Hemorrhoids

1. Definition

Hemorrhoids (also known as "piles") are abnormal engorgement, distension, and distal displacement (prolapse) of the anal vascular cushions ^[1][2].

Let's break that down from first principles:

• Anal vascular cushions are normal anatomical structures present in every human being. They are clusters of vascular tissue (arteriovenous sinusoids), smooth muscle (Treitz's muscle), and connective tissue (fibroelastic supporting tissue), lined by mucosa ^[1][2].

• Their components include: branches of the superior rectal artery, superior rectal veins, and a mucosal covering ^[2].

• Their normal function is twofold ^[1][2]:

  1. Aid in maintaining continence — they act as a "vascular plug" that swells to seal the anal canal at rest, contributing ~15–20% of resting anal canal pressure.
  2. Protect the sphincters and anus from the trauma of defecation — they cushion the anal canal during the passage of stool.

• These cushions are found in 3, 7, and 11 o'clock positions (with the patient in the lithotomy position, where 12 o'clock is suprapubic) — this corresponds to the three anatomical columns of submucosal arteriovenous plexus ^[3].

So hemorrhoids are NOT "new" growths — they are pre-existing normal structures that become pathological when the supporting fibroelastic connective tissue and smooth muscle degenerate, leading to caudal displacement, engorgement, and prolapse of the vascular cushions ^[2].

2. Epidemiology

• Prevalence: 4.4% of the US population are seen by physicians for symptomatic hemorrhoids ^[1].
• 49 per 100,000 US population undergo hemorrhoidectomy annually ^[1].
• Peak incidence is between ages 45–65 years ^[3].
• Equally affects males and females, though men are more likely to seek treatment ^[3].
• In Hong Kong, hemorrhoids are extremely common — the high-fibre traditional Chinese diet is increasingly replaced by Western-style low-fibre diets, and prolonged sitting (especially on the toilet with smartphone use) is culturally prevalent, contributing to high rates.
• The true prevalence is likely much higher than reported, as many patients self-manage with over-the-counter preparations and never present to a physician.

3. Risk Factors

Understanding risk factors requires understanding the two key pathological mechanisms: (a) degeneration of supporting tissue, and (b) increased venous pressure/engorgement.

4. Anatomy and Function of the Anal Canal

This is fundamental — you cannot understand hemorrhoids (or any perianal pathology) without mastering anal canal anatomy.

4.1 Basic Structure

• The anal canal measures approximately 4 cm long from the anal verge ^[3][4].
• The dentate (pectinate) line is the key landmark — it divides the upper 2/3 from the lower 1/3 of the anal canal ^[3][4].
• The dentate line represents the embryological junction between the hindgut endoderm (above) and the proctodeum ectoderm (below).

4.2 The Dentate Line — A Clinical Watershed

Everything changes at the dentate line. This is one of the most important tables in surgery:

^[3][4]

4.3 Anal Sphincter Complex

• Internal anal sphincter (IAS): Involuntary smooth muscle, continuation of the circular muscle layer of the rectum. Responsible for ~70–85% of resting anal tone. Controlled by autonomic innervation.
• External anal sphincter (EAS): Voluntary striated muscle (skeletal muscle). Innervated by the inferior rectal nerve (branch of pudendal nerve, S2–S4). Responsible for voluntary squeeze pressure and continence during coughing/straining.
• Puborectalis muscle: Part of levator ani; wraps around the anorectal junction creating the anorectal angle (~80–90°), critical for continence.

4.4 Arterial Supply

• The superior rectal artery (terminal branch of IMA) is the primary arterial supply to the hemorrhoidal cushions — its three terminal branches correspond to the 3, 7, and 11 o'clock positions of the hemorrhoidal cushions.
• Middle rectal artery (from internal iliac artery) — supplies the mid-anal canal.
• Inferior rectal artery (from internal pudendal artery) — supplies the lower anal canal.

4.5 Venous Drainage

• Internal hemorrhoidal (rectal) plexus — above the dentate line, drains via superior rectal veins → inferior mesenteric vein → portal vein.
• External hemorrhoidal (rectal) plexus — below the dentate line, drains via middle and inferior rectal veins → internal iliac vein → IVC.
• These two plexuses are connected — they form an important portosystemic anastomosis.

5. Pathophysiology

The traditional "varicose vein" theory (hemorrhoids = varicose veins of the rectum) is outdated and incorrect. The modern understanding is the "sliding anal cushion" theory ^[2][3]:

The Sliding Anal Cushion Theory

Step-by-step:

1. Degeneration of supporting fibroelastic tissue and smooth muscle (Treitz's muscle) → the scaffolding that holds the anal cushions in place weakens ^[2].
2. Anal cushions are displaced caudally (slide downward toward and beyond the anal verge) ^[2].
3. Dilation and engorgement of the arteriovenous plexuses → the sinusoidal channels within the cushion become congested because their venous outflow is impaired by the displaced tissue ^[2].
4. Mucosal trauma during passage of stool → fragile engorged mucosa bleeds (bright red arterial blood from the AV sinusoids).
5. Progressive prolapse → stretching of the already weakened fibromuscular support → worsening grade.

Contributing factors amplifying this cycle:

• Straining → shearing force on cushions + venous engorgement
• Hard stools → mechanical trauma to engorged mucosa
• Acute thrombosis: venous stasis within the engorged plexus → clot formation → painful large, swollen, irreducible mass with marked anal sphincter contraction ^[2]

6. Classification

6.1 By Location (Relative to the Dentate Line)

^[1][2][3]

Mixed type: Both internal and external components; usually found in pregnancy; treated as external ^[2].

