Edaravone combined with hyperbaric oxygen therapy in delayed encephalopathy after acute carbon monoxide poisoning: A meta-analysis.

BACKGROUND: The use of both edaravone (EDA) and hyperbaric oxygen therapy (HBOT) is increasingly prevalent in the treatment of delayed encephalopathy after carbon monoxide poisoning (DEACMP). This meta-analysis aims to evaluate the efficacy of using EDA and HBOT in combination with HBOT alone in the treatment of DEACMP. METHODS: We searched and included all randomized controlled trials (RCTs) published before November 6, 2023, from 12 Chinese and English databases and clinical trial centers in China and the United States. The main outcome indicator was the total effective rate. The secondary outcome indicators included the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), National Institutes of Health Stroke Scale (NIHSS), Barthel Index (BI), Hasegawa Dementia Scale (HDS), Fugl-Meyer Assessment (FMA), Superoxide Dismutase (SOD), and Malondialdehyde (MDA). Statistical measures utilized include risk ratios (RR), weighted mean difference (WMD), and 95 % confidence intervals (95 % CI). RESULTS: Thirty studies involving a combined total of 2075 participants were ultimately incorporated. It was observed that the combination of EDA with HBOT for the treatment of DEACMP demonstrated an improvement in the total effective rate (RR: 1.25; 95 % CI: 1.20-1.31; P < 0.01), MMSE (WMD: 3.67; 95 % CI: 2.59-4.76; P < 0.01), MoCA (WMD: 4.38; 95 % CI: 4.00-4.76; P < 0.01), BI (WMD: 10.94; 95 % CI: 5.23-16.66; P < 0.01), HDS (WMD: 6.80; 95 % CI: 4.05-9.55; P < 0.01), FMA (WMD: 8.91; 95 % CI: 7.22-10.60; P < 0.01), SOD (WMD: 18.45; 95 % CI: 16.93-19.98; P < 0.01); and a reduction in NIHSS (WMD: -4.12; 95 % CI: -4.93 to -3.30; P < 0.01) and MDA (WMD: -3.05; 95 % CI: -3.43 to -2.68; P < 0.01). CONCLUSION: Low-quality evidence suggests that for DEACMP, compared to using HBOT alone, the combined use of EDA and HBOT may be associated with better cognition and activity of daily living. In the future, conducting more meticulously designed multicenter and large-sample RCTs to substantiate our conclusions is essential.

CARDIOGENIC SHOCK AND GLOBUS PALLIDUS INJURY AS A PRESENTATION OF CARBON MONOXIDE POISONING.

Carbon monoxide poisoning is one of the leading causes of mortality and morbidity by poisoning in the world. Signs and symptoms are nonspecific and related to impaired oxygen delivery to tissues, with the brain being the most affected organ due to its high oxygen demand. CO-Hb is a poor indicator of severity and long-term outcome, with clinicians relying more on clinical features such as level of consciousness and need for intubation, organ dysfunction and shock and also pH level. A 45-year-old female was found unconscious in her home with the fireplace lit and smoke all over the house. She was last seen well 18 hours before. She was brought to the emergency department and was admitted to the ICU in coma and cardiogenic shock, with a metabolic acidosis with hyperlactacidemia and a CO-Hb level of 15.5%. Laboratorial investigation revealed hepatic cytolysis, acute renal failure, rhabdomyolysis and a troponin I level of 338 ng/L. ECG showed no acute myocardial ischemia. Echocardiogram revealed diffuse hypokinesia with an ejection fraction of 25%. Head CT scan showed bilateral and symmetrical hypodensities of the globus pallidus. The patient underwent hyperbaric oxygen treatment with full neurological and cardiac recovery, allowing extubation 48 hours after admission. This rare severe case of coma due to carbon monoxide intoxication with globus pallidus injury and cardiogenic shock was successfully treated with hyperbaric oxygen, showing that it can be the right treatment choice in these cases, with an excellent impact on neurological and cardiac outcome.

