Clinical features and predictors of delayed neurological syndrome in carbon monoxide poisoning: the AMICO study. / Caracterización clínica y factores predictivos de desarrollo de síndrome neurológico tardío en la intoxicación por monóxido de carbono: estudio AMICO.

OBJECTIVES: To identify predictors for developing delayed neurological syndrome (DNS) after an initial episode of carbon monoxide (CO) poisoning in the interest of detecting patients most likely to develop DNS so that they can be followed. MATERIAL AND METHODS: Retrospective review of cases of CO poisoning treated in the past 10 years in the emergency departments of 4 hospitals in the AMICO study (Spanish acronym for the multicenter analysis of CO poisoning). We analyzed demographic characteristics of the patients and the clinical characteristics of the initial episode. The records of the cohort of patients with available follow-up information were reviewed to find cases of DNS. Data were analyzed by multivariant analysis to determine the relationship to characteristics of the initial exposure to CO. RESULTS: A total of 240 cases were identified. The median (interquartile range) age of the patients was 36.2 years (17.6-49.6 years); 108 patients (45.0%) were men, and the poisoning was accidental in 223 cases (92.9%). The median carboxyhemoglobin concentration on presentation was 12.7% (6.2%-18.7%). Follow-up details were available for 44 patients (18.3%). Eleven of those patients (25%) developed DNS. A low initial Glasgow Coma Scale score predicted the development of DNS with an odds ratio (OR) of 0.61 (95% CI, 0.41-0.92) and an area under the receiver operating characteristic curve of 0.876 (95% CI, 0.761-0.990) (P .001). CONCLUSION: The initial Glasgow Coma Scale score seems to be a clinical predictor of DNS after CO poisoning. We consider it important to establish follow-up protocols for patients with CO poisoning treated in hospital EDs.

OBJETIVO: Identificar factores pronósticos de desarrollo de síndrome neurológico tardío (SNT) después de un episodio inicial de intoxicación por monóxido de carbono (ICO), con el fin detectar precozmente a la población más susceptible y facilitar su acceso a un seguimiento específico. METODO: Revisión retrospectiva de todos los casos de ICO que acudieron a los servicios de urgencias (SU) de 4 hospitales durante los últimos 10 años. Se analizaron datos demográficos y características clínicas en el momento del episodio. En la cohorte de pacientes con datos de seguimiento disponibles, se evaluó la aparición de SNT y su relación con diferentes variables en la exposición inicial al CO a través de técnicas de análisis multivariante. RESULTADOS: Se identificaron 240 pacientes. La mediana de edad fue de 36,2 años (17,6-49,6). De ellos 108 (45,0%) eran hombres y 223 casos (92,9%) fueron accidentales. El nivel medio de COHb fue del 12,7% (6,2-18,7). En 44 (18,3%) episodios se disponía de datos de un seguimiento específico. En esta cohorte, 11 (25%) pacientes desarrollaron SNT. Una puntuación inicial más baja en la Escala Coma de Glasgow (GCS) (OR: 0,61, IC 95%: 0,41-0,92) fue predictor independiente del desarrollo del SNT, con un ABC en la curva COR de 0,876 (IC 95%: 0,761-0,990, p 0,001). CONCLUSIONES: Una puntuación inicial baja en la GCS parece ser un predictor clínico de desarrollo de SNT en la ICO. Dada la incidencia de SNT, consideramos fundamental establecer protocolos de seguimiento específico de estos pacientes tras su asistencia inicial en los SU.

Optic nerve sheath diameter measurements to predict delayed neurological sequelae after carbon monoxide poisoning.

