Radiation therapy: Managing GI tract complications

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Applied Evidence

Radiation therapy: Managing GI tract complications

J Fam Pract. 2017 August;66(8):E1-E7

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References

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The stomach

The stomach is relatively resistant to XRT injury. Although XRT therapy can cause a transient decrease in acid output, there are rarely significant short- or long-term consequences with conventional therapeutic dosing (less than 50 gray).¹¹

The liver

Hepatic resistance to radiation is relatively high; however, liver toxicity has been reported at low doses, an effect that is seen largely following bone marrow transplantation.²⁴ Acute histologic XRT-related liver injury changes consist of severe pan-lobar congestion leading to hemorrhagic necrosis, cell atrophy, and perivascular fibrosis, as well as sclerosis of central and sublobular hepatic veins. The majority of patients will show reversal of the histologic changes within 3 months; however, approximately 25% to 40% of patients,²⁵ depending on total XRT dose to the liver and other technical factors, will experience progressive and chronic changes resulting in liver atrophy, severe perivascular injury, and fibrosis of the portal vein or bile ducts.

Besides hyperbaric oxygen, there are no evidence-based preventive or therapeutic treatments that address the underlying mechanisms of radiation-related GI tract injury.

The clinical symptoms of acute liver injury may include right upper quadrant pain, ascites, jaundice, veno-occlusive disease, or Budd-Chiari syndrome.²⁵ The major chronic complication of XRT-related liver injury is progressive fibrosis, which may advance to cirrhosis.

Small bowel

The small bowel is the most radiosensitive GI tract organ due to high cell turnover, which makes it very susceptible to XRT-related injury.^4,8,10,26-28 Under 3 gray, ≤20% of patients will develop radiation enteropathy, while at >5 gray, the incidence rises progressively with dose, and a majority of patients will be symptomatic.²⁹ The degree to which the bowel is healthy before XRT can be an important factor in developing enteropathy. Parenthetically, treatment with a full bladder may also help displace some of the loops from the field of XRT and decrease injury.

Acute XRT-related injury of the small bowel includes mucosal necrosis (ie, direct cell death) and ulcerations that may present as diarrhea, pain, malabsorption, weight loss, bleeding, and perforation.^4,8,10,26-28 Fortunately, in most patients, these are self-limited and can be managed symptomatically. Loperamide is the first-line medication for diarrhea, although Lomotil (diphenoxylate/atropine) may also be used if necessary.^4,8,10,26-28 Nutrition may be challenging in severe cases, and if dietary modifications and supplementation do not prove sufficient, home parenteral nutrition is required.

Over time, chronic small bowel pathology may develop, including strictures in 3% to 15%, fistulae in 0.6% to 4.8%, secondary neoplasia in up to 10%, dysmotility- or adhesion-related small intestinal bacterial overgrowth in up to 45%, and malabsorption with associated nutritional deficiency in up to 63%.^26-28 Other common XRT-related complications are chronic pain, which could be due to adhesions or ischemia, small intestinal bacterial overgrowth, or partial bowel obstruction, and telangiectasias that result with acute or chronic blood loss.¹³