Search

Chorangiomas of the placenta, benign tumors of chorionic tissue, are a rare placental cause of adverse fetal and maternal outcomes. We describe the case of a large placental chorangioma leading to polyhydramnios as well as consecutive preterm birth and high output cardiac failure of the newborn. Derived from a literature review, we suggest instructions for diagnosis and optimal prenatal care in case of a a suspected placental chorangioma.Plazentare Chorangiome sind als benigne Tumore des Choriongewebes seltene Ursache fetaler und maternaler Morbidität. Wir beschreiben den Fall eines großen plazentaren Chorangioms, das zu einem Polyhydramnion, konsekutiver Frühgeburt und kindlicher High-Output-Herzinsuffizienz führte. Aus einer Literaturrecherche leiten wir zudem Hinweise zur Diagnostik und Empfehlungen zur optimalen Schwangerschaftsbetreuung bei Verdacht auf Chorioangiom ab.

Maternal floor infarction/massive perivillous fibrin deposition (MFI/MFD), chronic histiocytic intervillositis (CHIV) and villitis of unknown etiology (VUE) are lesions of the placenta which are characterized morphologically. The cause is thought to be pathological immunotolerance/rejection reaction at the fetomaternal interface. The risk of recurrence is elevated and the lesions can lead to severe pediatric diseases.This article provides an overview of the pathological and anatomical characteristics of each of these lesions, including diagnostic criteria, suspected etiology, clinical relevance and suggested therapy options.A selective search of the literature was carried out and experiences from own diagnostic clientele are presented.While MFI/MFD and CHIV occur more rarely, VUE is relatively common occurring in up to 15 % of placentas at term. Both MFI/MFD and CHIV can occur in the first and second trimester, while VUE typically manifests in the third trimester. All lesions can lead to intrauterine growth retardation or abortion and have a tendency towards disease recurrence. Furthermore, VUE and MFI/MFD can be associated with an adverse neurodevelopmental outcome in the children. For all these entities potential therapy strategies have been reported, which are mainly based on anticoagulation and immunosuppression in subsequent pregnancies.

Intrauterine death is a multifactorial major complication during pregnancy. In this retrospective analysis the pathological anatomical findings of fetuses and placentas as well as maternal factors were evaluated.A retrospective screening of post-mortem examinations, corresponding placental examinations and clinical data on maternal status (1998-2008) was carried out. A classification of all findings was made with the ReCoDe system and induced abortions and cases with incomplete data were excluded from the study.A total of 84 pregnancies involving 87 fetuses (9 siblings) were evaluated. The median gestation age was 20 weeks (range 12-41). The evaluation based on the ReCoDe system revealed that intrauterine death was mainly associated with placental diseases (n = 63) and to a lesser extent with fetal malformations (n = 15) or maternal diseases (n = 4). Idiopathic cases were rare (n = 2).Placental examination is important for explaining intrauterine death because in most cases an association with placental diseases can be found but fetal malformation and maternal diseases must be taken into account.

Placental-mediated pregnancy complications (PmC) like preeclampsia, intrauterine growth restriction and placental abruption are common causes of fetal and maternal morbidity and mortality. The high prevalence of hereditary thrombophilias in case-control studies associated with pathological morphological findings of the placenta in these cases gave evidence for the association between hereditary thrombophilias and PmC. However, data from the literature are inconsistent, since subsequent prospective cohort studies could not demonstrate significant associations between inherited thrombophilia and PmC. Because of the multifactorial aetiology of PmC it may be difficult to prove, that hereditary thrombophilias are independent risk factors for PmC. Current guidelines do not recommend screening for inherited thrombophilias in patients with previous PmC. Evidence from current in vitro studies have shown, that heparin has beneficial non-anticoagulatory effects on trophoblast invasion. Retrospective case-control studies and recently published randomised controlled cohort studies have shown, that prophylactic administration of low-molecular-weight heparin (LWH), started in early pregnancy, may lead to a significant reduction in the incidence of PmC in subsequent pregnancies in patients with and without hereditary thrombophilias and previous PmC.Large, well-designed multicenter studies are needed to elucidate the role of hereditary thrombophilias in cases of PmC and to confirm the benefit of LWH for subsequent pregnancy outcomes.