OBJECTIVES: Delayed neurological sequelae are a major complication of carbon monoxide poisoning. However, today there is still no objective screening tool for predicting delayed neurological sequelae in patients with carbon monoxide poisoning. The present study aimed to assess the usefulness of optic nerve sheath diameter measurements in predicting delayed neurological sequelae after carbon monoxide poisoning. METHODS: In this retrospective study, patients with a diagnosis of carbon monoxide poisoning in the emergency department from 2010 to 2021 were included in the study. Right and left optic nerve sheath diameters were calculated based on cranial computed tomography scans, and the presence of delayed neurological sequelae was evaluated. RESULTS: The mean (± standard deviation) optic nerve sheath diameter in patients who developed delayed neurological sequelae was statistically significantly greater on both the right and left compared to patients who did not develop delayed neurological sequelae (right; 5.02 ± 0.06 mm versus 4.89 ± 0.07 mm, P < 0.001; left; 5.03 ± 0.09 mm versus 4.85 ± 0.10 mm, P < 0.001). A multivariate linear regression analysis revealed that carboxyhemoglobin and both right and left optic nerve sheath diameter were the factors associated with the delayed neurological sequelae. DISCUSSION: The present study revealed that optic nerve sheath diameter measurements may be a useful screening tool to predict delayed neurological sequelae after carbon monoxide poisoning. The ability to predict a poor neurological prognosis in carbon monoxide poisoning is important for initiating early rehabilitation interventions and make help future trials. Limitations of this study include that normal optic nerve sheath diameters are not well established, and that not every patient underwent computed tomography. CONCLUSIONS: Optic nerve sheath diameters measurements may be a helpful screening tool for predicting delayed neurological sequelae after carbon monoxide poisoning.

Hyperbaric oxygen for the treatment of carbon monoxide-induced delayed neurological sequelae: a case report and review of the literature.

Introduction: Hyperbaric oxygen treatment (HBOT) remains a recognised treatment for acute carbon monoxide (CO) poisoning, but the utility of HBOT in treating CO-induced delayed neurological sequelae (DNS) is not yet established. Case description: A 26-year old woman presented with reduced consciousness secondary to CO exposure from burning charcoal. She underwent a single session of HBOT with US Navy Treatment Table 5 within six hours of presentation, with full neurological recovery. Eight weeks later, she represented with progressive, debilitating neurological symptoms mimicking Parkinsonism. Magnetic resonance imaging of her brain demonstrated changes consistent with hypoxic ischaemic encephalopathy. The patient underwent 20 sessions of HBOT at 203 kPa (2 atmospheres absolute) for 115 minutes, and received intravenous methylprednisolone 1 g per day for three days. The patient's neurological symptoms completely resolved, and she returned to full-time professional work with no further recurrence. Discussion: Delayed neurological sequelae is a well-described complication of CO poisoning. In this case, the patient's debilitating neurocognitive symptoms resolved following HBOT. Existing literature on treatment of CO-induced DNS with HBOT consists mainly of small-scale studies and case reports, many of which similarly suggest that HBOT is effective in treating this complication. However, a large, randomised trial is required to adequately determine the effectiveness of HBOT in the treatment of CO-induced DNS, and an optimal treatment protocol.

Waterpipe vs non-Waterpipe carbon monoxide poisoning: Comparison of patient characteristics, clinical presentation and outcomes.

OBJECTIVE: The aim of this study is to describe the difference between carboxyhemoglobin (CO-Hb) acute poisoning caused by waterpipe vs non-waterpipe exposures as they relate to demographics, clinical presentations and outcome of patients. DESIGN: Retrospective cohort study conducted in the Emergency Department (ED) at the Lebanon. PATIENTS: All adult patients presenting with a CO-Hb level ≥ 10 between January 2019 and August 2023 with exposure types stratified as waterpipe or non-waterpipe. MEASUREMENTS AND MAIN RESULTS: 111 ED visits were identified. Among these, 73.9% were attributed to waterpipe exposure, while 26.1% were non-waterpipe sources. These included cigarette smoking (17.2%), burning coal (24.1%), fire incidents (3.6%), gas leaks (6.9%), heating device use (10.3%), and undocumented sources (37.9%). Patients with waterpipe-related carbon monoxide exposure were younger (41 vs 50 years, p = 0.015) women (63.4 vs 41.4%, p = 0.039) with less comorbidities compared to non-waterpipe exposures (22.2 vs 41.4%, p = 0.047). Waterpipe smokers were more likely to present during the summer (42.7 vs 13.8%, p = 0.002) and have shorter ED length of stays (3.9 vs 4.5 h, p = 0.03). A higher percentage of waterpipe smokers presented with syncope (52.4 vs 17.2%, p = 0.001) whereas cough/dyspnea were more common in non-waterpipe exposures (31 vs 9.8%, p = 0.006). The initial CO-Hb level was found to be significantly higher in waterpipe exposure as compared to non-waterpipe (19.7 vs 13.7, p = 0.004). Non-waterpipe exposures were more likely to be admitted to the hospital (24.1 vs 4.9%, p = 0.015). Waterpipe smokers had significantly higher odds of experiencing syncope, with a 5.74-fold increase in risk compared to those exposed to non-waterpipe sources (p = 0.004) irrespective of their CO-Hb level. Furthermore, males had significantly lower odds of syncope as compared to females, following carbon monoxide exposure (aOR 0.31, 95% CI 0.13-0.74). CONCLUSION: CO-Hb poisoning related to waterpipe smoking has distinctive features. Syncope is a commonly associated presentation that should solicit a focused social history in communities where waterpipe smoking is common. Furthermore, CO-Hb poisoning should remain on the differential in patients presenting with headache, syncope, dizziness, vomiting or shortness of breath, even outside of the non-waterpipe exposure peaks of winter season.

