Haemorrhoids

Meet the patient

A 52-year-old man comes to the surgical outpatient clinic embarrassed but not worried: for three months he has been wiping bright red blood off the toilet paper after a hard stool, sometimes a few drops dripping into the bowl. There is no pain, no weight loss, no change in bowel habit — just years of straining on a low-fibre diet.[1]

The single question that decides his next six weeks is the one that decides every rectal-bleeding case: is this just his cushions, or is it the cancer that cushions always mimic? Hold that question and the whole topic falls into place.[1]

Thomson's three cushions — normal anatomy mislabelled a disease

Haemorrhoids are normal anatomy that engorges — not a growth, not a varicose vein. Thomson's 1975 thesis ended a century of argument by proving that every anal canal holds three discrete vascular cushions at the 3, 7, and 11 o'clock positions (left lateral, right posterior, right anterior in lithotomy), built from arteriovenous communications, connective tissue, and smooth muscle.[4]

These cushions are universal and physiological. They contribute roughly 15 to 20 per cent of resting anal continence by acting as compliant seals that fill the canal at rest, and they only become haemorrhoidal disease when sustained pressure engorges them, fragments their anchoring tissue, and pushes them distally to bleed and prolapse.[4]

The cushions hang from a fibroelastic scaffold held up by the muscularis submucosae ani (Treitz's muscle) and the suspensory ligament of the anal cushions (Parks's ligament). When that scaffold gives way — from straining, ageing, or pregnancy — the cushions slide, and a Grade II pile is born.[1]

[1]

The dentate line — one line that decides pain and treatment

One embryological boundary decides whether a pile bleeds silently or screams, and whether you may band it. The dentate (pectinate) line sits about 2 cm proximal to the anal verge — the junction of endoderm above (proximal gut) and ectoderm below (proctodeum). Above and below it the epithelium, blood supply, lymphatics, and innervation all differ, and every clinical and surgical decision flows from that split.[1]

Above the line is visceral, autonomic, insensate — so an internal pile bleeds painlessly and a rubber band placed there hurts no more than a pinch. Below the line is somatic, inferior-rectal-nerve territory, exquisitely sensitive — so a thrombosed external pile is agonising, and a band placed below the line is a cardinal surgical error.[1]

The vascular map follows the same line and explains the surgery. Above: the superior rectal artery (terminal branch of the inferior mesenteric artery) and superior rectal vein draining into the portal system — which is why portal hypertension engorges these vessels. At the line the middle rectal vessels (internal iliac) bridge the portosystemic circulation. Below: the inferior rectal artery and vein (internal pudendal). Lymphatics drain above to the inferior mesenteric and para-aortic nodes, and below to the superficial inguinal nodes — a distinction that matters when staging an anal versus a rectal tumour.[1]

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The classic trap: reaching for the bander on a lump you have not scoped. A band placed below the dentate line on somatic, pain-sensitive anoderm produces agony the patient will not forgive — remove it immediately and re-place above the line under vision.[1]

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Goligher grades I to IV — the ladder in four lines

Prolapse, not bleeding, decides whether you band in the clinic or cut in theatre — and Goligher's four grades order internal piles by how far they have fallen. Every examiner expects them reproduced verbatim.[1][2]

[1]

By anatomy, piles are also internal (mucosa-covered, above the line), external (anoderm-covered, below), and mixed (interno-external) — an internal component and a perianal skin tag communicating across the line and prolapsing together.[1]

Two situations sit outside the grades and carry their own logic. A thrombosed external haemorrhoid is a sudden, acutely painful, firm, purple perianal lump from clot in an external cushion; pain peaks at about 48 hours and eases over 1 to 2 weeks. A strangulated internal haemorrhoid is a Grade IV prolapse incarcerated outside the sphincter, with oedema, thrombosis, and a real risk of necrosis — a surgical emergency.[1]

Why the blood is bright red — the arterial secret

The blood is bright red because the cushions are arteriovenous shunts, not veins. This is Thomson's single most examinable insight: the cushions are masses of submucosal tissue carrying arteriovenous communications without an intervening capillary bed, fed at near-systemic arterial pressure. So haemorrhoidal bleeding is brisk and bright red — not the dark, sluggish ooze of a pure vein — and a small pile can stain the bowl alarmingly.[4]

