Early diagnosis, meticulous pre-op prep, and definitive extirpative surgery are key.
Dr Lockwood, Editor-in-Chief, is Dean of the Morsani College of Medicine and Senior Vice President of USF Health, University of South Florida, Tampa.
I admit I am a bit of an adrenaline junkie and this may account for my fascination with what is now termed morbidly adherent placenta (MAP), formerly designated as placenta accreta, increta, and percreta. In accreta, the anchoring trophoblast attaches not to the decidua basalis but directly to the myometrium. In the case of placenta increta, trophoblasts penetrate into the myometrium, whereas in percreta, they penetrate through the myometrium to the serosa or adjacent organs.
During the course of my career I have seen massive intraperitoneal hemorrhage from placenta percreta at 14 weeks and yet nearly bloodless cesarean hysterectomies for the same diagnosis at 36 weeks. I have become convinced that early, accurate diagnosis, meticulous preoperative preparation, and definitive extirpative surgery are the keys to optimal outcomes.
One of the mainstays of my approach over the past 20 years has been the nearly universal use of intraoperative intermittent occlusion of the internal iliac arteries using balloon catheters placed preoperatively. However, recent studies have called into question the utility of this approach. In addition, there is growing evidence that conservative management is appropriate in select cases. Thus, while MAP has become an epidemic we are only now perfecting rational management strategies.
NEXT: Pathogenensis of MAP >>
Cesarean delivery (CD) and placenta previa are the primary risk factors for MAP. In a prospective cohort study of more than 30,000 women undergoing CD without labor by the National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network, women having ≥ 4 CDs had a 9- to 30-fold increased risk of placenta accreta and a 4- to 15-fold higher risk of hysterectomy.1 Indeed the risk of accreta increased from 0.03% in women without a placenta previa who were having their first CD to 67% among those with a previa having their fourth CD.
Because both conditions result in placentation at sites of reduced or absent decidua, the condition can be thought of as a disorder of impaired decidualization.
Decidualization of endometrial stromal cells occurs in response to rising luteal phase progesterone and persists throughout gestation. The decidua normally poses a barrier to excessive trophoblast invasion by limiting access to tropho-trophic hormones such as insulin growth factors and vascular endothelial growth factor, impeding trophoblast-associated proteolysis, and imposing a tenacious basement-like extracellular matrix.2,3
Equally important, the decidua creates a hemostatic milieu to prevent hemorrhage during placentation and following delivery by elaborating high levels of the primary initiator of clotting, tissue factor, and the primary inhibitor of fibrinolysis, type-1 plasminogen-activator inhibitor (PAI-1).3,4 Thus, the absence of decidua accounts for both the extraordinary trophoblastic invasiveness seen in MAP and the massive hemorrhage accompanying such deliveries.
As noted, one approach to prevention of potentially massive MAP-associated hemorrhage has been the use of prophylactic internal iliac artery balloon catheterization. The theory behind this intervention is that inflation of the balloon dramatically reduces uterine blood flow, allowing for less intraoperative blood loss, clearer operative fields, and easier, more expeditious surgery.
Tan and colleagues reported on 11 MAP patients who underwent CD after bilateral internal iliac artery occlusive balloon placement, comparing them to 14 MAP patients undergoing CD without such placement.5 They found that balloon catheters resulted in 40% less blood loss (2011 mL vs 3316 mL; P < 0.04), 52% less blood transfused (1058 mL vs 2211 mL; P = 0.005) and a shorter duration of surgery (P < 0.05). In contrast, neither Levin and colleagues nor Shrivastava and associates demonstrated reductions in blood loss, units transfused, or hospital stays with the use of prophylactic occlusive balloon catheters in such patients.6,7
Salim and colleagues recently reported on the first randomized clinical trial of preoperative prophylactic balloon catheters for women undergoing CD in the setting of MAP.8 In the intervention group, catheters were placed in the anterior division of the internal iliac arteries, while the control group received no catheters. The primary outcome was number of packed red blood cell (pRBC) units transfused. Patients were delivered at 34 to 35 weeks following administration of corticosteroids. Either cesarean hysterectomy (C-hys) or conservative management was offered, depending on intraoperative findings. Between 2009 and 2015, 13 women were randomized to the intervention group and 14 to the control group.
Among the former patients, MAP was confirmed in 12 patients and 6 (50%) underwent C-hys, while 12 control patients had a confirmed MAP and 7 (58%) underwent C-hys. Among intervention patients with confirmed MAP, an average of 5.6 pRBC units were transfused and 5259 mL of blood was lost. In contrast, control patients with confirmed MAP received 4.8 units of pRBCs and had 5296 mL of blood loss. Neither these findings nor any other perioperative outcome was statistically different between the 2 groups.
While the numbers of patients studied were small and the degree of MAP-associated pathology modest, as suggested by the relatively large number of patients conservatively managed, these findings certainly do not indicate an overwhelming and universal utility to preoperative prophylactic iliac artery balloon catheter placement.
