Abdominal tuberculosis is a common extrapulmonary manifestation of tuberculosis that most commonly involves the ileocaecal region of the small intestine. It can present with nonspecific constitutional symptoms like fever, weight loss, or abdominal pain. Diagnosis is challenging as findings can mimic other diseases like Crohn's disease, but imaging modalities like ultrasound, CT scan, and barium studies can reveal features suggestive of abdominal tuberculosis like enlarged lymph nodes, bowel wall thickening, strictures, and ascites. Blood tests are often nonspecific but may show elevated ESR or mild anemia. Sputum tests have low yield for diagnosis but help evaluate for concurrent pulmonary tuberculosis. Tissue sampling is often needed for confirmation.

1. ABDOMINAL TUBERCULOSIS

2. TUBERCULOSIS
 Major health problem
 7-10 million new cases annually
 6% of deaths world wide
 Abdominal tuberculosis is a common extrapulmonary
manifestation of tuberculosis.
 Of non HIV patients 10 – 15 % have extrapulmonary manifestations of
tuberculosis .
 HIV infected patients > 50% have extra pulmonary manifestations of
tuberculosis
There is a resurgence of abdominal tuberculosis due to multidrug resistance and co
existence of HIV – AIDS.

3.  In India, around 3 – 20 % of all cases of bowel obstruction are due
to tuberculosis.
 Tuberculosis accounts for 5 – 9 % of all small intestinal perforations
in India, second commonest cause after typhoid fever.
 Abdominal tuberculosis is an important cause of Malabsorption
syndrome in India.

4. 4
• Epidemiology:
– Both gender: equally affected
– Most common age: 35-45 years
• Riskfactors:
– Alcoholic liver disease
– HIV infection
• 9% of all new TB cases are related to HIV
– Advanced age
– Low socioeconomic status

5. Etiology
Mycobacterium tuberculosis
Pathogen for most cases of abdominal tuberculosis
Mycobacterium bovis
Cause in small percentage of cases, in developing countries.
Transmitted by unpasteurized diary products.
 Mycobacterium Avium complex
more likely in HIV infected patients

6. Agent

8. Mode of infection
Swallowing of
infected sputum
Hematogenous spread
from pulmonary focus
Ingestion of contaminated
milk products
Direct spread from
adjacent organs
Pathogenesis of abdominal TB

9. Potential fates..
The bacilli have 4 potential fates:
1. They may be killed by the immune system,
2. They may multiply and cause primary TB,
3. They may become dormant and remain
asymptomatic, or
4. They may proliferate after a latency period
(reactivation disease).
9

10. Intestinal
49%
Peritoneal
42%
Nodal
4%
Solid visceral
5%
Abdominal tuberculosis
Others
1.3%

11. 1. Intestinal tuberculosis
Ileocaecal
region
Small bowel
& colon

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

13. 1. Intestinal tuberculosis
Ileocaecal region Ileal region
• Ulcerative 60%
• Hypertrophic 10%
• Ulcerohypertrophic 30%
• Stricture type

14. • Most common site of abdominal tuberculosis
due to:
– Stasis
– Abundant payer’s patches
– Alkaline media
– Bacterial contact time is more
– Minimal digestive activity
– Maximum absorption in the area
Ileocaecal Tuberculosis

15. A. Ulcerative type (60%)
– Secondary to pulmonary tuberculosis
– Old malnutritioned people
– Virulent organism
– Poor body resistance
– Multiple circumferential transverse ulcers (Girdle
ulcers) with skip leisons
– Commonly in ileum
– Rarely in caecum
Ileocaecal tuberculosis

16. – Napkin ring strictures in longstanding ulcers
(common in ileum)
– Intestinal nodes involvement with caseation and
abscess
– May present with blood in stools, diarrhoea, loss
of appetite and reduced weight
– Complications:
• Acute: Ulcer perforation
• Chronic: Stricture  Subacute obstruction
Ileocaecal Tuberculosis

17. Ileocaecal Tuberculosis

18. B. Hyperplastic Type -10%
• Primary GIT tuberculosis
• Less virulent organism
• Good body resistance
• Chronic granulomatous lesions in ileoceacal region
• Fibroblastic activity in submucosa and subserosa causes
thickening of bowel wall with lymph node enlargement
• Presenting as Mass in Right Iliac Fossa (Nodular fixed and
firm mass)
• Caseation is very rare
• No primary lesion in the chest
Ileocaecal Tuberculosis

