Tuberculosis remains a major public health problem in India, with 40% of Indians harbouring the tuberculosis bacilli and over 2 million new cases reported in 2010 according to WHO. Gastrointestinal tuberculosis is not uncommon, with the ileocecal region being the most commonly involved site due to physiological factors that allow bacterial growth. Complications of gastrointestinal tuberculosis include obstruction, perforation, and malabsorption resulting from strictures, hyperplastic lesions, and inflammation.

1. 

4. 
 40% of Indians harbour tb bacilli
 In 2010,
Global Incidence – 9.4million
In india – 2.3million
Prevalence in India is 3.1 million
3,20,000 deaths…
-WHO

5. TB declared as notifiable disease by
INDIAN GOVERNMENT on may9th
2012
http://articles.timesofindia.indiatimes.com/2012-05-
09/india/31640562_1_mdr-tb-tb-cases-tb-diagnosis

6. 

7. Risk Factors
 Case series involving 60 patients
 38% Cirrhosis

 33% Renal Failure with Peritoneal Dialysis
 27% Diabetes Mellitus
 18% Underlying Malignancy
 10% Systemic Corticosteroids
 2% AIDS
 12% No Risk Factors
http://www.med.unc.edu

8. 

9. 

10. 24th march 1882
World TB DAY

11. PATHOGENESIS

12. STAGE 1
ESTABLISHMENT

ALVEOLAR MACROPHAGE
INGESTS TB BACILLI

13.  M. tuberculosis blocks phagolysosome formation by
inhbiting Ca2+ signals and the recruitment and
assembly of the proteins that mediate phagosome-
lysosome fusion
Fratti RA, et al. J cell Biol 2001

14. 
 Racial differences in macrophages microbicidal
enzymes. Africans have macrophages less capable of
destroying tb bacilli.
 Mutations in NRAMP-1 gene involved in pushing
out Fe2+ ions from the phagolysosome.
Cellier MF, et al. Microbes Infect 2007;
9:1662.

15. STAGE 2 SYMBIOSIS

Tubercle bacilli ingested
By non activated newly recruited
Monocytes.

16. STAGE 2 SYMBIOSIS

 Incapable alveolar macrophage bursts.
 New monocytes from blood are recruited to the site
mainly by c5a, Monocyte Chemoattractant protein-
1(MCP-1)
 TB bacilli multiplies in these non activated
monocytes.
 7-21 days (<3weeks) – primary TB.
 Comes to an end when Th1 cells enters the site

17. Secrete IFN γ Activates
Macrophages
T-
CELL
Kills the inactivated
macrophages which were
allowing the tb bacilli growth
inside them…

18. CMI or DTH???
Main difference is concentration of
antigen required….

19. STAGE 3 EARLY STAGES
OF CASEOUS NECROSIS

Non activated
Macrophages which
allowed the growth of
TB bacilli are killed by
DTH mediated by T-cells
Forming solid caseous
necrosis

20. up-regulation of ICAM-1, ELAM-1, VCAM-1, and
other adhesion molecules
Activated endothelial cells presents tuberculin like
antigen to macrophage
Leading to endothelial injury and its consequences
J Leukoc Biol. 1996;60:692–703.

21. DTH AND CMI

• T-CELLS
DTH
• DESTROYS INACTIVATED
MACROPHAGES IN WHICH BACILLI
MULTIPLIES
• INITIALLY BENEFICIAL
• MACROPHAGES and T-CELLS
CMI
• BACILLI MULTIPLYING INSIDE
ACTIVATED MACROPHAGES ARE
DESTROYED
• BENEFICIAL TO THE HOST

22. STAGE 3 EARLY STAGES
OF CASEOUS NECROSIS

TB bacilli remains live
but cannot multiply in
solid caseous material.
TB bacilli escaping from
the edges of caseous
necrosis are engulfed by
macrophages and
caseous centre enlarges.

23. STAGE 4 INTERPLAY OF
CMI AND DTH

ACTIVATED MACROPHAGES
WALLS OFF THE EXPANDING
CAVITY AND PREVENTS
FURTHER INCREASE IN
SIZE IN HOST WITH GOOD
CMI.

24. POOR CMI

IN HOST WITH POOR CMI
DTH CONTINUES DESTROYS THE
BACILLI
AND LUNG TISSUE TOO.
TB BACILL SPREADS THROUGH
LYMPHATIC AND
HEMATOGENOUS ROUTE TO
OTHER ORGANS.

