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The pathogenesis of pulmonary sequestration is still debated. Despite the obvious correlation of ELS with other congenital diseases,some cases of ILS seemed to be acquired after birth. This is based on the finding that there was a paucity of cases in a neonatal autopsy series, and the observation that pulmonary inflammation can stimulate collateral circulation to the lung [6]. In contrast, most of the cases with ELS were diagnosed within the first year of life,with or without the development of respiratory compromise . ELS also has higher incidence of associated congenital anomalies than ILS. In a series of 28 cases among children and adults,associated malformations occurred in 43% ofELS and 17% of ILS cases. The clinical features of pulmonary sequestrations vary, depending on the type of malformations, age at presentation and the size of the sequestered lung.On prenatal ultrasound,pulmonary sequestration commonly presents as an incidental finding of an echogenic thoracic mass that can be small or occupy most of the hemithorax. Mediastinal shift is often seen in cases of large pulmonary sequestration. Hydrops may develop in a minority of patients,possibly due to vascular compression. There is no validated predictive factor currently to estimate the progression of pulmonary sequestration and the risk of developing hydrops. ELS typically presents in symptomatic newborns with respiratory compromise. Recurrent pneumonia is less commonly reported, and most patients remain asymptomatic throughout the course. Most cases of postnatal ELS were identified during evaluation of an associated anomaly. ILS is usually detected in adolescents with recurrent pneumonia or signs of airway infection, like fever and productive cough. It is rarely diagnosed in the perinatal period. When patients with ILS become older, hemoptysis and chest pain may occur. If the aberrant artery supplying a sequestered lung is large, heart failure can develop in rare cases a result of high cardiac output.