EXIT (ex-utero intrapartum treatment) procedure is a fetal survival-increasing modification of cesarean section. Previously we found an increase incidence of fetal vascular malperfusion (FVM) in placentas from EXIT procedures which indicates the underlying stasis of fetal blood flow in such cases. This retrospective analysis analyzes the impact of the recently introduced CD34 immunostain for the FVM diagnosis in placentas from EXIT procedures.
Objectives and Methods
A total of 105 placentas from EXIT procedures (48 to airway, 43 to ECMO and 14 to resection) were studied. In 73 older cases, the placental histological diagnosis of segmental FVM was made on H&E stained placental sections only (segmental villous avascularity) (Group 1), while in 32 most recent cases, the CD34 component of a double E-cadherin/CD34 immunostain slides was also routinely used to detect the early FVM (endothelial fragmentation, villous hypovascularity) (Group 2). 23 clinical and 47 independent placental phenotypes were compared by χ2 or ANOVA, where appropriate.
There was no statistical significance between the groups in rates of segmental villous avascularity (29 vs. 34%), but performing CD34 immunostain resulted in adding and/or upgrading 12 more cases of segmental FVM in Group 2, thus increasing the sensitivity of placental examination for FVM by 37%. There were no other statistically significantly differences in clinical (except for congenital diaphragmatic hernias statistically significantly more common in Group 2, 34 vs 56%, p=0.03) and placental phenotypes, proving the otherwise comparability of the groups.
The use of CD34 immunostain increases the sensitivity of placental examination for FVM by 1/3, which may improve the neonatal management by revealing the increased likelihood of the potentially life-threatening neonatal complications.
To retrospectively statistically compare clinical and placental phenotypes of nonmacerated fetuses and live-born perinatal deaths in 3rd trimester pregnancies.
Twenty-five clinical and 47 placental phenotypes were statistically compared among 93 cases of nonmacerated (intrapartum, or recent antepartum death) 3rd trimester fetal deaths (Group 1), 118 3rd trimester neonatal deaths (Group 2) and 4285 cases without perinatal mortality (Group 3).
Sixteen clinical and placental phenotypes were statistically significantly different between Group 3 and the two groups of perinatal deaths, which included eight placental phenotypes of fetal vascular malperfusion and eight other placental phenotypes of various etiology (amnion nodosum, 2-vessel umbilical cord, villous edema, increased extracellular matrix of chorionic villi, erythroblasts in fetal blood and trophoblastic lesions of shallow placentation). Statistically significant differences between Groups 1 and 2 were scant (oligohydramnios, fetal malformations, cesarean sections, hypercoiled umbilical cord and amnion nodosum being more common in the latter, and retroplacental hematoma more common in the former).
Placental examination in neonatal mortality shows thrombotic pathology related to umbilical cord compromise and features of shallow placental implantation that are similar to those in nonmacerated stillbirth; however, the features of placental abruption were more common in recent antepartum death, as were the features related to neonatal congenital malformations in neonatal deaths.
An approximate analytical solution of the radial Schrödinger equation for the generalized Hulthén potential is obtained by applying an improved approximation of the centrifugal term. The bound state energy eigenvalues and the normalized eigenfunctions are given in terms of hypergeometric polynomials. The results for arbitrary quantum numbers n r and l with different values of the screening parameter δ are compared with those obtained by the numerical method, asymptotic iteration, the Nikiforov-Uvarov method, the exact quantization rule, and variational methods. The results obtained by the method proposed in this work are in a good agreement with those obtained by other approximate methods.
The analytic expression of the Wigner function for bound eigenstates of the Hulthén potential in quantum phase space is obtained and presented by plotting this function for a few quantum states. In addition, the correct marginal distributions of the Wigner function in spherical coordinates are determined analytically.
Applying an improved approximation scheme to the centrifugal term, the approximate analytical solutions of the Schrödinger equation for the Eckart potential are presented. Bound state energy eigenvalues and the corresponding eigenfunctions are obtained in closed forms for the arbitrary radial and angular momentum quantum numbers, and different values of the screening parameter. The results are compared with those obtained by the other approximate and numerical methods. It is shown that the present method is systematic, more efficient and accurate.
Aim: To study the relation of retention of dead fetus resulting in its maceration and gestational age at delivery to placental diagnosis.
Methods: Some 75 clinicoplacental phenotypes have been retrospectively analyzed in 520 consecutive stillbirths, 329 macerated and 191 nonmacerated, and at three gestational age interval cohorts (330 second trimester, 102 preterm third trimester, and 88 term). Chi-square and clustering methods (Ward dendrograms and multidimensional scaling) were used for statistical analysis.
Results: Maternal diabetes mellitus, induction of labor, fetal growth restriction, various umbilical cord abnormalities, and placental clusters of sclerotic/hemosiderotic chorionic villi were more common in macerated stillbirths, while clinicoplacental signs and symptoms of ascending infection and placental abruption, i.e., retroplacental hematoma, premature rupture of membranes, and acute chorioamnionitis in nonmacerated stillbirths. Placental abnormalities were less common in the second trimester, other than the acute chorioamnionitis. Patterns of chronic hypoxic placental injury were common in preterm third trimester, while signs of in-utero hypoxia (abnormal cardiotocography, meconium, and histological erythroblastosis of fetal blood) in term pregnancy. In addition to classical statistics, the clustering analyses added new information to placental investigation of cause of stillbirth.
Conclusions: Macerated third trimester stillbirths have multifactorial etiology more likely than the second trimester stillbirths and the likely stasis-induced fetal thrombotic vasculopathy secondary to occult umbilical cord compromise should be sought in placental investigation in such cases. Nonmacerated stillbirths are associated with ascending infection and placental abruption.
Premature closure of the foramen ovale, 4-chamber
cardiac hypertrophy, and renal vein/vena cava thrombosis
were found at autopsy of a stillborn dizygotic twin
at 36 weeks gestational age. Review of the original prenatal
sonograms showed features suggestive of early
closure of the foramen ovale. Homozygosity for the
5,10 methylene tetrahydrofolate reductase mutation was
shown only in the affected twin after the parents were
found to be heterozygous for the mutation. The difference in outcome of the twins following prenatal treatment
with beta mimetics and corticosteroids for preterm
labor may be related to the added susceptibility factor
for thromboembolism associated with presumed hyperhomocysteinemia
in the proband which was not shared
by the surviving healthy twin. The role of premature
closure of the foramen ovale and prenatal treatment are
discussed but remain uncertain.