El rol del laboratorio en los hallazgos de intoxicación y exposición a monóxido de carbono / The role of the laboratory in findings of carbon monoxide poisoning and exposure

El monóxido de carbono es un gas altamente tóxico que se origina principalmente por la combustión incompleta de combustibles fósiles. La intoxicación presenta síntomas inespecíficos que solapan otras patologías y por lo tanto es indispensable la confirmación mediante la medición de la carboxihemoglobina en sangre. El laboratorio incorporó la determinación en el informe del estado ácido base a partir de octubre del 2018, debido a que previamente el médico debía solicitarla frente a la sospecha de una intoxicación. El objetivo del trabajo fue evaluar si esta medida implementada por el laboratorio contribuyó a mejorar el diagnóstico de intoxicación por CO, analizar las características de los pacientes con COHb mayor o igual a 5% y definir un valor de reporte inmediato para la COHb. El 46% de los casos con COHb mayor o igual a 5% no se relacionaban con una intoxicación y/o exposición a CO. De los casos de intoxicación se encontró que el 77% fueron diagnosticados a partir de la sospecha médica y un 23% por hallazgo del laboratorio. Se concluyó que es de mucha utilidad el rol del laboratorio en detectar aquellos casos que no fueron evidentes clínicamente. Existen ciertas patologías como las oncológicas o la enfermedad de Wilson donde se vieron valores elevados de COHb sin presentar intoxicación y se definió finalmente, como valor de reporte inmediato 7% para la COHb. (AU)

Carbon monoxide is a highly toxic gas that originates mainly from incomplete combustion of fossil fuels. Intoxication causes nonspecific symptoms that overlap with other conditions and, therefore, confirmation by measuring blood carboxyhemoglobin is essential. The laboratory incorporated the measurement in the acid-base status report as of October 2018, as it was previously required to be requested by the physician in case of suspected intoxication. The aim of this study was to evaluate whether this measure implemented by the laboratory contributed to the improvement of the diagnosis of CO intoxication, to analyze the characteristics of patients with COHb greater than or equal to 5% and to define an immediate reporting value for COHb. Overall, 46% of the cases with COHb greater than or equal to 5% were not related to CO poisoning and/or exposure. Of the cases of intoxication, 77% were diagnosed based on medical suspicion and 23% on laboratory findings. It was concluded that the laboratory has a useful role in detecting cases that were not clinically evident. There are certain diseases including different types of cancer or Wilson's disease where elevated COHb values were seen without intoxication and finally, 7% for COHb was defined as the immediate reporting value (AU)

Intoxicación por monóxido de carbono: estudio observacional de pacientes que acudieron a Urgencias durante 2020 / Carbon monoxide poisoning: an observational study of patients admitted to Emergency Department during 2020

El objetivo fue describir las intoxicaciones monóxido de carbono. Se diseñó un corte transversal que incluyó una muestra consecutiva de mediciones de carboxihemoglobina (COHb), realizadas Enero y Diciembre 2020 en la Central de Emergencias del Hospital Italiano de Buenos Aires. Se utilizaron bases secundarias y revisión manual de historias clínicas para recolección de varia-bles de interés. Durante el período de estudio hubo 20 pacientes confirmados, con media de 50 años (DE 20), 55% sexo masculino, 20% tabaquistas, y una única embarazada. El 70% correspondieron al trimestre Junio-Julio-Agosto. La fuente de intoxicación más frecuente se debió a accidentes domésticos (calefón, estufa, brasero, hornalla, salamandra) que representaron el 50% de los casos, 30% por incendios, y el 20% restante explicado por tabaco o factor desconocido. Los estudios de laboratorio más solicitados fueron: 95% recuento de glóbulos blancos, 85% glucemia, 70% CPK, y 55% troponina. Los hallazgos relevantes fueron COHb con mediana de 7.15%, CPK con mediana de 89 U/mL, y troponina con mediana de 8.5 pg/mL. La totalidad se realizó electrocardiograma: 15% presentaron arritmia como hallazgo patológico, y ninguno isquemia. En cuanto la presentación clínica: 30% presentó cefalea, 15% síncope, 15% coma, 10% mareos y 10% convulsiones. Sólo 25% tuvieron tomografía y 15% resonancia de cerebro, sin hallazgos críticos. Sin embargo, 15% fueron derivados para trata-miento con cámara hiperbárica. La mayoría ocurrieron en invierno y explicados por accidentes domésticos. Será necesario un fortalecimiento del rol preventivo que apunte al control de la instalación y el buen funcionamiento de artefactos, como mantener los ambientes bien ventilados (AU)

