Background:Several studies have clearly demonstrated a significantly higher incidence of persistent pulmonary hypertension of the newborn (PPHN) in neonates delivered by caesarean section (CS) compared to those delive...Background:Several studies have clearly demonstrated a significantly higher incidence of persistent pulmonary hypertension of the newborn (PPHN) in neonates delivered by caesarean section (CS) compared to those delivered vaginally.The pathophysiological factors underlying the link between CS and PPHN are still poorly understood.In this review,we describe the mechanisms that could explain the association between CS delivery and subsequent PPHN,as well as potential preventive measures.Data sources:A literature search was conducted by electronic scanning of databases such as PubMed and Web of Science using the key words 'persistent pulmonary hypertension of the newborn','caesarean section','iatrogenic prematarity','oxidative stress','late preterm','labor' and 'vasoaetive agents'.Results:Iatrogenic prematurity,higher rates of late preterm delivery and lack of physiological changes of labor play an important role in the association between CS and PPHN.CS delivery also results in limited endogenous pulmonary vasodilator synthesis and lower levels of protective anti-oxidants in the neonates.In addition,CS delivery exposes infants to a higher risk of respiratory distress syndrome and its concomitant increase in endothelin-1 levels,which might indirectly lead to a higher risk of developing PPHN.We believe that neonates delivered by CS are exposed to a combination of these pathophysiological events,culminating in an endpoint of respiratory distress,hypoxia,acidosis,and delayed transition and thereby increased risks of PPHN.The use of antenatal corticosteroids prior to elective CS in late preterm deliveries,promoting accurate informed-consent process,delaying elective CS to 39 weeks of gestation or beyond and antenatal maternal anti-oxidant supplementation could potentially mitigate the effects of CS delivery and minimize CS-related PPHN.Conclusions:The link between CS delivery and PPHN is complex.In view of the rising rates of CS worldwide,there is an urgent need to further explore the mechanisms linking CS to PPHN and experimentally test therapeutic options in order to allow effective targeted interventions.展开更多
Background To summarize the experience of management of persistent pulmonary hypertension of the newborn (PPHN) with extracorporeal membrane oxygenation (ECMO) support.Methods We presented three neonates with PPHN sup...Background To summarize the experience of management of persistent pulmonary hypertension of the newborn (PPHN) with extracorporeal membrane oxygenation (ECMO) support.Methods We presented three neonates with PPHN supported by ECMO in our center.Medical records and patient management notes were retrospectively reviewed.Results For two neonates with congenital diaphragmatic hernia (CDH),diaphragm repair surgery was done under ECMO support.One patient was weaned from ECMO after 73 hours,and recovered well at the last follow-up after 1 year.The other patient was weaned from ECMO after 167 hours,and he died from septic shock 21 days after decannulation.For the neonate with idiopathic PPHN,ECMO was withdrawn successfully.Conclusions ECMO is an effective rescue means for refractory PPHN.Appropriate intervention timing,accurate coagulation,and volume management are important.展开更多
Most congenital heart disease(CHD)is readily recognisable in the newborn.Forewarned by previous fetal scanning,the presence of a murmur,tachypnoea,cyanosis and/or differential pulses and saturations all point to a car...Most congenital heart disease(CHD)is readily recognisable in the newborn.Forewarned by previous fetal scanning,the presence of a murmur,tachypnoea,cyanosis and/or differential pulses and saturations all point to a cardiac abnormality.Yet serious heart disease may be missed on a fetal scan.There may be no murmur or clinical cyanosis,and tachypneoa may be attributed to non-cardiac causes.Tachypnoea on day 1 is usually non-cardiac except arising from ventricular failure or a large systemic arteriovenous fistula.A patent ductus arteriosus(PDA)may support either pulmonary or systemic duct dependent circulations.The initially high pulmonary vascular resistance(PVR)limits shunts so that murmurs even from large communications between the systemic and pulmonary circulations take days/weeks to develop.At times despite expert input,serious CHD maybe difficult to diagnose and warrants close interaction between the neonatologist and cardiologist to reach a timely diagnosis.Such conditions include obstructed total anomalous pulmonary venous connections(TAPVC)and the need to distinguish it from persistent pulmonary hypertension in the newborn(PPHN)–the treatment of the former is surgical the latter medical.A large duct shunting right to left may overshadow a suspected hypoplastic aortic isthmus and/or coarctation.Is the right to left shunting because of severe aortic obstruction or resulting from a high PVR with little obstruction.The diagnosis of pulmonary vein stenosis(PVS)remains problematic often developing in premature infants with ongoing bronchopulmonary dysplasia(BPD),still being cared for by the neonatologist.While there are other diagnostic dilemmas including deciding the contribution of a recognised CHD in a sick neonate,this paper will focus on the above-mentioned conditions with suggestions on what may be done to arrive at a timely diagnosis to achieve optimal outcomes.展开更多
文摘Background:Several studies have clearly demonstrated a significantly higher incidence of persistent pulmonary hypertension of the newborn (PPHN) in neonates delivered by caesarean section (CS) compared to those delivered vaginally.The pathophysiological factors underlying the link between CS and PPHN are still poorly understood.In this review,we describe the mechanisms that could explain the association between CS delivery and subsequent PPHN,as well as potential preventive measures.Data sources:A literature search was conducted by electronic scanning of databases such as PubMed and Web of Science using the key words 'persistent pulmonary hypertension of the newborn','caesarean section','iatrogenic prematarity','oxidative stress','late preterm','labor' and 'vasoaetive agents'.Results:Iatrogenic prematurity,higher rates of late preterm delivery and lack of physiological changes of labor play an important role in the association between CS and PPHN.CS delivery also results in limited endogenous pulmonary vasodilator synthesis and lower levels of protective anti-oxidants in the neonates.In addition,CS delivery exposes infants to a higher risk of respiratory distress syndrome and its concomitant increase in endothelin-1 levels,which might indirectly lead to a higher risk of developing PPHN.We believe that neonates delivered by CS are exposed to a combination of these pathophysiological events,culminating in an endpoint of respiratory distress,hypoxia,acidosis,and delayed transition and thereby increased risks of PPHN.The use of antenatal corticosteroids prior to elective CS in late preterm deliveries,promoting accurate informed-consent process,delaying elective CS to 39 weeks of gestation or beyond and antenatal maternal anti-oxidant supplementation could potentially mitigate the effects of CS delivery and minimize CS-related PPHN.Conclusions:The link between CS delivery and PPHN is complex.In view of the rising rates of CS worldwide,there is an urgent need to further explore the mechanisms linking CS to PPHN and experimentally test therapeutic options in order to allow effective targeted interventions.