26. STAGE 5 LIQUEFACTION
AND CAVITY
FORMATION

the large quantities of bacilli and their antigens in the liquefied
caseum overwhelm a formerly effective CMI, causing progression of
the disease and the destruction of local tissues, including the wall of
an adjacent bronchus.

27. 
 when the caseum liquefies, the entering
macrophages do not function effectively.
 Possibly, the entering macrophages are killed by
toxic fatty acids originating from host cells, or the
bacilli, or both.
 CAUSE OF LIQUEFACTION???
REF: Hemsworth GR, Kochan I. Secretion of antimycobacterial fatty acids by
normal and activated macrophages. Infect Immun. 1978;19:170–177.

28. 

29. GENERAL INVESTIGATIONS

. Types of specimens:
1.Pulmonary specimens
-Sputum
-Gastric lavage
-Transtracheal aspirations
-Bronchoscopy
-Laryngeal swabbing
2.Urine specimens
3.Tissue and body fluid specimens
4.Blood specimens
5.Wounds, skin lesions, and aspirates

30. Microscopy
 Sputum smears stained by
Z-N stain 
 What is Smear Positivity
 All patients who have
submitted two
Specimens and found to
be positive for
identification of AFB
 Detecting AFB by
fluorochrome stain using
fluorescence microscopy

31.  Culturing for isolation of
Mycobacterium spp
continues to be a Gold
standard
 Agar based 4-6weeks
 egg based
 BACTEC – 14.8days
 MGIT- 13.3days

32. NEWER METHODS

 PCR SENSITIVITY-92% SPECIFICITY-99%
 INTERFERON –γ release assays.
QuantiFERON- TB SPOT
TB
SENSITIVITY-81% SENSITIVITY-87.5%
SPECIFICITY-91.2% SPECIFICITY-86.3%

33. GASTROINTESTINAL
TUBERCULOSIS

34. 
 Epidemiology
 Pathogenesis
 Clinical features
 Diagnosis

35. Epidemiology

 Upto 1% of hospital admissions
 More common in immuno-suppressed
 Isolated abdominal tuberculosis:
 Unselected autopsy series- 0.02 - 5.1%
 Higher prevalence in females in India (3:1–4:1)
 Mainly disease of young adults
 ~ 2/3 of pt. are 21-40 yr old

36. TB & HIV

 Incidence severity of
abdominal TB will increase with
the HIV epidemic
 HIV – 50 % develop abdominal TB

37. Pathogenesis

 Mechanisms by which M. tuberculosis reach the GIT:
 Hematogenous spread from primary lung focus
 Ingestion of bacilli in sputum from active
pulmonary focus.
 Direct spread from adjacent organs.
 Via lymph channels from infected LN
 In India, organism from all intestinal lesions – M.
tuberculosis and not M. bovis.

38. Types

 Ulcerative
 Hyperplastic
 Ulcerohyperplastic
 Diffuse colitis
 Sclerotic

39. PATHOLOGY
Most active inflammation in submucosa.
Bacilli in depth of mucosal glands
Inflammatory reaction
Phagocytes carry bacilli to Peyers Patches
Formation of tubercle
Tubercles undergo necrosis

40. PATHOLOGY

Submucosal tubercles enlarge
Endarteritis & edema
Sloughing
Ulcer formation
Accumulation of collagenous tissue
Thickening & Stenosis

41. PATHOLOGY

Inflammatory process in submucosa penetrates to serosa
Tubercles on serosal surface
Bacilli reach lymphatics
Bacilli via lymphatics
Lymphatic obstruction Regional lymph nodes
of mesentery and bowel • Hyperplasia
Thick fixed mass • Caseation necrosis
• Calcification

42. Order of Frequency

Ileum > caecum > ascending colon > jejunum
>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
 More than one site may be involved

43. 
 Bhansali - ileum involved in 102 and caecum in 100 of 196
pt.
 Prakash - ileocaecal involvement in 162 of 300 pt.
 Most common site - ILEOCAECAL REGION
WHY?

44. 
 Increased physiological stasis
 Increased rate of fluid and electrolyte absorption
 Minimal digestive activity
 Abundance of lymphoid tissue at this site.

