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体外膜肺氧合(ECMO)支持下的先天性膈疝婴儿的表面活性剂(贝拉克坦)治疗:持续性表面活性剂缺乏的证据

Surfactant (beractant) therapy for infants with congenital diaphragmatic hernia on ECMO: evidence of persistent surfactant deficiency.

作者信息

Lotze A, Knight G R, Anderson K D, Hull W M, Whitsett J A, O'Donnell R M, Martin G, Bulas D I, Short B L

机构信息

Department of Neonataology, George Washington University School of Medicine and Health Sciences, Washington, DC.

出版信息

J Pediatr Surg. 1994 Mar;29(3):407-12. doi: 10.1016/0022-3468(94)90580-0.

DOI:10.1016/0022-3468(94)90580-0
PMID:8201510
Abstract

Infants with congenital diaphragmatic hernia (CDH) on extracorporeal membrane oxygenation (ECMO) can have initial lung atelectasis which, in survivors, gradually improves over time. To test the hypothesis that these patients could benefit from surfactant therapy, infants with CDH (born at > 34 weeks' gestation) on ECMO received either four doses of modified bovine lung surfactant extract (beractant) (surfactant group, n = 9) or an equal volume of air (control group, n = 8). Tracheal aspirate surfactant protein-A (SP-A) concentrations were initially low, and then increased over time in both CDH groups (P = .0021); however, levels remained low when compared with those of infants on ECMO who had other diagnoses (P = .04). Lung compliance (CL), time to extubation, time on oxygen, and total no. of hospital days were not different between the two groups. Infants with CDH had persistently elevated right ventricular pressure (RVP) at cessation of bypass when compared with non-CDH infants on ECMO (RVP = 53.25 mm Hg +/- 19.52 in the CDH group, 32.90 +/- 10.63 in the non-CDH group; P = .0121). The findings suggest that the postnatal surfactant deficiency may be more persistent in CDH infants than in non-CDH infants on ECMO. However, CDH remains a multifactorial condition, with delayed improvement, because of persistence of pulmonary hypertension, difficulties with vascular remodeling, degree of lung hypoplasia, or compromised respiratory mechanics.

摘要

患有先天性膈疝(CDH)且接受体外膜肺氧合(ECMO)治疗的婴儿起初可能会出现肺不张,不过存活下来的婴儿其肺不张情况会随着时间逐渐改善。为了验证这些患者可能从表面活性剂治疗中获益这一假设,对接受ECMO治疗的CDH婴儿(孕周>34周出生)给予四剂改良牛肺表面活性剂提取物(固尔苏)(表面活性剂组,n = 9)或等体积空气(对照组,n = 8)。两组CDH婴儿气管吸出物表面活性蛋白-A(SP-A)浓度起初都较低,之后随时间升高(P = .0021);然而,与患有其他诊断疾病且接受ECMO治疗的婴儿相比,其浓度仍较低(P = .04)。两组间肺顺应性(CL)、拔管时间、吸氧时间及住院总天数并无差异。与接受ECMO治疗的非CDH婴儿相比(CDH组右心室压力[RVP]=53.25 mmHg±19.52,非CDH组为32.90±10.63;P = .0121),接受ECMO治疗的CDH婴儿在体外循环停止时右心室压力持续升高。这些研究结果表明,与接受ECMO治疗的非CDH婴儿相比,出生后表面活性剂缺乏在CDH婴儿中可能持续时间更长。然而,由于肺动脉高压持续存在、血管重塑困难、肺发育不全程度或呼吸力学受损,CDH仍然是一种多因素疾病,改善延迟。

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