PowerPoint Presentation

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

TUBERCULOSIS ETIOPATHOGENESIS AND INVESTIGATIONS

WHY SHOULD WE KNOW ABOUT TB?? 40% of Indians harbour tb bacilliIn 2010, Global Incidence 9.4million In india 2.3millionPrevalence in India is 3.1 million3,20,000 deaths -WHOTB declared as notifiable disease by INDIAN GOVERNMENT on may9th 2012http://articles.timesofindia.indiatimes.com/2012-05-09/india/31640562_1_mdr-tb-tb-cases-tb-diagnosis

Risk Factors

Case series involving 60 patients

38% Cirrhosis

33% Renal Failure with Peritoneal Dialysis27% Diabetes Mellitus

18% Underlying Malignancy

10% Systemic Corticosteroids

2% AIDS

12% No Risk Factorshttp://www.med.unc.edu

24th march 1882World TB DAYPATHOGENESISSTAGE 1 ESTABLISHMENT

ALVEOLAR MACROPHAGE INGESTS TB BACILLIM. tuberculosis blocks phagolysosome formation by inhbiting Ca2+ signals and the recruitment and assembly of the proteins that mediate phagosome-lysosome fusionFratti 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 ingestedBy non activated newly recruitedMonocytes.STAGE 2 SYMBIOSISIncapable 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 ( 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 stasisIncreased rate of fluid and electrolyte absorptionMinimal digestive activity Abundance of lymphoid tissue at this site.

Clinical featuresConstitutional symptoms Fever (40%-70%)Weight loss (40%-90%)AnorexiaMalaisePain (80%-95%) Colicky (luminal stenosis)Continous ( LN involvement) Altered bowel habitsIleocecal TBColicky abdominal pain Ball rolling in abdomenBorborygmi Right iliac fossa lump - ileocaecal region, mesenteric fat and LN

Isolated Colonic TB9.2% of all cases

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

Anorectal TBHematochezia - most common symp. Due to mucosal trauma by stoolConstitutional symptoms ConstipationRectal strictureAnal fistula usually multiple

Gastroduodenal TBStomach and duodenum each ~ 1% of total cases Mimics PUD - shorter history, non response to t/tMimics gastric Ca. Duodenal obstruction - extrinsic compression by tuberculous LNHematemesis / Perforation / Fistulae / Obstructive jaundice Cx-Ray usually normalEndoscopic picture - non specific

Esophageal TBRare ~ 0.2% of total casesBy extension from adjacent LN Low grade fever / Dysphagia / Odynophagia / Midesophageal ulcer Mimics esophageal Ca

OBSTRUCTION

PERFORATION

MALABSORPTIONComplications Obstruction PathogenesisHyperplastic caecal TB Strictures (napkin ring) of the small intestineAdhesionsAdjacent LN involvement traction, narrowing and fixation of bowel loops.In India ~ 3% to 20% of bowel obstruction (Bhansali and Sethna).

Malabsorption 2nd most common cause in IndiaPathogenesisbacterial overgrowth in stagnant loop bile salt deconjugation diminished absorptive surface due to ulcerationinvolvement of lymphatics and LN75% pt with intestinal obstruction40% of those without (Tandon et al)

Perforation 5%-9% of SI perforations in India2nd commonest cause after typhoid Usually single and proximal to a strictureClue - 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 NodulesVariable sizes (2 to 6mm)Non friableMost common in caecum especially near IC valve. Tubercular ulcersLarge (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 stricturesDeformed and edematous ileocaecal valve

Esophageal TB Nodules

TB mass in stomach

T.B. ulceration with narrow lumenIs endoscopy diagnostic?8 10 Bx from ulcer edgelow yield on histopath as mainly submucosal disease Granulomas in 8%-48% Caseation in ~ 1/3 (33%-38%) of + casesAFB stains - variable Culture positivity in 40%Combination of histology & culture diagnosis in 80% ( S K Sharma)

Take home messageIleocecal TB is the most common intestinal TBCombination of histology & culture is necessary for diagnosis.Surgery is the only answer

PERITONEAL TUBERCULOSISAN OVERLOOKED DIAGNOSISDIAGNOSTIC CHALLENGESEPIDEMOLOGYPATHOGENESISCLINICAL PICTURECLINICAL PRESENTATION Case series involving 145 patients

73% Abdominal swelling (ascites) most common64% Abdominal pain 54% Fever and night sweats 44% Weight loss18% both pulmonary & abdominal TB Hepatomegaly and splenomegaly - uncommon

CLINICAL FEATURES 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% casesBarium studies . ultrasound and computed tomography.INVESTIGATIONSGross Appearance: Straw coloured . EXUDATIVE WBC cell count-500 and 1500cells/mm3 lymphocytosis.

LDH raised->90U/L

Protein > 3g /dl.

SAAG 15mm) with mesenteric lymph nodes- early sign Lymphadenopathy.(black arrow)

DIAGNOSTIC TOOL OF CHOICE?DIAGNOSTIC LAPROSCOPY

DIAGNOSTIC YEILDLAP FINDINGS PIT FALLS

Peritoneal carcinomatosis, sarcoidosis, starch peritonitis and Crohn's disease- MIMICK LAP FINDINGS.

More expensive. Requires expertise.poor isolation of organism complications -bleeding, infection and bowel perforationROLE 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 mycobacteriacharacteristic laparoscopic appearance itself, even in the absence of bacteriological confirmation, would be sufficient grounds for the diagnosis of TBP.

HIGH SPECIFICITY OF MACROSCOPIC APPEARANCEBUTTREATMENTMEDICAL vs SURGICALsolely pharmacological.

Four drug regimen:IsoniazidRifampinEthambutolPyrazinamide.

CAT I ATTResponse to therapy is manifested by resolution of symptoms and disappearance of ascitesUNCOMPLICATEDSurgery is reserved for complications or uncertainty in diagnosis.

MDR-TB not responsive to ATT.

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.DREADED COMPLICATION

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 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 TBPTuberculous peritonitis--do not miss itLaparoscopy, however, remains the best means of diagnosing the diseaseSOLID ORGAN TUBERCULOSISthe portal of entry :hematogenous dissemination miliary tuberculosis :hepatic artery focal liver tuberculosis :portal vein.HEPATIC TB three formsdiffuse hepatic involvement- most commongranulomatous hepatitisfocal/local tuberculoma or abscess- rareINVESTIGATIONSPercutaneous 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

It can occur due to disseminated or miliary form of the diseaseMost 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(