Diagnosis of Abdominal Tuberculosis : Role of Imaging

CLINICAL MEDICINE Diagnosis of Abdominal Tuberculosis : Role of Imaging Rita Sood* Tuberculosis has been declared a global emergency by the World Health Organization and is the most important communicable disease worldwide. The prevalence of extra-pulmonary tuberculosis seems to be rising, particularly due to increasing prevalence of acquired immunodeficiency syndrome (AIDS) 1,2. In patients with extrapulmonary tuberculosis, abdomen is involved in 11% of patients 3. Though potentially curable, abdominal tuberculosis continues to be a major cause of morbidity and mortality in India. In the abdomen, tuberculosis may affect the gastrointestinal tract, peritoneum, lymph nodes, and solid viscera. The disease can mimic various other gastrointestinal disorders, particularly inflammatory bowel disease, colonic malignancy, or other gastrointestinal infections. Because of the non-specific symptoms and signs, its diagnosis is often delayed. A high index of suspicion therefore needs to be maintained for an early diagnosis and timely treatment. Pathological spectrum of abdominal tuberculosis Abdominal tuberculosis denotes involvement of gastrointestinal tract (GIT), peritoneum, lymph nodes, and solid organs i.e., liver, spleen, and pancreas. The involvement of the gastrointestinal tract is seen in 65%-78% of patients of abdominal tuberculosis 4,5. The common sites of involvement in GIT are the terminal ileum and the ileocaecal region, followed by colon and jejunum. Rarely, tuberculosis may involve stomach, duodenum, and oesophagus. The intestinal lesions produced by tuberculosis are of three types ulcerative, hypertrophic, and stricturous. Strictures are usually * Additional Professor, Department of Medicine, All India Institute of Medical Sciences, Ansari Nagar, New Delhi-110 029. produced by the cicatricial healing of the ulcerative lesions. A combination of the three morphological forms of lesions i.e., ulcero-constrictive or ulcerohypertrophic may occur. Many of these patients of gastrointestinal tuberculosis have associated nodal and peritoneal involvement. Peritoneal involvement may be adhesive or ascitic. The nodal involvement due to tuberculosis is commonly mesenteric or retroperitoneal. The lymph nodes may show evidence of caseation or calcification. Intestinal, peritoneal, and nodal tuberculosis may occur together in varying permutations and combinations. Hepatosplenic tuberculosis is common as a part of disseminated and miliary tuberculosis. Macronodular form of hepatosplenic tuberculosis is an uncommon form of tuberculosis. Clinical spectrum The disease can present at any age but is seen most commonly in young adults. In children, the peritoneal and nodal form of tuberculosis is much more common than intestinal tuberculosis 6. The modes of presentation can vary from acute, acuteon-chronic or chronic, occasionally as an incidental finding on laparotomy for unrelated causes. The clinical presentation depends upon the site of disease and the type of pathological involvement. Ulcerative type of intestinal tuberculosis can present with chronic diarrhoea and features suggestive of malabsorption. Rectal bleeding is rare but has been reported particularly with colonic tuberculosis. Stricturous type of intestinal tuberculosis presents with features of recurrent subacute intestinal obstruction in the form of obstipation, vomiting, abdominal distension, and colicky abdominal pain. This may be associated with gurgling, feeling of ball of wind moving in the abdomen, and visible intestinal loops. These symptoms may get relieved spontaneously after passage of flatus or sometimes

patients can present with acute intestinal obstruction. Ano-rectal tuberculosis can present as strictures and fistula-in-ano. Tuberculous fistulae are usually multiple. In the caecum and large intestine, lesions are usually hypertrophic and present as either obstruction or as abdominal lump. Gastroduodenal tuberculosis may present as peptic ulcer with or without gastric outlet obstruction or perforation and may mimic malignancy. Microscopic involvement of the liver is common in patients with abdominal tuberculosis but focal lesions in the liver and spleen are generally seen as a part of disseminated tuberculosis. Tuberculosis at unusual sites like pancreas, and oesophagus, more commonly mimics the commoner diseases in those organs, e.g., malignancy. Peritoneal