L'intoxication au CO est une des causes principales de décès par empoisonnement dans le monde. Les signes, non spécifiques, sont dus à l'hypoxie cellulaire et le cerveau est le plus souvent atteint en raison de sa consommation d'oxygène élevée. Le taux d'HbCO est un indice peu fiable de la gravité initiale et du risque de séquelles si bien que l'on préfère se baser sur la clinique (conscience, nécessité d'intubation, dysfonctions d'organe, choc) et le pH sanguin. Une femme de 45 ans a été trouvée inconsciente à son domicile entièrement enfumé, cheminée allumée. Le dernier contact remontait à 18 heures. Elle a été hospitalisée en réanimation en coma et choc cardiogénique, avec une acidose lactique et une HbCO à 15,5%. La biologie retrouvait une cytolyse hépatique, une insuffisance rénale aiguë, une rhabdomyolyse et une troponine I à 338 ng/L. L'ECG ne trouvait pas d'ischémie, l'échocardiographie objectivait une hypokinésie globale et évaluait la fraction d'éjection à 25%. La TDM cérébrale montrait une hypodensité pallidale bilatérale. L'oxygénothérapie hyperbare (OHB) a permis une récupération neurologique et cardiaque complètes, permettant l'extubation à h48. Cette récupération complète après OHB confirme qu'il peut s'agir du traitement idoine des intoxications graves au CO, avec un excellent impact sur les devenirs cardiaque et neurologique.

Short and long-term outcomes of multidimensional physiotherapy in cases with acute compartment syndrome secondary to carbon monoxide poisoning with prolonged forearm compression.

BACKGROUND: Compartment syndrome following carbon monoxide (CO) poisoning and compression, can have a devastating impact on neuromuscular structures, depending on a time-based dosage. PURPOSE: To investigate multidimensional physiotherapy's short-term and long-term outcomes in identical twin cases who developed compartment syndrome due to CO poisoning and prolonged compression. STUDY DESIGN: Case report. METHODS: This study was conducted with two male cases, a 21-year-old identical twin. The loss of consciousness due to CO poisoning lasted for 15 hours. Case one had compartment syndrome that caused damage to the median and ulnar nerves in the right forearm, while Case two had compartment syndrome that caused damage to the radial nerve in the left forearm. No surgical intervention was performed (Fasciotomy etc). RESULTS: The disability, dexterity, hand health status, sensory-motor function, and edema were evaluated. Initial evaluations showed severe sensory and motor dysfunction, disability, and edema. Treatment included Complex decongestive physiotherapy, electrical stimulation, therapeutic ultrasound, orthotics, and exercises. On the 144th day (discharge day), both cases still exhibited weakness in functional strength and sensory loss compared to the uninjured side. At the ninth month, all parameters except strength were similar to the uninjured side in both cases. By the 53rd month, strength also reached normal values. CONCLUSIONS: Multidimensional physiotherapy effectively manages edema, improves sensory-motor function, and enhances hand function in the short and long term.

The Combination of Zhuli Decoction and N-butylphthalide Inhibits Cell Apoptosis Induced by CO Poisoning through the PI3K/AKT/GSK-3ß Signaling Pathway.

Carbon monoxide poisoning (COP) represents a significant global health burden, characterized by its morbidity and high mortality rates. The pathogenesis of COP-induced brain injury is complex, and effective treatment modalities are currently lacking. In this study, we employed network pharmacology to identify therapeutic targets and associated signaling pathways of Zhuli Decoction (ZLD) for COP. Subsequently, we conducted both in vitro and in vivo experiments to validate the therapeutic efficacy of ZLD in combination with N-butylphthalide (NBP) for acute COP-induced injury. Our network pharmacology analysis revealed that the primary components of ZLD exerted therapeutic effects through the modulation of multiple targets and pathways. The in vitro and in vivo experiments demonstrated that the combination of NBP and ZLD effectively inhibited apoptosis and up-regulated the activities of P-PI3K (Tyr458), P-AKT (Ser473), P-GSK-3ß (Ser9), and Bcl-2, thus leading to the protection of neuronal cells and improvement in cognitive function in rats following COP, which was better than the effects observed with NBP or ZLD alone. The rescue experiment further showed that LY294002, a PI3K inhibitor, significantly attenuated the therapeutic efficacy of NBP + ZLD. The neuroprotection effects of NBP and ZLD against COP-induced brain injury are closely linked to the activation of the PI3K/AKT/GSK-3ß signaling pathway.