Sonography is still the method of choice for imaging diseases in pregnant women. The changed physiognomy of the women increases the known limitations of sonography while the advantages of MRI (large field of view, excellent soft-tissue contrast, sensitive diagnosis of edema) are not affected. The available sequences allow the differentiation of various pathologies. Most of these can frequently be visualized without intravenous administration of contrast material. Although the significance of techniques like DWI and ASL has not yet been explored, initial descriptions are promising and MR imaging in pregnancy will be increasingly important in the future. Therefore, knowledge of the most frequent diseases in pregnancy and their image appearance is relevant to radiologists. The advantages of MRI in comparison to sonography and its important role in imaging pathologies of the acute abdomen in pregnancy are illustrated and discussed.

The differential diagnosis of villous forms of gestational trophoblastic disease (GTD) includes hydropic abortion, complete and partial hytatidiform mole and placental mesenchymal dysplasia. In addition to histologic criteria, p57(KIP2) immunohistochemistry might be helpful. Choriocarcinoma represents the most immature form of GTD. This and downregulation of HSP-27 might contribute to the high chemosensitivity, compared to placental site (PSTT) and epitheloid trophoblastic tumor (ETT). Within the differential diagnosis of the non-villous forms of GTD an algorithmic approach of immunohistochemistry is very helpful. With an incidence of 1.6% of all abortions within the first trimester the exaggerated placental site reaction (EPS) is rare. There is no molecular indication that the EPS represents a precursor lesion of PSTT. The morphologic prediction of the behaviour of PSTT is not well established. Factors which might be associated with adverse outcome are age35 years, interval since last pregnancy2 years, growth outside the uterus, deep myometrial invasion, destructive growth, extensive coagulative necrosis, presence of cells with clear cytoplasm, high mitotic rate and a Ki-67 labeling index50%. Recent molecular data suggest a neoplastic transformation of (cyto-) trophoblastic stem cells, within the pathogenesis of (non-villous) GTD. The detection of target molecules for a targeted therapy is currently irrelevant.

Hereditary hemoglobinopathies should be considered as differential diagnosis when examining placental specimens for fetal growth retardation and spontaneous abortion. They can cause various macroscopic and microscopic changes in the placenta that are relevant for routine pathology examination. The importance of interdisciplinary co-operation between obstetrics and pathology to achieve optimum diagnostics and therapy planning is demonstrated using the case of a pregnant woman with heterozygous genotype and her child with homozygous genotype. Within this context, the influence of hemoglobinopathies on placental pathology and fetal development are summarized and exemplified.

A 32-year-old para 3 patient is presented having suffered from a silent uterine rupture on the occasion of her second and third Caesarean sections. After the third Caesarean section, there was light uterine bleeding whilst the patient breastfed for five months. Amenorrhoea then ensued due to oral contraception. Regular clinical and ultrasound checks revealed negative serum beta-HCG values and retrovesicular resistance, which increased in size after 18 months and became symptomatic. Because the patient's family was complete, abdominal hysterectomy without adnexectomy was performed. Histology revealed a placental site trophoblastic tumour (PSTT). This is a rare tumour with malignant potential, whose prognosis depends on the stage of the primary tumour, the period of time between the last pregnancy and onset of disease, the patient's age, and the rate of mitosis, and whose progress cannot be assessed using the WHO Prognostic Index Score for Gestational Trophoblastic Disease. In therapeutic terms, hysterectomy is recommended. Chemosensitivity is low and, due to the infrequency of the tumours, the most suitable chemotherapy scheme is unknown. In the case of metastasising or recurrent PSTT, the EP/EMA regime has proved to be most effective.

