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Beckwith-Wiedemann syndrome (BWS) is an epigenetic disorder of imprinting on the chromosome 11p15 region that presents with clinical features, such as macroglossia, abdominal wall defects, neonatal hypoglycemia, hemihypertrophy, and embryonal tumors. Phyllodes tumors (PTs) are rare fibroepithelial tumors that account for 0.3% to 1% of breast tumors and present in women aged 35 to 55 years. Here we describe a rare case of metastatic malignant phyllodes tumor in a 27-year-old woman with BWS and uniparental disomy (UPD) of chromosome 11p15.5. To our knowledge, this is the first case report in literature to describe metastatic malignant phyllodes tumor in a woman with BWS. [ABSTRACT FROM AUTHOR]

The cause of meconium passage in utero is controversial, traditionally being considered evidence of fetal stress and hypoxia, and also associated with intra-amniotic inflammation/infection. It is now recognized to also occur in the absence of fetal stress. Autopsy studies have shown that many term stillborns (SB) have hypoxic/ischemic brain injury and other evidence of stress preceding the time period immediately before demise, including acute thymic involution (ATI); however, these findings, along with placental findings, have not been previously correlated with meconium-stained amniotic fluid (MSAF). 35 structurally normal singleton term SB (21 early term, 14 full/late term) with complete autopsies, including brain and placental examination, were identified. MSAF was visually identified at delivery and confirmed on the placental examination. Autopsy evaluation included brain injury and ATI. Placental evaluation included maternal and fetal vascular malperfusion and acute and chronic inflammatory lesions. Demographic and clinical features were compared. 18 (51%) SB had MSAF, and 17 (49%) had clear amniotic fluid (CAF). The was no significant difference in brain injury in the MSAF vs CAF group, including older gray matter injury (karyorrhexis) (67% vs 47%), recent gray matter injury (red neurons, but no karyorrhexis) (28% vs 35%), white matter injury (50% vs 29%), and hemorrhage (22% vs 24%). Severe ATI was more frequent in the MSAF vs CAF group (61% vs 24%, p =.04). There was no significant difference in placental lesions between groups, including acute maternal inflammation (39% vs 18%), acute fetal inflammation (6% vs 6%), fetal vascular malperfusion (11% vs 18%), maternal vascular malperfusion (39% vs 35%), and chronic inflammatory lesions (39% vs 29%). The MSAF group was more likely to be full/late term than early term (72% vs 28%), in contrast to the CAF group (6% vs 94%) (p =.0001). There was no difference in other clinical factors evaluated. 51% of term SB had MSAF, and, in contrast to the CAF group, these were significantly more likely to be full/late term. Brain injury was frequent in both MSAF and CAF groups, supporting hypoxia as the mechanism of demise in most of these SB. No placental lesions correlated with MSAF, including inflammation. This suggests that hypoxia is the cause of the MSAF in these SB, but that some additional biologic factor present in the full/late term SB, but not present in the early term SB, including possibly gastrointestinal maturation, is necessary for the meconium passage. [ABSTRACT FROM AUTHOR]

Case Presentation: A 22-year-old woman who was 36 weeks pregnant presented with a 4-day history of cough, hemoptysis, and exertional dyspnea. She had no fever, night sweats, or weight loss. The review of system was otherwise negative. Her medical history was notable for a spontaneous first-trimester abortion a year ago. At that time, she had a transvaginal ultrasound scan that showed a gestational sac with no fetal movement. A post-abortion ultrasound scan revealed no residual fetal parts. [ABSTRACT FROM AUTHOR]

Objective: Correlation of BPD with placental pathology is important for clarification of the multifactorial pathogenesis of BPD; however, previous reports have yielded varying results. We report placental findings in no/mild BPD compared to moderate/severe BPD, and with and without pulmonary hypertension (PH). Methods: Eligible infants were 230/7-276/7 weeks gestational age. BPD was defined by the need for oxygen at ≥28 days with severity based on need for respiratory support at ≥36 weeks. Acute and chronic inflammatory placental lesions and lesions of maternal and fetal vascular malperfusion were examined. Results: Of 246 eligible infants, 146 (59%) developed moderate/severe BPD. Thirty-four (23%) infants developed PH, all but 1 being in the moderate/severe BPD group. Chronic deciduitis (32% vs 16%, P =.003), chronic chorioamnionitis (23% vs 12%, P =.014), and ≥ 2 chronic inflammatory lesions (13% vs 3%, P =.007) were more frequent in the moderate/severe BPD group. Development of PH was associated with placental villous lesions of maternal vascular malperfusion (30% vs 15%, P =.047). Conclusions: The association of chronic inflammatory placental lesions with BPD severity has not been previously reported. This supports the injury responsible for BPD as beginning before birth in some neonates, possibly related to cytokines associated with these chronic inflammatory lesions. [ABSTRACT FROM AUTHOR]