tuberculosis often presents as abdominal distension and ascites or sometimes as a soft cystic lump due to loculated ascites. Lymph node involvement due to tuberculosis can present as a lump in central abdomen, or as vague abdominal pain. These focal symptoms depend upon the site of involvement and are often associated with systemic manifestations of tuberculosis in the form of lowgrade fever, malaise, night sweats, anaemia, and weight loss. These constitutional symptoms are present in about one-third of patients with abdominal tuberculosis 7. About one-third of patients may have tuberculous involvement of other organs or systems 5. The more common extra-abdominal sites are lungs, pleura, lymph nodes, and genito-urinary system. A physical examination may show features of ascites, lump abdomen, or visible peristalsis with dilated bowel loops. However, abdominal examination may not reveal any findings in a large number of patients. Differential diagnosis Because of a wide spectrum of clinical presentation, abdominal tuberculosis can mimic a large number of medical and surgical conditions. Abdominal tuberculosis should be considered in any patient with unexplained and chronic abdominal symptoms. In the hypertrophic form of intestinal tuberculosis, the clinical picture may mimic malignant neoplasms such as lymphoma or carcinoma. In the ulcero-hypertrophic form, it may mimic inflammatory bowel disease. The nodal form of abdominal tuberculosis may closely mimic lymphomas. Ascitic form can be difficult to distinguish from malignant peritoneal disease and sometimes ascites due to chronic liver disease. However, a high index of suspicion needs to be maintained for an early diagnosis and timely treatment. Investigations Haematological examination may show presence of anaemia and an elevated ESR. However, these are nonspecific findings and may not aid much in diagnosis. Tuberculin test may be positive but is of not much value as it does not differentiate between an active and inactive disease. Serological tests like soluble antigen fluorescent antibody (SAFA) and enzyme-linked immunosorbent assay (ELISA) are not sensitive and are non-specific and can only suggest a probable diagnosis 8. In patient with ascites, peritoneal fluid is straw coloured with proteins more than 30g/l, cells more than 1,000/cu.mm (mostly lymphocytes), ascitic/blood glucose ratio of less than 0.96, and adenosine deaminase (ADA) levels of more than 33 U/l 9,10. Acid fast bacilli (AFB) are rarely seen on smear but may be cultured from the ascitic fluid. The yield may be increased by culturing a litre of fluid concentrated by centrifugation. Confirmation of the diagnosis of tuberculosis at any site is ideally established by demonstrating AFB on smear or mycobacterial culture from the tissue or by demonstrating caseating granulomas at histopathology. Since abdominal tuberculosis is paucibacillary, the yield of organisms is low and characteristic histological changes are taken as diagnostic. However, getting a tissue for histology may not always be possible. 170 Journal, Indian Academy of Clinical Medicine Vol. 2, No. 3 July-September 2001

Radiological investigations Play a very important role in the diagnosis of abdominal tuberculosis. Plain X ray of the abdomen, both erect and supine may show the presence of multiple air-fluid levels and dilated bowel loops which signifies presence of obstruction. The pattern of dilated bowel loops alongwith clinical symptom profile may give clues to the site of obstruction. Enteroliths may form proximal to the site of obstruction. Calcification in the lymph nodes may also be evident. A radiograph of chest may show evidence of active or healed pulmonary tuberculosis in some patients. While finding of tuberculous lesions on chest x- ray support the diagnosis of abdominal tuberculosis, a normal chest x-ray does not rule it out. Barium contrast studies are often rewarding in patients suspected to have intestinal tuberculosis. Sharp and Goldman reported barium meal followthrough examination as the best diagnostic test, demonstrating bowel lesions highly suggestive of tuberculosis such as multiple strictures and distended caecum or terminal ileum in 84% of cases 11. The other radiologic findings that may be seen on small bowel study are mucosal irregularity and rapid emptying (ulcerative), flocculation and fragmentation of barium (malabsorption), dilated loops and