Ischemic pancolitis: recognizing a rare form of acute ischemic colitis

Ischemic colitis is the most common form of gastrointestinal ischemia.^1,2 The diagnosis, however, is often elusive, as patient signs and symptoms are nonspecific. Colonic involvement is usually segmental; ischemic colitis rarely involves the entire colon, but in such cases it is associated with increased morbidity and mortality.³

Case 1

A 62-year-old woman presented with septic shock and was referred after the results of an initial laparotomy were negative. Afterward, she was persistently hypotensive and required mechanical ventilation. Abdominal computed tomographic imaging revealed free air in her upper abdomen and diffuse thickening of the entire colon. Flexible sigmoidoscopy showed patchy areas of mucosal necrosis in the colon.

At a second laparotomy, the serosa of the rectosigmoid and splenic flexure were noted to be dusky red, with multiple perforations. A total colectomy and ileostomy were performed. Histological examination revealed extensive areas of full-thickness necrosis throughout the entire length of the colon.

Case 2

A 74-year-old woman was referred to our institution 2 weeks after a Hartman's resection for perforated segmental ischemic colitis. She developed abdominal distention and acute hemodynamic instability. Repeat emergency laparotomy revealed a grey colon proximal to the colostomy and patchy necrosis of the transverse colon. The cecum showed multiple areas of serosal ischemia. The results of histological examination indicated ischemic colitis involving the entire colon (Fig. 1).

FIG. 1. Ischemic colitis. Note the diffuse, continuous necrosis of the colonic epithelium with focal sparing of the base of the crypts (withering crypts), submucosal edema, vascular congestion, hemorrhage and fibrin thrombi.

Discussion

Ischemic colitis can be categorized as occlusive or nonocclusive.¹ Low-flow nonocclusive ischemia occurs most frequently in response to diminished cardiac output, shock, hypovolemia and the use of medications known to diminish splanchnic blood flow.² Critically ill patients are the most susceptible to ischemic colitis. The precise biological process leading to colonic ischemia remains unknown. The regions of the colon typically affected are shown in Fig. 2.²

FIG. 2. Incidences of colonic ischemia, by site. The data are from a 1999 review by S.V. Alapati and A.A. Mihas, published in volume 105 of Postgraduate Medicine , pages 177–80, 183–4 and 187.

Ischemic pancolitis is extremely rare, with only a handful of cases documented.^3,4 When Longo and colleagues³ reviewed cases of ischemic colitis over a period of 6 years, 12 of 43 patients presented with diffuse peritonitis and were found to have total colonic ischemia. The mortality rate for this group of patients was 75%. The authors concluded that the prognosis for total colonic ischemia is far worse than for segmental colonic ischemia, which, in their study, had an associated mortality of 22%.

Guivarc'h and associates⁴ reviewed 88 patients with ischemic colitis, of whom 18 had total colonic ischemia. The importance of perioperative colonoscopy was highlighted by these authors, as the endoscopic appearance of the mucosa, not the external appearance of the bowel, best revealed the extent of ischemic damage and in turn determined the extent of resection.

Both of our patients fared well, presumably because the pancolonic nature of the ischemia was recognized at their respective second laparotomy and the entire colon removed.

Conclusions

Ischemic pancolitis should be considered in the differential diagnosis of ischemic colitis, particularly in patients with a hypotensive prodrome. Although indications for surgery do not differ from those of segmental ischemia, vigilant examination of the entire colon at laparotomy as well as cautious pre- or intraoperative colonoscopy are necessary in order to recognize the diffuse nature of the disease and to initiate appropriate management.

This paper was presented as a poster at the annual meeting of the Canadian Association of General Surgeons, held in London, Ont., September 19–22, 2002.

Competing interests: None declared.

Correspondence to: Dr. Brian M. Taylor, London Health Sciences Centre — University Campus, 339 Windermere Rd., London ON N6A 5A5; fax 519 663-3068; brian.taylor@lhsc.on.ca

Accepted for publication Dec. 16, 2003