Differential diagnosis and prognosis of delayed neuropsychiatric sequelae after acute carbon monoxide poisoning in a patient with schizophrenia: A case report.

Background: Delayed neuropsychiatric sequelae (DNS) is a syndrome that appears days to weeks after acute carbon monoxide (CO) poisoning. DNS shows various neuropsychiatric symptoms, such as mental deterioration and parkinsonism. Case Presentation: Our case was a 37-year-old male with schizophrenia. He attempted suicide by CO poisoning and was brought to our emergency department (Day 0). He was ventilated with normobaric oxygen therapy for 3 days and moved to the psychiatric ward with clear consciousness. We restarted antipsychotics, and he gradually presented akinesia and rigidity. Additionally, around Day 32, he showed disorganized behaviors, mental deterioration, incontinence, and gait disturbance. Brain magnetic resonance imaging (MRI) showed slightly abnormal findings on Day 35. Although we suspected DNS on the clinical course and the MRI findings, catatonia and side-effects of antipsychotics were also considered. Finally, electroencephalography (EEG) on Day 38 with apparent abnormalities, including diffuse slow waves, resulted in our diagnosis of DNS, and he underwent hyperbaric oxygen therapy. His condition was dramatically improved, and his diffuse slow waves on EEG disappeared on Day 83. We also followed his clinical presentations and brain MRI until 33 months. Throughout the whole follow-up, his cognition, movement, and psychiatric symptoms remained stable. However, his brain MRI showed progressive atrophy in bilateral frontal lobes and increasing white matter lesions throughout the whole course. Conclusion: EEG, as well as brain MRI, may be crucial in the differential diagnosis of DNS in patients with complex conditions involving medications and severe mental illnesses.

Analysis of factors associated with the development of delayed encephalopathy following acute carbon monoxide poisoning.

In this study, we analyzed the factors influencing the development of delayed encephalopathy in patients with acute carbon monoxide poisoning (ACOP) (DEACMP) following conventional treatment such as hyperbaric oxygen therapy (HBOT). Between January 2012 and January 2022, we retrospectively analyzed 775 patients with ACOP, who were admitted to the Second Department of Rehabilitation Medicine and received HBOT in the Second Hospital of Hebei Medical University. These patients were divided into the non-DEACMP and DEACMP groups based on their follow-up; we then compared the general data, clinical characteristics, admission examination, and treatment between the two groups to identify risk factors for the development of DEACMP. The DEACMP group comprised of 168 cases, while the non-DEACMP group consisted of 607 cases. Univariate analysis showed that there were 20 possible prognostic factors in the non-DEACMP and DEACMP groups. The results of multivariable regression analyses suggested that the occurrence of DEACMP was significantly correlated with advanced age, the combination of multiple medical histories, the duration of CO exposure, the duration of coma, poisoning degree, the Interval between ACOP and the first HBOT, the total number of HBOTs, and the combination with rehabilitation treatment. DEACMP patients who are older, have more comorbidities, prolonged CO exposure, prolonged coma, severe intoxication, long intervals between ACOP and the first HBOT, fewer HBOT treatments, and who are not treated with a combination of rehabilitative therapies have a poor prognosis.

The Relationship between Fragmented QRS and Myocardial Injury in Patients with Acute Carbon Monoxide Poisoning.

