AIMS: Following intrauterine fetal death (IUFD), the placental fetal vessels undergo regressive changes. These changes are virtually indistinguishable from lesions that are the result of fetal vascular thrombosis (FVT). This study investigated the relation between these lesions and maternal thrombophilia. METHODS: Placenta slides of 65 IUFDs with known maternal thrombophilia test results (compound MTHFR C677T and A1298C heterozygosity, n = 10; MTHFR 677TT homozygosity, n = 3; protein S deficiency, n = 0; factor V Leiden mutation, n = 2; prothrombin gene mutation G20210A, n = 1; lupus anticoagulant, n = 2; antiphospholipid syndrome, n = 1; MTHFR C677T heterozygosity, n = 5; MTHFR A1298C heterozygosity, n = 4; and MTHFR 1298CC homozygosity, n = 2) and of 30 livebirths with positive maternal thrombophilia test results (n = 5, 2, 0, 9, 2, 0, 2, 7, 2 and 1, respectively, for those thrombophilias) were microscopically examined for septation, fetal vessel thrombosis, intimal fibrin cushions, avascular villi, haemorrhagic endovasculitis and fibromuscular sclerosis. RESULTS: Thirty of the 65 IUFDs had a positive maternal thrombophilia test; 22 of these 30 had FVT lesions. Thirty two of the 35 IUFDs with a negative maternal thrombophilia test had FVT lesions. Septation, defined as multiple lumens or 'recanalisation' in a placental vessel, was the lesion seen most often in IUFD (n = 41) whether by itself (n = 13) or in combination with other FVT lesions. Five of the 30 livebirths had FVT lesions but septation was not seen in any of the placentas from the 30 livebirths. FVT lesions did not have a significant relation with maternal thrombophilia. CONCLUSIONS: The finding of fetal vascular thrombosis lesions in stillbirths does not imply thrombophilia as the cause of the fetal death. Factors other than thrombophilia may play a role in the cause of FVT lesions.
AIMS: Following intrauterine fetal death (IUFD), the placental fetal vessels undergo regressive changes. These changes are virtually indistinguishable from lesions that are the result of fetal vascular thrombosis (FVT). This study investigated the relation between these lesions and maternal thrombophilia. METHODS: Placenta slides of 65 IUFDs with known maternal thrombophilia test results (compound MTHFRC677T and A1298C heterozygosity, n = 10; MTHFR 677TT homozygosity, n = 3; protein S deficiency, n = 0; factor V Leiden mutation, n = 2; prothrombin gene mutation G20210A, n = 1; lupus anticoagulant, n = 2; antiphospholipid syndrome, n = 1; MTHFRC677T heterozygosity, n = 5; MTHFRA1298C heterozygosity, n = 4; and MTHFR 1298CC homozygosity, n = 2) and of 30 livebirths with positive maternal thrombophilia test results (n = 5, 2, 0, 9, 2, 0, 2, 7, 2 and 1, respectively, for those thrombophilias) were microscopically examined for septation, fetal vessel thrombosis, intimal fibrin cushions, avascular villi, haemorrhagic endovasculitis and fibromuscular sclerosis. RESULTS: Thirty of the 65 IUFDs had a positive maternal thrombophilia test; 22 of these 30 had FVT lesions. Thirty two of the 35 IUFDs with a negative maternal thrombophilia test had FVT lesions. Septation, defined as multiple lumens or 'recanalisation' in a placental vessel, was the lesion seen most often in IUFD (n = 41) whether by itself (n = 13) or in combination with other FVT lesions. Five of the 30 livebirths had FVT lesions but septation was not seen in any of the placentas from the 30 livebirths. FVT lesions did not have a significant relation with maternal thrombophilia. CONCLUSIONS: The finding of fetal vascular thrombosis lesions in stillbirths does not imply thrombophilia as the cause of the fetal death. Factors other than thrombophilia may play a role in the cause of FVT lesions.