Complete rectal obstruction due to ischaemia following elective abdominal aortic aneurysm surgery

R.T. Gunasekera R. Ackroyd C.J. Stoddard
Department of Surgery, Royal Hallamshire Hospital, Glossop Road, Sheffield, S10 2JF,U.K.

Correspondence to: R. Ackroyd, Departmentof Surgery, Royal Hallamshire Hospital,Glossop Road, Sheffield, S10 2JF, U.K.

Introduction Case report

Discussion Conclusion References

Keywords: Rectal stricture, large bowel obstruction, ischaemic proctitis
Surg J R Coll Surg Edinb Irel., 1 April 2003, 114-117

Ischaemic rectal stricture formation is a rare but documented complication of aortic aneurysm surgery. We report the first case of acute large bowel obstruction secondary to this rare complication

INTRODUCTION
Acute ischaemic proctitis is a rare condition with only 39 cases described in the world literature whilst ischaemic rectal stricture formation has only been described on eleven previous occasions.^1-6 The latter is thought to be the extreme end of a spectrum of sequelae secondary to bowel ischaemia. Most cases have been associated with aortic or aortoiliac surgery and are probably secondary to hypotension, poor collateral blood supply following inferior mesenteric artery ligation and a compromised internal iliac circulation. The left half of the transverse colon and descending colon are supplied by the marginal artery (of Drummond), formed by the bifurcation of the left colic artery as it travels toward the splenic flexure.⁴ This artery is considered the most important collateral vessel as it is the artery with which the left colic artery anastomoses with the mid colic artery; a branch of the superior mesenteric artery. In between 5-22% of cases reported the mid colic artery is said to be absent, though in most it provides adequate collateral circulation between the left and right colic arteries.⁴

Prolonged ischaemia by any of the above mechanisms may result in mucosal ulceration and necrosis, leading to subsequent fibrosis and stricture formation. We report the first case of mechanical large bowel obstruction secondary to this pathophyisiological process and discuss the difficulties in diagnosis and management of the condition.

CASE REPORT
A 72-year-old male presented eight weeks following the elective repair of an abdominal aortic aneurysm, with a history of diarrhoea since surgery. The details of his pre-operative health and operative management are as follows. He was an ex-smoker who stopped smoking following a myocardial infarction 24 years earlier, and had been on medication for chronic (controlled) atrial fibrillation for 40 years. He walked over a mile a day and did not have a history of claudication or erectile dysfunction. There was no history of pre-existing gastrointestinal problems or of colonic surgery.

Examination prior to surgery revealed intact peripheral pulses; hence there had been no reason to perform a duplex Doppler scan. A spiral computerised tomography (CT) scan documented that the iliac vessels were calcified and were unsuitable for endovascular repair.

At laparotomy, the aortic aneurysm was noted to be juxta-renal; a 2cm right common iliac aneurysm was also present. All abdominal organs were normal. Suprarenal clamp time was 35 minutes, and a bifurcated 18x9mm (Sulzer-Vascutek gelsoft knitted polyester gelatin) graft was used for aorto-iliac reconstruction. Iliac backflow was brisk and perfusion was noted to be good on completion of the anastomosis. There was no record of any concerns about the colon at the end of the procedure.

With regards to the post-operative diarrhoea, toxin assay on stool cultures had been positive for clostridium difficile on two occasions and the patient had been treated with two separate courses of metronidazole. He then developed lower abdominal pain, abdominal distension and vomiting, as well as watery diarrhoea. Clinical examination of the abdomen was consistent with bowel obstruction and rectal examination revealed a large fixed mass typical of a carcinoma. In view of the fixity of the rectal lesion and the need to relieve the obstruction, a defunctioning procedure was planned.

Examination under anaesthesia (EUA) revealed an apparent tight stenosing annular rectal tumour 4-7cm from the anal verge. This barely admitted a fingertip and precluded passage of a rigid sigmoidoscope. Multiple biopsies were taken. The patient then proceeded to a laparotomy, which revealed a gaseously distended sigmoid colon but no tumour palpable above the peritoneal reflection. The rest of the colon appeared normal, but two liver lesions were also noted. A defunctioning sigmoid loop colostomy, therefore, was fashioned.

Histology revealed inflamed colonic mucosa, consistent with a benign inflammatory process with no evidence of dysplasia or malignancy. However, the presence of ulcerated polypoid granulation tissue, polymophs and histiocytes were suggestive of an ischaemic aetiology (Figures 1 and 2). Abdominal ultrasound showed the liver lesions to be simple hepatic cysts, rather than metastases. The carcinoembryonic antigen level was normal at 0.9ng/l.

Figure 1: Section of colonic mucosa showing fibrous tissue between crypts - courtesy of Dr.TJ Stephenson, Consultant Pathologist, Royal Hallamshire Hospital, Sheffield

Figure 2: Section of colonic mucosa showing capillary up-growth - courtesy of Dr. TJ Stephenson, Consultant Pathologist, Royal Hallamshire Hospital, Sheffield

Magnetic resonance imaging (MRI) of the pelvis showed an extensive lesion involving the entire rectum, which was fixed and unresectable (Figure 3). The rectum was rebiopsied but again there was no evidence of dysplasia or malignancy. The prostate specific antigen level was also normal. A further EUA two months later showed a completely obstructing rectal lesion. It was noted by the surgeon at the time that the lesion felt softer than what would be expected for a malignant lesion with similar involvement. Biopsies again showed ulcerated polypoid granulation tissue, with no dysplasia or malignancy. Histological features were not considered to be those of either ulcerative colitis or Crohn’s disease on either occasion. Three months following the initial presentation, the MRI was repeated, but again the appearances were similar with extensive rectal thickening noted. The patient still has a defunctioning stoma but, to date, remains well more than two years after the initial presentation and at present no further intervention is planned.

