Abdominal Tuberculosis
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Transcript of 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