Background and Objectives: Carbon monoxide (CO) intoxication is one of the most common causes of poisoning-related deaths and complications. Myocardial injury is an important complication of CO poisoning. In our study, we aimed to evaluate the relationship between the presence and prevalence of fragmented QRS (fQRS) and myocardial injury in patients with CO intoxication. Materials and Methods: We retrospectively evaluated patients who presented to the emergency department of our tertiary care center with CO intoxication between January 2020 and December 2023. In our study, we performed subgroup analyses according to the presence of myocardial injury and fQRS. We evaluated the parameters and risk factors associated with myocardial injury. Results: Myocardial injury was detected in 44 patients, and fQRS was detected in 38 patients. In the myocardial injury (+) group, the fQRS rate was 38.6%, and the median number of leads with fQRS was 3 (2-6) and was significantly higher than in the myocardial injury (-) group (p < 0.001). We found that carboxyhemoglobin had a significant positive correlation with troponin (p = 0.001) and pro-B-type natriuretic peptide (proBNP) (p = 0.009). As a result of multivariate analysis, we determined that age, creatinine, proBNP, fQRS, and ≥3 leads with fQRS are independent risk factors for myocardial injury. Conclusions: Myocardial injury in CO intoxication patients is associated with proBNP, the presence of fQRS, and the number of leads with fQRS. Age, creatinine level, proBNP, the presence of fQRS, and ≥3 leads with fQRS are independent risk factors for myocardial injury in patients with CO intoxication.

Carbon Monoxide-Related Vision Loss in an Acute Burn Patient.

Carbon monoxide poisoning can occur as part of smoke exposure in the burn population. Here we report the case of a 32-year-old, previously healthy male, with carbon monoxide-related blindness after smoke exposure in an apartment fire. Cerebral hypoperfusion was diagnosed using magnetic resonance imaging of the brain, and the patient was diagnosed with cortical visual impairment. He was treated with hyperbaric oxygen therapy following which he had partial recovery of his vision. There is a paucity of information regarding this phenomenon and its treatment.

Increased Long-Term Risk of Dementia in Patients With Carbon Monoxide Poisoning: A Systematic Review and Meta-Analysis of Cohort Studies.

OBJECTIVE: To assess whether carbon monoxide (CO) poisoning increases the incidence of dementia. METHODS: We searched the Cochrane Library, PubMed, and EMBASE from inception to 14 August 2022. Two authors independently selected studies, assessed the quality of included studies, and extracted data. Any disagreement was resolved by discussion with a third author. Only cohort study with an enough follow-up period was included for systematic reviews and meta-analysis. RESULTS: Thirty-three full texts were initially searched, but only three studies met our inclusion criteria, and they were comprised of 134,563 participants who were initially free of dementia. The follow-up period ranged from 9 to 12 years. We found that CO poisoning increased the risk of dementia incidence (adjusted hazard ratio 2.61, 95% confidence interval 1.56 to 4.36, p=0.0003). Subgroup analysis showed that the increased dementia risk was significant in males but not in females, and the highest risk was in young age group, followed by in middle age group, but not in the old one. CONCLUSION: Overall the evidence from prospective cohort studies supported a link between CO exposure and an increased dementia risk, although all the included studies were limited to Taiwanese population.

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.

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

Objetivos. 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. Métodos. 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. (AU)

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. 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). Conclusions. 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. (AU)

Carboxyhemoglobin half-life toxicokinetic profiles during and after normobaric oxygen therapy: On a swine model.

