Pathophysiology of Hemorrhoids
Hemorrhoids develop from abnormal swelling and prolapse of the normal anal cushions due to stretching of their suspensory muscles and dilation of the submucosal arteriovenous plexus, though the exact underlying cause remains unknown. 1
Normal Anatomy and Function
- Anal cushions are normal vascular structures consisting of connective tissue surrounding arteriovenous communications between terminal branches of the superior rectal arteries and rectal veins 2
- These cushions are suspended by smooth muscle arising from the conjoined longitudinal muscle layer 2
- They contribute 15-20% of resting anal pressure and play a role in fecal continence and anal canal sensitivity 2, 3
Pathophysiologic Mechanism
Structural Changes
- Symptomatic hemorrhoids arise when anal cushions become abnormally enlarged, leading to stretching of the suspensory muscles and prolapse of upper anal and lower rectal tissue through the anal canal 1, 2
- Disruption of the fibromuscular supporting layer in the submucosa, above the vascular cushions, represents the initial pathogenic event 3, 4
- Abnormal dilatation and distortion of the vascular channels, combined with destructive changes in the supporting connective tissue within the anal cushion, are paramount findings 5
Vascular Component
- Dilation of the submucosal arteriovenous plexus occurs within the subepithelial space 2
- Dysregulation of vascular tone and vascular hyperplasia appear to play important roles in hemorrhoidal development 5
- Hemorrhoids are NOT varicosities—they are vascular cushions composed of arterioles, venules, and arteriolar-venular communications that slide down, become congested and enlarged, and bleed 4
- The bright red bleeding characteristic of hemorrhoids is arteriolar in origin due to arterial oxygen tension from arteriovenous communications within the anal cushions 1, 4
Pressure Changes
- Elevated anal resting pressure has been consistently demonstrated in patients with hemorrhoids compared to controls 1, 2
- Whether this elevated pressure causes or results from enlarged hemorrhoids remains unclear, but resting tone normalizes after hemorrhoidectomy 1, 2
- Voluntary contraction pressure remains unchanged 1
- Ultraslow pressure waves are more common in patients with hemorrhoids 1
Contributing Factors (Lack of Rigorous Proof)
Important Caveat
The American Gastroenterological Association emphasizes that rigorous proof for most commonly believed risk factors is lacking, despite widespread clinical belief in their importance 1, 2, 6
Commonly Cited but Unproven Factors
- Inadequate fiber intake, prolonged sitting on the toilet, and chronic straining at stool are widely believed by clinicians to contribute, yet rigorous proof is lacking 1, 2, 6
- Constipation, diarrhea, pregnancy, and family history have all been proposed but none have been rigorously proven 1, 2
- Increased intra-abdominal pressure and prolonged straining are commonly cited predisposing factors 7
Special Population: Pregnancy
- Approximately 80% of pregnant persons develop hemorrhoids, more commonly during the third trimester due to compression of the rectum by the gravid uterus 2
- Only 0.2% of pregnant women require urgent hemorrhoidectomy for incarcerated prolapsed hemorrhoids 1, 2
Clinical Manifestations from Pathophysiology
Internal Hemorrhoids
- Prolapsed tissue is easily traumatized, leading to bleeding 1
- Prolapse of rectal mucosa leads to mucus deposition on perianal skin, causing itchiness and discomfort 1
External Hemorrhoids
- External hemorrhoids are asymptomatic unless they become thrombosed, presenting as an acutely painful perianal lump 1
- Thrombosed external hemorrhoids occasionally bleed when local pressure causes erosion through overlying skin 6
Key Clinical Pitfall
Portal hypertension has been shown NOT to be the cause of hemorrhoids, contrary to older teaching 4. This is a critical distinction, as hemorrhoids should not be attributed to liver disease or portal venous system pathology.