Hemorrhoids pathophysiology
Jump to navigation
Jump to search
|
Hemorrhoids Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Hemorrhoids pathophysiology On the Web |
|
American Roentgen Ray Society Images of Hemorrhoids pathophysiology |
|
Risk calculators and risk factors for Hemorrhoids pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Ahmed Younes M.B.B.CH [3]
Overview
Hemorrhoids are normal vascular and connective-tissue cushions of the anal canal; the term hemorrhoidal disease refers to these cushions when they become symptomatic.[1][2] The dominant current model is the "sliding anal cushion" theory, which replaced the older idea that hemorrhoids are varicose veins. In this model, the connective tissue and smooth muscle that anchor the cushions weaken. The cushions then slide downward (prolapse), become engorged, and bleed.[3][4] Bleeding from hemorrhoids is arterial in character because it comes from arteriovenous communications within the cushions. This is the rationale for artery-directed therapies.[3] The dentate line marks the boundary between the two types and explains their different symptoms. Internal hemorrhoids have visceral innervation, so they bleed and prolapse painlessly. External hemorrhoids have somatic innervation, so they are painful when thrombosed.[1]
Pathophysiology
Normal anatomy and physiology of the anal cushions
- Anal cushions are subepithelial vascular and connective-tissue structures present in everyone. They are called hemorrhoids clinically only when they become symptomatic.[1][2]
- The cushions surround direct arteriovenous communications between the terminal branches of the superior rectal artery and the superior, middle, and inferior rectal veins. This region is a site of portosystemic communication.[2][3]
- The classic positions are left lateral, right anterior, and right posterior. However, cadaver studies show this typical configuration in only about 19% of individuals.[2]
- The muscularis submucosae ani (Treitz muscle) suspends and anchors the cushions to the underlying sphincter. It arises from the conjoined longitudinal muscle and the internal anal sphincter.[3]
- The cushions contribute about 15–20% of resting anal canal pressure. They act as a compressible plug that completes anal closure, supports continence, and protects the sphincter during defecation.[3][1][4]
The dentate line and its clinical consequences
| Feature | Internal hemorrhoids | External hemorrhoids |
|---|---|---|
| Location | Above (proximal to) the dentate line | Below (distal to) the dentate line |
| Epithelium | Columnar/transitional | Squamous (anoderm) |
| Innervation | Visceral (autonomic); insensate | Somatic (pudendal nerve, S2–S4); pain-sensitive |
| Typical manifestation | Painless bleeding and prolapse; pain only if strangulated | Acute pain when thrombosed |
The dentate line lies about 3–4 cm proximal to the anal verge.[1][5][4]
Core mechanism: the sliding anal cushion model
The pathogenic sequence below reflects the current evidence-supported model. Its initiating cause is still incompletely understood.[2][3]
- Weakening of the supporting tissue: The muscularis submucosae and fibroelastic anchoring tissue weaken and fragment. This is driven by aging (starting as early as the 2nd–3rd decade), pregnancy, and chronic straining.[3][4][6]
- Distal displacement: With less support, the cushions slide distally (prolapse).[3]
- Vascular engorgement: Loss of support leads to venous engorgement, dilation of the internal hemorrhoidal plexus, and distention of the arteriovenous anastomoses. Plexus dilation is a consequence of support failure, not the initiating event.[1][2][4]
- Self-perpetuating cycle: During straining, stool pushes the cushions distally through the sphincter. This downward slippage further impairs venous return, causing more swelling and progressive tissue damage.[6][7]
- Bleeding: The prolapsed, redundant mucosa is easily traumatized, which causes painless bright-red bleeding. The blood is bright red because of the arterial oxygen tension in the arteriovenous communications, not because it is venous.[2][3]
- Anatomic enlargement does not equal disease. Many anatomically enlarged hemorrhoids are asymptomatic.[7][1]
- Experimental work implicates dysregulation of the extracellular matrix and fibroblasts in connective-tissue breakdown. Examples include downregulation of fibulin-5, LTBP-4, collagen, elastin, and α-smooth muscle actin. These findings are hypothesis-generating and not yet clinically actionable.[8]
Anal sphincter tone
