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Leading Article

Ind. J. Tub., 1991, 38, 119


Tuberculosis is still common in the developing world; so common that it must be considered in the differential diagnosis of a majority of the medical, surgical and gynaecological presentations.1 Abdominal tuberculosis too is quite common. Two large series from the UK23 have reported the prevalence in Asian immigrants as 16 and 36 per 100,000 population. While abdominal tuberculosis is one of the commonest forms of extra-pulmonary tuberculosis, it is ill understood and is being neglected all too often by clinicians and researchers. Surprisingly, even some text books on infectious diseases4^ and a monograph on inflammatory bowel disease6 make no mention of abdominal tuberculosis.

Clinical Features

As many as l/3rd of the patients with abdominal tuberculosis may present with an acute abdomen.3 , 8 Rolled up omentum, doughy abdomen, alternating constipation and diarrhoea are more commonly described in text books but are less frequently seen in clinical practice. The presence of associated pulmonary tuberculosis and/or peripheral tuberculous lymphadenitis is not so common as believed9 but should be looked for. The average age of Indian patients (26 years) is less than that in the whites (45 years)9. Does it mean that the Indian disease is different from that seen in the West?


It is not generally realised that abdominal tuberculosis denotes the involvement of the gastrointestinal tract, peritoneum and/or abdominal lymph nodes. Klimach and Ormerod3 while reporting 109 cases of gastrointestinal tuberculosis included as many as 42 cases in whom there were no gastrointestinal lesions. Bastani et al7 believe, incorrectly though, that it is pure gastrointestinal tuberculosis that has a more acute presentation. In a series of 90 cases of abdominal tuberculosis, more patients with peritoneal tuberculosis presented with acute abdomen than those with gastrointestinal lesions.8 Some authors9,10 describe abdominal rigidity and tenderness to be the most frequent signs-being present in as many as 2/3rd of the cases. However, Tandon et ai11 have found them in only 5% of their cases. The difference could perhaps be explained by the fact that the former series included more cases of peritoneal tuberculosis while the latter had mainly included cases with gastrointestinal lesions. It is also incorrect to say that obstruction and perforation are rare in abdominal tuberculosis.12,13 Abdominal tuberculosis should be considered as a possibility in any patient who presents with a lump, ascites, intestinal obstruction or peritonitis.

Sharp and Goldman2 wrongly advocate that non specific features like malaise, raised ESR and positive Mantoux test should be taken as diagnostic of abdominal tuberculosis in a difficult to diagnose abdominal problem in an Asian patient. Radiological studies too have a high false negative rate (ileal strictures are more likely to be missed)8 and may fail to differentiate between tuberculosis and carcinoma1. Besides, adhesions may be construed as intestinal lesions7. Blind percutaneous needle biopsy of the peritoneum,14 laparoscopic biopsy15 and peritoneal biopsy with a small grid iron incision in the right iliac fossa under local anaesthesia10 have been advocated but are hazardous to carry out except in patients with ascites. To sum up, while diagnosis of abdominal tuberculosis should always be kept in mind, a definite diagnosis needs careful and painstaking investigation. Therapeutic trial with anti-tuberculosis chemotherapy, though recommended16 is not really justified17. Although systemic symptoms like fever, anorexia and weight loss may subside within 4 to 6 weeks of anti-tuberculosis chemotherapy, bowel symptoms take much longer to respond18. Also, anti-tuberculosis chemotherapy, given for 4 to 6 weeks for purposes of trial, can alter the histological picture so much that subsequent differentiation from Crohn,s disease becomes difficult.19

