Christina Vogt

Comparison between prenatal ultrasound and postmortem findings in fetuses and infants with developmental anomalies

To determine if postmortem examinations of fetuses and infants change the diagnosis obtained at prenatal ultrasound and affect counseling of future pregnancies, and if there has been a change over recent years in the accuracy of prenatal ultrasound diagnosis.

How Important is Placental Examination in Cases of Perinatal Deaths

Research on stillbirths and placental pathology has traditionally been given low priority, causing a lack of understanding of the mechanisms leading to death. The purpose of this study was to gain knowledge on how many perinatal deaths relate to morphologic changes in the placenta, and what role the placenta plays in the pathogenesis of intrauterine, intrapartum, and neonatal deaths. The autopsy reports from 104 consecutive perinatal deaths in a 5-year period (2004–2008) were reviewed. Intrauterine, intrapartum, and neonatal deaths ranging from gestational age of 22 weeks up to 7 days postpartum were included. The following three questions were considered: Could placental examination (with autopsy) explain fetal/infant death; could the cause of death be explained by placental examination alone; and could the cause of death be explained with autopsy alone? The distribution of pathologic findings in the placenta was registered. The placenta had changes that could explain fetal/infant death in 69.2% of the cases. The cause of death could be explained by placental examination alone, without autopsy, in 48.1% of the cases. Only 16.3% of the deaths could be explained by autopsy alone. The most frequently observed diagnoses were infection (22.1%), degenerative changes (13.5%), and abruptio placentae (12.5%). To conclude, our study shows that placental examination in addition to autopsy is necessary in investigating the causes of perinatal deaths. Further research, including maternal and environmental factors, is needed to clarify the underlying causes of placental malfunction.

Longitudinal diffusion tensor and manganese-enhanced MRI detect delayed cerebral gray and white matter injury after hypoxia–ischemia and hyperoxia

Background:Hypoxia–ischemia (HI) induces delayed inflammation and long-term gray and white matter brain injury that may be altered by hyperoxia.Methods:HI and 2 h of hyperoxia (100% O2) or room air (21% O2) in 7-d-old (P7) rats were studied by magnetic resonance imaging at 7 Tesla during 42 d: apparent diffusion coefficient (ADC) maps on day 1; T1-weighted manganese-enhanced images on day 7; diffusion tensor images on days 21 and 42; and T2 maps at all time points.Results:The long-term brain tissue destruction on T2 maps was more severe in HI+hyperoxia than HI+room air. ADC was lower in HI+hyperoxia vs. HI+room air and sham and was correlated with long-term outcome. Manganese enhancement indicating inflammation was seen in both the groups along with more microglial activation in HI+hyperoxia on day 7. Fractional anisotropy (FA) in corpus callosum was lower and radial diffusivity was higher in HI+hyperoxia than that in HI+room air and sham on day 21. From day 21 to day 42, FA and radial diffusivity in HI+hyperoxia were unchanged, whereas in HI+room air, FA increased and radial diffusivity decreased to values similar to sham.Conclusion:Hyperoxia caused a more severe tissue destruction, delayed irreversible white matter injury, and increased inflammatory response resulting in a worsening in the trajectory of injury after HI in developing gray and white matter.

Thanatophoric Dysplasia: Autopsy Findings Over a 25-Year Period

The aim of our study was to retrospectively assess morphological findings in thanatophoric dysplasia, particularly, in how many cases were cerebral manifestations with temporal lobe dysplasia identified. We also wanted to register and analyze the proportions between lung, brain, and body weight. Criteria for inclusion were an autopsy performed during the period ranging from 1985 to 2009 with a diagnosis of thanatophoric dysplasia. During a 25-year period 25 cases of thanatophoric dysplasia were registered. Temporal lobe dysplasia was recognized in 52% of the cases, and after 1998 temporal lobe dysplasia was described in all cases. In 19 cases the brain/body weight ratio was increased, and in all cases the lung/body weight ratio was below the corresponding ratio calculated according to standard measurements. In all but one case the ratio of brain to lung weight was increased. This study focuses on morphological findings, stressing the importance of temporal lobe dysplasia in confirming a diagnosis of thanatophoric dysplasia. Lung/body, brain/body, and brain/lung weight ratios confirm macrocephaly and lung hypoplasia, which are constant findings in cases involving thanatophoric dysplasia. Femur and brain morphology inclusive histology remains the ultimate tool for confirmation of this lethal condition, although it has to be seen in a context inclusive of radiological examination.