The objective was to describe carbon monoxide poisoning. A cross sectional was designed, which included a consecutive sample of carboxyhemoglobin (COHb) measurements, carried from January to December 2020 at the Emergency Department of tHospital Italiano de Buenos Aires. Secondary databases and manual review of medical records were used to collect variables of interest. During the study period there were 20 confirmed patients, with a mean age of 50 (SD 20), mostly male (55%), 20% smokers, and only one pregnant woman, 70% corresponded to June-July-August. The most frequent source of poisoning was explained to domestic accidents (water heater, stove, brazier, stove, salamander) which represented 50% of cases, 30% due to fires, and the remaining 20% by tobacco or unknown factor. The most laboratory studies were: 95% white blood cell count, 85% glycemia, 70% CPK, and 55% troponin. Meanwhile, relevant findings were carboxyhemoglobin with a median of 7.15%, CPK with a median of 89 U/mL, and troponin with a median of 8.5 pg/mL. All underwent an electrocardiogram: 15% presented arrhythmia as a pathological finding, and none ischemia. Regarding the clinical presentation: 30% presented headache, 15% syncope, 15% coma, 10% dizziness and 10% seizures. Only 25% had brain tomography and 15% MRI, without pathological findings. However, 15% were referred for treatment with a hyperbaric chamber. Most of the cases occurred in winter and explained by domestic accidents. It will be necessary to strengthen the preventive role that aims to control the installation and the proper functioning of devices, such as keeping rooms well ventilated (AU)

Usefulness of a modified poisoning severity score for predicting prognosis in acute carbon monoxide poisoning.

INTRODUCTION: The poisoning severity score (PSS) was developed to grade the severity of various types of poisoning. However, in its current form, it requires investigating many variables, some of which have been found not to be associated with carbon monoxide (CO) poisoning severity. Therefore, in this study, we modified the PSS for CO poisoning and compared its usefulness to that of the original PSS, as an early prognostic factor of short-term outcome in CO poisoning patients. METHODS: This was a retrospective observational study conducted in patients with CO poisoning who visited the emergency department between January 2014 and December 2020. Patients' primary outcome was their Cerebral Performance Category (CPC) scale score at discharge, which classified those with CPC 1-2 as having a favorable outcome and those with CPC 3-5 as having a poor outcome. We calculated the patients' PSS and their CO-modified PSS by replacing blood and metabolic balance category in the original PSS with carboxyhemoglobin (COHb) and lactate levels, respectively. RESULTS: This study included 891 patients, of which 852 (95.6%) and 39 (4.4%) were classified into the favorable and poor outcome groups, respectively. Using multivariate analysis, the PSS (odds ratio [OR], 22.961; 95% confidence interval [CI], 10.641-49.546; p < 0.001) and CO-modified PSS (OR, 28.856; 95% CI, 12.874-64.679; p < 0.001) were both found to be associated with poor outcomes at hospital discharge. The areas under the receiver operating characteristic curves for the PSS and CO-modified PSS were 0.874 (95% CI, 0.850-0.895) and 0.881 (95% CI, 0.858-0.901), respectively. CONCLUSION: The CO-modified PSS, with fewer variables than the original PSS, was not inferior to predict poor outcomes, and if COHb level is considered together with other parameters, then it can be used both for predicting prognosis and in diagnosis.

Prediction of delayed neuropsychiatric sequelae after carbon monoxide poisoning via serial determination of serum neuron-specific enolase levels.

