Kerkhofs C, De Bruyn C, Mesens T, Theyskens C, Vanhoestenberghe M, Bruneel E, Van Holsbeke C, Bonnaerens A, Gyselaers W
Dept. Obstetrics & Gynecology, Ziekenhuis Oost Limburg, Genk, Belgium.
Dept. Neonatology, Ziekenhuis Oost Limburg, Genk, Belgium.
Facts Views Vis Obgyn. 2014;6(4):177-83.
Today, perinatal audit focuses basically on cases of perinatal mortality. In most centres in Western Europe, perinatal mortality is low. Identification of metabolic acidosis at birth may increase index cases eligible for evaluation of perinatal care, and this might improve quality of perinatal audit. The aim of this study is to assess the incidence of metabolic acidosis at birth in order to estimate its impact on perinatal audit.
Cord blood was analysed for every neonate born between January 1, 2010 and December 31, 2012 in Ziekenhuis Oost-Limburg, Genk. Acidosis was defined as an umbilical arterial pH ≤ 7.05 with or without a venous pH ≤ 7.17. Respiratory acidosis (RA) was defined as acidosis with normal base excess, and metabolic acidosis (MA) was defined as acidosis with an arterial or venous base excess ≤ -10 mmol/L. In case of failed cord blood sampling, 5 minute Apgar score ≤ 6 was considered as the clinical equivalent of MA. Retrospective chart review of obstetric and paediatric files was performed for all cases of MA, together with review of paediatric follow-up charts from at least 6 months after birth. Perinatal asphyxia was defined as biochemical evidence for MA at birth, associated with early onset neonatal encephalopathy and long-term symptoms of cerebral palsy.
In a total of 6614 babies, perinatal death up to 7 days of life occurred in 40 babies (6.0‰). Acidosis was present in 183 neonates (2.8%), of which 130 (2.0%) had RA and 53 (0.8%) had MA. Of the 173 neonates with unknown pH values, 6 had Apgar scores ≤ 6. Of 59 babies born with MA or its clinical equivalent, 52 (88.1%) showed no neurologic symptoms at birth. Two (3.4%) died in the early neonatal period, one after abruptio placentae and one due to chorioamnionitis and severe prematurity. Five (8.5%) MA babies had symptoms of early onset neonatal encephalopathy, which recovered in three (5.1%), and persisted long-term in two others (3.4%). The two babies with cerebral palsy (prevalence 1/3300) were both born after instrumental vaginal delivery for foetal distress.
In our study cohort, the incidence of perinatal mortality is 6‰. The incidence of metabolic acidosis is 9‰. Addition of cases of metabolic acidosis to those of mortality doubles index cases eligible for perinatal audit. The incidence of babies surviving with cerebral palsy after metabolic acidosis at birth is very low (0.3‰). Our results suggest that instrumental delivery for foetal distress might be a risk factor for metabolic acidosis with persisting neurologic dysfunction. Our study illustrates that identification of peripartum near-miss is useful for perinatal audit.
如今，围产期审计主要关注围产期死亡病例。在西欧的大多数中心，围产期死亡率较低。识别出生时的代谢性酸中毒可能会增加符合围产期护理评估条件的指标病例，这可能会提高围产期审计的质量。本研究的目的是评估出生时代谢性酸中毒的发生率，以估计其对围产期审计的影响。
对2010年1月1日至2012年12月31日在根克的东林堡医院出生的每例新生儿进行脐血分析。酸中毒定义为脐动脉pH值≤7.05，无论静脉pH值是否≤7.17。呼吸性酸中毒（RA）定义为碱剩余正常的酸中毒，代谢性酸中毒（MA）定义为动脉或静脉碱剩余≤ -10 mmol/L。如果脐血采样失败，则将5分钟阿氏评分≤6视为MA的临床等效情况。对所有MA病例进行产科和儿科病历的回顾性图表审查，并审查出生后至少6个月的儿科随访图表。围产期窒息定义为出生时MA的生化证据，并伴有早发性新生儿脑病和脑瘫的长期症状。
在总共6614例婴儿中，40例（6.0‰）在出生后7天内发生围产期死亡。183例新生儿（2.8%）存在酸中毒，其中130例（2.0%）为RA，53例（0.8%）为MA。在173例pH值未知的新生儿中，6例阿氏评分≤6。在59例出生时患有MA或其临床等效情况的婴儿中，52例（88.1%）出生时无神经症状。2例（3.4%）在新生儿早期死亡，1例死于胎盘早剥，1例死于绒毛膜羊膜炎和严重早产。5例（8.5%）MA婴儿有早发性新生儿脑病症状，其中3例（5.1%）恢复，另外2例（3.4%）症状长期持续。2例脑瘫婴儿（患病率1/3300）均因胎儿窘迫行器械助产分娩。
在我们研究队列中，围产期死亡率为6‰。代谢性酸中毒的发生率为9‰。将代谢性酸中毒病例添加到死亡病例中，使符合围产期审计条件的指标病例增加了一倍。出生时发生代谢性酸中毒后存活的脑瘫婴儿发生率非常低（0.3‰）。我们的结果表明，因胎儿窘迫行器械助产分娩可能是发生伴有持续神经功能障碍的代谢性酸中毒的危险因素。我们的研究表明，识别围产期接近死亡情况对围产期审计很有用。
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