ABDOMINAL TUBERCULOSIS A TO Z

1. ABDOMINAL
TUBERCULOSI
S
Dr.PRATEEK KUMAR
JUNIOR RESIDENT

2. Introduction
 Tuberculosis, a common disease in India
and other developing countries
 The extrapulmonary tuberculosis involves
11-16% of patients, out of which 3-4%
belong to abdominal tuberculosis
 Abdominal Tuberculosis is the 6th most
common type of extra-pulmonary
tuberculosis

3. Impact of HIV co-infection
 With the increasing incidence
of HIV infection there is
increase in both incidence and
severity of extrapulmonary
tuberculosis
 Extrapulmonary tuberculosis
alone or in association with
pulmonary disease has been
documented in 40-60% of all
cases

4.  HIV coexistence has dramatically
changed the etiological agents & the
pattern of presentation of abdominal
tuberculosis thus producing diagnostic
difficulties

5. Introduction
 24th March 1882- World Tb day
 TB declared as notifiable disease by
INDIAN GOVERNMENT on may9th 2012

6. Pathophysiology
Abdominal tuberculosis
Primary Secondary
 10 Abdominal TB results from ingestion of milk or food
infected with Mycobacterium bovis, has become
very rare these days.
 Mycobacterium tuberculosis is the pathogen in most
of the 20 cases
 Mycobacterium avium intracellulare(MAC) has
become a major pathogen in HIV coinfected patients

7. Modes of Transmission
1. Dissemination of primary pulmonary
tuberculosis in childhood
2. Swallowing of infected sputum in active
pulmonary tuberculosis
3. Hematogenous spread
4. Through lymphatics
5. Spread from infected adjacent organs
like fallopian tubes
6. Dissemination through bile from
tubercular granulomas of the liver

8. Pathology
Bacilli in depth of mucosal glandsBacilli in depth of mucosal glands
Inflammatory reactionInflammatory reaction
Phagocytes carry bacilli to Peyer’s PatchesPhagocytes carry bacilli to Peyer’s Patches
Formation of tubercleFormation of tubercle
Tubercles undergo necrosisTubercles undergo necrosis

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

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

11. Sites of involvement
• Gastrointestinal Tract: TB can involve
any part of GI tract from mouth to anus
• Peritoneum
• Lymph nodes
• Solid organs: liver, spleen, pancreas
• Omentum

12. Gastrointestinal Tuberculosis
Constitutes 70-78% cases of abdominal
tuberculosis
Most common site of gastrointestinal
tuberculosis is ileocaecal region
› Stasis
› Abundant payer’s patches
› Alkaline media
› Bacterial contact time is more
› Minimal digestive activity
› Maximum absorption in the area
But
why...?

13. Intestinal Tuberculosis
Characterisitc lesions produced are:
• Ulcerative
• Hypertrophic
• Stricturous or constrictive
• Diffuse colitis
• Combination of these forms can also occur
Ulcerative type
Adult patients who are malnourished
Multiple circumferential transverse ulcers (Girdle
ulcers) with skip leisons
Napkin ring strictures in longstanding ulcers

14. Hyperplastic Type:
 A low volume infection by less virulent organisms
in a host with good resistance & wound healing
capacity
 Chronic granulomatous lesions in ileoceacal
region
 Fibroblastic activity in submucosa and subserosa
causes thickening of bowel wall with lymph node
enlargement
Stricturous type:
 Characterised by strictures – multiple or single
Diffuse colitis:
 Rare form, very similar to ulceratice colitis

16.  Esophageal tuberculosis:
Very rare, usually occurs due to direct extension
from adjacent structures
 Gastric tuberculosis:
Rare, 80% patients have Ulcerative form
 Duodenal TB: rare, usual involvement is of
obstructive type (Extrinsic > luminal)
 Anal : perianal ulcerative lesions, fistula in ano,
perianal abscess

17. Peritoneal tuberculosis
Occurs in 4-10% patients of extrapulmonary
tuberculosis
Follows either direct spread of tuberculosis
from ruptured lymph nodes and intra
abdominal organs or Haematogenous
Seeding
Abdominal lymph nodal and peritoneal
tuberculosis may occur without gastrointestinal
involvement in about one third of the cases

18. Peritoneal tuberculosis
Peritoneal tuberculosis can occur in two
forms:
1) Acute –
Mimics acute abdomen
Due to perforation or rupture of mesenteric
lymph nodes
2) Chronic – ascitic / encysted / plastic / purulent

19. Peritoneal tuberculosis
Ascitic type:
Intense exudate causes ascitis
Common in children and young adults
Encysted type:
Exudation with minimal fibroblastic reaction
Ascites gets loculated due to fibrinous
deposition

20. Peritoneal tuberculosis
Plastic:
Extensive fibroblastic reaction
Widespread adhesions between coils of
intestine (matted intestines), abdominal
wall, Omentum
Purulent form:
Direct spread from adjacent organs e.g
tuberculous salpingitis

