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)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。     

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…     

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     

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), 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.     

Prognosis factors in severe bronchopulmonary dysplasia. A retrospective study of 65 premature infants with bronchopulmonary dysplasia

The annual incidence of bronchopulmonary dysplasia (BPD) is presently 1.3 case p. 1,000 alive births. The most severe forms of BPD are characterized by a prolonged oxygen-dependence and a spontaneous evolution marked by numerous complications which could be life-threatening. We studied retrospectively 65 premature infants with BPD who underwent ventilation for one month or more during the first weeks of life. Comparison between survivors and children deceased during the first year of life allowed for discerning 5 prognostic criteria: the nature and severity of initial respiratory disease, the respiratory improvement during the first trimester, the results of hematosis by age 3 months, the ability of maintaining and increasing the respiratory improvement while reducing the therapeutic management, the weight and head circumference gains. The respective parts and conditions of oxygen therapy and prolonged mechanical ventilation in severe cases of BPD are discussed.     

Vitamin A status of neonates with bronchopulmonary dysplasia

We prospectively assessed and compared the vitamin A status of two groups of preterm neonates (less than 1500 g birth weight, less than 32 wk gestation), one who developed clinical and radiographic evidence of bronchopulmonary dysplasia (BPD) (n = 10), and the other (control) who developed no significant lung disease (n = 8). The infants with BPD in this study required prolonged mechanical ventilation and supplemental O2 therapy, and had a higher incidence of cardiorespiratory complications when compared to controls. Their mean plasma vitamin A concentrations were significantly lower than those of controls at four sampling times in the 1st postnatal month. In contrast to the controls, infants with BPD showed a substantial decline in their plasma vitamin A concentrations from the initial values, and a high percentage of individual values of plasma vitamin A concentration in these infants were less than 10 micrograms/dl during the 8-wk postnatal period of observation. Delayed establishment of gastrointestinal feeding and a lower vitamin A intake in these infants relative to controls may have accounted for this decline. Our data show that preterm neonates who develop BPD have suboptimal plasma vitamin A concentrations for extended periods of time postnatally. We speculate that the necrotizing bronchiolitis and squamous metaplasia of conducting airways associated with vitamin A deficiency could influence the orderly repair of lung injury in susceptible neonates who are mechanically ventilated and could contribute to the pathophysiology of BPD in these infants.(ABSTRACT TRUNCATED AT 250 WORDS)