The Evaluation and Treatment of Hemorrhoids

A Guide for the Gastroenterologist

Robert A. Ganz

Disclosures

Clin Gastroenterol Hepatol. 2013;11(6):593-603. 

In This Article

Pathophysiology and Symptoms

Although hemorrhoidal cushions are normal anatomic structures, they are infrequently referred to until issues arise, and then the term hemorrhoid is meant as a pathologic process. The pathogenesis of hemorrhoids is not completely clear, but as stated by Kann et al,[3] "all etiologic factors work toward stretching and slippage of the hemorrhoidal tissue." As the supporting tissue of the anal cushions weakens, downward displacement of the cushions can occur, causing venous dilation and prolapse.[29,30] There is some controversy regarding the pathogenesis of symptomatic hemorrhoids, as Thomson[26] and Corman[31] propose the following possibilities:

  1. Deterioration of the anchoring connective tissue, as described by Thomson.

  2. Downward displacement or prolapse of the hemorrhoidal tissue.

  3. Abnormal distention of the arteriovenous anastomoses within the cushions.

  4. Abnormal dilatation of the veins of the internal hemorrhoidal venous plexus.

Any number of possible contributing factors leading to migration of the hemorrhoidal cushions has been suggested, including lack of dietary fiber, chronic straining, spending excess time on the commode, constipation, diarrhea, pregnancy, sedentary lifestyle, and a family history. Apart from pregnancy, none of these etiologies are supported by good evidence.[9,30] Others have discussed the role of pelvic floor dysfunction, particularly as that relates to elevated anal sphincter pressure, which has been demonstrated in some patients with symptomatic hemorrhoids. However, it is not clear whether these pressure changes are the cause or the result of hemorrhoids.[27,32,33]

As the overlying skin or mucosa is stretched, additional fibrous and sinusoidal tissue develops. With time, the anatomic structures supporting the muscularis submucosae weaken, leading to continued slippage and prolapse. As the redundant tissue moves toward the anal verge, it becomes susceptible to injury and allows symptoms to develop[11] (Figure 2).

Figure 2.

Illustration of internal hemorrhoid beginning to prolapse into the anal canal and external hemorrhoid. Courtesy of Iain Cleator, MD, Vancouver, BC, Canada.

The majority of hemorrhoidal symptoms arise from enlarged internal hemorrhoids, with bleeding as the most common presenting symptom.[9] As internal hemorrhoids prolapse through the anal canal, the tissue can become traumatized and friable, leading to bleeding. Hemorrhoids are arteriovenous plexuses, so the bleeding is typically bright red in color.[9,28] Blood that is darker in color suggests other, more proximal sources. Bleeding can be identified on the toilet paper or in the toilet bowl, is typically not mixed with stool, can drip or squirt out, and can be exacerbated by straining.[12,27] Hemorrhoids typically do not cause a positive Hemoccult test by themselves.[9,34,35] Internal hemorrhoids are covered with columnar mucosa, leading to mucous deposition on the perianal skin, which can also cause itching and perineal irritation. The prolapsing tissue can also impede the ability of the anal verge to "seal," and so fecal soiling can be noted as well.[8]

Internal hemorrhoids originate from points proximal to the dentate line and are covered by relatively insensate mucosa, so they are typically not painful. Internal hemorrhoids also rarely thrombose.[9] Hemorrhoid-associated pain usually comes from thrombosed external hemorrhoids, which can present as an acutely painful perianal swelling. External hemorrhoids are otherwise typically asymptomatic. With this in mind, if pain is one of the patient's symptoms, then it is recommended to look for coexistent complicating issues that may be the cause of perianal pain. These associated factors include entities such as anal fissures, solitary rectal ulcer syndrome, and a host of issues dealing with pelvic floor dysfunction (internal sphincter spasm, pelvic dyssynergia, proctalgia fugax, etc).[8]

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