病程长达一年的支气管肺发育不良一例

我院近两年使用肺表面活性物质加呼吸机抢救早产儿肺透明膜病共97例，治愈95例，2例家长放弃治疗。并发支气管肺发育不良(BPD)5例，4例住院2～3月后痊愈出院，其中1例住院时间长达205d，曾先后4次上机，需用氧时间长达1年，现报告如下。     

支气管肺发育不良

支气管肺发育不良（ＢＰＤ）由Ｎｏｒｔｈｗａｙ在１９６７年首次提出［１］,是继发于机械通气的一种慢性肺疾病,主要见于早产儿呼吸窘迫综合征（ＲＤＳ）,亦可见于其他疾病需长期机械通气治疗的新生儿。随着极低出生体重儿（ＶＬＢＷ）成活率的提高和机械通气的普遍开展,ＢＰＤ的发病率也随之升高,有关ＢＰＤ的研究取得了很大进展,死亡率有所下降,但仍是危害婴幼儿健康的一种严重疾病。本文将近年来ＢＰＤ的研究进展作一综述。 一、病因及发病机制１．肺发育不成熟：胎儿气道分支形成在孕２４周,此后肺泡逐渐形成,孕３０～４０周…     

支气管肺发育不良

支气管肺发育不良(BPD)是一种慢性肺疾病(CLD),通常发生于罹患肺透明膜病(HMD)、接受氧气、机械通气治疗的早产儿。在早期文献,此病被称为BPD,而近年来被称为CLD。2000年,在美国儿童健康和人类发展研究院(NICHD),心脏、肺和血液研究院(NHLBI)及少见病委员会共同举办的BPD研讨会上,多数人主张采用BPD命名,认为此命名可清楚的区别生命后期多种原因的CLD。     

支气管肺发育不良

支气管肺发育不良(BPD)是1967年由Naathway、Sosam和Porter介绍的一个专门名词,用来描述一些新生儿在延长呼吸机通气后发生的临床、X线检查及病理改变,有资料表明体重小于1000g的早产儿BPD发病率为44％。临床表现绝大多数是早产儿,在出生后的前几天使用过呼吸机,呼吸机的使用指征为由于呼吸窘迫综合征(RDS)所致的呼吸衰竭,但也用于肺炎、胎类吸入综合征(MAS)、动脉导管未闭或早产儿呼吸暂停。延长呼吸     

支气管肺发育不良

支气管肺发育不良（BPD）是一种慢性肺疾病（CLD），通常发生于罹患肺透明膜病（HMD）、接受氧气、机械通气治疗的早产儿。在早期文献，此病被称为BPD，而近年来被称为CLD。2000年，在美国儿童健康和人类发展研究院（NICHD），心脏、肺和血液研究院（NHLBI）及少见病委员会共同举办的BPD研讨会上，多数人主张采用BPD命名，认为此命名可清楚的区别生命后期多种原因的CLD。     

应用肺表面活性物质治疗支气管肺发育不良一例

患儿男 ,孕 31周早产儿 ,出生体重 195 0ｇ ,生后 1ｈ出现呼气性呻吟 ,呼吸困难逐渐加重 ,胸片符合新生儿肺透明膜病Ⅲ Ⅳ期。入院后行机械通气治疗。根据患儿肺透明膜病改善后机械通气参数不能下调、Ｘ线胸片一度好转后又出现弥漫条索及小囊状影、以及机械通气时间超过 2 8ｄ ,诊断为新生儿肺透明膜病合并支气管肺发育不良。给予激素治疗2个疗程后 ,呼吸机条件仍维持吸气峰压 (ＰＩＰ) 18～ 2 0ｃｍＨ2 Ｏ (1ｃｍＨ2 Ｏ =0 0 98ｋＰａ) ,吸入氧浓度 (ＦｉＯ2 )为 0 40～0 45 ,血气波动在ＰａＣＯ2 5 0～ 70ｍｍＨｇ (1ｍｍＨｇ =0 133…     