BACKGROUND: Neuron-specific enolase (NSE) is released into serum when nerve cells are damaged, and the levels thereof are used to determine neurological prognosis in patients who have suffered cardiac arrest or stroke. Delayed neuropsychiatric sequelae (DNS), a major complication of carbon monoxide poisoning (COP), can be caused by inflammatory response which is a mechanism of neuronal injury in cardiac arrest and stroke. NSE is known as a predictor of neurological prognosis in ischemic brain injury after cardiac arrest, and it is also reported as a predictor of DNS in acute COP. When serum NSE is measured serially in cardiac arrest patients, the best time to predict neurological prognosis is known at 48-72 h, but there are no studies analyzing serial serum NSE in acute COP. Thus, we explored whether serum NSE levels measured three times at 24 h intervals after COP predicted the development of DNS. METHODS: This prospective observational study was conducted on patients treated for COP from May 2018 to April 2020 in a tertiary care hospital in Korea. Neuron-specific enolase levels were assessed 24, 48, and 72 h after presentation at hospital. We used logistic regression to explore the association between NSE levels and DNS development. RESULTS: The NSE level was highest at 48 h, and the difference between the DNS group and the non-DNS group was greatest on the same time point. On multivariable logistic regression analysis, the NSE level at 48 h of >20.98 ng/mL (odds ratio [OR], 3.570; 95% confidence interval [CI], 1.412-9.026; P = .007) and the initial Glasgow Coma Scale (GCS) score of <9 (OR, 4.559; 95% CI, 1.658-0.12.540; P = .003) was statistically significant for DNS development. CONCLUSION: Early identification of those who will experience DNS in acute COP patients is clinically important for deciding treatment. In this study, we revealed that NSE level of >20.98 ng/mL at 48 h time point can be used as an independent predictor of DNS (OR, 3.570; 95% CI, 1.412-9.026; P = .007; AUC, 0.648).

Acute carbon monoxide poisoning with low saturation of carboxyhaemoglobin: a forensic retrospective study in Shanghai, China.

Carbon monoxide (CO) poisoning is a common cause of death, leading to morbidity and mortality worldwide. Features of the CO poisoning with low carboxyhemoglobin (COHb) levels remain to be characterized. This study collected a total of 307 CO poisoning cases from Shanghai Public Security Bureau, an official organization that handles the most complicated and life-threatening cases across Shanghai municipality in China, and regrouped these cases into three categories: group 1, 10% < COHb% < 30% (n = 58); group 2, 30% ≤ COHb% < 50% (n = 79); group 3, COHb% ≥ 50% (n = 170). Epidemiological, demographic, and forensic aspects of the CO poisoning cases, particularly those with low COHb levels, were analyzed. Our results showed that group 2 and 3 were mostly observed in younger victims (≤ 30 years), while group 1 equally distributed to all age groups (p = 0.03). All the CO poisoning from group 2 and 3 occurred in enclosed spaces, whereas cases from group 1 died additionally in outdoor spaces (p = 0.01). 81.03% of group 1 cases died in fire circumstances, while only 45.57% from group 2 and 30.59% from group 3 were fire-related (p = 0.00). Accordingly, group 1 was mostly related with fire burns, while group 2 or 3 were largely associated with gas leakage (p = 0.00). A combination with alcohol, but not other psychotropic drugs, associated with significant higher levels of blood COHb% in fire-unrelated (p = 0.021) but not fire-related cases (p = 0.23). Five extremely low COHb% (< 30%)-related poisoning deaths were negative of any cardiopulmonary pathology and psychoactive substances. In conclusion, CO poisoning with low COHb% significantly associates with fire circumstances and outdoor spaces and has no age preference. Further diagnostic markers mandates to be identified in order to avoid disputes in cases of extremely low COHb%-related poisoning.

Serum NSE and S100B protein levels for evaluating the impaired consciousness in patients with acute carbon monoxide poisoning.

ABSTRACT: The aim of this study was to investigate the associations between the levels of neuron-specific enolase (NSE) and S100B protein and coma duration, and evaluate the optimal cut-off values for prediction coma duration ≥ 72 hours in patients with acute carbon monoxide poisoning (ACOP).A total of 60 patients with ACOP were divided into 3 following groups according to their status of consciousness and coma duration at admission: Awake group [Glasgow Coma Scale score (GCS score) ≥ 13 points], Coma < 72 hours group (GCS score < 13 points and coma duration < 72 h), and Coma ≥ 72 hours group (GCS score < 13 points and coma duration ≥ 72 h). The levels of serum NSE and S100B protein were measured after admission.There were significant differences in GCS score, carbon monoxide (CO) exposure time, NSE, and S100B levels between the Coma ≥ 72 h group and the Awake group, and between the Coma < 72 h group and the Awake group. Significant differences in GCS score, NSE, and S100B levels were also found between Coma ≥ 72 h group and Coma < 72 h group. Correlation analysis showed that NSE and S100B were positively correlated (rs = 0.590, P < .01); NSE and S100B were negatively correlated with GCS score (rs = -0.583, rs = -0.590, respectively, both P < .01). The areas under the curve (AUCs) of NSE, S100B, and GCS score to predict the coma duration ≥ 72 hours were 0.754, 0.791, and 0.785, respectively. Pairwise comparisons did not show differences among the 3 groups (all P > .05). The sensitivity and specificity of NSE prediction with a cut-off value of 13 µg/L were 80% and 64%, respectively, and those of S100B prediction with a cut-off value of 0.43 µg/L were 70% and 88%, respectively.The NSE and S100B protein levels were significantly correlated with the degree of impaired consciousness and had the same clinical value in predicting coma duration of ≥ 72 hours in patients with ACOP.