45. Clinical features
 Constitutional symptoms

 Fever (40%-70%)
 Weight loss (40%-90%)
 Anorexia
 Malaise
 Pain (80%-95%)
 Colicky (luminal stenosis)
 Continous ( LN involvement)
 Altered bowel habits

46. Ileocecal TB

 Colicky abdominal pain
 Ball rolling in abdomen
 Borborygmi
 Right iliac fossa lump - ileocaecal region, mesenteric fat
and LN

47. Isolated Colonic TB

 9.2% of all cases
 Multifocal involvement in ~ 1/3 (28% to 44%)

48. Anorectal TB

 Hematochezia - most common symp. Due to mucosal
trauma by stool
 Constitutional symptoms
 Constipation
 Rectal stricture
 Anal fistula – usually multiple

49. Gastroduodenal TB
 of total cases
 Stomach and duodenum each ~ 1%
 Mimics PUD - shorter history, non response to t/t
 Mimics gastric Ca.
 Duodenal obstruction - extrinsic compression by tuberculous
LN
 Hematemesis / Perforation / Fistulae / Obstructive jaundice
 Cx-Ray usually normal
 Endoscopic picture - non specific

50. Esophageal TB

 Rare ~ 0.2% of total cases
 By extension from adjacent LN
 Low grade fever / Dysphagia / Odynophagia /
Midesophageal ulcer
 Mimics esophageal Ca

51. Complications

 OBSTRUCTION
 PERFORATION
 MALABSORPTION

52. Obstruction

 Pathogenesis
 Hyperplastic caecal TB
 Strictures (napkin ring) of the small intestine
 Adhesions
 Adjacent LN involvement traction, narrowing
and fixation of bowel loops.
 In India ~ 3% to 20% of bowel obstruction
(Bhansali and Sethna).

53. Malabsorption

2nd most common cause in India
 Pathogenesis
 bacterial overgrowth in stagnant loop
 bile salt deconjugation
 diminished absorptive surface due to ulceration
 involvement of lymphatics and LN
75% pt with intestinal obstruction
40% of those without (Tandon et al)

54. Perforation

 5%-9% of SI perforations in India
 2nd commonest cause after typhoid
 Usually single and proximal to a stricture
 Clue - Chest x-ray,
 Pneumoperitoneum in ~ 50% cases

55. 
Investigations

56. 

57. 

58. Intestinal TB cont.
 CT scan shows thickening

of the cecum with pericecal
inflammatory changes.
Mesenteric lymph nodes are
also evident (arrows).

59. Endoscopy
 Nodules

 Variable sizes (2 to 6mm)
 Non friable
 Most common in caecum especially near IC valve.
 Tubercular ulcers
 Large (10 to 20mm) or small (3 to 5mm)
 Located between the nodules
 Single or multiple
 Transversely oriented / circumferential contrast to
Crohns
 Healing of these ‘girdle ulcers’ strictures
 Deformed and edematous ileocaecal valve

60. 
Esophageal TB Nodules
TB mass in stomach T.B. ulceration with narrow lumen

61. 
Is endoscopy diagnostic?

62. 
 8 –10 Bx from ulcer edge
 low yield on histopath as mainly submucosal disease
 Granulomas in 8%-48%
 Caseation in ~ 1/3 (33%-38%) of + cases
 AFB stains - variable
 Culture positivity in 40%
 Combination of histology & culture diagnosis in 80% (
S K Sharma)

63. Take home message

 Ileocecal TB is the most common intestinal TB
 Combination of histology & culture is necessary for diagnosis.
 Surgery is the only answer

64. AN OVERLOOKED DIAGNOSIS

65. DIAGNOSTIC
CHALLENGES

Non specific presentation
Insidious presentation
Mimicks malignancy
Unhelpful labaratory tests

66. EPIDEMOLOGY
PATHOGENESIS
CLINICAL FEATURES
DIAGNOSIS
TREATMENT

67. EPIDEMOLOGY

6th most common extra pulmonary site
Incidence- 0.1% to 0.7% worldwide
Rising incidence
sexes are equally affected
35 and 45 years of age.

68. PATHOGENESIS

Activation of quiscent foci of infection(common)
Direct spread –mesentric Lymph nodes
–Intraabdominal organs
•Hematogenous spread from
–Primary pulmonary TB
–Miliary TB

69. 
CLINICAL PICTURE

70. CLINICAL
PRESENTATION

wet-ascitic dry-plastic form(less
fibrotic-fixed Encysted(loculated)
(most common) common)
• ascites •Mass formation • adhesions • localized
• ±peritonitis •Matting of bowel • „doughy feel‟ abdominal swelling
loops • tender abdominal
masses.

