Abdominal Tuberculosis
Abdominal Tuberculosis Pathophysiology/Pathology Who Gets Abdominal TB? How do they present? How do we make the diagnosis...
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
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”)
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.