- Patients with symptomatic hemorrhoids often have elevated anal resting pressure and increased internal sphincter tone. It is unresolved whether this is a cause or a consequence of hemorrhoidal disease.[7][3][2]
Arterial inflow
- The arteriovenous component is clinically important. Hemorrhoidal bleeding is arterial in character, and symptoms improve after the feeding arteries are ligated.[3]
- This is the mechanistic rationale for Doppler-guided hemorrhoidal artery ligation and rectal artery embolization.[3][9]
Portal hypertension
- Portal hypertension is not a primary mechanism of hemorrhoidal disease. Its role as a risk factor is minor or contested.[7]
- Anorectal varices caused by portal hypertension are a distinct entity with different management and should not be equated with hemorrhoids.[7]
Pathophysiologic basis of grading
- Internal hemorrhoids are graded by the degree of prolapse using the Goligher classification. Each grade reflects progressive loss of connective-tissue support:[4][1][9]
- Grade I: bleed but do not prolapse
- Grade II: prolapse with straining and reduce spontaneously
- Grade III: prolapse and require manual reduction
- Grade IV: prolapse and are irreducible, with risk of strangulation and necrosis
Clinical implications of the pathophysiology
- Pain: Internal hemorrhoids are insensate, so acute severe anal pain points to something else. Likely causes are a thrombosed external hemorrhoid, a strangulated internal hemorrhoid, or another diagnosis such as an anal fissure or anorectal abscess.[1][4]
- Office procedures: Banding, sclerotherapy, and infrared coagulation are placed at least 2 cm above the dentate line to avoid the pain-sensitive anoderm.[5]
- First-line therapy: Support failure aggravated by straining is the main driver. First-line therapy therefore targets this mechanism with increased dietary fiber and water and avoidance of straining.[1][4]
- Continence: The cushions supply part of resting anal tone, so aggressive excision may compromise continence.[3]
- Bleeding pattern: Bright-red, painless bleeding fits the hemorrhoidal mechanism. Blood mixed with stool or melena suggests a more proximal source and requires evaluation rather than attribution to hemorrhoids.[1]
Areas of uncertainty
- The initiating cause of symptomatic prolapse remains unknown.[2][3]
- Whether elevated sphincter pressure is a cause or a consequence is unresolved.[7]
- Epidemiologic associations conflict on whether constipation and straining or diarrhea are linked to hemorrhoidal disease.[6][3]
- Pathways involving the extracellular matrix and fibroblasts (fibulin-5, LTBP-4) have not been validated for human diagnosis or therapy.[8]
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 Ashburn JH (2025). "Hemorrhoidal Disease: A Review". JAMA. doi:10.1001/jama.2025.13083.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Madoff RD, Fleshman JW (2004). "American Gastroenterological Association technical review on the diagnosis and treatment of hemorrhoids". Gastroenterology. 126 (5): 1463–73. doi:10.1053/j.gastro.2004.03.008. PMID 15131807.
- ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 Ganz RA (2013). "The evaluation and treatment of hemorrhoids: a guide for the gastroenterologist". Clin Gastroenterol Hepatol. 11 (6): 593–603. doi:10.1016/j.cgh.2012.12.020. PMID 23333220.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Wald A, Bharucha AE, Limketkai B, Malcolm A, Remes-Troche JM, Whitehead WE, Zutshi M (2021). "ACG Clinical Guidelines: Management of Benign Anorectal Disorders". Am J Gastroenterol. 116 (10): 1987–2008. doi:10.14309/ajg.0000000000001507. PMID 34618700 Check
|pmid=value (help). - ↑ 5.0 5.1 Guttenplan M (2017). "The Evaluation and Office Management of Hemorrhoids for the Gastroenterologist". Curr Gastroenterol Rep. 19 (7): 30. doi:10.1007/s11894-017-0574-9. PMID 28567655.
- ↑ 6.0 6.1 6.2 Bharucha AE, Knowles CH, Malcolm A (2025). "An Evidence-Based Practical Review on Common Benign Anorectal Disorders: Hemorrhoids, Anal Fissure, Dyssynergic Defecation, and Fecal Incontinence". Gastroenterology.
- ↑ 7.0 7.1 7.2 7.3 7.4 7.5 Jacobs D (2014). "Clinical practice. Hemorrhoids". N Engl J Med. 371 (10): 944–51. doi:10.1056/NEJMcp1204188. PMID 25184866.
- ↑ 8.0 8.1 Zhao Y, Xiao K, Wu Y, et al. Fibulin-5 promotes fibroblast activation through LTBP-4 to improve the pathogenesis of hemorrhoids. BMC Gastroenterol. 2025.
- ↑ 9.0 9.1 Khan K, Lakshminarayan R, Yiasemidou M, Long J, Sayeed S, Smith GE, Hunter I, Chetter I (2024). "Endovascular rectal artery embolisation (RAE) for symptomatic haemorrhoids". Cochrane Database Syst Rev (5): CD014829. doi:10.1002/14651858.CD014829.