Background

The prevalence of hemorrhoidal disease is difficult to determine. Some estimate that up to 90% of patients may complain of hemorrhoidal symptoms at least once in their lifetime [1]. The incidence of hemorrhoids increases with age, with males affected twice as often as females. Age predisposes to a laxity of Treitz’s ligaments, with an average onset after age 30. There are hereditary predispositions; however, occupational predisposition has not been demonstrated. Low residue diets seen typically in industrialized countries have been described as contributing to symptomatic hemorrhoids, presumably by causing smaller hard stools. This is clearly not the only etiology however, as those patients with diarrhea may also develop symptomatic hemorrhoids. Diets high in fiber may reduce the risk of hemorrhoid congestion. Although increased intra-abdominal pressure such as that seen in chronic pulmonary disease, prostatism, and pelvic tumors has been postulated to contribute to symptomatic hemorrhoids, the actual incidence is no greater in these patients than is found in the general population.

Data from the National Center for Health Statistics estimate that 10 million people in the United States have had symptomatic hemorrhoids; however, this may actually underestimate the problem, because the majority of patients may not seek professional care, preferring self-medication instead. Those who eventually seek medical care complaining of hemorrhoids often have another reason for their complaint. In one recent audit, only 20% of patients initially believed to have symptomatic hemorrhoids when presenting to their physician actually had hemorrhoids as the etiology of their complaints [2, 3, 4]. The most common presenting symptom is bleeding. It usually happens toward the end of defecation and is often bright red and painless. Prolapse and thrombosis may also occur. The patient may also complain of swelling and itching, but pain may also be present if there is thrombosis involving the external hemorrhoids [1, 5].

Pathophysiology and Anatomy

The anal canal is the terminal portion of the gastrointestinal tract. It begins approximately 2 cm proximal to the dentate line and extends to the anal verge. Anatomists and surgeons differ on the “definition” of the anal canal. The anatomic anal canal starts at the dentate line and extends to the anal verge, whereas the surgical anal canal includes the anatomic anal canal and the tissue 2 cm proximal to the dentate line (see Fig. 3.1). The lining of the surgical anal canal transitions from columnar mucosa above the dentate line to squamous epithelium containing hair follicles and sweat glands at the anal verge. The transitional zone, 0.5–1 cm above the dentate line, contains an abundance of nerve endings and is responsible for fine sensory discrimination [1, 6].

Figure 3.1.
figure 1

Surgical anal canal

Full size image

Hemorrhoids are cushions of vascular tissue arising above the dentate line (insensate) and extending to the anal verge (sensate). Microscopically, hemorrhoids are sinusoids (vascular structures without muscular walls) with a blood supply arising from the middle and inferior rectal arteries. Bleeding from hemorrhoids is arterial, arising from the presinusoidal arterial plexus, as evidenced by the bright red color, and having an arterial pH. The hemorrhoids arise in three main positions: right posterior, right anterior, and left lateral, which is coincident with the terminal branches of the hemorrhoidal vessels. Normal engorgement of these cushions contributes to the maintenance of continence.

It has been suggested that chronic straining secondary to constipation or occasionally diarrhea may result in pathologic hemorrhoids. Eventually, with repeated straining, the hemorrhoids may lose their attachment (Treitz’s ligaments) to the underlying rectal wall, leading to the prolapse of the tissue into the anal canal. The engorged tissue becomes more friable, which may contribute to bleeding. These tissues communicate with the superficial subcutaneous venules at the anal verge, which may result in external hemorrhoidal dilation [6, 7, 8]. Internal hemorrhoids are classified by history and not by physical examination, as follows:

  • Grade I—bleeding without prolapse.

  • Grade II—prolapse with spontaneous reduction.

  • Grade III—prolapse with manual reduction.

  • Grade IV—incarcerated, irreducible prolapse.

The utility of this system is that it correlates well with management recommendations; i.e., Grade I and II hemorrhoids are often successfully treated by non-operative means, while Grade III and Grade IV hemorrhoids are more likely to require surgery. Investigators have suggested that those patients with symptomatic hemorrhoids have higher anal canal pressures. Anal canal pressures were measured in symptomatic and asymptomatic patients, demonstrating significantly higher pressures in the symptomatic patients. These patients had a fall in their resting pressures following treatment for the hemorrhoids, but still remained higher than asymptomatic controls. The magnitude of the pressure elevation did not correlate with the duration of symptoms or degree of prolapse [9, 10, 11, 12].

Treatment Options

Early disease (Grade I and early Grade II) is often managed with medications designed to cause vasoconstriction and treat inflammation for the engorged friable hemorrhoid. More advanced disease frequently requires operative management which may include sclerotherapy, cryosurgery, infrared coagulation, rubber band ligation, and various modes of surgical excision. These therapies attempt to remove the redundant tissue and create cicatrices to fix the remaining mucosa within the anal canal once again.