Hemorrhaging during pregnancy is often fulminant and life-threatening for mother and child. Of maternal deaths occurring during pregnancy, 25% are caused by hemorrhaging. All physicians involved in the interdisciplinary treatment of hemorrhaging during pregnancy need to be familiar with the specific pathophysiology of hemostatic changes during pregnancy, e.g. elevated hemostatic capacity, reduced anti-coagulation activity and severe alterations of the fibrinolysis system. Therapists must be able to perform a consequent, goal-directed interdisciplinary approach to prevent adverse maternal and fetal outcomes. The major issues of therapy are causal obstetric treatment of the bleeding, early detection and therapy of hyperfibrinolysis, optimization of fibrinogen and platelet levels and knowledge of the possibilities of a targeted coagulation therapy.

Perinatal brain damage has a diverse and complex aetiology. Over the past decades, much progress has been made in this research field. In this article, I offer a discussion of seven dimensions of aetiological perinatal brain damage research: (1) hypoxia-ischaemia vs. inflammation; (2) "classic" vs. "remote" intrauterine infection; (3) focal vs. diffuse white matter damage; (4) maternal vs. foetal inflammatory response; (5) clinical vs. experimental data; (6) bacterial vs. viral infection; and (7) preterm vs. term delivery. Despite these complexities, it is hoped that obstetricians, neonatologists, and neuropaediatricians will agree on a perinatal neuroprotective strategy in the near future.

Chorangiomas are regarded as hamartous lesions of the placenta which may complicate a pregnancy if they grow large. The etiology of these lesion is still unclear. We suspected a link between the development of chorangiomas and an increase of the expression of the angiogenic growth factor bfgf and angiopoietin-1 within the tumour.We examined 20 placentas without tumour, 19 placentas with solitary chorangiomas and 10 placentas with multiple chorangiomas (chorangiomatosis) with respect of the difference in clinical complications, regarding the expression of bfgf and angiopoietin-1 and with regard to the proliferation rate.The expression of the growth factors in solitary chorangiomas did not differ from that in the normal placental tissue. Both groups showed moderate expression of growth factors. In placentas with multiple chorangiomas all cases were associated with a strong expression of bfgf and angiopoietin-1. Proliferating cells and fibroblasts were seen more often in placentas with chorangiomatosis. There were clinical differences with regard to the maternal age. The mean age in case of normal placentas was 24 years, in placentas with solitary chorangiomas 32 years and for placentas with multiple chorangiomas 28 years. There were more complications such as HELLP-syndrome, diabetes, preterm birth and additional maturational arrest of the placenta in case of chorangiomas.There is a link between the development of multiple chorangiomas and an increase of the expression of bfgf and angiopoietin-1 in the placenta. In our study there is no correlation between multiple tumours and complications of pregnancy.

We describe an unusual type of cellular chorangioma with a high rate of proliferating cells and mitosis and high expression of the growth factor BFGF. The tumor was observed in the placenta of a 26-year-old gravida 1 with help syndrome. The pregnancy was terminated at 35+5 weeks by elective caesarean section. Chorangiomas are hamartoma malformations of the placenta which in some cases may be large enough to influence the course of pregnancy and associated complications are hydramnion, gestosis or hemorrhage. Complications for the fetus are due to hemodynamic alterations caused by the formation of an arteriovenous shunt. Because the histogenesis of the tumor is still unknown, we examined the expression of the growth factors VEGF and BFGF. The number of cells with an expression of VEGF in placental tissue and in the chorangioma was uniform, but the number of cells with an expression of BFGF was much higher in the chorangioma than in the placenta. We conclude that BFGF may have an influence on the growth of chorangiomas. There was no difference between the chorangioma and the placenta in the rate of apoptosis-inhibited cells.