This same arterial fact is why the bleeding can occasionally be dramatic. The patient describes blood on the toilet paper, dripping into the bowl, or on the surface of the stool — never mixed in, never melaena. Mixing-in, dark blood, or clots all point away from piles toward a proximal source and demand endoscopy.[1]

Etymology for viva gold: haem is Greek for blood and rhoos means flowing — so the word literally names the symptom, a flowing of blood, which is exactly how the patient presents.[4]

The mantra so far: above the line painless, below the line painful; grade I to II band, grade III to IV excise; never assume rectal bleeding is piles over 40.[1]

The classic trap — never assume bleeding is piles over 40

Assuming rectal bleeding is piles without looking is the single most dangerous error in proctology — because piles and colorectal cancer share the same opening symptom. The disciplined habit is to never attribute bleeding to haemorrhoids until other causes are actively excluded by history, examination, and, where indicated, endoscopy.[1][2]

The rule every candidate must state: any patient over 40 (some guidelines say 45) with new rectal bleeding, or any patient of any age with an alarm feature — weight loss, change in bowel habit, iron-deficiency anaemia, family history of colorectal cancer, or blood mixed with stool — gets a digital rectal exam, a proctoscopy, and a colonoscopy. Reassurance alone in these patients misses cancer.[2]

The mimics, each with a discriminator:[1][2]

How common, and who strains into piles

Haemorrhoidal disease is one of the commonest surgical complaints — and almost everything that raises intra-abdominal pressure feeds it. The point prevalence is roughly 4 to 5 per cent, climbing with age so that more than half of those over 50 have some symptomatic disease; the peak age is 45 to 65, and the sexes are roughly equal, though women often date the onset to pregnancy.[1]

The unifying mechanism of every recognised risk factor is sustained elevation of intra-abdominal and intra-rectal pressure transmitting to the cushions and, over time, shredding their anchoring tissue:[1]

• Constipation and chronic straining — the dominant factor; hard stool and prolonged toilet-sitting force the cushions down.
• Low-fibre diet — hard, low-bulk stools that demand straining; common in urban Indian diets short on roughage.
• Prolonged sitting on the toilet (phone, reading) — sustains the gravitational and pressure load.
• Pregnancy — the gravid uterus compresses pelvic veins, and progesterone vascularly engorges and loosens the support.
• Obesity, chronic diarrhoea (especially IBD), heavy lifting (porters, weightlifters), chronic cough, BPH with straining to void, anal intercourse.
• Portal hypertension and cirrhosis — engorges the portosystemic anastomoses; note this produces rectal varices, a distinct entity, not haemorrhoids.
• Ageing (progressive loss of connective-tissue support) and a weak familial tendency.[1]

Pathophysiology — two theories, one cascade

Two theories explain how normal cushions become piles, and the modern synthesis uses both. Thomson's vascular cushion theory (1975) established that the cushions are rich arteriovenous communications fed at high flow by terminal branches of the superior rectal artery — which is why the bleeding is bright red and arterial, not venous.[4] The sliding anal cushion theory adds the mechanics: chronic straining and ageing degenerate the muscularis submucosae ani (Treitz's muscle) and the suspensory ligament (Parks's ligament), so the cushions lose their mooring, slide distally, and prolapse.[1]

The cascade runs the same way every time. Repeated rises in intra-abdominal pressure raise hydrostatic pressure in the superior haemorrhoidal vessels at the portosystemic anastomosis; the cushions engorge, their anchoring tissue fragments, and they slide downward and prolapse during defecation. With repeated episodes they fail to reduce — the patient drifts from Grade II to III to IV. Trauma from stool then tears the thinned, engorged mucosa, producing the characteristic bright-red bleeding on the paper or in the bowl.[1]

Thrombosis is the external-cushion parallel. When an external pile's venous return is obstructed by acute straining, a thrombus forms, producing the tender, firm, purple perianal lump. As the thrombus organises it may erode through the skin and discharge a dark clot — a sign that spontaneous resolution is near.[1]

