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ABDOMINAL TUBERCULOSIS DR. KAMAL ABDOMINAL TUBERCULOSIS DR. KAMAL

ABDOMINAL TUBERCULOSIS DR. KAMAL - PowerPoint Presentation

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ABDOMINAL TUBERCULOSIS DR. KAMAL - PPT Presentation

JR 2 ND YEAR PULMONARY MEDICINE GASTROINTESTINAL TUBERCULOSIS Tuberculosis enteritis as a complication of pulmonary TB was appreciated by HIPPOCRATES s in the 5 th century BC Diarrhea attacking a person with phthisis is a mortal symptom ID: 628414

abdominal amp present tuberculosis amp abdominal tuberculosis present diagnosis thickening form ileocaecal bowel intestinal ulcers due perforation att small lymph common cases

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Slide1

ABDOMINALTUBERCULOSIS

DR. KAMALJR 2ND YEARPULMONARY MEDICINESlide2

GASTROINTESTINAL TUBERCULOSIS

Tuberculosis enteritis as a complication of pulmonary T.B. was appreciated by

HIPPOCRATES

s

in the 5

th century B.C.

Diarrhea attacking a person with phthisis is a mortal symptom

(Walsh, 1909)

Slide3

Abdominal TB can involve any part of GIT from mouth to anus, the peritoneum and pancreato-billiary system.

Total EP TB accounts for about 10-12% of total no. of TB cases, out of which 11-16% are abdominal koch.Sixth most frequent EP TB after lymphatics, genitourinary, bone & joint, milliary & meningeal TB.Caused by M. tuberculosis, M.

bovis & NTM.Age group 20-40 most commonly affected & slight female preponderance has been described.Slide4

HIV & TB

Before era of HIV infection > 80% TB was confined to lung

Extrapulmonary

TB increases with HIV

40 –60% TB in HIV+ pt

are extrapulmonary

Globally, proportion of co-infected pt > 8 %

~ 0.4 million people in India are co-infected.

In one study, 16.6% abdominal TB pt in Bombay

was

HIV +.Slide5

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 Rare Mechanism:

Contiguous spread of infection from a fallopian tube

TB peritonitis as complication of peritoneal dialysis

PATHOGENESISSlide6

DISTRIBUTION OF TUBERCULOUS LESIONS

Ileum >

caecum

> ascending colon > jejunum

>appendix > sigmoid > rectum > duodenum

> stomach >

oesophagus

More than one site may be involvedSlide7

Most common site - ileocaecal region

Increased physiological stasisIncreased rate of fluid and electrolyte absorptionMinimal digestive activity permitting greater contact time between the organism & mucosal surface. Abundance of lymphoid tissue at this site(

peyer’s patches) & microfold cell ( M cell )Slide8

Most active site of inflammation is submucosaBacilli in glands Inflamatory

reaction Phagocytes carry Bacilli in Peyer’s patch formation of tubercles Necrosis of tubercles Enlarges Endarteritis, edema & sloughing Ulcer formation& Accumulation of collagenous tissue Thickening & stenosis

PATHOLOGYSlide9

It can be acute or chronicACUTE TUBERCULOSIS PERITONITISPresent as acute abdomen & are often subjected to emergency surgery

On opening abdomen , straw colored fluid may be present & tubercles may be found to be scattered on the peritoneum & greater omentum.PERITONEAL TB

OMENTUM SCATTERED WITH TUBERCLESSlide10

ASCITIC FORM : Insidious in onset , abdominal pain usually absent , rolled up greater omentum

infiltrated with tubercles may be felt as transverse mass.ENCYSTED(LOCULATED ) FORM: There is localized swelling & diagnosis is usually retrospective .FIBROUS FORM: Widespread adhesion may cause coils of intestine to be matted together & distended which act as blind loop leading to steatorrohoea, malabsorpation syndrome & abdominal pain.