19. B. Hyperplastic Type -10%
Ileocaecal Tuberculosis

20. 20
 30% of patients
 Inflammatory mass with thickened and
ulcerated mucosa
 Commonly in ileocaecal region
 Cone shaped deformity of caecum
 Shortening of ascending colon
 Thickening of ileocaecal valve
C. Ulcerohypertrophic type-30%

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

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

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

24. Clinical Features
• Mainly disease of young adults
• ~ 2/3 of pt. are 21-40 yr old
• Sex incidence equal.
Indian studies  slight female predominance
• Clinical presentation  Acute / Chronic / Acute
on Chronic.

25. • Constitutional symptoms
– fever, night sweats, anorexia, weight loss, failure to
thrive(in children), malaise, anaemia, lethargy,
lassitude
– Observed in 30% patients
• Atypical symptoms
– Lower GI bleed, fistulas, PID like pain, dysphagia
• Pain (80%-95%)
– Colicky (luminal stenosis)
– Continous ( LN involvement)

26. • Diarrhoea (11%-20%)
• Constipation
• Alternating constipation and diarrhoea
• Abdominal mass
– in right iliac fossa (35%)
– Hard, nodular, fixed, nontender mass mimicing ca
caecum
• Subacute intestinal obstruction (20%)
26

27. 1. Ca Caecum
2. Appendicular mass
3. Lymph node mass
4. Psoas abscess
5. Crohn’s disease
Differential Diagnosis

28. Diagnosis: intestinal TB or CD
• They can present exactly with same clinical
pictures (same age group, symptoms and
signs)
• Same radiological findings and same
endoscopic findings
• Mostly with same pathological findings
• So how can we make the diagnosis?

29. Blood tests
• No specific diagnostic blood tests available
• Common blood parameters:
– Elevated ESR
• Almost always raised but not exceed 60 mm/hr
– Mild anemia
• normochromic/ normocytic
– Mild leukocytosis
– Raised CRP
– Hypoproteinemia
– Hypoalbuminemia

30. Tuberculinskin test
A +ve tuberculin skin test has been reported in 55 to
100 % pts. with abdominal tuberculosis. However in
areas where TB is highly endemic , +ve tst neither
confirms the diagnosis of abdominal TB nor excludes
it
30

31. QUANTI-FERON TB TEST
 Whole blood cytokine assay
 Approved by U.S. food and drug administration as an aid
in the diagnosis of latent TB infection
 Recommended for screening for latent TB infection in
population at low risk of TB.
 The test‘s performance will probably be enhanced by
use of antigen such as ESAT-6 and CPF-10 that are
present in M. tuberculosis but absent in others.
31

32. Concomitant PTB
• Concomitant PTB
– Present in 15-25% only
• Sputum smear and culture
for AFB:
– Low diagnostic yield
• Abnormal CXR:
– 19-83%
– Average = 38%

33. 33
– Thickened bowel wall
– Loculated ascites
– Interloop ascites-club sandwitch sign
– Mesenteric thickening hyperechoic >15mm
– Lymph node enlargement
– Pulled up caecum (Pseudokidney sign)
USG abdomen

34. USG abdomen
Ascites Right lower quadrant mass
consisting of matted bowel

35. COMPUTED TOMOGRAPHY
• Abdominal lymphadenopathy -commonest
manifestation
• Enlarged lymph nodes
– mesenteric,
– peri-portal,
– peri-pancreatic, and
– upper para-aortic groups of nodes.

36. CECT
• The CECT have been described as –
peripheral rim enhancement,
non-homogenous enhancement,
homogenous enhancement and
homogenous non-enhancement, in that order of
frequency.
• Different patterns are seen same nodal group,
possibly related to the different stages of the
pathological process.

37. CECT
• Conglomerate mass of
6cm.
• Enlarged nodes with
hypo enhancing areas
are seen.

38. CECT
• presence of nodal calcification in the absence
of a known primary tumour in patients from
endemic areas suggests a tubercular aetiology
.
• CECT imaging criteria differentiating
abdominal lymph node enlargement due to
tuberculosis or lymphoma suggested some
differences in the anatomic distribution and
the CT enhancement patterns

39. CECT
CECT FINDINGS Tuberculosis lymphoma
Lymph nodes lesser omental,
mesenteric, and upper
para-aortic
lower para-aortic lymph
nodes
Lymphadenopathy features peripheral rim
enhancement, frequently
with a multilocular
appearance
homogenous
attenuation.