strictures, displaced loops (enlarged lymph nodes), and adherent fixed loops (adhesive peritoneal disease). The thickening of the ileocaecal valve lips and/or wide gaping of the valve with narrowing of the terminal ileum (Fleischner sign) has been described as characteristic of tuberculosis 12. The mucosal details possible with double contrast barium examination allows visualisation of the ulceration in the early stages of the disease. These ulcers are shallow with characteristic elevated margins. With progression, the ulcers may become confluent. In ileocaecal tuberculosis, double-contrast barium enema may show a deformed (irregular, shortened, narrowed) caecum, deformed and incompetent ileocaecal valve, dilated ileum and a distorted ileo-caecal junction with increased (obtuse) ileocaecal angle, a shortened ascending colon and an upwardly displaced caecum 13. In a study conducted by us, barium studies were helpful in 18 out of 24 (75%) patients suspected to have intestinal tuberculosis 14. Findings included dilated bowel loops, strictures, deformed and pulled-up caecum, ulceration of ileum, bowel wall thickening, and extrinsic compression by lymph nodes. Thus, contrast barium studies seem to have a good diagnostic yield, when performed in patients with suspected intestinal involvement. Imaging plays a very important role in the diagnosis of abdominal tuberculosis particularly extra-intestinal disease. Ultrasonography Ultrasonography being a widely available investigation, is now a low threshold diagnostic procedure for all patients suspected to have abdominal tuberculosis. It can accurately demonstrate small quantities of ascitic fluid and is an effective method for detection of peritoneal disease. The reported findings include multiple, thin, complete and incomplete septae, visible echogenic debris seen as fine strands or particulate matter within the fluid 15,16 (Fig. 1). These strands of septae may be due to high fibrin content of the exudative ascitic fluid. Septae have also been reported in a few cases of malignant ascites 17. Peritoneal thickening and nodularity are the other sonographic features of abdominal tuberculosis. The other conditions that may give rise to these findings are peritoneal mesothelioma, peritoneal carcinomatosis, and sometimes pyogenic peritonitis and haemoperitoneum. Omental cakes and adhesions which, in addition to peritoneal thickening, are the sonographic features of peritoneal mesothelioma can also be detected in patients with tuberculous peritonitis. However, in mesothelioma the ascites is disproportionately small in relation to the degree of tumour dissemination 18. In peritoneal mesothelioma, there Journal, Indian Academy of Clinical Medicine Vol. 2, No. 3 July-September 2001 171

may be adhesive bands between parietal peritoneum and bowel loops, but these bands are thick and immobile unlike fine mobile septae in tuberculous peritonitis. Peritoneal tubercles are usually very small and rarely detected by ultrasound. echogenicity combined with mesenteric lymphadenopathy has been reported as the characteristic sonographic feature of early abdominal tuberculosis19 (Fig. 2). Pathologically, this mesenteric thickening results from lymphadenopathy, fat deposition, and oedema due to lymphatic obstruction which makes it more echogenic 20. Omental thickening with altered echogenicity was also reported. Ultrasonography is also sensitive to detect abnormalities in intestinal tuberculosis21. The findings reported included dilated small bowel loops and bowel wall thickening. Diseased intestine is recognised as non- specific bowel wall thickening showing as a hypoechoic halo measuring more than 5 mm. Occasionally, ulceration may be visible. Ultrasonography may also be useful for guiding procedures like ascitic tap and fine needle aspiration cytology or biopsy from the lymph nodes or hypertrophic lesions. Fig. 1 : Sonogram showing loculated ascites with thin echogenic incomplete septations within. Lymphadenopathy in abdominal tuberculosis usually occurs in mesenteric, peri-pancreatic, periportal, and para-aortic groups of lymph nodes. The distribution reflects the lymphatic drainage of sites in the small bowel and liver that have been seeded haematogenously. The nodes may be seen as conglomerate masses and/or as scattered enlarged nodes with hypoechoic or anechoic centres because of necrosis. The involvement of retroperitoneal nodes and lesions not confined