{"paper_id":"03c8d580-3285-4e4c-9230-40fb3bbe1b54","body_text":"A 30 year-old P0 +1  lady who was referred to the\ngynaecology clinic, whose complaints were inability\nto conceive for 8 years duration and progressive\nabdominal distension of 2 years duration. She had a\nhistory of severe, chronic cyclical dysmenorrhoea\nwarranting occasional hospitalization. There was no\nhistory suggestive of weight loss, nausea, vomiting or\nchange in bowel habit. However, she experienced early\nsatiety and occasional bloating. She attained menarche\nat 14 years and menstruated for 5 days in a regular 30\ndays cycle. Her sexual debut was at 17 years. She had\nbeen on combined oral contraceptive pills\n(microgynon) in the preceding 12 months. She was\nthe 2 nd  wife of a polygamous union. The other two\nwives had two children each. There was a history of\nvoluntary termination of pregnancy about 8 years\nearlier.\nClinical examination revealed a healthy young lady with\na distended abdomen. Fluid thrill was positive. Digital\nrectal examination was essentially normal. Vaginal\nexamination was difficult and unremarkable due to\nthe distension, limiting access to the uterus and adnexae.\nHer vital signs were normal. Laboratory investigations\nrevealed a packed cell volume of 38%, white blood\ncell count of 14,600/mm 3 , (Polymorphonuclear\nneutrophils were 90%, lymphocytes were 7% and\nmonocytes 3%). Liver function tests, Electrolytes &\nUrea were within normal limits. Her Carcinoma antigen\n-125 was markedly elevated at 118u/ml (Reference\n<35). A chest X-ray was performed to exclude possible\npleural effusion and was essentially normal.\nAbdominopelvic ultrasound revealed marked\nabdominal collection with normal looking uterus and\novaries. There were no pelvic masses and other\nabdominal organs were unremarkable. A diagnosis of\nmassive ascites probably due to an intra-abdominal\nmalignancy was made in a patient with background\nhistory of infertility. In view of her stable clinical\ncondition and reassuring abdomino-pelvic ultrasound,\na decision was taken to further evaluate the peritoneal\ncavity. She subsequently had laparoscopy and drainage\nof 6 litres of endometriotic ascites. Findings were\nmassive chocolatey ascites, dense pelvic adhesions,\nmultiple endometriotic deposits along the anterior\nabdominal wall, pelvic side wall, large bowel, ovaries,\nuterus and the Pouch of Douglas. The ascitic fluid was\nsent for cytology and she was commenced on medical\nmanagement for endometriosis with subcutaneous\ngoserelin injection (zoladex) 10.8mg every 13 weeks\nfor 6 months.\nCytology revealed sheets of epithelial cells and\nfragments of loosely arranged spindled stroma. There\nwas no atypia. She was followed up at the gynaecology\nclinic for 12 months and she demonstrated sustained\nclinical improvement and was referred for assisted\nconception in view of the tubal disease.\n\nThe occurrence of endometriotic ascites is extremely\nrare 1  and the first documented case was by Brews in\n1954 1 . Few studies have been reported since then.\nAppleby et al. in 2014 2  reported a case of intestinal\nendometriosis occurring in the presence of\nhaemorrhagic ascites. A similar finding of\nhaemorrhagic ascites managed by drainage, gonadotrophin\nreleasing hormone analogues (GnRH) and subsequent successful assisted reproduction was\nreported in 2014 by Bignall and colleagues 3 .\nVarious theories have been propounded for this rare\npresentation and has been suggested to include the\ncontinuous release of endometrial cells from a ruptured\nchocolate cyst into the peritoneal cavity. Pelvic\nendometriosis is a recognised cause of low grade pelvic\ninflammation with varied manifestations 4 . Acute\nabdomen may result from chronic peritoneal irritation\nvia chemical inflammation induced by the\nendometrioma 5 . The chemical irritation caused by these\ndeposits leads to increased white blood cell count,\nelevated C-reactive protein and carcinoma antigen -\n125 levels. This may mimic the presence of an intraabdominal\nmalignancy and may pose a challenge to\nclinical diagnosis. The most common endometriotic\nsites, in decreasing order, are the ovaries, anterior/\nposterior cul-de-sac, broad ligaments, uterosacral\nligaments, uterus, fallopian tubes, sigmoid colon and\nappendix. The symptoms of endometriosis are often\ncorrelated with the site of the implant and an unusual\npresentation of hemoperitoneum has been described\nin literature 6 , 7 .