We reviewed the data of 38 neonates who died of respiratory failure. Paraffin sections of the autopsy lung samples were examined with HE staining or immunolabeling for CD34, CD68 and CK to observe the development of the pulmonary vessels and detect potential pulmonary vascular diseases (PVDs). Five cases were identified to have PVDs, including pulmonary hypertensive vascular remodeling in 3 cases and alveolar capillary dysplasia in 2 cases. The result indicated that PVD was one of the important reasons for respiratory failure in these neonates.
Death ; Humans ; Infant, Newborn ; Lung ; pathology ; Lung Diseases ; diagnosis ; Persistent Fetal Circulation Syndrome ; pathology ; Pulmonary Alveoli ; abnormalities ; pathology ; Respiratory Insufficiency ; mortality ; Vascular Diseases ; diagnosis ; Vascular Remodeling

OBJECTIVETo investigate the effect of premature rupture of the membrane (PROM) on neonatal complications in premature infants.

METHODSThe registration information of 7684 preterm infants with gestational age <37 weeks were collected from the cooperative units in the task group between January 1, 2014 to December 31, 2014. Specially trained personnel from each cooperative units filled in the unified form in a standardized format to record the gender, gestational age, birth weight, PROM, placental abruption, antenatal corticosteroid, Apgar score, amniotic fluid pollution, and complications of the infants. The data were analyzed comparatively between the cases with PROM and those without (control).

RESULTSThe preterm mortality rate was significantly lower but the incidences of ICH, NEC, ROP and BPD were significantly higher in PROM group than in the control group (P<0.05). The 95% confidence interval of the OR value was <1 for mortality, and was >1 for ICH, NEC, ROP and BPD. After adjustment for gestational age, birth weight, gender, mode of delivery, placental abruption, placenta previa, prenatal hormones, gestational diabetes mellitus (GDM), gestational period hypertension and 5-min Apgar score <7, the incidences of NEC, ROP and BPD were significantly different between the two groups (P<0.05) with 95% confidence interval of OR value >1, but the mortality rate and incidence of ICH were not significantly different between the two groups (P>0.05).

CONCLUSIONPROM is a risk factor for NEC, ROP and BPD in preterm infants, and adequate intervention of PROM can reduce the incidences of such complications as NEC, ROP and BPD in the infants.

Apgar Score ; Birth Weight ; Female ; Fetal Membranes, Premature Rupture ; pathology ; Gestational Age ; Humans ; Incidence ; Infant, Newborn ; Infant, Newborn, Diseases ; etiology ; Infant, Premature ; Pregnancy ; Risk Factors

OBJECTIVETo improve the diagnostic accuracy of fetal pulmonary venous abnormalities through the analysis of the fetal pulmonary vein anatomy.

METHODS234 cases of congenital cardiac abnormalities were detected by echocardiography during pregnancy in An Zhen Hospital, Capital Medical University from May 2010 to August 2015. Autopsy was then performed. The type of fetal pulmonary venous malformation, cardiac abnormalities, systemic venous malformations, and other internal organs deformities were documented.

RESULTSThere were ninteen cases of pulmonary venous malformations among the 234 cases of fetal congenital heart disease. These included two cases of congenital pulmonary venous hypoplasia (CPVH) or atresia, four cases of partial anomalous pulmonary venous drainage (PAPVD), seven cases of total anomalous pulmonary venous drainage (TAPVD), five cases of atresia of common pulmonary vein (CPV), one case of congenital pulmonary venous hypoplasia with total anomalous pulmonary venous drainage. There were eleven cases with single ventricle, eight cases with right aortic arch, seven cases with single atrium and six cases with pulmonary valve stenosis. Eleven cases had pulmonary hypoplasia and nine cases had abnormal spleen.

CONCLUSIONSThere are many variations in pulmonary venous abnormalities associated with severe and complex cardiac abnormalities and internal organs malformation. Care should be exercised during autopsy examination to look for all branches of the pulmonary vein.