Spontaneous preterm labor is an obstetrical syndrome accounting for approximately 65–70% of preterm births, the latter being the most frequent cause of neonatal death and the second most frequent cause of death in children less than five years of age worldwide. The purpose of this study was to determine and compare to uncomplicated pregnancies (1) the frequency of placental disorders of villous maturation in spontaneous preterm labor; (2) the frequency of other placental morphologic characteristics associated with the preterm labor syndrome; and (3) the distribution of these lesions according to gestational age at delivery and their severity. A case-control study of singleton pregnant women was conducted that included (1) uncomplicated pregnancies (controls, n=944) and (2) pregnancies with spontaneous preterm labor (cases, n=438). All placentas underwent histopathologic examination. Patients with chronic maternal diseases (e.g., chronic hypertension, diabetes mellitus, renal disease, thyroid disease, asthma, autoimmune disease, and coagulopathies), fetal malformations, chromosomal abnormalities, multifetal gestation, preeclampsia, eclampsia, preterm prelabor rupture of the fetal membranes, gestational hypertension, gestational diabetes mellitus, and HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome were excluded from the study. Compared to the controls, the most prevalent placental lesions among the cases were the disorders of villous maturation (31.8% [106/333] including delayed villous maturation 18.6% [62/333] vs. 1.4% [6/442], q<0.0001, prevalence ratio 13.7; and accelerated villous maturation 13.2% [44/333] vs. 0% [0/442], q<0.001). Other lesions in decreasing order of prevalence included hypercapillarized villi (15.6% [68/435] vs. 3.5% [33/938], q<0.001, prevalence ratio 4.4); nucleated red blood cells (1.1% [5/437] vs. 0% [0/938], q<0.01); chronic inflammatory lesions (47.9% [210/438] vs. 29.9% [282/944], q<0.0001, prevalence ratio 1.6); fetal inflammatory response (30.1% [132/438] vs. 23.2% [219/944], q<0.05, prevalence ratio 1.3); maternal inflammatory response (45.5% [195/438] vs. 36.1% [341/944], q<0.01, prevalence ratio 1.2); and maternal vascular malperfusion (44.5% [195/438] vs. 35.7% [337/944], q<0.01, prevalence ratio 1.2). Accelerated villous maturation did not show gestational age-dependent association with any other placental lesion while delayed villous maturation showed a gestational age-dependent association with acute placental inflammation (q-value=0.005). Disorders of villous maturation are present in nearly one-third of the cases of spontaneous preterm labor. [ABSTRACT FROM AUTHOR]

Objective: The aims of this study were to ascertain the frequency of disorders of villous maturation in fetal death and to also delineate other placental histopathologic lesions in fetal death. Methods: This was a retrospective observational cohort study of fetal deaths occurring among women between January 2004 and January 2016 at Hutzel Women's Hospital, Detroit, MI, USA. Cases comprised fetuses with death beyond 20 weeks' gestation. Fetal deaths with congenital anomalies and multiple gestations were excluded. Controls included pregnant women without medical/obstetrical complications and delivered singleton, term (37–42 weeks) neonate with 5-min Apgar score ≥7 and birthweight between the 10th and 90th percentiles. Results: Ninety-two percent (132/143) of placentas with fetal death showed placental histologic lesions. Fetal deaths were associated with (1) higher frequency of disorders of villous maturation [44.0% (64/143) vs. 1.0% (4/405), P < 0.0001, prevalence ratio, 44.6; delayed villous maturation, 22% (31/143); accelerated villous maturation, 20% (28/143); and maturation arrest, 4% (5/143)]; (2) higher frequency of maternal vascular malperfusion lesions [75.5% (108/143) vs. 35.7% (337/944), P < 0.0001, prevalence ratio, 2.1] and fetal vascular malperfusion lesions [88.1% (126/143) vs. 19.7% (186/944), P < 0.0001, prevalence ratio, 4.5]; (3) higher frequency of placental histologic patterns suggestive of hypoxia [59.0% (85/143) vs. 9.3% (82/942), P < 0.0001, prevalence ratio, 6.8]; and (4) higher frequency of chronic inflammatory lesions [53.1% (76/143) vs. 29.9% (282/944), P < 0.001, prevalence ratio 1.8]. Conclusion: This study demonstrates that placentas of women with fetal death were 44 times more likely to present disorders of villous maturation compared to placentas of those with normal pregnancy. This suggests that the burden of placental disorders of villous maturation lesions is substantial. [ABSTRACT FROM AUTHOR]