to one anatomic area of drainage are more suggestive of lymphoma. A thickening of the small bowel mesentery of 15 mm or more and an increase in mesenteric 172 Fig. 2 : Echogenic mesenteric thickening (within calipers) and small round lymph nodes interspersed within the mesentery. Computed tomography Though findings are nonspecific, computed tomography (CT) has an advantage over ultrasound in that it examines a range of abdominal structures. Till a few years ago, the only feature of abdominal tuberculosis reported on CT was the nonspecific appearance of high density ascites22. Over the years, a number of reports have been published highlighting the wide spectrum of abnormalities demonstrated on CT. The most common findings on CT that Journal, Indian Academy of Clinical Medicine Vol. 2, No. 3 July-September 2001

are highly suggestive of abdominal tuberculosis are high density ascites, lymphadenopathy, bowel wall thickening, and irregular soft tissue densities in the omental area23-26. Abdominal lymphadenopathy is the commonest manifestation of tuberculosis on CT. As mentioned earlier, the lymph nodes involved most commonly include mesenteric, peri-portal, peri-pancreatic, and upper para-aortic groups of nodes (Fig. 3). Fig. 4 : CECT abdomen showing multiple hypodense mesenteric nodes having enhancing peripheral rim. Fig. 3 : CT scan at the level of porta showing multiple hypodense nodes showing peripheral rim enhancement in tuberculous lymphadenitis. The contrast enhancement of tuberculous lymph nodes on contrast-enhanced CT (CECT) have been described as (four patterns) - peripheral rim enhancement, non-homogenous enhancement, homogenous enhancement and homogenous non-enhancement, in that order of frequency27. Different patterns of contrast enhancement could be seen within the same nodal group, possibly related to the different stages of the pathological process. Though not pathognomonic, the pattern of peripheral rim enhancement, could be highly suggestive of tuberculosis in an appropriate clinical setting (Fig. 4). A similar pattern can however be seen in malignant adenopathy, especially in metastasis from testicular tumours, Whipple s disease, and rarely in lymphoma following radiotherapy28. The presence of nodal calcification in the absence of a known primary tumour in Journal, Indian Academy of Clinical Medicine Vol. 2, No. 3 patients from endemic areas suggests a tubercular aetiology (Fig. 5). A study to evaluate CECT imaging criteria differentiating abdominal lymph node enlargement due to tuberculosis or lymphoma suggested some differences in the anatomic distribution and the CT enhancement patterns29. Tuberculosis predominantly involved lesser omental, mesenteric, and upper para-aortic lymph nodes whereas lower para-aortic lymph nodes were involved more often in Hodgkin s and non-hodgkin s lymphoma. Tuberculous lymphadenopathy commonly showed peripheral rim enhancement, frequently with a multilocular appearance, whereas lymphomatous adenopathy characteristically showed homogenous attenuation. Fig. 5 : Tuberculous lymphadenitis showing multiple lymph nodes at porta with amorphous calcification. July-September 2001 173

Ascites in abdominal tuberculosis can either be free or loculated. Characteristically, it is a high density ascites which could be because of high protein and cellular contents of the fluid. A similar peritoneal appearance may occur in carcinomatosis and mesothelioma. Recently, the CT features that can help in differentiating tuberculous peritonitis from peritoneal carcinomatosis have been described. A smooth peritoneum with minimal thickening and marked enhancement after contrast suggests tuberculous peritonitis whereas nodular and irregular peritoneal thickening suggests the presence of peritoneal carcinomatosis 30 (Fig. 6). Mesenteric involvement and presence of macronodules (> 5mm in diameter), a thin omental line (fibrous wall covering the infiltrated omentum), peritoneal or extraperitoneal masses with low density centres and calcification, and splenomegaly or splenic calcification have been more commonly seen with tuberculous peritonitis 31. Pelvic tuberculous peritonitis can sometimes mimic pelvic inflammatory disease. The diagnosis of tuberculosis is suggestive when loculated fluid collections are detected in the presence of omental infiltration, peritoneal enhancement, transperitoneal reaction, and mesenteric or bowel involvement. Bowel wall