Neuropsychiatric sequelae of acute carbon monoxide poisoning: The predictive role of neuron specific enolase and glial fibrillary acidic protein.

BACKGROUND: Acute carbon monoxide (CO) poisoning is one of the most common poisons worldwide and neuropsychiatric sequelae (NS) are the most frequent form of its morbidity. OBJECTIVES: This study aimed to measure the percentage of patients liable to NS, to evaluate the cognitive profile of patients with NS and to assess the role of neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP) in predicting the development of NS after acute CO poisoning. METHODS: This prospective study included 50 patients with acute CO poisoning presented to the Poison Control Center, Ain Shams University Hospitals during the period from beginning of November 2015 till the end of January 2017. Patients' demographic characteristics, clinical manifestations and blood carboxyhemoglobin levels were recorded. Serum levels of NSE and GFAP were determined on admission. Every patient was invited to participate in a follow-up visit at a dedicated outpatient clinic one month after CO exposure. During the visit, a complete neurological examination, as well as a psychiatric evaluation using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders version 4 Axis-I were performed for detection of neurological and psychiatric disorders. Wechsler memory scale test was administrated for detection of cognitive deficits. The patients were divided into two groups based on the presence or absence of NS. RESULTS: Cognitive impairment was found in 38 % of patients in the NS group. The serum levels of NSE and GFAP were significantly high in the NS group in comparison to the non-NS group. Receiver operating characteristic curves (ROC) determined the cut-off level of NSE at 39 ng/mL achieved 100 % sensitivity with 88.64 % specificity to predict the development of NS after acute CO poisoning while GFAP had 95.24 % sensitivity and 69.23 % specificity at a cut-off value of 2.8 ng/mL. CONCLUSION: NSE and GFAP could be useful in the early identification of patients at risk of developing NS after CO poisoning helping in treatment plans and thus improving quality of care.

Development of delayed neurologic sequelae in acute carbon monoxide poisoning cases caused by briquette-based kotatsu: A case-control study.

ABSTRACT: Briquette-based kotatsu, a traditional Japanese heating system, is still used in rural areas and has been linked to the development of acute carbon monoxide (CO) poisoning. This study aimed to investigate the occurrence of delayed neurologic sequelae (DNS) in patients with acute CO poisoning caused by briquette-based kotatsu.This retrospective study included 17 patients treated for acute CO poisoning due to briquette-based kotatsu, between April 2017 and March 2020. Patients were divided into either a sequelae group (3 patients) or a non-sequelae group (14 patients) based on the presence or absence, respectively, of DNS. Demographic data, kotatsu characteristics, clinical findings, and therapies were compared between the 2 groups.Significant differences were noted in patient posture during their initial discovery. Specifically, all non-sequelae patients only had their legs under the kotatsu quilt and all sequelae patients had their entire bodies under the kotatsu quilt (P = .001). There were no statistically significant differences in carbon monoxide levels in hemoglobin (CO-Hb) or the creatine-kinase myocardial band (CK-MB), between the 2 groups; however, troponin-I levels were significantly higher in the sequelae group (P = .026). Abnormal head imaging findings were noted in 2 sequelae-group patients, with a significant difference between the groups (P = .025).We speculate that acute CO poisoning, caused by briquette-based kotatsu, may lead to DNS more frequently in patients in who cover their entire body with the kotatsu quilt and are found in this position. Patients should be warned about the dangers of acute CO poisoning when using briquette-based kotatsu.

Non-invasive monitoring of carboxyhemoglobin during hyperbaric oxygen therapy.

