MSC - F. Surgery Answers 2025

Others:

Proctosigmoidoscopy (if tolerated or under anesthesia) – to rule out internal opening or secondary pathology (e.g., tumor, Crohn's)

Treatment:

Surgical intervention is mandatory – no role for antibiotics alone.

Principles of Surgery:

1.Immediate Incision and Drainage (I&D):

Under general anesthesia

Radial or semilunar incision over the point of maximal tenderness or fluctuation

Adequate drainage must be ensured

2.Eliminate Internal Opening (if identified):

Only in subcutaneous paraproctitis – Gabriel's operation (simultaneous drainage + internal opening excision)

In other types: dealt with later during definitive surgery for fistula

3.Special Cases:

Horseshoe abscess (posterior, bilateral): requires bilateral semilunar incisions (Fig. 22)

Postoperative Care:

Sitz baths

Stool softeners, laxatives

Analgesics

Broad-spectrum antibiotics (if systemic signs of infection or immunocompromised)

Complications:

Chronic fistula-in-ano (in 70–75% if internal opening not addressed)

Sepsis (if delayed treatment)

Recurrence

Incontinence (if sphincter injured)

13.Anaerobic paraproctitis: features of the clinic, diagnosis and treatment.

Definition:

A rapidly progressive, necrotizing infection of the perirectal tissues caused by anaerobic bacteria, characterized by tissue destruction, sepsis, and high mortality.

Most severe form of paraproctitis

Mortality rate: 10–30% or higher

More common in males

Strong association with diabetes mellitus and immunosuppression

Etiology:

Caused by anaerobic organisms, both:

Clostridial: Clostridium perfringens (gas gangrene-like features)

Non-clostridial: Bacteroides, Fusobacterium, Peptostreptococcus, etc.

Predisposing factors:

Diabetes mellitus

Immunosuppression (HIV, malignancy, corticosteroids)

Local trauma or surgical manipulation

Chronic perianal infections

Pathogenesis:

Entry through anal crypts or existing fissures/abscesses

Rapid spread due to low oxygen tension in perianal tissues

Toxin production → tissue necrosis, vascular thrombosis, systemic toxicity

Gas formation in tissues (esp. clostridial infections)

Impaired host immunity allows rapid anaerobic proliferation

Forms (3 clinical types):

1.Putrefactive form – less aggressive; localized necrosis

2.Progressive gangrenous form – extensive necrosis and soft tissue destruction (similar to Fournier’s gangrene)

3.Anaerobic lymphangitis – lymphatic spread with systemic sepsis

Clinical Presentation:

Early Stage:

Sudden onset of severe perianal pain

High fever (38–40°C)

Tachycardia, chills, malaise

Perineal fullness, pressure Advanced Stage (3–7 days):

Rapidly spreading edema, erythema, and crepitus

Necrosis of skin, subcutaneous fat, fascial planes (perineum, genitalia, thighs)

Foul-smelling discharge and gas in tissues

Systemic toxicity: hypotension, septic shock

Grave general condition

Diagnosis:

Clinical Examination:

Signs of necrotizing soft tissue infection (NSTI) in perineum

Blackish or purplish skin, blistering, discharge of gas and pus

Palpable crepitus (subcutaneous gas)

Rectal exam: pain, bogginess (done only if tolerated)

Laboratory:

Leukocytosis, anemia, hypoproteinemia

Elevated CRP, procalcitonin

Lactate ↑, metabolic acidosis

Microbiology:

Gas-liquid chromatography, microscopy of smears for early detection

Culture and sensitivity (takes 5–7 days)

Imaging (if time permits before surgery):

CT scan: shows gas in soft tissues, abscess pockets, fascial spread

MRI: delineates deep fascial involvement (if not contraindicated by time)

Treatment:

This is a surgical emergency. Delay = death.