It is a generally held concept that finding increased aspirated amniotic fluid squames at autopsy supports a diagnosis of acute fetal asphyxia, the massive aspiration of squames being an indicator of terminal gasping. To evaluate this concept, we identified autopsies on 15 third-trimester stillborns with clinical acute placental abruption (acute asphyxia); 13 also had thymic petechiae and none had severe acute thymic involution, findings also supporting acute asphyxia. Thirty third-trimester stillborns with findings supporting a subacute or chronic mode of death, including severe thymic involution and absence of thymic petechiae, comprised the comparison group. Intra-alveolar squames were scored as 0, no squames; 1+, scattered squames singly or in small groups; and 2+, squames in many alveoli, at least focally in compacted clusters. In all cases, the squames were patchily distributed, and none received a score of 0. In the abruption group, the intra-alveolar squames were scored as 1+ in 12 (80%) and as 2+ in 3 (20%) cases, while in the comparison group, the squames were scored as 1+ in 20 (67%) and 2+ in 10 (33%) cases (P = NS). There was also no difference in the quantification of intra-alveolar squames in term compared to preterm stillborns. In conclusion, quantification of intra-alveolar squames did not aid in separating an acute mode of death (acute asphyxia) from subacute or chronic modes of death. [ABSTRACT FROM AUTHOR]

Objective: To determine frequency, stage and grade of placental histologic acute maternal inflammatory response (MIR) and fetal inflammatory response (FIR) in meconium-stained amniotic fluid (MSAF) in our predominantly African-American population.Methods: Term placentas with MSAF (n = 310) were evaluated for MIR/FIR, including stage/grade, and compared with placentas with clear amniotic fluid (AF) (n = 250). MIR/FIR were also evaluated in thick compared to thin MSAF subgroups. Selected demographic and clinical features were compared.Results: MIR and FIR were present in 57.7 and 40.3% of the MSAF compared to 44.0 and 29.2% of the clear AF group, respectively (p = .001 and .008). MIR with FIR was present in 35.8% of the MSAF compared to 25.2% of the clear AF group (p = .008); however, there was no significant difference in frequency of MIR without FIR between groups. There was no significant difference in frequency of MIR/FIR in thick compared to thin MSAF; however, thick MSAF was associated with higher FIR stage compared to thin MSAF (29.2 versus 5.4%, p = .004). This association was not seen with MIR stage or MIR/FIR grade.Conclusions: Histologic MIR and FIR are frequent findings in MSAF. Thick MSAF is associated with higher FIR stage when compared to thin MSAF. [ABSTRACT FROM AUTHOR]

Objective: To determine the frequency and type of histopathologic lesions in placentas delivered by women with a normal pregnancy outcome. Methods: This retrospective cohort study included placental samples from 944 women with a singleton gestation who delivered at term without obstetrical complications. Placental lesions were classified into the following four categories as defined by the Society for Pediatric Pathology and by our unit: (1) acute placental inflammation, (2) chronic placental inflammation, (3) maternal vascular malperfusion and (4) fetal vascular malperfusion. Results: (1) Seventy-eight percent of the placentas had lesions consistent with inflammatory or vascular lesions; (2) acute inflammatory lesions were the most prevalent, observed in 42.3% of the placentas, but only 1.0% of the lesions were severe; (3) acute inflammatory lesions were more common in the placentas of women with labor than in those without labor; (4) chronic inflammatory lesions of the placenta were present in 29.9%; and (5) maternal and fetal vascular lesions of malperfusion were detected in 35.7% and 19.7%, respectively. Two or more lesions with maternal or fetal vascular features consistent with malperfusion (high-burden lesions) were present in 7.4% and 0.7%, respectively. Conclusion: Most placentas had lesions consistent with inflammatory or vascular lesions, but severe and/or high-burden lesions were infrequent. Mild placental lesions may be interpreted either as acute changes associated with parturition or as representative of a subclinical pathological process (intra-amniotic infection or sterile intra-amniotic inflammation) that did not affect the clinical course of pregnancy. [ABSTRACT FROM AUTHOR]