thickening is a non-specific manifestation of abdominal tuberculosis. The most common CT finding is a mural thickening affecting the ileocaecal region, either limited to terminal ileum, caecum, or both the regions (Fig. 7). Though nonspecific, when associated with other suggestive features, it can be helpful in diagnosis of abdominal tuberculosis. Diffuse bowel wall thickening can also occur due to intestinal involvement by lymphomas. The other CT features reported to be highly suggestive of abdominal tuberculosis are irregular soft tissue densities in the omental area, low density masses surrounded by thick solid rims, and a disorganized appearance of soft tissue densities, fluid and bowel loops forming a poorly defined mass 23. Involvement of the liver and spleen in miliary tuberculosis may appear on CT as tiny low density foci widely scattered throughout the organ. The macronodular form of hepatosplenic tuberculosis may be seen as multiple low attenuation (15-50 HU), 1-3 cm round lesions or simple tumour like masses. The lesions may show peripheral enhancement after i-v contrast administration 32. The tuberculous involvement of the pancreas may show as well defined hypoechoic areas on ultrasonography and as hypodense necrotic regions within the enlarged pancreas 13. Our study on the role of ultrasonography and CT abdomen in abdominal tuberculosis suggested that CT was more accurate than ultrasound in Fig. 6 : An axial scan through pelvis showing presence of free ascites surrounded by smoothly thickened and enhancing peritoneum. Fig. 7 : CECT abdomen showing diffuse circumferential mural thickening of caecum. 174 Journal, Indian Academy of Clinical Medicine Vol. 2, No. 3 July-September 2001

detecting abnormalities like peri-portal and peripancreatic lymph nodes, and bowel wall thickening 11. This may be due to the disturbance of the sonographic window by bowel gas. However, bowel wall dilatation was better appreciated on ultrasound than CT scan. Therefore, while CT appears to be more sensitive and specific, ultrasound has the advantage of being less expensive, widely available, and easy to perform. Knowledge about the utility of magnetic resonance imaging (MRI) in abdominal tuberculosis is very limited. MRI when compared to CT added no additional information 33. Endoscopy may be useful in cases of GI tuberculosis where lesions are accessible. Endoscopic appearances in tuberculosis include hyperaemic nodular friable mucosa, irregular ulcers with sharply defined margins and undermined edges, and pseudopolyps. These may mimic inflammatory bowel disease and malignancy. Endoscopic biopsy may not reveal granulomas in all cases, as the lesions are submucosal 34. Biopsies from the edges and the base of the ulcer or multiple biopsies from the same site may increase the yield. Endoscopic biopsy specimens may be subjected to polymerase chain reaction for detection of AFB 35. In peritoneal tuberculosis, laparoscopic appearances of thickened peritoneum alongwith whitish to yellowish miliary tubercles studded over the peritoneum and other viscera have been found to be more helpful in diagnosis of tuberculosis than either histological or bacteriological examination 36. Reports have described a number of patients in whom tuberculosis could not be diagnosed during life but was revealed only at necropsy 37,38. This occurs mostly when there are small intestinal strictures which are not amenable to endoscopic biopsies or adhesive peritoneal lesions where ascitic tap or laparoscopic biopsy cannot be performed. Therapeutic trial of antitubercular treatment (ATT) is recommended by some authors in suspected cases of abdominal tuberculosis, when diagnosis cannot be proven. However, sometimes it may lead to a delay in diagnosis and treatment of conditions like malignancy, lymphoma, and Crohn s disease which can mimic tuberculosis clinically and radiologically. Recurrence of obstructive symptoms requiring surgery has been observed in some patients who were put on ATT for obstructive symptoms 20. In circumstances where clinical suspicion is strong, but results of investigations are equivocal, a diagnostic laparatomy may be a safer option. This may allow concurrent treatment of intestinal lesions. The imaging has proven to be a very useful modality for diagnosis of extra-intestinal disease. Where clinical suspicion is strong and imaging features are suggestive, a therapeutic trial of ATT may