Hemorrhoids are normal vascular and connective-tissue cushions of the anal canal. The term hemorrhoidal disease (HD) refers to these cushions when they become symptomatic.^[1] According to the current “sliding anal cushion” model, the supporting connective tissue and smooth muscle weaken with age and straining. The cushions then prolapse, become engorged, and bleed. This model has replaced the older view of hemorrhoids as varicose veins.^[2][3] Hemorrhoids are classified relative to the dentate line as internal, external, or mixed. Internal hemorrhoids are further graded I–IV by degree of prolapse using the Goligher classification.^[4] Internal hemorrhoids have visceral innervation, so they typically cause painless bleeding and prolapse. External hemorrhoids have somatic innervation and become painful when thrombosed.^[1]

HD is the most common anorectal disorder in adults, with an estimated global pooled prevalence of about 26%. In the United States, it affects approximately 10 million people and accounts for nearly 4 million office and emergency department visits each year.^[5][6] The most consistent risk factors are constipation with straining or prolonged toilet sitting, increasing age, and pregnancy. Common symptoms include hematochezia, prolapse, anal discharge, and pain when an external hemorrhoid thromboses. Diagnosis is made by inspection, digital rectal examination, and anoscopy. Rectal bleeding or anemia should not be attributed to hemorrhoids until colorectal cancer and other sources have been excluded.^[7]

Treatment escalates by grade. First-line therapy for all grades is increased dietary fiber and fluid intake with correction of defecation habits. Rubber band ligation is the first-line office procedure for grade I–III internal hemorrhoids. Excisional hemorrhoidectomy is the most durable option for refractory grade III, grade IV, and mixed disease.^[4] HD usually follows a relapsing–remitting course with an excellent prognosis, and only about 10% of patients ultimately require surgery.^[1]

Hemorrhoids were first documented by ancient Egyptians more than 3,700 years ago.

Hemorrhoids are classified by anatomic origin relative to the dentate line as internal, external, or mixed. Internal hemorrhoids are further graded I–IV by degree of prolapse using the Goligher classification. Grade I bleeds without prolapse; grade IV is irreducible. Location and grade together determine the stepwise escalation from conservative therapy to office-based procedures to surgery. External hemorrhoidal disease is not graded and becomes clinically relevant mainly when acutely thrombosed.^[1][4]

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][8] 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.^[2][3] Bleeding from hemorrhoids is arterial in character because it comes from arteriovenous communications within the cushions. This is the rationale for artery-directed therapies.^[2] 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]

No single cause has been identified. Disease reflects risk factors acting through two linked mechanisms: degeneration of the supporting tissue, and increased anorectal or intra-abdominal venous pressure.^[9][1] The best-supported associations are:

• Disordered defecation, including constipation, straining, and prolonged toilet sitting
• Increasing age
• Pregnancy and parity
• Smoking and hypertension, which are small but independent correlates in large screening data^[10]

The roles of obesity, diet, physical activity, diarrhea, and portal hypertension remain inconsistent. Anatomic hemorrhoids are common and often asymptomatic. Associations derived from endoscopic prevalence studies therefore may not apply directly to symptomatic disease.^[11]

Hemorrhoids should be differentiated from other diseases that cause anal discomfort and pain with defecation such as rectal cancer, anal fissure, anal abscess, and anal fistula.

Hemorrhoidal disease (HD) is the most common anorectal disorder in adults and one of the most frequent outpatient gastrointestinal diagnoses.^[12][6] Reported prevalence ranges from about 4% to nearly 40%. Most of this spread comes from differences in case definition and ascertainment method (self-report, physician examination, or endoscopy), not from true biological differences between populations.^[5][13]

• The largest meta-analysis to date covered 150 studies and about 9 million individuals. It estimated a global pooled point prevalence of approximately 26%.^[5]
• Prevalence rises with age and is modestly higher in women, mainly because of pregnancy and parity.^[5][10]
• In the United States, HD affects approximately 10 million people. It accounts for nearly 4 million office and emergency department visits each year.^[1][6]
• True prevalence is unknown, because many affected individuals are asymptomatic or self-treat and never seek care.^[5][6]

Current models attribute it mainly to age- and strain-related degeneration of the supporting connective tissue and anchoring (Treitz) muscle, with vascular engorgement as a secondary feature. This replaces the older varicose-vein (venous stasis) model.^[3][14] The most consistent risk factors are increasing age, constipation with straining or hard stools, and the late-pregnancy and peripartum period. Prior HD is a strong predictor of HD during pregnancy. Higher adiposity has genetic support for a causal role, even though observational data are inconsistent.^[10][15]. In cirrhosis with portal hypertension, HD is more prevalent but must be distinguished from rectal varices, which are a separate entity.^[16]

According to the USPSTF, screening for hemorrhoids is not recommended.