6.2 Goligher Grading of Internal Hemorrhoids

This is the most widely used classification. You need to know this! ^[2]

^[2][3][4]

7. Clinical Features

7.1 Symptoms

7.2 Signs

7.3 Characteristics of Bleeding by Type

7.4 External Hemorrhoids — Special Note

External hemorrhoids are described as a "5-day, painful, self-curing lesion" ^[3]:

• Acute thrombosis → peak pain in first 48–72 hours
• Spontaneous resolution over ~5 days as the clot organizes and is reabsorbed
• Leaves behind a residual skin tag

7.5 Relationship of Blood with Stool (Localizing Bleeding Source)

This is a high-yield concept from the LGIB approach ^[5]:

8. Examination Findings

8.1 PR (Per Rectal) Examination

Digital rectal examination (DRE) is essential ^[2][3]:

• Inspection: Look for prolapsed piles, associated skin tags, perianal excoriation, fissures, thrombosed hemorrhoids, condylomata, sinuses, or scars ^[2].
• Palpation: Assess pain, induration, any mass or lesion, anal tone (reflects IAS) and squeeze pressure (reflects EAS — ask patient to squeeze your finger) ^[2]. Also palpate the prostate (males) or rectovaginal septum (females).

8.2 Proctoscopy

• Proctoscopy is the key investigation for diagnosing internal hemorrhoids, especially Grade I and II ^[2].
• Allows direct visualization of the hemorrhoidal cushions at the 3, 7, and 11 o'clock positions.
• Can assess degree of prolapse and bleeding.
• Also useful for performing office-based procedures (rubber band ligation, sclerotherapy).

8.3 Flexible Sigmoidoscopy ± Colonoscopy

Required if risk of malignancy ^[2]:

• PR bleeding in age > 45 years
• Change in bowel habit / tenesmus
• Family history of CRC

9. Differentiating Hemorrhoids from Look-Alikes

9.1 Acute Painful Anal Mass — Differential Diagnosis

This is a common clinical scenario and exam question ^[2]:

10. Summary of the Clinical Approach (Pre-Diagnosis/Management)

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p22–27) ^[2] Senior notes: maxim.md (Haemorrhoids section, pp. 109–111) ^[3] Senior notes: felixlai.md (Hemorrhoids section, pp. 745–750) ^[4] Senior notes: felixlai.md (Anatomy and Risk Factors, pp. 745–746) ^[5] Senior notes: maxim.md (LGIB section, p. 158); Lecture slides: GC 186. Lower and diffuse abdominal pain fresh blood in stool.pdf

Differential Diagnosis of Hemorrhoids

The differential diagnosis of hemorrhoids must be considered in two distinct clinical scenarios:

1. The patient presenting with per-rectal (PR) bleeding — the most common hemorrhoid symptom, but shared with many other conditions.
2. The patient presenting with a painful perianal mass — the acute presentation.

The golden rule, stated in the previous section and worth repeating:

The approach to the differential diagnosis is best organized by the presenting symptom and then by anatomical location (working proximally from the anal verge).

A. Differential Diagnosis of PR Bleeding (Fresh Blood Per Rectum)

This is the clinical scenario where hemorrhoids most commonly enter the differential. The lecture slides list the common symptoms of anal pathology as: bleeding (usually fresh blood), anal pain, discharge (blood or purulent), prolapse, perianal mass, pruritus ani, incontinence ^[1].

Before diving into individual diagnoses, recall the localizing principle from history-taking ^[5][6]:

^[5][6]

Now let's work through each differential systematically.

1. Colorectal Carcinoma (CRC)

This is the most important diagnosis to exclude — it is the reason we never just label PR bleeding as "hemorrhoids" without investigation.

• Why it mimics hemorrhoids: CRC can present with bright red PR bleeding, especially left-sided or rectal tumours. Patients may dismiss it as "just piles."
• How to differentiate: Look for constitutional symptoms (weight loss, anorexia, fatigue), change in bowel habits (e.g., alternating diarrhoea and constipation), change in stool calibre, tenesmus, intestinal obstruction (IO) symptoms, metastatic symptoms (e.g., jaundice, SOB, bone pain), family history, previous colonoscopy/FOBT results ^[5][6].
• Pathophysiology of bleeding: Tumour grows into the bowel lumen → overlying mucosal erosion or ulceration → bleeding. Bleeding may be occult (iron deficiency anaemia, FOBT positive) or overt (hematochezia, rarely melena from right-sided lesions) ^[6].
• Key point: Bleeding from CRC is typically mixed with stool (proximal lesions) or may coat the stool (rectal lesions), unlike the pure outlet-type dripping seen with hemorrhoids.

2. Diverticular Disease (Diverticular Bleeding)

• Epidemiology: Most common cause of lower GI bleeding overall (15–55%) ^[6][7]. However, hemorrhoids remain the most common cause in patients < 50 years ^[7].
• Pathophysiology: Colonic diverticula are sac-like protrusions of the mucosa and submucosa through the muscular wall at points of nutrient artery penetration. The penetrating vessels (vasa recta) are draped over the dome of the diverticulum and are separated from the bowel lumen only by mucosa — this makes them vulnerable to rupture into the bowel lumen ^[7].
• How it presents: Painless profuse hematochezia ^[5][6] — classically large-volume, sudden-onset, bright red or maroon blood, often without preceding symptoms. This is typically much more profuse than hemorrhoidal bleeding.
• How to differentiate from hemorrhoids: Volume and pattern. Diverticular bleeding is usually abrupt, profuse, and self-limiting (80% stops spontaneously). Hemorrhoidal bleeding is smaller volume, outlet-type (on paper, dripping, coating stool), and recurrent with defecation.
• Hong Kong relevance: Right-sided diverticula are common in Asians (compared to left-sided predominance in Western populations) and have a higher risk of hemorrhage ^[7].
• Important: Diverticular bleeding typically occurs in the absence of diverticulitis — bleeding and inflammation are separate complications of diverticular disease ^[7].
• Risk factors: Advanced age, obesity, hypertension, hyperlipidaemia, IHD, chronic renal insufficiency, use of aspirin or NSAIDs ^[7].