be justified. However, laparotomy is definitely indicated where malignancy cannot be ruled out with certainty. In many patients, it may not be possible to rule out malignancy even at laparotomy. A frozen section examination may help in such cases. A mesenteric lymph node should always be removed in such cases as caseation and granulomas are much more likely to be present in lymph nodes than intestinal lesions 4,20. Management All patients with abdominal tuberculosis should be given standard full course of ATT. Conventional regimens suggest ATT for 12 to 18 months 39. However, the use of short course regimens for 6-9 months have been found to be equally effective 40. Patients with peritoneal, nodal, or ulcerative intestinal disease are usually treated with drugs (ATT). Some authors have recommended the addition of corticosteroids in patients with peritoneal disease in order to reduce subsequent complications of adhesions 41. No controlled studies have been performed to show their benefit. Patients with intestinal obstruction due to strictures and hypertrophic lesions require surgical treatment 42. However, some reports have shown successful treatment of obstructing intestinal Journal, Indian Academy of Clinical Medicine Vol. 2, No. 3 July-September 2001 175

lesions with ATT alone 40,43. Though patients usually report improvement in systemic symptoms in few weeks, relief of intestinal symptoms may require a much longer duration. A number of patients with abdominal tuberculosis who present with acute abdomen require emergency surgical intervention 44. Subacute intestinal obstruction or acute-on-chronic obstruction responds usually to conservative management and patients can be investigated later and managed electively. The surgical procedures recommended presently for the management of intestinal tuberculosis are largely conservative, as it is a systemic disease. A number of surgical procedures are recommended depending upon the type and extent of intestinal lesions 45. A description of these is beyond the scope of this article. Despite being a treatable disease, abdominal tuberculosis carries a mortality of 4-12% which is largely due to associated problems of malnutrition, anaemia, and hypoalbuminaemia and due to acute complications. A high clinical index of suspicion and judicious use of diagnostic procedures can certainly help in timely diagnosis and treatment and thus reduce the mortality of this curable but potentially lethal disease 46. References 1. Kahana LM. The modern face of tuberculosis. Can J Surg 1986; 29: 393-4. 2. Goldman KP. AIDS and tuberculosis. Tubercle 1988; 69: 71-2. 3. Anonymous. Management of non-respiratory tuberculosis. Lancet 1986; 1: 1423-4. 4. Bhansali SK. Abdominal tuberculosis. Experience with 300 cases. Am J Gastroenterol 1977; 67: 324-37. 5. Vij JC, Malhotra V, Choudhary V et al. A Clinico-pathological study of abdominal tuberculosis. Indian J Tuberculosis 1992; 39: 213-20. 6. Sharma AK, Aggarwal LD, Sharma CS, Sarin YK. Abdominal tuberculosis in children: Experience over a decade. Indian Paediatr 1993; 30: 1149-53. 7. Tandon RK, Sarin SK, Bose SL, Berry M, Tandon BN. A Clinico-radiological reappraisal of intestinal tuberculosischanging porofile? Gastroenterol Jpn 1986; 21: 17-22. 8. Bhargava DK, Dasarathy S, Shriniwas et al. Evaluation of enzyme-linked immunosorbent assay using mycobacterial saline-extracted antigen for the serodiagnosis of abdominal tuberculosis. Am J Gastroenterol 1992; 87:105-8. 9. Wilkins EGL. Tuberculous peritonitis: diagnostic value of the ascitic/blood glucose ratio. Tubercle 1984; 65: 47-52. 10. Dwivedi M, Misra SP, Misra V, Kumar R. Value of adenosine deaminase estimation in the diagnosis of tubercuous ascites. Am J Gastroenterol 1990; 85: 1123-5. 11. Sharp JF, Goldman M. Abdominal tuberculosis in East Birmingham: A 16 year study. Postgrad Med J 1987; 63: 539-42. 12. Carera GF, Young S, Lewicki AM. Intestinal tuberculosis. Gastrointest Radiol 1976; 1: 147-55. 13. Kapoor VK, Chattopadhyay TK, Sharma LK. Radiology of abdominal tuberculosis. Australas Radiol 1988; 32: 365-7. 14. Baba CS, Sood R, Jain R, Sharma MP. Clinico-pathological spectrum of abdominal tuberculosis and usefulness of ultrasound and computed tomograhy in its diagnosis. Thesis for MD Medicine, AIIMS, New Delhi, 1999 (personal communication). 15. Gompels BM, Darlington LG. Ultrasonic diagnosis of tuberculous peritonitis. Br J Radiol 1979; 51: 1018-9. 