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Neil B. Hampson - One of the best experts on this subject based on the ideXlab platform.

  • cost of accidental Carbon Monoxide Poisoning a preventable expense
    Preventive medicine reports, 2016
    Co-Authors: Neil B. Hampson
    Abstract:

    Carbon Monoxide (CO) Poisoning is common in the United States, accounting for hundreds of deaths and thousands of emergency department visits annually. It is believed that most accidental CO Poisoning is preventable through public education, warning labels on consumer products, and uniform use of residential CO alarms. However, cost effectiveness of these prevention strategies has not been demonstrated in the United States to date. It was the objective of this study to estimate societal cost of accidental CO Poisoning and evaluate the cost-effectiveness of universal installation of residential CO alarms. Published studies and data from the English language literature were used in to estimate direct hospital costs and lost earnings resulting from accidental CO Poisoning. The study was performed in the US in 2015. Approximately 6600 individuals are estimated to sustain long-term cognitive sequela annually, with total loss in earnings of approximately $925 million, 334 individuals die from accidental, non-fire related CO Poisoning with an average loss of 26 years of productivity accounting for $355 million, and 2800 are hospitalized with acute medical care costs of $33 million. Available data indicate that accidental CO Poisoning in the US conservatively costs society over $1.3 billion, resulting from direct hospital costs and lost earnings. Further, it demonstrates a positive cost-benefit ratio for the uniform use of residential CO alarms.

  • toxic co ingestions in intentional Carbon Monoxide Poisoning
    Journal of Emergency Medicine, 2013
    Co-Authors: Neil B. Hampson, Diana Bodwin
    Abstract:

    Abstract 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.

  • practice recommendations in the diagnosis management and prevention of Carbon Monoxide Poisoning
    American Journal of Respiratory and Critical Care Medicine, 2012
    Co-Authors: Neil B. Hampson, Stephen R. Thom, Claude A Piantadosi, Lindell K. Weaver
    Abstract:

    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.

  • recipients of hyperbaric oxygen treatment for Carbon Monoxide Poisoning and exposure circumstances
    American Journal of Emergency Medicine, 2012
    Co-Authors: Jacquelyn H Clower, Neil B. Hampson, Shahed Iqbal, Fuyuen Y Yip
    Abstract:

    Abstract Background Unintentional Carbon Monoxide Poisoning is preventable. Severe cases are often referred for hyperbaric oxygen treatment. To guide prevention efforts and treatment practices, this study provides some of the most detailed current information about patients with Carbon Monoxide Poisoning who have been treated at hyperbaric facilities across the United States and the circumstances surrounding their exposures. This study can help improve efforts to prevent Carbon Monoxide Poisoning and enhance treatment practices. Methods From August 2008 to January 2010, nonidentifiable, patient-level data were reported by 87 hyperbaric facilities in 39 states via an online reporting system. This reporting system was developed collaboratively by the Undersea and Hyperbaric Medical Society and the Centers for Disease Control and Prevention. Results Among the 864 patients reported to receive hyperbaric oxygen treatment for unintentional, non–fire-related, Carbon Monoxide Poisoning, most of the patients were white men aged between 18 and 44 years. Only 10% of patients reported the presence of a Carbon Monoxide alarm at their exposure location, and 75% reported being part of a group exposure. Nineteen patients (2%) reported a prior Carbon Monoxide exposure. About half (55%) of the patients treated were discharged after treatment; 41% were hospitalized. Conclusions The findings in this report expand the knowledge about patients with Carbon Monoxide Poisoning. These results suggest that prevention efforts, such as educating the public about using Carbon Monoxide alarms and targeting the most at-risk populations, may help reduce the number of exposures, the number of persons with chronic cognitive sequelae, and the resulting burden on the health care system.

