Massive haemorrhage due to colitis 57 Postgrad Med J: first published as 10.1136/pgmj.72.843.57 on 1 January 1996. Downloaded from Massive haemorrhage due to colitis secondary to nonsteroidal anti-inflammatory drugs

E Sacanella, F Mufioz, F Cardellach, R Estruch, O Mir6, A Urbano-Marquez

Summary A case of massive haemorrhage due to colitis induced by nonsteroidal anti- inflammatory drugs in a 74-year-old man is reported. ::I:. Keywords: colitis, intestinal bleeding, ketorolac, non- steroidal anti-inflammatory drugs

:ii :ii: The adverse effects of nonsteroidal anti-

inflammatory drugs (NSAIDs) such as damage .ii. to gastroduodenal mucosa or renal failure are well established."12 In recent several years, iiii· reports have related these drugs with the ii!: development of small bowel and colon

diseases.3"7 .iiii.'':::: A case of massive lower intestinal bleeding ·iiii··ir: '1·. due to NSAID intake is reported in a patient who also had an aneurysm of the abdominal ii. '·:· aorta. 3 Case report u A 74-year-old man was admitted to the hospital .iii: with haematochezia. Five months previously, the had of severe and Figure AbdominalX-ray patient complained http://pmj.bmj.com/ progressive back pain and different NSAIDs (diclofenac, naproxen, aceclofenac) were alter- natively prescribed. Four days before admis- sion the patient presented with severe lower intestinal bleeding and visited another hospital. hypotensive, diaphoretic and pale. Although No previous episodes of gastrointestinal plasma expanders and packed red cells were bleeding or other digestive symptoms were infused the patient remained hypotensive reported, but the NSAIDs were discontinued. because of bleeding recurrence. Rupture of the on October 1, 2021 by guest. Protected copyright. A rectosigmoidoscopy was performed. No aortic aneurysm into the bowel was suspected lesions were observed, although blood was and emergency laparotomy was performed. An present in the colon. Bleeding stopped spon- unruptured aortic aneurysm was found and taneously and the patient was transferred to our replaced with a prosthesis. Both mesenteric hospital. arteries were macroscopically normal. During Physicial examination disclosed mild skin surgery, strong life-support management pallor and spontaneous and persistent bilateral allowed normalisation of the arterial pressure. lumbar pain which increased with mobilisation Three days later, colonoscopy disclosed large of the spine. The respiratory and cardiocir- bloody ulcerations widely distributed in the Department of culatory systems were normal. A tender pul- colon, although the rectal mucosa was normal. Internal Medicine, satile mass of 6 cm was found in the abdomen. of several revealed Hospital Clinic i Histologic study specimens Provincial, Villarroel, Blood analysis revealed an erythrocyte mononuclear infiltrate in the mucosa with no 170. Barcelona 08036, sedimentation rate of 54 mm/h, haematocrit evidence ofmalignancy or inflammatory bowel Spain 0.33 1/1, haemoglobin 105 g/l and mean corpus- disease. Non-specific colitis was diagnosed. E Sacanella cular volume 93 fl. An abdominal X-ray The possible association between pancolitis F Munoz (figure) disclosed a calcified aortic aneurysm and NSAID administration led to discontinua- F Cardellach and tion of ketorolac. 24 hours R Estruch generalised osteoporosis. Bleeding stopped O Mir6 Two days after admission, ketorolac (30 mg/ later. Another colonoscopy performed 14 days A Urbano-Marquez day) was started because of severe back pain. later showed mild improvement of the ulcera- Forty-eight hours later life-threatening lower tions. Two months after discharge the patient Accepted 28 June 1995 intestinal bleeding recurred; the patient was remains asymptomatic. 58 Sacanella, Munioz, Cardellach, et al.