40. CECT
• Ascites can be free or loculated.
• Characteristically, it is a high density ascites which
could be because of high protein and cellular contents
of the fluid.
• Mesenteric involvement and presence of
macronodules (> 5mm in diameter),
a thin omental line (fibrous wall covering the infiltrated
omentum),
peritoneal or extraperitoneal masses with low density
centres and calcification,
and splenomegaly or splenic calcification have been more
commonly seen with tuberculous peritonitis.

41. CECT
• High density ascitic fluid
• Peritonial and
mesenteric thickening
and enhancement are
seen.

42. CECT
• The diagnosis of tuberculosis is suggestive
when
loculated fluid collections are detected in the
presence of omental infiltration,
peritoneal enhancement,
transperitoneal reaction, and
mesenteric or bowel involvement.
mural thickening affecting the ileocaecal region.

43. CECT
• Multiple small
hypoenhancing focci in
liver parenchyma.

44. Computer tomography scan
Gross ascites

45. 45
Thickened omentum
Computer tomography scan

46. 46
Loculated ascites
Computer tomography scan

47. 47
Thickened ileocaecal bowel
Computer tomography scan

48. 48
Enlarged paraaortic LN
Computer tomography scan

49. 49
• Tubercles in spleen & liver
Computer tomography scan

50. • Barium study Xray (barium enema or barium follow through x-
ray)
– Pulled up caecum, conical caecum, pulled down hepatic
flexure
– Obtuse ileocaecal angle; straightening (Goose neck)
– Steirlin sign: Hurrying of barium due to rapid flow and lack
of barium in inflamed site
– Fleischner sign (Inverted umbrella sign): Narrow ileum
with thickened ileocaecal valve
– Napkin leisons- ulcers and strictures in the terminal ileum
– Increased transient time:Hypersegmentation(chicken
intestine)
– Mega Ileum: Dilatation of proximal ileum

51. Contrast study
Stricture in ileocaecal region Stricture in descending colon
• Good for intestinal tuberculosis affecting small or large bowel

52. Barium enema:
• increased (obtuse)
ileocaecal angle
• retracted, fibrosed
caecum (“goose neck
deformity”) ;

55. • Barium
Study
showing
Mega Ileum

56. Endoscopy
 Colonoscopy is of value to rule out malignancy.
 It is easiest and most direct method in establishing
the diagnosis.
 Shows mucosal nodules or ulcers , deformed ileo
caecal valve, mucosal oedema and pseudopolyps
and occasionally diffuse colitis. Biopsy can be taken
to confirm diagnosis.
 Capsule endoscopy is also useful to see small
intestine pathology in difficult cases .
56

57. 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
57

58. 58

59. 59

60. 60

61. 61

63. Microbiology and histology exam
Definitive diagnosis:
• Ziehl-Neelsen stain for
AFB
• Tissue culture for
mycobacteria
• Caseating granulomas on
histology

64. Tissue Biopsy
• Peritoneal tapping
• Endoscopic biopsy
• Laparoscopy
• Laparotomy
Histological
exam
Microbiological
Smear & culture

65. Molecular Methods
• Polymerase chain reaction (PCR)
– PCR analysis for Mycobacterium tuberculosis
complex in tissues
– Reported as 100% sensitivity in some series

66. Peritoneal tapping
• Ziehl-Neelsen stain: 3% positive
– At least 5000 bacteria/ ml is required
• Culture for AFB: 35% positive
– At least 10 bacteria is required
– 66-83% positive if 1L of ascitic fluid is cultured after centrifugation

67. Diagnostic laproscopy
Direct visualization
Collect acsitic fluid
Take biopsy from mass, omentum or peritoneum
is very useful method of investigation .
 Transabdominal peritoneoscopy is visualization of
the peritoneal cavity using endoscope through
small incision in the abdomen.
 It aids in visualization ,to collect ascitic fluid for
analysis and to biopsy.
Diagnostic laproscopy

68. 68

69. 1. Obstruction 20%
2. Malabsoprption, blind loop syndrome
3. Dissemination of tuberculosis
4. Cold abscess formation
5. Hemorrhage
6. Perforation
7. Fecal fistula
Complications