Most symptomatic hemorrhoids follow a relapsing–remitting course with an excellent overall prognosis, and only about 10% of patients ultimately require surgery.^[1] Asymptomatic or incidentally detected hemorrhoids need no treatment.^[1][3] The main complications of the disease are thrombosis of external hemorrhoids, strangulation of irreducible (grade IV) prolapse with risk of gangrene and perineal sepsis, iron-deficiency anemia from chronic bleeding, and pruritus ani with soiling.^[14][7] Treatment-related complications include pain and delayed bleeding after rubber band ligation, and urinary retention, fecal incontinence, and anal stricture after hemorrhoidectomy. Perineal sepsis after office procedures is rare but can be fatal.^[4] Recurrence rises as treatment becomes less invasive. Excisional hemorrhoidectomy has the lowest recurrence (2%–10%), and its advantage over rubber band ligation is concentrated in grade III disease.^[1][17][18] Rectal bleeding or anemia should never be attributed to hemorrhoids until colorectal cancer and other sources have been excluded.^[7]

Symptoms of hemorrhoids include pain with defecation, hematochezia, and anal discharge.

Patients with acute prolapsed or thrombosed hemorrhoids usually appear ill and in pain. Physical examination of patients with hemorrhoids is usually remarkable for protruding mass from the anus or palpable mass on digital rectal exam.

There are no specific diagnostic lab findings associated with hemorrhoids. However, complete blood count may show anemia in the case of chronic bleeding.

There are no X-ray, MRI or ultrasound findings associated with hemorrhoids.

There are no other diagnostic imaging studies of significance for hemorrhoids.

Anoscopy is mandatory to visualize internal hemorrhoids as they are not visible on inspection of the anal verge or palapable on performing digital rectal exam.

Medical (non-procedural) therapy is the appropriate initial management for symptomatic hemorrhoidal disease of all grades and is often definitive for grade I–II internal hemorrhoids.^[14][12] Increased dietary fiber and fluid intake with correction of defecation habits is first-line therapy with the strongest supporting evidence; it reduces persistent symptoms and bleeding but does not improve prolapse, pain, or pruritus.^[4][19] Topical preparations are low-risk symptomatic adjuncts supported only by low-quality evidence.^[4] Oral flavonoid phlebotonics reduce bleeding, pruritus, and discharge in randomized trials, but symptoms frequently recur after discontinuation and these agents are not FDA-approved in the United States.^[20][1] Patients who fail an adequate trial of medical therapy, or who have high-grade prolapse, should be referred for office-based procedures or surgery.^[3]

Procedural treatment of hemorrhoidal disease is reserved for symptomatic internal hemorrhoids that fail conservative therapy and for selected external or mixed disease. Conservative therapy includes dietary fiber 20–30 g/day, adequate fluid intake, avoiding straining and prolonged toilet sitting, and optional phlebotonics. Treatment escalates by grade, starting with the least invasive option. Office-based procedures are used for grade I–III internal hemorrhoids. Surgery is used for refractory grade III, grade IV, mixed internal–external disease, and acutely thrombosed external hemorrhoids.^[1][3][4] About 10% of patients with hemorrhoidal disease eventually undergo surgery.^[1] Rubber band ligation is the first-line office procedure. Excisional hemorrhoidectomy is the most durable operation but causes the most postoperative pain. Non-excisional techniques, such as Doppler-guided hemorrhoidal artery ligation, laser hemorrhoidoplasty, and radiofrequency ablation, cause less pain but have higher recurrence rates. Stapled hemorrhoidopexy is not recommended as routine first-line surgery.^[4][21]

Primary prevention of hemorrhoids may include drinking excessive fluids, regular exercise, practicing better posture, and reduction of bowel movement straining and time. Eating a high-fiber diet can make stools softer and easier to pass, reducing the pressure on hemorrhoids caused by straining.

The secondary preventive measures for hemorrhoids are similar to primary preventive measures.

Hemorrhoids were first discovered by ancient Egyptians more than 3,700 years ago.

• Hemorrhoids were known 3,700 years ago by ancient Egyptians. A recipe for an ointment made of ground acacia leaves was described in an ancient Egyptian manuscript.
• The ancient Greek medical textbook “Hippocratic Corpus” described a maneuver that is similar to rubber band ligation as we know it today.
• Roman encyclopedist Aulus Cornelius Celsus described band ligation and discussed possible complications. The Roman surgeon Galen suggested severing the connection between arteries and veins in an attempt to relieve the pain and the spread of infection.
• During the sixth century, hemorrhoids were known as Saint Fiacre’s curse after a saint who developed them after working in his farm.
• In 1398, the word “hemorrhoids” was first used in English after the French word “emorroides,” which developed from the Latin word “hæmorrhoida”. “Hæmorrhoida” means liable to bleeding.