3. Angiodysplasia (Arteriovenous Malformation)

• Epidemiology: Most common cause of lower GI bleeding in patients > 65 years ^[7][8].
• Pathophysiology: Dilated, tortuous submucosal vessels whose walls are composed of endothelial cells lacking smooth muscle — these are acquired degenerative lesions where chronic peristaltic contraction causes intermittent obstruction of submucosal veins → loss of pre-capillary sphincter competence → formation of small AVMs ^[7][8].
• Location: Most commonly right-sided (caecum, ascending colon) ^[8].
• How it presents: Bleeding is usually occult (FOBT-positive stools, iron deficiency anaemia) but can be overt with hematochezia or melena. Bleeding is venous in origin and tends to be less massive than diverticular bleeding ^[7].
• How to differentiate from hemorrhoids: Angiodysplasia bleeding is not outlet-type, often presents as occult bleeding with anaemia rather than bright red blood on paper, and typically occurs in elderly patients.
• Associations: ESRD, von Willebrand disease, aortic stenosis (Heyde syndrome — acquired Type 2A vWD from high shear stress across stenotic valve) ^[8].
• Colonoscopy: Cherry red spots ^[8]. Angiography: "mother-in-law phenomenon" (early filling, delayed emptying) ^[8].

4. Inflammatory Bowel Disease (IBD)

• Types: Crohn's disease and ulcerative colitis.
• How it presents: Bloody diarrhoea, abdominal pain (cramping), urgency, tenesmus, mucus in stool, constitutional symptoms (fever, weight loss, fatigue).
• How to differentiate from hemorrhoids: IBD bleeding is typically mixed with stool and accompanied by diarrhoea, mucus, systemic symptoms, and often extraintestinal manifestations (joints, eyes, skin, liver). Hemorrhoidal bleeding is painless outlet-type bleeding without systemic features.
• Important caveat: Crohn's disease and ulcerative colitis should not be misdiagnosed as infectious or ischaemic colitis since therapy is different ^[7].

5. Anal Fissure (Fissure-in-Ano)

This is a very common differential for hemorrhoids — both cause bright red PR bleeding and perianal symptoms, but the clinical picture is quite different.

• Definition: A tear in the mucosal lining below the dentate line ^[9].
• Pathophysiology: Local trauma (constipation, vaginal delivery) → pain → internal anal sphincter (IAS) spasm → impaired healing → vicious cycle ^[9]. The posterior midline (6 o'clock position) is the least perfused area of the anal canal, explaining why most fissures occur at 6 o'clock (posterior midline) ^[9]. About 10% occur at 12 o'clock (anterior), typically after vaginal delivery.
• Clinical features from lecture slides: Pain on defecation, fresh rectal bleeding. Diagnosis is by spreading the buttock to reveal the fissure. Rectal examination and proctoscopy are painful and not indicated ^[1][9].
• How to differentiate from hemorrhoids: The key distinguishing feature is pain. Anal fissure causes severe, tearing pain during and after defecation — this creates a vicious cycle (pain → avoidance of defecation → harder stools → more trauma). Hemorrhoidal bleeding is painless (unless complicated). The bleeding in fissure is also limited to a small amount on toilet paper or surface of stool ^[9], similar to hemorrhoids but always accompanied by significant pain.
• Chronic fissure triad: Fissure + sentinel pile (skin tag at distal end) + hypertrophied anal papillae (at proximal end) ^[9].

6. Anorectal Abscess

• Definition: Acute phase manifestation of a collection of purulent material arising from glandular crypts in the anus or rectum ^[10]. The chronic phase of the same suppurative process is an anorectal fistula ^[10].
• Pathophysiology: Usually cryptoglandular infection — anal glands at the dentate line become blocked → infection → abscess formation, which can spread through tissue planes ^[10].
• Clinical features from lecture slides: Pain, swelling, drainage, constipation, urinary difficulties ^[1][10]. The pain is constant and not necessarily associated with bowel movements — unlike fissure (pain on defecation) or hemorrhoids (painless unless complicated) ^[10]. Associated with fever and malaise ^[10].
• How to differentiate from hemorrhoids: Abscess presents with a tender, fluctuant, warm perianal swelling with systemic signs (fever). Hemorrhoids are soft, compressible, and not associated with fever or purulent discharge.
• Sites: Perianal (20%), intersphincteric (18%), ischiorectal (60%), supralevator (2%) ^[10].

7. Fistula-in-Ano (Anorectal Fistula)

• Definition: Abnormal communication between the anal canal (usually at the dentate line where the infected crypt was) and the perianal skin. It is the chronic phase of anorectal sepsis ^[10].
• Clinical features from lecture slides: Drainage, pain, bleeding, swelling, decrease in pain with drainage, external opening visible, PR examination reveals induration with a cord-like structure ^[1].
• How to differentiate from hemorrhoids: The chronic intermittent purulent discharge and the palpable cord-like tract on DRE are pathognomonic. Hemorrhoids do not drain pus and do not have external openings.

8. Rectal Prolapse (Rectal Procidentia)

• Definition: Protrusion of all layers of the rectum through the anus (complete) or protrusion of mucosa only (partial/mucosal prolapse) ^[11].
• How it mimics hemorrhoids: Both present as a prolapsing mass through the anus. This is a classic clinical and exam question — differentiating prolapsed hemorrhoids from rectal prolapse.
• Key differentiating feature on inspection:
  • Rectal prolapse: concentric CIRCULAR mucosal folds (full-thickness wall with its circumferential mucosal pattern)
  • Prolapsed hemorrhoids: RADIAL mucosal folds (individual cushions protrude at 3, 7, 11 o'clock with normal intervening skin/mucosa)
• Epidemiology: Majority affects elderly women ^[11].
• Associated symptoms: Faecal incontinence (75%), constipation (15–65%), mucus/stool discharge, incomplete evacuation ^[11].

9. Colitis (Infectious / Ischaemic / Radiation)

• Infectious colitis: Dysentery-type illness with bloody diarrhoea, fever, cramping — usually acute onset, travel history, sick contacts.
• Ischaemic colitis: Typically in elderly patients with vascular risk factors. Sudden crampy left-sided abdominal pain followed by bloody diarrhoea. Watershed areas (splenic flexure) most vulnerable.
• Radiation telangiectasia and proctitis: Radiation therapy for abdominal/pelvic cancers (e.g., cervical, prostate) can lead to lower GI bleeding. Acute radiation injury often occurs within 6 weeks of therapy ^[7]. Chronic radiation proctitis may present months to years later.

