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COVID-19 , Accidente Cerebrovascular , Muerte Encefálica , Niño , Mortalidad Hospitalaria , Humanos , SARS-CoV-2RESUMEN
OBJECTIVE: Delayed neuropsychiatric syndrome may occur after carbon monoxide poisoning has completely healed. The literature on indicators to predict delayed neuropsychiatric syndrome in pediatric patients is limited. The aim of the study is to investigate the effectiveness of complete blood count parameters, neutrophil/lymphocyte ratio, platelet/lymphocyte ratio, systemic immune inflammation index, glucose/potassium ratio, venous blood gas parameters, and carboxyhemoglobin in predicting delayed neuropsychiatric syndrome in children with carbon monoxide poisoning due to coal-burning stove. MATERIALS AND METHODS: The patients admitted to the pediatric emergency department with acute carbon monoxide poisoning between 2014 and 2019 were analyzed. The patients were divided into 2 groups as delayed neuropsychiatric syndrome (+) and delayed neuropsychiatric syndrome (-). Neutrophil/lymphocyte ratio, platelet/lymphocyte ratio, systemic immune inflammation index (platelet count×neutrophil count/lymphocyte count), and glucose/ potassium ratio were calculated. RESULTS: Of the 137 patients, 46 were diagnosed with delayed neuropsychiatric syndrome within 1 year of carbon monoxide poisoning. A control group was formed from 137 age- and sexmatched children. Glasgow Coma Scale < 15 was found in 11% of patients with delayed neuropsychiatric syndrome (-) and 8.7% of patients with delayed neuropsychiatric syndrome (+) (P = .773). Blood glucose, potassium, glucose/potassium ratio, platelet/lymphocyte ratio, white blood cell, neutrophil count, lymphocyte count, neutrophil/lymphocyte ratio, systemic immune inflammation index, venous partial pressure of carbon dioxide, carboxyhemoglobin, and methemoglobinemia levels were significantly different between control, delayed neuropsychiatric syndrome (+), and delayed neuropsychiatric syndrome (-) groups (P < .05). The most effective predictors for delayed neuropsychiatric syndrome were systemic immune inflammation index (area under the curve = 0.852; cut-off value > 1120; sensitivity = 89.1%; specificity = 75.8%), neutrophil (area under the curve = 0.841; cut-off value > 8000/mm3; sensitivity = 78.2%; specificity = 79.1%), and neutrophil/lymphocyte ratio (area under the curve = 0.828; cut-off value > 4; sensitivity = 78.2%; specificity = 75.5%). CONCLUSION: About one-third of children with carbon monoxide poisoning due to coal-burning stove develop delayed neuropsychiatric syndrome. Systemic immune inflammation index, neutrophil count, and neutrophil/lymphocyte ratio obtained immediately after the poisoning in the pediatric emergency department may be effective predictors for delayed neuropsychiatric syndrome.
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OBJECTIVE: The aim of this study is to investigate the relationship between exposure to acute air pollution and meteorological factors on the frequency of epileptic attacks in children. METHODS: This retrospective study was carried using patient files from a children's hospital in Diyarbakir, one of the largest cities in Turkey. In the present study, the possible relationship between epileptic attacks seen in children over a 10-year period, two air polluting factors (PM10 and SO2), and the meteorological factors (air pressure, humidity, precipitation, wind speed) affecting them were investigated. The effects of different variables on the number of epilepsy patients admitted to the pediatric emergency department were also evaluated through four different models utilizing Poisson Regression Analysis. RESULTS: According to Model 2 and 3, the strongest relationship of the four Poisson Regression models, there was a significantly increased risk of pediatric emergency department admissions for seizures associated with a 10 µm/m3 increase in PM10 (IRR=1.020; 95% CI: 1.018-1.022); IRR= 1.071; 95% CI: 1.050-1.081; respectively) and 10 µm/m3 increase in SO2 (IRR=1.162; 95%CI: 1.151-1.173; IRR=1.092; 95% CI: 1.042-1.120; respectively). In Model 2, a 1 m/s increase in wind speed decrease the risk of daily of epileptic attack admitted to the emergency department and a 1 °C increase in temperature increased the risk of daily of epileptic attack admitted to the emergency department (IRR=0.840; 95% CI; 0.714-0.987; IRR=1.033; 95%CI: 1.007-1.059; respectively). In Model 3, 1% increase in humidity and 1 m/s increase in wind speed increased the number of daily epileptic attack admitted to the emergency department (IRR=1.008; 95%CI: 1.004-1.011; IRR=1.169; 95%CI: 1.056-1.294; respectively). The daily number of epilepsy patients was statistically significantly affected by the autumn (95%CI: 10.017-19.845) and winter (95%CI: -0.279 to 13.292) seasons. CONCLUSION: Meteorological factors and air pollutants affect the number of pediatric patients admitted to the pediatric emergency department with epilepsy attacks.