Hemorrhoids are classified by anatomic origin relative to the dentate line as internal, external, or mixed. Internal hemorrhoids are further graded I–IV by degree of prolapse using the Goligher classification. Grade I bleeds without prolapse; grade IV is irreducible. Location and grade together determine the stepwise escalation from conservative therapy to office-based procedures to surgery. External hemorrhoidal disease is not graded and becomes clinically relevant mainly when acutely thrombosed.^[1][2]

Vascular anal cushions are normal structures that contribute to continence and anal sensation. They are termed hemorrhoidal disease only when they enlarge, bleed, or prolapse symptomatically.^[3] Classification has two axes:

• Anatomic location, which applies to all hemorrhoids.
• Grade of prolapse, which applies to internal hemorrhoids only.

• Perianal pruritus is not specific to external hemorrhoids. Mucoid discharge from prolapsing internal hemorrhoids is a common cause.^[1][5]

Internal hemorrhoids are graded by degree of prolapse. This four-grade system is the Goligher classification and is the one used by the ACG, ASCRS, and Cochrane sources.^[3][2][6] Painless bleeding can occur with internal hemorrhoids of any grade.^[7]

• Grade distribution in endoscopic populations is weighted toward low grades. In a colonoscopy cohort of patients with internal hemorrhoidal disease, 72.9% were grade I, 18.4% grade II, 8.2% grade III, and 0.53% grade IV.^[1]

• Assign both location and grade before treatment. Use external inspection at rest and with straining, digital rectal examination, and anoscopy; grade cannot be assigned reliably without visualizing prolapse.^[1][2]
• Classification guides treatment only in symptomatic disease. Asymptomatic hemorrhoids of any grade require no treatment.^[1]
• External and grade IV disease are not candidates for banding. Ligation below the dentate line causes severe somatic pain.^[3][5]
• Significant pain should prompt reassessment for thrombosed external hemorrhoid, strangulated internal prolapse, or an alternative diagnosis such as anal fissure or anorectal abscess.^[5]
• Do not attribute rectal bleeding to hemorrhoids by default. Bleeding from colorectal cancer is often misattributed to hemorrhoids; evaluate with colonoscopy when alarm features or unexplained bleeding are present.^[2][4][9]
• Avoid over-grading. Do not mistake rectal mucosal prolapse or external skin tags for high-grade internal hemorrhoids.^[5]

• It captures only prolapse. It does not capture bleeding severity, symptom burden, or external/mixed components, and it has inter-observer variability.^[6]
• Symptom-based and supplementary systems have been proposed, but none has displaced Goligher grading in current guidelines.^[6]
• Grade III management overlaps between office-based and surgical approaches. Evidence for Doppler-guided ligation is low quality.^[3]

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]

• 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 lies about 3–4 cm proximal to the anal verge.^[1][5][4]

The pathogenic sequence below reflects the current evidence-supported model. Its initiating cause is still incompletely understood.^[2][3]

1. 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]
2. Distal displacement: With less support, the cushions slide distally (prolapse).^[3]
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]
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]
5. 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]

• 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]

• 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 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]

• 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

• 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]

• 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]

Hemorrhoids are normal vascular cushions of the anal canal. Hemorrhoidal disease develops when the connective tissue anchoring these cushions deteriorates and the underlying arteriovenous plexuses become engorged, causing bleeding and prolapse.^[1][2] No single cause has been identified. Disease reflects risk factors acting through two linked mechanisms: degeneration of the supporting tissue, and increased anorectal or intra-abdominal venous pressure.^[3][4] The best-supported associations are:

• Disordered defecation, including constipation, straining, and prolonged toilet sitting
• Increasing age
• Pregnancy and parity
• Smoking and hypertension, which are small but independent correlates in large screening data^[5]

The roles of obesity, diet, physical activity, diarrhea, and portal hypertension remain inconsistent. Anatomic hemorrhoids are common and often asymptomatic. Associations derived from endoscopic prevalence studies therefore may not apply directly to symptomatic disease.^[6]