Delayed neuropsychiatric syndrome after carbon monoxide poisoning. / Forsinket nevropsykiatrisk syndrom etter kullosforgiftning.

Background: Delayed neuropsychiatric syndrome (DNS) is a well-known complication following carbon monoxide (CO) poisoning and develops in up to 50 % of adult survivors. The syndrome is probably immunologically mediated. Common symptoms are slowness, Parkinsonism and cognitive impairment. Case presentation: A woman in her forties started to show gradually increasing symptoms of DNS a few days after an episode of severe CO poisoning. She received methylprednisolone 1 g intravenously on 3 consecutive days at around 7 weeks after the poisoning, with an immediate positive response to motor deficit symptoms. Thereafter, she gradually recovered and returned to full-time employment 4.5 months after the steroid treatment. Interpretation: The role of steroids in this patient's recovery is uncertain. However, successful high-dose steroid treatment for patients with ongoing DNS progression after CO poisoning has been reported previously in the literature. The authors recommend more attention to the risk of DNS after CO poisoning and further research on treatment options.

Carbon monoxide related deaths: A Verona case series. When cooperation becomes compulsory.

INTRODUCTION: Carbon monoxide (CO) poisoning is a significant concern in forensic medicine, as it often presents unique challenges in terms of diagnosis, investigation, and determination of the cause of death. CO is a colourless, odourless, and tasteless gas that can be lethal when inhaled in high concentrations. It binds strongly to haemoglobin, forming carboxyhaemoglobin (COHb), which reduces the oxygen-carrying capacity of the blood, leading to tissue hypoxia and ultimately death. MATERIALS AND METHODS: Circumstantial data, medical history information, autopsy findings, and toxicological analysis results related to 24 CO poisoning cases at the Institute of Legal Medicine in Verona were collected and analysed. The data were examined in an integrated manner to identify correlations and common patterns. A comparison was also made with the data available in the literature. RESULTS: The male gender was confirmed to be the most frequently involved. COHb levels were found to be less than 50% in 6 cases. Three individuals had concurrent cardiovascular pathologies, while 11 subjects tested positive for various substances, including alcohol, benzodiazepines, and morphine. In most cases, the manner of fatal intoxication was accidental, although 6 suicides and 1 homicide are reported. CONCLUSIONS: The Verona case series demonstrates that deaths due to CO poisoning require a multidisciplinary approach. The integration of diverse expertise is essential for assessing the manner of death. This approach enables a comprehensive evaluation of the available data, aids in distinguishing between accidental, suicidal, and homicidal deaths, and ensures accurate and reliable forensic conclusions.

Aspectos por considerar en autopsias por intoxicación aguda con monóxido de carbono, el asesino silente. A propósito de dos casos / Aspects to consider in autopsies for acute carbon monoxide poisoning, the silent killer. About two cases

El monóxido de carbono (CO) es un gas que se produce durante la combustión incompleta de diferentes materiales orgánicos. Una vez que se inhala, se absorbe hacia la sangre, ejerciendo su efecto a nivel sistémico. Se une fuertemente a la hemoglobina, y forma la carboxihemoglobina lo que provoca una disminución del transporte de oxígeno a los tejidos y dependiendo de su concentración puede ser mortal. Los hallazgos comúnmente encontrados en la autopsia son color rojo cereza en la piel y órganos, así como edema pulmonar, entre otros. El diagnóstico de intoxicación por CO se basa en la medición post mortem de carboxihemoglobina en sangre, por lo que se deben tomar muestras para cuantificar estos niveles. Con respecto al manejo en estos casos, se presenta dos casos correspondientes a la autopsia médica legal en las que se estableció como causa de muerte la intoxicación por monóxido de carbono.

