ABDOMINAL

TUBERCULOSI
S

Dr.PRATEEK KUMAR
JUNIOR RESIDENT
 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
 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
 HIV coexistence has dramatically
changed the etiological agents & the
pattern of presentation of abdominal
tuberculosis thus producing diagnostic
difficulties
Introduction

 24th March 1882- World Tb day

 TB declared as notifiable disease by

INDIAN GOVERNMENT on may9th 2012
 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
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
Pathology

Bacilli
Bacilli in
in depth
depth of
of mucosal
mucosal glands
glands

Inflammatory
Inflammatory reaction
reaction

Phagocytes
Phagocytes carry
carry bacilli to Peyer’s
Peyer’s Patches
Patches

Formation
Formation of
of tubercle
tubercle

Tubercles
Tubercles undergo
undergo necrosis
Pathology
Submucosal tubercles enlarge

Endarteritis & edema

Sloughing

Ulcer formation

Accumulation of collagenous tissue

Thickening & Stenosis

 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
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
 Gastrointestinal Tuberculosis
Constitutes 70-78% cases of abdominal
tuberculosis
Most common site of gastrointestinal
tuberculosis is ileocaecal region
But
› Stasis
why...?
› Abundant payer’s patches
› Alkaline media
› Bacterial contact time is more
› Minimal digestive activity
› Maximum absorption in the area
 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
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
 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
 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
 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
 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
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
 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
 Tuberculous Mesenteric
Lymphadenitis
5 types of lymph node involvement may be
seen
• Acute mesenteric lymphadenitis
• Pseudo-mesenteric cyst
• Tabes mesenterica
• Chronic Lymphadenitis
• Calcified lesion
 Solid organ TB
Involvement of liver and spleen occurs as a part
of disseminated and miliary tuberculosis
 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
 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
CLINICAL PRESENTATIONS OF
ABDOMINAL TUBERCULOSIS
 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
 Dissemination of tuberculosis
 Cold abscess formation
 Hemorrhage
 Fecal fistula
 Gastric outlet obstruction
 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
 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
 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
Plain X ray abdomen:
• Intestinal obstruction
• Calcified lymph nodes
• Hollow viscus perforation
• Calcified Granuloma in liver
 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
 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
 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
Loss of normal
ileocaecal angle
and dilated terminal
ileum, appearing
suspended from a
retracted fibrosed
caecum – goose
neck deformity
 Barium oesophagogram-ulcerative
oesophagitis, stricture, pseudo tumour
masses, fistula, sinus, traction
diverticulae
 Duodenal tuberculosis-segmental
narrowing, widening of the “C” loop due to
lymphadenopathy
 Investigations
 Ultrasound Abdomen
Mainly used for extraintestinal lesions
(peritoneal & lymph nodes)
• Thickening of bowel wall
Tuberculosis Crohn’s disease Malignancy
Fluid&concentric
• Uniform collection in the pelvis
Eccentric with thick
at mesentric Variegated appearance
border
septa
• Loculated ascitis
• Interloop ascitis – “club sandwich” or
“sliced bread” sign
• 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
• 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
 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
 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
 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
 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
 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%
 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
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
• The detection &
quantification of IFN-Υ by
ELISA is used to identify
in vitro response
Indian scenario
 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
 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– Levels
HIV Coinfection cells may
to activate
be normalthe
Malignant Ascites – Levels may be falsely
macrophages & increase their bactericidal activity.
high
High IFN-Υ levels have been found in tubercular
ascites
 Combining both ADA & IFN-Υ estimation in ascitic
fluid increase sensitivity & specificty of diagnosis
 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
 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
 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
 Tubercular ascites with
underlying Cirrhosis
 3 of the 5 first line anti tubercular drugs are
hepatotoxic ( Z> R>H )
 HOW TOdrugs can lead to
Use of these hepatotoxic
• worsening LFT
TREAT
• decompensation of stable cirrhosis
THEN...?
• fulminant hepatic failure
 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
 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
 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
 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
 Treatment

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