• Connective-tissue degeneration (sliding-cushion model): Age, chronic straining, and pregnancy weaken the anchoring connective tissue, so the cushions bulge and descend. During defecation, stool pushes the prolapsing tissue through the sphincter, which impairs venous return and causes cyclical swelling, trauma, and bleeding.^[3][2] This model has replaced the older view of hemorrhoids as simple varicose veins.^[1]
• Increased venous and intra-abdominal pressure: Sustained pressure (straining, pregnancy, raised intra-abdominal pressure) dilates the submucosal vascular plexus and stretches its fibroelastic support.^[4]
• Anal sphincter tone: Basal anal pressures are higher in patients with hemorrhoids than in controls across manometric studies. Whether this is a cause or a consequence remains uncertain.^[7]
• Anatomic vs symptomatic disease: In a colorectal cancer screening population, 38.9% of 976 adults had hemorrhoids at colonoscopy, but only 44.7% of these reported symptoms.^[6] Why some anatomic hemorrhoids become symptomatic is not well understood.^[3]

• Obesity: Findings conflict across studies.
  • In an Austrian screening cohort, each 1-unit increase in body mass index raised hemorrhoid risk by 3.5%.^[6]
  • In a Korean cohort, overweight was associated with hemorrhoids, but the effect of adiposity differed by sex and parity.^[5]
  • In a US colonoscopy cohort, neither overweight nor obesity was associated with hemorrhoids.^[8]
• Dietary fiber: Among fiber subtypes, only high grain-fiber intake was associated with lower prevalence (quartile 4 vs 1: OR 0.78; 95% CI 0.62–0.98).^[8] Direct evidence that low dietary fiber causes hemorrhoids is limited.
• Spicy food: Spicy food did not worsen hemorrhoidal symptoms in a randomized trial, contrary to common teaching.^[3]
• Physical activity and sedentary behavior: Sedentary behavior was paradoxically associated with lower risk (OR 0.80; 95% CI 0.65–0.98). Physical activity showed no significant association.^[8]
• Diarrhea and bowel frequency: An older case-control study suggested that diarrhea, rather than constipation, was associated with hemorrhoids.^[9] Frequent bowel movements were not associated with hemorrhoids in a later colonoscopy cohort.^[8] Constipation is therefore not the only relevant bowel disturbance, but no single bowel pattern is clearly causal.^[1]
• Direction of the constipation association: Constipation is more common in patients with hemorrhoids. However, hemorrhoids were not significantly more prevalent in constipated patients than in controls (OR 2.37; 95% CI 0.67–8.44). This suggests shared mechanisms, such as dyssynergic defecation and straining, rather than a simple one-way causal relationship.^[7]
• Straining: Straining was not independently associated with endoscopic hemorrhoids after adjustment in the smartphone cohort.^[10] This conflicts with traditional teaching.
• Portal hypertension and cirrhosis:
  • One review reports higher hemorrhoid prevalence in cirrhosis with portal hypertension (59%) than without it (19%).^[4] An older case-control study found no association with cirrhosis.^[9]
  • Clinically significant portal hypertension can produce anorectal varices. These are portosystemic collaterals, distinct from hemorrhoids, and must be distinguished before bleeding is attributed to hemorrhoids.^[4][11]

The following conditions are traditionally listed because they plausibly raise intra-abdominal or pelvic venous pressure:^[12]

• Chronic cough
• Heavy lifting
• Ascites
• Pelvic space-occupying lesions
• Straining related to bladder outlet obstruction

These factors have not been validated as independent risk factors in controlled epidemiologic studies.

Hemorrhoids should be differentiated from other diseases that cause anal discomfort and pain with defecation such as rectal cancer, anal fissure, anal abscess, and anal fistula.

Hemorrhoids should be differentiated from other diseases that cause anal discomfort and pain with defecation such as anal fissure, rectal prolapse and perianal abscess.