The named trap — rectal varices are NOT haemorrhoids. In portal hypertension, submucosal portosystemic collaterals extend proximally from the anorectal junction into the rectum and can bleed massively and life-threateningly. They do not arise from the anal cushions, and must not be banded or excised like piles — they need endoscopic variceal banding, TIPSS, or suture ligation. Confusing the two risks catastrophic bleeding.[1]

At the bedside — inspection, DRE, proctoscopy

Suspected piles are confirmed by three bedside steps in order — inspection, digital rectal examination, and proctoscopy — with endoscopy reserved for excluding proximal disease. Skip any step and you miss cancer and fail the station.[1]

Inspection of the perianal skin (left lateral or lithotomy) looks for external tags, a thrombosed external pile (the purple tender lump), prolapsed internal piles, fissures (posterior midline), sentinel tags, fistula openings, condylomata, and any mass. Ask the patient to bear down to reveal a Grade II or III prolapse invisible at rest.[1]

Digital rectal examination is non-negotiable, and has two jobs:[1]

• Internal piles are usually not palpable — they are soft and collapse when the patient is not straining. A palpable pile is more often a tumour, a thrombosed external pile, or a hypertrophied papilla.
• DRE exists to exclude other pathology: anal fissure (posterior midline tear — defer if exquisitely tender and refer for examination under anaesthesia), rectal mass (cancer, polyp), prostate, pelvic floor tone, and the anocutaneous (S4) reflex (a scratch at the verge should contract the external sphincter).[1]

Proctoscopy (anoscopy) is the definitive bedside test for internal piles. The rigid proctoscope shows the cushions at 3, 7, and 11 o'clock, lets you grade them and see whether they bleed on contact, and permits rubber band ligation at the same sitting. A rigid sigmoidoscopy to 25 cm should accompany it to inspect the rectum for proctitis, tumours, and polyps.[1]

Investigations — confirming nothing, excluding everything

Haemorrhoids are a clinical diagnosis — investigations exist to exclude other pathology and to quantify the consequences of bleeding, not to confirm piles.[1]

• Full blood count — check for iron-deficiency anaemia from chronic loss. Anaemia attributed to piles is a red flag mandating full colonic evaluation, because piles alone rarely drop the haemoglobin — colorectal cancer must be excluded.
• Coagulation screen and platelets — if anticoagulated, liver disease, or a bleeding history, before any invasive intervention.
• Colonoscopy — for any patient over 40 to 45 with rectal bleeding, or younger with alarm features, to exclude proximal pathology above all colorectal cancer, polyps, and IBD.
• Flexible sigmoidoscopy — an acceptable alternative when colonoscopy is unavailable or contraindicated in a young patient with typical bleeding.
• STI screen — if sexually transmitted anal pathology (gonococcus, syphilis, HPV, herpes) is suspected.[2]

No imaging is routinely required. In the rare case of massive lower-GI bleeding with an unclear source, CT angiography localises the bleeding point and guides intervention.[1]

The ladder by grade — fibre for all, band for I to III, cut for III to IV

Definitive treatment is a ladder that maps onto the Goligher grade — office measures for I to II, surgery for III to IV — and every patient, whatever the grade, starts with the same baseline.[1][2]

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Rubber band ligation (Barron's banding) is the standard office procedure for Grade II and III (and Grade I with troublesome bleeding). A band goes on the pedicle above the dentate line — painless — causing ischaemic necrosis; the tissue sloughs at 5 to 7 days, leaving a fibrotic ulcer. Success is about 70 to 80 per cent for Grade II; band no more than one or two piles per session. The complications are the trap: pain (band too low — remove it at once), secondary bleeding at day 5 to 7 when tissue sloughs, and the rare but lethal pelvic sepsis and Fournier's gangrene — any fever, severe pain, or urinary retention after banding is an emergency.[1]

Injection sclerotherapy — 5 per cent phenol in almond (arachis) oil, 2 to 3 mL into the submucosa above the pedicle — causes slow fibrosis that tethers the mucosa and fixes the cushion. Used for Grade I and early II with bleeding; less effective than banding for prolapse, and avoid in nut allergy. Infrared coagulation (tungsten-halogen heat) suits small bleeding Grade I to II piles; cryotherapy and bipolar diathermy are largely historical.[1]

