Clinical Significance and Treatment of Massive Intervillous Fibrin Deposition Associated with Recurrent Fetal Growth Retardation

Abstract

Retrospective examinations of 8,139 placentae were performed to clarify the relationship between placental disorders with massive intervillous fibrin deposition (MIFD) and intrauterine growth retardation (IUGR). Although the incidence of MIFD was low (0.4%), the small-for-date (SFD) birth rate in the MIFD group was significantly higher than that in the control group (62.9 vs. 8.3%; p < 0.001). Seventeen of 35 patients in the MIFD group had no clinical complications. MIFD itself was thought to be the main cause of IUGR in these patients. 78.4% of multiparae in the MIFD group gave unsuccessful obstetrical histories such as intrauterine fetal death and fetal growth retardation. Four of 6 patients with a history of MIFD and SFD delivery in a previous pregnancy repeated the same episode. These data indicate the MIFD recurrence rate in subsequent pregnancies must be high. Patients with a history of both SFD delivery and MIFD in previous pregnancies were defined as high-risk patients and they were given orally 30 mg of aspirin and 150 mg of dipyridamole daily and/or daily intravenous injection of 10,000 IU heparin during pregnancy. As a result, MIFD did not recur in all cases of the treated group and 87.5% (7/8) of the treated group could deliver approximate-for-date infants compared with 33.3% (2/6) of the untreated group (p < 0.05). These results indicate that anticoagulant and antiplatelet therapies are extremely effective for prevention of MIFD and IUGR due to MIFD.

Perinatal outcome of placental massive perivillous fibrin deposition: a case–control study

“…This strong association has already been stressed, with growth restriction rates ranging from 31% to 100%, depending on the author. [2][3][4][5][6]12 Some portion of these variations may be explained by the different curves and cut off points used. The cases of growth restriction observed in our series were mainly vascular placental, because 60% of them had abnormal umbilical artery Doppler spectra, including more than 15% with reverse flow or absent diastole.…”

“…The risk of recurrence is high in the first-trimester abortion, but it seems to be lower when MFD is observed in second-trimester or third-trimester placentas, at around 14%. [2][3][4][5][6][7] The absence of studies comparing these cases with a control population has prevented the formal establishment of a relation between these lesions and the clinical manifestations observed. To improve knowledge of the clinical consequences associated with MFD and to determine if outcome differs according to the extent of fibrin deposition, we conducted a retrospective comparative clinicopathologic study.…”

A mouse model of spontaneous preterm birth based on the genetic ablation of biglycan and decorin

“…The placentae of infants with in utero growth restriction display decreased biglycan and decorin as well as thrombosis (Murthi et al 2010, Swan et al 2010, Fuke et al 1994), while the glycosaminoglycan chains on biglycan and decorin display anticoagulant activity (He et al 2008). Thus, the absence of biglycan and decorin in the placenta may lead to thrombosis and fibrosis of the placenta with subsequent in utero growth restriction.…”

Diverse Placental Pathologies as the Main Causes of Fetal Death

“…Occurrence of fetal thrombotic vasculopathy was 2.8% compared with 1% reported earlier 21 and 1.2% for maternal floor infarction/massive perivillous fibrin deposition compared with 0.4% earlier. 30 Although they are infrequent, identifying these placental pathologies as the origin of mechanism is clinically relevant because some of these may be associated with a high recurrence risk and some may be amenable to preventive therapies in the future. 31 Umbilical cord complications (5.2%) were observed mainly from mid-third trimester onward, with less fetal space in utero.…”