Chorangioma is a benign angiomatous tumor of the placenta occurring with a frequency of approximately 1 % of all examined placentas. Pregnancies especially with large chorangiomas are frequently complicated by abruptio placentae, premature labour, fetal anaemia, hydrops, cardiomegaly and polyhydramnios. We here report a case of an extremely rare chorangiomatosis. Multiple chorangiomas measuring up to 1.5 cm comprised approximately one third of the placenta. A caesarean section had to be performed at 36 weeks of gestation because of uteroplacental insufficiency with oligohydramnios. Displacement of normal placental parenchyma by chorangiomatosis as a cause of uteroplacental insufficiency is very likely. Colour doppler imaging allows early diagnosis and management of chorangiomas. Thus, in our case early diagnosis of uteroplacental insufficiency was rendered. Principally, early diagnosis of fetal hazard due to myocardial insufficiency of the fetus is feasible. In-utero-endoscopy permits prenatal laser devascularisation of large chorangiomas. In the reported case the pregnancy was closely monitored with colour flow imaging. The diagnosis of uteroplacental insufficiency was established because of abnormal blood flow of the uterine arteries and abnormal fetal heart rate (FHR). At the same time fetal cardiomegaly and pathologic blood flow of the ductus venosus in terms of beginning fetal myocardial insufficiency was recognized. Consequently, caesarean section could be performed opportune.

Triploidy describes the presence of threefold haploid chromosome set and is a frequent cause of early abortion. Only few pregnancies reach the second trimester.Prenatal diagnosis of a fetus in the 28th week of gestation with a hypotriploidy and with characteristic ultrasonographic features is presented. An enlarged placenta with molar changes, an oligohydramnion, severe growth retardation and minor cardiac anomalies were observed by ultrasound. Before prenatal karyotyping could be performed, immediate cesarian section was necessary due to massive intraplacentar hemorrhage resulting in a decrease of the hemoglobin level. The diagnosis of triploidy was confirmed postnatally by cytogenetic analysis of lymphocytes, the child died after 3 days.Ultrasonographic and clinical features for the diagnosis of triploidy are presented. Etiology of the rare karyotype 68,XX is discussed.

1. A 26-year-old secondgravida presented at 26 weeks' gestation with severe vaginal bleeding. A caesarean was performed which led to a 880 g female infant with multiple malformations (Wolf-Hirschhorn-Syndrome). It deceased short time later. 2. A 27-year-old second-gravida at 37 weeks' gestation delivered a 1520 g infant by caesarean which was made because of fetal asphyxia. In both cases investigation of the placenta showed capillary chorioangioma. Chorioangiomas are the most common tumors of the placenta. Occasionally they are associated with fetal anomalies and growth retardation. Depending on size complications during delivery must be considered.

We investigated the morphologically distinct forms of inflammatory infiltration of the placenta both histologically and immunohistologically (n = 24). Our material included cases of membraneous inflammation (chorioamnionitis), inflammatory infiltration of arteries in the chorionic membrane, basal and intervillous placentitis. NACE staining was used to detect myeloid cells and monoclonal antibodies (LCA, CD3, CD8, CD20, CD68). To detect lymphoid and macrophageal cells we also measured the proliferation activity with MiB 1. In cases of chorioamnionitis and subchorial demarcation and in the arteries of the chorionic membranes the main inflammatory cell is the myeloid cell (most often the mature neutrophil granulocyte). T-lymphocytes were only occasionally found. In cases of intervillous placentitis, on the other hand, lymphocytic infiltration predominates, consisting of T-lymphocytes which are mostly CD8 negative, and some monocytes and macrophages. Basal inflammation in the demarcation zone was characterized by T-lymphocytes. We interpret this as indicating basal demarcation. According to our histological and immunohistological observations, "asphyxial infiltrates" are abortive forms of a placental (bacteriological) inflammation, possibly infective in origin. We do not consider asphyxial infiltration to be a separate entity with its own causal pathogenesis.

