围产儿宫内窘迫的临床病理分析(附210例尸检资料)

目的 明确围产儿宫内窘迫死亡的主要致病因素及其所引起的并发症等对预后的影响，为降低病死率提供依据。方法 对围产儿官内窘迫的210例尸检资料进行全面复查，主要观察肺和脑病变，并结合临床重点分析了宫内窘迫的主要致病因素、并发症等。结果 在官内窘迫的致病因素中以综合因素最为多见；若以单一因素统计，脐带因素居首位，其次为胎盘和母体因素。形态学上计有：胎粪吸入综合征170例(81.0％)，羊水吸入36例(17．1％)，缺氧综合征仅4例(1．9％)。210例中59例伴吸人性肺炎(胎粪吸人性肺炎48例，羊水吸人性肺炎11例)。在宫内窘迫致死的患儿中，常见的并发症依次为缺氧缺血性脑病、弥漫性肺出血及致死性畸形等。结论 宫内窘迫并发缺氧缺血性脑病、弥漫性肺出血、肺部感染和致死性畸形是导致围产儿死亡的重要因素。     

安宝治疗产时胎儿窘迫40例临床分析

目的探讨安宝治疗产时胎儿窘迫效果.方法对40例诊断为产时胎儿窘迫并准备行剖宫产终止妊娠的病例作为研究组,术前给予安宝治疗;并随机选择40例符合相同条件的病例作为对照组.观察治疗后产妇的心率变化、宫缩抑制情况、异常胎监图形恢复情况、新生儿出生后Apgar评分和脐静脉血pH.结果应用安宝后产妇虽有心率加速,但无一例＞130/min,无一例自诉不适;用药后宫缩显著抑制(P＜0.01);异常胎监图形明显恢复(P＜0.01);新生儿窒息发生率显著低于对照组(P＜0.05),新生儿出生后1分钟Apgar评分显著高于对照组(P＜0.05);脐静脉血pH虽高于对照组,但无统计学差异,估计与例数偏少有关.结论安宝通过有效抑制宫缩、改善子宫-胎盘血流灌注,对于产时胎儿窘迫者用药是安全、有效的.     

非糖尿病性巨大胎儿368例临床分析

目的 分析非糖尿病性巨大胎儿的相关危险因素,为临床预测巨大胎儿及选择恰当的分娩方式提供依据.方法 回顾性分析南京军区南京总医院2006年1月至2007年12月期间出生的368例非糖尿病性巨大胎儿的临床资料,分析孕母的年龄、身高、基础体重、孕周、孕产次、分娩时体重、孕期增重、宫高、腹围及胎儿的股骨长、双顶径、分娩方式等,并与新生儿出生体重进行相关及回归分析.结果 非糖尿病性巨大胎儿的发生率为13.23%(368/2781).基础体重、分娩时体重、孕期增重、宫高、腹围、双顶径、股骨长、宫高+腹围、双顶径+股骨长是产前诊断非糖尿病性巨大胎儿的相关因素,而宫高及双顶径+股骨长相关性最为显著.非糖尿病性巨大胎儿与正常体重儿分娩方式差异无统计学意义.结论 结合宫高及双顶径+股骨长能够提高非糖尿病性巨大胎儿的产前预测率.巨大胎儿并不是剖宫产的绝对指征.     

胎儿心电图诊断胎儿宫内窘迫的临床价值

本文总结了>36孕周高危妊娠的胎儿心电图(FECG)共30例。同时分别作NST和B超监测,并以上述两项结果作对照。经过分析认为:FECG是反映胎儿在于宫内是否正常的一种客观检查指标。异常FECG提示胎儿宫內缺氧,FQRS>0.05秒或FST段改变时要注意脐带绕颈和羊水过少;而FQRS振幅>30μV时要注意羊水过少或胎儿体重≥3500g,并认为FQRS>0.05秒,振幅>30μV及FST段改变,可作为异常FECG的重要指标。其检出胎儿异常率和敏感性与NST和B超比较有显著差异(P<0.01)。     

胎儿持续性心动过缓15例临床分析

目的 了解胎儿持续性心动过缓常见的发病原因及新生儿预后.方法 回顾性分析2013年1月至2020年1月在北京大学第一医院经胎儿超声心动检查诊断的胎儿持续性心动过缓病例15例的临床资料.结果 ①15例胎儿中,胎儿心动过缓合并胎儿心脏畸形3例,均选择终止妊娠;②房室传导阻滞8例,5例母体血清自身抗体anti-Ro(SS-A...     