早产儿支气管肺发育不良25例

目的 探讨早产儿支气管肺发育不良(BID)的危险因素及早期诊断和治疗.方法 回顾性分析本院2003年9月-2007年12月住院BPD患儿25例的临床资料,对患儿的原发病、合并症、临床诊断和治疗进行分析,并对患儿出院12个月内进行随访,分析BPD发生的重要因素及早期诊治的效果.结果 25例中胎龄26～27周2例,28～30周17例,31～32周5例,35周1例;出生体质量700～1 000 g9例,1 001～1 500 g 12例,1 501～2 000 g4例.诊断BPD前并感染15例、动脉导管未闭10例.最早拟诊时间出生13 d.20例接受地塞米松治疗,经治疗24例好转出院,1例放弃治疗后死亡.结论 早产、极低出生体质量、并感染、机械通气、动脉导管未闭等是BPD发生的重要因素,对易感患儿进行严密监测、早期诊断、防治感染、及时关闭导管、及时应用利尿剂和地塞米松是预防和治疗BPD的重要措施.     

长期机械通气致支气管肺发育不良一例

患儿,男,30小时,因进行性呼吸困难、紫绀、呻吟26小时入院。孕32周早产,体重1.96kg,查体:R80次/分,鼻扇,呻吟,三凹征明显,呼吸暂停,面色青灰,双肺呼吸音低,心脏无杂音。血气示pH7.308,PCO_27.05kPa,PO_23.99kPa,HCO_3~- 26mEq/L,SaO_229.5％。生后28小时胸片双肺细颗粒阴影,可见支气管充气象。入院诊     

支气管肺发育不良的研究进展

支气管肺发育不良(BPD)是早产儿最常见的严重呼吸系统疾病。随着产前糖皮质激素的应用、呼吸支持的改善、肺表面活性物质(PS)的应用,经典型BPD发病率有所降低,新型BPD发生率有所增多,其发病机制主要是在基因易感性的基础上,宫内和出生后的多重打击引起促炎、抗炎因子的级联反应,对发育不成熟的肺引起损伤,以及损伤后血管化失调和肺组织异常修复。在治疗上无满意的治疗策略,目前常采用的方法包括保持适当的血氧含量,允许性高碳酸血症,早期使用无创呼吸支持,使用气管内插管-PS使用-尽早拔管改用无创呼吸支持模式,常用药物为咖啡因、类固醇、外源性PS等,但具体效果仍存在争议。     

支气管肺发育不良的研究进展

支气管肺发育不良(BPD)是威胁早产儿健康问题的主要原因.随着新生儿治疗新技术的不断应用,"新"BPD已经替代了"老"BPD.BPD的发生涉及多种因素的相互作用,很多预防和治疗策略已用于BPD.

Abstract：

Bronchopulmonary dysplasia(BPD) is one of the main causes which threatend the health of preterm infants. As neonatal intensive care improved, the "new" BPD have replaced the" old" BPD. The development of BPD involved many factors, and several preventative and therapeutic strategies have been used in BPD.     

支气管肺发育不良早产儿生后1年内神经行为发育的临床分析

目的 探讨支气管肺发育不良（BPD）对早产儿生后1年内神经行为发育的影响。方法 回顾性选取2017年9月至2019年12月间出生胎龄 < 34周，并完成纠正胎龄40周及3、6、12月龄神经行为发育随访的早产儿为研究对象。根据诊断分为BPD组（n=23）和非BPD组（n=27），比较两组患儿不同时点的神经行为发育结果。结果 BPD组与非BPD组患儿纠正胎龄40周时新生儿神经行为测定评分差异无统计学意义（P > 0.05）。Gesell发育量表中，BPD组纠正胎龄3、6、12月龄时精细动作、适应性行为、社交行为能区发育商（DQ）及总DQ低于非BPD组（P < 0.05）；两组患儿纠正胎龄6月龄时言语能区DQ高于纠正胎龄12月龄（P < 0.017），纠正胎龄6月龄时社交行为能区DQ高于纠正胎龄3月龄（P < 0.017），纠正胎龄12月龄时适应性行为能区DQ高于纠正胎龄3、6月龄（P < 0.017）。Bayley发育量表Ⅱ中，两组患儿各时点智力和运动发展指数差异无统计学意义（P > 0.05），纠正胎龄3月龄时智力发展指数高于纠正胎龄6、12月龄（P < 0.001）。结论 BPD早产儿在生后1年内较非BPD早产儿存在神经发育落后，临床需给予重视。     

