<unk> ’s ability to cause<unk>  in utero stems from its ability to limit vitamin K activation.<unk>  binds to and blocks the enzyme Vitamin K epoxide reductase which is usually responsible for activating vitamin K during vitamin K recycling. Vitamin K, once activated, is able to add a carboxylic acid group to glutamate residues of certain proteins which assists in correct protein folding. Without active vitamin K, a fetus exposed to<unk>  is unable to produce large quantities of clotting and bone growth factors. Without vitamin K, clotting factors II, VII, IX and X are unable to be produced. Without these vital parts of the coagulation cascade a durable fibrin plug cannot form to block fluid escaping from damaged or permeable vasculature. Anemia is common in fetuses exposed to<unk>  as blood constantly seeps into the interstitial fluid or amniotic cavity. High doses of<unk>  and heavy bleeding lead to abortion and stillbirth. Osteocalcin is another protein dependent on vitamin K for correct folding and function. Osteocalcin is normally secreted by osteoblast cells and plays a role in aiding correct bone mineralization and bone maturation. In the presence of<unk>  and subsequent absence of vitamin K and active osteocalcin, bone mineralization and growth are stunted.
Fetal warfarin syndrome
Neonatal sepsis
Fetal hydantoin syndrome
Shaken baby syndrome
Neonatal stroke
Fetal trimethadione syndrome
Neonatal meningitis
Uremic fetor