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Gut. 2007 December; 56(12): 1759.
PMCID: PMC2095704


Carry on with the pills

[filled triangle] Norberto L, Polese L, Cillo U, et al. A randomized study comparing ligation with propranolol for primary prophylaxis of variceal bleeding in candidates for liver transplantation. Liver Transp 2007;13:1272–8.

Although beta‐blockers have a proven efficacy in preventing bleeding from varices, significant numbers of patients have either contraindications or intolerance to these drugs. Endoscopic variceal ligation can obliterate varices within about a month and hence ligation offers a distinct advantage over long‐term treatment with propranolol. Norberto et al conducted a randomised controlled trial comparing these two interventions for patients awaiting liver transplantation.

Sixty‐two patients (mean age 52.6 years) with Child B‐C cirrhosis (32 due to hepatitis C) and high‐risk varices were randomised to receive propranolol or banding. During a mean follow‐up period of 14.6 months there was no significant difference between the two groups in overall mortality (three in each group) and transplantation rate (14 vs 10 in the banding and propranolol groups, respectively). One patient in the banding group and two receiving propranolol died due to bleeding. Adverse events (two instances of post‐banding ulcer bleeding and five of drug intolerance) were similar in the two groups. However, the cost of banding (US$4289 (SD 285); £2114 (SD 140); €3023 (SD 201)) was significantly higher than the cost of beta‐blocker treatment (US$1425 (SD 460); £703 (SD 227); €1005 (SD 324); p<0.001). Although the authors conclude that both modalities of primary prophylaxis were equally effective in this sub‐group of patients, the study reminds clinicians of the potentially fatal complications of variceal ligation. Overall, banding for primary prevention is best reserved for selected patients who are unsuitable for beta‐blocker treatment.

Pre‐pouch ileitis: more evidence for ulcerative colitis in the small bowel?

[filled triangle] Calabrese C, Fabbri A, Gionchetti P, et al. Controlled study using wireless capsule endoscopy for the evaluation of the small intestine in chronic refractory pouchitis. Aliment Pharmacol Ther 2007;25:1311–6.

[filled triangle] Bell AJ, Price AB, Forbes A, et al. Pre‐pouch ileitis: a disease of the ileum in ulcerative colitis after restorative proctocolectomy. Colorectal Dis 2006;8:402–10.

Ulcerative colitis is already known to affect the small intestinal mucosa in the form of backwash ileitis and pouchitis. The group from Bologna, Italy, evaluated 16 patients with chronic refractory pouchitis and a control group of 8 patients with normal pouches using wireless capsule endoscopy, as well as conventional pouch endoscopy and small bowel follow‐through. They found ileal lesions above the pouch on capsule endoscopy in all patients with chronic refractory pouchitis (aphthae in 18%, erosions in 16%, erythema and oedema in 24%, atrophy in 12%, deep fissuring ulcers in 20% and also scars, polyps or cobblestoning in a few). In one patient with duodenal lesions, histology at gastroscopy showed mucosal inflammation not diagnostic of Crohn's disease. In contrast, the control group had no abnormalities other than localised oedema in three (27%) in the mid‐jejunum. Bacteriology showed no abnormalities in the patients with ileitis. Eight patients with chronic refractory pouchitis were given infliximab and seven had complete resolution of ileitis at capsule endoscopy 3 months later.

This study is complemented by a paper from Bell et al. This was a retrospective survey of 571 patients who had ileoanal pouches. In 19 (3%) there was evidence of ileal inflammation extending up to 50 cm proximal to the pouch. In three of these, Crohn's disease was diagnosed and one had non‐steroidal‐related inflammation. The remaining 15 had non‐specific ileitis histologically. Only half of these patients had pouchitis however, so it appears that pre‐pouch ileitis is not confined to patients with pouchitis. Only 2 of the 15 had back‐wash ileitis prior to colectomy.

So what do we know about pre‐pouch ileitis? Ileal inflammation appears to be an uncommon finding after ileo‐anal pouch anastomosis for ulcerative colitis but it is much more common in patients with pouchitis and severity is maximal in the distal small bowel. Histology and bacteriology to date give no clues to aetiology but it responds to immunosuppressive treatment. It is assumed that these lesions do not occur in patients with end‐ileostomies, although no comparable studies have been done. If the lesions are confined to those with pouches, then the implication is that the altered bacterial flora of the pouch is affecting the susceptible mucosa of the ileum. Yet more evidence that surgery can't cure colitis and that the whole of the gut can be affected by ulcerative “colitis”.

Stoma or no stoma? That is the question…

[filled triangle] Matthiessen P, Hallböök O, Rutegård J, et al. Defunctioning stoma reduces symptomatic anastomotic leakage after low anterior resection of the rectum for cancer: a randomized multicenter trial. Ann Surg 2007;246:207–14.

The role of the defunctioning stoma in reducing anastomotic leakage following operations such as low anterior resection for rectal cancer or ileoanal pouch procedures is controversial and has not been assessed in any randomised trial of sufficient size. Current surgical practice usually dictates a tailored approach, allowing clinicians to avoid a stoma in well patients who have undergone a technically straightforward procedure. Clearly this is desirable for the patients but the consequences of an anastomotic leak under these circumstances could be devastating.

This multicentre, randomised trial from Sweden provides clear evidence that stomas can reduce anastomotic leak and is, therefore, an important addition to the body of surgical literature in this area. From December 1999 to June 2005, 234 patients were randomised to defunctioning loop stoma or no stoma groups. Inclusion criteria for randomisation were: expected survival >6 months; a low anastomosis ([less-than-or-eq, slant]7 cm from the anal verge); the absence of major intra‐operative adverse events; and a technically straightforward anastomosis. Patients randomised to the defunctioning stoma group had a leakage rate of 10.3% (12 of 116) and those in the no stoma group had a leakage rate of 28.0% (33 of 118) (OR 3.4; 95% CI 1.6 to 6.9; p< 0.001). The need for urgent abdominal re‐operation was 8.6% (10 of 116) for those randomised to the stoma group and 25.4% (30 of 118) for those without (p<0.001).

It is difficult to change surgical practice based on a single trial but this article provides compelling evidence in support of a defunctioning stoma following operation for low rectal cancer. A three‐fold increase in leak and need for emergency re‐operation when a stoma is avoided is clearly an important message for all surgeons. Although this study has not investigated other surgical procedures such as the ileoanal pouch and there are fundamental clinical differences between these operations, it is tempting to extrapolate these results and at least consider defunctioning all patients with low anastomoses.

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