Placenta accreta occurs when all or part of the placenta attaches abnormally to the myometrium (the muscular layer of the uterine wall). Three grades of abnormal placental attachment are defined according to the depth of attachment and invasion into the muscular layers of the uterus:

Accreta – chorionic villi attached to the myometrium, rather than being restricted within the decidua basalis. Increta – chorionic villi invaded into the myometrium. Percreta – chorionic villi invaded through the perimetrium (uterine serosa).Because of abnormal attachment to the myometrium, placenta accreta is associated with an increased risk of heavy bleeding at the time of attempted vaginal delivery. The need for transfusion of blood products is frequent, and surgical removal of the uterus (hysterectomy) is sometimes required to control life-threatening bleeding.Rates of placenta accreta are increasing. As of 2016, placenta accreta affects an estimated 1 in 272 pregnancies. Risk factors
An important risk factor for placenta accreta is placenta previa in the presence of a uterine scar. Placenta previa is an independent risk factor for placenta accreta. Additional reported risk factors for placenta accreta include maternal age and multiparity, other prior uterine surgery, prior uterine curettage, uterine irradiation, endometrial ablation, Asherman syndrome, uterine leiomyomata, uterine anomalies, and smoking. The condition is increased in incidence by the presence of scar tissue i.e. Ashermans syndrome usually from past uterine surgery, especially from a past dilation and curettage, (which is used for many indications including miscarriage, termination, and postpartum hemorrhage), myomectomy, or caesarean section.
Other commonly reported symptoms include anterior pituitary dysfunction, visual field defects, headache/pain, and ophthalmoplegia. Treatment
Treatment options depend on the type of tumor and on its size:

Prolactinomas are most often treated with cabergoline or bromocriptine (both dopamine agonists), which decrease tumor size as well as alleviates symptoms, followed by serial imaging to detect any increase in size. Treatment, where the tumor is large, can be with radiation therapy, proton therapy or surgery, and patients generally respond well. Unlike prolactinomas, thyrotrophic adenomas characteristically respond poorly to dopamine agonist treatment. Somatotrophic adenomas respond to octreotide or lanreotide, which are long-acting somatostatin analogs. These somatostatin receptor analogs inhibit secretion of growth hormone. They were found to be about 50–55% effective in reducing tumor mass and reducing growth hormone and insulin like growth factor 1 (IGF-1) levels in studies. The growth hormone receptor antagonist pegvisomant is also used in the treatment of somatotrophic adenomas. Pegvisomant blocks the action of growth hormone. It can either be used as monotherapy or combined with a somatostatin analog. Surgery is a common treatment for pituitary tumors. The normal approach is trans-sphenoidal adenectomy, which usually can remove the tumor without affecting the brain or optic nerves. Radiation is also used to treat pituitary adenomas. Examples include external beam or proton beam radiation therapy or stereotactic radiosurgery. External radiation of pituitary adenomas can arrest tumor growth for several years but pituitary failure develops within 10 years in most patients necessitating lifelong hormone replacement.