Objective: Examine the association between placental inflammation and neonatal infections, and 25OH vitamin D (25OH D) levels at birth among very low birth weight infants (VLBWI).Study Design: Serum 25OH D levels were measured in 89 VLBWI (≤1250 g) and 47 mothers on day one, and in 78 infants on day 21. Placentas were examined for maternal and fetal inflammation. Infants were divided into deficient (≤10 ng/ml) and adequate (>10 ng/ml) groups based on 25OH D levels on day 1.Results: Mean ± SD maternal levels of 25OH D (21 ± 9 ng/ml) correlated with infants' levels (15 ± 8 ng/ml), (p < .001). 25OH D levels were lower in deficient (32/89) than in adequate group (8 ± 2 versus 20 ± 7 ng/ml, p = .011). Infants' 25OH D levels rose significantly by day 21 (p < .001). Univariate analyses showed no differences between infant groups in maternal or fetal inflammation, or neonatal infections (p > .05). Logistic regression analyses revealed no association between deficient 25OH D levels and the odds of maternal or fetal inflammation or other infections. Levels of 25OH D did not correlate with severity of placental inflammation.Conclusions: Deficient levels of 25OH D at birth are not associated with the occurrence of placental inflammation or neonatal infections among VLBWI. [ABSTRACT FROM AUTHOR]

Problem To determine whether amniotic fluid ( AF) CXCL10 concentration is associated with histologic chronic chorioamnionitis in patients with preterm labor ( PTL) and preterm prelabor rupture of the membranes ( PROM). Method of Study This study included 168 women who had an episode of PTL or preterm PROM. AF interleukin (IL)-6 and CXCL10 concentrations were determined by immunoassay. Results (i) Increased AF CXCL10 concentration was associated with chronic ( OR: 4.8; 95% CI: 1.7-14), but not acute chorioamnionitis; (ii) increased AF IL-6 concentration was associated with acute ( OR: 4.2; 95% CI: 1.3-13.7) but not chronic chorioamnionitis; and (iii) an increase in AF CXCL10 concentration was associated with placental lesions consistent with maternal anti-fetal rejection ( OR: 3.7; 95% CI: 1.3-10.4). (iv) All patients with elevated AF CXCL10 and IL-6 delivered preterm. Conclusion Increased AF CXCL10 concentration is associated with chronic chorioamnionitis or maternal anti-fetal rejection, whereas increased AF IL-6 concentration is associated with acute histologic chorioamnionitis. [ABSTRACT FROM AUTHOR]

Background: Skeletal ciliopathies comprise a spectrum of ciliary malfunction disorders that have a profound effect on the skeleton. Most common among these disorders is short rib polydactyly syndrome (SRPS), a recessively inherited perinatal lethal condition characterized by a long narrow chest, markedly shortened long bones, polydactyly and, often, multi-organ system involvement. SRPS shows extensive locus heterogeneity with mutations in genes encoding proteins that participate in cilia formation and/or function. Results: Herein we describe mutations in IFT43, a satellite member of the retrograde IFT-A complex, that produce a form of SRPS with unusual bending of the ribs and appendicular bones. These newly described IFT43 mutations disrupted cilia formation, produced abnormalities in cartilage growth plate architecture thus contributing to altered endochondral ossifcation. We further show that the IFT43 SRPS phenotype is similar to SRPS resulting from mutations in the gene encoding IFT121 (WDR35), a direct interactor with IFT43. Conclusions: This study defnes a new IFT43-associated phenotype, identifying an additional locus for SRPS. The data demonstrate that IFT43 is essential for ciliogenesis and that the mutations disrupted the orderly proliferation and diferentiation of growth plate chondrocytes, resulting in a severe effect on endochondral ossifcation and mineralization. Phenotypic similarities with SRPS cases resulting from mutations in the gene encoding the IFT43 direct interacting protein IFT121 suggests that similar mechanisms may be disrupted by defects in these two IFT-A satellite interactors. [ABSTRACT FROM AUTHOR]

