1. Abdominal tuberculosis is the third most common form of extrapulmonary tuberculosis, affecting the gastrointestinal tract, peritoneum, and solid organs. 2. It is usually caused by ingesting infected food or milk, or from hematogenous or contiguous spread from active pulmonary lesions. Common symptoms include abdominal pain, weight loss, and fever. 3. Diagnosis involves ascitic fluid analysis, imaging studies, biopsy, and culture of the bacteria. Treatment consists of a multi-drug antibiotic regimen over 6-9 months, with surgery sometimes needed for complications like strictures or perforations.

1. INTRODUCTION
• Most common form of extrapulmonary
tuberculosis (3 to 4%)
• Defined as tuberculosis infection of the
abdomen including gastrointestinal tract,
peritoneum, omentum, mesentery and its
nodes, liver, spleen and pancreas
• Mycobacterium tuberculosis is the most
frequently isolated organism

2. PATHOPYSIOLOGY
• Ingestion of milk or infected food
• Swallowing of sputum in active PTB
• Hematogenous spread from active pulmonary
lesion, miliary tuberculosis
• Contiguous spread from infected foci like
fallopian tubes, mesenteric lymph node
• Very rarely as a consequence of peritoneal
dialysis

3. CLASSIFICATION OF THE ABDOMINAL
TUBERCULOSIS
• Gastrointestinal tuberculosis
Ulcerative
Hypertrophic
Sclerotic or fibrous
Diffuse colitis
Peritoneal tuberculosis
Acute
Chronic
• 1. Ascitic form
• 2. Encysted form
• 3. Fibrous form

4. .
• Tuberculosis of the mesentery and its contents
• Tuberculosis of the solid viscera
Liver
Pancreas
Spleen
• Miscellaneous
Retroperitoneal lymph node tuberculosis

5. GASTROINTESTINAL TB
• Constitutes 70 to80% of abdominal tuberculosis
• Any region of the gastro intestinal tract from mouth to
anus can be involved
• Ileoceacalarea most commonly affected
• It can be of ulcerative, hypertrophic, diffuse colitis,
ulcerohypertrophic, and sclerotic forms
• Entero-enteric, entero-vesicaland entero-
cutaneousfistula can occur
• Luminal narrowing is often caused by adjacent
lymphadenitis which results in traction
diverticulaformation, narrowing and sinus tract
formation

7. GESTRIINTESTINAL TB
• Ulcerative form
• Usually occurs in adult patients whoare malnourished
• Ulcers lie transverse “girdle ulcers”
• Areas of the normal appearing mucosamay be found
• Healing and fibrosis results in stricture
• Hypertrophic form
• Commonly occurs in young patients who are relatively
well nourished
• Characterised by extensive inflammation and fibrosis
which often results in adherence of bowel, mesentery
and lymph nodes

9. GESTROINTESTINAL TB
• Clinical features
• 20 to 40 yrs age group most often affected
• A slight female preponderance
• Most common symptom is abdominl pain others
include abdominal distention, wt.loss anorexia, fever,
diarrhoea or constipation borborygmi, bleeding per
rectum
• Signs include anemia, malnutrition, abdominal
tenderness, ascites, mass in the right iliac fossa features
of intestinal obstruction
• Classic doughy abdomen described only in 6 to 11% in
Indian studies

10. GESTRIINTESTINAL TB
• Oesophageal tuberculosis
• Very rare, upper part is involved more often than lower
part, commonly present with dysphagiaand
odynophagia
• Gastric tuberculosis
• Rare due to the presence of gastric acid
• Ulcerative form is the commonest
• Duodenal tuberculosis (MAC infection)
• Tuberculosis of Appendix
• Anal tuberculosis
• Mostly ulcerative, may be lupoid, verrucus, miliary
lesion
• Multiple fistulae with inguinal lymphadenopathy

11. PERITONEAL TB
• Acute tuberculousperitonitis
• Chronic tuberculousperitonitis
• Ascitic form
• Insidious in onset, abdominal pain usualyabsent, rolled
up omentum infiltrated with tubercle may felt as a
transverse solid mass
• Encysted (loculated) form
• Fibrous form
• Wide spread adhesions may cause coils of intestine
matted together and distended, they may act as blind
loop

