ppt on Hemorrhoids, anal fissure, anal fistula, anal abscess.

1. HEMORRHOIDS
KABIR BANSAL
57
BATCH 2017

2. Definition
• Hemorrhoids, also called piles, arise from a cushion of dilated
arteriovenous blood vessels and connective tissue in the anal canal
that may abnormally enlarge or protrude.
• Hemorrhoids are divided into three categories: internal (above the
dentate line), external (below the dentate line), or mixed (above and
below the dentate line).

3. ANATOMY OF ANAL CANAL
• Anal cushions --
• Areas of thickened anal mucosa that consist of arteriovenous blood vessels
(corpus cavernosum recti), smooth muscle (e.g., Treitz muscle), and
fibroelastic tissue (e.g., collagen, elastic fibers)
• Located at 11, 7 and 3 o'clock in the lithotomy position (right anterior, right
posterior, and left lateral position)
• Defecation causes contraction of supportive structures (e.g., Treitz muscle)
→ compression of anal cushions → increased diameter of the anal canal
for adequate passage of stool

4. .

5. ANATOMY OF ANAL CANAL
• Anal columns: longitudinal folds of mucous membrane that are fused
at their inferior ends.
• Anal sinuses: small, mucus-secreting pouches between the anal
columns above the anal valves
• Dentate line-Circular separation line formed by the fusion of anal
valves (hindgut-proctodeum junction)
• Divides anal canal into an upper and lower part

6. .

7. EXTERNAL ANAL SPHINCTERS
• External anal sphincter
• Composed of--
1. Subcutaneous external sphincter: surrounds lower third of anal canal
2. Superficial external sphincter
3. Deep external sphincter
• Consists of skeletal muscle and functions to open and close the anal canal
and opening
• Innervated by the pudendal nerve and under voluntary control

8. INTERNAL ANAL SPHINCTER
• Internal anal sphincter
• Surrounds upper two-thirds of anal canal
• Consists of involuntary circular smooth muscle and is responsible for
∼ 85% of the resting pressure of the anal canal
• Innervated by the enteric nervous system

9. .

11. ETIOLOGY
• Excessive straining (e.g., from chronic constipation, frequent bowel
movements, chronic cough, heavy lifting, benign prostatic
hyperplasia)
• Extended periods of sitting (e.g., due to occupation or sedentary
lifestyle)
• Connective tissue disorder (e.g., Ehlers-Danlos syndrome,
scleroderma)
• Pregnancy

12. INTERNAL HEMORRHOIDS
• Prolapse of internal hemorrhoids, with possible incarceration and
strangulation, may cause pain by triggering an anal sphincter complex spasm.
→ possible ischemia and necrosis of internal hemorrhoids → worsening anal
sphincter complex spasm → potential external hemorrhoid thrombosis →
cutaneous pain
• Develop above the dentate line, which is not innervated by cutaneous
nerves; distension does not cause pain.
• Bleeding and/or prolapsed internal hemorrhoids irritate sensitive perianal
skin → perianal itching

13. EXTERNAL HEMORRHOIDS
• Develop below the dentate line, which is innervated by cutaneous
nerves; distention of this innervated skin due to a clot or edema results
in severe pain.
• Acute thrombosis triggers cutaneous pain, lasting 7–14 days →
thrombosis resolves → residual skin or skin tags of distended anal skin

14. .

15. .

17. LOCATIONS

18. LOCATIONS

19. CLINICAL FEATURES
• Internal hemorrhoids--
• Often painless, bright red bleeding at the end of defecation
(potentially dull, aching pain with severe sphincter spasm)
• Perianal mass in the event of prolapse
• Pruritus
• Discharge (containing mucus or fecal debris)
• Ulceration (in grade IV)

20. CLINICAL FEATURES
• External hemorrhoids--
• Painful perianal mass
• Pruritus

21. DIAGNOSIS
• Clinical examination
• Inspect perianal area for external hemorrhoids and prolapsed internal
hemorrhoids; exclude other conditions (e.g., anal skin tags, polyps).
• Digital rectal examination may show abnormal masses or tenderness
or bleeding.

