Clinical Characteristics Analysis Of 25 Full-term Neonates With Respiratory Distress Syndrome

Objective: To improve understanding of clinical characteristics and risk factors for respiratory distress syndrome/RDS in full-term neonates. Methods: According to RDS diagnostic criteria , we choose cases among the full-term neonates who were admitted to our NICU award and received assistant ventilation after intubation from 1st January 2006 to 31st December 2006, then retrospectively study and analyze the clinical data of those eligible cases. Results: Clinical characteristics: ①Onset timing window is broad, from birth to 14 hours after birth.②In 25 eligible cases , 12(48%) had patent ductus arteriosus/PDA , 11(44%)had pulmonary airleak , 9(36 %)had pulmonary arterial hypertension/PH , 8(32%) had hypoxic-ischemic encephalopathy/HIE, 6(24%) had intracranial hemorrhage. ③Mean assistant ventilation time is 120.24±45.73 hours. ④24 babies in 25 eligible cases recovered and returned home after proper assistant ventilation in time, only one died Risk factors for RDS in full- term neonates: in 25 eligible cases , 23(92%, OR 17.25) neonates were carried out by caesarean section/CS, including 21 (84%) before the onset of labor; 14 (56%, OR 11.45) babies had asphyxia history; 3(12%) had aspiration history; 1(4%, OR 2.63) is a twin; 1(4%) had a mother with gestational diabetes history. The ratio of male and female patients was 18:7 (OR 2.14). Conclusions: RDS in full-term neonates has broad onset timing window, high incidence of complications, long duration of assistant ventilation. CS especially CS before the onset of labor, asphyxia, male, and so on are risk factors for RDS in full-term neonates. Strict command of selective CS indication, choice of right CS timing and change of the CS mode may decrease the incidence of RDS in full- term babies. Given early diagnosis, proper assistant ventilation in time, most cases of RDS in full-term neonates would have good prognosis.The toxic effect of bilirubin to neurological system (bilirubin encephalopathy) is apt to induce death or severe neurological sequealae.So pediatrians always pay great attention to the management of hyperbilirubinemia .Due to the increase of preterm survival rate and early discharge of neonate ,the prevalence of bilirubin encephalopathy abroad has risen up in recent 10 years. And bilirubin-induced neurotoxicity and its molecular mechanisms have caught researchers' eye once again. This review elaborates current research advances in bilirubin-induced neurotoxicity and its molecular mechanisms from different aspects below :apoptosis , glumatate excitory toxicity, NO and mitochondrial role.