Autopsy ; Female ; Fetal Diseases ; Heart Defects, Congenital ; diagnosis ; Humans ; Pregnancy ; Pulmonary Veins ; abnormalities ; Spleen ; pathology

BACKGROUNDPreeclampsia is a multifactorial disease during pregnancy. Dysregulated lipid metabolism may be related to some preeclampsia. We investigated the relationship between triglycerides (TGs) and liver injury in different preeclampsia-like mouse models and their potential common pathways.

METHODSPreeclampsia-like models (Nw-nitro-L-arginine-methyl ester [L-NAME], lipopolysaccharide [LPS], apolipoprotein C-III [Apo] transgnic mice + L-NAME, β2 glycoprotein I [βGPI]) were used in four experimental groups: L-NAME (LN), LPS, Apo-LN and βGPI, respectively, and controls received saline (LN-C, LPS-C, Apo-C, βGPI-C). The first three models were established in preimplantation (PI), early-, mid- and late-gestation (EG, MG and LG). βGPI and controls were injected before implantation. Mean arterial pressure (MAP), 24-hour urine protein, placental and fetal weight, serum TGs, total cholesterol (TC) and pathologic liver and trophocyte changes were assessed.

RESULTSMAP and proteinuria were significantly increased in the experimental groups. Placenta and fetal weight in PI, EP and MP subgroups were significantly lower than LP. Serum TGs significantly increased in most groups but controls. TC was not different between experimental and control groups. Spotty hepatic cell necrosis was observed in PI, EG, MG in LN, Apo-LN and βGPI, but no morphologic changes were observed in the LPS group. Similar trophoblastic mitochondrial damage was observed in every experimental group.

CONCLUSIONSEarlier preeclampsia onset causes a higher MAP and urine protein level, and more severe placental and fetal damage. Preeclampsia-like models generated by varied means lead to different changes in lipid metabolism and associated with liver injury. Trophoblastic mitochondrial damage may be the common terminal pathway in different preeclampsia-like models.

Animals ; Cholesterol ; blood ; Disease Models, Animal ; Female ; Fetal Weight ; physiology ; Liver ; injuries ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondrial Diseases ; blood ; pathology ; Placenta ; metabolism ; Pre-Eclampsia ; blood ; pathology ; Pregnancy ; Triglycerides ; blood ; Trophoblasts ; pathology

OBJECTIVETo investigate the prenatal ultrasonic manifestations of fetal gray matter heterotopias (FGMH) and evaluate the optimal method its prenatal diagnosis.

METHODSThe prenatal and postnatal ultrasound images and MRI images were analyzed for a fetus with a definitive diagnosis of FGMH. The detection rates of FGMH by prenatal ultrasound and MRI reported in literature were compared.

RESULTSWe identified 11 reports of FGMH from 1998 to 2015, involving 43 cases with prenatal diagnoses. Of the total of 44 cases (including our case), 32 that had been confirmed postpartum had prenatal ultrasound and MRI data, which showed a significantly lower detection rates of FGMH by prenatal ultrasound than by MRI (43.8% vs 93.8%, P<0.001).

CONCLUSIONPrenatal ultrasound can only detect subependymal heterotopia with characteristic manifestations, and the detection of other types of FGMH relies on MRI, which is currently the best option for prenatal diagnosis of FGMH.

Classical Lissencephalies and Subcortical Band Heterotopias ; diagnosis ; Female ; Fetal Diseases ; diagnosis ; Fetus ; Gray Matter ; pathology ; Humans ; Magnetic Resonance Imaging ; Pregnancy ; Prenatal Diagnosis ; Ultrasonography, Prenatal

OBJECTIVETo investigate the clinicopathological characteristics, diagnostic criteria and differential diagnosis of placental chorioangioma.

METHODSTwenty-five cases of placental chorioangioma were analyzed for their clinical data, histomorphology and immumohisto chemical staining. Relevant literature was reviewed.

RESULTSThe average age of the 25 patients was 29 years. Fourteen patients had full-term pregnancy, 10 had preterm labor, and 1 had intrauterine fetal death. Nineteen patients had pregnancy complications. The tumors presented as red or dusty pink nodules with clear borders. The tumor size ranged from 1 to 16 cm. Microscopically, the tumors possessed abundant capillaries or cavernous blood spaces lined by hyperplastic endothelial cells. These cells were positive for CD34 and Ki-67 index < 10%.