Electronic fetal heart rate monitoring during cesarean section in cases of fetal distress

Twelve fetuses in whom the diagnosis of fetal distress was made during first stage of labor were included in the study. All 12 patients underwent urgent cesarean section during which fetal heart rate (FHR) was recorded continuously. In 50% of the cases, marked improvement of FHR was registered early in the course of the operation. Improvement in fetal status is attributed to adequate oxygenation and cessation of uterine activity.     

Pathological analysis of 76 placentae in fetal distress

The result of pathological analysis of 76 placentae and their appendices from clinically diagnosed fetal distress in year 1985-1989 is here presented. The findings could be classified into 4 groups; lesions due to disturbance of maternal blood flow and villous ischemia or hypoxia; retardation of development and malformation of villi; lesions due to haematogenous and ascending infection and pathological changes of the umbilical cord. The clinical significance of these pathological changes was discussed. We suggested that some lesions such as villous growth retardation, placental haemangioma, choriangiosis, infection of the placenta, single umbilical artery etc, could cause fetal distress, and villitis, single umbilical artery could sufficiently impair placental function so as to retard fetal growth or cause fetal malformation. The etiology of some placental lesions needs further study.     

妊娠期肝内胆汁淤积症发生死胎的临床因素分析

Objective To investigate the clinical features,critical laboratory parameters,and fetal monitoring methods in intrahepatic cholestasis of pregnancy(ICP).Methods A retrospective analysis of 21 cases of ICP suffered with fetal death in Women's hospital.School of Medicine.Zhejiang University from January 1999 to December 2010 were discussed.Results(1)The average age of ICP patients suffered with fetal death were(30.2±4.6)years old.Among them,4 cases were older than 35 years,six cases were multipara.oneo of them suffered stillbirth 2 year before.Twenty cases were singleton pregnancies and 1 cage was twin pregnancy.(2)All 21 cases of fetal death occurred in the third trimester,12 cases occurred before 37 weeks,9 cases after 37 weeks.Nine cases were diagnosed by ultrasound in outpatient clinics,fetal heart beat disappeared in 9 patients after admission because of ICP, two disappeared after labor, one during anesthesia before emergent surgery. Perinatal mortality rate of ICP was 0. 148% (21/14 184), and fetal death occurred from 29 to 41 weeks with an average gestational age of ( 33.8 ± 4. 2 ) weeks, ( 3 ) Puritus occurred in all 21 cases while 11 of them had pruritus all over the body. Ten pregnant women felt the fetal movement decreased or disappeared before diagnosis of fetal death. The glycocholic acid levels increased in all of the 21 cases. Among them, glycocholic acid levels in 11 cases were (21.49 -64. 48) μmol/L, while in 10 cases were ≥64. 48 μmol/L Serum bile acid levels elevated in 16 cases which had been analyzed ( the other 5 cases had not been checked ), and the highest level reached 270 μmol/L Serum alanine aminotransferase and aspartate aminotransferase were increased in 14 cases. Seven cases had their total bilirubin ＞21 μmoL/L, and 12 cases had their direct bilirubin levels significantly elevated. Among the 21 cases of ICP, 15 cases were in severe status, while the other 6 cases were mild. (4) Nine patients had no antepartum surveillance since fetal death were diagnosed before admission. The results of antepartum surveillance were as follows: 2 cases had nonreassuring nonstress test (NST), one had mild "V" type deceleration. Absence of diastolic flow in umbilical artery were found in 3 cases, and low fetal biophysical score was got in one case. ( 5 ) All 21 patients had vaginal delivery. Six of them delivered after natural contraction, and the remaining 14 cases delivered after oral intake of mifepristone and amniotic injection of ethacridine, or oxytocin induced labor within 48 hours, only one case delivered after additional dinoprostone suppositories. The appearance of fetus, placentas and membranes were normal, the lengths of umbilical cord were average. Four cases were found with cords binding the necks or the bodies. Eighteen cases had grade Ⅲ amniotic fluid with meconium-stained, and 2 cases complicated by oligohydramnios. Ten cases had their fetuses and placentas examined by pathologist. Among them, one case had multiple malformations, no more obvious pathological abnormalities were found in other fetuses. Pathologic examination showed that fibrin deposited around chorion and deciduas basalis, large vessels accompanied by calcification, degeneration,hemorrhagic infarction, and increased focal syncytial nodules could be seen in all of the ten placentas. Conclusions Fetal death in pregnant women with ICP of ten occurs after the contractions, Severe ICP may be a key factor that involved in the occurrence of fetal death. Up to now, there is no valid indicators in fetal monitoring, which can predict fetal death. Extensive assessment of the severity and careful antepartum surveillance should be achieved before timely termination of pregnancy.     

