The fetal prognosis is worse than the maternal prognosis; approximately 12% of fetuses affected by placental abruption die. 77% of fetuses that die from placental abruption die before birth; the remainder die due to complications of preterm birth.Without any form of medical intervention, as often happens in many parts of the world, placental abruption has a high maternal mortality rate. Mother
A large loss of blood may require a blood transfusion. If the mothers blood loss cannot be controlled, an emergency hysterectomy may become necessary. The uterus may not contract properly after delivery so the mother may need medication to help her uterus contract. The mother may develop a blood clotting disorder, disseminated intravascular coagulation. A severe case of shock may affect other organs, such as the liver, kidney, and pituitary gland. Diffuse cortical necrosis in the kidney is a serious and often fatal complication. Placental abruption may cause bleeding through the uterine muscle and into the mothers abdominal cavity, a condition called Couvelaire uterus. Maternal death. Baby
The baby may be born at a low birthweight. Preterm delivery (prior to 37 weeks gestation). The baby may be deprived of oxygen and thus develop asphyxia. Placental abruption may also result in death of the baby, or stillbirth. The newborn infant may have learning issues at later development stages, often requiring professional pedagogical aid. Epidemiology
Placental abruption occurs in approximately 0.2–1% of all pregnancies.
Fibrosis, also known as fibrotic scarring, is a pathological wound healing in which connective tissue replaces normal parenchymal tissue to the extent that it goes unchecked, leading to considerable tissue remodelling and the formation of permanent scar tissue.Repeated injuries, chronic inflammation and repair are susceptible to fibrosis where an accidental excessive accumulation of extracellular matrix components, such as the collagen is produced by fibroblasts, leading to the formation of a permanent fibrotic scar.In response to injury, this is called scarring, and if fibrosis arises from a single cell line, this is called a fibroma. Physiologically, fibrosis acts to deposit connective tissue, which can interfere with or totally inhibit the normal architecture and function of the underlying organ or tissue. Fibrosis can be used to describe the pathological state of excess deposition of fibrous tissue, as well as the process of connective tissue deposition in healing. Defined by the pathological accumulation of extracellular matrix (ECM) proteins, fibrosis results in scarring and thickening of the affected tissue — it is in essence an exaggerated wound healing response which interferes with normal organ function. Physiology
Fibrosis is similar to the process of scarring, in that both involve stimulated fibroblasts laying down connective tissue, including collagen and glycosaminoglycans. The process is initiated when immune cells such as macrophages release soluble factors that stimulate fibroblasts. The most well characterized pro-fibrotic mediator is TGF beta, which is released by macrophages as well as any damaged tissue between surfaces called interstitium.