70. TREATMENT
THERE ARE TWO MODILATIES OF TREATMENT:
1. Medical treatment
2. Surgical treatment
70

71. 71
The cornerstone of antituberculous therapy
is multidrug treatment to decrease the
duration of therapy and diminish the
likelihood that drug-resistant organisms will
develop
Medical treatment

72. 72
Antituberculosis Drugs
Drug/Formulation Adult Dosage (Daily) Main Adverse Effects
First-Line Drugs
Isoniazid (INH)[*] 5 mg/kg (max 300 mg) PO, IM, IV
Hepatic toxicity,
peripheral neuropathy
100, 300 mg tabs
50 mg/5 mL syrup
100 mg/mL injection
Rifampin (Rifadin, Rimactane) 10 mg/kg (max 600 mg) PO, IV Hepatic toxicity,
flulike syndrome,
pruritus
150, 300 mg caps
600 mg injection
powder

73. 73
Pyrazinamide 500 mg tabs 20-25 mg/kg PO Arthralgias, hepatic
toxicity, hyperuricemia,
gastrointestinal upset
Ethambutol[‡] (Myambutol) 100, 400
mg tabs
15-25 mg/kg PO
Decreased red-green color
discrimination, decreased
visual acuity
Drug/formulation Dosage Adverse effect

74. 74
Drug Dosage Adverse effect
streptomycin 15mg/kg IM Vestibular and auditory
toxicity, renal damage

75. 75
Second-Line Drugs
Capreomycin (Capastat) 15 mg/kg IM (max 1 g) Auditory and vestibular
toxicity, renal damage
Kanamycin (Kantrex and others) 15 mg/kg IM, IV (max 1 g) Auditory toxicity, renal
damage
Amikacin (Amikin) 15 mg/kg IM, IV (max 1 g) Auditory toxicity, renal
damage
Cycloserine[¶] (Seromycin and others)
10-15 mg/kg in two doses
(max 500 mg bid) PO
Psychiatric symptoms,
seizures
Ethionamide (Trecator-SC) 15-20 mg/kg in two doses
(max 500 mg bid) PO
Gastrointestinal and
hepatic toxicity,
hypothyroidism
Ciprofloxacin (Cipro and others) 750-1500 mg PO, IV Nausea, abdominal pain,
restlessness, confusion
Ofloxacin (Floxin) 600-800 mg PO, IV Nausea, abdominal pain,
restlessness, confusion
Drug Dosage Adverse effect

76. 76
Levofloxacin (Levaquin) 500-1000 mg PO, IV Nausea, abdominal pain,
restlessness, confusion
Gatifloxacin[¶] (Tequin) 400 mg PO, IV
Nausea, abdominal pain,
restlessness, confusion
Moxifloxacin[¶¶] (Avelox) 400 mg PO, IV
Nausea, abdominal pain,
restlessness, confusion
Aminosalicylic acid (PAS; Paser) 8-12 g in 2-3 doses PO Gastrointestinal
disturbance
Drug Dosage Adverse effect

77. Treatment categories according to
DOTS strategy:
77
Category of
treatment
Type of patient Regimen
Category I
New sputum smear- positive
- sputum smear negative
- extra-pulmonary
2(HRZE)3
4(HR)3
Category II
- Relapse
- Failure
- Defaulters
2(HRZES)3
1(HRZE)3
5(HRE)3

78. • Surgical Management:
– Indications:
• Intestinal obstruction
• Severe hemorrhage
• Acute abdomen (perforation)
• Intra-abdominal abscesses/ fistula formation
• Uncertain diagnosis
Treatment

79. • Surgical Management:
1. Limited 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
stricturiplasty
Treatment

80. • Surgical Management:
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
Treatment

81. • It is usually stricture type
• May be multiple
• Presents with intestinal obstruction
• Bowel adhesions, localization, fibrosis,
secondary infection are common
• Perforation (5%)
• Plain Xray – Multiple air fluid levels
• Resection and anastomosis/stricturoplasty
with Anti-tubercular drugs
Ileal Tuberculosis

