汕头大学医学院儿科学课件 新生儿呼吸窘迫综合征（英）.pptVIP

Definition Hyaline membrane disease， HMD Deficiency of pulmonary surfactant，PS Pulmonary alveoli collapse at the end of expiration Progressively aggravated respiratory distress shortly after birth Mainly in preterm infant Higher incidence rate with smaller gestational age Infant of DM mother, cesarean section, the second baby of twins Etiology PS are secreted by type II epithelial cells of pulmonary alveoli. Dipalmitoyllecithin（DPPC） is the main substance. Surfactant protein（SP） PS are produced from 18~20w till 35~36w when lung is mature. Etiology PS cover the inner surface of pulmonary alveoli, which can: decrease alveolar surface tension prevent alveoli collapse at the end of expiration keep functional residual capacity（FRC） keep stable pulmonary alveolus pressure decrease fluid exude from capillary to pulmonary alveoli Etiology Preterm birth pH of body fluid, body temperature, volume of pulmonary blood flow and hormone can influence PS secretion. Asphyxia, hypothermia, placenta previa, placental abruption and hypotension of mother, which can influence blood flow of fetus. High level insulin of IDM may resist the promotion effect of adrenal cortex hormone to PS synthesis Pathogenesis Clinical manifestation Respiratory distress 2~6h after birth: dyspnea, cyanosis, flaring of alaenasi, inspiratory three-concave sign, expiratory groan Progressively aggravated respiratory distress Flat thorax, low breath sound, wet rales Arterial duct opening at convalescence stage Condition will improve after 3d but the course will longer if complications exist. Assistant examination Laboratory examinations： foam test lecithin/sphingomyelin（L/S） blood gas analysis Chest X ray： frosted glass-like changes air bronchogram white lung color Doppler ultraphonic：PPHN, PDA Diagnosis Clinical manifestations Chest X ray Differential diagnosis wet lung group B streptococcal pneumonia diaphragmatic hernia Therapy General treatment： incubation monitoring of T, R, HR, BP, blood gas liquid and n