الفهرس 
Introduction
Lower Uterine SegmentOnly 14 pages are availabe for public view
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Abstract
The number of deliveries by Cesarean section has been increasing steadily worldwide in recent decades. Although it is often assumed that Cesarean section improves neonatal outcomes, there is no hard scientific evidence to support this view. The safety of Cesarean section, however, has increased owing to improvements in surgical and anesthetic techniques, increased safety of blood transfusion and routine use of antibiotics and thromboprophylaxis.
Cesarean section is also associated with long-term risks such as postoperative pelvic adhesions, uterine scar rupture, and placental complications such as placenta previa and accreta. The latter two complications are likely to be associated with the poor uterine scar healing following Cesarean sections. Uterine scar dehiscence may present as an acute event in the antenatal or intrapartum period, leading to significant fetal and maternal morbidity.
Gilliam et al., (2012) identified an increased risk of placenta previa with a history of Cesarean section. The consequences of abnormally adherent placenta are particularly severe, and they are responsible for 41–64% of all obstetric hysterectomies; 65% of these cases have a history of previous cesarean section. 80% of maternal deaths associated with placenta previa in the UK over the last 12 years occurred in women with a history of previous Cesarean section and abnormally adherent placenta. In recent years the first-trimester diagnosis of early pregnancy implantation into a deficient Cesarean section pregnancy’ has been used to describe this condition, which often leads to serious maternal morbidity due to severe hemorrhage. There is also evidence that viable Cesarean scar pregnancies have the potential to develop into placenta previa or accreta at term.
In summary, the incidence of placenta accreta has increased, probably explained by the increasing rate of CDs. This is concerning because current trends toward increased CDs, particularly cesarean on demand, may not take into account counseling gravid women regarding long-term consequences, including morbidity and even mortality, that may be associated with placenta accreta.
Placenta accreta occurs when the chorionic villi invade the myometrium abnormally. It is divided into three grades based on histopathology: placenta accreta (placenta accreta vera), where the chorionic villi are in contact with the myometrium, placenta increta where the chorionic villi invade the myometrium, and placenta percreta where the chorionic villi penetrate the uterine serosa.
Placenta accreta is important because of possible adverse complications: postpartum hemorrhage, sometimes necessitating hysterectomy and occasionally resulting in maternal death; retained placenta; uterine perforation; and recurrence in subsequent pregnancies. In placenta accreta, the placenta is abnormally adherent to the uterine wall in the absence of normal intervening decidua. Milder forms of placenta accreta often manifest clinically as retained placenta or require manual removal of the placenta. While severe cases can be diagnosed from hysterectomy specimen. It has been suggested that milder cases from deliveries not necessitating a hysterectomy also can be confirmed hiogically on placental examination by the finding of myometrial fibers in the basal plate.
Ultrasonography is the primary modality used for the evaluation of placenta accreta, with sensitivities ranging from 50% to 93%. A high-frequency transducer should be used via a transabdominal or translabial technique unless the patient has abnormal positioning of the placenta (previa), which may then necessitate a transvaginal examination. With the transabdominal technique, care should be taken to ensure that the bladder is full in order to have an appropriate acoustic window. With the transvaginal technique, the bladder should be left somewhat distended to evaluate the uterine bladder interface.
However, the sensitivity and specificity of transvaginal or transabdominal ultrasound and magnetic resonance imaging vary from 33% to 95% in different studies; they depend especially on placenta location. For these reasons, imaging should be considered only when placenta accreta is suspected for clinical reasons. It should be there systematically attempt to a careful and gentle intraoperative delivery of the placenta to confirm the diagnosis, even when placenta accreta is strongly suspected before labor.
Suspected placenta increta is the main indication for placental MRI.
Although the risk factors for placenta accreta are thus well established, the underlying mechanism leading to abnormal placental adhesions are less well understood, so the aim of work is to study the histopathological findings in placenta accreta using different histoplathological stains in the available CS hysterectomy specimen in a trial to investigate the possible pathogenesis of placenta accreta .This was performed at ECDU . Also to study the histological findings of the lower uterine segment in obstetric hysterectomy specimens for other cases rather than placenta accreta with or without cesarean delivery (CD) using different histological stains as a control.
In the current study it was found that:
Almost 50% of all cases were in 2012 and 2013 and the rest of cases from 2006 till 2010.
In current study 98% of all cases had at least one previous C.S which is a risk of placenta accreta.
The association of placenta previa and placenta accreta is well recognized as all cases had placenta previa.
In current study 54.4% cases had placenta previa centralis which is another risk of placenta accreta.
Advanced maternal age as the mean maternal age was 33years and grandmultiparity is a risk factor
In the current study history of dilatation and curettage was statistically significant (P-value <0.05)
In current study (71.7%) was diagnosed by ultrasound as adherent placenta where28.3% not diagnosed.
Sultanaet al., (2011) reported there are three variants of placenta accreta: 1) accreta: the placenta is attached to the myometrium 75%; 2) increta: the placenta extends into the myometrium 17%; and 3) percreta: the placenta extends through the entire myometrium and uterine serosa 7%.
While in the current study (10.8%) placenta previa, (28.3%) accreta, (54.4%)incerta, (6.5%)percreta.
Placenta increta and percreta were 61% as severe cases of adherent placenta (placenta accreta) usually need hysterectomy while milder degrees are usually treated conservatively.
In the current study the swirling pattern of myofiber disarray is best identified with the Masson trichrome stain with different degrees of fibrosis ranging from mild to severe.
(54.4%) of all cases are characterized by absence of decidua basalis which is statistically significant.
The abundant elastic fibers noted in all specimens stained with Orcein stain interpreted as indicative of abnormal wound healing as in figs( 30e ,30f ,31c ,31d ,32c, 33e, 36d, 37b, 37c ,37d ,39e ,40d ,41 c,41d ,41e, 42e).
Immunohistochemical findings that are coexpressed in vivo in the interstitial extra villous trophoblasts (iEVTs) penetrating beneath the basal plate in accreta, increta, and percreta cases as in figs (33a,33b, 34a,36a,40a) . The findings were suggestive of a striking similarity among accreta extra villous trophoblasts (EVTs)
In normal placentation, extravillous trophoblast invades the decidua controlled and converts the spiral arterioles of the endometrium to uteroplacental vessels.
Decidual tissue apparently limits placental growth. In placenta accreta normal decidua fails to form, most times locally because the subjacent endometrium is deficient and cannot decidualize. The trophoblast invades and penetrates into the myometrium.
In summary the possible pathogenesis of placenta accreta is almost due to previous uterine trauma (mostly CS) leads to either scaring or poor decidua. Scarring leads to hypoxia and EVT proliferation leading to increase VEGF and proteases leading to angiogenesis and degradation of exteracellular matrix respectively leading to trophoplastic invasion. Poor decidua or absent decidua leads to decrease tissue metalloproteinases and coagulation proteases this leads to decrease the protective mechanism of decidua against the expansine nature of EVT leading finally also to trophoplastic invasion.