tuberculous peritonitis

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Tuberculous Peritonitis

Overview

Tuberculous (TB) peritonitis is a form of extrapulmonary tuberculosis involving the peritoneal cavity. It accounts for about 0.5% of new TB cases and is the sixth most common site of extrapulmonary TB. Globally it is more prevalent in resource-poor countries, but incidence is rising in resource-rich countries due to immigration and immunosuppression. The abdomen is involved in approximately 11% of all extrapulmonary TB cases, with the peritoneum affected in 50-80% of abdominal TB cases.

Risk factors: HIV infection, cirrhosis, diabetes mellitus, underlying malignancy, and immunosuppression.

Pathogenesis

TB reaches the peritoneum by several routes:

Direct spread - from ruptured mesenteric lymph nodes (typically draining the ileocaecal region), intraabdominal organs, or fallopian tubes (genital TB in women)
Hematogenous seeding - most often from miliary TB, occasionally from cavitating pulmonary TB
Swallowed sputum - seeding via the gastrointestinal tract

Only one-third of patients with peritoneal TB have clinical or radiographic evidence of pulmonary disease at the time of presentation.

Morphological Forms

There are three recognised patterns:

Form	Frequency	Features
Wet / ascitic	~90%	Generalised or loculated ascites; multiple tubercle deposits on both peritoneal layers
Dry / plastic / fibrotic	Less common	Fibrotic fixed loops of bowel and omentum matted together; no ascites; may cause subacute intestinal obstruction
Mixed	Variable	Combination of fibrosis and loculated fluid

Clinical Features

Presentation is characteristically insidious, with symptoms present for weeks to months before diagnosis:

Abdominal pain and distension
Low-grade fever and night sweats
Weight loss and anorexia
Malaise

Abdominal tenderness is present in fewer than half of patients. Ascites is common in the wet form. An important diagnostic trap: TB peritonitis may present as a pelvic mass with elevated CA-125, closely mimicking metastatic ovarian cancer.

The condition may also present as acute peritonitis that is clinically indistinguishable from acute bacterial peritonitis.

Diagnosis

Ascitic Fluid Analysis

The typical profile of TB ascitic fluid:

Parameter	Finding
Appearance	Straw-coloured exudate
Protein	>25-30 g/L (high)
Serum-to-ascites albumin gradient (SAAG)	<1.1 g/dL (non-portal hypertension)
WBC	>500/mL
Differential	Lymphocytic predominance (>40-70%)
AFB smear	Positive in <3% of cases
AFB culture	Higher yield but takes 4-8 weeks

Key diagnostic tests:

Adenosine deaminase (ADA) in ascitic fluid - elevated in TB peritonitis; high sensitivity and specificity for distinguishing TB from peritoneal carcinomatosis. Caution: false negatives in HIV or cirrhosis; false positives in malignant ascites.
Ascitic fluid PCR (Xpert MTB/RIF) - highly sensitive and specific; rapid result
ELISPOT / interferon-gamma release assay (IGRA) - value in extrapulmonary TB still being established
QuantiFERON-Gold - poor test characteristics for active TB peritonitis, especially in BCG-vaccinated populations

Imaging

Ultrasound / CT scan - detects ascites, mesenteric and retroperitoneal lymphadenopathy, diffuse thickening of peritoneum, mesentery and omentum. CT may show a "wet" peritoneal pattern or matted bowel loops (dry form).

Definitive Diagnosis

Laparoscopy with peritoneal biopsy - nearly 100% sensitive; reveals scattered whitish peritoneal nodules (tubercles); biopsy shows caseating granulomas in >90% of cases. This is the gold standard when non-invasive tests are inconclusive.
Histopathology - caseating granulomas distinguish TB from other causes; also important to differentiate from peritoneal carcinomatosis and fat necrosis of pancreatitis.

Differential Diagnosis

Peritoneal carcinomatosis (malignant ascites): most common cause of lymphocytic ascites - 10x more frequent than TB. Peritoneal cytology is positive in >90% of carcinomatosis cases.
Ovarian cancer (CA-125 elevation overlap)
Crohn disease (intestinal fistulae)
Other infectious peritonitis (fungal, parasitic)
Primary bacterial peritonitis

Treatment

Standard Regimen (6 months total)

Intensive phase (2 months): Isoniazid (H) + Rifampin (R) + Pyrazinamide (Z) + Ethambutol (E) - i.e., HRZE
Continuation phase (4 months): Isoniazid + Rifampin (HR)

This is the same regimen used for pulmonary TB. Multidrug resistance may actually be higher for abdominal than for pulmonary TB, so local susceptibility testing is important. Resistant strains may require a longer course and additional agents.

Special considerations:

Cirrhotic patients - hepatotoxicity of first-line drugs (particularly isoniazid, rifampin, pyrazinamide) may require modification of the regimen
HIV co-infection - antiretroviral therapy (ART) timing must be coordinated with anti-TB therapy
Supportive care: nutrition and hydration are important adjuncts

Role of Surgery

Surgery is generally not required but may be needed for complications:

Intestinal obstruction (many cases resolve with anti-TB therapy alone)
Intestinal fistulae
Perforation

Supervision of therapy is critical - erratic treatment leads to emergence of resistant strains and must be overseen by public health personnel and physicians.

Summary of Key Points

TB peritonitis is often diagnosed late due to non-specific, insidious presentation
The wet (ascitic) form is most common (~90%)
Ascitic fluid is an exudate with lymphocytic predominance and elevated protein
AFB smear is almost never positive (<3%); culture takes weeks
ADA and Xpert MTB/RIF are the most useful rapid non-invasive tests
Laparoscopy + biopsy (showing caseating granulomas) is the gold standard
Treatment is standard 6-month anti-TB therapy (HRZE x 2 months, then HR x 4 months)
The key differential is peritoneal carcinomatosis - cytology resolves most cases

Sources: Sleisenger & Fordtran's Gastrointestinal and Liver Disease; Bailey & Love's Short Practice of Surgery, 28th Ed.; Harrison's Principles of Internal Medicine, 22nd Ed. (2025); Yamada's Textbook of Gastroenterology, 7th Ed.; Frameworks for Internal Medicine

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