1. Abdominal tuberculosis is a common extrapulmonary manifestation of tuberculosis that can involve the intestines, peritoneum, and lymph nodes. 2. Diagnosis is challenging as symptoms can mimic other diseases like Crohn's disease. Imaging findings on ultrasound and CT scan include lymphadenopathy, bowel thickening, ascites, and peritoneal involvement. 3. While blood tests are nonspecific, presence of ascites, omental thickening, and mesenteric adenopathy on CT scan are suggestive of abdominal tuberculosis.

1. ABDOMINAL TUBERCULOSIS

2. TUBERCULOSIS
Major health problem R .
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
'A
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. • Epidemiology:
- Both gender: equally affected
- Most common age: 35-45 years
• Riskfictors:
— Alcoholic liver disease
- HIV infection
• 9% of all new TB cases are related to HIV
— Advanced age
— Low socioeconomic status
4

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

6. Agent
■ Slightly curved,
rod shaped bacilli
■ 0.2 - 0.5 microns
in diameter; 2-4
microns in length
■ Acid fast - resists
decolorization with
acid/alcohol
■ Multiplies slowly
(every 1 8 - 2 4 hrs)
■ Thick lipid cell wall
■ Can remain
dormant for decades
■ Aerobic
■ Non-motile

7. Extra-pulmonary Tuberculosis
100
80
8
60
v
CL
40
20
0
------ ------------ - - - - -----------—>
Extra-Pulmonary
17.5%
v
v
Pulmonary
82.5%
S
Peritoneal 3.3 %
Meningeal 4.6 %
Miliary 7.3%
Other 9.8%
Bone/Joint 9.8 %
Genitourinary 119%
Pleural23 %
Adapted from
Mandell, et al.
Lymphatic 30 %
All Cases All Extra-pulmonary Cases

8. PathogenesisofabdominalTB
Ingestion of contaminated
milk products
Hematogenous spread
from pulmonary focus
Direct spread from
adjacent organs
Swallowing of
infected sputum

9. Potentialfates..
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. ‘Vbdomtnaituberculo
Nodal Solid v
4% 5
Others
1.3%

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

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
1
• Ulcerative 60%
• Hypertrophic 10%
• Ulcerohypertrophic 30%
Ileal region
I
• Stricture type

14. lleocaecal Tuberculosis
• 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

15. lleocaecal tuberculosis
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

16. IteocaecalTuberculosis
— 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

17. lleocaecalTuberculosis

18. lleocaecalTuberculosis
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

19. Ileocaecal Tuberculosis
B. Hyperplastic Type -10%

20. C. Ulcerohypertrophic type-30%
□ 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
20

21. PATHOLOGY
Most active inflammation in submucosa.

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

23. PATHOLOGY
Inflammatory process in submucosa penetrates to serosa
J Tubercles on serosal surface
i Bacilli reach lymphatics
I Bacilli via lymphatics I
Lym
of m
^ Tl
phatic obstruction
iesentery and bowel hick
fixed mass
Regional lymph nodes
• Hyperplasia
• Caseation necrosis
• Calcification

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

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. Tuberculinskintest
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

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

34. USGab
Ascites

35. domen
Right lower quadrant mass
consisting of matted bowel

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

37. 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.

38. CECT
• Conglomerate mass of
6cm.
• Enlarged nodes with
hypo enhancing areas are
seen.
Fig. 1: Contrast enhanced abdominal CT of a 21 year-old female patient demonstrates
multiple mesenteric lymphadenopathy forming a conglomerate mass (arrows) with 6 cm
in major axis. Most enlarged nodes have central hypoenhancing areas due to necrosis.

39. CECT
• presence of nodal calcification in the absence
of a known primary tumour in patients from
endemic areas suggests a tubercular aetiology
m
• 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

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

41. 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.

42. CECT
High density ascitic fluid
Peritonial and mesenteric
thickening and
enhancement are seen.
Fig. 11: Contrast enhanced abdominal CT of a 19 year-old female patient demonstrates
large volume of high density ascitic fluid (*). It is also visible pronounced peritoneal and
mesenteric thickening and enhancement (arrows).

43. 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.