1.Surgical Management (Immediate):

Wide surgical debridement under general anesthesia

Semilunar or radial incisions to:

o Drain abscess

o Remove all necrotic tissue

oDecompress fascial compartments

Repeat wound inspections/debridements may be required

If thigh involvement: additional incisions to track and drain fascial extensions

2.Antimicrobial Therapy:

Empiric high-dose, broad-spectrum antibiotics with anaerobic coverage:

oMetronidazole (obligatory)

o Piperacillin-tazobactam, carbapenems, or cefoperazone-sulbactam

oVancomycin (if MRSA risk)

Adjust based on culture

3.Antifungal Prophylaxis (especially in diabetics):

Fluconazole or Ketoconazole to prevent secondary fungal infections

4.Local Wound Care:

Modern antiseptics

Polyethylene glycol-based ointments

Hydrocolloid dressings, polyurethane foam

Aerosol applications

Use of:

oUltrasonic cavitation

o Low-intensity laser therapy

oOzonized irrigation

5.Supportive Therapy:

Disintoxication: IV fluids, vasopressors if needed

o External orifice (on perianal skin)

Clinical Picture:

Intermittent purulent or mucous discharge from external opening

Recurrent perianal pain, worse with defecation

Pruritus, skin maceration, occasional fecal/gas leak

Fever and malaise during exacerbations

The disease has a chronic undulating course: periods of remission interrupted by exacerbations

15.Chronic paraproctitis: classification, diagnosis and treatment.

Classification of Rectal Fistulas (By Parks, modified):

1.By anatomical relationship to sphincter: o Intersphincteric

o Transsphincteric o Suprasphincteric o Extrasphincteric

o Submucosal/subcutaneous (simpler, low-lying fistulas)

2.By tract orientation:

oAnterior / Posterior / Lateral

3.By complexity:

oSimple – low, single tract

oComplex – high, branching, multiple tracts, or associated with IBD, TB, or malignancy

4.By activity:

oActive (suppurating) vs. inactive (healed or epithelialized)

Diagnosis:

Clinical:

Purulent or serous discharge from a perianal opening

Palpable indurated tract

Pain during defecation or at rest in acute phases

Physical Examination:

Inspection of perianal region for external opening

Digital rectal exam: Palpate tract or induration

Fistula probing: To map tract (done carefully to avoid creation of false passage)

Instrumental:

Proctosigmoidoscopy: Identifies internal orifice, rules out other rectal pathology

Fistulography: Contrast study for complex/extrasphincteric fistulas

MRI pelvis: Gold standard in complex, recurrent, or Crohn’s-related fistulas

Endoanal ultrasound: Maps fistula path relative to sphincters

Sphincterometry: Measures sphincter tone (pre-op planning)

Treatment:

Conservative therapy is ineffective in achieving cure. Surgery is the definitive treatment.

Surgical Options (Based on Fistula Type):

1.Intersphincteric Fistulas:

Gabriel's operation (simple fistulectomy) o Excision of tract

o Internal opening is removed

oHealing by secondary intention

2.Low Transsphincteric Fistulas:

Gabriel’s operation with partial division and primary closure of sphincter fibers

3.High Transsphincteric & Extrasphincteric Fistulas (Complex):

Seton placement: Loose or cutting

Ligation of intersphincteric fistula tract (LIFT)

Advancement flap: Internal orifice is closed with a mucosal/submucosal flap

Fibrin glue, fistula plug: Biologic therapies (limited success)

4.Horseshoe or Multiple Fistulas:

Multiple incisions, drainage, fistulotomy or staged procedures

High risk of incontinence; sphincter-sparing strategies preferred

Postoperative Care:

Sitz baths, hygiene

Analgesia

Fiber-rich diet and stool softeners

Antibiotics if signs of infection or systemic symptoms

Wound dressing

Complications:

Recurrence (1–4%)

Anal incontinence (1–4%, depending on complexity and technique)

Delayed wound healing

Prognosis:

Excellent in intersphincteric/simple fistulas

Guarded in complex/extrasphincteric fistulas

Recurrence and sphincter damage risk increases with multiple surgeries or improper techniques

16.Epithelial coccygeal cyst: etiology, pathogenesis, clinic, diagnosis and treatment.

1. Epithelial Coccygeal Cyst (Pilonidal Disease)

Definition:

An epithelial coccygeal cyst, also known as a pilonidal sinus, is a congenital or acquired epithelial tract in the sacrococcygeal region, typically located midline in the intergluteal cleft, with one or more primary openings. It may remain asymptomatic or progress to inflammation, abscess formation, or chronic fistulous disease.

Etiology:

Congenital theory: Embryological epithelial invagination or remnant of the medullary canal.

Acquired theory (dominant modern view):

oHair penetration into subcutaneous tissue causes foreign body reaction.

oRisk factors:

Hirsutism

Obesity

Sedentary lifestyle

Deep natal cleft and poor hygiene