Adrenal histologic changes, including compact cell change (CCC), cystic change (CYC), and adrenal hemorrhage (AH), and their clinical correlations have only infrequently been investigated in stillbirth. We evaluated 75 third trimester singleton stillborns with complete autopsies (30 term and 45 preterm). A total of 58 had unexplained stillbirth and 17 had clinical placental abruption. The mothers were predominantly African-American (89%). CCC and CYC were diagnosed as cytoplasmic eosinophilia and cystic cavities in the definitive cortex, respectively. Adrenal changes were correlated with acute thymic involution (ATI), thymic petechiae, and clinical features, including abruption. CCC, CYC, and AH were present in 58 (77%), 51 (68%), and 15 (20%) of the 75 stillborns, respectively. CCC and CYC were frequently seen together (P<.001). CCC and CYC were associated with higher ATI grade (P<.001 and P=.010, respectively). The presence of CCC, but not CYC, was associated with absence of thymic petechiae (P=.013) and was more frequent with unexplained stillbirth compared to abruption (P=.017). AH was associated with lower ATI grade (P=.002), with thymic petechiae (P<.001), and with abruption (P=.004). CYC was associated with diabetes (P=.015). Overall, CCC and CYC were frequent findings and correlated with higher ATI grade, suggesting similar causes and time frames. CCC, but not CYC, correlated with unexplained stillbirth compared to abruption, but its high frequency in both groups limits its usefulness in their separation. AH was more frequent in the abruption group and correlated with lower ATI grade and thymic petechiae, supporting an association with sudden asphyxial death. [ABSTRACT FROM AUTHOR]

Objective: Complete placental abruption results rapidly in fetal death through acute asphyxia, and identification of thymic lesions at autopsy may help in confirming this diagnosis. Thymic petechiae are a marker for acute asphyxia, while absence of histologically identifiable acute thymic involution (ATI), which requires several hours to develop, may help in exclusion. Methods: We identified autopsies on 17 3rd trimester stillborns with clinical abruption; 58 stillborns with unexplained demise comprised the control group. Eighty-nine percent of the mothers were African–American. ATI was graded 0–4 (grades 0–1 and 3–4 were combined for analysis), and thymic petechiae were recorded. Results: In the abruption group, ATI grade 0–1 was more frequent than higher grades: 13 (77%) had ATI grade 0–1 compared to 1 (6%) with ATI grade 3–4 (p < 0.001). In contrast, in the control group, ATI grade 3–4 was more frequent than lower grades: 9 (16%) had ATI grade 0–1 compared to 30 (52%) with ATI grade 3–4 (p < 0.001). Thymic petechiae were more frequent in the abruption compared to control group [10 (59%) versus 2 (3%)] (p < 0.001), and were frequently seen with low ATI grade: 10 (83%) had ATI grade 0–1 (p < 0.001). Conclusions: The presence of thymic petechiae and ATI grade 0–1 correlates significantly with a clinical diagnosis of placental abruption. [ABSTRACT FROM PUBLISHER]

Objective: Acute atherosis is characterized by subendothelial lipid-filled foam cells, fibrinoid necrosis and perivascular lymphocytic infiltration. This lesion is generally confined to non-transformed spiral arteries and is frequently observed in patients with preeclampsia. However, the frequency of acute atherosis in the great obstetrical syndromes is unknown. The purpose of this study was to determine the frequency and topographic distribution of acute atherosis in placentas and placental bed biopsy samples obtained from women with normal pregnancy and those affected by the "great obstetrical syndromes". We also examined the relationship between acute atherosis and pregnancy outcome in patients with preeclampsia.Material and Methods: A retrospective cohort study of pregnant women who delivered between July 1998 and July 2014 at Hutzel Women's Hospital/Detroit Medical Center was conducted to examine 16, 345 placentas. Patients were classified into the following groups: (1) uncomplicated pregnancy; (2) spontaneous preterm labor (sPTL) and preterm prelabor rupture of membranes (PPROM); (3) preeclampsia; (4) gestational hypertension; (5) small-for-gestational age (SGA); (6) chronic hypertension; (5) fetal death; (6) spontaneous abortion and (7) others. A subset of patients had placental bed biopsy. The incidence of acute atherosis was compared among the different groups.Results: (1) The prevalence of acute atherosis in uncomplicated pregnancies was 0.4% (29/6961) based upon examination of nearly 7000 placentas; (2) the frequency of acute atherosis was 10.2% (181/1779) in preeclampsia, 9% (26/292) in fetal death, 2.5% (3/120) in midtrimester spontaneous abortion, 1.7% (22/1,298) in SGA neonates and 1.2% (23/1,841) in sPTL and PPROM; (3) among patients with preeclampsia, those with acute atherosis than in those without the lesion had significantly more severe disease, earlier onset, and a greater frequency of SGA neonates (p < 0.05 all) and (4) the lesion was more frequently observed in the decidua (parietalis or basalis) than in the decidual segment of the spiral arteries in patients with placental bed biopsies.Conclusions: Acute atherosis is rare in normal pregnancy, and occurs more frequently in patients with pregnancy complications, including preeclampsia, sPTL, preterm PROM, midtrimester spontaneous abortion, fetal death and SGA. [ABSTRACT FROM AUTHOR]