Investigations on acute carbon monoxide (CO) poisoning struggle to highlight a relevant discriminant criterion related to CO poisoning severity for predicting complications, such as delayed neurological syndromes. In this context, it remains difficult to demonstrate the superiority of one method of oxygen (O2) administration over others or to identify the optimal duration of normobaric 100% oxygen (NBO) treatment. Myoglobin, as hemoglobin, are a potential binding site for CO, which could be a source of extravascular CO storage that impacts the severity of CO poisoning. It is not possible in routine clinical practice to estimate this potential extravascular CO storage. Indirect means of doing so that are available in the first few hours of poisoning could include, for example, the carboxyhemoglobin half-life (COHbt1/2), which seems to be influenced itself by the level and duration of CO exposure affecting this store of CO within the body. However, before the elimination of CO can be assessed, the COHbt1/2 toxicokinetic model must be confirmed: research still debates whether this model mono- or bi-compartmental. The second indirect mean could be the assessment of a potential COHb rebound after COHb has returned to 5% and NBO treatment has stopped. Moreover, a COHb rebound could be considered to justify the duration of NBO treatment. On an experimental swine model exposed to moderate CO poisoning (940 ppm for ±118 min until COHb reached 30%), we first confirm that the COHb half-life follows a bi-compartmental model. Secondly, we observe for the first time a slight COHb rebound when COHb returns to 5% and oxygen therapy is stopped. On the basis of these two toxicokinetic characteristics in favor of extravascular CO storage, we recommend that COHbt1/2 is considered using the bi-compartmental model in future clinical studies that compare treatment effectiveness as a potential severity criterion to homogenize cohorts of the same severity. Moreover, from a general toxicokinetic point of view, we confirm that a treatment lasting less than 6 hours appears to be insufficient for treating moderate CO poisoning.

Gray matter atrophy and white matter lesions burden in delayed cognitive decline following carbon monoxide poisoning.

Gray matter (GM) atrophy and white matter (WM) lesions may contribute to cognitive decline in patients with delayed neurological sequelae (DNS) after carbon monoxide (CO) poisoning. However, there is currently a lack of evidence supporting this relationship. This study aimed to investigate the volume of GM, cortical thickness, and burden of WM lesions in 33 DNS patients with dementia, 24 DNS patients with mild cognitive impairment, and 51 healthy controls. Various methods, including voxel-based, deformation-based, surface-based, and atlas-based analyses, were used to examine GM structures. Furthermore, we explored the connection between GM volume changes, WM lesions burden, and cognitive decline. Compared to the healthy controls, both patient groups exhibited widespread GM atrophy in the cerebral cortices (for volume and cortical thickness), subcortical nuclei (for volume), and cerebellum (for volume) (p < .05 corrected for false discovery rate [FDR]). The total volume of GM atrophy in 31 subregions, which included the default mode network (DMN), visual network (VN), and cerebellar network (CN) (p < .05, FDR-corrected), independently contributed to the severity of cognitive impairment (p < .05). Additionally, WM lesions impacted cognitive decline through both direct and indirect effects, with the latter mediated by volume reduction in 16 subregions of cognitive networks (p < .05). These preliminary findings suggested that both GM atrophy and WM lesions were involved in cognitive decline in DNS patients following CO poisoning. Moreover, the reduction in the volume of DMN, VN, and posterior CN nodes mediated the WM lesions-induced cognitive decline.

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.

Clinical factors for delayed neuropsychiatric sequelae from acute carbon monoxide poisoning: a retrospective study.

