Shabana F. Pasha, MD
Which cells in the gastrointestinal tract are most prone to be damaged by radiation?
Crypt cells in the intestine as they have a high turnover rate.
When do acute and chronic radiation injury occur after radiation exposure?
Acute radiation injury occurs within 6 weeks of radiation exposure. Chronic radiation injury typically occurs 6 months after radiation exposure, but can occur up to 30 years after exposure.
What are the histopathological changes characteristic of acute radiation enteritis?
Inflammatory cell infiltrate, reduced crypt mitoses, crypt microabscesses, and ulceration.
What are the histopathological changes characteristic of chronic radiation injury?
Epithelial atrophy, obliterative endarteritis, submucosal fibrosis, mucosal ischemia, and necrosis.
What are the most common symptoms of acute radiation esophagitis?
Dysphagia, odynophagia, and substernal chest pain, typically occurring 2–3 weeks after initiation of radiation therapy.
How does radiation dosage correlate with esophageal symptoms and signs?
What other factors potentiate radiation-induced esophageal damage?
The manner of delivery with an accelerated fractionation schedule may result in more injury. Concomitant chemotherapy may also potentiate radiation injury and is particularly common with doxorubicin.
What are late effects of esophageal radiation injury?
Esophageal stricture and fistula formation.
What patient factors are associated with the development of chronic radiation enteritis?
Decreased body mass index, chronic co-morbidities (diabetes mellitus, hypertension, inflammatory bowel disease), smoking, and prior intestinal surgery.
What treatment factors are associated with the development of chronic radiation enteritis?
Radiation dose and fractionation, radiation technique, volume of small bowel irradiated, and concomitant chemotherapy.
What is the most common late manifestation of radiation-induced small bowel injury?
Partial small bowel obstruction.
What are the radiologic findings of chronic radiation enteritis on barium contrast radiography?
Mucosal edema, separation of intestinal loops, and flocculation.
What are the most common causes of diarrhea in patients with chronic radiation enteritis?
Malabsorption (lactose, bile salts, fat), small intestinal bacterial overgrowth, enteroenteric fistula, and gastrointestinal dysmotility.
What are the most common symptoms associated with the condition demonstrated in the figure?
Figure 6-1 See also color plate.
The figure demonstrates the typical endoscopic appearance of chronic radiation proctopathy. Rectal bleeding, tenesmus, and low-volume diarrhea are the most common symptoms.
What is the most serious complication after endoscopic therapy with argon plasma coagulation (APC) for chronic radiation proctopathy? When does this typically occur?
Rectourethral fistula. It occurs if aggressive APC treatment is performed within 6–24 months after radiation in patients with seed implants.
What is the most common location of radiation-induced rectal ulcers?
Anterior wall of the rectum, approximately 6–8 cm proximal to the anal verge.
What are the most common vascular abnormalities found in the gastrointestinal tract?
What are the characteristic histopathologic findings in an angioectasia?
Dilated thin-walled vessel lined with endothelium, with or without smooth muscle fibers.
What is being demonstrated in the figure and where in the colon are these lesions most commonly located?
Figure 6-2 See also color plate.
Angioectasia. Cecum and ascending colon.
True/False: Left-sided colonic angioectasia are more likely to bleed than those on the right side of the colon.
What percent of patients with colonic angioectasia have concomitant small bowel angioectasia?
What is the initial test of choice to evaluate the small bowel for angioectasia after a negative esophagogastroduodenoscopy (EGD) and colonoscopy in patients with obscure gastrointestinal bleeding?
Video capsule endoscopy.
What is Heyde syndrome?
Gastrointestinal bleeding from angioectasia in patients with aortic stenosis.
What is the proposed mechanism by which aortic stenosis leads to development of angioectasia?
Disruption of the vonWillebrand multimers during passage through the narrowed aortic valve leads to acquired vonWillebrand disease. It is considered that the increased prevalence of angioectasia in this setting is due to the increased detection rather than a true increased incidence, as the patients with this disease usually present with bleeding.
What are the clinical criteria for the diagnosis of hereditary hemorrhagic telangiectasia (HHT) aka Osler–Weber–Rendu syndrome?
Epistaxis, telangiectasias (multiple sites including lips, oral cavity, fingers, and nose), visceral vascular malformations (pulmonary, gastrointestinal, cerebral, or spinal), and family history (first-degree relative) of HHT.
At what age do patients with HHT present with gastrointestinal bleeding?
Fourth decade of life.
What are the histopathological changes typically seen in association with the condition shown in the figure?
Figure 6-3 See also color plate.
The figure demonstrates the typical appearance of gastric antral vascular ectasia (GAVE, aka “watermelon stomach”). Dilated capillaries with focal thrombosis, dilated and tortuous veins in the submucosa, and fibromuscular hyperplasia of the muscularis mucosa are the usual histological findings.
What conditions are associated with GAVE?
GAVE is usually seen in middle-aged and older women. It is associated with achlorhydria, atrophic gastritis, cirrhosis, CREST syndrome, and bone marrow transplantation.
What is the treatment of GAVE?
Supportive treatment with iron therapy and packed red blood cell (PRBC) transfusions, endoscopic ablation (eg, APC), and, rarely, antrectomy for refractory cases.
