Background: Hemroidsal disease is a common entity in the general population and in clinical practice. The most common cause of hematochezia in adults, it remains high in the differential diagnosis of almost any anorectal complaint.
Although hemroids are very common, their true prevalence is unknown. Their presence may be underestimated due to the large proportion of relatively asymptomatic patients. Conversely, many nonspecific anorectal symptoms can be reflexively, and falsely, attributed to hemroids without the appropriate workup.
The presentation of symptomatic hemroids may be acute, chronic, or relapsing.
Pathophysiology: Hemroids are a normal part of the human anorectum and arise from subepithelial connective tissue cushions within the Excretory Orifice canal.
Present in utero, these cushions surround and support distal anastomoses between the superior rectal arteries and the superior, middle, and inferior rectal veins. They also contain a subepithelial smooth muscle layer, contributing to the bulk of the cushions. Normal hemroidsal tissue accounts for approximately 15-20% of resting Excretory Orifice pressure and provides important sensory information, enabling the differentiation between solid, liquid, and gas.
Most people contain 3 of these cushions. Although classically described as lying in the right posterior (most common), right anterior, and left lateral positions, this combination is found in only 19% of patients. Hemroids can be found at any position within the rectum.
Hemroids are classified by their anatomic origin within the Excretory Orifice canal and by their position relative to the dentate line.
Internal hemroids develop above the dentate line from embryonic endoderm. They are covered by the simple columnar epithelium of Excretory Orifice mucosa and lack somatic sensory innervation.
External hemroids develop from ectoderm and arise distal to the dentate line. They are covered by stratified squamous epithelium and receive somatic sensory innervation from the inferior rectal nerve.
Mixed hemroids are confluent internal and external hemroids. Venous drainage of hemroidsal tissue mirrors embryologic origin:
Rich anastomoses exist between these 2 and the middle rectal vein, connecting the portal and systemic circulations.
Most symptoms arise from enlarged internal hemroids. Abnormal swelling of the Excretory Orifice cushions causes dilatation and engorgement of the arteriovenous plexuses. This leads to stretching of the suspensory muscles and eventual prolapse of rectal tissue through the Excretory Orifice canal. The engorged Excretory Orifice mucosa is easily traumatized, leading to rectal bleeding that is typically bright red due to high blood oxygen content within the arteriovenous anastomoses. Prolapse leads to soiling and mucus discharge (triggering pruritus) and predisposes to incarceration and strangulation.
Most clinicians use the grading system proposed by Banov et al in 1985, which classifies internal hemroids by their degree of prolapse into the Excretory Orifice canal. This system both correlates with symptoms and guides therapeutic approaches.
Grade I hemroids project into the Excretory Orifice canal and often bleed but do not prolapse.
Grade II hemroids may protrude beyond the Excretory Orifice verge with straining or defecating but reduce spontaneously when straining ceases.
Grade III hemroids protrude spontaneously or with straining and require manual reduction.
Grade IV hemroids chronically prolapse and cannot be reduced. They usually contain both internal and external components and may present with acute thrombosis or strangulation.