CHRONIC TUBERCULOSIS OF PERITONEUMSlide11

It is of following types:ULCERATIVE:

Usually occur in adults who are malnourishedUlcers may b solitary or multiple & usually lies transverse to the long axis of the gut girdle.Healing & fibrosis of the ulcers lead to formation of napkin ring stricture & obstructive symptomsFormation of fistula is thereGASTROINTESTINAL TB

TRANSVERSE ULCERSlide12

Usually occur in young adult who are relatively well nourished with low volume infection by less virulent organism.Caecum is most commonly affected site

There is extensive fibrosis & inflammation that often result in adherance of bowel , mesentry , lymph node into the mass. ULCEROHYPROTROPHIC FORM: Display features both of ulcerative & hypertrophic form

Hypertrophic formSlide13

Less common form of intestinal TBVery similar to ULCERATIVE COLITISSCLEROTIC FORM

It is associated with stricture formationDIFFUSE COLITIS

Resected

portion of

illeocaecalTBSlide14

Abdominal pain is the most common symptom & is most commonly located in right lower quadrant of abdoman. Patient with intestinal

obstructio has cramp like character.Diarrhoea : 11-20% of patient . Liquid to semisolid stool passed 6-8 times a day. Mucus is usually present. Diarrhoea alternating with constipation is present also present in some patient.Constitutional symptoms: fever , malaise , weight loss, anorexia.Other symptoms: moving lump in abdomen , nausea, vomiting, malaena

& constipation , menstural abnormalities.

SYMPTOMSSlide15

Most patient are ill & malnourished.Tenderness may be present mostly in right iliac fossa.

Palpable abdominal mass may be present which may be due to hyperplastic caecal TB, Lymph node enlargement & rolled up omentum.Classic doughy abdomen has been described in only 6-11% patients.Signs of peritonitis may be present when there is intestinal perforation.

SIGNSSlide16

Tuberculosis of esophagus

Rare ~ 0.2% of total cases

By extension from adjacent LN

Low grade fever /

Dysphagia

/

Odynophagia / Midesophageal

ulcer

Mimics esophageal Ca

Upper part is more commonly involved than lower part

Endoscopic

biopsy is must for confirmation of diagnosisSlide17

Rare due to presence of gastric acid and paucity of lymphoid organ.Ulcerative form is commonest & ulcers are found along lesser curvature.

Usually retrospective diagnosis & not suspected until time of surgeryDUODENAL TUBERCULOSISRare formUsually present with obstructive symptom which is more often due to extrinsic obstruction caused by lymph node or adhesion.Rare is obstructive jaundice.GASTRIC TUBERCULOSIS Slide18

Common with ileocaecal TB but isolated is rareAbdominal perforation may b presenting symptom

Diagnosed mostly on abdominal explorationANAL TBLesion are ulcerative,lupuoid & verrucus.Perianal ulcers are shallow with blue undermined edgesMay be associated with inguinal LAD.Fistula in ano

& perianal abscess may be present.

APPENDICULAR TBSlide19

Often associated with miliary TB & more often occur in immuno-compromised host

May present as acute or chronic pancreatitis or may mimic malignancy.FNAC & biopsy are helpfulPANCREATIC TBSlide20

Occur in disseminated or miliary form of TBMost common in HIV+ve

patientsCommon features are left upper quadrant abdominal pain, weight loss & diarrheaMay Present as hypersplenism or splenic abscessSPLENIC TBSlide21

One or more of the following four criteria must be fulfilled to diagnose abdominal TB.Histopathological

evidence of tubercles with caseation necrosis & AFB.Presence of M tuberculosis in sputum , tissue, or ascitic fluid.Clinical , radiological or operative evidence of proven TB elsewhere with good therapeutic response.Good therapeutic response to ATT.

DIAGNOSTIC CRITERIASlide22

HAEMATOLOGY & SERUM BIOCHEMISTRYAnaemia, leucopenia with relative

lymphocytosisESR is raised in 50-100% patientsLAB INVESTIGATION ARE NON SPECIFIC TUBERCULIN SKIN TEST: Positive in 55-100% cases.In area where TB is endemic it neither confirms the diagnosis nor exclude the diagnosis.CHEST X RAY: associated pulmonary TB has been described in 24-28% cases . Evidence of TB in chest x ray support the diagnosis but normal chest x ray does not rule it out.Slide23

PLAIN X RAY ABDOMEN:May show

calcified lymph nodes and granulomas dilated loops with fluid level, dilatation of terminal ileum AscitisPneumoperitoneum in intestinal perforation

X ray

abdoman

showing calcified LNSlide24

Straw coloured Protein >3g/

dLTLC of 150-4000/µl, Lymphocytes >70%SAAG < 1.1 g/DlAscitis to blood glucose ratio <1.1g/dlZN stain + in < 3% cases+ culture in < 20% cases

ASCITIC FLUID EXAMINATIONSlide25

ADA: Adenosine deaminase

ADA is increased due to stimulation of T-cells by mycobacterial AgSerum ADA > 54 U/LAscitic fluid ADA > 36 U/L

