Rare coexistence of placenta previa accreta and peritoneal adhesion: three-decade clinical observation

Abstract

Peritoneal adhesion makes abdominal surgery difficult. The recent increase in cesarean section (CS) is considered a main culprit for increase of placenta previa accreta (PPA) (accreta, increata, or percreta), which usually requires cesarean hysterectomy (CH). A recent article in this journal demonstrated that of 247 patients with placenta previa, 12 (4.9 %) required hysterectomy; 11 out of 12 had histologically confirmed placenta accreta [1]. We have devised some measures for CH [2, 3], which I have also described in this journal [2]. Briefly, we avoid administering uterotonic agents after infant delivery [2] and we employ ‘‘double distal edge pickup’’ mass ligation to ligate the medial side of the incised uterus [2]. If the placenta invades the bladder, we, without separating the bladder, intentionally cut the bladder wall and remove the uterus with the posterior bladder wall kept adhering to the uterus [3]. Even with these techniques, CH for PPA is always challenging. If peritoneal adhesion exists, it will make this difficult surgery more difficult. Laparotomy including CS sometimes leads to peritoneal adhesion, which makes next CS difficult. Since PPA usually occurs in patients with previous CS, it is likely that peritoneal adhesion and PPA tend to coexist. This is contrary to my observation derived from my three-decade tertiary obstetric center practice. My observation is that PPA does not, or at least rarely, accompanies peritoneal adhesion. Fortunately, no patients had severe adhesion requiring its adhesiolysis. This is in stark contrast to both previous data and our own data. Previous reports indicated that adhesion requiring surgical intervention such as adhesiolysis occurred in approximately one quarter (21-27 %) [4, 5] in repeat CS. I have performed approximately 40 CH for PPA during three decades, with almost all having a previous history of CS. Although the detailed surgical data have been missing during three decades and adhesion was not scored, the uterus could be easily exteriorized without adhesiolysis in all patients. This indicated that no PPA patients had adhesion of more than stage 3, with stage 4 being the full mark, according to the Myers and Bennett adhesion staging system [4]. Usually stage 3 and 4 adhesion are referred to as ‘‘clinically significant’’ adhesion [4]. Thus, whereas approximately one quarter of repeat CS patients had significant adhesion [4, 5], no PPA patients had it even though almost all had a previous CS history. I examined the surgical records of patients who underwent repeat CS without current PPA from July to December 2011 in this institute. Excluding the patients with the abdominal surgery history other than CS and those under steroid administration, 64 patients received repeat CS. Although its degree was not staged [4], peritoneal adhesion was present in 47 % (30/64), with 13 % (8/64) requiring surgical intervention. The mechanism for this observation is unclear; however, decreased wound healing may, at least partly, account for this phenomenon. Not well-healed CS scar leads to insufficient decidualization, which results in trophoblasts invading the uterine muscle layers, causing PPA [6]. Thus, decreased wound healing is considered to be a possible culprit for PPA. Wound healing consists of several steps: inflammatory cell mobilization to the site, fibroblast mobilization, and finally proliferation and regeneration of the corresponding tissue. Peritoneal adhesion formation S. Matsubara (&) Department of Obstetrics and Gynecology, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan e-mail: matsushi@jichi.ac.jp