  • Carbon Monoxide Poisoning from portable electric generators.
    American journal of preventive medicine, 2005
    Co-Authors: Neil B. Hampson, Jennette L. Zmaeff
    Abstract:

    Background While the overall death rate from unintentional Carbon Monoxide (CO) Poisoning has decreased in the United States due to improved automobile emissions controls and a decline in CO Poisonings from motor vehicles, exposures have not changed from some sources of CO. One of these is the operation of portable electrical generators in poorly ventilated spaces. This study sought to describe the population poisoned from CO produced by portable electric generators, and to determine the reasons that generators are operated in a hazardous fashion. Methods Cases of CO Poisoning referred for treatment with hyperbaric oxygen at Virginia Mason Medical Center in Seattle from November 1978 to March 2004 were reviewed. Those cases that resulted from portable generator use were selected for analysis. Results Sixty-three patients aged 2 to 85 years were treated for CO Poisoning from portable electric generators. They included 34 males and 29 females who were poisoned in 37 separate incidents. Thirty-four lost consciousness with the exposure. Of the 63 total patients, 60 spoke English. Generators were typically used when normal electrical service was disrupted by a storm or in remote locations. In 29 of 37 incidents, the generator was operated in the home environment, most commonly in the garage. Lack of awareness of the dangers of CO Poisoning or lack of knowledge of ventilation requirements were the most commonly identified reasons. Conclusions CO Poisoning from portable electric generators occurs in a characteristic population, in a few typical locations and for a limited number of reasons. This information may help target prevention efforts for this form of Poisoning, such as warning labels or educational programs.

Stephen R. Thom - One of the best experts on this subject based on the ideXlab platform.

  • practice recommendations in the diagnosis management and prevention of Carbon Monoxide Poisoning
    American Journal of Respiratory and Critical Care Medicine, 2012
    Co-Authors: Neil B. Hampson, Stephen R. Thom, Claude A Piantadosi, Lindell K. Weaver
    Abstract:

    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.

  • intravascular neutrophil activation due to Carbon Monoxide Poisoning
    American Journal of Respiratory and Critical Care Medicine, 2006
    Co-Authors: Stephen R. Thom, J. M. Clark, Veena M Bhopale, K R Hardy
    Abstract:

    Rationale: We hypothesized that platelet–neutrophil interactions occur as a result of acute Carbon Monoxide (CO) Poisoning, and subsequent neutrophil activation triggers events that cause neurologic sequelae. Objectives: To identify platelet–neutrophil interactions and neutrophil activation in patients and in animal models, and to establish the association between these intravascular events and changes linked to CO-mediated neurologic sequelae in an animal model. Measurements and Main Results: Blood was obtained from 50 consecutive patients. Abnormalities were variable depending on the carboxyhemoglobin level at study admission and duration of CO exposure. Platelet–neutrophil aggregates were detected and plasma myeloperoxidase (MPO) concentration was significantly elevated in those with confirmed CO Poisoning. Among patients exposed to CO for over 3 h, flow cytometry scans of neutrophils revealed increased surface expression of CD18 and, in some groups, MPO on the cell surface. Animal models revealed consistent evidence of platelet–neutrophil aggregates, neutrophil activation and surface MPO, and plasma MPO elevation. MPO was deposited along the brain vascular lining and colocalized with nitrotyrosine. CO Poisoning caused abnormalities in the charge pattern of myelin basic protein (MBP), changes linked to adaptive immunologic responses responsible for neurologic sequelae in this model. Changes did not occur in thrombocytopenic rats, those receiving tirofiban to inhibit platelet–neutrophil interactions, or those receiving l-nitroarginine methyl ester to inhibit nitric oxide synthesis. Alterations in MBP did not occur in CO-poisoned knockout mice lacking MPO. Conclusions: Acute CO Poisoning causes intravascular neutrophil activation due to interactions with platelets. MPO liberated by neutrophils mediates perivascular oxidative stress, which is linked to immune-mediated neurologic sequelae.

