Abdominal Tuberculosis

Causative Organisms and Pathogenesis

• Mycobacterium tuberculosis - responsible for the vast majority of cases
• Mycobacterium bovis - via contaminated dairy products (uncommon in Western countries)
• M. avium intracellulare - increasing with HIV co-infection

1. Swallowing of infected sputum (direct mucosal penetration) - the classic route
2. Ingestion of contaminated milk/food
3. Hematogenous (miliary) spread
4. Direct extension from adjacent organs (e.g., renal TB, fallopian tube TB in women)

Classification

A. Intestinal Tuberculosis

B. Tuberculosis of Mesenteric Lymph Nodes

• Chronic central abdominal pain/discomfort (enlarged nodes palpable to the right of the umbilicus)
• General symptoms: weight loss, anorexia, evening pyrexia
• Intestinal obstruction (loop adherent to caseating node)
• Mimicry of appendicitis (RIF pain, but Rovsing's sign negative, no high WBC/pulse)
• Pseudomesenteric cyst (cold abscess between mesenteric leaves after caseation)
• Calcified lymph nodes on plain X-ray

C. Tuberculous Peritonitis

1. Wet ascitic type (90%) - generalised or loculated exudative ascites; multiple tubercle deposits on both peritoneal layers
2. Dry/plastic type - fibrotic fixed loops with matted bowel and omentum; no ascites; presents with subacute intestinal obstruction
3. Mixed form

Clinical Features

• Chronic non-specific abdominal pain: 80-90% of patients
• Weight loss, fever (evening rise), night sweats
• Diarrhoea or constipation
• Blood in stool (occult bleeding more than frank haematochezia)
• Abdominal distension (ascites)

• Palpable RLQ mass in 25-50% (ileocaecal involvement)
• Perianal fistulae (should prompt evaluation for rectal TB)
• Enlarged, firm, discrete lymph nodes in the umbilical region (in mesenteric node disease)

Note: Chest film is often normal at the time of intestinal TB diagnosis - active concurrent pulmonary disease is now uncommon.

Histopathology

• AFB detected on acid-fast stain in ~20% of mucosal samples
• PCR (Xpert MTB/RIF): ~65% sensitivity, faster than culture

Investigations

Laboratory

• Raised inflammatory markers (ESR, CRP), mild anaemia, normal or mildly elevated WBC
• Mantoux / IGRA (IFN-γ release assay): positive does not confirm active disease; negative does not exclude it (especially in HIV or elderly)
• QuantiFERON-Gold: poor test characteristics for active peritoneal TB, particularly in BCG-vaccinated endemic populations

Ascitic Fluid Analysis (for peritoneal TB)

• Straw-coloured exudate
• Protein >25-30 g/L; low serum-ascites albumin gradient (<1.1 g/dL)
• WBC >500/mL with lymphocytic predominance (>40%)
• Adenosine deaminase (ADA): high sensitivity and specificity (cut-off ~30 U/L); distinguishes tuberculous from carcinomatous ascites
• Smear positivity is low; culture takes 4-8 weeks

Imaging

• Chest X-ray: pulmonary infiltration (may be normal)
• Abdominal ultrasound: loculated ascites, lymphadenopathy
• CT abdomen: thickened ileocaecal valve, asymmetric bowel wall thickening, massive lymphadenopathy with central/hypodense necrosis, peritoneal/omental thickening. Contracted caecum with disease on both sides of the valve.
• Barium meal and follow-through: non-filling of terminal ileum/caecum (due to narrowing and hypermotility); Stierlin sign - conification/narrowing of the caecum and loss of haustrations; subhepatic pull-up of caecum; multiple ileal strictures.

Endoscopy

• Colonoscopy with biopsy is the most useful diagnostic procedure
• Isolation precautions (mask) are required in the endoscopy suite
• Specimens for histopathology, AFB stain/PCR, and culture with drug sensitivities
• Endoscopic appearances: transverse ulcers, patulous (gaping) ileocaecal valve, pseudopolyps, scarring - contrast with Crohn's longitudinal ulcers, cobblestoning, and aphthous ulcers

Laparoscopy

• Near 100% sensitivity for peritoneal TB (lymphocytic ascites with fever = TB until proven otherwise)
• Typical appearance: "millet seed" peritoneal tubercles; peritoneal biopsy confirms caseating granulomas

Differential Diagnosis

Treatment

Medical (First-Line Anti-TB Therapy)

• Phase 1 (Intensive, 2 months): Isoniazid (H) + Rifampicin (R) + Pyrazinamide (Z) + Ethambutol (E) - 4 drugs
• Phase 2 (Continuation, 4 months): Isoniazid + Rifampicin - 2 drugs

• Ethambutol may be stopped once susceptibility to all drugs is confirmed
• Pyridoxine (vitamin B6) supplementation is co-prescribed to prevent isoniazid-induced peripheral neuropathy
• Patients at higher risk of relapse may be treated for up to 9 months
• Global treatment success rate: ~85%
• Hepatotoxicity of first-line drugs is a concern in cirrhotic patients with TB peritonitis
• TB is a reportable disease; public health notification is mandatory

• MDR-TB (resistant to H + R): ~3.4% of new cases
• XDR-TB: MDR + resistance to fluoroquinolones + injectable agents
• Second-line agents: bedaquiline, levofloxacin/moxifloxacin, clofazimine, cycloserine, delamanid, linezolid
• Treatment duration: 9-20 months depending on resistance pattern

Surgical Management

• Subacute intermittent obstruction not resolving on anti-TB drugs:
  • Limited ileocolic resection with anastomosis (terminal ileum to ascending colon) for ileocolic hyperplastic disease
  • Strictureplasty for short single ileal strictures
  • Right hemicolectomy for extensive ileocolic disease

• Vigorous resuscitation first (correct dehydration, anaemia, malnutrition)
• Minimum life-saving procedure: resection of diseased segment + proximal ileostomy + distal mucus fistula (anastomosis avoided due to high leak risk in active infection and poor general condition)
• One-stage resection and anastomosis only if patient general condition permits

Prognosis

• Prognosis depends primarily on immune status and promptness of therapy
• In untreated HIV-infected patients, disease progresses rapidly and is often fatal
• With appropriate early treatment, results are generally satisfactory even in immunocompromised patients
• Clinical response to anti-TB therapy often occurs within 2 weeks, though hypertrophic/mass lesions and strictures respond more slowly
• Intestinal obstruction may resolve with anti-TB treatment alone without surgery

Key Points Summary