Hemorrhoids
The internal hemorrhoidal plexus of veins is located in the submucosal space above the valves of Morgagni. The anal canal separates it from the external hemorrhoidal venous plexus, but the two spaces communicate under the anal canal, the submucosa of which is attached to underlying tissue to form the interhemorrhoidal depression. Whenever the internal hemorrhoidal plexus is enlarged, there is associated increase in supporting tissue mass, and the resultant venous swelling is called an internal hemorrhoid. When veins in the external hemorrhoidal plexus become enlarged or thrombosed, the resultant bluish mass is called an external hemorrhoid.
Both types of hemorrhoids are very common and are associated with increased hydrostatic pressure in the portal venous system, such as during pregnancy, straining at stool, or with cirrhosis. When internal hemorrhoids enlarge, pain is not a usual feature until the situation is complicated by thrombosis, infection, or erosion of the overlying mucosal surface. Most persons complain of bright red blood on the toilet tissue or coating the stool, with a feeling of vague anal discomfort. The discomfort is increased when the hemorrhoid enlarges or prolapses through the anus; prolapse is often accompanied by edema and sphincteric spasm. Prolapse, if not treated, usually becomes chronic as the muscularis stays stretched, and the patient complains of constant soiling of underclothing with very little pain. Prolapsed hemorrhoids may become infected or thrombosed; the overlying mucous membrane may bleed profusely as the result of the trauma of defecation.
External hemorrhoids, because they lie under the skin, are quite often painful, particularly if there is a sudden increase in their mass. These episodes result in a tender blue swelling at the anal verge due to thrombosis of a vein in the external plexus and need not be associated with enlargement of the internal veins. Since the thrombus usually lies at the level of the sphincteric muscles, anal spasm often occurs.
The diagnosis of internal and external hemorrhoids is made by inspection, digital examination, and direct vision through the anoscope and proctoscope. Since such lesions are very common, they must not be regarded as the cause of rectal bleeding or chronic hypochromic anemia until a thorough investigation has been made of the more proximal gastrointestinal tract. Acute blood loss can occasionally be attributed to internal hemorrhoids. Chronic anemia in the presence of large but not definitely bleeding hemorrhoids should provoke a search for a polyp, cancer, or ulcer.
Most hemorrhoids respond to conservative therapy such as sitz baths or other forms of moist heat, suppositories, stool softeners, and bed rest. Internal hemorrhoids which remain permanently prolapsed are best treated surgically; milder degrees of prolapse or enlargement with pruritus ani or intermittent bleeding can be successfully handled by banding or injection of sclerosing solutions. External hemorrhoids which become acutely thrombosed are treated by incision, extraction of the clot, and compression of the incised area following clot removal. No surgical procedure should be carried out in the presence of acute inflammation of the anus, ulcerative proctitis, or ulcerative colitis. Both proctoscopy and barium enema should always be performed before a patient is subjected to hemorrhoidectomy.