Abdominal wall endometriosis (AWE) is a rare type of endometriosis, with a reported incidence of 0.03–0.4% [4,5]. AWE results from a variety of obstetric and gynecologic surgeries, the majority of which are caesarean sections. The increasing number of caesarean sections and laparotomies are thus expected to increase the rate of AWE [6,7]. Surgery is the only curative therapy, and the removal of the lump also causes the chronic pain to disappear. During surgery, the different structures of the abdominal wall should be repaired in layers, and meshes should be inserted if necessary. The anatomical levels of the abdominal wall are skin, subcutaneous fat, anterior rectus abdominis sheath, rectus abdominis, posterior rectus abdominis sheath, and peritoneum from outside to inside . The lesions of abdominal wall endometriosis can invade all these layers, but we do not yet appreciate whether the layers invaded by the lesions impact basic clinical characters, the difficulty of surgery, or postoperative recovery, as there are no extant relevant studies. In this study we collected clinical data from 367 AWE patients who underwent operations at the Peking Union Medical College Hospital over the past 10 years, and compared them according to the level of tissue invasion.
The clinical triangle includes cyclical pain, a lump at the abdominal wall, and a history of caesarean section or similar gynecologic procedures . Local pain at the incision site of the abdominal wall during menstruation has been reported to be the most common complaint, but not all patients manifest painful symptoms related to the menstrual cycle [11, 12]; on rare occasions, a patient presents with skin changes . In our study, the preponderance of cases had a history of caesarean section (98.1%), all patients complained of abdominal wall masses (but not all patients had abdominal wall pain), and the relationship between pain and menstruation was unclear in some patients. Although there was no statistical difference among the three types of patients in latency period, latency for type III showed a tendency to be longer than that for other two types. Presumably because of the deeper location, the time needed to palpate the lesion and until the appearance of pain symptoms was delayed. We did, however, observe significant differences in the previous AWE resection of type III patients, and the proportion of relapsed type III patients was significantly higher than for types I or II. This shows that with deepening lesion invasion, there was a gradual increase in the risk of AWE recurrence.
Various rates for concurrent pelvic endometriosis have been reported in patients with AWE, ranging from 5.3–34% [14–16], which is similar to our results (17.7%). However, investigators have not previously analyzed these rates according to differing invasion layers. Our group analysis showed that the rate of concurrent pelvic endometriosis for type III was significantly higher than for the other two types. Among the 29 type III patients with pelvic endometriosis, 8 cases (27.6%) were found during intraoperative exploration. These data suggest that some patients who may have concurrent pelvic endometriosis cannot be diagnosed by auxiliary examination before surgery, and that the incidence of pelvic endometriosis concurrency may be underestimated. Because all type III patients underwent pelvic exploration during the surgical procedure, endometriomas that are typically difficult to uncover by imaging could then be located. This suggests that before surgery, clinicians should not only assess the level of invasion of intra-abdominal endometriotic lesions, but to also complete an assessment of whether the pelvic cavity is associated with the endometriosis; and if necessary, perform intraoperative treatment simultaneously. As we stated, AWE is principally secondary to caesarean section, and most authors have concluded that this rate is comparable to the rate of classical endometriosis in the general population and thus not relevant; however, it is very likely to be underestimated. Therefore, if endometriosis is found during caesarean section, more attention should be paid to the protection and cleaning of the caesarean section incision so as to reduce the risk of implanting the abdominal wall with endometrial fragments.
AWE masses are surrounded by connective tissue, and it is thus difficult for drugs to enter the lesion location, making the drug treatment ineffective. Surgical resection is therefore the primary treatment modality [17,18]. By comparing the three types of patients, we found that the deeper the level of invasion, the larger the diameter of the lesion during resection and the higher the risk of multiple lesions. This indicates that the deeper layers of the abdominal wall might be more favorable to the implantation and proliferation of the residual endometrial cells, which is not easy to diagnose early. We suggest two possible causes for the role of different invasion layers. First, the deep layer renders tissue irrigation difficult and induces much more endometrial cell contamination . The second cause is a larger nutrient supply. Endometrial cells require an adequate blood supply to survive in their ectopic sites, and angiogenesis plays an important role in the pathogenesis of endometriosis . Therefore, an enhanced blood supply would provide a relatively rich nutritional environment for the implantation and growth of residual endometrial cells, favoring the occurrence of AWE. For surgical patients, the location and diameter of the removed lesions are closely related to their intraoperative and postoperative treatment and prognosis. Intraoperative patch placement was concentrated in our type II and type III patients, and with the deepening of the level of lesion invasion, the proportion of patch placements in type III patients was significantly greater than for type II patients. The probability of drainage also gradually increased, the surgical duration was significantly prolonged, the likelihood of postoperative fever increased, and the length of hospital stay was correspondingly prolonged. Previous studies have confirmed that the size of the lesion is an independent risk factor for patch placement , and we herein confirmed that the level of lesion invasion also affected the placement of the patch. The level of lesion invasion thus exerts an impact on the difficulty of surgery and postoperative recovery.
Investigators have previously demonstrated that the recurrence rate of AWE is 4.3–11.4% [16,22–23], but there are no studies as yet in which comparisons were made between different types of AWE. In our study, the 5-year cumulative recurrence rate was 3.3%, and most of the recurrence sites were located in the fascia and rectus abdominis. With deeper lesion invasion, the risk of recurrence gradually increased, which may be due to the abundant blood supply in this area—providing a favorable environment for the implantation and continuous growth of the ectopic endometrium. Recurrence may also be due to a deeper location, accompanied by satellite lesions that were not visible to the naked eye, resulting in incomplete removal.