82. • Mimics ca rectum
• Occurs within 10 cmof anal verge
• Presents with tenesmus, diarrhoea and multiple
discahrging fistula in ano
• Fistula is painless, not indurated with undermined edges
• Shallow bluish ulcers with undermined edges
• Investigation:
– Sigmoidoscopy
– USG
– Discharge study
– fistulectomy and biopsy
• Treatment: Drugs, fistulectomy or sigmoid resection
Ano-Recto-Sigmoidal Tuberculosis

83. 2. Peritoneal Tuberculosis
Acute form Chronic form
Ascitic
Clear straw-coloured ascitic fluid
Fibrous
Intestines and viscera matted
together causing obstruction
Encysted
Matted intestines enclosing a
loculation of serous fluid
Purulent
Purulent ascitic fluid
Tuberculous peritonitis
• Acute abdomen
• Exploratory laparotomy
 ascitic fluid
 thickened omentum
 scattered tubercles

84. • It is post primary
• Becoming more common
• Activation of long standing latent foci
• Blood spread
• Can develop from diseased mesenteric lymph
nodes, intestines or fallopian tubes
Peritoneal Tuberculosis

85. Pathogenesis
Peritoneal seeding by tuberculosis bacilli
Granulomatous multiple whitish nodules(<5 mm) over
visceral and parietal peritoneum
• >95% of patients develop exudative free/ loculated ascitis
• Small group of patients … dry fibroadhesive (plastic)
Adhesions/ matting of bowel loops
Adenopathy, mesenteric omental thickening
(omental cake)
Purulent peritonitis
Secondary to tuberculous salpingitis
Abscess formation … lymph node, mesentery , omentum
Fistula formation…. Cutaneous/ enteric

86. • Basic pathology
– Enormous thickening of the parietal peritoneum
– Multiple tiny yellowish tubercles
– Dense adhesions in peritoneum and omentum
with small intestines
– May precipitate obstruction
– Thickening of bowel wall
Peritoneal Tuberculosis

87. 87

88. • Abdominal Cocoon Syndrome
– Dense adhesions in peritoneum and omentum
with contents inside as small bowel causing
intestinal obstruction
Peritoneal Tuberculosis

89. 89
Ascitic fluid analysis
-exudate with protein level >3gm/dl
-SAAG <1.1
-lymphocyte predominant cells with cell count as
high as 4000 / mm3
-AFB +ve seen only < 3%
-specific gravity > 1.016
-glucose < 30mg
-LDH > 90 units/lit
-ADA activity>33U/L in ascitic fluid

90. A. Acute type –mimics acute abdomen
– Rare
– On-table diagnosis
– Features of peritonitis
– Due to perforation or rupture of mesenteric lymph nodes
– Exploratory laparotomy reveals straw coloured fluid with
tubercles in the peritoneum, greater omentum and bowel
wall
– Fluid evacuated and sent for culture and AFB study
– Biopsy taken from omentum
– To be closed without drains
– ATD is started
Peritoneal Tuberculosis

91. A. Chronic
– Presents as
• Abdominal pain
• Fever
• Ascites
• Loss of appetite and weight
• Abdominal mass
• Doughy abdomen (10%)
– Types
a) Ascitic form
b) Encysted form
c) Plastic form
d) Purulent form
Peritoneal Tuberculosis

92. a) Ascitic peritoneal tuberculosis:
– Intense exudate caused ascitis
– Common in children and young adults
– Enormous abdominal distension
– May cause congenital hydrdocele, umbilical
hernia, shifting dullness, fluid thrill and mass
per abdomen
– Rolled up omentum and nodular due to
extensive fibrosis
Peritoneal Tuberculosis

93. a) Ascitic peritoneal tuberculosis:
– Asitic tap reveals straw coloured fluid from which
AFB can be isolated (<3%). Fluid is pale yellow,
clear, rich in lymphocytes with high specific
gravity
– Anti-tubercular drugs for one year
– Repeated tapping may be required initially as a
part of treatment
Peritoneal Tuberculosis

94. b) Encysted (Loculated) peritoneal tuberculosis
– Exudation with minimal fibroblastic reaction
– Ascites gets loculated due to fibrinous deposition
– Non shifting Dullness is the typical feature
– May present as intra-abdominal mass mimicing
ovorain cyst, mesenteric cyst
– USG guided aspiration and antitubercular drugs to be
given
Peritoneal Tuberculosis

