A 63-year-old female presented with epigastric pain, loss of appetite, abdominal bloating, regurgitation, and episodic projectile vomiting of five-year duration. These symptoms were aggravated particularly after meals. Her bowel opening was normal. The patient had lost 20 kilograms over five years. The patient had a background history of hypothyroidism for which she was on thyroxine replacement therapy. She was clinically euthyroid. She had undergone a vaginal hysterectomy for uterovaginal prolapse at the age of 39 years. There was no significant family history for bowel disorders.
On physical examination, she had a body mass index of 13. She was pale. There were peripheral stigmata of chronic malnutrition and vitamin B12 deficiency. She had a distended abdomen, visible peristalsis, and hyperacute bowel sounds. There was no clinically demonstrable free fluid in the abdomen. She had anaemia (haemoglobin-8.9 g/dl, haematocrit-27.3%, mean corpuscular volume-97.4 fl, mean corpuscular haemoglobin-31.6 pg, mean corpuscular haemoglobin concentration-325 g/l, and red cell distribution width-58.4 fl), with normal platelet (402 x 103/mul) and leucocyte (8.07 x 103/mul) counts. Blood picture showed macrocytic red cells and hypersegmented neutrophils. Abnormal chemical pathological investigations comprised of elevated C-reactive protein (20.1 mg/l), hypoproteinaemia (59 g/dl), hypoalbuminaemia (25.3 g/l), hypovitaminosis B12 (160 pg/ml), and hypocholesterolaemia (total cholesterol-125.5 mg/dl, HDL-32 mg/dl, LDL-66.3 mg/dl, and triglycerides-136.4% with normal VLDL-27.2 mg/dl). Serum ionized calcium was 2.41 mmol/l. Serum iron studies favoured anaemia of chronic disease (serum iron-95 mug/dl, total iron binding capacity-138 mug/dl, iron saturation-40.8%, and ferritin-238 mug/l). She was biochemically euthyroid (TSH-4.65 mIU/l). Ultrasonography was suggestive of subacute small intestinal obstruction with distended first part of the duodenum filled with fluid. Multiple tortuous small bowel loops were noted around the pancreas with increased peristalsis. Large bowel was distended with gas. There was no bowel wall thickening, mass lesions, or free fluid in the abdomen. Computed tomography (CT) of dual slice contiguous axial sections of the abdomen obtained after intravenous, oral, and rectal contrast administrations demonstrated mild dilatation of the first and second parts of the duodenum with no evidence of significant obstruction to distal passage of oral contrast. The stomach was not distended. A focal calcification of the segment VII of the liver was noted, which was likely to be an incidental finding. There was no CT evidence of an annular pancreas or superior mesenteric artery syndrome. A spiral CT was repeated after one week. It showed markedly distended proximal bowel loops involving the duodenum and the proximal jejunum. No definite transition point was identified. There was a whirl appearance seen in the mesentery and superior mesenteric venous branches around the superior mesenteric artery raising the suspicion of a possible midgut volvulus. Mild mesenteric engorgement was also seen. No definite CT evidence of diverticuli was seen. Upper gastrointestinal (UGI) endoscopy revealed multiple duodenal diverticuli with a small hiatus hernia. Barium meal and follow-through study revealed a slightly distended duodenum without evidence of obstruction or persistent narrowing. Magnetic resonance enterography revealed multiple dilated small bowel loops with loss of valvulae in the right side of the abdomen (Figure 1). There were numerous outpouchings arising from the small bowel.
However, with unexplained weight loss, we wanted to exclude a gastrointestinal malignancy and intestinal tuberculosis. We opted for laparotomy out of diagnostic laparoscopy and laparotomy. Multiple large diverticuli were noted extending from the first part of the duodenum to the proximal ileum (Figure 2). Diverticuli were measuring from 0.5-12.0 cm. There was macroscopic evidence of diverticulitis. There was gross gastric dilatation. Proximal small bowel was dilated without a definitive transition point. The rest of the terminal ileum and colon were normal macroscopically. Small bowel was not surgically resected because she was not a suitable candidate for a primary anastomosis as she had nutritional deprivation and the risk of short gut syndrome. We closed the abdomen without any surgical interventions. Because of macroscopic evidence of diverticulitis, intravenous cefuroxime 750 mg 8 hourly and intravenous metronidazole 500 mg 8 hourly were administered for 7 days and were converted to oral cefuroxime 500 mg 12 hourly and oral metronidazole 400 mg 8 hourly for another 21 days. She had an uneventful postoperative period. She received complementary parenteral nutrition with amino acids, electrolytes, dextrose, and lipid injectable emulsions followed by standard polymeric formulae containing whole proteins. Soluble fibres were gradually introduced to her diet. She received a high-calorie diet, initially 125% of the daily calorie requirement followed by 150% of the daily calorie requirement after one month. Thousand international units of vitamin B12 was administered intramuscularly every other day for five days, and oral vitamin B complex 1 mg three times a day was continued for six months, with folate and micronutrient replacement. Iron-rich food and standard formulae were used to supplement micronutrients such as selenium and zinc for six months. She had a remarkable recovery with no recurrence of symptoms following 10 months follow-up.