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Abdominal Tuberculosis Slide 1 Abdominal Tuberculosis Slide 2 Abdominal Tuberculosis Slide 3 Abdominal Tuberculosis Slide 4 Abdominal Tuberculosis Slide 5 Abdominal Tuberculosis Slide 6 Abdominal Tuberculosis Slide 7 Abdominal Tuberculosis Slide 8 Abdominal Tuberculosis Slide 9 Abdominal Tuberculosis Slide 10 Abdominal Tuberculosis Slide 11 Abdominal Tuberculosis Slide 12 Abdominal Tuberculosis Slide 13 Abdominal Tuberculosis Slide 14 Abdominal Tuberculosis Slide 15 Abdominal Tuberculosis Slide 16 Abdominal Tuberculosis Slide 17 Abdominal Tuberculosis Slide 18 Abdominal Tuberculosis Slide 19 Abdominal Tuberculosis Slide 20 Abdominal Tuberculosis Slide 21 Abdominal Tuberculosis Slide 22 Abdominal Tuberculosis Slide 23 Abdominal Tuberculosis Slide 24 Abdominal Tuberculosis Slide 25 Abdominal Tuberculosis Slide 26 Abdominal Tuberculosis Slide 27 Abdominal Tuberculosis Slide 28 Abdominal Tuberculosis Slide 29 Abdominal Tuberculosis Slide 30 Abdominal Tuberculosis Slide 31 Abdominal Tuberculosis Slide 32 Abdominal Tuberculosis Slide 33 Abdominal Tuberculosis Slide 34 Abdominal Tuberculosis Slide 35 Abdominal Tuberculosis Slide 36 Abdominal Tuberculosis Slide 37 Abdominal Tuberculosis Slide 38 Abdominal Tuberculosis Slide 39 Abdominal Tuberculosis Slide 40 Abdominal Tuberculosis Slide 41 Abdominal Tuberculosis Slide 42 Abdominal Tuberculosis Slide 43 Abdominal Tuberculosis Slide 44 Abdominal Tuberculosis Slide 45 Abdominal Tuberculosis Slide 46 Abdominal Tuberculosis Slide 47 Abdominal Tuberculosis Slide 48 Abdominal Tuberculosis Slide 49 Abdominal Tuberculosis Slide 50 Abdominal Tuberculosis Slide 51 Abdominal Tuberculosis Slide 52 Abdominal Tuberculosis Slide 53 Abdominal Tuberculosis Slide 54 Abdominal Tuberculosis Slide 55 Abdominal Tuberculosis Slide 56 Abdominal Tuberculosis Slide 57 Abdominal Tuberculosis Slide 58 Abdominal Tuberculosis Slide 59 Abdominal Tuberculosis Slide 60 Abdominal Tuberculosis Slide 61 Abdominal Tuberculosis Slide 62 Abdominal Tuberculosis Slide 63 Abdominal Tuberculosis Slide 64 Abdominal Tuberculosis Slide 65 Abdominal Tuberculosis Slide 66 Abdominal Tuberculosis Slide 67 Abdominal Tuberculosis Slide 68
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Abdominal tuberculosis
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Abdominal Tuberculosis

  2. 2. 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
  3. 3. 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
  4. 4.  HIV coexistence has dramatically changed the etiological agents & the pattern of presentation of abdominal tuberculosis thus producing diagnostic difficulties
  5. 5. Introduction  24th March 1882- World Tb day  TB declared as notifiable disease by INDIAN GOVERNMENT on may9th 2012
  6. 6. 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
  7. 7. Modes of Transmission 1. 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
  8. 8. Pathology Bacilli in depth of mucosal glandsBacilli 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
  9. 9. Pathology Submucosal tubercles enlarge Endarteritis & edema Sloughing Ulcer formation Accumulation of collagenous tissue Thickening & Stenosis
  10. 10. 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
  11. 11. 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
  12. 12. Gastrointestinal Tuberculosis Constitutes 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...?
  13. 13. Intestinal Tuberculosis Characterisitc lesions produced are: • Ulcerative • Hypertrophic • Stricturous or constrictive • Diffuse colitis • Combination of these forms can also occur Ulcerative type Adult patients who are malnourished Multiple circumferential transverse ulcers (Girdle ulcers) with skip leisons Napkin ring strictures in longstanding ulcers
  14. 14. 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
  15. 15.  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
  16. 16. 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
  17. 17. 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
  18. 18. 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
  19. 19. 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
  20. 20. 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
  21. 21. Tuberculous Mesenteric Lymphadenitis 5 types of lymph node involvement may be seen • Acute mesenteric lymphadenitis • Pseudo-mesenteric cyst • Tabes mesenterica • Chronic Lymphadenitis • Calcified lesion
  22. 22. Solid organ TB Involvement of liver and spleen occurs as a part of disseminated and miliary tuberculosis
  23. 23. 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
  24. 24. 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
  26. 26. 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
  27. 27.  Dissemination of tuberculosis  Cold abscess formation  Hemorrhage  Fecal fistula  Gastric outlet obstruction
  28. 28. 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
  29. 29. 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
  30. 30. 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
  31. 31. Plain X ray abdomen: • Intestinal obstruction • Calcified lymph nodes • Hollow viscus perforation • Calcified Granuloma in liver
  32. 32. 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
  33. 33.  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
  34. 34.  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
  35. 35. Loss of normal ileocaecal angle and dilated terminal ileum, appearing suspended from a retracted fibrosed caecum – goose neck deformity
  36. 36.  Barium oesophagogram-ulcerative oesophagitis, stricture, pseudo tumour masses, fistula, sinus, traction diverticulae  Duodenal tuberculosis-segmental narrowing, widening of the “C” loop due to lymphadenopathy
  37. 37. Investigations  Ultrasound Abdomen Mainly 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
  38. 38. • Mesenteric thickening ≥15mm with increased echogenicity • Lymph node enlargement Discrete or conglomerated Echotexture is mixed heterogenous, anechoic areas represent caseation Caseation and calcification is highly s/o tubercular etiology
  39. 39. • 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
  40. 40. 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
  41. 41. 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
  42. 42. 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
  43. 43.  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
  44. 44.  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%
  45. 45.  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
  46. 46. QUANTIFERON –TB GOLD ASSAY QuantiFERON-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
  47. 47. • The detection & quantification of IFN-Υ by ELISA is used to identify in vitro response
  48. 48. Indian scenario
  49. 49. Investigations Ascitic fluid analysis: ›Easy and cost effective ›Diagnose made easily from characteristic abnormalities seen in tubercular ascites ›Only difficulty is when there is underlying cirrhosis
  50. 50. 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 normal Malignant Ascites – Levels may be falsely high HIV Coinfection – Levels may be normal Malignant Ascites – Levels may be falsely high
  51. 51. 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
  52. 52. 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
  53. 53. 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
  54. 54. 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...?
  55. 55.  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 months Pyrazinamide 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
  56. 56.  Two hepatotoxic drugs: 9 months of Isoniazid, Rifampin & Ethambutol 2 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 drug 18-24 monthsof Streptomycin, Ethambutol and Quinolones
  57. 57. 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
  58. 58.  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
  59. 59. Treatment  Surgical Management: › Indications:  Intestinal obstruction  Severe hemorrhage  Acute abdomen (perforation)  Intra-abdominal abscesses/ fistula formation  Uncertain diagnosis
  60. 60. 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
  61. 61. 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
  62. 62. 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
  63. 63. Thank You
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