71. CLINICAL FEATURES

Case series involving 145 patients
 73% Abdominal swelling (ascites) – most common
 64% Abdominal pain
 54% Fever and night sweats
 44% Weight loss
 18% both pulmonary & abdominal TB
 Hepatomegaly and splenomegaly - uncommon

72. INVESTIGATIONS

 Haematological indices.
 Microbiological diagnosis.
 Ascitic fluid analysis.
 New diagnostic tools-Adenosine deaminase, Gene
amplification. Immunodiagnostic tests.
Imaging studies
 CXR- concomitant TB in less than 25% cases
 Barium studies .
 ultrasound and computed tomography.

73. Ascitic fluid analysis

 •Gross Appearance:
Straw coloured .
 EXUDATIVE
 WBC cell count- 500 and 1500 cells/mm3 – lymphocytosis.
 LDH raised-> 90 U/L
 Protein > 3g /dl.
 SAAG <1.1mg/dl
 RBC 7%.
 AFB stain +ve < 3 per cent of cases.
 positive culture is obtained in less than 20 per cent of cases

74. New diagnostic tools
 Adenosine deaminase.

 rapid and non-invasive
 Purine-degrading enzyme
 Assists with maturation and differentiation of T-
lymphoid cells.
 Raised- stimulation of T cells by the mycobacterial
antigens.

75. Adenosine deaminase
 •Cut-off value of 30 U/L
 94% Sensitive
 92% Specific.

FALSE VALUES-
 •In coinfection with HIV - normal or low.
 Falsely high values in malignant ascites.

76.  Gene amplification.- LCR & PCR in detecting AFB in
tissues.
 serological tests-

- ELISA to detect IgG to a 43 kDa antigen of M.
tuberculosis found it to be highly sensitive.
- High IFN-γ levels - detecting latent TB.
Elevated CA-125
-Not sensitive
Also raised in peritoneal
carcinomatosis, ovarian malignancy.
Can use to follow treatment response

77. Imaging studies

in obtaining peritoneal biopsies
safer and inexpensive alternative to
diagnostic laparoscopy.
high diagnostic yield approaching
95%

78.  Ultrasound-
superior to CT in revealing the multiple, fine, mobile

septations within the ascitic fluid
1. fluid -free or loculated;(echogenic debris)
2. “Club sandwich” or “sliced bread” sign.
3. Lymphadenopathy- caseation and
calcification.
4. Bowel wall thickening .
5. Pseudokidney sign

79. COMPUTED TOMOGRAPHY-
 ascitic fluid has high attenuation values .
 •Peritoneum(white arrow)
 –Smooth and uniform thickening
 –If nodular, think Peritoneal
Carcinomatosis.
 •Omentum(open arrow)
 –Smudged, omental cake or
nodular..
 •Mesentery
 –Loss of normal mesenteric
configuration
 -Thickened mesentery (>15 mm)
with mesenteric lymph nodes- early
sign
 •Lymphadenopathy.(black arrow)

80. 
DIAGNOSTIC TOOL
OF CHOICE?

81. DIAGNOSTIC
LAPROSCOPY


82. DIAGNOSTIC YEILD
on the
specificity in excess of 96%
laparoscopic appearance alone.
With histological findings-sensitivity- 93%
specificity- 98%
Peritoneal biopsies should always be examined
whenever possible for culture and sensitivity. - gold
standard

83. LAP FINDINGS

Thickened peritoneum with tubercles
(66%)
thickened and peritoneum with
adhesions (21%);
fibro-adhesive type – with tubercles
and adhesions 13%.

84. PIT FALLS

 Peritoneal carcinomatosis, sarcoidosis, starch
peritonitis and Crohn's disease - MIMICK LAP
FINDINGS.
 More expensive.
 Requires expertise.
 poor isolation of organism
 complications -bleeding, infection and bowel
perforation

85. 
ROLE OF
LAPAROTOMY?

86. 
 unnecessary
 with fibro-adhesive type of TBP when there is an
indication for a peritoneal biopsy.