Background: Delayed neuropsychiatric sequelae (DNS), which seriously affect the daily lives of patients, are the most common complications of carbon monoxide (CO) poisoning. No uniform screening tool is available for identifying high-risk groups. Therefore, in this study, we aimed to explore whether conventional laboratory indicators and imaging data from primary hospitals could predict the occurrence of DNS. Methods: This retrospective observational study was conducted in a single-center primary hospital from January 1, 2021 to May 31, 2023. Participants included patients aged >18 years with acute CO poisoning. Patients with complete recovery in the acute phase were followed up by telephone and outpatient visits, and the presence of DNS was determined according to the occurrence of new neurological symptoms within 6 weeks after discharge. We obtained demographic, laboratory, and imaging data from the medical records and performed a univariate analysis. A multivariate logistic regression model was used to identify independent clinical predictors of DNS. Results: A total of 73 patients were included in the study, of whom 25 (34.2%) developed DNS. Multivariate logistic regression analysis revealed that a longer duration of CO exposure (adjusted odds ratio (AOR): 1.262, 95% confidence interval (CI): 1.069-1.490) and the presence of acute brain lesions on diffusion-weighted imaging (DWI) (AOR: 5.117, 95% CI: 1.430-18.315) were independent risk factors for DNS. Receiver operating characteristic analyses of the duration of CO exposure were performed (area under the curve (AUC): 0.825; 95% CI: 0.731-0.918) with a cut-off value of 5.5 h, and DNS was predicted with a sensitivity of 96% and a specificity of 66.7%. Conclusion: High cranial DWI signal within 24 h and duration of poisoning longer than 5.5 h are independent predictors of DNS. The predictive effects of conventional laboratory indicators require further standardized and large-sample studies.

Neurological Sequelae After Acute Carbon Monoxide Poisoning.

Carbon monoxide poisoning (COP) is a common cause of death due to poisoning. After COP, a significant number of patients may develop a distinct type of neurological dysfunction called delayed neurological sequel (DNS). Recently, we came across a disaster of COP cases after a fire in a shared accommodation. The hostel was overcrowded and had a faulty air-conditioning/exhaust system. A total of five patients with loss of consciousness and shock were brought to us. They were diagnosed with acute COP based on their history of exposure to carbon monoxide (CO) and elevated carboxyhemoglobin levels in blood gas measurements. All patients were intubated and mechanically ventilated. Standard intensive care management was given to them, which included oxygenation, sedation, fluid resuscitation, and vasopressors. Their carboxyhemoglobin was rapidly reversed with normobaric oxygen therapy (NBO2). Three patients showed good response and neurological recovery after NBO2. Unfortunately, two patients developed DNS. DNS is a neuropsychological condition that may have cognitive, psychiatric, vestibulocochlear, motor, sensory, or diffuse demyelinating effects after COP. DNS is diagnosed in patients with a typical history of exposure to CO and a constellation of signs and symptoms. Neuroimaging, specifically magnetic resonance imaging of the brain with gadolinium contrast, is the method of choice for diagnosis. Treatment of DNS after COP begins with anticipation. All patients should receive appropriate oxygen therapy to bring down carboxyhemoglobin as soon as possible. Hyperbaric oxygen therapy (HBO2) for the treatment of COP and prevention of DNS is still debatable. In the available medical literature, there are conflicting recommendations regarding the use of HBO2 in COP/DNS. Moreover, apart from a lack of consensus, there is also a lack of clarity about optimum timing, duration, atmospheric pressure, and number of sessions of HBO2 in preventing DNS after COP. The development of DNS after COP is not directly responsible for mortality, but recovery sometimes takes a long time, which can contribute to increased morbidity and costs of treatment.

Prognostic value of systemic immune-inflammation index and monocyte-to-HDL-cholesterol ratio in early cardio-cerebral complications in elderly patients with acute severe carbon monoxide poisoning.

To investigate how effectively systemic immune-inflammation index (SII) and Monocyte-to-HDL-cholesterol ratio (MHR) predict the development of early cardio-cerebral complications in elderly patients who have experienced acute severe carbon monoxide poisoning (ASCMP). A retrospective analysis was conducted on 77 elderly patients with ASCMP admitted to the emergency department of Harrison International Peace Hospital from November 2020 to March 2022. The prevalence of early-onset complications among the 77 individuals was 38.96%. Binary Logistics regression analysis showed that SII and MHR were independent influencing factors of early cardio-cerebral complications in elderly patients with ASCMP. The complication group had a longer length of stay, a greater mortality rate, and a higher incidence of delayed encephalopathy after acute carbon monoxide poisoning (p < .05) than the non-complication group. The area under the curve (AUC) of SII and MHR in predicting early cardio-cerebral complications in elderly patients with ASCMP were 0.724 and 0.796, respectively, with 80.0% and 63.3% sensitivity, and 61.7% and 87.2% specificity. The incidence of early cardio-cerebral complications in elderly patients who had ASCMP is high and the prognosis is poor. SII and MHR can be utilized as independent predictors of early cardio-cerebral complications in elderly patients with ASCMP, allowing doctors to diagnose and treat cardio-cerebral complications earlier and improve prognosis.

