Harvey's Garden

Intestinal fistulas

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3 min read

Epidemiology & Risk Factors

  • Iatrogenic/Postoperative: Accounts for ~75–85% of all enterocutaneous fistulas (ECF); typically occurs after laparotomy, bowel resection, or lysis of adhesions.
  • Crohn Disease (CD): Most common non-surgical cause; transmural inflammation leads to fistula formation (enteroenteric, enterovesical, enterocutaneous, perianal).
  • Diverticulitis: Common etiology of enterovesical (colovesical) fistulas. c
  • Malignancy & Radiation: Tissue ischemia and necrosis predispose to barrier breakdown.
  • Trauma: Penetrating abdominal injuries.

Clinical Features

  • Enterocutaneous Fistula (ECF):
    • Drainage of enteric contents (succus entericus, bile, or fecal fluid) through surgical incision or abdominal wall defect.
    • Erythema & skin excoriation (severe chemical dermatitis from digestive enzymes).
  • Enterovesical Fistula: c
    • Pneumaturia (air in urine) and fecaluria (fecal matter in urine).
    • Recurrent, polymicrobial urinary tract infections (UTIs).
  • Enteroenteric/Enterocolic Fistula:
    • Diarrhea, weight loss, and malabsorption due to bypass of absorptive small bowel areas.
  • Aortoenteric Fistula:
    • Herald bleed (brief hematemesis/melena) followed by catastrophic, fatal gastrointestinal (GI) hemorrhage.
    • Typically occurs at the duodenum after abdominal aortic aneurysm (AAA) repair.

Diagnosis

  • Initial:
    • CT Abdomen/Pelvis w/ oral and IV contrast: Identifies fluid collections, abscesses, and defines the fistula tract.
    • Urinalysis (UA): In enterovesical fistulas, reveals pyuria, fecal debris, and polymicrobial bacteriuria.
  • Key Labs:
    • CBC: Leukocytosis (evaluates for sepsis or occult intra-abdominal abscess).
    • BMP: Evaluates severe electrolyte abnormalities (e.g., hyponatremia, hypokalemia, hypomagnesemia, metabolic acidosis).
    • Nutritional Markers: Serum albumin and prealbumin (essential to assess severity of malnutrition).
  • Confirmatory/Gold Standard:
    • Fistulogram: Water-soluble contrast injected into the skin opening under fluoroscopy to define tract anatomy.
    • CT Enterography/MR Enterography: Best for complex fistulas associated with Crohn disease.
    • Cystoscopy: Visualizes the fistulous opening in the bladder wall for suspected enterovesical fistulas.

Differential Diagnostics

  • Surgical Site Infection (SSI): Differentiated by purulent drainage without enteric/bilious fluid and absence of bowel tract communication on CT.
  • Abdominal Abscess: Differentiated by localized intra-abdominal fluid collection without a patent drainage tract to the skin.
  • Wound Dehiscence: Differentiated by separation of fascial layers with evisceration, but no active leakage of enteric contents (unless associated with bowel injury).

Management

  • Phase 1: Stabilization & Resuscitation (First-line):
    • IV Fluid Resuscitation: Aggressive isotonic fluids (e.g., Lactated Ringer’s) to replace volume losses, especially in high-output (>500 mL/day) ECFs.
    • Electrolyte Repletion: Prompt replacement of K+, Mg2+, and bicarbonate to correct metabolic acidosis.
    • Sepsis Control: Broad-spectrum IV antibiotics (e.g., Piperacillin/Tazobactam) and percutaneous drainage of any associated intra-abdominal abscesses.
    • Skin Protection: Wound care using specialized ostomy pouches, barrier creams, or negative pressure wound therapy (NPWT) to prevent chemical dermatitis.
  • Phase 2: Nutritional Optimization (Second-line):
    • Total Parenteral Nutrition (TPN): First-line nutritional support for high-output (>500 mL/day) fistulas or when enteral feeding increases output.
    • Bowel Rest: NPO status to reduce GI secretions and output.
    • Somatostatin Analogues (e.g., Octreotide): Used to reduce GI secretions and decrease time to spontaneous closure.
  • Phase 3: Definitive Intervention (Refractory):
    • Conservative Trial: Allow 4–6 weeks for spontaneous closure (highly likely in low-output, single-tract, non-radiated fistulas).
    • Surgical Resection (Definitive): Indicated if the fistula fails to close spontaneously after 6–12 weeks of optimal medical therapy, or if “FRIEND” factors are present.
      • FRIEND Mnemonic (factors preventing spontaneous closure): Foreign body, Radiation, Inflammatory bowel disease (CD) / Infection, Epithelialization of the tract, Neoplasm, Distal obstruction.

Complications

  • Severe Malnutrition: Rapid muscle wasting and cachexia due to large daily protein/caloric loss in bowel effluent.
  • Dehydration & Prerenal Azotemia: Caused by massive high-output fluid losses.
  • Electrolyte and Acid-Base Derangements: Severe hypokalemia, hypomagnesemia, and metabolic acidosis (due to loss of bicarbonate-rich pancreatic/biliary fluids).
  • Sepsis and Intra-abdominal Abscesses: Primary cause of mortality associated with fistulas.
  • Severe Necrotizing Dermatitis: Progressive destruction of abdominal wall skin from proteolytic enzymes in the effluent.

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