Objective: Acute atherosis is a lesion of the spiral arteries characterized by fibrinoid necrosis of the vessel wall, an accumulation of fat-containing macrophages, and a mononuclear perivascular infiltrate, which can be found in patients with preeclampsia, fetal death, small-for-gestational age, spontaneous preterm labor/premature prelabor rupture of membrane, and spontaneous mid-trimester abortion. This lesion is thought to decrease blood flow to the intervillous space which may lead to other vascular lesions of the placenta. The objective of this study was to test whether there is an association between acute atherosis and placental lesions that are consistent with maternal vascular underperfusion (MVU), amniotic fluid infection (AFI), fetal vascular thrombo-occlusive disease (FVTOD) or chronic inflammation. Material and methods: A retrospective cohort study of pregnant women who delivered between July 1998 and July 2014 at Hutzel Women’s Hospital/Detroit Medical Center was conducted examine 16 457 placentas. The frequency of placenta lesions (diagnosed using the criteria of the Perinatal Section of the Society for Pediatric Pathology) was compared between pregnancies with and without acute atherosis. Results: Among 16 457 women who were enrolled, 10.2% (1671/16 457) were excluded, leaving 14 786 women who contributed data for analysis. Among them, the prevalence of acute atherosis was 2.2% (326/14 786). Women with acute atherosis were more than six times as likely as those without to have placental lesions consistent with maternal underperfusion (adjusted odds ratio – aOR: 6.7; 95% CI 5.2–8.6). To a lesser degree, acute atherosis was also associated with greater risks of having either lesions consistent with FVTOD (aOR 1.7; 95% CI 1.2–2.3) or chronic chorioamnionitis (aOR 1.9; 95% CI 1.3–3), but not with other chronic inflammatory lesions, after adjusting for gestational age at delivery. In contrast, women with acute atherosis were 60% less likely to have lesions consistent with AFI, adjusting for gestational age at delivery (aOR 0.4; 95% CI 0.3–0.5). Conclusions: Acute atherosis is associated with increased risks of having placental lesions consistent with MVU, and to a lesser extent, chronic chorioamnionitis and those consistent with FVTOD. [ABSTRACT FROM AUTHOR]

Objective: With advances in therapy, more neonates with severe congenital anomalies are surviving, albeit some with neurologic disorders, possibly related to antenatal low brain blood flow. This autopsy series reports antenatal brain injury in neonates expiring due to severe anomalies, and provides correlation with umbilical cord blood gas and acid–base analysis. Methods: We identified autopsies of third trimester neonates expiring shortly following delivery due to severe anomalies or malformations. Brain injury classified as “older” included periventricular leukomalacia, gliosis and karyorrhectic neurons, and “recent” included red neurons and reactive glial changes. Results: We identified 22 cases (nine term, 13 preterm). 16 (73%) had brain injury, including 11 with older injury. Cord arterial blood was analyzed in 17, and six had pH <7 or base deficit >12 mmol/L. Four out of 5 (80%) neonates with neuronal necrosis compared to two out of 12 (17%) without had a pH <7 or base deficit >12 mmol/L (p = 0.03). Five out of nine (56%) neonates with white matter injury compared to one out of 8 (13%) without had pH <7 or base deficit >12 mmol/L (p = NS). Conclusions: Antenatal brain injury is frequent in neonates with severe congenital anomalies. Severely abnormal cord blood analysis results correlate significantly with neuronal necrosis and show a trend toward white matter injury; however, the absence of these abnormal results does not preclude the presence of brain injury. [ABSTRACT FROM AUTHOR]