Introduction: This study aimed to assess the capability of a pulse CO-oximeter to continuously monitor carboxyhemoglobin (COHb) during hyperbaric oxygen (HBO2) therapy. We estimated limits of agreement (LOA) between blood gas analysis and pulse CO-oximeter for COHb during HBO2 therapy in patients suffering from acute CO poisoning. Furthermore, we did a medicotechnical evaluation of the pulse CO-oximeter in hyperbaric conditions. Methods: We conducted a prospective, non-clinical, observational study in which we included n=10 patients with acute CO poisoning referred for HBO2 therapy. We did five repeated measurements of COHb for each patient during the HBO2 therapy. Bland-Altman analysis for multiple observations per individual was used to assess the agreement. The a priori LOA was ±6% for COHb. For the medicotechnical evaluation continuous measurements were obtained throughout each complete HBO2 therapy. The measurements were visually inspected and evaluated. Results: The Bland-Altman analysis showed that the pulse CO-oximeter overestimated COHb by 2.9 % [±1.0%] and the LOA was ±7.3% [±1.8%]. The continuous measurements by pulse CO-oximetry showed fluctuating levels of COHb and summarized saturations reached levels above 100%. Measurements were not affected by changes in pressure. Conclusion: To our knowledge, this study is the first to assess LOA and demonstrate use of a non-invasive method to measure COHb during HBO2 therapy. The pulse CO-oximeter performed within the manufactures reported LOA (±6%) despite hyperbaric conditions and was unaffected by changes in pressure. However, summarized saturations reached levels above 100%.

Hyperbaric oxygen therapy mobilized circulating stem cells and improved delayed encephalopathy after acute carbon monoxide poisoning with up-regulation of brain-derived neurotrophic factor.

Background Delayed encephalopathy (DE) is the most severe complication after acute carbon monoxide (CO) poisoning, which seriously affects the outcome of patients and leads to a high disability rate. Prior studies have shown that hyperbaric oxygen (HBO2) therapy is therapeutic for DE due to reducing immune-mediated neuropathology and thus improving cognitive performance. Methods In our present perspective study, five DE patients were treated regularly with HBO2 therapy. The mini-mental state examination (MMSE) and Barthel index (BI) were intermittently collected during their hospitalization for mental and physical status evaluation, the peripheral bloods were serially sampled to determine the concentration changes of circulating stem cells, as well as corresponding BDNF and neural markers. Results MMSE and BI showed series of improvements after multiple HBO2 therapies. The CD34+/CD90+ and CD34+/CD133+ dual positive cells, which were categorized as circulating stem cells, were observed an overall up-regulation since the beginning of the DE onset upon the application of HBO2 therapy. Characteristic neurotrophin BDNF, neural markers such as nestin and synaptophysin (SYP) were also up-regulated after exposure of HBO2. Conclusion The application of HBO2 therapy is of significance in improving the cognition of DE patients, along with mobilized circulating stem cells. We primarily infer that the CD34+/CD90+ and CD34+/CD133+ cells were mobilized by HBO2 exposure and have played a positive role in cognition improvement on DE patients by up-regulation of BDNF, nestin and SYP. The altering amount of circulating stem cells mobilized in peripheral blood could be a potential marker on predicting the outcome of DE.

Evaluation of the Cardioprotective Effect of Granulocyte Colony Stimulating Factor in Patients with Carbon Monoxide Poisoning.

BACKGROUND: Carbon monoxide (CO), which is well known as silent killer, has many toxic effects on organs with high rate of metabolism such as heart and brain. CO-induced cardiotoxicity resulted in a wide range of disabilities including electrocardiogram (ECG) abnormalities, elevation in level of cardiac enzymes, arrhythmias, impairment of left ventricular and myocardial infarction (MI). Cardio-protective effects of Granulocyte colony-stimulating factor (G-CSF) on infarcted heart was proved previously in various reports. OBJECTIVE: In this study, possible effect of G-CSF on cardiac function of patients with moderate to severe acute CO poisoning was investigated. METHODS: Cardioprotective effects of G-CSF in CO-poisoned patients was evaluated through ECG, Holter monitoring, echocardiography, and biochemical studies. Continuous intravenous infusion of G-CSF (90 µg/kg) and normal saline were administered respectively to treatment and placebo groups. RESULTS: The results demonstrated that in moderate to severe CO poisoning, myocardial injury is common. ECG changes (e.g., ST-segment and T-wave changes, QTC), cardiac arrhythmias (e.g., heart blocks and ventricular arrhythmias), serum level of Troponin I, left ventricular ejection fraction were determined after G-CSF administration. Frequencies of ST depression, inversion or flatting of T wave and QTC in ECG were significantly reduced after G-CSF treatment. In addition, incidence of cardiac arrhythmias due to CO poisoning were reduced after G-CSF treatment. However, G-CSF did not exert protective effects on TPI level and function of left ventricular in CO-poisoned patients. CONCLUSION: GCSF could probably reduce CO-induced cardiac ischemia in patients with acute CO poisoning. CLINICAL TRIAL REGISTRATION: The trial protocol was registered in the Iranian Registry of Clinical Trials (http://www.irct.ir) registry (Irct ID: IRCT201607232083N7).