Carbon monoxide (CO) is a gas that is produced during the incomplete combustion of different organic materials. Once inhaled, it is absorbed into the blood, exerting its effect at the systemic level. It strongly binds to hemoglobin, and forms carboxyhemoglobin, which causes a decrease in oxygen transport to the tissues and, depending on its concentration, can be fatal. The findings commonly found in the autopsy are cherry red color in the skin and organs, as well as pulmonary edema, among others. The diagnosis of CO poisoning is based on the postmortem measurement of carboxyhemoglobin in the blood, so samples must be taken to quantify these levels. Regarding the handling of these cases, two cases corresponding to the legal medical autopsy are presented in which carbon monoxide poisoning was established as the cause of death.

Sensorineural Hearing Loss due to Acute Carbon Monoxide Poisoning.

Carbon monoxide (CO) can cause "irreversible" severe-to-profound sensorineural hearing loss. However, there are few reports of detailed hearing test results. Here, we report a case of acute sensorineural hearing loss caused by acute CO poisoning with partial hearing recovery, evaluated by a detailed hearing examination. A 25-year-old woman was brought to the emergency department for attempted suicide. On admission, her consciousness was impaired, and she was treated for severe CO poisoning, including using hyperbaric-oxygen therapy. After regaining consciousness, symptoms of hearing loss and tinnitus were discovered, and a detailed audiological examination revealed bilateral hearing loss, suggesting cochlear damage. Steroids were systemically administered, and her hearing impairment was partially resolved. Sensorineural hearing loss caused by acute CO poisoning includes cochlear pathology and may be partially treatable. The early evaluation of hearing in patients with severe CO poisoning is advisable for early treatment.

Carbon monoxide poisoning: Diagnosis and management.

ABSTRACT: Diagnosis of carbon monoxide (CO) poisoning is challenging, as it is generally based on a history of present illness leading to clinical suspicion. CO is a tasteless, odorless, and colorless gas that has become known as the "silent killer." CO poisoning affects approximately 50,000 people in the United States each year and presents with wide range of nonspecific symptoms. Patients often do not know that they are being exposed to CO gas; it is therefore important to ask pertinent questions when taking a patient's history. Treatment consists of oxygen therapy. If a diagnosis is not made and treatment is not administered promptly, complications may occur.

The Critical Assessment of Oxidative Stress Parameters as Potential Biomarkers of Carbon Monoxide Poisoning.

In conventional clinical toxicology practice, the blood level of carboxyhemoglobin is a biomarker of carbon monoxide (CO) poisoning but does not correspond to the complete clinical picture and the severity of the poisoning. Taking into account articles suggesting the relationship between oxidative stress parameters and CO poisoning, it seems reasonable to consider this topic more broadly, including experimental biochemical data (oxidative stress parameters) and patients poisoned with CO. This article aimed to critically assess oxidative-stress-related parameters as potential biomarkers to evaluate the severity of CO poisoning and their possible role in the decision to treat. The critically set parameters were antioxidative, including catalase, 2,2-diphenyl-1-picryl-hydrazyl, glutathione, thiol and carbonyl groups. Our preliminary studies involved patients (n = 82) admitted to the Toxicology Clinical Department of the University Hospital of Jagiellonian University Medical College (Kraków, Poland) during 2015-2020. The poisoning was diagnosed based on medical history, clinical symptoms, and carboxyhemoglobin blood level. Blood samples for carboxyhemoglobin and antioxidative parameters were collected immediately after admission to the emergency department. To evaluate the severity of the poisoning, the Pach scale was applied. The final analysis included a significant decrease in catalase activity and a reduction in glutathione level in all poisoned patients based on the severity of the Pach scale: I°-III° compared to the control group. It follows from the experimental data that the poisoned patients had a significant increase in level due to thiol groups and the 2,2-diphenyl-1-picryl-hydrazyl radical, with no significant differences according to the severity of poisoning. The catalase-to-glutathione and thiol-to-glutathione ratios showed the most important differences between the poisoned patients and the control group, with a significant increase in the poisoned group. The ratios did not differentiate the severity of the poisoning. The carbonyl level was highest in the control group compared to the poisoned group but was not statistically significant. Our critical assessment shows that using oxidative-stress-related parameters to evaluate the severity of CO poisoning, the outcome, and treatment options is challenging.