CONCLUSIONSPlacental chorioangioma is a rare benign tumor of the placenta, and is associated with various pregnancy complications. Misdiagnosis of cell-rich type tumor should be avoided.

Adult ; Diagnosis, Differential ; Endothelial Cells ; pathology ; Female ; Fetal Death ; Hemangioma ; pathology ; Humans ; Infant, Newborn ; Placenta ; pathology ; Placenta Diseases ; pathology ; Pregnancy ; Pregnancy Complications, Neoplastic ; pathology ; Stillbirth

Acute atherosis is unique vascular changes of the placenta associated with poor placentation. It is characterized by subendothelial lipid-filled foam cells, fibrinoid necrosis of the arterial wall, perivascular lymphocytic infiltration, and it is histologically similar to early-stage atherosclerosis. Acute atherosis is rare in normal pregnancies, but is frequently observed in non- transformed spiral arteries in abnormal pregnancies, such as preeclampsia, small for gestational age (SGA), fetal death, spontaneous preterm labor and preterm premature rupture of membranes. In preeclampsia, spiral arteries fail to develop physiologic transformation and retain thick walls and a narrow lumen. Failure of physiologic transformation of spiral arteries is believed to be the main cause of uteroplacental ischemia, which can lead to the production of anti-angiogenic factors and induce endothelial dysfunction and eventually predispose the pregnancy to preeclampsia. Acute atherosis is more frequently observed in the spiral arteries of the decidua of the placenta (parietalis or basalis) than in the decidual or myometrial segments of the placental bed. The presence and deeper location of acute atherosis is associated with poorer pregnancy outcomes, more severe disease, earlier onset of preeclampsia, and a greater frequency of SGA neonates in patients with preeclampsia. Moreover, the idea that the presence of acute atherosis in the placenta may increase the risk of future cardiovascular disease in women with a history of preeclampsia is of growing concern. Therefore, placental examination is crucial for retrospective investigation of pregnancy complications and outcomes, and accurate placental pathology based on universal diagnostic criteria in patients with abnormal pregnancies is essential for clinicopathologic correlation.
Arteries* ; Atherosclerosis ; Cardiovascular Diseases ; Cholesterol ; Decidua ; Female ; Fetal Death ; Foam Cells ; Gestational Age ; Humans ; Infant, Newborn ; Ischemia ; Membranes ; Necrosis ; Obstetric Labor, Premature ; Pathology ; Placenta ; Placentation ; Pre-Eclampsia ; Pregnancy ; Pregnancy Complications ; Pregnancy Outcome ; Retrospective Studies ; Rupture

OBJECTIVECongenital heart defect is one of the most common birth defects. The isolated ventricular septal defect (VSD) has higher morbidity, and spontaneous closure may occur. Previously many studies about the prognosis of ventricular septal defect in childhood were conducted; in contrast, few studies on evolution and prognosis of ventricular septal defect from fetus to postnatal life have been available. This research aimed to determine the evolution of isolated ventricular septal defect during the period of fetus and postnatal life, and analyze the association between the diameter or location of VSD and the spontaneous closure of VSD.

METHODAll pregnant women seen at the prenatal diagnosis center of the West China Second Hospital were recruited. From June 2011 to June 2014, these participants underwent the fetal 2-dimensional and color Doppler echocardiographic examinations, and the fetuses with isolated VSD were included in the study, and those with other malformations or abnormal chromosome were excluded. This study was a prospective and longitudinal research. These fetuses were followed-up until the VSD closed spontaneously, or were surgically repaired or percutaneously closed. Outcomes of all the cases were recorded.