21. Tuberculous Lymphadenitis
 Accounts for about 25% cases of
extrapulmonary tuberculosis
 In abdomen, mainly mesenteric, peri-
pancreatic, periportal & upper para-aortic
group of lymph nodes involved
 Lymph node may show casseation or
calcification

22. Tuberculous Mesenteric
Lymphadenitis
5 types of lymph node involvement may be
seen
• Acute mesenteric lymphadenitis
• Pseudo-mesenteric cyst
• Tabes mesenterica
• Chronic Lymphadenitis
• Calcified lesion

23. Solid organ TB
Involvement of liver and spleen occurs as a part
of disseminated and miliary tuberculosis

24. Clinical manifestations
 Disease may present at any age but
commonly seen in young adults with slight
female predominance
 In children, peritoneal and nodal form of TB
is more common than intestinal TB
 It may present as
an acute disease or
a chronic illness or
an acute on chronic event

25. Symptoms
Constitutional localsymptoms
depending upon site involved
 Constitutional symptoms are:
• Fever
• Malaise
• Anemia
• Night sweats
• Loss of weight
• Pain abdomen: colicky if luminal compromise, dull and continuous when
mesenteric lymph nodes are involved

26. CLINICAL PRESENTATIONS OF
ABDOMINAL TUBERCULOSIS

27. Complications
 Intestinal Obstruction:
Most common complication
Mechanism: hyperplastic intestinal lesion, strictures,
adhesion and adjacent lymph node involvement
 Malabsoprption, blind loop syndrome:
Most important cause of malabsorption in India next to
tropical sprue
 Perforation:
2nd
commonest cause of small intestinal perforation,
first being typhoid fever
Usually single & proximal to a stricture

28.  Dissemination of tuberculosis
 Cold abscess formation
 Hemorrhage
 Fecal fistula
 Gastric outlet obstruction

29. 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

30. Diagnosis
 The key is . . . . . . . ‘High degree of suspicion’
with proper use of diagnostic modalities
 New criteria for the diagnosis were suggested
by Lingenfelser as follows:
1. Clinical features suggestive of TB
2. Imaging evidence indicative of abdominal TB
3. Histopathological or microbiological evidence
of TB and/or
4. Therapeutic response to ATT

31. Investigations
 Blood investgations:
• Anaemia
• Leucopenia with lymphocytosis
• Raised ESR
• Hypoalbuminemia
 Mantoux test:
Gives supportive evidence to the diagnosis
Positive in 50 – 70% cases
 Chest Xray: may reveal either healed or active pulmonary
tuberculosis

32. Plain X ray abdomen:
• Intestinal obstruction
• Calcified lymph nodes
• Hollow viscus perforation
• Calcified Granuloma in liver

33. Barium studies
 Very useful for intestinal tuberculosis
 Small bowel barium meal:
 Accelerated transit time & flocculation is the
earliest sign
 Hypersegmentation of the barium column
(chicken intestine)
 Localised areas of irregular thickened folds,
mucosal ulceration, dilated segments and
strictures

34.  Barium enema for colon and ileocaecal region:
 Thickened iliocaecal valve with a broad
triangular appearance with the base towards
the caecum (inverted umbrella sign or
(Fleischner’s sign)
 “Conical caecum”, shrunken in size and pulled
out of the iliac fossa due to contraction and
fibrosis of the mesocolon

35.  Loss of normal ileocaecal angle and dilated
terminal ileum, appearing suspended from
a retracted fibrosed caecum – goose neck
deformity
 Rapid transit and lack of barium retention
indicating acute
 inflammation - Sterlin’s sign
 Narrow beam of barium due to stenosis -
String’s sign

37. Loss of normal
ileocaecal angle
and dilated terminal
ileum, appearing
suspended from a
retracted fibrosed
caecum – goose
neck deformity

38.  Barium oesophagogram-ulcerative
oesophagitis, stricture, pseudo tumour
masses, fistula, sinus, traction
diverticulae
 Duodenal tuberculosis-segmental
narrowing, widening of the “C” loop due to
lymphadenopathy

39. Investigations
 Ultrasound Abdomen
Mainly used for extraintestinal lesions
(peritoneal & lymph nodes)
• Thickening of bowel wall
• Fluid collection in the pelvis with thick
septa
• Loculated ascitis
• Interloop ascitis – “club sandwich” or
“sliced bread” sign
Tuberculosis Crohn’s disease Malignancy
Uniform &concentric Eccentric at mesentric
border
Variegated appearance

40. • Mesenteric thickening ≥15mm
with increased echogenicity
• Lymph node enlargement
Discrete or conglomerated
Echotexture is mixed
heterogenous, anechoic
areas represent caseation
Caseation and calcification
is highly s/o tubercular
etiology

41. • Pulled up caecum to subhepatic position
(Pseudokidney sign)
USG can be used for guiding procedures like ascitic tap
or FNAC or biopsy from enlarged lymph
nodes/hypertrophic lesions