95. c) Plastic Peritoneal Tuberculosis
– Extensive fibroblastic reaction
– Widespread adhesions
– Between coils of intestine (matted intestines),
abdominal wall, omentum
– Obstruction  Distension of abdomen
– Colicky abdominal pain (recurrent)
– Diarrhoea, loss of weight, mass per abdomen
– Doughy abdomen
Peritoneal Tuberculosis

96. c) Plastic Peritoneal Tuberculosis
– Open or laproscopic biopsy (to rule out
peritoneal carcinomatosis)
– Anti-tubercular drugs
– Surgery to relieve obstruction by adhesolysis
Peritoneal Tuberculosis

97. d) Purulent peritoneal tuberculosis
– Direct spread from tuberculous salpingitis
– Mass per abdomen containing pus, omentum,
fallopian tubes, small and large bowel
– Cold abscess may get adherant to umbilicus
– May cause umbilical discharge
– Genitourinary tuberculosis usually present
– Anti-tubercular drugs with exporation of
umbilical fistula
Peritoneal Tuberculosis

98. 3. Nodal/ Glandular tuberculosis
A. Calcified lesion
B. Acute Mesenteric lymphadenitis
C. Pseudo-mesenteric cyst
D. Tabes mesenterica
E. Chronic Lymphadenitis
• Complications
– Abscess formation

99. 1. Calcified lesion:
– Along the line of the mesentery a single or multiple
calcified lesions
– Payer’s patches involved
– No active infection
– May be on right or left side (R>L)
– Antitubercular drugs
Tuberculous Mesenteric Lymphadenitis

100. 2. Acute mesenteric lymphadenits
– Common in children
– Mimics acute appendicitis
– Tender mass of lymph node palpapble in Right iliac
fossa which are matted and non-mobile
– Intestines adherant to caseating lymph nodes
obstruction
– Surgery for appendicitis or obstruction with lymph
node biopsy
– Antitubercular drugs
Tuberculous Mesenteric Lymphadenitis

101. 3. Pseudo-mesenteric cyst
– Caseating material collected between the layers of mesentery
– Forms cold abscess
– Mimicking a mesenteric cyst
4. Tabes mesenterica
– Massive enlargement of mesenteric lymph nodes due to
tuberculosis
5. Chronic Lyphadenitis
– Children
– Failure to thrive
– Protuberant abdomen and emaciation
– Lymph node on deep palpation in right iliac fossa
Tuberculous Mesenteric Lymphadenitis

102. 4. Solid visceral tuberculosis
Intraabdominal viscera:
 Liver‘
 Spleen
 Pancreas

103. • the portal of entry :hematogenous
dissemination
• miliary tuberculosis :hepatic artery
• focal liver tuberculosis :portal vein.
HEPATIC TB

104. three forms
• diffuse hepatic involvement- most common
• granulomatous hepatitis
• focal/local tuberculoma or abscess- rare

105. • INVESTIGATIONS
– Percutaneous liver biopsy.
– laparoscopy liver biopsy- cheesy white irregular
nodules.
– CT SCAN.

106. CT abdomen
– miliary micronodular with miliary calcifications
– Multiloculated cystic mass(cluster sign)

107. • MILIARY TB
– lesions are small 1 to 2 mm epitheloid
granulomas.
• TUBERCULOMA
Masses larger than 2mm in diameter

108. • It can occur due to disseminated or miliary form of
the 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)
SPLENIC TUBERCULOSIS

109. 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.

110. 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.

111. • 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)
PANCREATIC TB

113. A. Oesophageal (0.2% of abdominal)
B. Gastroduodenal(1%)
C. Retroperitoneal tuberculosis
5. Rare types

114. Esophageal Tuberculosis
• Extension of the disease from mediastinal lymph nodes or from pulmonary focus.
• Rarely without a primary contiguous focus.
• Ulceration, nodularity, stricture, sinus track formation, and fistulae with trachea or bronchus.
• Dysphagia, odynophagia, choking, and aspiration due to tracheoesophageal or
bronchoesophageal fistula and upper GI bleeding. Massive bleed from aortoesophageal fistula
has been reported.
• CXR and CT scan …. Active pulmonary lesions and mediastinal masses.
• Barium swallow …. Ulcerations, strictures, pseudotomor masses, fistulae, sinuses, and traction
diverticula.
• Upper GI Endoscopy with biopsy is the diagnostic procedure of choice.

115. THANK YOU