The patient, an 86-year-old woman with Alzheimer's dementia and hypertension, was chronically taking aspirin, amlodipine, and donepizil. She was admitted after an episode of hematochezia with orthostatic hypotension and a hemoglobin of 6.8 mg/dl. Her baseline hemoglobin 12 months prior had been 12.4 mg/dl. She received intravenous fluids and a total of five units of packed red blood cells for resuscitation. The aspirin and amlodipine were stopped. Nasogastric lavage of one liter produced neither blood nor bile. Hematochezia continued and she was transferred to the intensive care unit. She was started on continuous pantoprazole intravenous drip for possible upper gastrointestinal bleeding and prepared for upper and lower endoscopy with polyethylene glycol-electrolyte solution. The upper endoscopy showed multiple small (1-3 mm) antral erosions with no evidence of bleeding, and colonoscopy showed many diverticula scattered throughout the colon, but no blood was seen in the lumen or in the diverticula. No source of bleeding was identified. Her hematocrit stabilized with transfusions and conservative management. She was hospitalized for three days. She was discharged to a nursing home with a hemoglobin of 12.8 mg/dl and aspirin was restarted the day after discharge.
The patient was re-admitted three days later (day 6) with recurrent hematochezia and a hemoglobin of 10.5 mg/dl. The aspirin was stopped. Enteroscopy, performed on day 7 after the initial bleeding event, was normal to 50 cm past the pylorus with no evidence of bleeding. Colonoscopy showed multiple diverticula, none specifically bleeding, but maroon blood throughout the colon and maroon blood pooling in the cecum. The terminal ileum was not examined. Continued hematochezia led to a tagged RBC scan which showed increased tracer activity throughout the colon, specifically the ascending, transverse, and descending colon on delayed images at 6 h. The actual site of bleeding was not identified. It was felt by interventional radiologists that angiography would not localize the bleeding site as the bleeding rate was too slow. Capsule endoscopy was performed to further assess the small intestine as the patient continued to pass red blood and clots from the rectum. It showed two 2 mm angiodysplastic lesions not actively bleeding at 43 and 81 min, a small mucosal break at 89 min, and a few small submucosal hemorrhagic lesions at 120 min, all of which were not actively bleeding. There was no fresh or old blood seen in the lumen. The capsule reached the cecum at 2 h and 6 min.
Eight hours after the capsule endoscopy was completed, the patient had another episode of bright red blood per rectum. A third colonoscopy was performed after thorough polyethylene glycol preparation. It showed diverticulosis throughout the colon with trace amounts of old blood, but no bleeding site could be identified. Given persistent rectal bleed without evidence of blood in the small intestine or bleeding arteriovenous malformations on capsule endoscopy, we felt that the most likely source of bleeding was colonic diverticula. Our therapeutic options were limited since she was a poor surgical candidate given her age and dementia and since she had not been bleeding briskly enough on the tagged RBC scan for angiography to be helpful. Previous case reports have shown that therapeutic barium enema can successfully stop bleeding in patients diagnosed with presumptive diverticular bleed. For this reason, our patient was taken to the radiology suite for therapeutic high-density barium enema. 1,400 g of E-Z-HD barium sulfate (98% w/w, E-Z-EM, Westbury, N.Y., USA) were dissolved in 300 ml of tap water to prepare a final volume of 800 ml of 171.5% w/v suspension in water, and a Lafayette Aircon XL 3000 disposable air contrast enema kit (Mallinckrodt Inc., St. Louis, Mo., USA) was used to instill the high-density barium by gravity into the colon. Contrast was seen to reach the cecum, and numerous diverticula were noted scattered from the sigmoid colon to the cecum. The patient was asked to change position every 5 min by rolling 90 degrees to the next of four positions over a two-hour period, and at the end of the examination none of the barium could be expelled by the patient (fig. 1). No anti-motility agent such as glucagon was given prior to or during the procedure. Immediately after the procedure, normal saline at 175 ml/h was initiated. Eighteen hours after the procedure, treatment with polyethylene glycol 17 g mixed in 8 ounces of water p.o. bid and liberal oral fluids were added in an effort to clear the intraluminal barium and minimize any risk of colonic impaction. Ambulation was encouraged and the patient complied. She continued to pass large amounts of barium per rectum for 48 h and was able to tolerate clear liquids without any nausea, vomiting, or abdominal pain. She remained free of symptoms worrisome for obstruction, and daily abdominal films were obtained. The abdominal X-ray done 48 h after treatment showed barium remained in the diverticula throughout the colon but was largely cleared from the lumen proper (fig. 2). She remained hemodynamically stable without further evidence of bleeding. Her hematocrit remained stable. She was able to tolerate a regular diet and was discharged. Follow-up in the outpatient clinic two weeks later showed her to be doing well with no recurrence of hematochezia, and her hematocrit was stable at 12.1 mg/dl on day 16 (fig. 3). Follow-up blood counts on days 60, 76 and 120 showed no drop in hemoglobin, and the patient, the assisted living center staff, and the patient's children reported no further episodes of bleeding. Aspirin has been discontinued since she was discharged from the hospital.