Robison Nathan J, Hodgman Joan E, Barton Lorayne, Pavlova Zdena
Division of Neonatology, Department of Pediatrics Keck School of Medicine, Universisty of Southern California Los Angeles County, Los Angeles, CA 90033, USA.
J Perinatol. 2003 Mar;23(2):142-7. doi: 10.1038/sj.jp.7210863.
To investigate causes of death in infants who died after 28 days, beyond the neonatal period but before discharge from the nursery, to establish their clinical courses and causes of death and to attempt to find criteria for earlier identification of these infants.
We identified 30 such infants (12% of nursery deaths) from 1993 through 1998 and conducted a retrospective review of their records including placental pathology and autopsy reports when available. In all, 14 infants who weighed <or = 860 g at birth were matched with survivors.
The 30 infants divided almost equally into two groups. Of them 15 infants weighing >or = 880 g died of diverse congenital anomalies, including five with nonhemolytic hydrops and four with pulmonary hypoplasia. One infant without congenital anomaly weighed 3290 g. Support for this severely asphyxiated infant was withdrawn after 103 days because of progressive cortical atrophy. The remaining 14, the largest of which weighed 860 g, died of complications of prematurity, which we termed postponed neonatal deaths (PND). They followed a typical course of progressive multiple organ failure. All received assisted ventilation and postnatal steroids, developed chronic lung disease, and were on ventilation at the time of death. Renal insufficiency occurred late in the course. Acute infections and renal failure were the major proximal causes of death. When compared with surviving controls the PND were less likely to have received antenatal steroids and received more inotropic agents for cardiovascular support and more amphotericin for fungal infection; surgery for perforated bowel was confined to the PND.
The incidence of postneonatal nursery deaths has not changed in more than 20 years remaining at 11 to 12% of nursery deaths. Congenital anomaly was a prominent cause of death (50%). When infants without congenital anomalies (PND) were compared to surviving controls, no differences were found, which could reliably identify PND early in their course. The only potentially preventable factor was lack of antenatal steroid exposure in the PND.
调查出生28天后、新生儿期之后但在出院前死亡的婴儿的死因，明确其临床病程和死亡原因，并尝试找出早期识别这些婴儿的标准。
我们从1993年至1998年确定了30例此类婴儿（占保育室死亡人数的12%），并对其记录进行回顾性审查，包括胎盘病理学和尸检报告（如有）。总共将14例出生时体重≤860g的婴儿与存活者进行匹配。
30例婴儿几乎平均分为两组。其中15例体重≥880g的婴儿死于各种先天性异常，包括5例非溶血性水肿和4例肺发育不全。1例无先天性异常的婴儿体重为3290g。由于进行性皮质萎缩，对这名严重窒息的婴儿在103天后停止了支持治疗。其余14例，其中最大体重为860g，死于早产并发症，我们称之为延迟新生儿死亡（PND）。他们遵循典型的进行性多器官衰竭病程。所有婴儿均接受辅助通气和产后类固醇治疗，患慢性肺病，死亡时仍在通气。肾功能不全在病程后期出现。急性感染和肾衰竭是主要的近端死亡原因。与存活对照组相比，PND接受产前类固醇治疗的可能性较小，接受更多的强心剂用于心血管支持，接受更多的两性霉素用于真菌感染；肠穿孔手术仅限于PND。
新生儿期后保育室死亡的发生率在20多年来没有变化，仍占保育室死亡人数的11%至12%。先天性异常是一个突出的死亡原因（50%）。将无先天性异常的婴儿（PND）与存活对照组进行比较时，未发现可在病程早期可靠识别PND的差异。唯一可能可预防的因素是PND缺乏产前类固醇暴露。