Disease	History	Physical exam findings	Sample image
Hemorrhoids	External hemorrhoids External hemorrhoids are painful as the skin below the punctate line is sensitive to pain.[1] Blood clots may form in external hemorrhoids. Thrombosed external hemorrhoids cause bleeding, painful swelling, or a hard lump around the anus. When the blood clot dissolves, extra skin is left behind. This skin can become irritated or itch. Excessive straining, rubbing, or cleaning around the anus may make symptoms, such as itching and irritation, worse. Internal hemorrhoids The most common symptom of internal hemorrhoids is bright red blood on stool, on toilet paper, or in the toilet bowl after a bowel movement. Internal hemorrhoids that are not prolapsed are usually not painful. Prolapsed hemorrhoids often cause pain, discomfort, and anal itching	Skin examination Inspection of the anal verge may show scratch marks and skin tags. Inspection also may reveal external hemorrhoids or prolapsed internal hemorrhoids. Digital rectal examination Digital rectal examination reveals the size and location of hemorrhoids. Thrombosed hemorrhoids are tender to palpation. Internal hemorrhoids are not palpable by digital rectal examination and the use of anoscope is mandatory.
Anal fissure	Anal fissure usually presents with tearing pain with every bowel movement.[1] Pain usually lasts for minutes to hours after every bowel movement. Patient is typically afraid of going to the bathroom to avoid the pain, which leads to a viscious cycle. The fissure worsens the constipation and the constipation (hard stool) aggravates the fissure. About two-thirds of the patients present with bright red blood streaks on toilet papers or on the surface of stools. May be accompanied by pruritis and discharge.	Most fissures occur in the posterior midline of the anal canal.[2] Skin tags in the perianal area may accompany chronic anal fissures.
Rectal prolapse	Rectal prolapse most commonly occurs in multiparous females over 40 years old.[3] Appears as a progressive mass protrusion from the anus. The protrusion first appears with straining and defecation, then progresses to the degree when it is no longer replaced back. It presents with abdominal discomfort and incomplete defecation. Fecal incontinence and anal discharge. Pain is not usually present.	Mass protruding from the anus.[4] Concentric mucosal rings are characteristic of rectal prolapse.
Perianal abscess	Perianal abscess presents with severe, continuous, dull, aching pain in the perianal area.[5] Pain is exacerbated with bowel movements, but is not exclusive to it. Constipation due to fear of bowel movements. Fever, headache, and chills may accompany the pain. If the abscess starts to drain, discharge of purulent or bloody fluid may be noticed.	Flatulent, erythematous, and tender area of skin overlying the abscess. If abscess is deep, tenderness is elicited with digital rectal examination.
Anal cancer	Rectal bleeding is the most common presentation.[6] Mass sensation in the anus. Mucoid discharge may occur. Patient may give a history of anal condyloma (especially homosexual men).[7] Fecal incontinence.	On digital rectal examination, solid hemorrhagic mass that is firmly fixed to the surrounding structures is noted. Femoral and inguinal lymph nodes may show lymphadenopathy secondary to spread of cancer.
Condylomata acuminata	Patient may give a history of unprotected anal sex with an infected partner. Having multiple sexual partners is a risk factor and should be investigated.[8] Condyloma acuminata presents with painless warts that vary in size, shape, and color. Pruritis and discharge may accompany the warts.	Anal condyloma acuminata may be accompanied by cervical, vaginal, or even ororpharyngeal warts, so the patient should be examined thoroughly.[9]

Hemorrhoidal disease (HD) is the most common anorectal disorder in adults and one of the most frequent outpatient gastrointestinal diagnoses.^[1][2] Reported prevalence ranges from about 4% to nearly 40%. Most of this spread comes from differences in case definition and ascertainment method (self-report, physician examination, or endoscopy), not from true biological differences between populations.^[3][4]

• The largest meta-analysis to date covered 150 studies and about 9 million individuals. It estimated a global pooled point prevalence of approximately 26%.^[3]
• Prevalence rises with age and is modestly higher in women, mainly because of pregnancy and parity.^[3][5]
• In the United States, HD affects approximately 10 million people. It accounts for nearly 4 million office and emergency department visits each year.^[6][2]
• True prevalence is unknown, because many affected individuals are asymptomatic or self-treat and never seek care.^[3][2]

Prevalence estimates must be interpreted according to how hemorrhoids were ascertained. Endoscopic and physician-examination studies consistently report higher rates than symptom-based self-report or claims data.^[3][7]

• In the meta-analysis, general-population studies gave much lower pooled estimates (about 8%) than studies of patients with gastrointestinal complaints (about 29%). This pattern reflects referral and examination bias.^[3]
• About one in three American adults have hemorrhoids on screening colonoscopy, and most of these are incidental findings.^[2]
• Among patients evaluated for hematochezia or by proctoscopy, reported rates reach 64–86%.^[12]
• The widely quoted U.S. figure of about 4.4% (4,400 per 100,000) comes from a single 1990 analysis of self-reported data. It substantially underestimates burden compared with modern endoscopic and pooled data, and should be cited only as historical context.^[11][3][2]
• No contemporary, nationally representative U.S. prevalence study exists.^[2]

• Reported incidence ranges from about 708 to 1,225 per 100,000 person-years, depending on data source.^[7]
• Incidence is difficult to measure directly. Nationwide claims for invasive treatment have been used as an indirect surrogate.^[7]

• Prevalence increases with age:
  • In pooled case-control data, patients with HD were significantly older than controls.^[3]
  • Older age was an independent risk factor in a large Korean screening cohort.^[5]
• Pooled point prevalence is about 25% in adults and about 14% in children. The pediatric estimate is based on only five small datasets.^[3]
• The traditional teaching that HD “peaks” at 45–65 years comes from historical self-report and care-utilization data.^[11] It likely reflects care-seeking and procedural patterns rather than underlying prevalence.^[2][7]
• More than half of adults older than 50 years are commonly estimated to have had HD at some point.^[13]