Initial creatine kinase level as predictor for delayed neuropsychiatric sequelae associated with acute carbon monoxide poisoning.

INTRODUCTION: The primary goal of treating patients with carbon monoxide (CO) poisoning is preventing delayed neuropsychiatric sequelae (DNS). It is difficult to predict DNS because there is no precise diagnostic method in the early phase of CO poisoning. In this study, we aimed to investigate the optimal cut-off value for creatine kinase level to predict DNS. METHODS: This retrospective observational study included patients with CO poisoning visiting a single tertiary center from January to July 2018. They were divided into two groups according to the presence of DNS. We compared baseline characteristics with variables that could affect the presence of DNS. The optimal cut-off value of initial creatine kinase concentration for DNS was calculated. Additionally, multivariate analysis was performed to confirm whether creatine kinase could be an independent predictor of DNS. RESULTS: Of the 138 patients, 12 patients developed DNS. Univariate analysis showed significant differences in the Glasgow Coma Scale, duration of exposure, laboratory tests, abnormal finding on MRI in acute phase, the number of hyperbaric oxygen therapy sessions, and duration of hospitalization. Receiver operating characteristic analyses of creatine kinase were performed (AUC = 0.92; 95% CI, 0.86-0.96) with a cut-off value of 1603 U/L; DNS was predicted with a sensitivity of 91.7% and specificity of 88.1%. In multivariate analysis, the adjusted odds ratio of creatine kinase was 51.516. CONCLUSION: In patients with CO poisoning, initial creatine kinase concentrations of >1603 U/L can be used as an independent predictor of DNS.

Assessment of serum glucose/potassium ratio as a predictor for delayed neuropsychiatric syndrome of carbon monoxide poisoning.

INTRODUCTION: Carbon monoxide (CO) poisoning is a crucial cause of delayed neuropsychiatric syndrome (DNS). However, most biomarkers are not satisfactory for the prediction of DNS caused by CO poisoning. Thus, we evaluated the adequacy of the serum glucose/potassium (GLU/K) ratio, which may be an easy, quick, and readily available parameter that can be used in the emergency department for predicting DNS. METHODS: We evaluated 281 patients who were admitted to our emergency department between January 2012 and December 2018. The patients were divided into two groups: DNS (+) and DNS (-). The GLU/K was compared for the groups. RESULTS: Glucose, blood urea nitrogen, carboxyhemoglobin, and GLU/K ratios of patients in the DNS (+) group were statistically significantly higher than those patients in DNS (-) group (140 ± 34 vs. 110 ± 24, p < 0.001; 17.58 ± 6.14 vs. 14.27 ± 5.08, p = 0.003; 29 ± 5.1 vs. 18.9 ± 7.6, p < 0.001; and 38.35 ± 10.11 vs. 28.65 ± 6.53, p < 0.001, respectively). The area under the curve for GLU/K to predict DNS was measured as 0.791, and 35.9 as a cut-off value had 63.6% sensitivity and 89.6% specificity. CONCLUSIONS: DNS development in CO poisoning is a serious and feared complication. We suggest that the GLU/K ratio has a high potential as a rapid, easy preliminary marker for the exclusion of patients who will not subsequently develop DNS.

Patterns of cardiac dysfunction after carbon monoxide poisoning.