10. Other Anorectal Disorders

These are less common but important to keep in the differential ^[7]:

11. Anal Carcinoma (Expanded)

Worth expanding because it can masquerade as chronic hemorrhoids:

• Pathology: SCC below dentate line (80%), adenocarcinoma above dentate line (10%), others include melanoma ^[12].
• Risk factors: HPV infection (90%, especially HPV-16 and 18), HIV, smoking, immunocompromised, Crohn's disease ^[12].
• Clinical features: painful PR bleeding, pruritus, palpable mass. Examine for inguinal lymph nodes (superficial inguinal LN if tumour below dentate line) ^[12].
• Why it mimics hemorrhoids: Both can cause PR bleeding, pruritus, and a perianal mass. Any non-healing perianal lesion, especially with pain and lymphadenopathy, must be biopsied.

B. Differential Diagnosis of Acute Painful Anal/Perianal Mass

This is the second major clinical scenario. The lecture slides list the common symptoms: bleeding, anal pain, discharge, prolapse, perianal mass, pruritus ani, incontinence ^[1].

C. Differential Diagnosis Decision Algorithm

D. Summary Table: Key Differentiating Features

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p3, p27, p46, p50, p56) ^[2] Senior notes: maxim.md (Haemorrhoids section — Acute painful anal mass, pp. 110–111) ^[3] Senior notes: felixlai.md (Hemorrhoids section, pp. 745–750) ^[4] Senior notes: felixlai.md (Hemorrhoids — Clinical manifestation, p. 745) ^[5] Senior notes: maxim.md (LGIB section — DDx table, p. 158) ^[6] Lecture slides: GC 186. Lower and diffuse abdominal pain fresh blood in stool.pdf ^[7] Senior notes: felixlai.md (Lower GI bleeding — DDx, pp. 342–343) ^[8] Senior notes: maxim.md (Angiodysplasia section, p. 197) ^[9] Senior notes: maxim.md (Anal fissure section, pp. 111–112) ^[10] Senior notes: felixlai.md (Anorectal abscess, pp. 754–755) ^[11] Senior notes: felixlai.md (Rectal prolapse, pp. 761–762) ^[12] Senior notes: maxim.md (Anal carcinoma and Pilonidal sinus, p. 116)

Diagnosis of Hemorrhoids — Diagnostic Criteria, Algorithm and Investigations

A. Diagnostic Criteria

Hemorrhoids do not have formal standardized diagnostic criteria like, say, the Rome IV criteria for functional GI disorders. Instead, the diagnosis is made clinically through a combination of:

1. Compatible history (symptom pattern)
2. Physical examination (inspection, DRE)
3. Endoscopic visualization (proctoscopy — the definitive diagnostic tool)
4. Exclusion of sinister pathology (the most important step)

Let me walk through each of these from first principles.

B. Step 1 — History Taking (Clinical Diagnosis)

The history alone will often point strongly toward hemorrhoids, but never allows you to stop there. The approach to anorectal disease from the lecture slides is structured as follows:

History: present illness (anorectal symptoms: pain, bleeding, mass, prolapse), past health (medical diseases, previous surgery), family history, sexual history ^[1].

Key History Points for Hemorrhoids

The lecture slides on LGIB assessment emphasize a systematic bleeding severity assessment: "When did the bleeding start? First episode? Hematochezia? Melena? Recent endoscopy?" ^[6].

C. Step 2 — Physical Examination

The lecture slide on assessment of hemorrhoids states:

"Digital rectal examination (to exclude other rectal lesions). Proctoscopy: for diagnosis and assessment of severity. Rigid or flexible sigmoidoscopy to exclude proximal bowel lesion" ^[1].

Let me break each component down:

C1. Inspection

• Patient positioned in left lateral (Sims) position or lithotomy position.
• Look at the perianal skin and anal verge:
  • Skin tags — residual from previous thrombosed external hemorrhoids
  • Prolapsed hemorrhoids — engorged, purple-red, soft tissue protruding from the anus with radial mucosal folds (as opposed to circular folds of rectal prolapse)
  • Thrombosed external hemorrhoid — bluish, firm, tender subcutaneous lump at the anal verge
  • Fissure — linear tear, usually at posterior midline (6 o'clock)
  • External openings of fistula-in-ano — discharge, granulation tissue
  • Condylomata — warty lesions (HPV)
  • Excoriation — from chronic mucus discharge and scratching
• Ask the patient to bear down / strain — this may provoke prolapse of internal hemorrhoids, allowing you to grade them.

C2. Digital Rectal Examination (DRE)

DRE is performed to exclude other rectal lesions ^[1][3][4]:

• What DRE can assess:
  • Anal tone (reflects IAS function) and squeeze pressure (reflects EAS function — ask the patient to squeeze your finger) ^[2]
  • Presence of rectal masses (palpable tumour, polyp)
  • Induration, tenderness (abscess, fissure, carcinoma)
  • Prostate (males) or rectovaginal septum (females)
  • Stool colour — important in GI bleeding assessment

C3. Proctoscopy (The Key Diagnostic Tool)

Proctoscopy is the single most important investigation for diagnosis and assessment of severity of internal hemorrhoids ^[1][2]:

• Why proctoscopy? Internal hemorrhoids originate above the dentate line in the anal canal — a rigid proctoscope provides direct visualization of this area. The hemorrhoidal cushions at 3, 7, and 11 o'clock can be directly inspected for engorgement, prolapse, and active bleeding.
• How it works: A rigid tubular instrument with an obturator is inserted into the anal canal. The obturator is removed and the proctoscope is slowly withdrawn — the hemorrhoidal tissue prolapses into the lumen of the scope, allowing direct visualization.
• What to look for:
  • Engorged vascular cushions at 3, 7, 11 o'clock positions
  • Degree of prolapse (for Goligher grading)
  • Active bleeding or stigmata of recent hemorrhage
  • Other pathology (fissures, polyps, tumours)
• Also used therapeutically: Rubber band ligation, injection sclerotherapy, and infrared coagulation are all performed through a proctoscope.

D. Step 3 — Excluding Proximal Bowel Pathology (The "Must Not Miss" Step)

This is where the diagnostic approach transitions from "confirming hemorrhoids" to "ruling out cancer and other serious pathology." The lecture slides are emphatic:

"Common anorectal conditions are mostly benign. Colorectal neoplasm needs to be excluded. Diagnosis can usually be made by careful history and examination. Treatment is mainly for symptomatic control" ^[1].