42. Investigations
 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

43. Investigations
 CT Abdomen
 Better than USG for detecting
 High density ascites
 Lymphadenopathy with caseation
 Bowel wall thickening
 Irregular soft tissue densities in omental
area
 Tuberculosis of liver & spleen

46. Investigations
 Diagnostic laproscopy
› Direct visualization – inflammed
thickened peritoneum studded with
whitish yellow miliary tubercles
› Collect acsitic fluid
› Take biopsy from solid organs,
lymphnodes, omentum
or peritoneum

47.  FNAC
 In patients with palpable masses
 High diagnostic accuracy
 L-J culture of FNAC material increases the yield
further
 FNAC during colonoscopy adds to diagnostic
yield in ileocaecal or colonic TB

48.  Peritoneal Biopsy
 Blind percutaneous peritoneal needle biopsy
& open parietal peritoneal biopsy under LA
 Relatively safe, occasional bowel perforation
with blind needle biopsy
 Diagnostic accuracy is 80%

49.  Serodiagnosis:
 Histological & microbiological methods often
inadequate – paucibacillary disease
 Many serological tests have been developed,
but all have low predictive value
 PCR assay for detection of M. tuberculosis in
endoscopic biopsy specimen has shown
promising results

50. QUANTIFERON –TB GOLD ASSAY
QuantiFERON-TB Gold: Indirect blood test
for Mycobacterium tuberculosis complex
infection (both active & latent)
Measures cell-mediated immune response to
antigens simulating the mycobacterial proteins
Individuals infected with M. Tuberculosis complex
have lymphocytes in their blood that recognise
these specific antigens & in response secrete
IFN-Υ

51. • The detection &
quantification of IFN-Υ by
ELISA is used to identify
in vitro response

52. Indian scenario

53. Investigations
Ascitic fluid analysis:
›Easy and cost effective
›Diagnose made easily from characteristic abnormalities seen in tubercular
ascites
›Only difficulty is when there is underlying cirrhosis

54. ADA & IFN-Υ
 ADA is an enzyme present in T lymphocytes &
macrophages, hence its level increase due to
stimulation of T lymphocytes in response to CMI to
mycobacterial antigens.
 IFN-Υ is produced by T cells to activate the
macrophages & increase their bactericidal activity.
High IFN-Υ levels have been found in tubercular
ascites
 Combining both ADA & IFN-Υ estimation in ascitic
fluid increase sensitivity & specificty of diagnosis
HIV Coinfection – Levels may be normal
Malignant Ascites – Levels may be falsely
high
HIV Coinfection – Levels may be normal
Malignant Ascites – Levels may be falsely
high

55. Treatment
 Mediacal management: on same lines as for pulmonary
tuberculosis
› First line drugs:
 INH
 Rifampicin
 Pyrazinamide
 Ethambutol
› Second line drugs:
 Amikacin, kanamycin, PAS, Ciprofloxacin,
 Clarithrymycin, Azythromycin, Rifabutin
› Treatment to be continued for 6 months
› Supportive nutrition

56. Treatment
Role of corticosteroids:
 Used to decrease fibrosis during healing so
as to prevent development of obstruction,
but may delay healing and predispose to
perforation or further obstruction
 Current studies show that even obstructing
intestinal lesions can be successfully treated
with ATT, so use of steroids is declining
these days

57. HIV Coexistent Cases
 Treatment of TB should precede treatment of
HIV infection
 Patients already on HAART, should continue
same treatment with appropriate
adjustments in HAART and ATT
 Regimen is
2 (HRZE)3 + 7 (HR)3
 IRIS has been reported in 32-36% of
patients with HIV-TB coinfection

59. Tubercular ascites with
underlying Cirrhosis
 3 of the 5 first line anti tubercular drugs are
hepatotoxic ( Z> R>H )
 Use of these hepatotoxic drugs can lead to
• worsening LFT
• decompensation of stable cirrhosis
• fulminant hepatic failure
HOW TO
TREAT
THEN...?

60.  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

61.  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

62. 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

63.  No clear guidelines are available for cirrhotic
patients, general principle is to stop treatment if
a rising trend of LFTs is found on 2 consecutive
testing
 Any rise in serum bilirubin should be treated
cautiously and hepatotoxic treatment stopped
immediately
 Treatment can be restarted in a sequential
fashion once serum bilirubin & transaminase
return to normal

64. Treatment
 Surgical Management:
› Indications:
 Intestinal obstruction
 Severe hemorrhage
 Acute abdomen (perforation)
 Intra-abdominal abscesses/ fistula
formation
 Uncertain diagnosis

65. Treatment
 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

66. 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

67. Take Home Message
 Abdominal TB is increasing with increasing
incidence of HIV infection
 Peritoneum & ileocaecal region are
commonly affected by hematogenous spread
or ingestion of infected sputum
 Must exclude this treatable entity in all the
patients presenting with GI disease
 Antimicrobial therapy is the same as for
pulmonary TB

68. Thank You