Acute massive lower gastrointestinal bleeding from a rectal Dieulafoy-like lesion in a patient with chronic liver disease

摘要

Recurrent and life threatening gastrointestinal hemorrhage occur rarely from Dieulafoy’s lesions. Initially described in the gastric lesser curvature, these lesions have been described in other parts of the gastrointestinal tract. We report a case of acute massive lower gastrointestinal bleeding from a rectal Dieulafoy-like lesion in a patient with a history of chronic liver disease. An overview of the possible etiology and management of this rare presentation is presented. Introduction Dieulafoy’s lesions are a rare cause of massive and life threatening gastrointestinal (GI) hemorrhage. 1 Initially described in the lesser curvature of the stomach, this lesion has been described in other parts of the gastrointestinal tract, and in the bronchus. 1 We report a rare case of massive lower gastrointestinal bleeding from a rectal Dieulafoy-like lesion in a patient with a history of chronic liver disease (CLD). Case A 45 year old male with a history of alcohol abuse, chronic Hepatitis C infection, and liver cirrhosis with known esophageal varices and portal hypertension was seen in the emergency department. He presented with a 3 week history of upper abdominal pain, nausea, coffee ground emesis and passage of melena stools. He had no prior history of GI bleeding. His home medications included omeprazole, and antidepressants. On admission, hemoglobin was 5.9 g/dL, platelet count 99,000 and prothrombin time 19.9 sec. His pulse and blood pressure were 105 and 124/61 mmHg, respectively, without orthostatic changes. He was transferred to the Intensive Care Unit (ICU) due to concern for acute change in mental status, and was transfused with a total of 6 units of packed red blood cells (PRBC). Upper endoscopy done the following morning revealed non bleeding grade 1-2 esophageal varices and portal hypertensive gastropathy. On hospital day 3, he developed acute respiratory distress necessitating endoscopic intubation. The following day, he developed diarrhea and a rectal tube (Flexi-Seal, ConvaTec, Skillman, New Jersey) was inserted for ease of drainage. Diarrhea continued intermittently. He remained critically ill and was managed for alcohol withdrawal, acute respiratory distress syndrome (ARDS), and aspiration pneumonia. He was on lorazepam, thiamine, multivitamins, haloperidol, vancomycin and piperacillin-tazobactam. On day 14 of admission, he suddenly began passing bright red blood per rectum. The rectal tube was promptly taken off but he continued to bleed massively. Blood pressure was 80/62 mmHg and heart rate 92. Nasogastric aspirate revealed no blood. Physical examination revealed a distended but soft and non-tender abdomen. Examination of the anal region revealed active bleeding with lots of clots. Hemoglobin dropped to 6.7 g/dL from 9.2 g/dL, platelet count was 41, 000, and prothromin time 21.6sec. He was aggressively resuscitated with intravenous fluids, 6 units of PRBC, 6 units of fresh frozen plasma and one unit of platelets. Emergent colonoscopy revealed fresh blood coating the colon with large clots in the rectum. The ileum was clear of blood. Following meticulous lavage and thorough inspection, an area of active spurting of blood was identified in the distal rectum about 4 cm proximal to the anal verge, anterioly. Hemostasis was secured by injecting a total of 17 mL of 1:10,000 epinephrine interspersed with the application of 3 endoclips. (Figures 1-3) No visible erosion or ulceration was identified. There were no further bleeding episodes and he remained hemodynamically stable but critically ill. Three days after the episode, care was withdrawn in keeping with his family’s decision, and he passed peacefully thereafter. The cause of death was unrelated to the massive GI bleed episode.