Neonatal respiratory distress due to mumps.

We report an infant of 35 weeks'' gestation who developed severe respiratory distress and pneumonitis due to perinatal mumps virus infection.     

Acute respiratory distress syndrome

Background  

Acute respiratory distress syndrome (ARDS) is a common diagnosis among children admitted to pediatric intensive care units. This heterogeneous disorder has numerous pulmonary and non-pulmonary causes and is associated with a significant risk of mortality. Many supportive therapies exist for ARDS.     

Tracheo-oesophageal fistula and the respiratory distress syndrome

Four pre-term neonates with tracheo-oesophageal fistula required positive pressure ventilation because of the respiratory distress syndrome. Gastric rupture occurred in two patients, one of whom died. Ineffective ventilation was critically impaired by formation of a gastrostomy in a third patient, who also died. Direct ligation of the fistula in the fourth critically ill patient led to a dramatic improvement in gas exchange. When the resistance of the airways exceeds that of the fistula, gas escapes through the latter into the gastro-intestinal tract. Formation of a gastrostomy lowers intragastric pressure and thus the resistance to gas escape via the fistula; respiratory support is thus rendered ineffective. Effective ventilation is only possible after occlusion of the fistula, which we believe is best achieved by direct ligation. Offprint requests to: E. M. Kiely     

肺表面活性物质蛋白B基因多态性与新生儿呼吸窘迫综合征易感性的相关性研究

目的：研究肺表面活性物质蛋白（SP）B基因单核苷酸多态性分布以及与新生儿呼吸窘迫综合征（RDS）的关系。方法：选择88例RDS早产儿和未并发RDS的早产儿103例作为研究对象,采用DNA提取试剂盒提取DNA,应用聚合酶联反应-限制性片段长度多态性技术检测SP-B-18A/C、SP-B 1580C/T两个位点的单核苷酸多态性,分析两个位点多态性与RDS的关系。结果：SP-B -18A/C、SP-B 1580C/T两个位点在病例组和对照组中均存在多态性,与未并发RDS的早产儿对照组比较,RDS患儿SP-B 1580C/T位点基因型以CC型明显增多,（χ2=12.26,P0.05）。结论：SP-B 1580 位点C/T多态性与RDS有关,SP-B 1580C/T可能是RDS的易感基因,携带SP-B 1580位点C等位基因的个体患RDS的风险增加。SP-B-18A/C与RDS无关。     

Unexplained neonatal respiratory distress due to congenital surfactant deficiency

Genetic abnormalities of pulmonary surfactant were identified by DNA sequence analysis in 14 (12 full-term, 2 preterm) of 17 newborn infants with fatal respiratory distress of unknown etiology. Deficiency of adenosine triphosphate-binding cassette protein, member A3 (n = 12) was a more frequent cause of this phenotype than deficiency of surfactant protein B (n = 2).     

血清高迁移率族蛋白B1与新生儿呼吸窘迫综合征的相关性研究

目的探讨血清高迁移率族蛋白B1(HMGB1)水平与新生儿呼吸窘迫综合征(NRDS)的相关性。方法选取NRDS患儿35例(观察组)及正常新生儿35例(对照组),收集两组新生儿生后12~24 h内外周静脉血,采用酶联免疫法(ELISA)检测两组新生儿血清HMGB1水平。结果 NRDS患儿血清HMGB1水平高于对照组(P0.05),重度NRDS患儿血清HMGB1水平高于轻度患儿(P0.05),死亡的NRDS患儿血清HMGB1水平高于存活患儿(P0.05)。ROC曲线分析显示预测NRDS的AUC值为0.846(95%CI:0.755~0.936),血清HMGB1 625.3 pg/m L为预测NRDS的最佳界值,预测NRDS患儿死亡风险的AUC为0.916(95%CI:0.813~1.000),血清HMGB1 772.2 pg/L为预测NRDS患儿死亡的最佳界值。结论 NRDS患儿血清HMGB1水平显著升高,血清HMGB1可较好地预测NRDS的发生及预后。     