• Women have a slightly higher pooled point prevalence than men: 27.3% vs. 25.7%.^[3]
• Pooled case-control data showed no significant sex difference. Higher healthcare-seeking among women may partly inflate reported female prevalence.^[3]
• In a large Korean screening cohort:^[5]
  • Overall prevalence was slightly higher in women than men (17.2% vs. 16.3%).
  • The excess was confined to parous women (adjusted OR 1.06 vs. men).
  • Nulliparous women had lower prevalence than men (adjusted OR 0.92).
• The legacy statement that both sexes are “affected equally” is outdated. The modest female excess is driven largely by parity.^[5][3]

• Pooled prevalence in pregnant women is about 31%, the highest of any population subgroup in the meta-analysis.^[3]
• Pregnancy was associated with more than twice the odds of HD (unadjusted OR 2.6).^[3]
• Prevalence is higher in the postpartum period than in early pregnancy.^[3]
• Multiparity and cesarean delivery were not significantly associated with HD in pooled unadjusted analyses, although only two studies informed each estimate.^[3]
• Among parous women, higher body mass index and waist circumference were associated with HD.^[5]

Robust data on racial or ethnic differences in HD prevalence are not available.

• Pooled point prevalence by WHO region:^[3]
  • African region: 28.1% (highest)
  • Region of the Americas: 26.4%
  • European region: 26.0%
  • South-East Asia region: 23.4% (lowest)
• Prevalence was not associated with a country’s Human Development Index. The burden appears broadly similar across socioeconomic contexts.^[3]
• Country-level outliers mostly come from single studies and do not reliably represent national prevalence. Examples include about 53% in Germany and about 2.5% in Malaysia.^[3]

• In the United States:
  • HD is the third most common outpatient gastrointestinal diagnosis, with nearly 4 million office and emergency department visits annually.^[2]
  • It affects approximately 10 million people.^[6]
  • In 29 states covering about two-thirds of the U.S. population, there were 25,292 ambulatory surgery center visits for hemorrhoids in 2013 and 203,552 emergency department visits in 2014.^[2]
• The estimated annual economic burden is about $800 million, in the U.S. employer-insured population aged 18–64 years alone.^[7]
• Only a minority of patients undergo surgery.^[6]
• Death from hemorrhoids is exceedingly rare.^[14]

• Any quoted prevalence should be interpreted together with its ascertainment method and study population. Between-study heterogeneity in the meta-analysis was extreme (I² >99%).^[3]
• Hemorrhoids found on endoscopy are frequently asymptomatic. Symptoms commonly attributed to hemorrhoids are reported equally often by patients with and without them.^[2]
• Because hemorrhoids are so common, finding them does not establish them as the source of rectal bleeding. Colorectal cancer and other colorectal pathology must still be excluded where appropriate.^[1][2]
• Population-level associations with older age, pregnancy, constipation, and low grain-fiber intake are discussed in risk factors.^[3][8]

Hemorrhoidal disease (HD) is the symptomatic enlargement and distal displacement of the anal cushions. Current models attribute it mainly to age- and strain-related degeneration of the supporting connective tissue and anchoring (Treitz) muscle, with vascular engorgement as a secondary feature. This replaces the older varicose-vein (venous stasis) model.^[1][2] The most consistent risk factors are increasing age, constipation with straining or hard stools, and the late-pregnancy and peripartum period. Prior HD is a strong predictor of HD during pregnancy. Higher adiposity has genetic support for a causal role, even though observational data are inconsistent.^[3][4]. In cirrhosis with portal hypertension, HD is more prevalent but must be distinguished from rectal varices, which are a separate entity.^[5]

• Increasing age
• Constipation, straining, hard stools, incomplete evacuation
• Pregnancy (third trimester and postpartum)
• Parity / gravidity
• Prior hemorrhoidal disease
• Adiposity (BMI, waist circumference, body-fat %)
• Smoking,
• hypertension
• Chronic venous disease
• Portal hypertension

• Constipation, straining, hard stools, and incomplete evacuation are the best-supported modifiable factors, although effect sizes are modest.^[6]
• Prolonged toilet sitting is also implicated. The proposed mechanism is that raised intra-abdominal pressure and shear forces during straining are transmitted to the anal cushions.^[1]
• In care-seeking patients, constipation was among the variables most strongly associated with HD severity.^[7]
• Causality is weaker than traditionally taught. HD and constipation have different epidemiologic profiles, and some studies implicate diarrhea rather than constipation.^[2][8]

• HD is common in late pregnancy and the postpartum period. Reported frequency varies widely between studies, from 51% symptomatic in one survey cohort to as high as ≈80% in some reports.^[9][10]
• Contributing mechanisms include:
  