  • delayed neuropathology after Carbon Monoxide Poisoning is immune mediated
    Proceedings of the National Academy of Sciences of the United States of America, 2004
    Co-Authors: Stephen R. Thom, Veena M Bhopale, Donald Fisher, Jie Zhang, Phyllis A Gimotty
    Abstract:

    The neuropathological sequelae of Carbon Monoxide (CO) Poisoning cannot be explained by hypoxic stress alone. CO Poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes. Lymphocytes from CO-poisoned rats subsequently exhibit an auto-reactive proliferative response to MBP, and there is a significant increase in the number of activated microglia in brain. Rats rendered immunologically tolerant to MBP before CO Poisoning exhibit acute biochemical changes in MBP but no lymphocyte proliferative response or brain microglial activation. CO Poisoning causes a decrement in learning that is not observed in immunologically tolerant rats. These results demonstrate that delayed CO-mediated neuropathology is linked to an adaptive immunological response to chemically modified MBP.

  • hyperbaric oxygen therapy for acute Carbon Monoxide Poisoning
    The New England Journal of Medicine, 2002
    Co-Authors: Stephen R. Thom
    Abstract:

    Carbon Monoxide appears to be the leading cause of injury and death due to Poisoning worldwide.1 A colorless, odorless, tasteless gas, Carbon Monoxide is produced by the incomplete combustion of any Carbon-containing fuel. Prevention of Carbon Monoxide Poisoning requires 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 alarms.1 Despite the ubiquitous presence of Carbon Monoxide in our environment, its known threat to public health, and more than a century of scientific investigation, the mechanisms of injury and methods of treating Carbon Monoxide Poisoning are . . .

  • Carbon Monoxide Poisoning a public health perspective
    Toxicology, 2000
    Co-Authors: James A Raub, Neil B. Hampson, Monique Mathieunolf, Stephen R. Thom
    Abstract:

    Carbon Monoxide (CO) may be the cause of more than one-half of the fatal Poisonings reported in many countries; fatal cases also are grossly under-reported or misdiagnosed by medical professionals. Therefore, the precise number of individuals who have suffered from CO intoxication is not known. The health effects associated with exposure to CO range from the more subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO. The morbidity and mortality resulting from the latter exposures are described briefly to complete the picture of CO exposure in present-day society. The symptoms, signs, and prognosis of acute CO Poisoning correlate poorly with the level of carboxyhemoglobin (COHb) measured at the time of hospital admission; however, because CO Poisoning is a diagnosis frequently overlooked, the importance of measuring COHb in suspicious settings cannot be overstated. The early symptoms (headache, dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Complications occur frequently in CO Poisoning. Immediate death is most likely cardiac in origin because myocardial tissues are most sensitive to the hypoxic effects of CO. Severe Poisoning results in marked hypotension, lethal arrhythmias, and electrocardiographic changes. Pulmonary edema may occur. Neurological manifestation of acute CO Poisoning includes disorientation, confusion, and coma. Perhaps the most insidious effect of CO Poisoning is the development of delayed neuropsychiatric impairment within 2‐28 days after Poisoning and the slow resolution of neurobehavioral consequences. Carbon Monoxide Poisoning during pregnancy results in high risk for the mother by increasing the short-term complication rate and for the fetus by causing fetal death, developmental disorders, and chronic cerebral lesions. In conclusion, CO

Lindell K. Weaver - One of the best experts on this subject based on the ideXlab platform.

