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Thursday 3 May 2018

Hemorrhoids: Understanding their Pathophysiology



Hemorrhoids
Hemorrhoids are a normal parts of the anorectum structure and contribute to the mechanism of anal closure, thus providing natural adjustment of anal continence.

Formation of hemorrhoids is a common anorectal condition. It is the symptomatic enlargement and distal displacement of the anal cushions. Millions of people around the world are affected with this condition. And it is a major medical and socioeconomic problem.

Why do hemorrhoids occur?
Many factors are thought to be responsible for the hemorrhoidal development, including constipation and prolonged straining. The dilatation and distortion of the vascular channel, together with destructive changes in the supporting connective tissue within the anus is a cause of hemorrhoidal disease.

Some research suggests that inflammatory reaction and vascular hyperplasia may promote the development of hemorrhoids in the form of a lump on anus. This article reviews the pathophysiology hemorrhoidal disease briefly.

Pathophysiology of hemorrhoidal disease
The exact pathophysiology of the development of hemorrhoids is not well understood. In the beginning, the theory of varicose veins, which postulated that hemorrhoids were caused by varicose veins in the anal canal, was quite popular. However, it is obsolete now because hemorrhoids and anorectal varices are proven to be different. As a matter of fact, patients who have portal hypertension and varices are not found to have an increased incidence of hemorrhoidal development.

Now, sliding anal canal lining theory is more widely accepted for the development of hemorrhoids. The sliding anal canal theory is supported by other anatomic studies also, such as by the work of WHF Thomson. He popularized the term “cushions” to describe the complex nature of muscle, connective tissue, veins, arteries, and arteriovenous communications which form the hemorrhoids.

This theory says that a hemorrhoid develops when the supporting tissues of anal cushions disintegrate. Hemorrhoids are therefore described as the abnormal downward displacement of the anal cushions causing venous dilatation.

In a human anaorectal system, three major anal cushions exist. These are located in the right anterior, right posterior and left lateral aspect of the anal canal. In addition, many numbers of minor cushions lie between these major cushion. The anal cushions of patients undergo significant pathological changes after the development of hemorrhoids. These changes may include such as abnormal venous dilatation, vascular thrombosis, degenerative process in the collagen fibers and fibroelastic tissues, damage and rupture of the anal subepithelial muscle etc. A severe inflammatory reaction is also found to occur in hemorrhoidal changes. This may be accompanied with mucosal ulceration, ischemia and thrombosis.

More recently, increased microvascular density was found in certain tissues of hemorrhoids. This indicates that neovascularization may also play a role in the development of hemorrhoids.

Several enzymes that involve degradation of the supporting tissues in the anal cushions are being studied. Matrix metalloproteinase (MMP), a zinc-dependent proteinase, is one of the most potent enzymes among these enzymes. It is found that MMP can degrade extracellular proteins such as elastin, fibronectin, and collagen. MMP-9 was found to be higher in hemorrhoidal tissues.

These are some prominent theories that describe the formation of hemorrhoids. However, many other theories have been formulated and suggested to describe them. Accordingly, many therapeutic and surgical treatments of hemorrhoids have been developed that range from dietary and lifestyle modification to radical surgery, depending on the degree and severity of symptoms in a patient.

References:

  1. Hemorrhoids: From basic pathophysiology to clinical management, World J Gastroenterol
  2. Why Are Hemorrhoids Symptomatic? The Pathophysiology and Etiology of Hemorrhoids, Department of Surgery, University of Missouri–Kansas City


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