Rehospitalization in the first year of life among infants with bronchopulmonary dysplasia

OBJECTIVE: To describe rates and identify risk factors for rehospitalization during the first year of life among infants with bronchopulmonary dysplasia (BPD). STUDY DESIGN: This was a retrospective cohort study of infants born at a gestational age (GA) <33 weeks, between 1995 and 1999. BPD was defined as requirement of supplemental oxygen and/or mechanical ventilation at 36 weeks' corrected GA. The outcome was rehospitalization for any reason before first birthday. RESULTS: In the first year of life, 118 of 238 (49%) infants with BPD were rehospitalized, more than twice the rate of rehospitalization of the non-BPD population, which was 309 of 1359 (23%) (P=<.0001). No measured factor discriminated between those infants with BPD who were and were not rehospitalized, even when only rehospitalizations for respiratory diagnoses were considered. CONCLUSIONS: Among premature infants, BPD substantially increases the risk of rehospitalization during the first year of life. Neither demographic nor physiologic factors predicted rehospitalization among the infants with BPD. Other factors, such as air quality of home environment, passive smoking exposure, respiratory syncytial virus prophylaxis, breast-feeding status, and/or parenting and primary care management styles, should be examined in future studies.     

Management of bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) is a common and important complication of prematurity and is associated with significant mortality, morbidity and healthcare resource utilization. Despite advances in both perinatal and neonatal care the incidence of the condition continues to rise. The management of BPD and its related problems remains a major challenge to neonatologists and paediatricians. There is unlikely to be a single intervention which will dramatically alter the management of BPD and thus multiple interventions have been proposed to prevent and treat the disease. Many of these interventions are still not evidence based and some of those that are have been shown to have unacceptable long-term effects. It is useful to conceptualize BPD in three stages, namely (i) prevention, (ii) treatment of evolving BPD and (iii) treatment of established BPD. In this review current and potential future management approaches to BPD and the relevant evidence for these are discussed within the framework of these three stages.     

Management of bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD), also known as chronic lung disease of prematurity, and typically defined as the need for supplemental oxygen at 36 weeks' postmenstrual age, affects approximately 10% and 40% of very low birth weight and extremely low birth weight infants, respectively. Contributing factors include infection, oxygen exposure and ventilator induced lung injury, which can lead to impaired lung function. Several preventative and therapeutic strategies have been used in BPD, including lung protective ventilator strategies, and pharmacologic interventions. While many infants with BPD are treated with a wide variety of medications, little evidence for the efficacy of these treatments exist. This article will review current practice in the prevention and management of this complication of prematurity.     

Prevention of bronchopulmonary dysplasia

The clinical syndrome of bronchopulmonary dysplasia (BPD) in preterm infants results primarily from an arrest of lung vascular and alveolar development. The most likely mediators are proinflammatory cytokines that are induced by antenatal exposure to infection, postnatal ventilation, and oxygen exposure. New epidemiologic data suggest that attempts to avoid intubation and ventilation are the best ways to avoid severe BPD. The claim that one ventilation technique is better than another remains unconvincing, and any strategy that maintains the lung open and minimizes tidal volumes probably will be helpful. More adverse effects of postnatal steroids are being recognized. New insights into the pathophysiology of BPD and a new emphasis on minimizing ventilation and ventilator-mediated injury should improve outcomes for very preterm infants.