  • Venous congestion and rising intra-abdominal pressure from the gravid uterus
    
  • Progesterone-mediated smooth-muscle relaxation and slowed transit, which promote constipation
    
  • Expanded circulating volume^[10][11]
• Delivery-related and peripartum predictors identified in a prospective cohort include:^[12]
  • Prior perianal disease (hemorrhoids or anal fissure)
  • Constipation during pregnancy
  • Second-stage straining for more than 20 minutes
  • Birth weight greater than 3800 g
• In a randomized trial, dietary and behavioral counseling reduced postpartum HD (ITT RR 0.38; 95% CI 0.24–0.59).^[13]
• Gravidity alone was not associated with HD on controlled screening data. This underscores heterogeneity between populations.^[6]

• Observational data are inconsistent, including a null association in a large U.S. screening colonoscopy cohort.^[6]
• Two-sample Mendelian randomization supports a causal effect on HD of higher BMI, body-fat percentage, waist circumference, and waist-to-hip ratio. The findings were robust to adjustment for physical activity, and testing showed no evidence of reverse causation.^[4]
• The effect appears to be modified by sex and parity. BMI and waist circumference were positively associated with HD in parous women.^[3]

• HD is more prevalent in cirrhosis with portal hypertension (≈59%) than in cirrhosis without it (≈19%).^[14]
• Rectal varices are a distinct entity. They are portosystemic collaterals rather than degenerated anal cushions, and hemorrhoids occur independently of them.^[15][5]
• Distinguishing features:
  • Hemorrhoids: soft cushions at or near the dentate line, contiguous with the anal columns.
  • Rectal varices: tortuous, bluish, compressible submucosal veins, typically more than 4 cm above the anal verge and not contiguous with the anal columns. They are often accompanied by esophageal varices or ascites.^[5][16]
• Misclassifying rectal varices as hemorrhoids can lead to inappropriate banding or excision and potentially massive bleeding. In patients with portal hypertension and hematochezia, perform anorectal evaluation, with or without endoscopic ultrasound, before any intervention.^[5][16]

• Diarrhea vs constipation: which bowel disturbance drives HD remains disputed.^[2][8]
• Physical inactivity: sedentary behavior was paradoxically associated with lower HD risk in screening data, and the reason is unresolved.^[6]
• Diet: only grain fiber showed a protective signal in screening data. A “high-fat” component is not supported as a risk factor.^[6]
• Male sex: associated with HD severity in care-seeking populations.^[7] In population screening, however, prevalence was higher in women.^[3]
• Methodologic caveat: most data are cross-sectional. Colonoscopy-based ascertainment, including congestion related to bowel preparation, may overdiagnose or overstage HD.^[3][17]

• Most actionable lever: target straining and stool consistency with adequate dietary fiber and fluids, and limit time spent sitting on the toilet.^[1][14]
• Pregnancy: address constipation early. Bulking agents and osmotic laxatives are considered safe in pregnancy.^[11][10]
• Counseling: avoid presenting obesity, gravidity, or inactivity as definitive causes, because the evidence is mixed.^[6][4]
• Rectal bleeding in pregnancy or cirrhosis: examine the patient rather than attributing bleeding to hemorrhoids by default. In pregnancy, exclude anal fissure. In cirrhosis, exclude rectal varices.^[10][5]

There is insufficient evidence for screening patients for hemorrhoids.

There is insufficient evidence for screening patients for hemorrhoids.

Most symptomatic hemorrhoids follow a relapsing–remitting course with an excellent overall prognosis, and only about 10% of patients ultimately require surgery.^[1] Asymptomatic or incidentally detected hemorrhoids need no treatment.^[1][2] The main complications of the disease are thrombosis of external hemorrhoids, strangulation of irreducible (grade IV) prolapse with risk of gangrene and perineal sepsis, iron-deficiency anemia from chronic bleeding, and pruritus ani with soiling.^[3][4] Treatment-related complications include pain and delayed bleeding after rubber band ligation, and urinary retention, fecal incontinence, and anal stricture after hemorrhoidectomy. Perineal sepsis after office procedures is rare but can be fatal.^[5] Recurrence rises as treatment becomes less invasive. Excisional hemorrhoidectomy has the lowest recurrence (2%–10%), and its advantage over rubber band ligation is concentrated in grade III disease.^[1][6][7] Rectal bleeding or anemia should never be attributed to hemorrhoids until colorectal cancer and other sources have been excluded.^[4]

