. Published by Elsevier Inc.
Koren G, Sharav T, Pastuszak A, Garrettson LK, Hill K, Samson I, Rorem M, King A, Dolgin JE.
A multicenter, prospective study of fetal outcome following accidental carbon monoxide poisoning in pregnancy.
Reprod Toxicol. 1991;5(5):397-403. doi: 10.1016/0890-6238(91)90002-w.
Abstract/Text
We report the results of the first prospective, multicenter study of acute carbon monoxide (CO) poisoning in pregnancy. We collected and followed cases of CO poisoning occurring during pregnancy between December 1985 and March 1989. The sources of CO were malfunctioning furnaces (n = 16), hot water heaters (n = 7), car fumes (n = 6), and methylene chloride inhalation (n = 3). Pregnancy outcome was adversely affected in 3 of 5 pregnancies with severe toxicity; two stillbirths, and one cerebral palsy with tomographic findings consistent with ischemic damage. All adverse outcome occurred in cases treated with high flow oxygen, whereas the 2 cases of severe toxicity with normal outcomes followed hyperbaric oxygen therapy. All 31 babies exposed in utero to mild or moderate CO poisoning exhibited normal physical and neurobehavioral development. Severe maternal CO toxicity was associated with significantly more adverse fetal cases when compared to mild maternal toxicity (P less than 0.001). It is concluded that while severe CO poisoning poses serious short- and long-term fetal risk, mild accidental exposure is likely to result in normal fetal outcome. Because fetal accumulation of CO is higher and its elimination slower than in the maternal circulation, hyperbaric oxygen may decrease fetal hypoxia and improve outcome.