文摘Background To summarize the experience of management of persistent pulmonary hypertension of the newborn (PPHN) with extracorporeal membrane oxygenation (ECMO) support.Methods We presented three neonates with PPHN supported by ECMO in our center.Medical records and patient management notes were retrospectively reviewed.Results For two neonates with congenital diaphragmatic hernia (CDH),diaphragm repair surgery was done under ECMO support.One patient was weaned from ECMO after 73 hours,and recovered well at the last follow-up after 1 year.The other patient was weaned from ECMO after 167 hours,and he died from septic shock 21 days after decannulation.For the neonate with idiopathic PPHN,ECMO was withdrawn successfully.Conclusions ECMO is an effective rescue means for refractory PPHN.Appropriate intervention timing,accurate coagulation,and volume management are important.
文摘Most congenital heart disease(CHD)is readily recognisable in the newborn.Forewarned by previous fetal scanning,the presence of a murmur,tachypnoea,cyanosis and/or differential pulses and saturations all point to a cardiac abnormality.Yet serious heart disease may be missed on a fetal scan.There may be no murmur or clinical cyanosis,and tachypneoa may be attributed to non-cardiac causes.Tachypnoea on day 1 is usually non-cardiac except arising from ventricular failure or a large systemic arteriovenous fistula.A patent ductus arteriosus(PDA)may support either pulmonary or systemic duct dependent circulations.The initially high pulmonary vascular resistance(PVR)limits shunts so that murmurs even from large communications between the systemic and pulmonary circulations take days/weeks to develop.At times despite expert input,serious CHD maybe difficult to diagnose and warrants close interaction between the neonatologist and cardiologist to reach a timely diagnosis.Such conditions include obstructed total anomalous pulmonary venous connections(TAPVC)and the need to distinguish it from persistent pulmonary hypertension in the newborn(PPHN)–the treatment of the former is surgical the latter medical.A large duct shunting right to left may overshadow a suspected hypoplastic aortic isthmus and/or coarctation.Is the right to left shunting because of severe aortic obstruction or resulting from a high PVR with little obstruction.The diagnosis of pulmonary vein stenosis(PVS)remains problematic often developing in premature infants with ongoing bronchopulmonary dysplasia(BPD),still being cared for by the neonatologist.While there are other diagnostic dilemmas including deciding the contribution of a recognised CHD in a sick neonate,this paper will focus on the above-mentioned conditions with suggestions on what may be done to arrive at a timely diagnosis to achieve optimal outcomes.
文摘目的探讨新生儿持续肺动脉高压(persistent pulmonary hypertension of newborn,PPHN)患儿血清人CXC型趋化因子配体8(C-X-C motif chemokine ligand 8,CXCL8)、CXCL12与一氧化氮吸入治疗临床转归的关系。方法选择2021-08/2023-05月作者医院收治并给予一氧化氮吸入治疗的PPHN患儿135例为研究对象。根据患儿出院时临床转归结局分为死亡组(n=32)和存活组(n=103)。比较两组PPHN患儿血清CXCL8、CXCL12水平。单因素及多因素Logistic回归模型分析接受一氧化氮吸入治疗PPHN患儿临床转归的影响因素。受试者工作特征(receiver operating characteristic,ROC)曲线分析血清CXCL8、CXCL12对接受一氧化氮吸入治疗PPHN患儿临床转归的预测价值。结果死亡组患儿血清CXCL8、CXCL12水平显著高于存活组(P均<0.05)。多因素Logsitic回归分析结果显示,血清CXCL8水平升高、血清CXCL12水平升高、早产、出生时Apgar评分0~3分、合并并发症是接受一氧化氮吸入治疗的PPHN患儿死亡的危险因素,肺表面活性物质应用、吸入一氧化氮早期反应则是保护因素(P<0.05)。ROC曲线分析结果显示,血清CXCL8、CXCL12联合检测对接受一氧化氮吸入治疗的PPHN患儿死亡预测的曲线下面积(area under the curve,AUC)为0.828,大于血清CXCL8、CXCL12单独检测(AUC分别为0.762、0.714)。结论PPHN患儿血清CXCL8、CXCL12水平升高与接受一氧化氮治疗的不良临床转归有关,且CXCL8、CXCL12水平升高是PPHN患儿死亡的危险因素。CXCL8、CXCL12联合检测对接受一氧化氮治疗PPHN患儿死亡具有较高的预测价值。