87. 
ideal diagnostic test
requires the
demonstration of
mycobacteria

88. BUT…

 characteristic laparoscopic appearance itself, even
in the absence of bacteriological confirmation, would
be sufficient grounds for the diagnosis of TBP.
 HIGH SPECIFICITY OF MACROSCOPIC
APPEARANCE

89. 
TREATMENT

90. 
MEDICAL vs SURGICAL

91. UNCOMPLICATED
 solely pharmacological.

 Four drug regimen:
–Isoniazid
–Rifampin
–Ethambutol
–Pyrazinamide.
 CAT I ATT
 Response to therapy is manifested by resolution of
symptoms and disappearance of ascites

92. 
 Surgery is reserved for complications or uncertainty
in diagnosis.
 MDR-TB not responsive to ATT.

93. DREADED
COMPLICATION

ABDOMINAL COCOON SYNDROME-
 rare entity causing intestinal obstruction.
 Diagnosis done by imaging studies.
 Extensive bowel resection is associated with high morbidity.
 Symptomatic relief generally ensues following conservative
surgery, although recurrence has been reported.

94. 

95. 

96. 

97. 
ROLE OF
CORTICOSTEROIDS?

98. 
 four trials of adjuvant corticosteroids use in TBP and all
of them cited modest benefit.
 Alrajhi et al.85 reported considerably low morbidity and
complications in those treated with corticosteroids.
 pending need for prospective, well-controlled clinical
trials with long-term follow-ups to identify the category
of patients most likely to benefit from such therapy

99. Tuberculous peritonitis--
do not miss it

 requires a high index of suspicion because of the
subtle nature of the symptoms and signs.
 culture growth of the Mycobacterium remains the
„gold standard‟ for diagnosis.
 It is essential to recognize that a combination of
different diagnostic tests is used in order to arrive at
the diagnosis of TBP

100. 
Laparoscopy, however,
remains the best means
of diagnosing the
disease

101. 
SOLID ORGAN
TUBERCULOSIS

102. HEPATIC TB

 the portal of entry :hematogenous dissemination
 miliary tuberculosis :hepatic artery
 focal liver tuberculosis :portal vein.

103. 
three forms
 diffuse hepatic involvement- most common
 granulomatous hepatitis
 focal/local tuberculoma or abscess- rare

104. 
 INVESTIGATIONS
 Percutaneous liver biopsy.
 laparoscopy liver biopsy- cheesy white irregular
nodules.
 CT SCAN.

105. CT abdomen 
 miliary micronodular with miliary calcifications
 Multiloculated cystic mass(cluster sign)

106. 
 MILIARY TB
 lesions are small 1 to 2 mm epitheloid granulomas.
 TUBERCULOMA
Masses larger than 2mm in diameter

107. SPLENIC
TUBERCULOSIS
•
 or miliary form of the
It can occur due to disseminated
disease
• Most commonly encountered in HIV pt(developed
countries)
• Fever, weight loss, diarrhea, left upper abdominal
pain, splenomegaly
• Investigations
• Image-guided percutaneous needle biopsy is the gold
standard for diagnosis.
CECT-abdomen-multiple hypo echoic foci(<2cm)

108. Gross pathology of resected spleen showing innumerable caseating granulomas consistent
with splenic tuberculosis.
Mackowiak P A et al. Clin Infect Dis. 2011;52:418-420
The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases
Society of America. All rights reserved. For Permissions, please e-mail:
journals.permissions@oup.com.

109. Computed tomograph scan of the abdomen showing a spleen diffusely infiltrated by
small, hypodense lesions consistent with splenic granulomas.
Mackowiak P A et al. Clin Infect Dis. 2011;52:418-420
The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases
Society of America. All rights reserved. For Permissions, please e-mail:
journals.permissions@oup.com.

110. PANCREATIC TB

 It is rare
 Often associated with miliary TB &
immunocompromised pt
 Result from lymphohaematogenous dissemimation
after pulmonary exposure
 Anorexia,malaise fever,weight loss,mass
 Investication: FNAC & BIOPSY (CT guided)

111. 
 CT enhanced conrast-

112. RENAL TB

 Microscopic pyuria without bacteruria and with or
without hematuria.
 Progression of the disease  urine culture may be
+ve for tubercle bacilli.
 Cavitation of renal parenchyma may be seen.
 Standard anti TB therapy

114. Ovarian TB

 Fallopian tubes are affected in 94% of women with
genital tuberculosis.
 Salpingitis caused by hematogenous dissemination
is almost always bilateral .
 A tubo-ovarian abscess that extends through the
peritoneum into the extraperitoneal compartment
suggests tuberculosis

115. Ovarian TB
 Tuberculous tubo-ovarian
abscess
 (a) Contrast-enhanced CT
scan shows a
multiloculated mass with
peripheral enhancement
around centers .(arrow).
 (b) Coronal T2-weighted
MR image (7,200/90) shows
the abscess (arrows).