"Do not assume all the symptoms are attributable to hemorrhoids" ^[3].

D1. Rigid or Flexible Sigmoidoscopy

Rigid or flexible sigmoidoscopy is used to exclude proximal bowel lesion ^[1][3].

• Rigid sigmoidoscopy: Allows direct visualization of the rectum and distal sigmoid (up to ~25 cm). Quick, usually done without sedation. Can identify rectal tumours, proctitis, rectal varices, and solitary rectal ulcer.
• Flexible sigmoidoscopy: Reaches the splenic flexure (~60 cm). Better visualization and can biopsy suspicious lesions. However, does not examine the entire colon.

D2. Colonoscopy

Referral for colonoscopy is indicated when there are red flag features suggesting pathology beyond hemorrhoids ^[2][3]:

The lecture slides on intermittent/episodic PR bleeding state:

"Colonoscopy — current gold standard in detecting colonic neoplasm. Needs diet and bowel preparation ± sedation. Chance of perforation ≤ 0.1%. Therapeutic modalities (clipping, electrocoagulation, laser, argon plasma coagulation, sclerotherapy)" ^[6].

E. Step 4 — Laboratory Investigations

Hemorrhoids themselves do not require specific laboratory tests for diagnosis. However, investigations are essential for assessing the impact of bleeding and excluding other pathology:

The lecture slides state investigations should include: "Blood tests — haemoglobin and haematocrit, liver and renal function test, coagulation profile, type and screen" ^[6].

F. Additional Investigation Modalities (For Complex or Unclear Cases)

These are not routinely used for straightforward hemorrhoid diagnosis, but become relevant when the clinical picture is atypical or when acute LGIB requires localization:

G. Approach to Acute LGIB (When Hemorrhoids Are Part of the DDx)

For patients presenting with acute lower GI bleeding where hemorrhoids are one of several possible diagnoses, the lecture slide provides a comprehensive algorithm ^[6]. Let me integrate this:

Acute LGIB — Severity Assessment

The lecture slide framework: "History (When did the bleeding start? First episode? Hematochezia? Melena? Recent endoscopy?), Physical examination (vital signs, cardiopulmonary and abdominal examinations, including DRE — tachycardia? hypotension? syncope? gross blood on DRE? recurrent/ongoing hematochezia?), Laboratory tests (FBC, serum electrolytes, coagulation tests, type and cross match — Hb? Albumin? INR? PLT? Creatinine?), Co-morbidities (older age? need for RBC transfusion?), Concomitant medications (NSAIDs? antiplatelet agents? anticoagulants?)" ^[6].

Transfusion Targets (From Lecture Slides)

• If Hb < 7 g/dL, transfuse: target Hb 7–9 g/dL post-transfusion if no CVD ^[6]
• If Hb ≥ 8 g/dL and CVD present, transfuse: target Hb ≥ 10 g/dL ^[6]

Oakland Score

"Consider safe hospital discharge and outpatient evaluation if Oakland score < 8" ^[6]. The Oakland score predicts the probability of safe discharge in patients with acute LGIB based on age, sex, previous LGIB, DRE findings, heart rate, systolic BP, and haemoglobin.

H. Diagnostic Algorithm — Complete Flowchart

I. Summary of Investigation Hierarchy for Hemorrhoids

The investigations can be thought of in three tiers:

J. Interpretation of Key Findings

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p4, p13, p28, p77) ^[2] Senior notes: maxim.md (Haemorrhoids section — Examination, pp. 109–110) ^[3] Senior notes: felixlai.md (Hemorrhoids — Diagnosis, pp. 745–746) ^[4] Senior notes: felixlai.md (Hemorrhoids — Clinical manifestation and diagnosis, p. 745) ^[5] Senior notes: maxim.md (LGIB section — History taking, p. 158) ^[6] Lecture slides: GC 186. Lower and diffuse abdominal pain fresh blood in stool.pdf (p6, p20, p22, p38)

Management of Hemorrhoids — Algorithm and Treatment Modalities

A. Overarching Principles

Before diving into specific treatments, understand three governing principles that frame the entire management approach:

Principle 1: Conservative treatment for ALL patients ^[3]. Every hemorrhoid patient — regardless of grade — starts with lifestyle and dietary modification. Many will improve with conservative measures alone and never need procedural intervention.

Principle 2: Treatment is mainly for symptomatic control ^[1]. Remember, hemorrhoidal cushions are normal anatomy. We are not trying to eliminate them — we are trying to relieve symptoms (bleeding, prolapse, pain, pruritus). Asymptomatic hemorrhoids found incidentally do not require treatment.

Principle 3: Management is stepped — escalate only when the current level fails. The treatment ladder roughly follows the Goligher grading:

Grade I → Conservative + Medical ± Office procedures Grade II → Conservative + Medical + Office procedures (RBL) Grade III → Conservative + Medical + RBL ± Surgery Grade IV → Surgery

B. Management Algorithm — Overview

The treatment approach from the lecture slides ^[1] and senior notes ^[2][3] can be summarized in a grade-based escalation framework:

The senior notes provide a more detailed breakdown ^[3]:

^[3]

And the Goligher grading–management correlation from Maxim's notes ^[2]:

^[2]

C. Management Algorithm — Mermaid Diagram

D. Treatment Modalities — Detailed Breakdown

D1. Conservative Management (All Grades)

This is the foundation of hemorrhoid treatment. The lecture slide states: "Non-operative: diet modification: high fibre diet; sitz bath: for prolapsed haemorrhoids; ointments and suppositories: may help but some contain steroid" ^[1].

D1a. Lifestyle Modification

D1b. Sitz Baths

Sitz bath: for prolapsed haemorrhoids ^[1].

• What it is: Sitting in warm water covering the buttocks and hips (typically 10–15 minutes, 2–3 times daily and after bowel movements).
• Mechanism: Warm water relaxes the anal sphincter muscles and relieves sphincter spasm ^[3]. Patients with significant hemorrhoids tend to have elevated resting anal sphincter tone — relaxing this reduces venous congestion. Also relieves irritation, pruritus, and reduces inflammation and oedema ^[3].
• KMnO₄ (potassium permanganate) sitz bath ^[2] — acts as a topical antiseptic. Used as a very dilute solution (1:10,000) to keep the perianal area clean.