NSAID-induced colitis: clinical Summaryllearning points settings

* NSAIDs may have deleterious effects on Postgrad Med J: first published as 10.1136/pgmj.72.843.57 on 1 January 1996. Downloaded from * de novo colitis upper and lower gastrointestinal tract * proctitis after rectal administration ofNSAID * in every patient who consults for digestive * hypersensitivity colitis in atopic patients haemorrhage a detailed history ofdrugs * reactivation ofquiescent inflammatory bowel consumed must be performed disease * inflammatory bowel disease may be exacerbated by NSAIDs Box 1 * NSAIDs may induce colitis similar to inflammatory bowel disease

Discussion Box 2 The clinical settings in which NSAID-induced colitis may present are shown in box 1. 8 In our blood, although weight loss, abdominal pain or patient the diagnosis was supported by the fever may also be present.4 NSAID-induced chronological relationship between the colitis may affect any area of the colon and administration of the drug and the develop- perforation and haemorrhage are the most ment of gastrointestinal bleeding, with recur- severe complications.249" On review of the rence after re-exposure to the drug. Moreover, literature, no other cases presenting as massive the clinical and histologic improvement when haemorrhage and hypovolemic shock were ketorolac was removed confirmed the diag- found. nosis. The absence of clinical or histological The mechanism of NSAID-induced colitis data rule out other causes of ulcerative pan- may be related to the inhibition of intestinal colitis such as inflammatory bowel disease or prostaglandin synthesis.34 Diagnosis requires ischaemic colitis. To our knowledge, ketorolac exclusion of other causes, a relationship has not previously been associated with the between the length of drug administration and development of colitis, probably because of its the onset of symptoms, and resolution after relatively recent introduction in clinical prac- withdrawal ofthe drug.4 Discontinuation ofthe tice. drug and supportive management is the basic Colitis induced by NSAIDs is frequently treatment, although surgery may be required observed in elderly patients and symptoms on the presentation of severe complications. begin several months after drug intake. Most Re-exposure to NSAIDs must be avoided due patients have diarrhoea with occult or obvious to the high risk of relapse.

1 Soll AH. Nonsteroidal anti-inflammatory drugs and peptic 7 Bjarnason I, Zanelli G, Smith T, et al. Nonsteroidal ulcer disease. Ann Intern Med 1991; 114: 307-19. anti-inflammatory drug-induced intestinal inflammation in http://pmj.bmj.com/ 2 Flower RJ, Moncada S, Vane JR. Drug therapy of humans. Gastroenterology 1987; 93: 480-3. inflammation. In: Goodman, Gilman, eds. The phar- 8 Kaufmann HJ, Taubin HL. Nonsteroidal anti- macological basis of therapeutics. London: Macmillan, 1985; inflammatory drug activate quiescent inflammatory bowel pp 674-716. disease. Ann Intern Med 1987; 107: 513-6. 3 Aabakken L, Osnes M. Non-steroidal anti-inflammatory 9 Langman MJS, Morgan L, Warrall A. Use of anti- drug-induced disease in the distal ileum and large bowel. inflammatory drugs by patients admitted with small or large Scand J Gastroenterol 1989; 24 (suppl 163): 48-55. bowel perforations and hemorrhage. BMJ 1985; 290: 347-9. 4 Gibson GR, Whitacre EB, Ricotti CA. Colitis induced by 10 Saverymuttu SH, Thomas A, Grundy A, Maxwell JD. Ileal nonsteroidal anti-inflammatory drugs. Report of four cases strictising after long-term indomethacin (therapy) treat- and review of the literature. Arch Intern Med 1992; 152: ment. Postgrad Med J 1986; 62: 967-8. on October 1, 2021 by guest. Protected copyright. 625-32. 11 Bjamason I, Price AZ, Zanelli G, et al. Clinicopathological 5 Tanner AR, Raghunath AS. Colonic inflammation and features of nonsteroidal anti-inflammatory drug-induced nonsteroidal anti-inflammatory drug administration: an small intestinal strictures. Gastroenterology 1988; 94: assessment of the frequency of the problem. Digestion 1988; 1070-4. 41: 116- 120. 6 Allison MC, Howatson AG, Torrance CJ, Lee FD, Russell RI. Gastrointestinal damage associated with the use of nonsteroidal anti-inflammatory drugs. N Engl J Med 1992; 327: 749-54.