Considering the causal association of silent intrauterine infection and prematurity we investigated the possible effect of adjuvant antibiotic treatment of women with preterm labour on the appearance of inflammatory placental lesions. 140 patients with preterm labour in the 30 + 2 week of gestation (median; range: 17 + 2-34 + 6) without premature rupture of the membranes and detection of facultative-pathogenic micro-organisms in the vagina and/or in the canal of the cervix were enrolled in the study. 74 women were treated vaginally (polyvidone-iodine) in addition to intravenous tocolysis, 66 women were given ampicillin, cefotiam or erythromycin intravenously. After delivery the placentas were examined histologically and the frequency of inflammatory lesions was evaluated by use of 4 scores of classification. For statistical analysis the Fisher Exact- and the Wilcoxon Rank Sum Test were used. We found no differences concerning amnamnestic and perinatal parameters comparing the 2 groups of patients. With only one of the histological scores used (according to Salafia et al. [18]) we found a higher frequency of inflammatory placental lesion in the antibiotic treated group (12/66) in comparison to the vaginal treated group (4/74). Fifty patients of the antibiotics' group received the antibiotic during the last 10 days before birth. No differences in the frequency of inflammatory placental lesions were detectable in these patients when compared with the local treated group. However, we found a lower prolongation of gestation (calculated from the day of admission to the day of delivery, median: 7; range: 1-92 days) and a lower gestational age at delivery (median: 33 + 0; range: 22 + 2-39 + 6 weeks) in the patients receiving antibiotics during the last 10 days before birth in comparison to the local treated women (22; 1-138 days and 35 + 0; 23 + 4-41 + 5 weeks, respectively). There is the same incidence of inflammatory placental lesions in patients with preterm labour and facultative-pathogenic micro-organisms in the vagina and/or in the canal of the cervix who received adjuvant antibiotic treatment during pregnancy compared with patients who were treated vaginally with polyvidone-iodine.

An account is given of morphological issues relating to placental insufficiency. Variable manifestations of placental insufficiency in foetuses and newborns are described in some detail. Reference is made to morphological clues useful in diagnosing causes of placental insufficiency. It proved to be particularly difficult to find quantitatively recordable parameters for such diagnosis, comparable to morphological indicators resulting from various placental measurements or from determination of exchange area and thickness measurement of placental basal membranes. Most of these quantitative methods, after all, would not even be applicable to routine examination. All the other diagnostic criteria of placental insufficiency are part of obstetrics (placental hormone production, measurement of uterus circulation and of intervillous space). In a more specialized section of this paper, reference is made to various pathologico-anatomic patterns of placental disorders and their specific relevance to placental insufficiency. Circulatory disorders (maternal side), placental inflammation, impaired maturation and obliterative endarteriitis were the most common findings in this order.

Superinfected subchorionic haematomas are a rare septic focus in the 2nd trimenon. Symptoms being unspecific, the diagnosis has to be made by exclusion, in most cases. As the changes of a successful treatment of the manifest infection is poor, antibiotic prophylaxis as well as close laboratory controls and early antibiotic therapy should be discussed after sonographic diagnosis of an intrauterine haematoma. Two of our three patients reported on having suffered a miscarriage; only one pregnancy could be maintained after spontaneous depletion of the infected haemorrhage.

Benign and malignant tumours of the umbilical cord and placenta are the topics covered in Part XII of this general account under the above heading. Angiomas, angiofibromas and teratomas, all of them of rare occurrence, are the benign tumours, with the chorioangioma being the best known of them. The trophoblast tumours proper include chorionic epitheliomas and choriocarcinomas. While histological differentiation is not possible between these two, they still are biologically benign or malignant. They may develop in the wake of normal pregnancy or abortion or hydatidiform mole. Southeast Asia is a geographically preferred region for hydatidiform mole and chorionic epithelioma. Differentiated growth behaviours of trophoblast tumours are attributable to immunological aspects. It is certainly a rare event to have a high degree of tissue compatibility (HLA antigens) between tumour and maternal organism. This may at least offer an explanation for the low incidence of choriocarcinomas in the northern hemisphere. In Southeast Asia, efforts should be made to clear up the causative background of high incidence of hydatidiform mole, since the latter most probably is the basis for development of choriocarcinoma.