  • myositis associated with Carbon Monoxide Poisoning
    Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, 2019
    Co-Authors: Lindell K. Weaver, Christine L Oliver, Kayla Deru, Anat Stemmerrachamimov
    Abstract:

    Introduction Carbon Monoxide (CO) Poisoning causes hypoxia and inflammation, which could adversely affect muscle. We could find no published information about CO Poisoning causing myositis. Case report A 53-year-old previously healthy female semi truck driver had CO Poisoning from a faulty diesel engine exhaust intermittently over three months, culminating in an episode of acute CO Poisoning, with syncope after exiting the truck at the end of the three-month period. Neuropsychological symptoms immediately after the acute Poisoning event were followed by the development of fatigue, weakness and myalgias within two months and a diagnosis of "polymyositis" within four months. C-reactive protein and creatine kinase were elevated. Electromyogram showed pure myopathy without sensory abnormalities. Occult malignancy was ruled out. Thigh muscle biopsy revealed severe inflammatory myopathy and myonecrosis. Muscle specialist pathologists interpreted the biopsy as toxic or viral inflammatory myopathy, not polymyositis, with CO Poisoning as the likely etiology. She received steroids and mycophenolate. Nineteen months later, a repeat biopsy was negative for inflammation or myopathic process. Alternative diagnoses were ruled out by clinical investigation and her course over the next five years. Conclusion This patient's presentation and clinical course support a diagnosis of myositis from CO Poisoning, although it is possible that the myositis was either idiopathic or post-viral (without evidence of a causative virus).

  • Hyperbaric oxygen therapy for Carbon Monoxide Poisoning.
    Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society Inc, 2014
    Co-Authors: Lindell K. Weaver
    Abstract:

    Despite established exposure limits and safety standards, and the availability of Carbon Monoxide (CO) alarms, each year 50,000 people in the United States visit emergency departments for CO Poisoning. Carbon Monoxide Poisoning can occur from brief exposures to high levels of CO, or from longer exposures to lower levels. Common symptoms include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often go on to develop neurological problems, including cognitive sequelae, anxiety and depression, persistent headaches, dizziness, sleep problems, motor weakness, vestibular and balance problems, gaze abnormalities, peripheral neuropathies, hearing loss, tinnitus and Parkinsonian-like syndrome. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO Poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by the CO-induced adduct formation of myelin basic protein. Based upon three supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO Poisoning. Hyperbaric oxygen is indicated for CO Poisoning complicated by cyanide Poisoning, often concomitantly with smoke inhalation.

  • practice recommendations in the diagnosis management and prevention of Carbon Monoxide Poisoning
    American Journal of Respiratory and Critical Care Medicine, 2012
    Co-Authors: Neil B. Hampson, Stephen R. Thom, Claude A Piantadosi, Lindell K. Weaver
    Abstract:

    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.

  • Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning
    New England Journal of Medicine, 2002
    Co-Authors: Lindell K. Weaver, Karen J. Chan, Frank O. Thomas, C. Gregory Elliott, S. Churchill, James F. Orme, Terry P Clemmer, Ramona O. Hopkins, Alan H Morris
    Abstract:

    Background Patients with acute Carbon Monoxide Poisoning commonly have cognitive sequelae. We conducted a double-blind, randomized trial to evaluate the effect of hyperbaric-oxygen treatment on such cognitive sequelae. Methods We randomly assigned patients with symptomatic acute Carbon Monoxide Poisoning in equal proportions to three chamber sessions within a 24-hour period, consisting of either three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air. Oxygen treatments were administered from a high-flow reservoir through a face mask that prevented rebreathing or by endotracheal tube. Neuropsychological tests were administered immediately after chamber sessions 1 and 3, and 2 weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae six weeks after Carbon Monoxide Poisoning. Results The trial was stopped after the third of four scheduled interim analyses, at which point there were 76 patients in ea...

T Beppu - One of the best experts on this subject based on the ideXlab platform.

