INTRODUCTION: Colonic diaphragm disease is an uncommon condition usually associated with the long-term use of non-steroidal anti-inflammatory drugs. CASE PRESENTATION: A 48-year-old woman presented as an emergency patient with abdominal pain and vomiting. Past medical history included inflammatory bowel disease of ulcerative colitis type for which she was taking azathioprine and prednisolone. On examination, she was shocked with signs of peritonism. Following resuscitation, she was taken for a laparotomy upon which a small amount of turbid fluid was identified but there was no direct evidence of an intra-abdominal perforation. A peritoneal lavage was performed and she was taken to the intensive care unit. A repeat laparotomy was performed on the sixth postoperative day, following a clinical deterioration and again no leak was identified. Given the history of ulcerative colitis, the perforation was presumed to be of colonic origin and a total colectomy and ileostomy was performed. Histopathological examination of the colectomy specimen revealed extensive colonic diaphragm disease with 30 thin-walled diaphragms, one of which reduced the lumen to a pin-hole. No perforation was identified. CONCLUSION: To the best of the our knowledge, this is the first report of the development of colonic diaphragm disease in the absence of a history of non-steroidal anti-inflammatory drug ingestion. Given the history of ulcerative colitis we believe that the disease may have arisen as a result of the healing of the underlying inflamed colon rather than as a direct effect of non-steroidal anti-inflammatory drugs.
INTRODUCTION:Colonic diaphragm disease is an uncommon condition usually associated with the long-term use of non-steroidal anti-inflammatory drugs. CASE PRESENTATION: A 48-year-old woman presented as an emergency patient with abdominal pain and vomiting. Past medical history included inflammatory bowel disease of ulcerative colitis type for which she was taking azathioprine and prednisolone. On examination, she was shocked with signs of peritonism. Following resuscitation, she was taken for a laparotomy upon which a small amount of turbid fluid was identified but there was no direct evidence of an intra-abdominal perforation. A peritoneal lavage was performed and she was taken to the intensive care unit. A repeat laparotomy was performed on the sixth postoperative day, following a clinical deterioration and again no leak was identified. Given the history of ulcerative colitis, the perforation was presumed to be of colonic origin and a total colectomy and ileostomy was performed. Histopathological examination of the colectomy specimen revealed extensive colonic diaphragm disease with 30 thin-walled diaphragms, one of which reduced the lumen to a pin-hole. No perforation was identified. CONCLUSION: To the best of the our knowledge, this is the first report of the development of colonic diaphragm disease in the absence of a history of non-steroidal anti-inflammatory drug ingestion. Given the history of ulcerative colitis we believe that the disease may have arisen as a result of the healing of the underlying inflamed colon rather than as a direct effect of non-steroidal anti-inflammatory drugs.