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Contaminación del Aire , Epilepsia , Humanos , Niño , Estudios Retrospectivos , Contaminación del Aire/efectos adversos , Conceptos Meteorológicos , Servicio de Urgencia en Hospital , Convulsiones , Epilepsia/epidemiología , ChinaRESUMEN
PURPOSE: Our aim was to comparatively investigate the strain ratio and thickness of the Achilles tendon in children with cerebral palsy (CP), and to elucidate whether there is a correlation between biomechanical features of the Achilles tendon and strain ratio. METHODS: A total of 155 participants (72 CP patients and 83 healthy controls) who underwent real-time elastography of both Achilles tendons were studied. A linear transducer (4.8-11.0 MHz) was used to obtain the images. Correlation analysis between age, length, and thickness of the Achilles tendon, and strain ratio (SR) was performed by means of Pearson correlation and Spearman's rho tests. RESULTS: Comparison of results obtained from CP patients and controls showed that the length of the Achilles tendon was shorter (p < 0.001) and SR was higher (p < 0.001) in CP patients. In CP patients, there was a positive correlation between SR and age and between SR and the thickness and length of the Achilles tendon (p < 0.001 for all). Furthermore, the length of the tendon and age were positively associated (p < 0.001). ROC analysis revealed that the cut-off value for SR was 1.89. CONCLUSION: The results of the present study demonstrated that real-time elastography can constitute a simple, practical, and noninvasive method for evaluation of the elasticity of the Achilles tendon in children with CP.
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Tendón Calcáneo/diagnóstico por imagen , Parálisis Cerebral/complicaciones , Diagnóstico por Imagen de Elasticidad , Tendinopatía/diagnóstico por imagen , Tendón Calcáneo/fisiopatología , Adolescente , Fenómenos Biomecánicos , Parálisis Cerebral/fisiopatología , Niño , Preescolar , Estudios Transversales , Elasticidad/fisiología , Femenino , Humanos , Masculino , Tendinopatía/etiología , Tendinopatía/fisiopatologíaRESUMEN
OBJECTIVE: To identify the underlying etiology of 3 patients in a multiplex family with strokes, chronic immune-mediated peripheral neuropathy, and hemolysis. All had onset in infancy. METHODS: We performed genome-wide linkage analysis followed by whole exome sequencing (WES) in the proband, Sanger sequencing, and segregation analysis of putative mutations. In addition, we conducted flow cytometry studies to assess CD59 expression. RESULTS: In a 2-generation-3-affected family with early-onset immune-mediated axonal neuropathy, cerebrovascular event both in the anterior and posterior circulation, and chronic Coombs-negative hemolysis, we detected CD59 deleterious mutation as the underlying cause. Linkage analysis and homozygosity mapping using single nucleotide polymorphism (SNP) microarrays in the family followed by WES in one index case allowed identification of a homozygous missense mutation in the CD59 gene (c.A146T:p.Asp49Val). Sanger sequencing validated the mutation, showing cosegregation with the disease phenotype. Flow cytometry using blood cells in the 3 patients showed a lack of CD59 expression at the cell membrane compared to control and CD55 labeling. CONCLUSION: We added to the knowledge base about inherited CD59 deficiency.