Pathophysiology of respiratory distress syndrome

Respiratory distress syndrome (RDS) is a major cause of neonatal mortality and morbidity, especially in preterm infants. Its aetiology includes developmental immaturity of the lungs, particularly of the surfactant synthesizing system. Surfactant is produced, stored and recycled by type II pneumocytes and is detectable from about 24 weeks’ gestation. It is a mixture of phospholipids, neutral lipids and proteins and is spread as a film over the alveolar surface to lower surface tension and to prevent alveolar collapse. The resulting clinical correlates of RDS can be predicted from the immature lung structure and atelectasis which occur due to surfactant deficiency. Various clinical factors are known to dysregulate surfactant production and function, leading to the development of RDS. Apart from preventing the incidence of prematurity, antenatal steroids and prophylactic surfactant are of proven benefit in reducing the incidence of RDS.     

新生儿呼吸窘迫综合征的诊治

新生儿呼吸窘迫综合征(respiratory distress syndrome,RDS),又称新生儿肺透明膜病(hyaline membrane disease,HMD),是新生儿死亡的主要原因之一.RDS主要是因为缺乏肺表面活性物质(pulmonary surfactant,PS)引起.     

Management of respiratory distress syndrome

Respiratory distress syndrome is the most common pathology of preterm infants managed in neonatal intensive care units worldwide. Advances in neonatal intensive care, prenatal interventions, especially corticosteroid therapy, and postnatal respiratory support have considerably increased the survival of extremely premature infants. Despite these advances, epithelial lung injury and inflammation secondary to surfactant deficiency and as a consequence of mechanical ventilation ultimately leading to bronchopulmonary dysplasia has not significantly reduced. Animal studies have confirmed that the pathological cascade of inflammation is initiated within the first few breaths of life, more so in a surfactant-deficient lung. Hence early management is aimed at minimizing lung injury, starting in the delivery suite. Although a number of different modalities of ventilation are available for ongoing support, the principle is to administer controlled ventilation, avoiding overinflation, and to give just enough end expiratory pressure to prevent collapse of surfactant-deficient alveoli. Non-invasive ventilation is an invaluable tool both in the treatment of mild-to-moderate RDS and the prevention of post-extubation respiratory failure. Supportive treatment contributes equally to the outcome.     

Thymus size and its relationship to the respiratory distress syndrome.

Thymic size can be affected by both exogenous and endogenous glucocorticoids. The risk of respiratory distress syndrome is reduced after maternal steroid administration. To find whether fetal lung maturity correlates with size of the thymus, the cardiothymic:thoracic ratio was measured in 167 newborn infants with and without RDS. Mean CT/T was significantly greater (0.40 vs 0.35; P less than 0.001) in those babies with RDS. This relation was independent of gestational age, although an increase in CT/T with advancing gestational age was shown. Prepartum maternal steroid administration did not result in significant involution of the cardiothymic shadow when compared with control infants with and without RDS. The CT/T may be of use in predicting which premature babies are more likely to develop RDS.     

Minimizing the risk of respiratory distress syndrome

Respiratory distress syndrome, or hyaline membrane disease, remains one of the most significant causes of neonatal morbidity and mortality, despite advances in perinatal care. It is a condition predominantly affecting premature infants, with an incidence inversely related to gestational age. Whilst many infants will improve within a few days, more severely affected babies are at risk of developing chronic lung disease, and a range of extrapulmonary complications. Minimizing the risk of respiratory distress syndrome requires a combination of preventative strategies prior to and in the immediate aftermath of delivery and a balanced approach to treatment of established disease. The use of antenatal steroids and pulmonary surfactant have revolutionized perinatal medicine, however a number of controversies still exist for both treatments such as optimal dosing, timing, and repeat courses. This article reviews the current evidence for these treatments, as well as over viewing the other essential antenatal and perinatal concerns faced when managing an infant at risk of respiratory distress syndrome.     

Plasma progesterone in the respiratory distress syndrome

Seventeen newborns suffering from RDS (verified by X-ray and clinical parameters) had a mean plasma progesterone of 13.9±1.2 ng/ml (mean±S.E.) at 24 h of age. This is only 62% of the normal level (22.6±1.5 ng/ml).Supported by Turun Yliopistosäätiö