Ascitic fluid to serum ADA ratio > 0.985 Coinfection

with HIV

normal or low ADAFalse high values seen in malignant ascitis & chronic kidney disease.Slide26

Barium studiesEnteroclysis followed by barium enema is the best protocol

Increased transit time with hypersegmentation (chicken intestine) and flocculation is the earliest signLocalised areas of irregular thickened folds, mucosal ulceration, dilated segments and stricturesThickened iliocaecal valve with a broad triangular appearance with the base towards the caecum (inverted umbrella sign or (Fleischner’s

sign)Rapid transit and lack of barium retention (Sterlin’s sign)Narrow beam of barium due to

stenosis

(

string’s sign)Slide27

Conical caecum:- shrunken in size & pulled out of iliac fossa

Goose neck deformity- loss of normal ileocaecal angle & terminal dilated ileum appearing from retracted pulled up caecumBoth Stierlin & String sign is present in crohn’s disease Barium

oesophagogram-ulcerative oesophagitis, stricture, pseudo tumour masses, fistula, sinus, traction

diverticulae

Duodenal tuberculosis-segmental narrowing, widening of the “C” loop due to lymphadenopathySlide28

Group1: Highly s/o intestinal TB if one or more of the following features are presenta. Deformed ileocaecal

valve with dilatation of terminal ileumb. Contracted caecum with an abnormal ileocaecal valve and/or terminal ileumc. Stricture of the ascending colon with shortening of and involvement of ileocaecal regionBARIUM MEAL FOLLOW THROUGH FINDING IN INTESTINAL TBSlide29

GroupII: Suggestive of intestinal tuberculosis if one of the following feature present

a.Contracted caecumb.Ulceration or narrowing of the terminal ileumc.Stricture of the ascending colond.Multiple areas of dilatation, narrowing and matting of small bowel loopsGroupIII: Non-specific changesFeatures of matting, dilatation and mucosal thickening of small bowel loops

GroupIV: NormalstudySlide30

Multiple

tuberculous

strictures small intestine

Ba

. Meal follow-through

Yehia Aly, Cairo UniversityChicken intestine: hypersegmentation of small intestine

NARROWING OF INTESTINE: STRING’s SIGNSlide31

Often reveals a mass made up of matted loops of small bowel with thickened walls, diseased omentum

, mesentery and loculated asitesFine septae may be seen in the ascitic fluidInter loop ascites gives rise to charecteristic

“club sandwitch” appearance Mesenteric thickening is better detected in the presence of ascites

and is often seen as the

stellate sign” of bowel loops radiating from its rootIn intestinal tuberculosis bowel wall thickening is usually uniform and concentric as opposed to the eccentric thickening at the mesenteric border seen in Crohn’sdisease and the variegated appearance seen in malignancyABDOMINAL USGSlide32

Granulomas or absess in the liver ,pancreas or spleen

“Pseudo kidney sign” illeocaecal region pulled upto sub hepatic position

Usg abdoman showing lymphadenopathy

&

omental

thickeningUSG ABDOMAN SHOWING FREEFLUID & LADSlide33

CT is better than USG in detecting high dense ascites

of high attenuation 25-45 HU Abdominal lymphadenopathy is the commonest manifestation of tuberculosis on CTRetroperitoneal, peripancreatic, portahepatis, and mesenteric/omental lymph node enlargement may be evidentCaseous necrotising

lymph node appears as low attenuating necrotic centers and thick enhancing inflammatory rimOmental thickening is well seen as omental cake appearance . A fibrous wall can cover the

omentum

due to long standing inflammation & is called “

omental line”. An omental line is less common in malignancyCT ABDOMENSlide34

Preferential thickening of the medial caecal wall with an exophytic

mass engulfing the terminal ileum associated with massive lymphadenopathy is characteristic of tuberculosisShort segments of mural thickening with normal intervening bowel associated with ileocaecal involvement strongly suggest tuberculosisSlide35

CT SCAN OF PELVIS SHOWING ASCITIS & OMENTAL MASS

CT SCAN OF ABDOMAN SHOWING LOCULATED ASCITIS & MESENTRIC LN & STRANDS

CIRCUMFERENTIAL THICKENING OF CAECUM & NARROWING OF TERMINAL ILEUMSlide36

MRI:-has no added advantageEndoscopyColonoscopy:

- it is excellent tool for diagnosis.Ulceration is the most common finding. Ileocaecal valve may edematous or deformed. Nodules, ulcers, pseudopolyps may be seen. Mucosal nodules of variable sizes & ulcers in a discreate segment of colon , 4-8 cm in length are pathognomic. A combination of histology and culture can establish diagnosis in 80% of cases

Fine needle aspiration cytology : it can be done from lymph nodes , abscesses ,& focal lesion of viscera.Peritoneal biopsy- it can be blind or open parietal peritoneal biopsy under LA.