120 Pathology and Microbiology


studies of patients with abdominal tuberculosis. Surgical Treatment Surgical intervention may become necessary in abdominal tuberculosis for two reasonsdiagnostic and therapeutic. Diagnostic laparatomy becomes necessary for histopathological/microbiological diagnosis, more often in patients with peritoneal and/or lymph node tuberculosis.24 Therapeutic surgery is indicated for complications like intestinal obstruction (acute, acute-on-chronic, chronic), perforation and peritonitis. A textbook of surgery25 mentions that surgical therapy for hyperplastic lesions is rarely indicated and another (of tropical medicine) makes no mention of surgical treatment at all,26 but that is not true. ^ Strictureplasty27 may be performed in patients with multiple ileal strictures to preserve intestinal length, in selected cases. For hypertrophic ileocaecal lesions, the surgical procedure of choice is not a right hemicolectomy but a limited (segmental) resection,28 including only 5 cms of ascending colon, with ileoascending colostomy. Anti-tuberculosis Chemotherapy The regimen, doses and duration of antituberculosis chemotherapy for abdominal tuberculosis are becoming fairly standardized, but the role of steroids in preventing adhesion formation remains controversial.29 Cooke30 has recommended 12-18 months treatment but Dutt : et al31 found short course (9 months) regimens to be equally effective. Recently, Balasubramanian et al32 have shown in a controlled trial that a 6 month regimen is as effective as the conventional regimes in the treatment of abdominal tuberculosis. This can be accounted for by the progress made in the recent past in a clearer understanding of the role of multiple drugs, rhythm of administration, duration of treatment and the mode of action of anti-tuberculosis drugs on tubercle bacilli, wherever they are in the body. The site of the disease in abdomen, however, appears to be important in respect of the clinical response to chemotherapy. While peritoneal and nodal lesions respond well, the healing process in intestinal lesions may lead to increased fibrosis going on to intestinal obstruction.17,19 An increased occurrence of perforation has been reported in patients with intestinal tuberculosis

The pathology of abdominal tuberculosis is well understood--epithelioid cell granulomas, with Langhan,s giant cells, with or without central caseation necrosis. The histological findings of tuberculosis may be present only in the lymph nodes and not in intestinal lesions. Also, previous anti-tuberculosis chemotherapy may alter the histopathological picture19. A monograph on inflammatory bowel disease,20 surprisingly, says that only bacteriological studies.can differentiate gastrointestinal tuberculosis from Crohn,s disease. The relationship, if any, between abdominal tuberculosis and Crohn,s "disease (regional enteritis) remains a myth: many cases of so called regional enteritis could only be a manifestation of abdominal tuberculosis9 because mycobacteria like organisms have been isolated from patients with Crohn,s disease.21 Haddad et al9 go to the extent of saying that cases being presently diagnosed as regional enteritis are, in fact, abdominal tuberculosis and, in future, regional enteritis may be described as a variant of abdominal tuberculosis. However, there is sufficient evidence in support of a possible separate entity of regional enteritis. A large number of cases of inflammatory intestinal disease remain unclassified.22 Microbiological confirmation of tuberculous etiology is difficult, except in tuberculous peritonitis where processing of one litre of ascitic fluid may yield upto 80% positive results.23 The mycobacterial strains causing abdominal tuberculosis, at least in India, are of the human type." Etiopathogenesis The etiopathogenesis of abdominal tuberculosis-either through ingestion of bacilli, hematogenous spread from an active pulmonary focus or reactivation of a latent abdominal focus-does not explain why the gastro-intestinal tract is involved in some patients but in others the disease remains confined to peritoneum and/or lymph nodes; why do some patients develop ulcero-constrictive lesions, while others have hyperplastic masses and why do some patients with tuberculous peritonitis have frank ascites but others largely develop adhesions? The answers to these questions may come from immunological



who were on anti-tuberculosis treatment.33,34 However, Anand et al18 have shown that surgery was required in only 3 out of 39 patients with intestinal strictures treated with chemotherapy. The first country to eliminate tuberculosis will be the one which regards the disease a*s a serious problem, right to the end.35 We in India need to keep this message always in mind as tuberculosis is one of our "National" disease*

V.K. Kapoor Associate Professor, Surgical Gastroenterology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, P.B. 375, Lucknow-226 001. References 1. 2. 3. Cook G.C. Tuberculosis--certainly not a disease of the past (Editorial). Quart. J. Med.; 1985, 56, 519-21. Sharp J.F. Goldman M. Abdominal tuberculosis in East Birmingham--a 16 year study. Postgrad. Med. J. 1987; 63 : 539-42. Klimach O.E, Ormerod L.P. Gastrointestinal tuberculosis : a retrospective review of 109 cases in a district general hospital. Quart. J. Med; 1985,56, 569-78. Ramsay A.M., Emend R.T.D. Infectious Diseases. William Heinemann Medical Books Ltd, 1978. Sanford J.P., Luby J.P. Infectious Diseases: Grune and Stratton, 1978. Lee E.C.G. Surgery of Inflammatory Bowel Disease. (Clinical Surgery International-14). Churchil Livingstone 1987. Bastani B, Shariatizadeh M.R., Dehdashti F. Tuberculous peritonitis--a report of 30 cases and review of the literature. Quart. J. Med.; 1985. 56, 549-57. Palmer K.R., Patil D.H., Basran G.S., Riordan J.F. Silk D.B.A. Abdominal tuberculosis in urban Britain--a common disease. Gut; 1985, 26, 1296-1305. Haddad F.S., Ghossain A, Sawaya E, Nelson A.R. Abdominal tuberculosis. Dis. Colon. Rectum, 1987,30, 724-35. Das P., Shukla H.S. Clinical diagnosis of abdominal tuberculosis. Br. J. Surg. 1976, 63, 941-6. Tandon R.K., Sarin S.K., Bose S.L., Berry M. Tandon B.N. A clinicopathological appraisal of intestinal tuberculosis--changing profile? Gastroenterologica Japomca; 1986; 21, 17-22. Misiewicz J.J. et al. Atlas of Clinical Gastroenterology. London: Edward Arnold; 1987, 6.8-6.10.