The four operations — durability versus pain

Four operations, one trade-off: excisional surgery is the most durable but the most painful; stapled and THD spare the perianal skin at the cost of higher recurrence.[1][2][3]

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One-line discriminator beneath the table: open and painful but durable is Milligan-Morgan; closed and a little less sore is Ferguson; no wound, less pain, more recurrence is stapled; Doppler-guided, no wound, intermediate recurrence is THD.[2]

Milligan-Morgan (open) haemorrhoidectomy is the gold standard, dominant in the UK, India, and much of the world. The three primary pedicles at 3, 7, and 11 o'clock are excised with diathermy to the internal sphincter, the pedicle ligated, and the mucocutaneous wounds left open to heal by secondary intention, preserving skin bridges between wounds to prevent anal stenosis. Recurrence is under 5 per cent; the price is significant pain for 2 to 3 weeks.[1][2]

Ferguson (closed) haemorrhoidectomy uses the same excisional principle but closes the mucocutaneous defect primarily with a running absorbable suture — less pain, faster healing, popular in the US; wound breakdown may convert it to an open technique.[1]

Stapled haemorrhoidopexy (PPH) uses a circular stapler to excise a ring of rectal mucosa 2 to 4 cm above the dentate line, lifting the prolapsed cushions back up and interrupting their arterial inflow. With no perianal wound, pain is markedly less and recovery faster. The trade-off, fixed by the eTHoS trial, is a higher symptomatic recurrence rate and specific complications: staple-line bleeding, chronic pain, faecal urgency, rectovaginal fistula, and rarely full-thickness rectal wall excision or pelvic sepsis. Best suited to circumferential Grade III.[3]

[3]

Transanal haemorrhoidal dearterialisation (THD and HALO) uses a Doppler probe in a specialised proctoscope to locate the terminal branches of the superior rectal artery feeding each cushion, then suture-ligates them to cut inflow and hitches the prolapsing cushion back up by mucopexy. Minimal postoperative pain, no excisional wound, recurrence intermediate between stapling and excision; suits Grade II to IV. A systematic review found THD broadly comparable to stapled haemorrhoidopexy in symptom control with a favourable safety and pain profile.[5]

Laser haemorrhoidectomy (Nd:YAG or diode coagulation of the pedicle) is niche, expensive, and of limited evidence — know it exists, do not reach for it first.[1]

Thrombosed external haemorrhoid — the 72-hour fork

The timing of presentation decides everything: excise early, console late. Within 72 hours of onset, excision under local anaesthetic (1 to 2 per cent lignocaine, with or without adrenaline), removing an ellipse of overlying skin and the thrombosed vein en bloc, gives dramatic and immediate relief.[1]

After 72 hours the pain is already waning and conservative management wins: oral NSAIDs (ibuprofen 400 mg three times daily, or naproxen 500 mg twice daily), warm sitz baths two to three times daily, stool softeners, topical lignocaine 2 per cent gel, and topical glyceryl trinitrate 0.2 to 0.4 per cent ointment if anal spasm contributes. The thrombus organises and absorbs over 2 to 4 weeks; the skin may ulcerate and discharge the clot, and a residual skin tag may need later cosmetic excision.[1]

Strangulated internal — and the three emergencies

Piles rarely present as an emergency, but three scenarios demand urgent, structured management.[1]

Strangulated internal haemorrhoid is a Grade IV prolapse incarcerated outside the sphincter — venous return occluded, the cushion oedematous, thrombosed, and heading toward ulceration and necrosis. Give adequate analgesia and seek urgent surgical assessment; the preferred treatment, if the patient is fit, is urgent haemorrhoidectomy within 72 hours, which relieves pain definitively and removes necrotic tissue.[1]

Massive haemorrhoidal bleeding causing haemodynamic instability is uncommon but real. Resuscitate first — two large-bore cannulae, IV crystalloid, group and crossmatch, transfuse if shocked — then theatre for proctoscopy under anaesthesia to find the bleeding cushion; control is by suture ligation of the pedicle or balloon tamponade with a Foley catheter in the rectum as a bridge to definitive surgery.[1]

Thrombosed external haemorrhoid is the third emergency — handled by the 72-hour fork above.[1]

Three named traps in special populations

Pregnancy, portal hypertension, and Crohn's disease each carry a trap the examiner will probe.[1]