  • The role of MR imaging in assessment of brain damage from Carbon Monoxide Poisoning: a review of the literature
    2020
    Co-Authors: T Beppu
    Abstract:

    ABSTRACT SUMMARY: The aim of this article is to review how MR imaging and associated imaging modalities provide clinicopathologic information on brain damage after Carbon Monoxide Poisoning. Initially, many authors documented typical findings of conventional MR imaging in the gray matter structures such as the globus pallidus and in various regions of cerebral white matter. The focus of investigation has since shifted to observation of cerebral white matter areas that are more frequently detected on MR imaging and are more responsible for chronic symptoms than the gray matter. DWI has dramatically contributed to the ability to quantitatively assess cerebral white matter damage. Subsequently, DTI has enabled more sensitive evaluation than DWI and can demonstrate progressive pathologic changes in the early stage, allowing prediction of chronic conditions. In addition, MR spectroscopy reveals changes in metabolite levels, offering quantitative clinicopathologic information on brain damage after Carbon Monoxide Poisoning. ABBREVIATIONS: CO ϭ Carbon Monoxide; CWM ϭ cerebral white matter; DNS ϭ delayed neuropsychiatric sequelae; FA ϭ fractional anisotropy; GP ϭ globu

  • the role of mr imaging in assessment of brain damage from Carbon Monoxide Poisoning a review of the literature
    American Journal of Neuroradiology, 2014
    Co-Authors: T Beppu
    Abstract:

    SUMMARY: The aim of this article is to review how MR imaging and associated imaging modalities provide clinicopathologic information on brain damage after Carbon Monoxide Poisoning. Initially, many authors documented typical findings of conventional MR imaging in the gray matter structures such as the globus pallidus and in various regions of cerebral white matter. The focus of investigation has since shifted to observation of cerebral white matter areas that are more frequently detected on MR imaging and are more responsible for chronic symptoms than the gray matter. DWI has dramatically contributed to the ability to quantitatively assess cerebral white matter damage. Subsequently, DTI has enabled more sensitive evaluation than DWI and can demonstrate progressive pathologic changes in the early stage, allowing prediction of chronic conditions. In addition, MR spectroscopy reveals changes in metabolite levels, offering quantitative clinicopathologic information on brain damage after Carbon Monoxide Poisoning. ABBREVIATIONS: CO Carbon Monoxide; CWM cerebral white matter; DNS delayed neuropsychiatric sequelae; FA fractional anisotropy; GP globus pallidus; MBP myelin basic protein

How-ran Guo - One of the best experts on this subject based on the ideXlab platform.

  • Hyperbaric Oxygen Therapy Is Associated With Lower Short- and Long-Term Mortality in Patients With Carbon Monoxide Poisoning
    Chest, 2017
    Co-Authors: Chien Cheng Huang, Yi-chen Chen, Hung Jung Lin, Chien Chin Hsu, Jhi-joung Wang, Shih Bin Su, How-ran Guo
    Abstract:

    Background To date, there has been no consensus about the effect of hyperbaric oxygen therapy (HBOT) on the mortality of patients with Carbon Monoxide Poisoning (COP). This retrospective nationwide population-based cohort study from Taiwan was conducted to clarify this issue. Methods Using the Nationwide Poisoning Database, we identified 25,737 patients with COP diagnosed between 1999 and 2012, including 7,278 patients who received HBOT and 18,459 patients who did not. The mortality risks of the two cohorts were compared, including overall mortality, and stratified analyses by age, sex, underlying comorbidities, monthly income, suicide attempt, drug Poisoning, acute respiratory failure, and follow-up until 2013 were conducted. We also tried to identify independent mortality predictors and evaluated their effects. Results Patients who received HBOT had a lower mortality rate compared with patients who did not (adjusted hazard ratio [AHR], 0.74; 95% CI, 0.67-0.81) after adjusting for age, sex, underlying comorbidities, monthly income, and concomitant conditions, especially in patients younger than 20 years (AHR, 0.45; 95% CI, 0.26-0.80) and those with acute respiratory failure (AHR, 0.43; 95% CI, 0.35-0.53). The lower mortality rate was noted for a period of 4 years after treatment of the COP. Patients who received two or more sessions of HBOT had a lower mortality rate than did those who received HBOT only once. Older age, male sex, low monthly income, diabetes, malignancy, stroke, alcoholism, mental disorders, suicide attempts, and acute respiratory failure were also independent mortality predictors. Conclusions HBOT was associated with a lower mortality rate in patients with COP, especially in those who were younger than 20 years and those with acute respiratory failure. The results provide important references for decision-making in the treatment of COP.

