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January 10, 2011

There was a recent string on the SPP list server about the pathology of placenta accrete and its possible relationship to uterine atony. Several good ideas are there, but below are some additional comments. The first is mine in response to an e-mail.



There is a literature of studies trying to understand the pathology of accrete such as Placenta 29:639-645 (the list of controls included uterine atony which might be debatable as a control) and Dr. Yee Khong has also written about it, Placenta 8:399-409 and Obstet Gynecol 82:17-22.  The relationship of uterine atony to accreta is an interesting question. I am not sure if I understand David’s distinction on percreta. I had sort of agreed with those who felt percreta was an accident of the thinned lower uterine segment especially with C section scar. There probably is some room for rethinking the problem. What exactly does the healed C section look like in ordinary hysterectomy. What allows the uterus to remain contracted for so long after delivery, is it just the loss of intrauterine volume and a natural tone or is there an active mechanism. What is the role of all the mast cells in the myometrium? Is there permanent thrombosis in the arterial tree of the placenta bed within a reasonable time after delivery, or is sustained contraction the only significant mechanism? If increased trophoblastic invasive cells stop uterine contraction do they do it mechanically or chemically? How fast do myometrial cells return to their prelabor phenotype, that is loose gap junctions, oxytocin receptors etc? In placenta creta, is there always a preexisting abnormality of the decidua?


The following are some comments by Dr. Stewart Cramer at Rochester General Hospital


1. I had so much trouble seeing villi in contact with myometrium that for decades I have been doing keratin and actin immunostains on all the incretas. Never once did I see a case where villi were not preceded into the myometrium by nonvillous trophoblast. So I long ago ceased to believe that villi invade myometrium.


2.In my teaching of OB residents about placentation, I used to tell them that the trophoblastic shell gives rise to nonvillous trophhoblast on one side, and villous trophoblast on the other. I had a nice case showing this, but the flash drive with this photo died and I didn't have backup, unfortunately.

    The nonvillous trophoblast is interstitial (to anchor the placenta to the wall), and endovascular (to redirect blood flow into the intervillous space).

    The villous trophoblast is for gas exchange and nutrient exchange.

        In my experience, the relationship of nonvillous trophoblast to villous trophoblast in placenta increta is the same as in normal placentas. So Increta is a disease of NONVILLOUS trophoblast, in my opinion.


3. An old paper in Lab Investigation showed that decidua makes massive amounts of basement membranes proteins. And of course placentas have collagenases, etc. So I have always thought of increta in terms of a balance of collagenases,etc. vs. decidual basement membrane proteins as a barrier to life-threatening invasion of interstitial nonvillous trophoblast. 


4.  One more turn of that screw is that the body has natural inhibitors (a la anti-trypsin deficiency) to collagenases, etc.. So a mutation analagous to A1AT deficiency might coneivably tip the balance so as to promote increta. I once actually advocated investigation of this idea in the literature, many years ago. As far as I know, this has been pretty much ignored, although Benirschke cited the idea in order to dismiss it.


5. I have multiple gross photos showing that incretas and even accretas can do their morbid adherence all the way up to the fundus, so I have serious doubts about the focal decidual deficency idea as it relates to previa and prior C-sections. Those may be predisposing factors, but I think the problem is inherent in the nonvillous trophoblast itself.


6. I can pick up a uterus off the dissecting table by pulling up on the membranes with a forceps in both accreta and increta cases. I'd call that pretty darn morbid adherence. When I see this grossly, I diagnose chorion accreta, although I am not aware that such an entity is in the textbooks. One look at my gross photo and my clinicians don't need a textbook or literature reference to believe that the membranes are morbidly adherent as well as the placenta.


7. I have a couple of cases where the radiologist diagnosed accreta, and the gynecoligst did a hysterectomy rather than try to remove the placenta. My assignment at Ob Grand Rounds was to show the pathology which correlated with what the sonographer saw. I am not aware that any of the standard texts actually discusses this radiologic-pathologic correlation in accreta and increta. My own effort to do that leads to very different ideas than what I have read or heard from others.


The following comments are from Dr. David Gryspan.


Let me deconstruct the definition of accreta on the basis of the fact that the described pathology (abutment of placental basal plate on myometrium) doesn’t fully explain the clinical presentation – for as you say- even once the palcenta accrete is delivered  bleeding may persist.


Thus, whereas percreta is an anatomical problem essentially defined by the absence of formation of a basal plate and thus intrusion of chorionic villi as far as there is (blood filled) space, accreta is more elusive. Let’s become semantically liberal and for an instant say that Accreta is a more of a clinical problem with two commonalities: 1) An overly adherent placenta-that after separation has only relatively subtle abnormality and 2) (sometimes) post-partum bleeding. In percreta the hysterectomy is anticipated; in accrete it is often precipitous. And in the latter the pathologist is occasionally left to attempt to find anatomical justification for a momentous clinical decision with the challenge that the dramatic clinical presentation (severe post-partum bleeding) is accompanied by relatively subtle histology. This problem was reflected in one of the posted comments and I think it may be under-appreciated in clinical medicine.

I just reviewed with a colleague in our archival cases one accreta and one case of hysterectomy done in second trimester for cervical carcinoma- as a control for “normal” implantation. In the ”normal”  there was some invasion of intermediate trophoblast into the superficial myometrium (under the decidua) but it was relatively limited whereas in the accreta case besides the mutli-focal direct appostion of basal plate on myometrium without intervening decidua there was relatively extensive invasion of intermediate trophoblast into the superficial myomterium with a concomitant remodeling effect that suggested to my imagination why bleeding couldn’t be stopped (but I am biased). To me this raises the possibility that some cases variably diagnosed as  uterine atony, post-partum hemorrhage, delayed placental separation and accreta may all be part of a similar spectrum where the placenta pathology per-se doesn’t hold the full answer for the uterine bleeding but the underlying uterus might; however, even those features may be subtle.


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