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ABDOMINAL TUBERCULOSIS

HOD : Prof. Dr. Vasanthakumar MS.,


UNIT CHIEF : Prof. Dr.Ravindran MS.,
ASSISTANT PROFESSORS: Dr.Vishwanathan MS.,
Dr.Muthulakshmi
MS.,
PRESENTED BY
Dr.Pradeep Pathogenesis & Investigations
Dr.Dhanaraj Gastrointestinal TB
Dr.Sudish- Peritoneal & Solid Organ TB
Dr.Adarsh- Surgery in TB

TUBERCULOSIS
ETIOPATHOGENESIS AND INVESTIGATIONS

WHY SHOULD WE
KNOW ABOUT
TB??


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

TB declared as notifiable disease


by INDIAN GOVERNMENT on
may9th 2012

http://articles.timesofindia.indiatimes.com/2012-05-09/india/316405
62_1_mdr-tb-tb-cases-tb-diagnosis

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.ed

24th march
1882
World TB DAY

PATHOGENESIS

STAGE 1
ESTABLISHMENT

ALVEOLAR MACROPHAGE
INGESTS TB BACILLI

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


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.

STAGE 2 SYMBIOSIS

Tubercle bacilli ingested


By non activated newly recruited
Monocytes.

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

Secrete IFN

Activates
Macrophag
es

TCELL
Kills the inactivated
macrophages which were
allowing the tb bacilli
growth inside them

WHAT IS THE
INITIAL RESPONSE
OF THE HOST??

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

STAGE 3 EARLY STAGES OF CASEOUS


NECROSIS

Non activated
Macrophages which
allowed the growth of
TB bacilli are killed by
DTH mediated by Tcells
Forming solid caseous
necrosis

If DTH is directed towards


the TB bacilli then why so
much of tissue
destruction occurs??

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;60:692703.

DTH AND CMI

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.

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.

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.

1.ARE HOSTS WITH POOR


CMI ARE MORE INFECTIVE??
2.ROLE OF STEROIDS IN
ABDOMINAL TB??

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.


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;19:170177.

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

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

Culturing for isolation


of Mycobacterium spp
continues to be a Gold
standard

Agar based
4egg based
6weeks
BACTEC 14.8days
MGIT- 13.3days

NEWER METHODS

PCR SENSITIVITY-92% SPECIFICITY-99%


INTERFERON release assays.

QuantiFERONTB
SENSITIVITY-81%
SPECIFICITY-91.2%

TB SPOT
SENSITIVITY-87.5%
SPECIFICITY-86.3%

GASTROINTESTINAL
TUBERCULOSIS

Epidemiology
Pathogenesis
Clinical features
Diagnosis

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 (3:14:1)
Mainly disease of young adults
~ 2/3 of pt. are 21-40 yr old

TB & HIV

Incidence severity of
abdominal TB will increase with
the HIV epidemic

HIV 50 % develop abdominal TB

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.

Types

Ulcerative
Hyperplastic
Ulcerohyperplastic
Diffuse colitis
Sclerotic

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

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
of mesentery and bowel
Thick fixed mass

Regional lymph nodes


Hyperplasia
Caseation necrosis
Calcification

Order of Frequency

Ileum > caecum > ascending colon > jejunum


>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
More than one site may be involved

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?


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

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

Ileocecal TB

Colicky abdominal pain


Ball rolling in abdomen
Borborygmi
Right iliac fossa lump - ileocaecal region,
and LN

mesenteric fat

Isolated Colonic TB

9.2% of all cases


Multifocal involvement in ~ 1/3 (28% to 44%)

Anorectal TB

Hematochezia - most common symp. Due to mucosal


trauma by stool
Constitutional symptoms
Constipation
Rectal stricture
Anal fistula usually multiple

Gastroduodenal TB

Stomach and duodenum each ~ 1% of total cases

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

Esophageal TB

Rare ~ 0.2% of total cases


By extension from adjacent LN
Low grade fever / Dysphagia / Odynophagia /
Midesophageal ulcer
Mimics esophageal Ca

Complications

OBSTRUCTION
PERFORATION
MALABSORPTION

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
(Bhansali and Sethna).

bowel obstruction

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)

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


Investigations

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

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

TB mass in stomach

Esophageal TB Nodules

T.B. ulceration with narrow lumen


Is endoscopy diagnostic?

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)

Take home message

Ileocecal TB is the most common intestinal TB


Combination of histology & culture is necessary for diagnosis.
Surgery is the only answer

PERITONEAL
TUBERCULOSIS

AN

OVERLOOKED
DIAGNOSIS

DIAGNOSTIC
CHALLENGES

Non specific presentation


Insidious presentation
Mimicks malignancy
Unhelpful labaratory tests

EPIDEMOLOGY
PATHOGENESIS

CLINICAL FEATURES
DIAGNOSIS
TREATMENT

EPIDEMOLOGY

6th most common extra pulmonary site


Incidence- 0.1% to 0.7% worldwide
Rising incidence
sexes are equally affected
35 and 45years of age.