\nIt is estimated that about 10-15% of reproductive aged\nwomen suffer from pelvic endometriosis  8 .\nDysmenorrhoea, deep dyspareunia, dyschezia and\ndysuria are the most frequently reported symptoms.\nDespite its prevalence, the disease is still poorly\nunderstood, evidenced by lack of diagnostic blood\ntests and inconclusive evidence of a relationship\nbetween the extent of the disease and its symptomatology 8 .\nSeveral pathogenic theories have been\nproposed and none of these theories have been able\nto entirely explain the clinical presentation of the\nvarious types of endometriosis 9 . The retrograde\nmenstruation theory provides the most lucid\nexplanation of the aetiopathogenesis of pelvic\nendometriosis, suggesting a transtubal retrograde flow\nof endometrial fragments onto the peritoneum and\nabdominal organs. It has been suggested that the\nnumber and amount of menstrual flow in conjunction\nwith both genetic and environmental factors, determine\nthe degree of phenotypic expression of the disease 9 .\nThe association between infertility and endometriosis\nis well established in literature, but a definite cause-effect\nrelationship remains controversial 10 . The\nprevalence of endometriosis increases to as high as\n25%–50% in women with infertility and 30–50% of\nwomen with endometriosis have infertility 11 , 12 . Severe\npelvic endometriosis is known to distort pelvic\nanatomy, impair oocyte release and pick-up, alter sperm\nmotility as well as fertilization and embryo transport 13 .\nThe role of mild disease however remains elusive and\nmay be related to the expression of inflammatory\ncytokines, growth and angiogenic factors as well as\nthe expression of aberrant genes 13 .\nOur patient had secondary infertility and had never\nbeen investigated. She only presented because of the\ndiscomfort associated with the progressive abdominal\nswelling. Late presentation is not an uncommon finding\nin the tropics where health insurance is limited. She\nhad a history of chronic pelvic pain and this should\nhave been an early warning sign of endometriosis. The\npresence of gross ascites and elevated carcinoma\nantigen-125 values made it imperative to screen for\nthe possibility of an intra-abdominal malignancy via\nan abdominopelvic ultrasound, which did not reveal\nany pelvic masses. The decision to do laparoscopy was\npremised on the need to further evaluate the peritoneal\ncavity, drain the ascites and obtain tissue biopsy.\nLaparoscopy has the advantage of minimal tissue\nhandling as well as providing a panoramic view of\nthe peritoneal cavity.\nMedical management was instituted in this case in view\nof the extensive endometrial deposits and the desire\nto conceive. This aims to create either a pseudo\npregnancy or a pseudo menopausal state thereby\nhalting the progression of the irritation from the\nendometriotic deposits. The pseudo menopausal state\nwas favoured in this case and goserelin (zoladex) a\nGnRH analogue was the drug of choice. Goserelin is\nuseful in pituitary downregulation in preparation for\nassisted conception and has been shown to be a quicker,\nmore convenient and effective alternative to multiple\ndoses of buserelin (suprefact) 14 .\n\nEndometriosis is prevalent amongst infertile women\nand may present in a bizarre manner. Endometriotic\nascites is very rare and may pose a diagnostic challenge\nin resource poor settings where delayed presentation\nis quite common. Excluding intra-abdominal\nmalignancies and instituting appropriate treatment in a\ntimely fashion would halt the progression of the\ndisease. Early recourse to assisted reproduction should\nbe considered in patients with extensive disease and\nconcomitant tubal disease.","source_license":"CC0","license_restricted":false}