13. 14. 15. 16. 17. 18. 19. 20.


4. 5. 6. 7.



24. 25. 26. 27.


9. 10. 11.

28. 29.



Rains A.J.H., Mann C.V. Baily and Love,s Short Practice of Surgery. London: ELBS & HK Lewis & Co, 1988,1050-1051. Levine H. Needle biopsy diagnosis of tuberculous peritonitis. Am. Rev. Resp. Dis. 1968. 97, 889-94. Wolfe J.H.N., Behn A.R., Jackson B.T. Tuberculous peritonitis* and role of diagnostic laparoscopy. Lancet; 1979,1, 852-3. Anand B.S., Nanda R, Sachdeva G.K. Response of tubercular strictures to anti-tuberculosis treatment. Gut, 1988, 29, 62-9. Schofield P.F. Abdominal tuberculosis. Gut, 1985,26, 1275-8. Anand B.S. Distinguishing Crohn,s disease from intestinal tuberculosis. Natl. Med. J. India. 1989, 2,170-5. Tandon H.D., Prakash A. Pathology of intestinal tuberculosis and its distinction from Crohn,s disease. Gut, 1972,13, 260-9. Carlson H.C. Radiology on inflammatory bowel disease. In Kirsner J.B. Shorter R.G. Eds. Inflammatory Bowel Disease. Philadelphia : Lea and Febiger 1988, 416. Chiodini R.J., Van Kruiningen J.H., Merkal R,S., Thayer W.R., Coutu J.A. Characteristics of an unclassified Mycobacterium species isolated from patients with Crohn,s disease. J. Clin. Microbiol; 1984, 20, 966-71. Tandon H.D. The pathology of intestinal tuberculosis and distinction from other diseases causing stricture. Trop. Gastroenterol, 1981, 2 , 77-93. Singh M.M., Bhargava A.N., Jain K.P., Tuberculous peritonitis. An evaluation of pathogenetic mechanisms, diagnostic procedures and therapeutic measures. N. Engl. J. Med. 1969,281, 1091-4. Bhansali S.K. Abdominal tuberculosis. Experiences with 300 cases. AM. J. Gastroenterol; 1972,67,324-37. Schwartz S.I. Principles of Surgery : McGraw Hill; 1984,1152-1153. Woodruff A.W. Medicine in the Tropics. Churchill Livingstone; 1974, 451-3. Katariya R.N, Sood S, Rao P.G., Rao P.L.N.G. Stricture-plasty for tubercular strictures of the gastrointestinal tract. Br. J. Surg. 1977, 64, 4968. Puiari B.D. Modified -surgical procedures in intestinal tuberculosis. Br. J. Surg, 1979, 66,1801. Fox W. Short course chemotherapy for pulmonary tuberculosis and some problems of its programme application with particular reference to India. Lung India, 1984, 2,161-74. Cooke NJ. Treatment of tuberculosis. Br. Med. J. 1985, 291, 497-8.






Dutt A.K, Moers D, Stead W.W. Short course chemotherapy for extra pulmonary tuberculosis. Nine years experience. Ann. Intern. Med; 1986, 104,7-12. Balasubramanian R, Ramachandran R, Joseph P, Nagarajan M, Thiruvengadam K.V, Tripathy S.P, Prabhakar R. Interim results of a controlled clinical study of abdominal tuberculosis. Ind. J. Tub. 1989,36, 117-22. Tabrisky J, Lindstrom R.R., Peters R, Lachman



R.S. Tuberculous enteritis. Review of a protean disease. Am. J. Gastroenterol; 1975; 63, 49-57. Jayaswal R, Jena P.K, Gopinathan V.P, Chauhan M.S. Recurrent acute tuberculous perforations of small intestine associated with miliary tuberculosis of lung. J. Assoc. Physicians India; 1986; 34. 817-8. Home N.W. Problems of tuberculosis in

decline. Br. Med. J 1984; 288,1249-51.



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