D2. Medical Treatment

D2a. Laxatives / Stool Softeners

The aim is to produce soft, well-formed stools that pass easily without straining — thereby breaking the pathological cycle of straining → venous engorgement → mucosal trauma → bleeding.

^[3]

D2b. Topical Agents

D2c. Venoactive Agents (Phlebotonics)

• Class: Heterogeneous class of plant extracts, primarily flavonoids ^[3].
• Example: Daflon (micronized purified flavonoid fraction — 90% diosmin + 10% hesperidin) ^[3].
• Mechanism: Improves venous tone, reduces microvascular permeability, enhances lymphatic activity, and improves microcirculatory nutritive flow ^[3].
• Indication: Primarily used to treat acutely inflamed and bleeding hemorrhoids ^[3]. Can reduce bleeding episodes and symptom severity.
• Classification: Categorized as a medical food, not as a drug ^[3]. Has good safety profile.
• Evidence: Meta-analyses show that phlebotonics significantly reduce bleeding, pruritus, discharge, and overall symptom scores in hemorrhoidal disease.

D3. Office-Based Procedures

These are interventional procedures performed in the outpatient/office setting, typically without general anaesthesia. They work because internal hemorrhoids have visceral innervation (no somatic pain sensation) — so procedures applied above the dentate line are tolerable without anaesthesia ^[3].

D3a. Rubber Band Ligation (RBL) — The Most Important Office Procedure

Rubber band ligation (RBL) is the most commonly performed office-based procedure ^[2][3][4]:

• How it works: Apply rubber bands to strangulate the pile by Barron's bander → ischaemic necrosis of the piles → slough off within 10 days ^[2]. The necrosed tissue and band fall off, leaving an ulcer that heals with fibrosis, fixing the residual tissue in place and preventing re-prolapse.
• Administration: Up to 3 bandings at ≥ 1 cm above the dentate line ^[2]. Why above the dentate line? Because the area above the dentate line has visceral innervation — placing bands here is tolerable. Banding below the dentate line would cause excruciating pain (somatic innervation).
• Efficacy: 70% resolve, 30% recur ^[2].
• Indications: Symptomatic Grade II/III internal hemorrhoids ^[2]. Also used for Grade I hemorrhoids with persistent bleeding despite conservative treatment ^[3][4].
• Advantages: Inexpensive, easy to perform, rarely causes serious complications. Compared with sclerotherapy and infrared coagulation, RBL is more effective and requires fewer treatment sessions ^[4].
• NOT recommended for Grade IV hemorrhoids — surgery is the best treatment for these ^[4].
• Only for internal hemorrhoids — external hemorrhoids are NOT amenable to banding ^[4] (somatic innervation → too painful; also, banding external tissue risks full-thickness skin necrosis).

Contraindications for RBL:

Complications of RBL:

• Pain — most frequent, occurring in ~8% ^[4]. Usually mild and self-limiting. Indicates the band may have been placed too close to the dentate line.
• Bleeding — 7–10 days post-banding due to sloughing of ligated haemorrhoids ^[2]. Usually minor, but can be significant in coagulopathic patients.
• Delayed haemorrhage ^[4]
• Post-banding sepsis ^[2] — rare but potentially fatal. Presents with fever, perineal pain, and urinary retention 3–7 days post-procedure. Requires urgent IV antibiotics and debridement.
• Urinary retention ^[4]
• Haemorrhoidal thrombosis ^[4]

Practical notes on RBL:

• Usually only one haemorrhoidal column should be treated at a time to minimize excessive tissue necrosis ^[4]. Multiple columns can be banded if tolerated.
• If multiple sessions are needed, repeat banding should be performed at 3–4 week intervals to allow swelling and ulcerations to subside ^[4].
• If ineffective after repeated attempts → proceed to surgery ^[4].

D3b. Injection Sclerotherapy

• Method: Injection of sclerosants such as phenol (5%) in vegetable oil (or almond oil) submucosally into the hemorrhoidal tissue ^[2][4].
• Mechanism: Causes an intense inflammatory reaction → destroys redundant submucosal tissue → fibrosis → obliterates vascular channels and fixes the position of the hemorrhoidal cushion (prevents prolapse) ^[2][4].
• Indications: Grade I and II hemorrhoids. Critically, indicated in patients with coagulopathies, on antiplatelets or anticoagulants, immunocompromised, or with portal hypertension* — where RBL is contraindicated due to high risk of delayed bleeding ^[4]. Sclerotherapy is better studied than infrared coagulation in the literature for these groups ^[4].
• Status: Largely abandoned now in routine practice — risk of allergy to nuts and intraprostatic injection ^[2]. However, still used in special populations where RBL is contraindicated.

D3c. Infrared Coagulation

• Method: Direct application of infrared light waves to haemorrhoidal tissues ^[4].
• Mechanism: Infrared energy causes coagulation necrosis of the tissue → subsequent fibrosis → fixes the hemorrhoidal cushion.
• Indications: Grade I and II hemorrhoids ^[4]. Candidates include patients who cannot tolerate RBL or as an alternative.
• Compared to RBL: Less effective and requires more treatment sessions. Used less frequently.

D3d. Haemorrhoidal Artery Ligation Operation (HALO)

May be Doppler-guided (DG-HALO) to identify feeding vessels ^[2]:

• Method: A Doppler ultrasound probe is used to identify the terminal branches of the superior rectal artery supplying the hemorrhoidal cushions. These arteries are then ligated with sutures through a specially designed proctoscope.
• Mechanism: Reduces arterial inflow to the hemorrhoidal cushion → decompression → shrinkage. May be combined with mucopexy (stitching the prolapsed mucosa back into position).
• Indications: Mainly for bleeding symptoms, indicated for Grade II/III haemorrhoids ^[2].
• Lowest post-operative complications, but highest recurrence rate ^[2]. This makes it suitable for patients who prioritize minimal invasiveness and accept a higher chance of needing re-treatment.

