ABDOMINAL TUBERCULOSIS

1. ABDOMINALTUBERCULOSIS DR. KAMAL JR 2ND YEAR PULMONARY MEDICINE

2. GASTROINTESTINAL TUBERCULOSIS Tuberculosis enteritis as a complication of pulmonary T.B. was appreciated by HIPPOCRATESs in the 5th century B.C. Diarrhea attacking a person with phthisis is a mortal symptom (Walsh, 1909)

3. 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.

4. 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 +.

5. 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 • Rare Mechanism: • Contiguous spread of infection from a fallopian tube • TB peritonitis as complication of peritoneal dialysis

6. DISTRIBUTION OF TUBERCULOUS LESIONS Ileum > caecum > ascending colon > jejunum >appendix > sigmoid > rectum > duodenum > stomach > oesophagus • More than one site may be involved

7. Most common site - ileocaecal region • Increased physiological stasis • Increased rate of fluid and electrolyte absorption • Minimal 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 )

8. PATHOLOGY Most active site of inflammation is submucosa Bacilli 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

9. PERITONEAL TB It can be acute or chronic ACUTE TUBERCULOSIS PERITONITIS Present 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. OMENTUM SCATTERED WITH TUBERCLES

10. CHRONIC TUBERCULOSIS OF PERITONEUM • 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.

11. GASTROINTESTINAL TB It is of following types: ULCERATIVE: • Usually occur in adults who are malnourished • Ulcers 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 symptoms • Formation of fistula is there TRANSVERSE ULCER

12. Hypertrophic form • 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

13. DIFFUSE COLITIS • Less common form of intestinal TB • Very similar to ULCERATIVE COLITIS SCLEROTIC FORM • It is associated with stricture formation Resected portion of illeocaecalTB

14. SYMPTOMS • 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.

15. SIGNS • 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 hyperplasticcaecal 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.

16. 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 diagnosis

17. GASTRIC TUBERCULOSIS • 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 surgery DUODENAL TUBERCULOSIS Rare form Usually present with obstructive symptom which is more often due to extrinsic obstruction caused by lymph node or adhesion. Rare is obstructive jaundice.

18. APPENDICULAR TB • Common with ileocaecal TB but isolated is rare • Abdominal perforation may b presenting symptom • Diagnosed mostly on abdominal exploration ANAL TB • Lesion are ulcerative,lupuoid & verrucus. • Perianal ulcers are shallow with blue undermined edges • May be associated with inguinal LAD. • Fistula in ano & perianal abscess may be present.

19. PANCREATIC TB • 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 helpful

20. SPLENIC TB • Occur in disseminated or miliary form of TB • Most common in HIV+ve patients • Common features are left upper quadrant abdominal pain, weight loss & diarrhea • May Present as hypersplenism or splenic abscess

21. DIAGNOSTIC CRITERIA 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.

22. HAEMATOLOGY & SERUM BIOCHEMISTRY • Anaemia, leucopenia with relative lymphocytosis • ESR is raised in 50-100% patients LAB 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.

23. PLAIN X RAY ABDOMEN: May show • calcified lymph nodes and granulomas • dilated loops with fluid level, dilatation of terminal ileum • Ascitis • Pneumoperitoneum in intestinal perforation X ray abdoman showing calcified LN

24. ASCITIC FLUID EXAMINATION • Straw coloured • Protein >3g/dL • TLC of 150-4000/µl, Lymphocytes >70% • SAAG < 1.1 g/Dl • Ascitis to blood glucose ratio <1.1g/dl • ZN stain + in < 3% cases • + culture in < 20% cases

25. ADA is increased due to stimulation of T-cells by mycobacterial Ag • Serum ADA > 54 U/L • Ascitic fluid ADA > 36 U/L • Ascitic fluid to serum ADA ratio > 0.985 • Coinfection with HIV  normal or low ADA • False high values seen in malignant ascitis & chronic kidney disease. ADA: Adenosine deaminase

26. Barium studies • Enteroclysis followed by barium enema is the best protocol • Increased transit time with hypersegmentation (chicken intestine) and flocculation is the earliest sign • Localised areas of irregular thickened folds, mucosal ulceration, dilated segments and strictures • Thickened 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)

27. 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 caecum Both 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 lymphadenopathy

28. BARIUM MEAL FOLLOW THROUGH FINDING IN INTESTINAL TB • Group1: Highly s/o intestinal TB if one or more of the following features are present • a. Deformed ileocaecal valve with dilatation of terminal ileum • b. Contracted caecum with an abnormal ileocaecal valve and/or terminal ileum • c. Stricture of the ascending colon with shortening of and involvement of ileocaecal region

