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Colorectal varices and congestive rectopathy or colopathy have been erratically reported in patients with portal hypertension. The clinical importance of these entities has not been described. We assessed the changes in the venous system of the rectum by endoscopy and rectal endosonography (EUS). We also assessed the role of factors such as etiology of portal hypertension, grade of esophageal varices, sclerotherapy, and liver disease severity on the occurrence of these vascular changes.We studied changes in the venous system of the rectum using endoscopy and EUS in 60 patients with portal hypertension (cirrhotic 41, noncirrhotic 19). Ten patients with irritable bowel syndrome and 6 patients with hemorrhoids served as controls. Rectal varices were classified as tortuous, nodular, and tumorous. Corresponding appearances on rectal EUS were classified as single or discrete multiple, multiple, and innumerable submucosal veins, respectively. Evidence of congestive rectopathy was also recorded.Prevalence of rectal varices was 43.3% on endoscopy (73% tortuous, 19% nodular, and 8% tumorous) and 75% on EUS (p0.0005). The latter showed corresponding appearances of submucosal veins in 25 of 26 patients and detected submucosal veins not identified at endoscopy in 19 other patients. Congestive rectopathy was found in 38.3% of patients. Multiple small dilated vessels in the submucosa were seen in 23.3% patients on rectal EUS. The development of these vascular changes was significantly influenced by sclerotherapy, but not by higher grade of esophageal varices, the etiology of portal hypertension, or severity of liver disease.Changes in the rectal venous system are common, with rectal EUS being superior to endoscopy in detecting early, as well as florid, changes.

Rectal endoscopic ultrasonography was performed using an ultrasound fiberscope in 20 patients with cirrhotic portal hypertension (6 alcoholic patients, 4 patients with hepatitis B surface antigen positive, and 10 cryptogenic patients) and in 10 patients with irritable bowel syndrome as controls. Rectal varices were diagnosed endoscopically when either tortuous or saccular distended veins were seen beneath the mucosa. At rectal endoscopic ultrasonography rectal varices were seen as rounded or oval echo-free structures in the submucosa. Rectal endoscopic ultrasonography also showed perirectal veins outside the rectal wall. Rectal varices were detected by endoscopy in 9 patients and by rectal endoscopic ultrasonography in 17 patients. Rectal endoscopic ultrasonography also detected submucosal veins in 3 of 10 controls. The number and size of submucosal veins seen on rectal endoscopic ultrasonography in patients with portal hypertension were greater than in controls (p0.01 for both number and size). The size of perirectal veins was greater in patients than in controls (p0.05), although their number was no different (p = NS). A perforating vein communicating between a submucosal and perirectal vein was seen in only one patient. Rectal wall thickness was not different in patients and controls (p = NS). Rectal endoscopic ultrasonography was superior to endoscopy in detecting the presence (85% versus 45%, p0.01), and number (p0.01) of rectal varices. Our study suggests that rectal endoscopic ultrasonography is useful in detecting changes in rectal and perirectal vasculature in patients with cirrhotic portal hypertension.