妊娠期肝内胆汁淤积症发生死胎的临床因素分析

Objective To investigate the clinical features,critical laboratory parameters,and fetal monitoring methods in intrahepatic cholestasis of pregnancy(ICP).Methods A retrospective analysis of 21 cases of ICP suffered with fetal death in Women's hospital.School of Medicine.Zhejiang University from January 1999 to December 2010 were discussed.Results(1)The average age of ICP patients suffered with fetal death were(30.2±4.6)years old.Among them,4 cases were older than 35 years,six cases were multipara.oneo of them suffered stillbirth 2 year before.Twenty cases were singleton pregnancies and 1 cage was twin pregnancy.(2)All 21 cases of fetal death occurred in the third trimester,12 cases occurred before 37 weeks,9 cases after 37 weeks.Nine cases were diagnosed by ultrasound in outpatient clinics,fetal heart beat disappeared in 9 patients after admission because of ICP, two disappeared after labor, one during anesthesia before emergent surgery. Perinatal mortality rate of ICP was 0. 148% (21/14 184), and fetal death occurred from 29 to 41 weeks with an average gestational age of ( 33.8 ± 4. 2 ) weeks, ( 3 ) Puritus occurred in all 21 cases while 11 of them had pruritus all over the body. Ten pregnant women felt the fetal movement decreased or disappeared before diagnosis of fetal death. The glycocholic acid levels increased in all of the 21 cases. Among them, glycocholic acid levels in 11 cases were (21.49 -64. 48) μmol/L, while in 10 cases were ≥64. 48 μmol/L Serum bile acid levels elevated in 16 cases which had been analyzed ( the other 5 cases had not been checked ), and the highest level reached 270 μmol/L Serum alanine aminotransferase and aspartate aminotransferase were increased in 14 cases. Seven cases had their total bilirubin ＞21 μmoL/L, and 12 cases had their direct bilirubin levels significantly elevated. Among the 21 cases of ICP, 15 cases were in severe status, while the other 6 cases were mild. (4) Nine patients had no antepartum surveillance since fetal death were diagnosed before admission. The results of antepartum surveillance were as follows: 2 cases had nonreassuring nonstress test (NST), one had mild "V" type deceleration. Absence of diastolic flow in umbilical artery were found in 3 cases, and low fetal biophysical score was got in one case. ( 5 ) All 21 patients had vaginal delivery. Six of them delivered after natural contraction, and the remaining 14 cases delivered after oral intake of mifepristone and amniotic injection of ethacridine, or oxytocin induced labor within 48 hours, only one case delivered after additional dinoprostone suppositories. The appearance of fetus, placentas and membranes were normal, the lengths of umbilical cord were average. Four cases were found with cords binding the necks or the bodies. Eighteen cases had grade Ⅲ amniotic fluid with meconium-stained, and 2 cases complicated by oligohydramnios. Ten cases had their fetuses and placentas examined by pathologist. Among them, one case had multiple malformations, no more obvious pathological abnormalities were found in other fetuses. Pathologic examination showed that fibrin deposited around chorion and deciduas basalis, large vessels accompanied by calcification, degeneration,hemorrhagic infarction, and increased focal syncytial nodules could be seen in all of the ten placentas. Conclusions Fetal death in pregnant women with ICP of ten occurs after the contractions, Severe ICP may be a key factor that involved in the occurrence of fetal death. Up to now, there is no valid indicators in fetal monitoring, which can predict fetal death. Extensive assessment of the severity and careful antepartum surveillance should be achieved before timely termination of pregnancy.     