22. DIAGNOSIS
• Anoscopy
• For assessing the anus and distal rectum
• Useful when hemorrhoids are suspected but rectal examination is
inconclusive [5]
• In addition, proctoscopy may be used to support anoscopy findings.
• Other procedures
• Flexible sigmoidoscopy, colonoscopy, or barium enema: to exclude suspected
malignancy (especially in patients over the age of 40), presence of risk factors
for colorectal cancer, or red flags for colorectal cancer

23. .

24. CONSERVATIVE TREATMENT
• Indications: grade I–II internal hemorrhoids and external hemorrhoids
• Interventions
• Lifestyle modifications: weight loss, exercise, high fiber diet, avoid fatty and spicy
foods, increase water intake
• Alter stool habits (e.g., avoid excessive straining or > 5 min periods on the toilet)
• Sitz baths
• Stool softeners (e.g., docusate)
• Topical or suppository analgesia (e.g., lidocaine)
• Topical anti-inflammatory (e.g., hydrocortisone, especially with pruritus, but no longer
than 1 week)
• Topical antispasmodic agents (e.g., nitroglycerin)

25. OUTPATIENT TREATMENT
• Indications: all internal hemorrhoids with symptoms persisting
despite conservative treatment and grade III internal hemorrhoids
• Interventions
• Rubber band ligation (RBL)
• Sclerotherapy (5% phenol in almond oil injected in submucosa above
dentate line)
• Infrared coagulation

26. SURGICAL TREATMENT
• Indications: grade III-IV internal hemorrhoids and no improvement of
condition after clinical interventions
• Interventions
• Arterial ligation of hemorrhoids (HAL)
• Submucosal hemorrhoidectomy-
1-Ferguson approach (closed approach )
2-Milligan-Morgan approach (open approach )
• Stapled hemorrhoidopexy (e.g., using the Longo procedure): only
effective for internal hemorrhoids

27. STAPLED
HEMORRHOIDOPEXY

28. ANAL FISSURE

29. DEFINITION
• Longitudinal tear of the anal canal; distal to the dentate line

30. ETIOLOGY
• PRIMARY (DUE TO LOCAL TRAUMA)
• Location: 90% of all anal fissures located at the posterior commissure (6
o'clock in the lithotomy position)
• Types of trauma:
• Chronic spasm/increased tone in the internal anal sphincter
• Low fiber intake
• Chronic constipation or diarrhea
• Anal sex
• Vaginal delivery

31. ETIOLOGY
• SECONDARY (DUE TO UNDERLYING DISEASE)
• Location: may occur lateral or anterior to the posterior commissure
• Underlying conditions:
• Previous anal surgery (e.g., possible stenosis of anal canal)
• Inflammatory bowel disease (IBD; e.g., Crohn's disease)
• Granulomatous disease (e.g., tuberculosis)
• Infections (e.g., chlamydia, HIV)
• Malignancy(e.g., leukemia)

32. PATHOPHYSIOLOGY
• Overdistension or disease of the anal mucosa → laceration of the anoderm
• Spasm of the exposed internal anal sphincter leads to pulling along the
laceration, which impairs healing and worsens the extent of laceration with
each bowel movement.
• The resultant pain results in voluntary avoidance of defecation and
constipation, which worsens distension of the anal mucosa.
• The posterior commissure is believed to have a very poor blood supply,
which predisposes it to ischemia (exacerbated by poor perfusion during
increased anal pressure).

33. CLINICAL FEATURES
• Sharp, severe pain during defecation
• Rectal bleeding (often bright red and minimal; should not be
confused with other types of bleeding such as in colorectal cancer or
hemorrhoids)
• Perianal pruritus
• Chronic constipation

34. ACUTE
FISTULA

35. CHRONIC
FISTULA

36. DIAGNOSIS
• Clinical examination
• Superficial or deep laceration in anterior, lateral, or posterior anal canal
• In addition, chronic fissures may present with fibrotic and infective changes:-
• Wide, raised edges
• Skin tags (sentinel pile) at the fissure's distal end
• Hypertrophied anal papillae at the fissure's proximal end
• Clinical history:
• Digital rectal examination: if diagnosis is uncertain or to exclude a suspected underlying pathology (e.g.,
rectal tumor)
• Anoscopy
• Indicated if clinical findings are unclear or if symptoms persist despite adequate treatment
• Possible biopsy and histological investigation (to exclude a carcinoma, especially when presentation is
atypical)