  • lack of pupil reflex and loss of consciousness predict 30 day neurological sequelae in patients with Carbon Monoxide Poisoning
    PLOS ONE, 2015
    Co-Authors: Jian Fang Zou, Hung Jung Lin, How-ran Guo, Qiming Guo, Hua Shao, Maofeng Liu, Fengling Liu, Lixin Dai, Chien Cheng Huang
    Abstract:

    Background Predicting the neurological sequelae of Carbon Monoxide Poisoning (COP) has not been well studied. We investigated the independent predictors of neurological sequelae in patients with COP and combined these predictors to predict the prognosis. Methods This study was conducted at four hospitals in Shandong Province, China. Data were retrospectively collected from 258 patients with COP between November 1990 and October 2011. Thirty-day neurological sequelae were the primary endpoints. Results A lack of pupil reflex and a loss of consciousness appear to be independent predictors for neurological sequelae in patients with COP. The presence of either one had a sensitivity of 77.0% (95% confidence interval [CI]: 69.3–83.2), a specificity of 47.1% (95% CI: 38.3–56.0), positive predictive value (PPV) of 62.9% (95% CI: 55.2–70.1), and a negative predictive value (NPV) of 63.6% (95% CI: 52.6–73.4). With both predictors present, the sensitivity was 11.5% (95% CI: 6.9 to 18.3), the specificity was 99.2 (95% CI: 94.7–100.0), the PPV was 94.1% (95% CI: 69.2–99.7), and the NPV was 49.0% (95% CI: 42.5–55.5). Conclusions The risk for neurological sequelae apparently increased with the number of independent predictors. In patients with both predictors, the risk for neurological sequelae was 94.1%. Almost all (99.2%) patients with neither predictor had no neurological sequelae. This finding may help physicians make decisions about and dispositions for patients with COP. For patients with a higher risk, earlier treatment and more appropriate utilization of health care services, including hyperbaric oxygen, should be considered.

  • a positive babinski reflex predicts delayed neuropsychiatric sequelae in chinese patients with Carbon Monoxide Poisoning
    BioMed Research International, 2014
    Co-Authors: Jian Fang Zou, Hung Jung Lin, How-ran Guo, Qiming Guo, Hua Shao, Maofeng Liu, Fengling Liu, Lixin Dai, Min Hsien Chung, Tzu Meng Yang
    Abstract:

    As the human population increased in China, the Carbon Monoxide is a serious environmental toxin in public health. However, predicting the delayed neuropsychiatric sequelae (DNS) of Carbon Monoxide Poisoning (COP) has not been well studied. We investigated the independent predictors of DNS in patients with COP. This study was conducted at four hospitals in China. Data were retrospectively collected from 258 patients with COP between November 1990 and October 2011. DNS was the primary endpoint. A positive Babinski reflex was the independent predictor for DNS: sensitivity = 53.8% (95% confidence interval [CI]: 26.1–79.6), specificity = 88.6% (95% CI: 83.7–92.1), positive predictive value (PPV) = 20.0% (95% CI: 9.1–37.5), and negative predictive value (NPV) = 97.3% (95% CI: 94.0–98.9). The area under the receiver operating characteristic curve = 0.712 (95% CI: 0.544–0.880). A positive Babinski reflex was very memorable, immediately available, and applicable in clinical practice. Even when the sensitivity and PPV of a positive Babinski reflex were unsatisfactory, it had a good specificity and NPV for excluding the risk of DNS. In patients without a positive Babinski reflex, the risk for DNS was only 2.7%. This finding may help physicians make decisions about dispositions for patients with COP.