Pregnancy-related piles — common in the third trimester from mechanical and hormonal factors. Manage conservatively (fibre, fluids, stool softeners, topical agents); most resolve or markedly improve within weeks of delivery. Defer banding and excisional surgery unless the pile is strangulated; if surgery is unavoidable, the second trimester is safest, with obstetric and anaesthetic input.[1]

Portal hypertension and cirrhosis — the named trap: rectal varices are NOT piles. Distinguish rectal varices (submucosal portosystemic collaterals that may bleed massively) from coincidental haemorrhoids. Varices are managed with endoscopic variceal banding, TIPSS, or suture ligation — never by haemorrhoidectomy or routine banding. Different origin, different bleeding potential, different treatment.[1]

Inflammatory bowel disease — the named trap: excising in active Crohn's is a disaster. Excisional haemorrhoidectomy in active Crohn's risks non-healing wounds, fistula, and incontinence. Manage conservatively until the IBD is quiescent; only then consider surgery, and with great caution.[1]

The remaining groups: immunocompromised patients (HIV, chemotherapy, transplant) — avoid surgery for fear of sepsis and poor healing; favour conservative and office measures, optimise immune status first, use antibiotic prophylaxis, and expect slower healing. Paediatric piles are rare and should trigger a search for portal hypertension or chronic constipation. Circumferential (rosette) prolapse suits stapled haemorrhoidopexy or a tailored Milligan-Morgan with careful skin bridges. Anticoagulated patients — continuing anticoagulants does not significantly increase bleeding after banding for most, but warfarin and DOACs should be reviewed; favour cautery techniques and warn about delayed bleeding.[1]

Complications — of the disease and of the treatment

Complications come in three lists: of the disease, of the band, and of the knife.[1]

Of the disease itself: iron-deficiency anaemia from chronic loss (mandates colonoscopy to exclude cancer), thrombosis of an external cushion, strangulation and gangrene of a Grade IV prolapse progressing to sepsis, and incontinence and soiling from large prolapsing piles disrupting sphincter closure.[1]

Of rubber band ligation: severe pain (band too low, below the dentate line — remove it immediately), secondary bleeding at day 5 to 7 when tissue sloughs (usually self-limiting; severe bleeding needs suture ligation under anaesthesia), and the rare but lethal pelvic sepsis and Fournier's gangrene — any fever, severe pain, or urinary retention after banding is an emergency.[1]

Of haemorrhoidectomy:[1]

• Pain — the dominant drawback; 2 to 3 weeks after Milligan-Morgan, somewhat less after Ferguson, stapled, or THD.
• Urinary retention — the commonest reason for overnight admission after day-case haemorrhoidectomy; managed with analgesia and, if needed, temporary catheterisation.
• Bleeding — primary (intra-operative, inadequately secured pedicle) and secondary (day 7 to 10, infection or sloughing); secondary bleeding can be torrential — warn the patient to attend urgently.
• Anal stenosis — from over-resection of anoderm leaving insufficient skin bridges (the whitehead deformity); prevented by always preserving skin bridges.
• Incontinence — from inadvertent internal sphincter injury, especially in repeated or aggressive surgery.
• Recurrence — about 5 to 10 per cent after excisional haemorrhoidectomy; higher (15 to 20 per cent) after stapled haemorrhoidopexy, as eTHoS confirmed.[3]
• Infection, fissure, and fistula — less common but recognised.[1]

Prognosis, prevention, and the message every patient leaves with

Piles are benign, chronic, and relapsing — only about 10 to 20 per cent of symptomatic patients ever need surgery. Recurrence shapes the long term: under 5 to 10 per cent after excisional surgery, 30 to 50 per cent over 5 years after banding (often re-banded), and about 15 to 20 per cent after stapling, as eTHoS confirmed; THD sits between.[1][3]

Prevention is the half of management patients carry home, and the message every patient should leave with: high-fibre diet (25 to 30 g per day), adequate fluid (about 2 L per day), avoiding straining and prolonged toilet-sitting, treating constipation promptly with bulk-forming laxatives, regular exercise, and answering the call to stool rather than delaying.[1]

