Abdominal Tuberculosis

Abdominal Tuberculosis Pathophysiology/Pathology Who Gets Abdominal TB? How do they present? How do we make the diagnosis? What are some of the complications? What are the principles of treatment?

Pathophysiology/ Pathology Intestinal TB Organism • Mycobacterium tuberculosis most common • Mycobacterium bovis rare Routes of infection • Ingestion of sputum: MTB acid resistant • Lymphohaematogenous • Contiguous spread (rare) Areas involved • Most commonly involves distal ileum & caecum • Less commonly: ileum, jejunum, colon, anorectum, proximal small bowel rare. • Tracheoesophageal fistula

Pathophysiology/ Pathology Intestinal TB

Pathological manifestations • Hypertrophic/ ulcerative/ ulcerohypertrophic/ mesenteric thickening/ strictures • Mucosa: transverse, usually superficial, granuloma in base • Vascular involvement: intestinal ischeamia, pseudoaneurysms, haemorrhage, PVT

Peritoneum & Nodal Disease

• Haematogenous spread, reactivation of granuloma, rupture of mesenteric glands, fallopian tubes (rare). • Three types: predominant ascites, fibrotic, encysted • Mesenteric & para-aortic glands: may occur in absence of overt intestinal disease

Who Gets Abdominal TB? Mostly adults (third & fourth decades) Children 10-20% In South Africa > 50% of children 25g/l) Serum-ascites albumin gradient LDH ADA

Cell count Culture (yield 10-30%) Chylous peritonitis Co-existent liver cirrhosis may complicate interpretation

Case Study Ascites  Albumin 14g/l (serum albumin 20g/l)  Total protein 22g/l  Numerous lymphocytes were present  No malignant cells were present  Adenosine deaminase (ADA) 42u/l  Lactate dehydrogenase (LDH) 99u/l  Triglycerides 3.5mmol/l (serum triglycerides 1.1mmol/l)

Case Study Presumptive diagnosis: abdominal tuberculosis  presence of acid-fast bacilli in enlarged cervical lymph nodes  presence of a chyloperitoneum in a patient living in a tuberculosis endemic area  chest radiograph not typical of pulmonary tuberculosis but was consistent with the diagnosis.

How do we make the diagnosis? Do we need histology/culture? Is evidence of tuberculosis in an extra-abdominal source enough? Invasive diagnosis FNA Laparoscopy Laparotomy Endoscopy

Therapeutic trial

What strategy would you use for this patient?

How do we make the diagnosis? Therapeutic trial Where is this appropriate? High prevalence Presentation consistent with abdominal tuberculosis (“typical”)

Caveats “atypical” clinical presentation Monitor response carefully General condition Fever Ascites Abdominal mass Lymphnodes Nutrition

Incorrect diagnosis e.g. portal hypertension, malignancy

What are some of the complications?

What are some of the complications? Intestinal Obstruction Inflammatory Strictures Adhesions

Perforation Fistula formation Malabsorption Ulceration

Lymphatic Intestinal lymphangiectasia

Vascular Portal vein thrombosis Mesenteric artery aneurysms

What are the principles of treatment? Nutritional support Ascites Poor response to diuretics

Anti-Tb drugs 4 drugs intensive phase/ 2 drugs consolidation 6 months

Surgery Diagnostic Obstruction not responding to conservative measures Perforation Fistula Haemorrhage

Case Study Treatment  Dietary support  low fat diet with high medium chain fatty acid content and high protein (TPN if refractory ascites).  Care should be taken to meet the essential fatty acid requirements.  Concomitant nutritional deficiencies of protein, minerals and trace elements corrected.

Antituberculosis treatment  isoniazid, rifampicin, pyrazinamide, and ethambutol.

Case Study Clinical Course During the following three weeks ascites, general well being, appetite and weight-gain improved.

During the following 4 weeks glandular enlargement resolved ascites was no longer clinically detectable.

 The culture of the fine needle aspirate grew M. Tuberculosis.