The invisible killer: fetal vascular malperfusion in stillbirths without macroscopic cord abnormalities.

OBJECTIVE

The aim was to evaluate the association between fetal vascular malperfusion (FVM) and the umbilical cord characteristics in stillbirth. FVM is a category of placental lesions consistent with restriction/interruption of fetal blood flow, frequently associated with a "cord accident". In some stillbirths, gross umbilical cord abnormalities unravel at birth, helping to elucidate the cause of death; however, other cases do not show any structural alterations and therefore these cases do not have an obvious cause of death.

METHODS

Retrospective histopathological evaluation of singleton antepartum stillbirths affected by of FVM. Clinical and histopathological findings were compared among cases with or without gross umbilical cord abnormalities.

RESULTS

One hundred and three cases were evaluated. Forty-eight cases (48/103; 46.6%) of stillbirth with FVM showed gross umbilical cord abnormalities, whereas 55/103 cases (53.4%) did not show any gross anomalies. Clinical risk factors for stillbirth were equally distributed between cases. Notably, the main histological lesion observed in cases without gross umbilical cord abnormalities was fatal thrombosis of the fetal vessels along the cord-placental vascular tree. This finding implies that the absence of macroscopic cord anomalies is not a sufficient criterion to exclude reduction/interruption of fetal blood flow and cord accidents as a potential cause of stillbirth.

CONCLUSION

Knowing the cause of fetal death is paramount both for bereaved parents and clinicians, helping in stillbirth acceptance and future prevention strategies. Our findings show the occurrence of FVM in cases without macroscopic umbilical cord anomalies. Therefore, an in-depth placental histopathological examination is mandatory to unravel signs of fetal blood flow obstruction in cases in which umbilical cord looks grossly normal. This knowledge helps parents, and health care providers in the real identification of the pathogenesis of fetal death, as the first step for personalized future actions of stillbirth prevention.