12. PANCRATIC TB

14. HEPATOBILIARY TB
• In a patient with PUO, marked elevation of serum
alkaline phosphatase(3 to 6 times) with mild elevation
of s.transaminases, normal PT, s.albuminand a slight
increase in bilirubin hepatic tuberculosis should be
suspected
• Clinical syndromes of Hepatobiliary tuberculosis
• Congenital tuberculosis
• Primary hepatic tuberculosis
• Disseminated/miliary tuberculosis
• Tuberculoma
• Tuberculosis of biliary tract
• Hepatic failure
• Granulomatous hepatitis
• Tuberculous pylephlebitis

16. DIFFRENTIAL DIAGNOSIS
Malabsorption
• Coeliac disease
• Lymphoma
• Immuno proliferative small intestinal diseae
Mass
• Appendicular mass
• Actinomycosis
• Crohn’sdisease
• Caecalcarcinoma
• Lymphoma
Ascites
• Cardiac disease
• Renal disease
• Hepatic diseae
• malignacy

17. INVESTIGATION
• Hematology &serum biochemistry
Anemia, raised ESR, hypoalbumenemia, leucopenia
with relative lymphocytosis, normal serum transminase
level, raised serum ALP
• Ascitic fluid examination
Exudative, fluid protein>3gm%, SAAG<1.1 Ascitic/blood
glucose ratio<0.96, WBC count usually 140 to
4000cells/mm³ consist of lymphocytes predominantly,
AFB(+<3%), culture(+<20%), IFN-γincreased
ADA((98%sensitivity&95%specificity
at cut off value 32 IU/L), PCR
• Mantoux test (positive in 50 to 100%)

19. .
• Culture medium
Lowenstein-Jensen
Middlebrook7H11
Liquid medium
• QuantiFERON-TB test(QFT)
• BACTEC radiometric system
• MycobacterialGrowth indicator tubes
• Animal pathogenicity
• PCR assay
• Ligasechain reaction

21. .
• Imaging studies
• Chest skiagram (associated PTB in 24 to 28%)
• Plain X-ray abdomen
• May show calcified lymph nodes or granulomas in
the liver, spleen, pancreas. Other features include
dilated loops with fluid levels, dilatation of terminal
ileum and ascites . Pneumoperitoneummay be
evident in patients with intestinal perforation

22. .

23. .• Barium studies
• Enteroclysis followed by barium enema is the best protocol
• Increased transit time with hypersegmentation (chicken
intestine) and flocculation is the earliest sign
• Localised areas of irregular thickened folds, mucosal
ulceration, dilated segments and strictures
• Thickened iliocaecal valve with a broad triangular appearance
with the base towards the caecum (inverted umbrella sign or
(Fleischner’ssign)
• Rapid transit and lack of barium retension(Sterlin’ssign)
• Narrow beam of barium due to stenosis(string’s sign)
• Barium oesophagogram-ulcerative oesophagitis, stricture,
pseudo tumourmasses, fistula, sinus, traction diverticulae
• Duodenal tuberculosis-segmental narrowing, widening of the
“C” loop due to lymphadenopathy

24. .

25. BERIUM MEAL FOLLO THROUGH FINDING
IN INTESTINAL TB
• Group1: Highly s/o intestinal TB if one or more of
the following features are present
• a. Deformed ileocaecal valve with dilatation of
terminal ileum
• b. Contracted caecum with an abnormal ileocaecal
valve and/or terminal ileum
• c. Stricture of the ascending colon with shortening
of and involvement of ileocaecal region

27. .
• GroupII:Suggestiveofintestinaltuberculosisifon
eofthefollowingfeaturesispresent
• a.Contractedcaecum
• b.Ulcerationornarrowingoftheterminalileum
• c.Strictureoftheascendingcolon
• d.Multipleareasofdilatation,narrowingandmatt
ingofsmallbowelloops

28. .
• GroupIII:Non-specificchanges
• Featuresofmatting,dilatationandmucosalthick
eningofsmallbowelloops
• GroupIV:Normal study

29. .• Abdominal sonography
• Often reveals a mass made up of matted loops of small
bowel with thickened walls, diseased omentum,
mesentery and loculated asites
• Fine septaemay be seen in the asciticfluid
• Interloopascites gives rise to charecteristic“club
sandwitch” appearance
• Mesenteric thickening is better detected in the
presence of ascites and is often seen as the
“stellatesign” of bowel loops radiating from its root
• In intestinal tuberculosis bowel wall thickening is
usually uniform and concentric as opposed to the
eccentric thickening at the mesenteric border seen in
Crohn’sdisease and the variegated appearance seen in
malignancy
• Granulomas or absessin the liver ,pancreas or spleen