D4. Surgical Treatment

Indications for surgical hemorrhoidectomy from the lecture slides ^[1]:

Severe haemorrhoids (3rd or 4th degree), mixed internal and external haemorrhoids, failure of other treatments, patient preference, in conjunction with another procedure ^[1]

From the senior notes, additional indications ^[3]:

• 2nd degree hemorrhoids that failed non-operative treatments
• Fibrosed hemorrhoids
• Hemorrhoidal bleeding leading to anaemia

D4a. Conventional Excisional Hemorrhoidectomy

This is the gold standard surgical treatment with the highest cure rate.

• Efficacy: 95% resolve ^[2].
• Pre-op preparation: stool softener, enema ^[2].
• Position: prone jackknife or lithotomy ^[2].
• Anaesthesia: perianal / spinal / general anaesthesia ^[2].

Approach: 3-leaf clover excision — excise the three main hemorrhoidal cushions (at 3, 7, 11 o'clock) leaving adequate mucocutaneous bridges between excision sites. Avoid circumferential excision — prone to stenosis ^[2].

Two main techniques:

Indications for conventional hemorrhoidectomy: Internal ≥ Grade III or external ^[2]. Also for symptomatic internal/external haemorrhoids refractory to other treatments ^[2].

D4b. Stapled Hemorrhoidopexy (Stapled Hemorrhoidectomy / PPH)

"Using the stapling device to remove a ring of rectal mucosa and submucosa with the creation of a mucosal anastomosis above the dentate line. Haemorrhoids are not excised. Haemorrhoidal tissues pulled back into the anal canal from the prolapsed position. Interruption of blood supply to the haemorrhoids" ^[1].

Let me break this down from first principles:

• How it works: A circular stapler is introduced through the anal canal. It excises a circumferential ring (doughnut) of rectal mucosa and submucosa above the hemorrhoidal cushions. The stapler simultaneously creates an anastomosis. This achieves two things:
  1. Repositions the prolapsed hemorrhoidal tissue back into the anal canal (hemorrhoidopexy — "pexy" = fixation)
  2. Interrupts the blood supply to the hemorrhoidal cushions (the excised doughnut contains the feeding vessels)
• The hemorrhoids are not excised — they shrink in situ as their blood supply is cut off and they are pulled back into anatomical position.
• Indication: Internal hemorrhoids only ^[2].
• Less favoured now due to poorer long-term outcomes ^[2].

D5. Management of Acute / Emergency Presentations

D5a. Symptomatic Grade IV Internal Hemorrhoids (Acutely Prolapsed)

Hyperosmolar solution (gauze with lignocaine + cold water + dextrose) or warm water sitz bath to reduce size of haemorrhoids before surgery ^[2].

• Why hyperosmolar solution? The high osmolarity of the dextrose solution draws fluid out of the oedematous, engorged hemorrhoidal tissue by osmosis → reduces swelling → makes the tissue more amenable to reduction or subsequent surgical excision.
• Why lignocaine? Provides local anaesthesia for pain relief.
• Once adequately reduced → proceed to elective surgical hemorrhoidectomy.

D5b. Thrombosed External Hemorrhoids

Thrombosed (external) haemorrhoids ^[2]:

• Why topical nifedipine? Nifedipine is a calcium channel blocker → relaxes the internal anal sphincter smooth muscle → reduces sphincter spasm → relieves pain and improves venous drainage.

E. Post-Operative Complications

Post-operative complications ^[3][2]:

F. Summary: Treatment Ladder at a Glance

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p29, p30, p31, p33, p36, p77) ^[2] Senior notes: maxim.md (Haemorrhoids management section, pp. 109–111) ^[3] Senior notes: felixlai.md (Hemorrhoids — Treatment, pp. 746–750) ^[4] Senior notes: felixlai.md (Hemorrhoids — Office-based procedures, pp. 748–749)

Complications of Hemorrhoids

Complications of hemorrhoids fall into two categories:

1. Complications of the disease itself — what happens when hemorrhoids are left untreated or progress
2. Complications of treatment — what happens after office-based procedures or surgery

Both are important for exams. Let's work through each from first principles.

A. Complications of Hemorrhoidal Disease

The senior notes list the following complications ^[3]:

Strangulation and thrombosis, gangrene, ulceration, fibrosis, portal pyaemia

Let me explain each one mechanistically, because understanding the "why" makes these easy to remember.

1. Thrombosis

• What happens: Venous stasis within the engorged hemorrhoidal plexus → blood pools and clots → thrombus forms within the hemorrhoidal vascular cushion.
• Why it happens: The sluggish flow in the dilated, congested AV sinusoids creates the conditions of Virchow's triad (stasis, endothelial injury from chronic trauma, hypercoagulability is not typically a factor but the other two are sufficient). Sphincter spasm from the prolapsed tissue further impedes venous drainage, worsening the stasis.
• Clinical presentation: Acute onset of severe perianal pain + swollen, tense, bluish mass. For external hemorrhoids: the classic painful bluish perianal mass ^[2]. For internal hemorrhoids: thrombosis usually occurs in the context of prolapse (Grade III/IV) where the tissue becomes trapped outside.
• Recall from clinical features: Pain occurs only when complications are present (thrombosis, prolapse) ^[1]. Thrombosis is the most common reason uncomplicated hemorrhoids become painful.
• Natural history of thrombosed external hemorrhoids: The "5-day, painful, self-curing lesion" ^[3] — peak pain in the first 48–72 hours, then the clot gradually organizes and is reabsorbed. The residual stretched skin becomes a skin tag (forms skin tag after 48 hours ^[2]).

2. Strangulation

• What happens: A prolapsed internal hemorrhoid (typically Grade III or IV) protrudes through the anal canal → the anal sphincter contracts around the base of the prolapsed tissue → venous outflow is completely obstructed while arterial inflow initially continues → the tissue becomes massively engorged, oedematous, and trapped (incarcerated).
• Why it happens: The sphincter acts like a tourniquet. Initially, arterial blood still enters (arteries have higher pressure than the constrictive force of the sphincter), but venous return is blocked (veins have lower pressure). This creates a vicious cycle: arterial inflow without venous outflow → progressive engorgement → more oedema → even more pressure → eventually arterial supply is also compromised.
• Clinical presentation: Acutely painful, swollen, tense, irreducible hemorrhoidal mass. The tissue appears dark purple or dusky. Patient is in significant distress with marked sphincter spasm.
• This is a surgical emergency — if not reduced, strangulation progresses to gangrene (see below).