37. TREATMENT
• CONSERVATIVE-
• First-line treatment for most anal fissures
• Includes:
• Dietary improvement (e.g., adequate ingestion of dietary fiber and water)
• Stool softeners (e.g., docusate)
• Anti-inflammatory and analgesic creams and/or suppositories (e.g., 2% lidocaine
jelly)
• Sitz baths
• Local anesthetic injection
• Topical vasodilator therapy: calcium channel blocker gel (e.g., nifedipine) or glyceryl
trinitrate ointment (GTN)

38. TREATMENT
• SURGICAL-
• Indicated when conservative treatment is unsuccessful
• The risk of fecal incontinence (e.g., high in multiparous or elderly patients) determines
the type of surgical intervention.
• Low risk-
• Sphincterotomy (e.g., lateral internal sphincterotomy)
• Anal dilatation (although there is a high risk of fecal incontinence with this procedure)
• High risk-
• Anal advancement flap
• Fissurectomy (excision of the fissure)

39. ANAL ABSCESS AND FISTULAS
• Anal abscesses are the acute manifestation of a purulent infection in the
perirectal area, while anal fistulas are the chronic manifestation of such
infections.
• An anal abscess is a pus-filled cavity that most commonly develops from an
infected anal crypt gland following obstruction and bacterial overgrowth.
• An anorectal abscess may heal spontaneously following drainage into the
anal canal. In about 30–60% of cases, anal abscesses progress into fistulas,
which are ductal connections between the abscess and the anal canal or the
perianal skin.

40. ETIOLOGY
• Most common cause: flow obstruction and infection of the anal crypt glands (90% of
cases)
• Less common causes
• Chronic inflammatory bowel disease (IBD): Crohn's disease, ulcerative colitis (less
commonly)
• Acute infections of the gastrointestinal tract: e.g., complicated diverticulitis, acute
appendicitis
• Radiation-induced proctitis
• Iatrogenic
• Foreign body
• Malignancy: e.g., colorectal cancer

41. PATHOLOGY
• Typical development
• Obstruction of anal glands by thick debris → stasis and bacterial
overgrowth → abscess formation
• Abscess may extend into adjacent perirectal spaces → possible fistula
formation , bacteremia and sepsis

42. CLINICAL FEATURES
• Abscesses
• Perianal abscess-
• Dull perianal discomfort and pruritus
• Erythematous, subcutaneous mass near the anus found by manual inspection
• Perirectal abscess-
• Rectal or perirectal drainage (bloody, purulent, or mucoid)
• Severe pain, fever, and chills
• Pain exacerbation with sitting and defecation

43. ANAL ABSCESS

44. .

45. CLINICAL FEATURES
• Fistulas
• Purulent drainage (from anal canal or surrounding perianal skin)
• Pain during defecation
• Digital rectal examination: fluctuant, indurated mass, pain with
pressure

46. .

47. DIAGNOSIS
• Digital rectal examination: fluctuant, indurated mass, pain with pressure
• CT/MRI or anal ultrasonography: confirmatory tests for deeper abscesses
• Further testing: to identify possible fistulae and comorbidities (malignancy,
IBD)
• Endoscopy
• MRI
• Fistula probe (with methylene blue)

48. TREATMENT
• ABSCESSES
• Early surgical incision and drainage
• Postoperative
• Sitz baths
• Analgesics and stool softeners
• Antibiotics: indicated in immunocompromised individuals

49. TREATMENT
• FISTULAE
• Fistulotomy (standard approach)
• Possible seton placement (enables adequate drainage and fibrosis)
• Possible fibrin glue or fistula plug
• Additional administration of antibiotics and immunosuppressants in
patients with Crohn's disease

50. .
SENTON PLACEMENT
IN ANAL FISTULA

51. .
FISTULA PLUG