With the increased application and efficacy of radiation therapy in the management of patients with gastrointestinal, genitourinary, and retroperitoneal malignancies, normal tissue response to this treatment is important. Intestinal tolerance is a major factor limiting radiation treatment of tumours of the abdomen and pelvis. Small and large bowel complications (both acute and long-term) are closely related to radiation therapy techniques. Acute complications are correlated with volume of bowel irradiated and fraction size, while long-term complications are related not only to the volume of bowel treated and fraction size but also to total dose of radiation administered. Table 1 319 summarizes the incidence of long-term severe small bowel complications stratified to the parameters of total dose, fraction size, and volume and design of the radiation fields from a number of different series. As the data show, severe small bowel complications occur with high frequency in patients treated with large fields and high doses of radiation. Limiting small bowel irradiation to 45 to 50.4 Gy in 1.8 Gy fractions and large bowel irradiation to 55 to 60 Gy in 1.8 Gy fractions, with the use of carefully designed fields and technique, should limit complications to less than 5 per cent of patients. Other reported predisposing factors to long-term radiation injury include obesity, diabetes mellitus, hypertension, pelvic inflammatory disease, prior abdominal or pelvic surgery, and the use of concurrent chemotherapy during radiation therapy. Acute and long-term complications occur with distinct clinical courses and pathological manifestations.

Gastrointestinal symptoms are common during the course of radiation treatment to the pelvis and/or abdomen. Large bowel symptoms consist of an acute proctocolitis with diarrhoea and tenesmus. Sigmoidoscopsy during treatment frequently shows an inflamed, oedematous, and friable mucosa. Acute small bowel reactions may result in nausea, abdominal cramps, and watery diarrhoea, primarily due to the depletion of actively dividing cells in what is otherwise a stable cell renewal system. In the small bowel, loss of the mucosal cells results in malabsorption of various substances including fat, carbohydrate, protein, and bile salts. In the large bowel, failure of fluid adsorption results in watery diarrhoea.

Although occasionally severe, these symptoms are usually self limited and managed by the use of antispasmodic and anticholinergic medications. Some patients with symptoms refractory to these drugs may respond to a bile sequestrating agents (such as cholestyramine), although such reports are anecdotal. In a double blind placebo controlled trial, buffered acetysalicylate was effective in improving gastrointestinal symptoms in patients who had undergone curative radiotherapy for malignant gynaecological disease. The prevalence and severity of radiation induced diarrhoea may also be reduced by using an elemental diet or total parenteral nutrition during therapy.

Long term complications include obstruction, perforation, bleeding, malabsorption, and fistulae. The latent period between completion of radiation therapy and the subsequent development of these complications is usually 6 to 24 months but chronic radiation enteritis can occur many years after the original treatment. Colicky abdominal pain is the most common symptom, and generally precedes bloody diarrhoea, tenesmus, steatorrhoea, and weight loss. Less commonly, patients present with an acute obstruction or perforation of the small or large bowel.

Pathological study of bowel affected by chronic radiation enteritis demonstrates obliterative endarteritis of the small vessels in the intestinal wall, submucosal fibrosis, and lymphatic dilatation. Perhaps the injury sustained by endothelial and connective tissue in the intestinal wall leads to progressive ischaemia of the intestinal wall. Ischaemia then leads to mucosal ulceration, necrosis of the intestinal wall with subsequent bleeding, perforation, stricture, and fistula formation, alone or in combination.

Radiation enteritis can also be progressive: in a series of 51 patients reported by Galland, only 24 patients remained symptom free after the first manifestation and treatment, whereas 20 patients developed second, third, or more gastrointestinal problems. Bleeding appeared to be a less ominous presentation: no new complications followed a bleeding episode, while 33 per cent of those with stricture and 89 per cent of those with perforation or fistula later manifested new lesions.