Thoracic cavity fluid as an alternative specimen for carboxyhaemoglobin measurement in post-mortem toxicology.

Post-mortem blood is most frequently used for the measurement of carboxyhaemoglobin (COHb) in post-mortem forensic cases, when investigating suspected inhalation of carbon monoxide (CO). However, in many post-mortem cases (especially severe burns and charring deaths), adequate blood specimens are not always available for toxicological analyses. Here, the availability of an alternative specimen for COHb analysis is required. This study investigated the suitability of thoracic cavity fluid (TCF) as an alternative specimen for the measurement of COHb. TCF and comparative blood samples from fifteen potential CO toxicity cases were collected into green-top tubes (containing lithium heparin) and analysed immediately after collection using a validated method on the ABL825 FLEX Radiometer CO-oximeter. Pearson's correlation coefficient indicated a strong positive relationship between the two specimens (r = 0.975, n = 10, p < 0.001). A statistical agreement between COHb concentrations from blood and TCF was demonstrated using the Bland-Altman plot, with a slight bias of 1.54 % when blood was taken as the standard. This study found that TCF would be a suitable alternative to blood for the measurement of COHb using the ABL825 FLEX blood gas analyser.

Hydranencephaly following carbon monoxide poisoning during pregnancy: An uncommon and potentially fatal complication in infant.

BACKGROUND: Hydranencephaly is a rare malformation of the brain system with an incidence of 0.5 per 1000 births. Its principal etiologies are bilateral occlusion of the internal carotid arteries and congenital infections. CASE: We reported an uncommon case of hydranencephaly diagnosed in 50-day old infant and attributable to carbon monoxide (CO) poisoning during the first trimester of pregnancy. CONCLUSIONS: We recommend a prompt diagnosis and management of CO poisoning in pregnant women since it can dramatically affect both the fetus and mother.

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)

Accuracy of pulse CO-oximetry to evaluate blood carboxyhemoglobin level: a systematic review and meta-analysis of diagnostic test accuracy studies.

Carbon monoxide (CO) poisoning is one of the most common causes of poisoning death and its diagnosis requires an elevated carboxyhemoglobin (COHb) level. Noninvasive CO saturation by pulse oximetry (SpCO) has been available since 2005 and has the advantage of being portable and easy to use, but its accuracy in determining blood COHb level is controversial. To evaluate the accuracy of SpCO (index test) to estimate COHb (reference test). Systematic review and meta-analysis of diagnostic test accuracy (DTA) studies. Four electronic databases were searched (Medline, Embase, Cochrane Central Register of Controlled Trials, and OpenGrey) on 2 August 2022. All studies of all designs published since the 2000s evaluating the accuracy and reliability of SpCO measurement compared to blood COHb levels in human volunteers or ill patients, including children, were included. The primary outcome was to assess the diagnostic accuracy of SpCO for estimating COHb by blood sampling by modeling receiver operating characteristic (ROC) curves and calculating sensitivity and specificity (primary measures). The secondary measures were to calculate the limits of agreement (LOA) and the mean bias. This systematic review was conducted according to the Preferred Reporting Items for a Systematic Review and Meta-analysis-DTA 2018 guidelines and has been registered on International Prospective Register of Systematic Reviews (PROSPERO, CRD42020177940). The risk of bias was evaluated using the Quality Assessment of Diagnostic Accuracy Studies-2 tool. Twenty-one studies were eligible for the systematic review; 11 could be included for the quantitative analysis of the primary measures and 18 for the secondary measures. No publication bias was found. The area under the summary ROC curve was equal to 86%. The mean sensitivity and specificity were 0.77, 95% confidence interval (CI, 0.66-0.85) and 0.83, 95% CI (0.74-0.89), respectively (2089 subjects and 3381 observations). The mean bias was 0.75% and the LOA was -7.08% to 8.57%, 95% CI (-8.89 to 10.38) (2794 subjects and 4646 observations). Noninvasive measurement of COHb (SpCO) using current pulse CO oximeters do not seem to be highly accurate to estimate blood COHb (moderate sensitivity and specificity, large LOA). They should probably not be used to confirm (rule-in) or exclude (rule-out) CO poisoning with certainty.