44. CECT
Multiple small
hypoenhancing focci in
liver parenchyma.

45. Computertomographyscan
Gross ascites

46. Computertomographyscan
Thickened omentum
45

47. Computertomographyscan
Loculated ascites
46

48. Thickened ileocaecal bowel
47

49. Computertomographyscan
Enlarged paraaortic LN
48

50. Computertomographyscan
• Tubercles in spleen & liver
49

51. • 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

52. Contraststudy
Good for intestinal tuberculosis affecting small or large bowel
Stricture in ileocaecal region Stricture in descending colon

53. Barium enema:
• increased (obtuse)
ileocaecal angle
• retracted, fibrosed
caecum ("goose neck
deformity") ;

55. Ileocecal tuberculosis. Radiograph
obtained with peroral pneumocolon
technique demonstrates a conical and
shrunken cecum (straight arrow)
retracted out of the iliac fossa by
contraction of the mesocolon. Note also
the narrowing of the terminal ileum
(curved arrow).

57. • Barium
Study
showing
Mega Ileum

58. 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

59. □ 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

63. 61

66. Definitive diagnosis:
• Ziehl-Neelsen stain for
AFB
• Tissue culture for
mycobacteria
• Caseating granulomas
on histology

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

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

69. 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

70. Diagnostic laproscopy
□ 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.

71. 68

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

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

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

75. Antituberculosis Drugs
Drug/Form ulation Adult Dosage (Daily) Main Adverse Effects
First-Line Drugs
Hepatic toxicity,
Isoniazid (INH)[*] 5
mg/kg (max 300 mg)
PO, IM, IV 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
72

76. 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
73

78. Adverse effect
Vestibular and auditory
toxicity, renal damage
74

79. Second-Line Drugs
Drug Dosage Adverse effect
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
10-15 mg/kg in two doses Psychiatric symptoms,
Cycloserine™ (Seromycin and others) (max 500 mg bid) PO seizures
Ethionamide (Trecator-SC) 15-20 mg/kg in two doses Gastrointestinal and
(max 500 mg bid) PO 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

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

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

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

83. Treatment
• 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

84. Treatment
• 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

85. Ileal Tuberculosis
• 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

86. Ano-Recto-SigmoidalTuberculosis
• 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

87. 2.PeritonealTuberculosis
1 1
Acute form Chronic form
I
Tuberculous peritonitis
• Acute abdomen
• Exploratory laparotomy
> ascitic fluid
> thickened
omentum
> scattered
tubercles
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

88. Peritoneal Tuberculosis
• 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

89. Pathogenesis
Peritoneal seeding by tuberculosis bacilli
4
Granulomatous multiple whitish npdules(<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 omeHtal thickening (omental cake)
Purulent peritonitis
Secondary to tuberculous salpingitis
Abscess formation ... lymph nOde, mesentery , omentum
Fistula formation.. Cutaneous/ enteric

90. Peritoneal Tuberculosis
• 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

91. 87

92. PeritonealTuberculosis
• Abdominal Cocoon Syndrome
— Dense adhesions in peritoneum and omentum
with contents inside as small bowel causing
intestinal obstruction

93. 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
89

94. PeritonealTuberculosis
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

95. PeritonealTuberculosis
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

96. Peritoneal Tuberculosis
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

97. PeritonealTuberculosis
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

98. Peritoneal Tuberculosis
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

99. Peritoneal Tuberculosis
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

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

101. Peritoneal Tuberculosis
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

102. 3.Nodal/Glandulartuberculosis
A. Calcified lesion
B. Acute Mesenteric lymphadeniti:
C. Pseudo-mesenteric cyst
D. Tabes mesenterica
n#
E. Chronic Lymphadenitis
• Complications
— Abscess formation

103. Tuberculous Mesenteric Lymphadenitis
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

104. TuberculousMesentericLymphadenitis
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

105. TuberculousMesentericLymphadenitis
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

106. 4.Solidvisceraltuberculosis
Intraabdominal viscera:
□ Liver‘
□ Spleen
□ Pancreas

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

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

109. • INVESTIGATIONS
- Percutaneous liver biopsy.
- laparoscopy liver biopsy- cheesy white irregular
nodules.
- CTSCAN.

110. CT abdomen
— miliary micronodular with miliary calcifications
- Multiloculated cystic mass(cluster sign)

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

112. SPLENIC TUBERCULOSIS
• 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)

113. 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
Clinical Infectious Diseases
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.

114. 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
Clinical Infectious Diseases
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.

115. 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)

117. 5.Raretypes
A. Oesophageal (0.2% of abdominal)
B. Gastroduodenal(1%)
C. Retroperitoneal tuberculosis

118. • 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.

119. THANKYOU