The medical and surgical treatment of chronic radiation enteritis is complex and requires individual management. Isolated damage to the rectum or rectosigmoid junction can often be managed with a low residue diet and steroid suppositories, but damage to the large intestine is frequently associated with significant injuries to the distal part of the small intestine. In the management of lesions of the small intestine, antispasmodics, anticholinergics, broad spectrum antibiotics, cholestyramine, and salicylazosulphapyridine have been used but responses to these agents have been anecdotal and based on a small number of patients. The use of a low fat diet, a low residue diet, or a gluten and lactose free diet with low fat as well as elemental diets have all been reported to be useful in selected patients with chronic radiation enteritis. A randomized study comparing total parenteral nutrition, with or without methylprednisone, with enteral nutrition for patients with severe chronic small bowel radiation enteritis found the former to be beneficial, with improvement in nutritional, radiological, and clinical parameters. The efficacy of total parenteral nutrition administration appeared to be enhanced by use of methylprednisone.

Before definitive surgical treatment is embarked upon, the status of the original malignancy and the extent of radiation damage should be assessed. Sepsis, malnutrition, and biochemical abnormalities should be corrected. Although wide resection and primary anastomosis may be appropriate for patients with single, discrete areas of radiation induced pathology manifested as obstruction, perforation, or bleeding, the majority of patients have more generalized radiation damage. Those who present with radiation induced perforation of the small bowel should be treated as emergencies, with avoidance of primary anastomosis. Exteriorization of the involved segments may be the optimal procedure in this situation, even though a further operation will be necessary to reconstitute the alimentary tract. An enteric fistula can sometimes be managed conservatively but such management is rarely successful. Gastrointestinal bypass without extensive resection of the involved bowel has less mortality and a higher success rate.

Abdominal and pelvic radiotherapy is increasingly used in the curative treatment of many abdominal and pelvic malignancies. Bowel tolerance is a major limitation to this treatment. Long-term complications occur less frequently than acute complications but are substantially more serious. Efforts must be made to minimize long-term bowel complications: these include the use of modern radiation treatment planning and techniques. Surgical measures to exclude the small bowel from the radiation field—absorbable mesh, ectopic implant, cystopexy, and omental flap—have shown encouraging results in reducing the amount of small bowel in the radiation field and thus reducing the incidence of small bowel injury.

Galland RB, Spencer J. Natural history and surgical management of radiation enteritis. Br J Surg 1987; 74: 742–7.

Gunderson LL, Martenson JA. Gastrointestinal tract radiation tolerance. Frontiers Radiat Ther Oncol 1989; 23: 277–98.

Gunderson LL, Russell AH, Llewellyn HJ, Doppke KP, Tepper JE. Treatment planning for colorectal cancer: radiation and surgical techniques and value of small-bowel films. Int J Radiat Oncol Biol Phys 1985; 11: 1379–93.

Hoskins RB, et al. Adjuvant postoperative radiotherapy in carcinoma of the rectum and rectosigmoid. Cancer 1985; 55: 61–71.

Kinsella TJ, Bloomer WD. Tolerance of the intestine to radiation therapy. Surg Gynecol Obstet 1980; 151: 273–84.

Loiudice TA, Lang JA. Treatment of radiation enteritis. J Gastroenterol 1983; 78: 481–7.

Mennie AT, et al. Treatment of radiation-induced gastrointestinal distress with acetylsalicylate. Lancet 1975; 942–3.

Minsky BD, Cohen AM. Minimizing the toxicity of pelvic radiation therapy in rectal cancer. Oncology 1988; 2: 21–5.

Piver MS, Barlow JJ. High dose irradiation to biopsy confirmed aortic node metastases from carcinoma of the uterine cervix. Cancer 1977; 39: 1243–6.

Sher ME, Bauer J. Radiation-induced enteropathy. Gastroenterology 1990; 85: 121–8.

Smith DH, DeCosse JJ. Radiation damage to the small intestine. World J Surg 1986; 10: 189–94.

Taylor Whartor J, Facog WJ III, Facog TGD, Facog FNR, Fletcher GH. Preirradiation cellotomy and extended field irradiation for invasive carcinoma of the cervix. Obstet Gynecol 1976; 49: 333–8.

Vigliotti A, Richard TA, Romsdahl MM, Withers HR, Oswald MJ. Postoperative adjuvant radiotherapy for adenocarcinoma of the rectum and rectosigmoid. Int J Radiat Oncol Biol Phys 1986; 13: 999–1006.

Yeoh EK, Horowitz M. Radiation enteritis. Surg Gynecol Obstet 1987; 165: 373–9.