妊娠期肝内胆汁淤积症发生死胎的临床因素分析

目的 探讨妊娠期肝内胆汁淤积症(ICP)孕妇发生胎儿死亡的临床特点、实验室指标及胎儿监护手段.方法 对1999年1月至2010年12月浙江大学医学院附属妇产科医院收治的发生死胎的21例ICP孕妇的临床资料进行回顾性分析.结果 (1)21例ICP孕妇的平均年龄(30.2±4.6)岁,其中＞35岁者4例;经产妇6例,1例2年前因ICP发生死胎而引产1次;20例单胎妊娠,1例双胎妊娠.(2)21例ICP孕妇的死胎均发生在孕晚期,胎儿死亡的孕周为29～41周,平均(33.8±4.2)周.12例发生在孕29～37周,9例发生在孕37周后.9例为门诊B超检查时确诊胎死宫内;9例因诊断ICP入院治疗期间发生胎心消失;2例临产后胎心消失;1例胎心监护提示V型减速,拟行急诊刮宫产术于麻醉期间胎心消失.在所有ICP孕妇中围产儿死亡率为0.148%(21/14 184).(3)21例ICP孕妇均有皮肤瘙痒,其中11例有全身皮肤瘙痒.10例在发生死胎前自觉胎动减少或消失.21例ICP孕妇血清甘胆酸水平均升高,其中21.49～64.48 μmol/L 11例,t≥64.48 μmol/L 10例.血清总胆汁酸水平升高16例(另5例未检查),最高达270μmoL/L.血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶水平升高14例,总胆红素＞21μmol/L 7例,直接胆红素升高12例.21例ICP孕妇中,重度15例,轻度6例.(4)9例孕妇门诊即确诊宫内死胎未做胎心监护,其余12例住院检查结果 为:胎心监护结果 可疑2例,无应激试验(NST)提示胎心轻度V型减速1例,B超提示脐动脉舒张期血流缺如3例,胎儿生物物理指标评分低值1例.(5)21例ICP孕妇均经阴道分娩.6例为自然宫缩娩出死胎,其余15例予米非司酮配合依沙吖啶羊膜腔注射或缩宫素引产,14例在48 h内成功娩出死胎,仅1例追加地诺前列酮栓后引产成功.所有死胎外观无异常,脐带长度均在正常范围,有4例脐带绕颈或绕体.胎盘胎膜外观无异常,18例羊水Ⅲ度胎粪污染,2例合并羊水过少.10例行死胎及胎盘病理检查,其中1例合并多发畸形,其余死胎病理检查未见明显异常,10例胎盘病理检查均有绒毛膜周围或底蜕膜、大血管周围的纤维蛋白沉积,同时伴有钙化、退行性变、红色梗死及局灶性合体细胞结节增多.结论 ICP孕妇发生死胎的孕周常在孕晚期,时间常在正常宫缩后,ICP重度可能是发生死胎的关键因素;尚无有效的胎儿监护指标可预测死胎的发生.因此,应综合评估病情,加强胎儿监护,适时终止妊娠.

