A 53-year-old lady presented following a collapse at home. In the ambulance she became unresponsive with a temperature 33.4oC, heart rate of 95 beats per minute and un-recordable blood pressure. On arrival active resuscitation commenced and a brief history of three days of severe, intermittent abdominal pain, absolute constipation, and reduced urine output was noted. Prior to this recent deterioration the patient had been well, with no weight loss or change in appetite. She had a past medical history of hypertension, osteoporosis, a previous appendicectomy; and a 20-pack year smoking history. She denied any dyspeptic symptoms prior to her admission, and had never taken any antacids. Her medications on admission were regular beta blocker, regular long term bisphosphonates and paracetamol on as required basis. On inspection the patient appeared of a normal body habitus, with a BMI of 22 and examination revealed a peritonitic abdomen.
Blood tests from admission revealed grossly elevated inflammatory markers (CRP>500mg/L), neutrophilia and acute kidney failure. Her blood gas showed metabolic acidosis with a high lactate (12.7mmol/L), and low base excess (−21.8 mmol/L) and bicarbonate (6.9mmol/L).
Due to her severe acute renal impairment no contrast was initially used for imaging. CT scan of her abdomen performed on admission revealed extensive free peritoneal fluid and also fluid adjacent to the right kidney in the retro peritoneum (Figure1). There was no evidence of any free air, obstruction, perforation or abdominal aortic aneurysm, with no evidence for small bowel ischaemia. Furthermore an ascitic tap was performed which revealed a clear straw coloured fluid with a very high lactate dehydrogenase, and normal protein. It did not yield growth of any organisms.
Despite optimal management in the intensive care unit the patient’s inflammatory markers, creatinine and alanine aminotranserase all continued to rise, and urine output remained minimal. In light of her clinical deterioration, 12 hours after admission the patient underwent an urgent diagnostic laparoscopy.
Intraoperatively approximately 3 litres of free intraperitoneal purulent bile stained fluid filled the abdomen, and multiple fibrinous exudates surrounded the entire small bowel. A 162 cm section of distal small bowel appeared ischemic, and an anterior duodenal (D1) perforation was identified. The procedure was converted to a laparotomy in view of the findings. The D1 perforation was repaired using an omental patch, and the ischemic bowel wrapped in warm saline-soaked packs, with minimal benefit. The distal 162cm of dead small bowel was resected, and because of her critical condition the neodistal small bowel had a few viable slightly dusky patches left behind for a relook the following day. A washout was performed and a laparostomy using a saline bag was applied.
One day post-operatively the patient was dialysed and kept intubated due to unresolving metabolic acidosis. During the second laparotomy another 50cm of small bowel appeared ischaemia and was resected. 2 meters of healthy small bowel was left in situ. An ileocaecal anastomosis was made, a washout performed, and the abdominal wound closed.
Two weeks after her initial laparotomy the patient had an endoscopy for a nasojejunal tube insertion. The omental patch repair was performed during laparotomy for duodenal perforated ulcer. However, once endoscopy was performed few days after the first laparotomy for naso-jejunal feeding tube insertion, a small hole was identified near the D1 repair site and was clipped (Figure2). A repeat endoscopy a week later showed closure of the duodenal defect and a 1cm healing ulcer. The patient made a slowly recovery and she was discharged few weeks later.
Histology showed haemorrhagic infarction in sections of small bowel with ischaemic changes throughout the submucosa and muscle coat, with normal appearing Mesenteric vessels.