Today's post is written in response to the questions raised by the reader below...
Anonymous has left a new comment on your post "Hypoplastic Right Heart Syndrome (HRHS): A Reader'...":
Dear Dr T
I am 40 and pregnant for the 8th time. I have 2 kids both delivered by cesarean section and have had 3 D & C's, the most recent in March 2009. My second trimester blood work at 15 weeks for my current pregnancy showed elevated hCG (2.4MoM), AFP (2.4 MoM) and inhibin A (2.3MoM). Also uE3 (estriol) was 0.59 MoM. My first trimester blood work was normal (hCG 0.9MoM and PAPP-A 1.1MoM). Amniocentesis done at 17 weeks showed no fetal chromosome problems and fetal (amniotic fluid) AFP was 1.13 MoM (which is normal). I would like to know if I am at risk of placenta accreta or worse and how easy is it to diagnose this condition by ultrasound. I have my 20 week scan next week. I was told after the second trimester blood work that I may be at risk for growth restriction but no one has mentioned placenta accreta.
To M Dec 17: That is an excellent question! As we will discuss below, you are at increased risk for placenta accreta because of your multiple uterine procedures and the abnormalities of your midtrimester serum screening might just be a hint that such an abnormality of placentation has occurred.
The first question that should be addressed is what is a placenta accreta? To understand this requires a basic understanding of the uterine anatomy. The innermost lining of the uterus is called the endometrium. This is a thin layer of a variety of very hormonally responsive cells that grow, proliferate, and finally regress (resulting in a ‘period’ if a pregnancy does not occur) during the normal menstrual cycle. Under the influence of progesterone, following ovulation in the second half of the cycle, the endometrium becomes ‘decidualized’ in preparation for the reception of an early embryo if a pregnancy does occur. The embryo attaches to and burrows into the endometrium and almost immediately begins to produce the cells that will eventually become the placenta. These cells, called trophoblasts, spread out within the endometrium (but not through it) and also invade the portion of the maternal blood vessels (spiral arterioles) that are contained within the endometrium to form the large vascular bed containing mother’s blood that will eventually bathe the placental villi and supply nutritional needs to the baby.
Beneath the endometrium is the myometrium. The myometrium contains multiple thick layers of smooth muscle cells that give the uterus its ability to contract and makes up the bulk of the uterus. Outside the myometrium is another very thin layer of cells called the uterine serosa. This is contiguous with the peritoneal lining of the abdomen and isolates the uterus from other structures within the abdominal cavity. Under normal circumstances, as the placenta develops, it grows only within the endometrium and is clearly separated from the myometrium by a structure called Nitabuch’s layer and the deepest layer of the endometrium called the decidua basalis. This separation is important, because under normal circumstances, after the birth of the baby, the placenta cleanly separates from the endometrium at this level and the maternal blood vessels that have been invaded by the trophoblasts within the endometrium rapidly contract, controlling maternal hemorrhage from the placental bed. A placenta accreta occurs when the placenta grows beneath where Nitabuch’s layer and the decidua basalis should be, anchoring the placenta to the myometrium from which it cannot readily separate following the delivery of the baby. Deeper invasion into the myometrium is called a placenta increta and if the placenta invades all the way through the uterus and the serosa, this is termed a placenta percreta. Placenta accreta occurs in about 75%-80% of such cases, placenta increta in about 15%, and placenta percreta in about 5%.
There are several mechanisms one might imagine that could lead to the development of a placenta accreta in an otherwise normal pregnancy. For example, the placental trophoblasts might not be able to respond to the normal signals that limit their growth and invasiveness and/or the maternal immune system might not be able to generate the appropriate signals. However, more often, it appears that defects in the endometrium, areas in which the endometrium has been damaged, attenuated, scarred, or denuded, placing the trophoblasts in close or direct contact with tissue layers not ordinarily ‘equipped’ to limit trophoblast invasiveness, are the primary reason placenta accreta, increta, and percreta occur. Such endometrial defects are usually the consequence of a variety of uterine operative procedures including D&Cs, myomectomies, extensive surgery for endometriosis, removal/correction of congenital uterine abnormalities (Mullerian abnormalities) such as septums, and endometrial ablation, or as the result of Asherman’s syndrome. Higher parity and advanced maternal age are also associated with increased risk for placenta accreta. In recent years, cesarean section has come to the fore as the primary factor contributing to the development of placenta accreta. Indeed, there is a clear association between previous cesarean section, a placenta previa, and the risk for a placenta accreta. Almost 25 years ago, Clark and colleagues (Obstet Gynecol 1985;66:89-92) showed that the risk of a placenta previa increases with the number of previous cesarean deliveries and that women who had four or more cesareans had a risk as high as 67% for a placenta accreta.
Accompanying placenta accreta are risks for both the mother and baby during pregnancy and at delivery. Placenta accreta is associated with bleeding, usually in third trimester, premature delivery, premature rupture of membranes, and necessity for cesarean delivery. Severe hemorrhage can occur as well as uterine rupture prior to the onset of labor, resulting in risk for fetal and maternal death. Obviously, severe hemorrhage can also occur at the time of delivery, requiring transfusion with blood products and even hysterectomy. If the placenta has invaded through the uterine wall (placenta percreta) into adjacent structures such as the bladder, bowel, or the broad ligament in which the major blood vessels supplying the uterus are enclosed, this can be an extremely challenging surgical procedure, especially if there is extensive intraperitoneal scarring from previous cesarean sections.
Sometimes the diagnosis of placenta accreta is very easy to make, especially when the placenta is overlying a previous uterine scar in the lower segment, there is not a clear separation between placenta and the myometrium (uterine muscle) and there is evidence of infiltration, into or through, the uterine muscle seen by ultrasound (Lerner, et al., Ultrasound Obstet Gynecol 1995;5:198-201). More often it is not a simple diagnosis. Only a small portion of the placenta might be involved or the myometrial invasion is on the lateral or posterior uterine walls. Efforts have been made to employ MRI to help sort out the suspected diagnosis (Palacios, et al., Acta Obstet Gynecol Scand 2005;84:716-724). This is safe enough in pregnancy and can be very helpful at times. Furthermore, unexplained elevations in the serum analytes (MSAFP and hCG) in midtrimester (the question raised by our reader) can sometimes be a hint that an accreta has occurred (Hung, et al., Obstet Gynecol. 1999;93:545-50).
Review of the management options for placenta accreta is beyond the scope of today’s discussion but perhaps can be the topic for another post in the future. However, the importance of maintaining a low threshold for suspicion in patients who have the risk factors noted above, taking steps to establish the diagnosis, and careful preparation for delivery if a placenta accreta is suspected cannot be underestimated to minimize morbidity and to optimize maternal and fetal outcome.