29. GroupII: Suggestive of intestinal tuberculosis if one of the following feature present • a.Contractedcaecum • b.Ulceration or narrowing of the terminal ileum • c.Stricture of the ascending colon • d.Multiple areas of dilatation, narrowing and matting of small bowel loops • GroupIII: Non-specific changes • Features of matting, dilatation and mucosal thickening of small bowel loops • GroupIV: Normalstudy

30. Multiple tuberculous strictures small intestine Ba. Meal follow-through YehiaAly, Cairo University Chicken intestine: hypersegmentation of small intestine NARROWING OF INTESTINE: STRING’s SIGN

31. ABDOMINAL USG • Often reveals a mass made up of matted loops of small bowel with thickened walls, diseased omentum, mesentery and loculatedasites • Fine septae may be seen in the ascitic fluid • Inter 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 root • In 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 malignancy

32. Granulomas or absess in the liver ,pancreas or spleen • “Pseudo kidney sign” illeocaecal region pulled upto sub hepatic position USG ABDOMAN SHOWING FREE FLUID & LAD Usgabdoman showing lymphadenopathy & omental thickening

33. CT ABDOMEN • 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 CT • Retroperitoneal, peripancreatic, portahepatis, and mesenteric/omental lymph node enlargement may be evident • Caseousnecrotising lymph node appears as low attenuating necrotic centers and thick enhancing inflammatory rim • Omental 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 malignancy

34. Preferential thickening of the medial caecal wall with an exophytic mass engulfing the terminal ileum associated with massive lymphadenopathy is characteristic of tuberculosis • Short segments of mural thickening with normal intervening bowel associated with ileocaecal involvement strongly suggest tuberculosis

35. CT SCAN OF PELVIS SHOWING ASCITIS & OMENTAL MASS CIRCUMFERENTIAL THICKENING OF CAECUM & NARROWING OF TERMINAL ILEUM CT SCAN OF ABDOMAN SHOWING LOCULATED ASCITIS & MESENTRIC LN & STRANDS

36. MRI:-has no added advantage Endoscopy • 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.

38. 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. tuberculosis Diagnostic accuracy as a single test is questionable

39. TREATMENT • 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

40. DIFFERENTIAL DIAGNOSIS Malabsorption • Coeliac disease • Lymphoma • Immunoproliferative small intestinal diseae • Crohn’s disease MASS • Appendicular mass • Actinomycosis • Caecal carcinoma • Lymphoma Ascites • Cardiac disease • Renal disease • Hepatic disease • malignacy

41. COMPLICATIONS 1. OBSTRUCTION : Most common complication Pathogenesis • Hyperplasticcaecal TB • Strictures of the small intestine--- commonly multiple • Adhesions • Adjacent LN involvement  traction, narrowing and fixation of bowel loops.

42. 2. PERFORATION: 2nd commonest cause after typhoid Usually single and proximal to a stricture Clue - TB Chest x-ray, h/o SAIO Pneumoperitoneum in ~ 50% cases • 3. MALABSORPTION: • Pathogenesis • bacterial overgrowth in stagnant loop • bile salt deconjugation • diminished absorptive surface due to ulceration • involvement of lymphatics and LN

43. TREATMENT • 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

44. DIFFICULTY IN DIAGNOSIS OF ABDOMINAL TB • TUBERCULOSIS • CXRAY show previous or active TB. • Involvement of fewer than 4 segments, patulous ileocaecalvalve,transverse ulcers , scars & pseudopolyp . • Granulomas: Multiple(mean no. 5.35 per site), large(>0.05 mm^2), confluent & in submucosal region • Preferential thickening of ileocaecal valve & medial wall of caecum • CROHN’s DISEASE Feautres like arthralgia, arthritis, eythemanodosum are more common • Anorectal fissures, longitudnal ulcers, apthous ulcers, cobblestone Infrequent(mean no : 0.75) , small(95µm) & mucosal granuloma Thickening is more uniform & lesser thickening of the bowel

45. TO DIAGNOSE REOCCURENCE OF ABDOMINAL KOCH • Abdominal koch is most difficult type of TB to diagnose & its reoccurence is even more difficult to diagnose as • BMFT changes like pulled up caecum, fibrosis, remain even after initial treatment • There are no specific sign & symptom & mimicks many other disease • Often patient do not have previous record to differentiate between new & old finding • No role of Montoux in reoccurence & ELISA also remain positive even after treatment.

46. HOW TO DIAGNOSE REOCCURENCE • Usually on basis of clinical signs & symptoms • High clinical suspicion • Proved from biopsy / HPE or culture positive • As one of the diagnostic criteria is RELIEF OF SYMPTOMS WITH THERAPEUTIC TRIAL OF ATT so sometime diagnosis is retrospective