Laparoscopy

:-most effective method. 80 to 95% diagnostic accuracy. Characteristic finding include multiple, yellowish-white

miliary nodules over peritoneum, erythematous, thickened and hyperemic peritoneum , turbid ascitis & adhesions. chances of perforation are higher when patients with fibroadhesive disease are subjected to laproscopy.Slide37
Slide38

IMMUNOLOGICAL TEST

Bhargava et al used ELISA with monoclonal Ab against 38 kDa protein Found a senstivity of 81% and specificity of 88% & diagnostic accuracy of 84%.However, ELISA remain positive even after therapy, the response to mycobacteria is variable & its reproducibility is poor.

PCR:Amplification of 340 bp nucleotide seq

located within the 38

kDa

protein gene of M. tuberculosisDiagnostic accuracy as a single test is questionableSlide39

Medical treatment Earlier 8-12 month of ATT given now it has been observed that A six month short-course ATT is as effective as standard 12 month regimen

Corticosteroids-role not well established Surgical treatmentTo manage complication such as Obstruction , perforation and massive hemorrhageStrictures by stricturoplasty or resectionPerforation by resection and anastomosisBypass surgery not indicated

Surgery followed by full course of ATT

TREATMENT

39Slide40

MalabsorptionCoeliac

diseaseLymphomaImmunoproliferative small intestinal diseae Crohn’s diseaseMASSAppendicular massActinomycosis

Caecal carcinomaLymphomaAscites

Cardiac disease

Renal disease

Hepatic diseasemalignacyDIFFERENTIAL DIAGNOSISSlide41

1. OBSTRUCTION : Most common complication

PathogenesisHyperplastic caecal TB Strictures of the small intestine--- commonly multiple

AdhesionsAdjacent LN involvement 

traction, narrowing and fixation of bowel loops.

COMPLICATIONSSlide42

2. PERFORATION

: 2nd commonest cause after typhoid Usually single and proximal to a strictureClue - TB Chest x-ray, h/o SAIOPneumoperitoneum in ~ 50% cases

3. MALABSORPTION

:

Pathogenesis

bacterial overgrowth in stagnant loop bile salt deconjugation diminished absorptive surface due to ulcerationinvolvement of lymphatics and LNSlide43

43

Medical treatment

. Earlier 8-12 month of ATT given now it has been observed that A six month short-course ATT is as effective as standard 12 month regimen

Corticosteroids-role not well established

Surgical treatment

To manage complication such as

Obstruction,perforation and

massive hemorrhage

Strictures by stricturoplasty or resection

Perforation by resection and anastomosis

Bypass surgery not indicated

Surgery followed by full course of ATT

TREATMENTSlide44

DIFFICULTY IN DIAGNOSIS OF ABDOMINAL TB

TUBERCULOSISCXRAY show previous or active TB.Involvement of fewer than 4 segments, patulous ileocaecal valve,transverse ulcers , scars & pseudopolyp .Granulomas

:Multiple(mean no. 5.35 per site), large(>0.05 mm^2), confluent & in submucosal regionPreferential

thickening

of

ileocaecal valve & medial wall of caecumCROHN’s DISEASEFeautres like arthralgia, arthritis, eythema nodosum are more commonAnorectal fissures, longitudnal ulcers, apthous ulcers, cobblestone

Infrequent(mean no : 0.75) , small(95µm) & mucosal granulomaThickening is more uniform & lesser thickening of the bowel Slide45

Abdominal koch is most difficult type of TB to diagnose & its reoccurence

is even more difficult to diagnose asBMFT changes like pulled up caecum, fibrosis, remain even after initial treatmentThere are no specific sign & symptom & mimicks many other disease Often patient do not have previous record to differentiate between new & old findingNo role of Montoux in reoccurence

& ELISA also remain positive even after treatment.

TO DIAGNOSE REOCCURENCE OF ABDOMINAL KOCHSlide46

HOW TO DIAGNOSE REOCCURENCEUsually on basis of clinical signs & symptomsHigh clinical suspicion

Proved from biopsy / HPE or culture positiveAs one of the diagnostic criteria is RELIEF OF SYMPTOMS WITH THERAPEUTIC TRIAL OF ATT so sometime diagnosis is retrospectiveSlide47