868 parturitions were examined to determine the relation between the clinical mastitis around partition and the loosening process of the placenta in the bovine. The occurrence of mastitis in heifers and cows around parturition was 18.7%. The frequency of retained placenta in animals with mastitis was significantly higher (p less than 0.01) than that in animals without mastitis influenced the loosening process of the afterbirth. The results support an hypothesis, that mastitis and retentio secundinarum can regard as signs of the decrease in the activity of the immune system.

Part X of this review is devoted to the remaining pathologico-anatomic patterns which are associated with regressive alterations. Increased syncytial proliferation is the most important aspect within that complex, since it may be a consequence of intervillous and intravillous hypoxia and may thus provide a clue to effects of that kind. Placental calcification may be subdivided by two major groups. The first is relating to "dystrophic" calcification following the same rules in the placenta as it does in other places, in other words, it is calcification of necrotic tissue portions or acidotic areas of decreased circulation. Calcification may just as well occur to particular structures of the placenta, such as the epithelial basal membrane, syncytial proliferations or in walls of vessels. Placental cysts usually are localized at the placental base (in septa), their development being owed to hypoxic events during ontogenesis. They actually are pseudocysts. Placental icterus (along with severe maternal icterus) is macroscopically identifiable with unambiguity. The biliary pigment, histologically, is localized in HOFBAUER cells. Additional reference is made to melanin deposits (in concomitance with congenital giant naevus) and placental alterations in conjunction with rare metabolic disorders.

Intra-uterine fetal death along with discontinuation of fetal circulation is followed by intraplacental processes which result in the following pathologico-anatomic pattern: Fetal vessels in terminal villi are doomed to collapse, with the major arteries being occluded due to proliferation. This is followed by substantial proliferation of connective tissue in peripheral villi, and by total disappearance of capillaries in terminal villi. Possible remnants of cytotrophoblast are lost from trophoblast epithelium, with the syncytiotrophoblast undergoing proliferation. Multiple syncytial proliferations were recorded from cases in which some time had passed from the event of intra-uterine fetal death. Stromal fibrosis is introduced by transient activation of mesenchyma of the terminal villi. Complete regression with totally fibrosed (collagenized) villi, vascular occlusion of stem villi, numerous spots of syncytial proliferation, and increased deposition of intervillous fibrin ist the morphological equivalent of missed abortion. Stromal fibrosis of terminal villi is a consequence of regression after intra-uterine fetal death or may possibly result from impairment of placental circulation of different causative background. Certain forms of fibrosis may possibly develop via stromatic edema (e.g. diabetes mellitus, blood group incompatibility, immunological disorders) together with edema-activated mesenchymal proliferation. Edema of villous stroma may be of diffuse or focal manifestation in the terminal villi and in advanced cases may affect all parts of the placenta. It is usually linked to diseases in which the entire fetoplacental unit is prone to edematization (maternal diabetes mellitus). Severe stromatic edema leads to formation of so-called stromatic ducts in which edema liquid is accumulated but is incapable of flowing out for absence of lymphatic drainage of the placenta.

A four year old cow with an enlargement of the uterus of unknown cause was submitted to the clinic. The cow had a pyonecrotizing myometritis and placental retention following an injury of the birth canal. The final diagnosis was only made after pathological examination.

Thus far ten patients with connatal neuroblastoma and metastases in the placenta have been reported. Our patient suffered from neuroblastoma stage IV-S and expired on the first day of life due to hepatic failure from massive metastatic involvement of this organ. Metastases from the placenta into the mother have thus far never occurred, neither in our case nor in any patient reported in the literature.