An endoscopy is performed on a 43-year-old man with long-standing alcoholism and stigmata of chronic liver disease on physical exam. Describe the mucosal changes seen on endoscopy. What is the most likely diagnosis?
Figure 6-4 See also color plate.
Snake skin or mosaic appearance of the mucosa in the gastric body and fundus is seen. The most likely diagnosis in this case is portal hypertensive gastropathy.
What is the treatment of portal hypertensive gastropathy (PHG)?
Supportive treatment with iron supplementation, PRBC transfusions, and nonselective beta blockers; transjugular intrahepatic portosystemic shunt (TIPS) for refractory cases.
What is a Dieulafoy lesion?
It is a dilated aberrant submucosal artery. Focal pressure from the artery can lead to erosion of the overlying mucosa causing severe and often intermittent GI bleeding. Although the most common location is 6 cm distal to the gastroesophageal junction along the lesser curvature, Dieulafoy lesions have been described throughout the GI tract.
What diseases are associated with cutaneous vascular nevi and gastrointestinal bleeding?
Blue Rubber Bleb Nevus syndrome and Klippel–Trenaunay–Weber syndrome.
What gastrointestinal lesions are seen in Blue Rubber Bleb Nevus syndrome?
Venous malformations, most commonly located in the small bowel.
What is superior mesenteric artery syndrome?
Impingement of the superior mesenteric artery on the duodenum, when the angle between the root of the spinal muscular atrophy (SMA) and aorta is narrowed to less than 25 degrees. It usually occurs after rapid weight loss in adults. Symptoms include postprandial epigastric pain, vomiting, and early satiety.
What is celiac artery compression syndrome?
Celiac artery compression syndrome, also referred to as median arcuate ligament syndrome and Dunbar syndrome, is characterized by postprandial abdominal pain thought to be related to compression of the celiac artery by fibers of the median arcuate ligament.
True/False: The etiology of celiac artery compression syndrome remains a source of controversy.
True. Indeed, even the existence of this syndrome remains a source of controversy. As a consequence, so do the diagnosis and treatment.
What are the clinical findings in celiac axis compression syndrome?
Postprandial epigastric pain, diarrhea, weight loss, and presence of an abdominal bruit that increases with expiration. The characteristic radiologic finding is compression of the celiac axis by the median arcuate ligament.
What are the risk factors for acute mesenteric ischemia?
Advanced age, atherosclerosis, cardiac arrhythmias, low cardiac output states, valvular heart disease, and intra-abdominal malignancy.
What are the causes of acute mesenteric ischemia?
Superior mesenteric artery embolism (50%), superior mesenteric artery thrombosis, mesenteric venous thrombosis, and nonocclusive ischemia.
What is the classical clinical presentation of acute mesenteric ischemia?
Severe abdominal pain (periumbilical) out of proportion to the physical examination.
What is the gold standard test in the diagnosis of acute mesenteric ischemia?
Mesenteric angiography; multidetector CT angiography is a noninvasive alternative.
Intestinal angina, sitophobia, and weight loss are the classical findings of what vascular disorder?
Chronic mesenteric ischemia. Sitophobia refers to a fear of eating.
True/False: In patients with classic chronic mesenteric ischemia, two of the three mesenteric vessels must typically be occluded or severely stenotic for the patient to experience symptoms of abdominal pain because of the extensive collateral network of the bowel.
What is the mechanism of injury to the colon in ischemic colitis?
Hypoxia due to nonocclusive ischemia followed by reperfusion injury with release of oxygen-free radicals and toxins.
True/False: Mesenteric angiography is an important test in the diagnosis of ischemic colitis.
False, for reasons noted in the preceding question.
What proportion of patients with ischemic colitis develop gangrenous colitis?
What are the most common locations where ischemic colitis occurs?
Splenic flexure and sigmoid colon.
Why is isolated ischemic colitis of the right colon associated with a worse prognosis than other areas of the colon?
A large proportion of these patients have silent superior mesenteric artery obstructive disease and are at risk for acute mesenteric ischemia of the small intestine.
What is the classical clinical triad seen in Henoch–Schonlein purpura?
Abdominal pain, arthritis, and palpable purpura.
What are the gastrointestinal manifestations in Behcet’s disease?
Ulcerations in the terminal ileum, cecum, ascending colon, and esophagus that mimic Crohn’s disease clinically and endoscopically. Pancreatitis may also occur.
• • • SUGGESTED READINGS • • •
Czito BG, Willett CG. Radiation injury. In: Feldman M, Friedman L, Brandt L, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Philadelphia, PA: Saunders Elsevier; 2010:639-651.
Coia AR, Myerson RJ, Tepper JE. Late effects of radiation therapy on the gastrointestinal tract. Int J Radiation Oncology Biol Phys. 1995;31:1213-1236.
Brandt LJ, Landis CS. Vascular lesions of the gastrointestinal tract. In: Feldman M, Friedman L, Brandt L, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Philadelphia, PA: Saunders Elsevier; 2010:593-608.
American Gastroenterological Association Medical Position Statement: Guidelines on intestinal ischemia. Gastroenterology. 2000;118:951.