Figure 3: MRI image (horizontal section) at level of seminal vesicles (seen above) showing rectal “stranding”, indicative of fibrosis - Courtesy of Dr. A Blakeborough, Consultant Radiologist, Royal Hallamshire Hospital, Sheffield

DISCUSSION
Acute ischaemic colitis is a recognised complication of aortic surgery, with commonly quoted prevalence rates of 0.7% for elective and 2% for emergency aneurysm repairs.⁷ However, colonoscopic evaluation post-aortic surgery suggests that the condition may be far more common than previously thought, with up to 60% of patients undergoing emergency aneurysm repair showing signs of ischaemia.^8,9 On the other hand, it is extremely rare for the rectum to be affected. Only 39 cases of acute ischaemic proctitis have been reported, and in only 11 of these was the condition complicated by rectal stricture formation (see Table 1).^1-6 In none of these cases was the stricture severe enough to cause large bowel obstruction.

There are various theories regarding the aetiology of acute ischaemic proctitis. It may occur where blood flow has been compromised or where collateral circulation is inadequate. Hence, it is more common following complex aorto-iliac procedures. High ligation of the inferior mesenteric artery avoids interruption of anastomotic channels, allowing secondary supply of the rectum from the left colic and sigmoidal vessels.¹ Similar collateral supply between internal and external iliac arteries may help protect the rectum from ischaemia.

There is a spectrum of disease severity, ranging from superficial mucosal ulceration and ischaemia to frank rectal gangrene and perforation. The degree of damage is variable and dependent on the severity of the ischaemia. Submucosal haematomata are said to be pathognomonic. Clinical indicators of ischaemia of the colon or rectum include early bowel action, diarrhoea, and rectal bleeding. Lax or absent anal sphincter tone may be a more specific indicator of acute ischaemic proctitis and frequent digital rectal examination has been suggested for patients at high risk.² Infectious causes need exclusion using toxin assay and stool culture. Plain radiography may show thumb printing or other evidence of ischaemic bowel. Magnetic resonance imaging may show extensive soft tissue stranding. Contrast studies, though useful in diagnosing strictures in general, may have little role in the acute situation because of the inherent risk of perforation in a compromised bowel.

Labelled white cell scans have been proposed as an alternative means of diagnosis, defining the extent and severity of ischaemia.¹ Laser Doppler flowmetry has been used to detect early signs of ischaemia and D-lactate has been identified as a predictor of colonic ischaemia.^10,11 Superficial damage may be treated conservatively with sulphasalazine and intravenous antibiotics with close monitoring with proctosigmoidoscopy.² Severe ischaemia and obstruction may require a defunctioning procedure.²

CONCLUSION
Rectal stricture formation is a rare complication of aortic surgery and can, if extreme, lead to large bowel obstruction. It is a difficult condition to diagnose and can cause much confusion in a clinical setting if it presents late. Awareness of risk factors for acute ischaemic proctitis and its associated symptoms enhances its early diagnosis. The acute phase is best managed conservatively, but symptomatic strictures may require dilatation, myotomy or most commonly colostomy formation.^1,3 This is the recommended treatment when surgery is considered for significant stricture formation. There is little or no role for subsequent resection of the rectum, as retention of the fibrosed rectum does not appear to result in any increased morbidity.²

REFERENCES
1. Lane TM, Bently PG. Case Report: Rectal Strictures following abdominal aortic aneurysm surgery. Ann R Coll Surg Engl 2000; 82: 421-23.
2. Nelson RL, Briley S, Schuler JJ, Abcarian H. Acute ischaemic proctitis. Dis Colon Rectum 1992; 35: 375-80.
3. Smith RF. Ischaemia of the colon as a complication in the surgery of the abdominal aorta. Arch Surg 1960; 80: 808-16.
4. Bernstein WC, Bernstein EF. Ischaemic ulcerative colitis following inferior mesenteric arterial ligation. Dis Colon Rectum 1963; 6: 54-61.
5. Birnbaum W. Colonic and rectal ischaemia following abdominal aneurysectomy. Dis Colon Rectum 1964; 7: 293-302.
6. Orr G, Jones PF. Ischaemic proctitis followed by rectal stricture. Br J Surg 1982; 69: 433-34.
7. Schroeder T, Christoffersen JK, Andersen J, Bille S, Gravgaard E, Kimose HH et al. Ischaemic colitis complicating reconstruction of the abdominal aorta. Surg Gynecol Obstet 1985; 169: 299-303.
8. Bast TJ, van der Biezen JJ, Scherpenisse J, Eikelboom JC. Ischaemic disease of the colon and rectum after surgery for abdominal aortic aneurysm: a prospective study of the incidence and risk factors. Eur J Vasc Surg 1990; 4: 253-57.
9. Hagihara PF, Ernst CB, Griffen WO Jr. Incidence of ischaemic colitis following abdominal aortic reconstruction. Surg Gynecol Obstet 1979; 149: 571-73.
10. Sakakibara Y, Jikuya T, Saito EM et al. Does Doppler flowmetry aid in the prevention of ischaemic colitis in abdominal aortic aneurysm surgery? Thorac Cardiovasc Surg 1997; 45: 12-14.
11. Poeze M, Froon AH, Greve JW, Ramsay G et al. D-Lactate as an early marker of intestinal ischaemia after ruptured abdominal aortic aneurysm repair. Br J Surg 1998; 85: 1221-24.

Copyright: 14 January 2003