**7. Abdominal wall endometriosis**

Abdominal wall endometriosis is defined as endometrial tissue within the abdominal wall, superficial to the peritoneum. This entity occurs in 0.03 to 1.08% of women with previous history of obstetric or gynaecologic procedures, particularly after histerotomy The time from surgery to the onset of symptoms ranges from months to 17.5 years, with an average of 30 months. The association between abdominal wall endometriosis and pelvic endometriosis is found in 2.5% - 25% of the cases (Bektas *et al.*, 2010; Horton *et al.*, 2008).

The pathogenesis of abdominal wall endometriosis is explained by a combination of theories: (i) Iatrogrenic direct implantation during the surgical procedure, endometrial tissue is seeded into the wound; this theory alone is not enough to completely explain the physiopathology, given the low incidence of this disease and the reports of endometriosis without previous surgery, (ii) endometrial cells may reach a caesarean section via lymphatic or hematogenous routes, (iii) coelomic metaplasia and, (iv) cell immunity change theory (Bektas *et al.*, 2010). Malignant transformation of abdominal wall endometriosis is a rare complication (1%).

nonjuxtaposed vaginal and colorectal sutures are major factors in preventing and facilitating the conservative treatment of anastomotic leaks, and the increased use of preoperative endoscopic ureteral double pig-tail stenting may help to prevent delayed ureteral ischemic necrosis related to extensive ureterolysis. The most frequent specific complication of compete surgery for low rectal endometriosis is transient peripheral neurogenic bladder. The inferior hypogastric nerves are recognized and preserved during surgery but may

The recurrence of symptoms for follow-up periods of 2-5 years varies between 4% and 54%. The recurrence of pain requiring surgery is 0% to 34%. Proven bowel endometriosis recurrence is 0-25% (De Cicco *et al.*, 2011; Dousset *et al.*, 2010), and is higher for dissection off the rectal wall (22.2%) that anterior rectal wall excision (5.2%) and segmental rectal resection (0-4.7%) (Brouwer & Woods, 2007; Dousset *et al.*, 2010). Recurrence of endometriosis can be explained by the significant proportion of rectal lesions that extend into the submucosa (36%) (Brouwer & Woods, 2007). The overall improvement in pain-related symptoms is of 87%-94% and in quality of life assessment of 90% (Dousset *et al.*, 2010). Dousset y cols (2010) believe that the very low recurrence in rectal endometriosis is related to a "carcinologic" surgical approach: (i) all additional extrarectal sites of endometriosis were removed, (ii) total mesorectal excision and en-bloc resection of the rectal nodule together with posterior vaginal fornix and uterosacral to ensure free anterior and circumferential resection margins, (iii) rectal section at least 2-cm below the endometriotic nodule, and (iv) all additional intestinal and urologic endometriotic deposits were resected with 2-cm-free surgical

The results of several series show that with a multidisciplinary approach (gynaecologic, gastrointestinal and urologist surgeons, radiologist) to the management of endometriosis involving the rectum and radical surgery to excise the disease as completely as possible at one operation, excellent results can be achieved with low morbidity and recurrence

Abdominal wall endometriosis is defined as endometrial tissue within the abdominal wall, superficial to the peritoneum. This entity occurs in 0.03 to 1.08% of women with previous history of obstetric or gynaecologic procedures, particularly after histerotomy The time from surgery to the onset of symptoms ranges from months to 17.5 years, with an average of 30 months. The association between abdominal wall endometriosis and pelvic endometriosis is found in 2.5% - 25% of the cases (Bektas *et al.*, 2010; Horton *et al.*,

The pathogenesis of abdominal wall endometriosis is explained by a combination of theories: (i) Iatrogrenic direct implantation during the surgical procedure, endometrial tissue is seeded into the wound; this theory alone is not enough to completely explain the physiopathology, given the low incidence of this disease and the reports of endometriosis without previous surgery, (ii) endometrial cells may reach a caesarean section via lymphatic or hematogenous routes, (iii) coelomic metaplasia and, (iv) cell immunity change theory (Bektas *et al.*, 2010). Malignant transformation of abdominal wall endometriosis is a rare

(Brouwer & Woods, 2007; De Cicco *et al.*, 2011; Dousset *et al.*, 2010).

**7. Abdominal wall endometriosis** 

require resection in cases with lateral pelvic wall invasion (Dousset *et al.*, 2010).

margins.

2008).

complication (1%).

It should always be considered when a mass appears in or near a caesarean section scar or other gynaecologic operative procedure sites, in the umbilicus or in the inguinal region, more so when pain accompanying the patient's menstrual cycle. The diagnosis may become difficult if cyclical pain is not present (43%). Also be diagnosed in patients without previous surgery. Moreover, abdominal wall endometriosis patients are often referred to the general surgeons and were diagnosed after surgical techniques such as appendectomy, inguinal hernia repair, or laparoscopic procedures. Accurate preoperative diagnosis varies between 20% and 50% (Bektas *et al.*, 2010; Horton *et al.*, 2008).

Additional studies such as ultrasound, CT scan, MRI, or fine-needle aspiration may be obtained if the lesion is very large, there is concern for fascial involvement, or if the diagnosis is in doubt. This information may assist with surgical planning especially when an abdominal wall reconstruction is anticipated (Veeraswamy *et al.*, 2010). Ultrasonography is the most commonly used investigational procedure for abdominal masses; the mass may appear hypoechoic and heterogeneous with scattered internal echoes, solid, or with cystic changes. The findings on computed tomography scan depend on the phase of the menstrual cycle, the proportions of stromal and glandular elements, the amount of bleeding, and the degree of surrounding and fibrotic response, without pathognomonic findings. Owing to the relatively vascular nature of these lesions, enhancement often occurs when intravenous contrast material is used. Magnetic resonance imaging enables very small lesions to be detected and can distinguish the hemorrhagic signal of endometriotic lesions. Fine needle aspiration cytology can confirm the diagnosis and eliminate the possibility of malignancy. This is justified only in cases of large masses, doubtful diagnosis and atypical clinical manifestations. However, its use is still controversial of the risk of causing new implants at the puncture site (Bektas *et al.*, 2010; Horton *et al.*, 2008).

The treatment of choice is surgical excision with at least 1 cm margin, even for recurrent cases and, if necessary, placement of mesh for fascia defects. A combination of surgical reexcision with hormonal therapy is also recommended (Bektas *et al.*, 2010; Horton *et al.*, 2008).

During violation of endometrial cavity, inoculum of endometrial tissue spill and implant on the abdominal wound. Thus, it is strongly recommended that the abdominal wound be cleaned at the conclusion of the cesarean section. Other recommendations are delivering the uterus outside the abdomen to repair, not using the same suture material to close the abdomen as used for uterine closure, not swabbing out the uterine cavity following the delivery of the placenta or discarding the swab used to clean the endometrial cavity after delivery of placenta, or using wound edge protector to separate the edges of the incision from contact with the patient's abdominal contents, instruments, and gloves during the procedure (Bektas *et al.*, 2010; Horton *et al.*, 2008).