Given the rapidly increasing prevalence of MAP, from 1 in 2000 deliveries in the 1980s to 1 in 500 today,9 efforts at preserving the uterus to permit additional childbearing have increased. Sentilhes and associates conducted a retrospective multicenter study of 167 conservatively managed patients with placenta accreta from 1993 to 2007 in 40 French university hospitals.10
Conservative treatment was successful in 78.4% (95% CI: 71.4–84.4%). Severe maternal morbidity occurred in 6.0% (95% CI: 2.9–10.7%), including one woman who died of myelosuppression and nephrotoxicity after intraumbilical methotrexate administration. Spontaneous placental resorption occurred in 75.0% of cases (95% CI: 66.1–82.6%), with a median delay from delivery of 13.5 weeks (range 4–60 weeks). While initial conservative management efforts were limited to placenta accreta, more recently this approach has been extended to cases of placenta percreta with less favorable results.
Clausen and colleagues recently reviewed 19 published cases of conservatively managed placenta percreta and reported that 58% of affected patients eventually required hysterectomy for delayed infection or hemorrhage.11
What then is the optimal management of patients with MAP? First, precision in diagnosis is crucial. Patients with prior CDs, particularly those with placenta previa, should be carefully evaluated for sonographic evidence of accreta. Magnetic resonance imaging can be employed to better define the extent of invasion.
The defect should be carefully mapped, not only to avoid disrupting the placenta during delivery, but to ascertain if it is likely to be so focal as to be amendable to en bloc wedge excision or more dispersed but still superficial enough to permit conservative management, leaving the placenta in situ in motivated, fully informed patients. In the latter cases, delayed hysteroscopic resection maybe an option12 but methotrexate should not be used. In all other cases the placenta should be left undisturbed, the cesarean incision repaired and an expeditious C-hys performed.
Preoperatively, establish 2 large-bore intravenous access points, employ pneumatic compression boots, ensure adequate quantities of readily available pRBCs, fresh frozen plasma, platelets, and cryoprecipitate, and have your team trained in implementing a massive hemorrhage protocol. Use of a cell saver seems reasonable, especially when the diagnosis is percreta. Finally, I would still recommend preoperative placement of prophylactic balloon catheters when there is a high degree of suspicion for percreta, especially involving adjacent organs.
1. Silver RM, Landon MB, Rouse DJ, et al; National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Maternal morbidity associated with multiple repeat cesarean deliveries. Obstet Gynecol. 2006;107(6):1226–1232.
2. Irwin JC, Giudice LC. Insulin-like growth factor binding protein-1 binds to placental cytotrophoblast alpha5beta1 integrin and inhibits cytotrophoblast invasion into decidualized endometrial stromal cultures. Growth Horm IGF Res. 1998;8(1):21–31.
3. Lockwood CJ, Krikun G, Caze R, et al. Decidual cell-expressed tissue factor in human pregnancy and its involvement in hemostasis and preeclampsia-related angiogenesis. Ann N Y Acad Sci. 2008;1127:67–72. Review.
4. Schatz F, Krikun G, Runic R, et al. Implications of decidualization-associated protease expression in implantation and menstruation. Semin Reprod Endocrinol. 1999;17(1):3-12.
5. Tan CH, Tay KH, Sheah K, et al. Perioperative endovascular internal iliac artery occlusion balloon placement in management of placenta accreta. AJR Am J Roentgenol. 2007;189(5):1158–1163.
6. Levine AB, Kuhlman K, Bonn J. Placenta accreta: comparison of cases managed with and without pelvic artery balloon catheters. J Matern Fetal Med. 1999;8(4):173–176.V.
7. Shrivastava V, Nageotte M, Major C, et al. Case-control comparison of cesarean hysterectomy with and without prophylactic placement of intravascular balloon catheters for placenta accreta. Am J Obstet Gynecol. 2007;197(4):402.e1–5.
8. Salim R, Chulski A, Romano S, et al. Precesarean prophylactic balloon catheters for suspected placenta accreta: a randomized controlled trial. Obstet Gynecol. 2015;126(5):1022–1028.
9. Silver RM, Fox KA, Barton JR, et al. Center of excellence for placenta accreta. Am J Obstet Gynecol. 2015;212(5):561–568. Review.
10. Sentilhes L, Ambroselli C, Kayem G, et al. Maternal outcome after conservative treatment of placenta accreta. Obstet Gynecol. 2010;115(3):526–534.
11. Clausen C, Lönn L, Langhoff-Roos J. Management of placenta percreta: a review of published cases. Acta Obstet Gynecol Scand. 2014;93(2):138–143. Review.
12. Hequet D, Morel O, Soyer P, et al. Delayed hysteroscopic resection of retained tissues and uterine conservation after conservative treatment for placenta accreta. Aust N Z J Obstet Gynaecol. 2013;53(6):580–583.