Objective: To describe the structural sequelae of carbon monoxide (CO) poisoning on the heart assessed using stress cardiac MRI (CMR). CO poisoning is common. While acute cardiac injury is frequent among survivors, the mid- and long-term effects of CO on the myocardium are unclear. Methods: CMR studies performed between the years 2005 and 2014 for a primary diagnosis of CO poisoning at a tertiary care center were reviewed by an experienced cardiologist. Variables of interest were compared between patients with normal and abnormal studies to identify factors associated with cardiac dysfunction. Results: Eighty-eight patients underwent stress CMR, age 34 years (range 11-70); 49% were male, 74 had acute poisoning and 14 had chronic poisoning (CO exposure for longer than 24 hours). Time from CO poisoning to imaging was 24 months (1 day-120 months). Patients were stratified into four categories, which included those with acute poisoning imaged: ≤12 months; 12-60 months; >60 months from the event; and those with chronic poisoning. Overall, 26 studies (30%) were abnormal. The most common findings were: left ventricular systolic dysfunction in 14 patients, right ventricular systolic dysfunction in nine, and LV dilatation in six. Abnormalities were mild in most cases and were equally prevalent in all four patient categories. Dyspnea at the time of follow-up was more frequent among those with abnormal studies. Conclusion: Mild alterations in ventricular structure and function are frequent in survivors of CO poisoning. Myocardial scarring is rare, suggesting that acute hypoxic injury may not fully explain these abnormalities.

Successful use of hyperbaric oxygen therapy for limb salvage of acute limb ischemia as a complication of acute carbon monoxide poisoning.

Acute limb ischemia (ALI) as a complication of acute carbon monoxide (CO) poisoning is rare. Several reports have utilized hyperbaric oxygen therapy (HBO2) as an adjunctive therapy for peripheral arterial diseases. However, no study has yet described the use of HBO2 for ALI precipitated by CO poisoning. Herein we report successful limb salvage achieved with adjunctive HBO2 and conventional therapies in a patient with CO-induced ALI. A 69-year-old man was admitted with acute CO poisoning; ALI of both lower extremities occurred on hospitalization day 3. Pre-existing risk factors for ALI other than CO were not definite. After conventional treatments including catheter-directed thrombolysis and endovascular thrombectomy, the right-side lesion remained and a left-side lesion was newly developed. In addition to prior therapies, 47 sessions of serial HBO2 were administered as adjunctive therapy, resulting in limb salvage. Acute CO poisoning can cause ALI as a rare complication. HBO2 may be utilized as an adjunctive treatment in ALI.

Comparison of non-invasive CPAP with mask use in carbon monoxide poisoning.

BACKGROUND: Carbon monoxide (CO) is one of the major causes of poisoning worldwide. We aimed to investigate the efficacy of the continuous positive airway pressure (CPAP) use in CO poisoning. METHODS: After CO poisoning, one group of patients was treated with a non-rebreather mask (NRB) and another group using the CPAP mode of mechanical ventilation (CPAP). All patients received at least 90 minute treatment. The carboxyhemoglobin saturation (SpCO) levels of all patients were measured from the fingertips with a portable CO-oximeter at 0, 30, 60 and 90 min. The rates of changes in the serially measured SpCO values were obtained using the Wilcoxon signed-rank test. RESULTS: A total of 45 patients (24 in NRB and 21 in CPAP group) completed the study. The median initial SpCO levels were 24% (21-33) in NRB group, 25% (21-32) in CPAP group, with no statistically significant difference (p 0.323). At the 30th, 60th, and 90th minutes of treatment, significantly lower values were obtained from CPAP than NRB (p < 0.001). The COHb half-life was decreased significantly by CPAP [105(70-190) vs 45(30-120), p < 0.001]. In CPAP group, the fastest decline in the SpCO level was observed for the interval of 0-30 min [Median difference: 8(3-14), p < 0.001]. CONCLUSIONS: CPAP lowered the amount of CO in the blood faster than the mask; therefore, it may be effective in the treatment of CO poisoning.

Blood carboxyhemoglobin elimination curve, half-lifetime, and arterial-venous differences in acute phase of carbon monoxide poisoning in ovine smoke inhalation injury model.