Many 3rd-trimester stillbirths are unexplained, including the time course of the illness. Histologic acute thymic involution (ATI), when graded, correlates with duration of acute illness (grade 0, <12 hours; grade 4, >72 hours). Histologic brain injury is also common in stillbirth. We investigated ATI in unexplained stillbirth and correlated it with neuropathologic injury by identifying 58 autopsies of unexplained, 3rd-trimester stillboms (preterm, n = 24; term, n = 34) that included brain examination and graded ATI from 0 (resting state) to 4 (pronounced lymphodepletion). Gray matter injury (GMI) and white matter injury (WMI) were classified as older, recent, or absent, and ATI was correlated with GMI, WMI, thymic weight, and clinical data. Nine cases (16%) had ATI grade 0-1; 19 (33%), grade 2; 24 (41%), grade 3; and 6 (10%), grade 4. Older GMI and WMI were present in 39 (67%) and 10 (17%) stillborns, respectively. Higher ATI grade correlated significantly with older GMI (P < 0.001) and WMI (P = 0.014). The ATI grade was higher in the small-forgestational stillboms compared with the appropriate- or large-for-gestational stillboms (P = 0.017) but did not correlate significantly with gestational age or other clinical or demographic factors evaluated. The ATI grades 2-4 were found in 84% of the stillborns, consistent with onset of acute illness between 24 and >72 hours before demise. Higher ATI grade correlated significantly with older brain injury, suggesting similar time of onset and shared underlying pathophysiologic events, the specific nature of which remains unclear. [ABSTRACT FROM AUTHOR]

Objective: To examine the association between an umbilical artery notch and fetal deterioration in monochorionic/monoamniotic (MC/MA) twins. Methods: Six MC/MA twin pregnancies were admitted at 24-28 weeks of gestation for close fetal surveillance until elective delivery at 32 weeks or earlier in the presence of signs of fetal deterioration. Ultrasound (US) examinations were performed twice weekly. The presence of cord entanglement, umbilical artery notch, abnormal Doppler parameters, a non-reassuring fetal heart rate pattern, or an abnormal fetal biophysical profile were evaluated. Results: Umbilical cord entanglement was observed on US in all pregnancies. The presence of an umbilical artery notch was noted in four out of six pregnancies and in two of them an umbilical artery notch was seen in both twins. The umbilical artery pulsatility index was normal in all fetuses. Doppler parameters of the middle cerebral artery and ductus venosus, fetal biophysical profile and fetal heart rate monitoring remained normal until delivery in all pregnancies. All neonates experienced morbidity related to prematurity; however, all were discharged home in good condition. Conclusion: The presence of an umbilical artery notch and cord entanglement, without other signs of fetal deterioration, are not indicative of an adverse perinatal outcome. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The lesion termed 'placental infarction hematoma' is associated with fetal death and adverse perinatal outcome. Such a lesion has been associated with a high risk of fetal death and abruption placentae. The fetal and placental hemodynamic changes associated with placental infarction hematoma have not been reported. This paper describes a case of early and severe growth restriction with preeclampsia, and progressive deterioration of the fetal and placental Doppler parameters in the presence of a placental infarction hematoma. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objective: Third trimester fetal deaths occurring in the hospital at the time of delivery are unusual. We report an autopsy series of such cases with emphasis on neuropathological injury and other lesions predating delivery. Methods: We identified autopsies performed on third trimester fetuses documented to be alive shortly before delivery, but that expired during, or very close to, time of delivery, and we correlate autopsy and placental findings. Fetuses with major congenital anomalies were excluded. Results: Ten cases were identified (6 term, 4 preterm). All were delivered by cesarean section and had attempted resuscitation. Established or recent brain injury was identified in 9 of 10 cases, including 3 with established neuronal damage and 1 with periventricular leukomalacia. Additional autopsy findings included thymic involution in eight (five mild; three severe), myocardial infarcts in two; intrathoracic petechiae in five, and ascites or pleural or pericardial effusions in six. Severe thymic involution and myocardial infarcts correlated with established brain injury. Placental lesions adaptive to decreased oxygenation (increased nucleated red blood cells or villous hypervascularity) were seen in five cases and correlated with established brain injury. Acute chorioamnionitis with funisitis was present in one, and chronic inflammatory placental lesions were present in six. Conclusions: These findings indicate brain injury predated the time period immediately before delivery in 9 of 10 fetuses, and in the fetuses with established brain injury the onset of acute illness was possibly >72 h before delivery. [ABSTRACT FROM AUTHOR]