Guidelines, trials, and regional deltas

The ASCRS Clinical Practice Guidelines for the Management of Hemorrhoids (Davis et al., 2018) are the most widely cited consensus and recommend dietary modification first-line for all grades, rubber band ligation as the preferred office procedure for Grade I to III, excisional haemorrhoidectomy for Grade III to IV or failed banding, stapled haemorrhoidopexy for circumferential Grade II to III accepting less pain but higher recurrence, and THD as an alternative for Grade II to III with a favourable pain profile.[2]

The eTHoS trial (Watson et al., 2017) — the definitive pragmatic multicentre RCT comparing stapled haemorrhoidopexy with traditional excisional surgery — confirmed that stapling gives less short-term pain but a higher rate of symptomatic recurrence, shifting equipoise back toward excisional surgery for durable cure, especially in Grade IV.[3]

THD versus stapled (Sajid et al., 2012) — a systematic review — found broadly comparable symptom control, with THD offering a favourable safety and pain profile.[5]

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The mantra

The mantra: above the line painless, below the line painful; grade I to II band, grade III to IV excise; never assume rectal bleeding is piles over 40.[1]

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Ward-round test — three stems, thirty seconds each

Stem 1 — painless bright-red blood on the paper (answer)

A 52-year-old with three months of painless bright-red blood on the toilet paper and dripping into the bowl, constipated, no weight loss, no change in bowel habit. Proctoscopy shows a bleeding Grade II internal pile at 7 o'clock. What is your management — and what must you do first for the bleeding to count as fully worked up?[1]

Model: First, exclude colorectal cancer by DRE, proctoscopy (done — confirms the pile), and — because he is over 40 with new rectal bleeding — colonoscopy; the proctoscopy finding does not remove that obligation. Then treat the Grade II pile with rubber band ligation above the dentate line (painless), plus baseline fibre (25 to 30 g per day), fluids, and a bulk-forming laxative. Safety-net for red flags (change in bowel habit, weight loss, dark or mixed blood).[2]

Stem 2 — the patient in agony after banding (answer)

Four hours after rubber band ligation a patient phones in severe perianal pain and cannot pass urine. What happened, and what do you do?[1]

Model: The band was placed below the dentate line on somatic, pain-sensitive anoderm — the cardinal error — and urinary retention is the reflex response to severe anal pain. Remove the band immediately and re-place it above the line under vision once pain settles. If fever, worsening pain, or retention persist after removal, assume pelvic sepsis or Fournier's gangrene until proven otherwise — urgent review and admission.[1]

Stem 3 — the cirrhotic with a bleeding pile (answer)

A 60-year-old with cirrhosis and portal hypertension has massive painless rectal bleeding. Proctoscopy shows a purplish submucosal vessel extending up into the rectum from the anorectal junction. The registrar plans to band it as a haemorrhoid. What is the right call?[1]

Model: This is a rectal varix, not a haemorrhoid — a submucosal portosystemic collateral from portal hypertension that can bleed massively. It does not arise from the anal cushions and must not be banded or excised like a pile, which risks catastrophic bleeding. Manage as a portosystemic varix with endoscopic variceal banding, TIPSS, or suture ligation under anaesthesia. The two entities have different origins, different bleeding potential, and different treatment.[1]

[1] [2]

References

1. [1]Lohsiriwat V Hemorrhoids: from basic pathophysiology to clinical management World J Gastroenterol, 2012.PMID 22563187
2. [2]Davis BR, Lee-Kong SA, Migaly J, Feingold DL, Steele SR The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Hemorrhoids Dis Colon Rectum, 2018.PMID 29420423
3. [3]Watson AJ, Cook JA, Hudson NC, et al. A pragmatic multicentre randomised controlled trial comparing stapled haemorrhoidopexy with traditional excisional surgery for haemorrhoidal disease: the eTHoS study Health Technol Assess, 2017.PMID 29205150
4. [4]Thomson WH The nature of haemorrhoids Br J Surg, 1975.PMID 1174785
5. [5]Sajid MS, Parampalli U, Whitehouse P, Sains P, McFall MR, Baig MK A systematic review comparing transanal haemorrhoidal de-arterialisation to stapled haemorrhoidopexy in the management of haemorrhoidal disease Tech Coloproctol, 2012.PMID 22183450