Disorders of intervillous circulation are covered in this sixth part of the account of Pathology of the Placenta. Proposed in this paper are a new setup and modified nomenclature in which the term of "infarction" is definitely abandoned, as there can be neither genuinely anaemic nor haemorrhagic infarction in the placenta. Alterations which we consider as a formally pathogenetic chain are discussed by the order of focus of villous collapse, reticular intervillous fibrin deposition, and chronic disorder of intervillous circulation. These should be distinguished from subchorionic fibrin deposition, a special case of chronic circulatory disorder. Reference is finally made to intervillous haemorrhage and retroplacental haemorrhage (premature detachment of the placenta). An attempt is made, in conclusion, to give an account of the causative genesis of impairment to intervillous circulation together with various pathologic-anatomic findings recordable from myometrial and decidual arteries.

Discussed are circulatory disorders as well as pathologico-anatomic findings recordable from fetal vessels of the placenta. Thorough reference is first made to obliterative endoarteritis of the greater arteries. Its forms are described, with formal and causative pathogenesis being discussed. Conclusive coverage of causative pathogenesis has proved to be possible only for unambiguously determined inflammatory manifestations (rubella, lues). The second major complex covers alterations to greater and minor fetal vessels which are characterized by central parietal thrombosis (possibly associated with fetal asphyxia) and peripherally disseminated intravasal coagulation (associated with peripartal shock or other conditions). Included in the latter group of alterations are congenital pulmonary hyaline membranes (perhaps also some membranes of postnatal origin) which are, as well, considered as shock equivalent.

A general account of routes of infection is followed by reference to localisations of placental infection. The most common routes of infection are transmembrane, transdecidual, haematogenico-maternal, and haematogenico-foetal. Intra-uterine infections with placental involvement may be caused by several types of pathogens, with particular reference being made to listeriosis, tuberculosis, and lues, while virus infections may be associated with rubella and cytomegaly and protozoonosis with toxoplasmosis. Unambiguous morphological traces are left in the placenta merely by few of these "specific" infections. A possible pathogen, therefore, can be rarely concluded from the type of inflammatory placental involvement. Reference is also made to "villitis of unknown aetiology", an aetiologically obscure, probably haematogenico-maternal infection of the placenta. Introduction of this term to histological routine diagnosis is recommended. This account of placental inflammation is completed by explanations on relationships between inflammation and impaired maturation of the placenta as well as between inflammation and intervillous fibrin deposition or chronic disorders of intervillous circulation.

In Part IV of this review of placental pathology, reference is made to impaired maturation of the placenta under special clinical conditions. Foetal erythroblastosis is only of minor importance, in that context, today, while similar placental alterations may result from foetal hydrops of different genesis, including immunological causes. A detailed account is given of diabetic impairment of maturation together with possible placental diagnosis of diabetes. Cases of diabetes mellitus with concomitant EPH gestosis were found to be more strongly determined for placental differentiation by EPH gestosis. Reference, finally, is made to disturbed placental differentiation under conditions of EPH gestosis with or without concomitant impairment of intervillous circulation.

Chorioangiomas are relatively frequent, benign and highly vasculated tumours of the placenta. In a few rare cases they show an excessive growth. Placental necrosis, preterm delivery and foetal asphyxia are well-known complications. Another severe complication is maternal thrombocytopenia, leading to serious thrombopathia. In cases with unfavourable examination conditions, it may be difficult to distinguish ultrasonographically between a chorioangioma and foetal elements. In our case, final diagnosis of a 10 by 9 cm chorioangioma became possible by the use of Doppler ultrasound. Arterial and venous signals were seen all over the tumour. During the following period of observation, the tumour did not grow and pregnancy was uneventful. Diagnosis of chorioangiomas should be made as early as possible to enable the obstetrician to adjust the management of pregnancy to complications that can be expected.