117. 
 A 24 yr old female comes with pain RIF, MANTRELS
7/10 diagnosed as acute appendicitis.
 On opening an inflammed appendix is found but
studded with tubercles, omentum and caecum show
multiple tubercles
Do we do appendicectomy ?

118. 
 Patient comes with features of perforation peritonitis
 On opening TB peritonitis with ileac perforation
with a stricture of about 3 cm 2 feet distal to
perforation
Primary closure?
Stricturoplasty?
Resection?

119. 
 A 60 yr old male, known case of pulmonary TB
presenting with acute intestinal obstruction
 On opening ileocecal mass with peritonium and
omentum showing features of TB
Rt hemicolectomy?
Limited resection?
Bypass?

120. 
 Patent known case of pulmonary TB , presenting
with ascites and subacute obstruction.
 On diagnostic Lap we find Milliary TB with multiple
adhesions
Do we do adhesiolysis?

121. Appendicectomy

 Removing the appendix is a safe procedure even if
microscopic evidence of tuberculosis is present
 Delay in treatment can cause significant morbidity
•Singapore Med J 2011; 52(2) : 91
•Abrams & Holden, 1964

122. Stricturoplasty/
Resection

 Both procedures were equally effective and had
equal morbidity in cases of intestinal tuberculous
strictures.
Zafar A et al ,Rawalpindi General Hospital, Rawalpindi
 Stricturoplasty is superior to resection anastomosis
in cases of multiple strictures as it conserves gut
length
 Stricturoplasty can even be performed safely in cases
with coexistent gut perforation.
J Coll Physicians Surg Pak 2003 May;13(5):277-9

123. Stricturoplasty

 Stricturoplasty is a simple, quick, and safe operative
technique to manage tuberculous small intestinal
strictures, in combination with limited resection or as
a sole procedure
Abrar Hussain Zaid et al
 Stricturoplasty is suggested in pyloroduodenal and
ileocaecal lesions
Katariya et al

124. Perforation primary closure?

 The results of oversewing alone are poor
 Bhansali et al.,1968
 Resection anastomosis is the best method in
treating perforations
 N.O. Aston and A.M. de Costa, Postgraduate Medical
Journal (1985) 61, 251-252
 In critically ill is oval excision of the perforated
area with a transverse anastomosis reinforced by an
omental patch
 Pujari, 1979

125. 
Resection Anastomosis
Is it safe?

126. 
Annals of Surgery November 1964

127. 
 Two-stage procedures
 Reversal of stoma in a well-prepared gut with ATT
cover
Muhammad Saaiq et al

128. 
 Turkish Journal of Trauma & Emergency Surgery vol
17 2011
 Rankie et al
 Recio et al
 Piechaud et al
 Asian J Surg 2002:25(2):145-8

129. 
 Resection is a safe and effective procedure in treating
abdominal TB complications.

130. 
 Resection of a tuberculous lesion where feasible is
the procedure of choice

131. How much to resect?

 With effective ATT limited and conservative
resections give good results
•Journal of the College of Physicians and Surgeons Pakistan 2008, Vol. 18 (7): 393-396
•P Agarwal et al , BHJ 2000

132. Fistulas

 Low output fistulas without distal obstruction
ATT wait and watch
 High output fistulas
 Fistulas with distal obstruction
 Fistulas not responding to conservative management
Surgery
Saudi J Gastroenterol. 2010 October; 16(4): 305.

133. Adhesiolysis / ATT

 Adhesive intestinal lesions may be relieved with
antitubercular drugs alone without surgery.
 Anand et al
 Balasubramaniam et al

134. To summarise

 Tuberculous peritonitis once diagnosed is usually
not a surgical disease.
 Resection of diseased segment is the best method
 Stricturoplasty and Resection anastomosis are safe
procedures
 Limited resection is advised with ATT cover
 Chemotherapy has no substitute and is essential
after surgery.

135. 
Thank You