16. Denton T, Hossain. A radiological study of abdominal tuberculosis in a Saudi population, with special reference to ultrasound and computed tomography. Clinical Radiology 1993; 47: 409-14. 17. Kedar RP, Shah PP, Shivde RS, Malde HM. Sonographic findings in gastrointestinal and peritoneal tuberculosis. Clin Radiol 1994; 49: 24-9. 18. Reuter K, Ratopoulas V, Reale F et al. Diagnosis of peritoneal mesothelioma-computed tomography, sonography and find needle aspiration biopsy. AJR 1983; 140: 1189-94. 19. Jain R, Sawhney S, Bhargava DK, Berry M. Diagnosis of abdominal tuberculosis: sonographic findings in patients with early disease. AJR 1995; 165: 1391-5. 20. Tandon HD, Prakash A. Pathology of intestinal tuberculosis and its distinction from Crohn s disease. Gut 1972; 13: 260-9. 21. Lee DH, Ko YT, Yoon Y, Lim JH. Sonographic findings of intestinal tuberculosis. J Ultrasound Med 1993; 12: 537-40. 22. Stanley RJ. Fluid characterization with computed tomography in: Moss AA, Goldberg HI (eds) Computed tomography, ultrasound and x ray: an integrated approach. New York: Academic Press, 1980: 65-6. 23. Epstein BM, Mann JH. CT of abdominal tuberculosis. AJR 1982; 139: 861-6. 24. Hulnick DH, Megibow AJ, Naidich DP et al. Abdominal tuberculosis: CT evaluation. Radiology 1985; 157: 199-204. 25. Bankier AA, Fleischmann D, Weismayr MN et al. Update: Abdominal tuberculosis unusual findings on CT. Clinical Radiology 1995; 50: 223-8. 26. Suri S, Gupta S, Suri R. Computed tomography in abdominal tuberculosis - pictorial review. Br J Radiol 1999; 72: 92-8. 27. Pombo F, Rodriguez E, Mato J et al. Patterns of contrast enhancement of tuberculous lymph nodes demonstrated by computed tomography. Clinical Radiology 1992; 46: 13-7. 28. Scatarige JC, Fishman EK, Kerhajdr FP et al. Low attenuation nodal metastasis in testicular carcinoma. JCAT 1983; 7: 682-7. 29. Yang ZG, Min PQ, Sone S et al. Tuberculosis versus lymphomas in the abdominal lymph nodes: evaluation with contrast-enhanced CT. AJR 1999; 172: 619-23. 30. Rodriguez E, Pombo F. Peritoneal tuberculosis versus peritoneal carcinomatosis: Distinction based on CT findings. JCAT 1996; 20: 269-72. 176 Journal, Indian Academy of Clinical Medicine Vol. 2, No. 3 July-September 2001

31. Ha HK, Jung HL, Lee MS et al. CT differentiation of tuberculous peritonitis and peritoneal carcinomatosis. AJR 1996; 167: 743-8. 32. Buxi TBS, Vohra RB, Sujatha Y et al. CT appearances in macronodular hepatosplenic tuberculosis: A review with additional new cases. Comput Med Imag Graph 1992; 16: 381-7. 33. Zirinsky K, Auh YH, Kneeland JB et al. Computed tomography, sonography and MR imaging of abdominal tuberculosis. JCAT 1985; 9: 961-3. 34. Singh V, Kumar P, Kamal J et al. Clinico-colonoscopic profile of colonic tuberculosis. Am J Gastroenterol 1996; 91: 565-8. 35. Anand BS, Schneider FE, EI-Zaatari FA et al. Diagnosis of intestinal tuberculosis by polymerase chain reaction on endoscopic biopsy specimens. Am J Gastroenterol 1994; 89: 2248-9. 36. Bhargava DK, Shriniwas, Chopra P et al. Peritoneal tuberculosis : laparoscopic pattern and its diagnostic accuracy. Am J Gastroenterol 1992; 87: 109-12. 37. Klimach OE, Ormerod LP. Gastrointestinal tuberculosis : A retrospective review of 109 cases in a district general hospital. Q J Med 1985; 56: 569-78. 38. Palmar KR, Patil JH, Basran S et al. Abdominal tuberculosis in urban Britain : A common disease. Gut 1985; 26: 1296-305. 39. Cooke NJ. Treatment of tuberculosis. BMJ 1985; 291: 497-8. 40. Balasubramanian R, Ramachandran R, Joseph P et al. Interim results of a clinical study of abdominal tuberculosis. Indian J Tubercul 1989; 36: 117-21. 41. Singh MM, Bhargava AN, Jain KP. Tuberculous peritonitis. An evaluation of pathogenic mechanisms, diagnostic procedures and therapeutic measures. N Engl J Med 1969; 281: 1091-94. 42. Kapoor VK, Sharma LK. Abdominal tuberculosis. Br J Surg 1988; 75: 2-3. 43. Anand BS, Nanda R, Sachdev K. Response of tuberculous strictures to antituberculous treatment. Gut 1988; 29: 62-9. 44. Kapoor VK, Gupta S, Sikora SS et al. Acute tubercular abdomen. Indian J Surg 1991; 55: 71-5. 45. Kapoor VK. Abdominal tuberculosis classic disease revisited. Postgrad Med J 1998; 74: 459-67. 46. Lingenfelser T, Zak J, Marks IN et al. Abdominal tuberculosis: still a potentially lethal disease. Am J Gastroenterol 1993; 88: 744-50. Journal, Indian Academy of Clinical Medicine Vol. 2, No. 3 July-September 2001 177