Smoke inhalation injury (SII) affects more than 50,000 people annually causing carbon monoxide (CO) poisoning. Although the increased blood level of carboxyhemoglobin (CO-Hb) is frequently used to confirm the diagnosis of SII, knowledge of its elimination in the acute phase is still limited. The aim of this study is to determine CO-Hb elimination rates and their differences in arterial (aCO-Hb) and mixed-venous (vCO-Hb) blood following severe SII in a clinically relevant ovine model. Forty-three chronically instrumented female sheep were subjected to SII (12 breaths, 4 sets) through tracheostomy tube under anesthesia and analgesia. After the SII, sheep were awakened and placed on a mechanical ventilator (FiO2 = 1.0, tidal volume 12 mL/kg, and PEEP = 5cmH2O) and monitored. Arterial and mixed-venous blood samples were withdrawn simultaneously for blood gas analysis at various time points to determine CO-HB half-lifetime and an elimination curve. The mean of highest aCO-Hb level during SII was 70.8 ± 13.9%. The aCO-Hb elimination curve showed an approximated exponential decay during the first 60 min. Per mixed linear regression model analysis, aCO-Hb significantly (p < 0.001) declined (4.3%/minute) with a decay constant lambda of 0.044. With this lambda, mean lifetime and half-lifetime of aCO-Hb were 22.7 and 15.7 min, respectively. The aCO-Hb was significantly lower compared to vCO-Hb at all-time points (0-180 min). To our knowledge, this is the first report describing CO-Hb elimination curve in the acute phase after severe SII in the clinically relevant ovine model. Our data shows that CO-Hb is decreasing in linear manner with supportive mechanical ventilation (0-60 min). The results may help to understand CO-Hb elimination curve in the acute phase and improvement of pre-hospital and initial clinical care in patients with CO poisoning.

Carbon monoxide poisoning can act as a stress test to reveal underlying coronary artery disease: case report.

Carbon monoxide (CO) poisoning presents with many different cardiac effects, but one important presentation is its effect as a CO stress test to reveal underlying coronary artery disease (CAD). There are a limited number of publications detailing this phenomenon, but after CO intoxication it is important to suspect CAD in association with mild troponin leak or non-ST segment elevation myocardial infarction (NSTEMI) shown on electrocardiogram (EKG). We recently treated three patients with CO poisoning who had underlying CAD. In the first case a man presented to the emergency department with CO toxicity and an ST segment elevation myocardial infarction (STEMI), resulting in emergent angioplasty and the discovery of severe CAD. The second case involved an individual who presented with CO poisoning with rising troponin levels. An angioplasty discovered a stable 90% occlusion. The third case was a patient with CO poisoning and transient inferior T wave inversion EKG with borderline troponin elevation. Angioplasty showed only 30% occlusion, so the patient's presentation was likely due to direct CO cardiac toxicity. These cases demonstrate the varied presentations that CO poisoning can have on patients with underlying heart disease.

Carbon monoxide poisoning.

Despite established exposure limits and safety standards as well as 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 can 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 develop brain injury manifested by 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, Parkinsonian-like syndrome, and other problems. In addition, some will have cardiac issues or other ailments. 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.

Evaluation of hepatic injury in acute carbon monoxide-poisoned patients in emergency department.

INTRODUCTION: The affinity of hemoglobin for carbon monoxide (CO) is 250 times higher than that for oxygen. Therefore, exposure to CO leads to a reduction in oxygen delivery to tissues, resulting in cellular hypoxia and affects whole body. Hepatic dysfunction in critically ill patients is related to poor outcome, but few studies have been conducted on this subject that occurs after CO poisoning. This study aims to conduct a study of hepatic injury in CO-poisoned patients in emergency department (ED). METHODS: This retrospective observational study collected data from patients who were diagnosed with acute CO poisoning at the ED between June 2011 and May 2018 in local tertiary-care hospital (Wonju, Republic of Korea). The primary end point of this study was to describe the prevalence of hepatic injury in acute CO-poisoned patients. The secondary goals were to investigate the recovery trends of hepatic injury caused by acute CO poisoning and the relation to neurologic outcome and mortality. RESULTS: Eight hundred ninety-four patients were enrolled in the final analysis, 128 cases (14.3%) had subclinical hepatic injury and 15 (1.6%) cases had hepatic injury. The relationship with mortality was not statistically significant. However, the hepatic injury group was higher incidence of intensive care unit admission and other complications. Patients in the hepatic injury group recovered through conservative management within 1 week of being admitted to the ED. CONCLUSIONS: While CO-induced hepatic injury is relatively uncommon, it can be associated with complications and poor neurologic outcome. However, CO-induced hepatic injury was not found to have a statistically significant effect on mortality rate.