Introduction: Due to its severe toxicity, carbon monoxide poisoning is an emergency that leads to cardiac and brain involvement, and emergency physicians should aim to master this diagnosis. This study is intended to ...Introduction: Due to its severe toxicity, carbon monoxide poisoning is an emergency that leads to cardiac and brain involvement, and emergency physicians should aim to master this diagnosis. This study is intended to describe the expected prevalence of these severe toxicities in the emergency department. Materials and Methods: A retrospective cohort of consecutive patients over 16 years of age presenting with carbon monoxide poisoning to the emergency department of the Hospital Universitario Austral, Argentina, during the period from January 2018 to June 2022. The prevalence of myocardial and brain toxicity was assessed regarding percentage, continuous variables with mean and standard deviation, categorical variables with percentage and absolute frequency. Positive findings of acute neurological toxicity included seizures, syncope and coma, while cardiovascular toxicity encompassed acute myocardial infarction (MI) diagnosed by electrocardiogram or elevated troponin levels, arrhythmias, and the development of pulmonary edema/ congestive heart failure (CHF) confirmed by chest X-ray with suggestive signs or clinically compatible symptoms. Patients were followed-up for 90 days to estimate hospitalization and mortality. Results: A total of 67 patients were evaluated;44.77% of them were males with a mean age of 38.5 ± 14.97 years. The prevalence of acute myocardial toxicity was 7.46% (n: 5). Among these patients, 3 had overweight as a risk factor, and 3 showed ECG abnormalities with negative T-waves. The prevalence of acute brain toxicity was 8.9% (n: 6). In total, 37% (n: 25) of patients met the criteria for hyperbaric oxygen therapy, of which 32% (n: 8) underwent more than one session. A total of 7.46% of patients (n: 5) required hospitalization. Mortality at 90 days was 0%. Conclusion: Among the patients who presented to the emergency department, the prevalence of acute myocardial toxicity was 7.46% (n: 5), which is lower than the prevalence reported in other studies to date. The prevalence of acute brain toxicity was 8.9% (n: 6), and there are no studies describing the prevalence of acute brain toxicity in the emergency department to date. There were no fatalities in our series.展开更多
Currently, there is no known optimal therapy for carbon monoxide （CO） poisoning and CO-associated delayed neu- rological sequelae. Hyperbaric oxygen therapy （HBOT） is a well-known treatment method, but its use for...Currently, there is no known optimal therapy for carbon monoxide （CO） poisoning and CO-associated delayed neu- rological sequelae. Hyperbaric oxygen therapy （HBOT） is a well-known treatment method, but its use for CO poison- ing patients is controversial to use due to lack of evidences regarding its efficacy. Thus, it is unlikely that HBOT alone will be accepted as the standard treatment method. In this article, current and potential treatment methods of CO poi- soning are presented as well as the tentative multi-factorial pathophysiology. A series of treatments are suggested for use as a bundle therapy, with targeted temperature management as the base treatment method. Such a therapy holds a great potential, especially for the cases where HBOT is not readily available. We suggest further investigations for elucidating the effects of these suggested treatments and their roles in terms of the complex pathophysiology of CO poisoning. Future ac- ceptance of this therapy based on the improved scientific and clinical knowledge may result in injury prevention and mini- mization of the signs and the symptoms in CO poisoning.展开更多
BACKGROUND Delayed post hypoxic leukoencephalopathy syndrome(DPHLS),also known as Grinker’s myelinopathy,is a rare but significant neurological condition that manifests days to weeks after a hypoxic event.Characteriz...BACKGROUND Delayed post hypoxic leukoencephalopathy syndrome(DPHLS),also known as Grinker’s myelinopathy,is a rare but significant neurological condition that manifests days to weeks after a hypoxic event.Characterized by delayed onset of neurological and cognitive deficits,DPHLS presents substantial diagnostic and therapeutic challenges.AIM To consolidate current knowledge on pathophysiology,clinical features,diagnostic approaches,and management strategies for DPHLS,providing a comprehensive overview and highlighting gaps for future research.METHODS Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes guidelines,we systematically searched PubMed,ScienceDirect and Hinari databases using terms related to delayed post-hypoxic leukoencephalopathy.Inclusion criteria were original research articles,case reports,and case series involving human subjects with detailed clinical,neuroimaging,or pathological data on DPHLS.Data were extracted on study characteristics,participant demographics,clinical features,neuroimaging findings,pathological findings,treatment,and outcomes.The quality assessment was performed using the Joanna Briggs Institute critical appraisal checklist.RESULTS A total of 73 cases were reviewed.Common comorbidities included schizoaffective disorder,bipolar disorder,hypertension,and substance use disorder.The primary causes of hypoxia were benzodiazepine overdose,opioid overdose,polysubstance overdose,and carbon monoxide(CO)poisoning.Symptoms frequently include decreased level of consciousness,psychomotor agitation,cognitive decline,parkinsonism,and encephalopathy.Neuroimaging commonly revealed diffuse T2 hyperintensities in cerebral white matter,sometimes involving the basal ganglia and the globus pallidus.Magnetic resonance spectroscopy often showed decreased N-acetylaspartate,elevated choline,choline-to-creatinine ratio,and normal or elevated lactate.Treatment is often supportive,including amantadine,an antioxidant cocktail,and steroids.Hyperbaric oxygen therapy may be beneficial in those with CO poisoning.Parkinsonism was often treated with levodopa.Most of the patients had substantial recovery over the course of months and many cases had some residual neurocognitive deficits.CONCLUSION DPHLS remains a complex and multifaceted condition with various etiologies and clinical manifestations.Early recognition and appropriate management are crucial to improving patient outcomes.Future research should focus on standardizing diagnostic criteria,using advanced imaging techniques,and exploring therapeutic interventions to improve understanding and treatment of DPHLS.Conducting prospective cohort studies and developing biomarkers for early diagnosis and monitoring will be essential to advance patient care.展开更多