If a severe uterine inflammation is diagnosed 15 days post partum in a cow with retained placenta by clinical examination, it has to be assumed that this inflammation was already manifest two days before (in the discussed case at the time of purchase). By an external examination of the animal this genital inflammation cannot be seen, if there is no vaginal discharge or dried uterine fluids at the tail and around the vulva. The inflammation is the consequence of the placental retention, even if there has been veterinary assistance (manual removal of the retained placenta, antibiotic treatment of the uterus) in time. After manual removal of the placenta, part of it is normally left in the tips of the uterine horns; they cannot be reached by the veterinarian's hand. Even by additional means - like application of oxytocin, lifting the abdomen of the cow with the aid of a plank or trying to invert the tip of the uterine horn - the fetal membranes cannot always be totally removed. The statement that the placenta has been totally removed, is correct only if the end of the chorionic membranes could be clearly identified. Each placental retention in cattle carries the risk of reduced fertility. If a cow is sold a few days post partum, this defect, which can reduce the animal's breeding value, may be unnoticed.

In cases with different umbilical cord anomalies the influence of foetoplacental resistance on the flow velocity wave forms is discussed. If there is no anastomosis between the two umbilical arteries, the end-diastolic flow velocities depend on the volume of the foetoplacental vessel tree, i.e. higher resistance indices (RI) are found in the arteria with the smaller placental area. If there is only one umbilical artery, the peripheral resistance is reduced to 50%, because the part of the placenta part belonging to this solitary umbilical artery is twofold compared to cases with two umbilical arteries. This leads to a higher perfusion pressure gradient with higher flow velocities and lower RI values, resulting in an underestimation of the foetoplacental resistance. In cases of thrombosis of chorionic membrane vessels or stem villi vessels, placental regions are excluded from the perfusion, followed by an increasing foetoplacental resistance in the same manner as it happens in slowly developing failures of villus maturation. This means that the presented cases of umbilical cord anomalies and function disorders of allantois vessels can be interpreted as an in-vivo model to show pressure and resistance parameters in foetoplacental circulation.

Normal maturation of the placenta (signs of maturation) and disorders in maturation are covered in the third part of this account of placental pathology. Impairment of maturation should be related to pregnancy age and intrauterine fetal development. A historic account is given of various classifications so far applied to impaired placental maturation, and a new setup is recommended for introduction to routine diagnosis.

In a prospective study we performed a breast-stimulation-test (BST) in 136 patients. Sufficient contractions could be achieved in 89.7%. A hyperstimulation was seen in 5.8% of the patients. We could not find a false negative BST-result. The duration of the BST was significantly shorter compared to the OBT. The new noninvasive method was well accepted by patients and staff-members, leading to a new management of fetal surveillance in patients beyond 40 weeks of pregnancy.

Results of DHAS-tests are calculated according to 4 methods (recovery of injected DHAS as total oestrogens measured in 24 hour urine specimens; changes of oestrogen excretion peaks measured in two hour intervals; recovery of injected DHAS as total oestrogens measured in 2 hour urine specimens; classification according to a scheme of oestrogen excretion pattern measured in two hour intervals). The results are critically compared with the general development of pregnancy and with the condition of the newborn. The discrepancies observed show that the DHAS-test is of little practical value.

The ante partum FHR-pattern of a 26 years old primigravida with signs of umbilical cord compression combined with placental insufficiency is presented and discussed. The difficulty in interpreting the CTG-tracings in this special case is stressed.

After the explosion accident on July 10, 1976 in Seveso (Italy), material from 30 interrupted pregnancies and from 4 spontaneous abortions was investigated by embryological and histomorphological studies. No indications of mutagenic, teratogenic or fetotoxic effects of TCDD could be found. The cases of spontaneous abortion, albeit more suspect for dioxin damage, showed different morphological alterations obviously due to a variety of causative factors independent of TCDD. On the other hand it is not possible to exclude entirely an embryotoxic effect of TCDD because in the majority of cases the fetal tissues were incomplete.