• Asymptomatic disease: Hemorrhoidal tissue is common and often silent. In an Austrian screening colonoscopy cohort, 38.9% of patients had internal hemorrhoidal tissue, and 55.3% of these were asymptomatic. Asymptomatic hemorrhoids require no intervention and carry an excellent prognosis.^[1][2]
• Symptomatic internal disease: Usually presents with painless bleeding and/or prolapse and follows a relapsing–remitting course that responds to conservative and office-based measures.^[1] Prolapse grade (I, within the canal; II, spontaneous reduction; III, manual reduction; IV, irreducible) broadly predicts the intensity of treatment required and the risk of recurrence.^[1]
• Thrombosed external hemorrhoids: Most resolve with conservative management over days to weeks, often leaving a residual skin tag. After about 72 hours the thrombus organizes and the overlying hematoma liquefies. Excision within 48–72 hours shortens symptomatic pain and reduces recurrence compared with conservative care.^[3][2]
• Progression to strangulation: Irreducible (grade IV) prolapse can be trapped by anal sphincter spasm, causing venous congestion and strangulation. If untreated, this can progress to necrosis and life-threatening perineal sepsis. It is uncommon, but it is the main reason untreated advanced disease is dangerous.^[4][3]

• Thrombosis: Acute, sharply painful, bluish-purple perianal mass (external hemorrhoids). Erosion of the thrombus may cause bright-red bleeding.^[1]
• Strangulation and necrosis/gangrene: Results from irreducible prolapse with vascular compromise and may progress to life-threatening infection. Management is almost always inpatient and ranges from analgesia and antibiotics to emergency excision.^[3]
• Iron-deficiency anemia: Results from chronic bleeding. Rarely, acute severe bleeding requires transfusion. Anemia mandates full colonic evaluation and should never be attributed to hemorrhoids alone.^[4]
• Pruritus ani, mucous discharge, and fecal seepage/soiling: Caused by prolapse and by skin tags that impede anal hygiene.^[3]
• Residual skin tags: Common after a thrombosed external hemorrhoid resolves. They are a cosmetic and hygienic problem, not a dangerous one.^[1]
• Infection: Significant infection or abscess is not a routine complication of uncomplicated hemorrhoids. It is essentially confined to strangulation/necrosis and to rare post-procedural perineal sepsis.^[2][3]

• The overall prognosis is excellent, and most patients never require surgery (~10% do).^[1]
• Recurrence is the main prognostic trade-off: it rises as treatment becomes less invasive. In a 1,958-patient cohort (mean follow-up 42 months), treatment received was the main independent predictor of recurrence. Rubber band ligation had the highest recurrence and the lowest complication rate, and excisional hemorrhoidectomy had the lowest recurrence.^[7]

• In a Cochrane analysis, excision was superior to rubber band ligation for grade III disease (RR 1.23; 95% CI 1.04–1.45) but not for grade II disease (RR 1.07; 95% CI 0.94–1.21).^[1]
• In the Dutch multicenter HollAND RCT in grade III disease (n = 87), recurrence was 47.5% after rubber band ligation versus 6.1% after hemorrhoidectomy (absolute difference 41%; 95% CI 24%–59%). Banding was not noninferior in quality-adjusted life years, but patients had less pain and returned to work sooner (1 vs 9 days).^[6]
• Grade III disease is therefore a genuine decision point rather than an automatic surgical referral. Patients choosing banding should be counseled on the quantified recurrence penalty.^[6][5]

• Optimal first-line treatment for grade III disease: Society guidance allows both office-based rubber band ligation and excision. The pivotal RCT was small and terminated early (n = 87).^[6][5]
• Bleeding risk with antithrombotic therapy: Systematic reviews suggest increased post-banding bleeding, but a retrospective clopidogrel cohort found no significant difference. The optimal timing for holding and resuming agents is unresolved.^[5]
• Conservative adjuncts: Efficacy of sitz baths, suppositories, and topical anesthetics/steroids rests on scarce evidence despite widespread use.^[3]
• Newer sclerosants: Polidocanol foam may rival rubber band ligation with lower recurrence and fewer complications, based on small trials that need confirmation.^[11]

• Significant pain with internal hemorrhoids suggests strangulation or a thrombosed external component. Otherwise, suspect an alternative diagnosis such as anal fissure.^[3]
• Strangulated hemorrhoids lack concentric mucosal folds and cannot be reduced, which distinguishes them from full-thickness rectal prolapse.^[4]
• The characteristic delayed-hemorrhage windows are 10–14 days after rubber band ligation and 7–10 days after hemorrhoidectomy.^[5][1]
• Fever, severe anal pain, and urinary difficulty after banding suggest perineal sepsis and require urgent examination under anesthesia and antibiotics.^[5]
• Limiting perioperative intravenous fluids to less than 750 mL and providing adequate analgesia reduces urinary retention after hemorrhoidectomy.^[5]