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This study focused to investigate a possible association of extensive umbilical hypercoiling (displaying an umbilical coiling index [UCI] of at least 1.0 coils/cm), clinical outcome, and associated pathoanatomical placental lesions. Of the 771 singleton placentas from the second and third trimesters submitted for pathoanatomical evaluation, 15 cases (2%) displayed extensive hypercoiling. There was an association of excessive hypercoiling with hypotrophy of fetuses and children (11 cases) and fetal demise (12 cases). Thin cord syndrome and umbilical stricture were observed in 9 cases and 4 cases, respectively. Seven of the 15 cases with excessive umbilical hypercoiling showed increased placental fibrin deposition (47% of the cases with hypercoiling), in 4 cases sufficient for rendering the diagnosis of massive perivillous fibrin deposition. Signs of maternal vascular malperfusion (n = 6) and chorangiosis (n = 2) were also detected in cases with hypercoiling. Recurrence of excessive umbilical hypercoiling was observed in 2 families, suggesting a genetic predisposition for the development of this lesion. Extensive hypercoiling could be a hitherto underrecognized pathogenetic factor for the development of massive perivillous fibrin deposition. A high UCI measured in the second trimester by ultrasound may be predictive of fetal hypotrophy, and intensified fetal monitoring is warranted, particularly if there is a history of hypercoiling and adverse fetal outcome.

Massive perivillous fibrin deposition (MFD) is a morphologically defined severe placental lesion associated with perinatal morbidity and mortality. The etiology is unknown, and recurrence risk in subsequent pregnancies is assumed to be high. In most cases, a pathologic immune reaction is supposed to be responsible for the lesion. We report a case of a pregnant woman's suffering from hand, foot, and mouth disease in the 20th gestational week. Subsequently, MFD developed in the placenta and was followed by intrauterine growth restriction and stillbirth in the 29th gestational week. Enterovirus A with high homology to Coxsackievirus A16 was detected in the placenta by means of immunohistochemisty and reverse transcription polymerase chain reaction. This infection could be a rare cause of MFD and should be taken into consideration in the differential diagnosis of the individual etiology. Recurrence risk of virus-related MFD is expected to be lower than in MFD without infectious association.

Background: 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., Aim: 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., Material and Methods: A selective search of the literature was carried out and experiences from own diagnostic clientele are presented., Results and Discussion: 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.