A 19-years-old female presented to our center with a one-month history of abdominal pain which was generalized and associated with progressive abdominal distension, pain on passing stool, and difficulty in breathing on lying flat. There was no history of cough, fever nor chest pain. She denied any abnormal vaginal discharge.
Nine months ago she had a cesarean section due to obstructed labour in a peripheral hospital after which she developed peritonitis and was referred to our center. She underwent an emergency midline laparotomy whereby a gauze was found in the peritoneal cavity with multiple pus pockets and a biopsy of the omentum was obtained to rule out malignancy. This was complicated by a burst abdomen five days later for which she was operated on again followed by delayed wound healing. She was then discharged only to develop abdominal pain and distension in the current presentation.
On admission, she was fully conscious and alert, mildly pale, and tachypnoeic with a respiratory rate of 26 breaths/min, an axillary temperature of 36  C, blood pressure of 98/67 mm Hg, pulse rate of 137 beats/min and was saturating at 97 % on room air. She also had bilateral, non-tender lower limb pitting edema up to the level of her knees.
Her abdomen was globally distended with a healed midline and Pfannenstiel surgical scars from previous surgeries, symmetrical abdominal contours, tenderness over the umbilical and flank areas with a dull percussion note, and positive fluid-thrill. Her bowel sounds were heard normally. Her cardiovascular exam revealed a gallop rhythm with raised JVP with no hepato-jugular reflux. There were no positive findings in her respiratory examination. Ascitic fluid tapping was done under sterile conditions using a large bore cannula (16G) attached to a collecting bag and drained 5 L of milk-like fluid (chyle) (Fig. 1).
Her laboratory investigations revealed a white blood cell count of 5.91 x 109/L, hemoglobin of 16.2 g/dL, and a platelet count of 437 x 109/L. Her hepatitis panel was negative for hepatitis B and C. Her aspartate transaminase of 16.09 U/L, alanine transaminase of 20.88 U/L and serum albumin of 22.1 g/L. Her serum creatinine was 75 mumol/L, BUN of 1.01 mmol/L, lactate dehydrogenase of 350.54 IU/L, and Prolactin of 317.5 mug/L. Peritoneal fluid triglyceride level was 201 mg/dL, negative gram-stain, serum-ascites-albumin-gradient of 1.2 g/dL and Gene Xpert was negative for Mycobacterium tuberculosis. Cytology of peritoneal fluid revealed an inflammatory effusion mixed with fresh RBC. Histology of the omental specimen ruled out malignancy. Ultrasound of the abdomen revealed a massive anechoic collection in the whole abdomen with an impression of ascites. CT scan of the abdomen and pelvis revealed a substantial amount of free fluid within the peritoneum, suggestive of severe ascites (Fig. 2). The echocardiogram showed a small pericardial effusion with an ejection fraction of 66 %.
Throughout admission, she was kept on oral spironolactone and furosemide for the ascites as well as Ceftriaxone, Metronidazole, and Gentamicin to prevent spontaneous bacterial peritonitis. She faired well on conservative management, whereby she was discharged on oral furosemide, and spironolactone and was advised on a high-protein diet. She was reviewed weekly at the surgical outpatient unit initially and was tapped of which the frequency of ascetic tapping gradually decreased over two months from 2.5 L/week to less than 500 mL/week. She is currently on observation with no medical intervention.