Correlation between Time to Hyperbaric Oxygen Therapy and Delayed Neurological Sequelae in Acute Carbon Monoxide Poisoning Patients.

Carbon monoxide (CO) is one of the most common causes of intoxication. Delayed neurologic sequelae (DNS) have a major impact on prognosis of CO poisoning patients. Hyperbaric oxygen therapy (HBOT) is widely used to treat DNS. However, there is no consensus regarding the optimal timing of HBOT. This prospective study enrolled patients who visited the hospital from November 2019 to October 2022. The cutoff value for the latency to HBOT after CO exposure was determined, and the area under the receiver operating characteristic curve (AUC) was estimated. In total, 167 patients were divided into non-DNS and DNS groups. The initial Glasgow Coma Scale (GCS) score, CO exposure time, latency to HBOT after CO exposure, median length of hospital stay (p < 0.001) and creatine kinase (p = 0.016) showed significant differences. A GCS score ≤ 9 had an odds ratio (OR) of 5.059 (95% confidence interval [CI]: 1.602-15.976, p = 0.006), and latency to HBOT after CO exposure ≥ 200 min had an OR of 18.971 (95% CI: 4.310-83.508, p < 0.001). The AUC was 0.8235 (95% CI: 0.7504-0.8966). A GCS score ≤ 9 and latency to HBOT ≥ 200 min may be significant risk factors for DNS.

Carbon Monoxide Poisoning: From Microbes to Therapeutics.

Carbon monoxide (CO) poisoning leads to 50,000-100,000 emergency room visits and 1,500-2,000 deaths each year in the United States alone. Even with treatment, survivors often suffer from long-term cardiac and neurocognitive deficits, highlighting a clear unmet medical need for novel therapeutic strategies that reduce morbidity and mortality associated with CO poisoning. This review examines the prevalence and impact of CO poisoning and pathophysiology in humans and highlights recent advances in therapeutic strategies that accelerate CO clearance and mitigate toxicity. We focus on recent developments of high-affinity molecules that take advantage of the uniquely strong interaction between CO and heme to selectively bind and sequester CO in preclinical models. These scavengers, which employ heme-binding scaffolds ranging from organic small molecules to hemoproteins derived from humans and potentially even microorganisms, show promise as field-deployable antidotes that may rapidly accelerate CO clearance and improve outcomes for survivors of acute CO poisoning.

Targeting Ferroptosis Promotes Functional Recovery by Mitigating White Matter Injury Following Acute Carbon Monoxide Poisoning.

Survivors experiencing acute carbon monoxide poisoning (ACMP) tend to develop white matter injury (WMI). The mechanism of ACMP-induced WMI remains unclear. Considering the role of ferroptosis in initiating oligodendrocyte damage to deteriorate WMI, exploring therapeutic options to attenuate ferroptosis is a feasible approach to alleviating WMI. Our results indicated that ACMP induced accumulation of iron and reactive oxygen species (ROS) eventually leading to WMI and motor impairment after ACMP. Furthermore, ferrostatin-1 reduced iron and ROS deposition to alleviate ferroptosis, thereafter reducing WMI to promote the recovery of motor function. The nuclear factor erythroid-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway was found to be involved in alleviating ferroptosis as seen with the administration of ferrostatin-1. The present study rationalizes that targeting ferroptosis to alleviate WMI is a feasible therapeutic strategy for managing ACMP.