abdominal tuberculosis

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 Transmission1. 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 in depth of mucosal glands Bacilli 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

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

Lymphatic obstruction of mesentery and bowel Thick fixed mass

Regional lymph nodes Hyperplasia Caseation necrosis Calcification

Bacilli via lymphatics

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 TuberculosisConstitutes 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...?

Intestinal TuberculosisCharacterisitc lesions produced are:• Ulcerative• Hypertrophic• Stricturous or constrictive• Diffuse colitis• Combination of these forms can also occur

Ulcerative typeAdult 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 TBInvolvement 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 AbdomenMainly 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

• Mesenteric thickening ≥15mm with increased echogenicity

• Lymph node enlargementDiscrete or conglomeratedEchotexture is mixed

heterogenous, anechoic areas represent caseationCaseation 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 ASSAYQuantiFERON-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

InvestigationsAscitic 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 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 normalMalignant Ascites – Levels may be falsely

high

HIV Coinfection – Levels may be normalMalignant Ascites – Levels may be falsely

high

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 )

Use of these hepatotoxic drugs can lead to • worsening LFT• decompensation of stable cirrhosis• fulminant hepatic failure

HOW TO TREAT

THEN...?

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 monthsPyrazinamide 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 & Ethambutol2 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 drug18-24 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