RESULTThere were 234 fetuses with isolated VSD who were recruited in our research cohort. Twelve of 234 lost to follow-up, 5 of 234 were still in uterus. Totally 217 fetuses were followed up. One hundred eighty-nine of 217 (87.1%) cases were delivered. The pregnancies were terminated in 28 of 217 (12.9%) cases. Ten cases died after birth. Of the 179 delivered cases, the rate of VSD spontaneous closure was 45.2% (81/179), the VSD of 49 cases (27.4%, 49/179) spontaneously closed in uterus. The VSD of 17.9% (32/179) cases spontaneously closed after birth and those of 75% (24/32) cases closed in the first year of life. Furthermore, these participants were divided into 3 groups according to the diameter of VSD in fetus. There were 87 cases in ≤ 2.0 mm group, 51 spontaneously closed (59%, 51/87) and 30 of 84 spontaneously closed (36%, 30/84) in 2.1-5.0 mm group. There were no spontaneous closure in > 5.0 mm group. There was a significant difference in spontaneous closure rate between the 3 groups (χ(2) = 15.200, P = 0.001). Nevertheless, these participants were divided into 2 groups according to the location of VSD in fetus (perimembrane VSD (P-VSD) group and muscular VSD (M-VSD) group). There were 152 cases in P-VSD group, 69 spontaneously closed (45.4%, 69/152) and 12 of 27 spontaneously closed (44%, 12/27) in M-VSD group. There was no significant difference in spontaneous closure between P-VSD and M-VSD (χ(2) = 0.008, P = 0.950).

CONCLUSIONThere was a high spontaneous closure rate of VSD in the period of late pregnancy. The most of postnatal VSD were spontaneously closed within one year of age. The spontaneous closure rates of fetal VSD with different diameter were different. The spontaneous closure rate of VSD with smaller diameter was higher.

China ; Chromosome Aberrations ; Echocardiography, Doppler, Color ; Female ; Fetal Diseases ; diagnostic imaging ; pathology ; Fetus ; Heart Septal Defects, Ventricular ; diagnostic imaging ; pathology ; Humans ; Lost to Follow-Up ; Pregnancy ; Prenatal Diagnosis ; Prognosis ; Prospective Studies

OBJECTIVETo investigate the etiology, pathogenesis, clinicopathologic characteristics, clinical prognosis and treatment of Dandy-Walker syndrome.

METHODSNine cases of Dandy-Walker syndrome were included in the study. The autopsy findings and clinical history were evaluated along with review of the literature. The causes, pathogenetic mechanism, pathologic features and prognosis of Dandy-Walker syndrome were analyzed.

RESULTSAmong 9 Dandy-Walker syndrome cases, six patients presented with variants of Dandy-Walker complex and 3 cases had classic Dandy-Walker malformation. In addition, 4 patients presented with combined lateral ventricle expansion and multiple malformations were seen in 7 cases. Combined umbilical cord abnormality was noted in 4 patients with variant of Dandy-Walker complex and combined placental abnormality was seen in one classic Dandy-Walker syndrome.

CONCLUSIONSDandy-Walker syndrome is a rare disease. In addition to complex pathogenesis with possible genetic and environmental antigenic etiologies, placental and umbilical cord abnormality may be also related to its development.

Abortion, Induced ; Autopsy ; Dandy-Walker Syndrome ; diagnostic imaging ; pathology ; Female ; Fetal Diseases ; diagnostic imaging ; pathology ; Fetus ; pathology ; Gestational Age ; Humans ; Lateral Ventricles ; pathology ; Male ; Placental Insufficiency ; pathology ; Pregnancy ; Retrospective Studies ; Ultrasonography, Prenatal

Intrahepatic cholestasis of pregnancy (ICP) is an unique complication in pregnancy, which usually manifests in the second or third trimester, and mainly harms the fetus. Its pathogenesis is not yet clear, and placental pathological changes are insufficient to explain the clinical phenomenon.Recent studies had shown that the important cause of perinatal deaths may be the damage to the placental structure and function caused by the high bile acid level. In addition, the change of placental structure and function, umbilical cord factors, and endocrine changes can also cause the fetal development and intrauterine hypoxia. In recent years related researches focus on the toxic effect of bile acid on fetus heart, lungs, brain, liver, and other important organs, the placental vascular pathology, hemodynamic changes, umbilical cord blood vessel factors and the endocrine changes.
Bile Acids and Salts ; metabolism ; Cholestasis, Intrahepatic ; metabolism ; pathology ; Female ; Fetal Diseases ; etiology ; metabolism ; Fetus ; metabolism ; Humans ; Maternal-Fetal Exchange ; Placenta ; pathology ; Pregnancy ; Pregnancy Complications ; metabolism ; pathology ; Umbilical Cord ; metabolism ; pathology