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Abdominal Tuberculosis

Dr. Irshad Ali Khan PGT GST III PIMS

Epidemiology
Every year:

7-10 million new cases 6 % deaths

Abdominal T.B is the commonest extra

pulmonary manifestation Incidence in west in on rise due to


Immigrants Aging HIV infection

Extra-pulmonary manifestations

Non HIV patients: 10-15 % HIV patients: 50%

Re-emergence of the intestinal variant due to

Incomplete therapy Multi drug resistance Increased incidence of HIV infection

Routes of abdominal Kocks


Direct Ingestion

Infected sputum (M. tuberculosis) Dietary products e.g. unpasturised milk, M. bovis)

Haematogenous spread

Secondry to pulmonary TB

Direct extension from the contiguous organ

e.g through fallopian tubes

Pathogenesis
After ingestion the organism is trapped in the

Peyers patches
It

undergoes inflammatory enlargement Leads to transverse mucosal ulceration Element of endarteritis Ultimately may lead to bowel perforation
Mesenteric lymph node infected Enlarge and caseate Intra abdominal abscess formation

Pathogenesis
Fibrosis may follow leading to napkin ring

strictures Extensive inflammation of submucosa and subserosa at ICJ hyperplastic form Adjacent bowel loops, mesentery, and nodes adhere a mass intestinal cocoon

Pathogenesis
Peritoneal involvement takes the form of the

numerous tubercles on the peritoneum and intestine Omentum thickens to form a rolled-up omentum Ascites is usually present

Pathogenesis
Haematogenous involvement presents as

multiple parenchymal abcesses with organomegaly of the liver, spleen, and pancreas. Contagious spread from the
Spine Genitourinary tract Parietal wall Retro peritoneum

Peritoneal
Wet type: Ascites Generalized Loculated Dry plastic Mesenteric thickening Caseous lymph node Fibrous adhesions

Peritoneal

Fibrotic fixed type


Mass formation of the omentum Matting of the bowel loops

Acute primary peritonitis

Mesenteric Involvement

Mass Abscess Nodal

Solid Organ

Liver, Spleen, Pancreas


Localized abscess Multiple miliary form

Pre and post ATT Therapy