3. Gangrene

• What happens: Prolonged strangulation → complete arterial ischaemia → tissue necrosis (gangrene) of the prolapsed hemorrhoidal tissue.
• Why it happens: The progression is: prolapse → strangulation (venous obstruction) → continued arterial inflow → massive engorgement → eventually arterial inflow also obstructed → ischaemia → infarction → gangrene. Superimposed bacterial infection accelerates the necrotic process.
• Clinical presentation: The prolapsed hemorrhoidal mass becomes black, necrotic, foul-smelling, and extremely painful. There may be surrounding cellulitis and systemic signs of sepsis (fever, tachycardia).
• Management: This is an emergency. Requires urgent surgical hemorrhoidectomy — specifically the Open (Milligan-Morgan) technique is preferred for acute gangrenous haemorrhoids because leaving the wound open prevents further tissue oedema and necrosis ^[2] (closing a wound over necrotic, infected tissue would trap the infection and worsen the situation).

4. Ulceration

• What happens: The mucosal surface of a prolapsed hemorrhoid is exposed to the external environment and subjected to repeated mechanical trauma (clothing friction, sitting, defecation) → the fragile columnar mucosa ulcerates.
• Why it happens: Columnar epithelium (above the dentate line) is not designed to withstand the dry, abrasive environment outside the anal canal. Unlike squamous epithelium (which is tough and stratified), columnar epithelium is thin and delicate. When chronically prolapsed, it becomes traumatized and eroded.
• Clinical significance: Ulcerated hemorrhoids bleed more readily and are vulnerable to secondary infection. The ulceration can also cause pain (exposed submucosa is sensitive) and mucus discharge.

5. Fibrosis

• What happens: Chronic, repeated episodes of thrombosis, inflammation, and ulceration → fibrotic scarring replaces the normal vascular and connective tissue of the hemorrhoidal cushion.
• Why it happens: This is the normal wound-healing response to chronic injury — inflammation → granulation tissue → fibrosis. The hemorrhoidal cushion becomes firm and non-compressible rather than soft and vascular.
• Clinical significance: Fibrosed hemorrhoids are firm, whitish, and do not respond well to conservative measures or office-based procedures (rubber band ligation is less effective on fibrotic tissue). Fibrosed hemorrhoids are listed as a specific indication for surgical treatment ^[3]. The fibrotic tissue also predisposes to chronic skin tags.

6. Portal Pyaemia

• What happens: Bacterial infection of the hemorrhoidal tissue (e.g., from ulceration or post-procedural sepsis) → bacteria enter the superior rectal veins → ascend via the inferior mesenteric vein → reach the portal vein → seed the liver → portal pyaemia (septic thrombophlebitis of the portal venous system) → potentially liver abscess.
• Why it happens: Recall from the anatomy section that internal hemorrhoids drain via the superior rectal veins → portal venous system ^[3]. This direct connection between the anal canal and the portal system means that any septic process in the hemorrhoidal tissue can, in theory, seed the liver via the portal blood.
• Clinical significance: This is extremely rare but potentially fatal. Presents with high spiking fevers, rigors, right upper quadrant pain, jaundice, and hepatomegaly. The liver abscess(es) are typically multiple. Requires aggressive IV antibiotics and possibly percutaneous drainage.
• "Pyaemia" = "pyo" (pus) + "haemia" (blood) — literally pus in the blood. Portal pyaemia specifically means septic emboli travelling through the portal venous system.

7. Iron Deficiency Anaemia (from Chronic Bleeding)

Although not listed in the classic "complications" list, this is clinically important:

• What happens: Chronic, recurrent hemorrhoidal bleeding (even if small volume per episode) → cumulative blood loss over months to years → depletion of iron stores → iron deficiency anaemia.
• Clinical significance: Hemorrhoidal bleeding leading to anaemia is a specific indication for surgical treatment ^[3]. Any patient with hemorrhoids and anaemia should also have a colonoscopy to exclude a coexisting proximal colonic malignancy as the cause of the anaemia — hemorrhoids alone uncommonly cause significant anaemia.

B. Complications of Hemorrhoid Treatment

B1. Complications of Rubber Band Ligation

B2. Complications of Hemorrhoidectomy

The lecture slide lists the complications of hemorrhoidectomy as:

Bleeding, urine retention, pain, faecal impaction, infection, anal tags, anal stenosis, incontinence ^[1]

Let me explain each:

B3. Complications of Stapled Hemorrhoidopexy

The lecture slide is specific about this:

"Complications can be serious (rectal perforation, severe pelvic sepsis, rectovaginal fistula). More recurrence than conventional haemorrhoidectomy" ^[1]

C. Summary: Natural History of Untreated Hemorrhoids

Understanding the complications allows you to trace the natural history of progressive untreated hemorrhoidal disease:

Grade I (bleeds) → Grade II (prolapse, spontaneous reduction) → Grade III (manual reduction)
→ Grade IV (irreducible) → Strangulation → Thrombosis → Gangrene
                                                          ↘ Ulceration → Chronic bleeding → Anaemia
                                                          ↘ Fibrosis → Skin tags
                                                          ↘ Secondary infection → Portal pyaemia (rare)

This progression is driven by the same underlying mechanism throughout: progressive degeneration of fibroelastic support → worsening prolapse → increasing venous congestion → increasing vulnerability to mechanical trauma, thrombosis, and ischaemia.

D. Complications Summary Table

References

^[1] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p27, p33, p35, p40) ^[2] Senior notes: maxim.md (Haemorrhoids — Complications and management, pp. 110–111) ^[3] Senior notes: felixlai.md (Hemorrhoids — Complications, p. 750; Treatment, pp. 749–750) ^[4] Senior notes: felixlai.md (Hemorrhoids — Office-based procedures and complications, pp. 748–749)