Abnormal gyration of the temporal lobe and megalencephaly are typical features of thanatophoric dysplasia and can be visualized prenatally by ultrasound

Autopsies of fetuses with thanatophoric dysplasia (TD) have shown abnormal gyration of the temporal lobes. In addition, the head is relatively large compared with the abdomen. We evaluated by ultrasound six consecutive cases of TD at 19 + 0 to 19 + 6 gestational weeks based on last menstrual period. We observed abnormal and deep transverse sulci in the temporal lobes in all cases; these features were confirmed at autopsy. We performed biometric assessment, including biparietal diameter (BPD) and mean abdominal diameter (MAD). For each MAD value in the TD fetuses, we computed mean and SD of the corresponding BPD values from a population‐based registry in the relevant age range, and used them to calculate Z‐scores for each BPD/MAD ratio. In the general population, the average BPD/MAD ratio was 1.05. In the TD fetuses, the mean BPD was 51.5 (range, 49–54) mm, the MAD was 45 (range, 41–47) mm and the BPD/MAD ratio was 1.15 (range, 1.09–1.20). The average Z‐score of the ratios for TD fetuses was 2.44 (range, 1.05–3.39). The ratios for the TD fetuses were significantly higher than were the population ratios (P = 0.016). At autopsy, the mean brain‐to‐body weight ratio was 20.6% (range, 15.4–24.1%), which was greater than the corresponding mean ratio of 14.9% in normal fetuses. We conclude that abnormal and deep transverse gyration of the temporal lobes can be visualized by ultrasound in mid‐second‐trimester fetuses with TD. Due to megalencephaly, fetuses with TD have significantly different body proportions, with a larger BPD compared with normal fetuses. Copyright

Correlation between prenatal ultrasound and postmortem findings in 1029 fetuses following termination of pregnancy

A prenatal ultrasound examination and a postmortem examination provide the basis for correct diagnosis in fetuses terminated due to congenital anomalies. The aim of this study was to correlate fetal anomalies detected by ultrasound examination with those identified at autopsy following termination of pregnancy (TOP) over a 30‐year period, and to evaluate the correlation between findings at different gestational ages and assess these trends over time.

Prenatal examination and postmortem findings in fetuses with gastroschisis and omphalocele

This study compares prenatal ultrasound examination and autopsy findings in fetuses and infants with gastroschisis and omphalocele.

Explaining Fetal Death—What are the Contributions of Fetal Autopsy and Placenta Examination?

The aim of our study was to categorize fetal deaths by different diagnostic groups and see to what extent an autopsy of a presumably normal fetus contributes to the final diagnosis and how many unexplained fetal deaths remain unexplained after examination of the placenta. We reviewed autopsy reports of 351 fetuses with a gestational age of 12 or more weeks at the Department of Pathology and Medical Genetics at St Olavs Hospital during the years 2001 through 2010. In our records, 38.5% (135 of 351) of the deaths were due to noninfectious placenta causes, 31.6% (111 of 351) were caused by infections, and 29.9% (105 of 351) of the fetal deaths remained unexplained after autopsy. We also found that an inconclusive report was more common early in pregnancy. The incidence of fetal loss due to circulatory disturbances in the placenta increased toward term. Infections were evenly distributed in intrauterine fetal deaths, although in spontaneous abortions, they were more frequent during the second trimester. For both explained and unexplained deaths, we observed a bimodal distribution, with peaks in the early second trimester and late third trimester toward term.

Colposcopy and additive diagnostic value of biopsies from colposcopy‐negative areas to detect cervical dysplasia

We evaluated colposcopy in the routine diagnostic workup of women with abnormal cervical cytology, as well as the diagnostic value of endocervical curettage material and biopsies taken from colposcopy‐positive and colposcopy‐negative quadrants of the cervix.

Maternal and fetal insulin levels at birth in women with polycystic ovary syndrome: data from a randomized controlled study on metformin.

CONTEXT Metformin is suggested to reduce pregnancy complications in women with polycystic ovary syndrome (PCOS). Metformin crosses the placenta and therapeutic concentrations are measured in the fetal circulation. Whether metformin treatment in pregnant PCOS women affects maternal and fetal insulin concentrations at birth is not clarified. OBJECTIVES To investigate the possible effect of metformin on insulin concentrations in umbilical cord blood and the possible association between maternal and fetal insulin concentrations. DESIGN Post-hoc analysis of a subgroup of PCOS women participating in a double-blind randomized controlled trial. SETTING University hospital setting. PARTICIPANTS Women with PCOS (n=118), aged 19-39 years. MAIN OUTCOME MEASURES Maternal and umbilical cord insulin concentrations immediately after birth. RESULTS At delivery women randomized to metformin had lower insulin concentrations than those randomized to placebo (259±209 vs 361±261 pmol/l; P=0.020). No difference was found in insulin concentrations in umbilical venous (P=0.95) and arterial (P=0.39) blood between the metformin and placebo groups. The arteriovenous difference was also equal between the groups (P=0.38). Insulin concentrations were higher in the umbilical vein than in the umbilical artery independent of randomization (70±51 vs 45±48 pmol/l; P<0.0005). CONCLUSIONS In PCOS, metformin treatment during pregnancy resulted in lower maternal insulin concentrations at delivery. Metformin treatment did not affect fetal insulin concentrations. Higher insulin concentrations in the umbilical vein indicate that the placenta somehow secretes insulin to the fetus. The possibility of placental insulin secretion to the fetus deserves further investigations.