Systemic Venous Air Emboli After Emergent Hyperbaric Therapy for Carbon Monoxide Poisoning.

BACKGROUND A venous air embolism is a rare condition but could have a disastrous effect on vital organs. It usually occurs due to iatrogenic sources, such as central venous catheter insertion, neurosurgery, and other invasive procedures. In most cases, hyperbaric oxygen therapy (HBOT) is the best treatment for those conditions. However, multiple venous air emboli after hyperbaric oxygen therapy has not been reported in the literature. CASE REPORT An 82-yr-old woman came to the Emergency Department after inhalation of fumes at the scene of a house fire. She had dizziness and nausea. Her vital signs were normal at the time of presentation. She received HBOT for carbon monoxide poisoning. Soon after the HBOT, the patient started to have dizziness, abdominal pain, and leg pains. Computed tomography scans showed multiple systemic venous air emboli throughout the portal venous system and femoral veins. The air emboli totally disappeared after HBOT with a longer ascent time. CONCLUSIONS To the best of our knowledge, this is the first case of multiple systemic venous air bubbles after emergent HBOT. Physicians should be aware of any kind of complications when treating patients who need HBOT in the emergent setting. Although decompression sickness following HBOT is extremely rare, it should not be ignored by emergency physicians.

Clinical and Laboratory Characteristics Predicting the Severity of Carbon Monoxide Poisoning in Children: A Single-Center Retrospective Study.

OBJECTIVES: Carbon monoxide poisoning (COP) is extremely common throughout the world. The purpose of this study was to assess the demographic, clinical, and laboratory characteristics predicting the severity COP in children. METHODS: The study included 380 children diagnosed with COP between January 2017 and January 2021 and 380 healthy controls. Carbon monoxide poisoning was diagnosed based on the medical history and a carboxyhemoglobin (COHb) level of more than 5%. The patients were classified as mild (COHb 10%), moderate (COHb 10%-25%), or severely (COHb > 25%) poisoned. RESULTS: The mean age of the severe group was 8.60 ± 6.30, for the moderate group was 9.50 ± 5.81, for the mild group was 8.79 ± 5.94, and for the control group was 8.95 ± 5.98. The most common place of exposure was at home and all cases were affected accidentally. The coal stove was the most common source of exposure, followed by natural gas. The most common symptoms were nausea/vomiting, vertigo, and headache. Neurologic symptoms such as syncope, confusion, dyspnea, and seizures were more common in the severe group. A total of 91.3% of the children had hyperbaric oxygen therapy, 3.8% were intubated, and 3.8% were transferred to intensive care in the severe group, whereas no death or sequela was observed. Mean platelet volume and red cell distribution width had the highest area under the curve in the receiver operating characteristic analysis (0.659; 0.379). A positive and low statistically significant relationship was found between COHb levels and troponin and lactate levels in the severe group ( P < 0.05). CONCLUSIONS: Carbon monoxide poisoning progressed more severely in children presented with neurological symptoms and have elevated red cell distribution width and mean platelet volume. Even in severe COP cases, satisfactory results have been obtained with early and appropriate treatment.

Screening patients for unintentional carbon monoxide exposure in the Emergency Department: a cross-sectional multi-centre study.

BACKGROUND: Low-level exposure to carbon monoxide (CO) is a significant health concern but is difficult to diagnose. This main study aim was to establish the prevalence of low-level CO poisoning in Emergency Department (ED) patients. METHODS: A prospective cross-sectional study of patients with symptoms of CO exposure was conducted in four UK EDs between December 2018 and March 2020. Data on symptoms, a CO screening tool and carboxyhaemoglobin were collected. An investigation of participants' homes was undertaken to identify sources of CO exposure. RESULTS: Based on an ED assessment of 4175 participants, the prevalence of suspected CO exposure was 0.62% (95% CI; 0.41-0.91%). CO testing in homes confirmed 1 case of CO presence and 21 probable cases. Normal levels of carboxyhaemoglobin were found in 19 cases of probable exposure and in the confirmed case. CONCLUSION: This study provides evidence that ED patients with symptoms suggestive of CO poisoning but no history of CO exposure are at risk from CO poisoning. The findings suggest components of the CO screening tool may be an indicator of CO exposure over and above elevated COHb. Clinicians should have a high index of suspicion for CO exposure so that this important diagnosis is not missed.