31. .• Abdominal computerised tomography
• CT is better than USG in detecting high dense ascites
• Abdominal lymphadenopathy is the commonest
manifestation of tuberculosis on CT
• Retroperitoneal, peripancreatic, portahepatis, and
mesenteric/omentallymph node enlargement may be evident
• Caseous necrosing lymph node appears as low attenuating,
necrotic centers and thick, enhancing inflammatory rim
• Preferential thickening of the medial caecalwall with an
exophytic mass engulfing the terminal ileum associated with
massive lymphadenopathy is characteristic of tuberculosis
• Short segments of mural thickening with normal intervening
bowel associated with ileocaecal involvement strongly
suggest tuberculosis

32. .

33. .• MRI:-has no added advantage
• Endoscopy
• Fine needle aspiration cytology
• Peritoneal biopsy
• Laparoscopy:-most effective method. 80 to 95%
diagnostic accuracy. Characteristic finding include
multiple, yellowish-white miliary nodules over
peritoneum, erythematous, thickened and
hyperemic peritoneum

34. .

35. .
• Colonoscopy
• › Excellent tool for suspected colonic & terminal
• ileal involvement
• › Mucosal nodules (2-6mm) & ulcers in a
• discrete segment of 4-8 cm, with normal or
• hyperemic intervening mucosa are
• pathognomic
• › Other findings: strictures, deformed ileocaecal
• valve, mucosal oedema, pseudopolyps and
• diffuse colitis
• › Biopsy can be taken to eslablish the diagnosis

37. .• DIFFERENTIAL DIAGNOSIS
• Abdominal TB may mimic any of the following
• conditions:
• 1. Malignant neoplasms: lymphoma, carcinoma
• 2. Inflammatory bowel disease e.g crohn’s
• disease
• 3. Ascites: hepatic/ cardiac/ renal/ malignant
• 4. Ileocaecal mass: appendicular lump, CA
• caecum
• 5. Malabsorption syndromes

38. TREATMENT
• Medical treatment
•
• There are two categories of treatment:
• A) cirrhotic patients with essentialy normal
• baseline LFTs (Child A cirrhosis)
• Treat with standard 4 drug regime for 2 months f/b 2
• drugs regime for 4 months
• Pyrazinamide being most hepatotoxic can be
• avoided and a 9 month 3 drug regime may be used
• B) Cirrhotic patients with altered baseline LFTs
• (Childs B & C)
• One or two hepatotoxic drugs may be used in
• moderately severe disease ( Child B cirrhosis)
• but totally avoided in decompensated cirrhosis

39. .
• Two hepatotoxic drugs:
• 9 months of Isoniazid, Rifampin & Ethambutol
• 2 months of Isoniazid, Rifampin, Ethambutol &
• Streptomycin f/b 6 months of Isoniazid & Rifampin
• One hepatotoxic drug:
• 2 months of Isoniazid, Ethambutol & Streptomycin
f/b 10
• months of Isoniazid& Ethambutol
• No hepatotoxic drug
• 18-24 monthsof Streptomycin, Ethambutol and
Quinolones

40. • Hepatotoxicity
• Regular LFT monitoring recommended in all
• patients on ATT
• In the general population, the criteria for
• stopping anti tubercular treatment is
• • AST / ALT > 3times upper limit of normal
• and symptomatic
• • AST / ALT > 5times upper limit of normal
• even if asymptomatic.
• • Any rise in bilirubin

41. .
• Surgical Management:
• 1. Ileocaecal resection with 5 cm margin
• 2. Stricturoplasty- single stricture
• 3. Single strictutre with friable bowel : Resection
• 4. Multiple Strictures: Resection and
anastomosis
• 5. Multiple strictures with long segment gaps:
• Multiple stricturoplasty

42. .
• 6. Early perforation: resection and anastomosis
• (due to friable bowels)
• 7. Perforation with severe contamination:
resection
• with colostomy
• 8. Adhesiolysis by laproscopy (Very difficult
• procedure)
• 9. Drainage of abscesses and treatment for
fistula
• in ano