文摘Introduction: Due to its severe toxicity, carbon monoxide poisoning is an emergency that leads to cardiac and brain involvement, and emergency physicians should aim to master this diagnosis. This study is intended to describe the expected prevalence of these severe toxicities in the emergency department. Materials and Methods: A retrospective cohort of consecutive patients over 16 years of age presenting with carbon monoxide poisoning to the emergency department of the Hospital Universitario Austral, Argentina, during the period from January 2018 to June 2022. The prevalence of myocardial and brain toxicity was assessed regarding percentage, continuous variables with mean and standard deviation, categorical variables with percentage and absolute frequency. Positive findings of acute neurological toxicity included seizures, syncope and coma, while cardiovascular toxicity encompassed acute myocardial infarction (MI) diagnosed by electrocardiogram or elevated troponin levels, arrhythmias, and the development of pulmonary edema/ congestive heart failure (CHF) confirmed by chest X-ray with suggestive signs or clinically compatible symptoms. Patients were followed-up for 90 days to estimate hospitalization and mortality. Results: A total of 67 patients were evaluated;44.77% of them were males with a mean age of 38.5 ± 14.97 years. The prevalence of acute myocardial toxicity was 7.46% (n: 5). Among these patients, 3 had overweight as a risk factor, and 3 showed ECG abnormalities with negative T-waves. The prevalence of acute brain toxicity was 8.9% (n: 6). In total, 37% (n: 25) of patients met the criteria for hyperbaric oxygen therapy, of which 32% (n: 8) underwent more than one session. A total of 7.46% of patients (n: 5) required hospitalization. Mortality at 90 days was 0%. Conclusion: Among the patients who presented to the emergency department, the prevalence of acute myocardial toxicity was 7.46% (n: 5), which is lower than the prevalence reported in other studies to date. The prevalence of acute brain toxicity was 8.9% (n: 6), and there are no studies describing the prevalence of acute brain toxicity in the emergency department to date. There were no fatalities in our series.
文摘Currently, there is no known optimal therapy for carbon monoxide （CO） poisoning and CO-associated delayed neu- rological sequelae. Hyperbaric oxygen therapy （HBOT） is a well-known treatment method, but its use for CO poison- ing patients is controversial to use due to lack of evidences regarding its efficacy. Thus, it is unlikely that HBOT alone will be accepted as the standard treatment method. In this article, current and potential treatment methods of CO poi- soning are presented as well as the tentative multi-factorial pathophysiology. A series of treatments are suggested for use as a bundle therapy, with targeted temperature management as the base treatment method. Such a therapy holds a great potential, especially for the cases where HBOT is not readily available. We suggest further investigations for elucidating the effects of these suggested treatments and their roles in terms of the complex pathophysiology of CO poisoning. Future ac- ceptance of this therapy based on the improved scientific and clinical knowledge may result in injury prevention and mini- mization of the signs and the symptoms in CO poisoning.
文摘BACKGROUND Delayed post hypoxic leukoencephalopathy syndrome(DPHLS),also known as Grinker’s myelinopathy,is a rare but significant neurological condition that manifests days to weeks after a hypoxic event.Characterized by delayed onset of neurological and cognitive deficits,DPHLS presents substantial diagnostic and therapeutic challenges.AIM To consolidate current knowledge on pathophysiology,clinical features,diagnostic approaches,and management strategies for DPHLS,providing a comprehensive overview and highlighting gaps for future research.METHODS Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes guidelines,we systematically searched PubMed,ScienceDirect and Hinari databases using terms related to delayed post-hypoxic leukoencephalopathy.Inclusion criteria were original research articles,case reports,and case series involving human subjects with detailed clinical,neuroimaging,or pathological data on DPHLS.Data were extracted on study characteristics,participant demographics,clinical features,neuroimaging findings,pathological findings,treatment,and outcomes.The quality assessment was performed using the Joanna Briggs Institute critical appraisal checklist.RESULTS A total of 73 cases were reviewed.Common comorbidities included schizoaffective disorder,bipolar disorder,hypertension,and substance use disorder.The primary causes of hypoxia were benzodiazepine overdose,opioid overdose,polysubstance overdose,and carbon monoxide(CO)poisoning.Symptoms frequently include decreased level of consciousness,psychomotor agitation,cognitive decline,parkinsonism,and encephalopathy.Neuroimaging commonly revealed diffuse T2 hyperintensities in cerebral white matter,sometimes involving the basal ganglia and the globus pallidus.Magnetic resonance spectroscopy often showed decreased N-acetylaspartate,elevated choline,choline-to-creatinine ratio,and normal or elevated lactate.Treatment is often supportive,including amantadine,an antioxidant cocktail,and steroids.Hyperbaric oxygen therapy may be beneficial in those with CO poisoning.Parkinsonism was often treated with levodopa.Most of the patients had substantial recovery over the course of months and many cases had some residual neurocognitive deficits.CONCLUSION DPHLS remains a complex and multifaceted condition with various etiologies and clinical manifestations.Early recognition and appropriate management are crucial to improving patient outcomes.Future research should focus on standardizing diagnostic criteria,using advanced imaging techniques,and exploring therapeutic interventions to improve understanding and treatment of DPHLS.Conducting prospective cohort studies and developing biomarkers for early diagnosis and monitoring will be essential to advance patient care.