A case of hemangioma of the umbilical cord with an associated amnionic epithelial inclusion cyst (4.5 cm in maximum dimension), diagnosed by pathological examination at 26 weeks of gestation following in utero fetal demise, is reported. These are both uncommon lesions of the umbilical cord, and to our knowledge, have not been reported together. Prenatal ultrasound at 20 weeks of gestation had shown no fetal or placental abnormalities. The cyst formation may have been secondary to the hemangioma, possibly the result of damage to the amnion caused by the associated edema and myxomatous degeneration of Wharton's jelly. [ABSTRACT FROM AUTHOR]

We report the neuropathologic findings and clinicopathologic associations in 63 3rd trimester singleton stillborn fetuses. All were ≥28 weeks estimated gestational age (EGA) with complete autopsies, including placental examination. Fetuses with chromosomal abnormalities, major congenital anomalies, and intrapartum demise were excluded. The cases were divided into those with abruption (n = 12) and those with unexplained fetal demise (n = 51). The latter group was then subdivided by gestational age with 3 subgroups (preterm 28 to <32 weeks EGA (n = 16), preterm 32 to <37 weeks EGA (n = 13), and term 37-41 weeks EGA (n = 22). Each group was further subdivided as appropriate-for-gestational age/large-for-gestational age (AGA/LGA) or small-for-gestational age (SGA). Placental lesions were also evaluated and correlated with brain lesions. Established or recent injury involving gray or white matter was seen in 88% of the fetuses with unexplained demise versus 42% with abruption (P = 0.001). The most common form of brain injury was established gray matter damage, seen in 65% of the fetuses with unexplained demise versus 25% with abruption (P = 0.021), the most common pattern being established pontosubicular neuronal necrosis plus established neuronal necrosis in other sites. There was no significant difference in the frequency of brain injury between the SGA fetuses and AGA/LGA fetuses or between the unexplained stillbirth preterm and term subgroups, and there was no unequivocal correlation between placental lesions and brain lesions. Brain injury, most frequently established gray matter damage, is seen in the majority of stillborn infants with unexplained demise, indicating that the brain injury predates the period immediately before death. [ABSTRACT FROM AUTHOR]

We report 51 placentas diagnosed with eosinophilic/T-cell chorionic vasculitis (E/TCV), an unusual form of chorionic vasculitis characterized by an infiltrate composed predominantly of CD3++ T cells and eosinophils. The placentas were all 3rd trimester, with 48 (94.1%%) being term. Forty-seven (92.2%%) were singleton placentas, and the remaining 4 were twins. The E/TCV was limited to 1 chorionic surface vessel in 40 (78.4%%) and involved 50%% or less of the vessel circumference in 30 (58.8%%) placentas. The inflammation faced the intervillous space in 12 (23.5%%) and the amniotic cavity in 8 (15.7%%) and had no distinct predominant direction in the remaining 31 (60.8%%) placentas. Twelve (25.5%%) placentas showed mural thrombi or intramural fibrin in association with the E/TCV. One hundred six term singleton placentas were selected as the control group, and the 47 singleton placentas with E/TCV made up the study group for comparison of demographic and histopathologic features. Villitis of unknown etiology was identified more frequently in study group placentas (20 [[42.6%%]]) compared with control group placentas (14 [[13.2%%]]) ( P < 0.001). Vascular changes of fetal vascular thrombo-occlusive disease were identified away from the E/TCV more frequently in study group placentas (8 [[17.0%%]]) compared with control group placentas (4 [[3.8%%]]) ( P == 0.008). There were no significant differences in the frequencies of other placental lesions studied, including acute inflammatory lesions and lesions related to maternal underperfusion. There were no significant differences in maternal age, race, parity, birth weight, allergy history, blood type, or medication use. [ABSTRACT FROM AUTHOR]