PATHOGENESIS

Activation of quiscent foci of


infection(common)

Direct spread mesentric Lymph nodes


Intraabdominal organs
Hematogenous spread from
Primary pulmonary TB
Miliary TB


CLINICAL PICTURE

CLINICAL
PRESENTATION

wet-ascitic
(most common)
ascites
peritonitis

fibrotic-fixed
Mass formation
Matting of bowel
loops

dry-plastic
form(less
common)
adhesions
doughy feel
tender
abdominal
masses.

Encysted(loculate
d)
localized
abdominal
swelling

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

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.

Ascitic fluid analysis

Gross Appearance:
Straw coloured .

EXUDATIVE
WBC cell count-500 and 1500cells/mm3 lymphocytosis.
LDH raised->90U/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

New diagnostic tools

Adenosine deaminase.

rapid and non-invasive

Purine-degrading enzyme
Assists with maturation and differentiation of Tlymphoid cells.

Raised- stimulation of T cells by the


mycobacterial antigens.

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.

Gene amplification.- LCR & PCR in detecting AFB


in tissues.
serological tests-

- ELISA todetect IgG to a 43kDa antigen ofM.


tuberculosisfound it to be highly sensitive.
- High IFN-levels- detecting latent TB.

Elevated CA-125
-Not sensitive
Also raised in peritoneal carcinomatosis,
ovarian malignancy.
Can use to follow treatment response

Imaging studies

in obtaining peritoneal biopsies

safer and inexpensive


alternative to diagnostic
laparoscopy.

high diagnostic yield


approaching 95%

Ultrasoundsuperior to CT in revealing the multiple, fine,


mobile septationswithin 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

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 (>15mm) with
mesenteric lymph nodes- early sign

Lymphadenopathy.(black arrow)


DIAGNOSTIC TOOL
OF CHOICE?

DIAGNOSTIC
LAPROSCOPY

DIAGNOSTIC YEILD

LAP FINDINGS

PIT FALLS

Peritoneal carcinomatosis, sarcoidosis,


starch peritonitis and Crohn's diseaseMIMICK LAP FINDINGS.
More expensive.
Requires expertise.
poor isolation of organism
complications -bleeding, infection and bowel
perforation


ROLE OF
LAPAROTOMY?


unnecessary

with fibro-adhesive type of TBP when there


is an indication for a peritoneal biopsy.


ideal diagnostic test
requires the
demonstration of
mycobacteria

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


TREATMENT


MEDICAL vs SURGICAL

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


Surgery is reserved for complications or
uncertainty in diagnosis.

MDR-TB not responsive to ATT.

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.


ROLE OF
CORTICOSTEROIDS?


four trials of adjuvant corticosteroids use in TBP and
all of them cited modest benefit.

Alrajhiet al.85reported 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

Tuberculous
peritonitis--do not
it
miss

requires a high index of suspicion because of


the subtle nature of the symptoms and signs.

culture growth of theMycobacteriumremains


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

Laparoscopy,

however, remains the


best means of
diagnosing the
disease


SOLID ORGAN
TUBERCULOSIS

HEPATIC TB

the portal of entry :hematogenous


dissemination
miliary tuberculosis :hepatic artery
focal liver tuberculosis :portal vein.


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


INVESTIGATIONS
Percutaneous liver biopsy.
laparoscopy liver biopsy- cheesy white irregular
nodules.

CT SCAN.

CT abdomen

miliary micronodular with miliary calcifications

Multiloculated cystic mass(cluster sign)


MILIARY TB

lesions are small 1 to 2 mm epitheloid


granulomas.

TUBERCULOMA
Masses larger than 2mm in diameter

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 biopsyis the


gold standard for diagnosis.
CECT-abdomen-multiple hypo echoic foci(<2cm)

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.

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.

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)

CT enhanced conrast-

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

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

Ovarian TB
Tuberculous tuboovarian 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).

Surgeons
Viewpoint


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 ?


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?


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?


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?

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

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 Pak2003 May;13(5):277-9

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
Katariyaet al

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


Resection Anastomosis
Is it safe?

Annals of Surgery November


Two-stage procedures
Reversal of stoma in a well-prepared gut with
ATT cover

Muhammad Saaiq et al


Turkish Journal of Trauma & Emergency
Surgery vol 17 2011
Rankie et al
Recio et al
Piechaud et al
Asian J Surg2002:25(2):145-8


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


Resection of a tuberculous lesion where
feasible is the procedure of choice

How much to resect?

With effective ATT limited and conservative


resections give good results

ournal of the College of Physicians and Surgeons Pakistan 2008, Vol. 18 (7): 393
Agarwal et al , BHJ 2000

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.

Adhesiolysis / ATT

Adhesive intestinal lesions may be relieved


with antitubercular drugs alone without
surgery.

Anand et al
Balasubramaniam et al

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.


Thank You