Abstract：

Objective To investigate the clinical features,critical laboratory parameters,and fetal monitoring methods in intrahepatic cholestasis of pregnancy(ICP).Methods A retrospective analysis of 21 cases of ICP suffered with fetal death in Women's hospital.School of Medicine.Zhejiang University from January 1999 to December 2010 were discussed.Results(1)The average age of ICP patients suffered with fetal death were(30.2±4.6)years old.Among them,4 cases were older than 35 years,six cases were multipara.oneo of them suffered stillbirth 2 year before.Twenty cases were singleton pregnancies and 1 cage was twin pregnancy.(2)All 21 cases of fetal death occurred in the third trimester,12 cases occurred before 37 weeks,9 cases after 37 weeks.Nine cases were diagnosed by ultrasound in outpatient clinics,fetal heart beat disappeared in 9 patients after admission because of ICP, two disappeared after labor, one during anesthesia before emergent surgery. Perinatal mortality rate of ICP was 0. 148% (21/14 184), and fetal death occurred from 29 to 41 weeks with an average gestational age of ( 33.8 ± 4. 2 ) weeks, ( 3 ) Puritus occurred in all 21 cases while 11 of them had pruritus all over the body. Ten pregnant women felt the fetal movement decreased or disappeared before diagnosis of fetal death. The glycocholic acid levels increased in all of the 21 cases. Among them, glycocholic acid levels in 11 cases were (21.49 -64. 48) μmol/L, while in 10 cases were ≥64. 48 μmol/L Serum bile acid levels elevated in 16 cases which had been analyzed ( the other 5 cases had not been checked ), and the highest level reached 270 μmol/L Serum alanine aminotransferase and aspartate aminotransferase were increased in 14 cases. Seven cases had their total bilirubin ＞21 μmoL/L, and 12 cases had their direct bilirubin levels significantly elevated. Among the 21 cases of ICP, 15 cases were in severe status, while the other 6 cases were mild. (4) Nine patients had no antepartum surveillance since fetal death were diagnosed before admission. The results of antepartum surveillance were as follows: 2 cases had nonreassuring nonstress test (NST), one had mild "V" type deceleration. Absence of diastolic flow in umbilical artery were found in 3 cases, and low fetal biophysical score was got in one case. ( 5 ) All 21 patients had vaginal delivery. Six of them delivered after natural contraction, and the remaining 14 cases delivered after oral intake of mifepristone and amniotic injection of ethacridine, or oxytocin induced labor within 48 hours, only one case delivered after additional dinoprostone suppositories. The appearance of fetus, placentas and membranes were normal, the lengths of umbilical cord were average. Four cases were found with cords binding the necks or the bodies. Eighteen cases had grade Ⅲ amniotic fluid with meconium-stained, and 2 cases complicated by oligohydramnios. Ten cases had their fetuses and placentas examined by pathologist. Among them, one case had multiple malformations, no more obvious pathological abnormalities were found in other fetuses. Pathologic examination showed that fibrin deposited around chorion and deciduas basalis, large vessels accompanied by calcification, degeneration,hemorrhagic infarction, and increased focal syncytial nodules could be seen in all of the ten placentas. Conclusions Fetal death in pregnant women with ICP of ten occurs after the contractions, Severe ICP may be a key factor that involved in the occurrence of fetal death. Up to now, there is no valid indicators in fetal monitoring, which can predict fetal death. Extensive assessment of the severity and careful antepartum surveillance should be achieved before timely termination of pregnancy.     

Acute fetal distress

Three different clinical patterns of acute fetal distress may be observed during labor: an ante-partum hypoxia with a persistent nonreactive and "fixed" fetal heart rate (FHR) on admission to the hospital, a progressive intra-partum asphyxia manifested, as the labor continues, by a substantial rise in baseline heart rate, a loss of variability and repetitive severe variable or late decelerations, and finally, as a result of a catastrophic event, a sudden prolonged FHR deceleration to approximately 60 beats per minute lasting until delivery. However the majority of fetuses with nonreassuring tracings of FHR are neurologically intact, as evidenced by the high false-positive rate of electronic fetal monitoring (EFM). Therefore the diagnosis of fetal distress must be corroborated by complementary methods, such as continuous recording of the fetal electrocardiogram or computed-assisted EFM, fetal pulse oximetry or fetal scalp sampling with immediate determination of blood gases or lactates. Defavorable outcome of an acute fetal distress leading to neonatal encephalopathy or death is best predicted by a persisting low Apgar score (<3) for more than 5 minutes and by a severe metabolic acidosis (umbilical artery pH<7,00 and base-excess>-12mmol/l).     

Lipid peroxidation in nuchal cord cases: implication for fetal distress

Objective. To examine whether nuchal cord affects fetal lipid peroxidation and cord arterial blood gases, and thus to determine whether lipid peroxidation can show intrapartum distress.

Methods. Pregnant women giving birth to a baby with nuchal cord (n = 32) formed the study group and others without this condition made up the control group (n = 36). The maternal malondialdehyde levels (MDA) before and after delivery as well as fetal umbilical cord MDA and arterial blood gases were measured in both the groups.

Results. Mean cord MDA level was higher in the study group (p < 0.02) and was significantly higher than maternal MDA level after birth within the same group (p = 0.007). Cord blood gases as well as neonatal and labour characteristics showed no difference, except for variable decelerations, which were 2.2 times more common in the study group. Correlations between maternal MDA levels before and after delivery, umbilical cord MDA and arterial blood gases were non-significant in the nuchal cord group.

Conclusions. During delivery, nuchal cord increases lipid peroxidation without causing significant fetal acidemia. Level of lipid peroxidation may be a more sensitive indicator of intrapartum distress than results of acid–base studies.