The term abdominal tuberculosis includes tuberculous infection of the gastrointestinal tract, the mesentry, its nodes, and omentum, the peritoneum, and the solid organs related to the gastrointestinal tract, such as the liver and spleen. Genitourinary tuberculosis, which itself is a separate entity is not discussed here.

Abdominal tuberculosis is rare in the Western population and is declining in incidence in certain parts of India. In developed countries the disease is largely limited to immigrants from areas of the world endemic for tuberculosis. Strict control of tuberculosis in dairy herds and pasteurization of milk have almost eliminated bovine tuberculosis in many countries; however, despite efforts aimed at effective treatment of tuberculosis, the disease is not uncommon in developing countries.

Tuberculosis was recognized as early as the fourth century bc, and was known as phthisis, lupus, scrofula, or Pott's disease, until the identity was established by Robert Koch in 1882. Hippocrates stated that ‘phthisical persons die if diarrhoea sets in and it is a mortal symptom’; the severity of intestinal tuberculosis was known even at that time.

Mycobacterium tuberculosis causes almost all cases of abdominal tuberculosis in developed nations. The other pathogenic species, Mycobacterium bovis has been largely eliminated by public health measures and is rarely encountered. The tubercle bacillus is a Gram-positive, aerobic, non-motile, non-spore bearing organism, and it is identified by the Ziehl - Neelson acid-fast differential staining method. The organism is cultured in Lowenstein - Jensen medium for 4 weeks. Several other atypical or anonymous mycobacteria whose pathogenicity is not yet established have been identified. The virulence of Mycobacterium tuberculosis is established by guinea-pig inoculation.

Intestinal tuberculosis has been found in 6 to 90 per cent of patients with pulmonary tuberculosis. Intestinal infection is more prevalent in populations from lower socioeconomic strata, contributing factors being poor hygiene, crowded living conditions and poor nutrition. The incidence is higher in those with caseo-pneumonic and late disease than in those with fibrotic lesions or early disease. There is a sharp contrast in the incidence of intestinal tuberculosis between the West and India: 15 of 4222 patients admitted to the University of Michigan for tuberculosis had intestinal tuberculosis over a 22-year period, compared to 300 cases over 14 years in one Indian series, and 557 cases over 12 years in another series.

Tuberculosis may spread to abdomen by several routes. Ingestion of food contaminated with bacilli may cause primary intestinal tuberculosis. The incidence of this route of infection is decreasing. Secondary intestinal disease arises from swallowed sputum containing the bacilli. Its development is influenced by the virulence and quantity of bacilli ingested and the resistance of the individual to the bacilli. The peritoneum and mesenteric nodes and the intestine may become infected during the bacteraemic phase that can occur during primary pulmonary tuberculosis. The infecting bacteria may also spread from infected adjacent organs, such as the fallopian tube. When the intestine becomes infected by retrograde lymphatic spread from the mesenteric lymph nodes, the nodal disease is considered to be primary and intestinal involvement secondary. This is supported by the fact that the early intestinal lesion is usually found in the submucosa, overlying mucosa being normal. In addition, more advanced lesions with caseation are found often in the mesenteric node rather than in the intestine. The bacteria may also be disseminated in the bile, as they are sequestrated and excreted or excreted from granuloma in the liver.

The terminal ileum and ileocaecal junction are the sites most commonly affected by tuberculosis. The other regions to be affected are, in decreasing order of frequency, colon, jejunum, rectum and anal canal, duodenum, stomach, and oesophagus. The site of predilection is dictated by the abundance of lympoid tissue, rate of absorption of the intestinal contents, prolonged stasis, providing longer time of contact with mucosa, and reduced digestive activity.

Intestinal ulcers are usually deep and transversely placed in the direction of the lymphatics. Multiple ulcers are commonly seen in the ileum with normal areas in between. The slow progression of the ulcer is associated with the appearance of an inflammatory mass around the bowel. The infected part of the gut is thickened and the serosal surface is studded with tubercles. There is often a marked increase in mesenteric fat, with fat wrapping around the bowel. The regional nodes become enlarged and may caseate, leading to mesenteric abscess formation. Perforation is rare; when it occurs it is often confined by the perilesional inflammatory mass.

In hyperplastic intestinal tuberculosis, a fibroblastic reaction occurs in the submucosa and subserosa, resulting in thickening of the bowel. Along with the adjacent mesentery, lymph nodes, and omentum this forms a mass. The hyperplastic lesion may develop as a result of reduced virulence of the organism and increased host resistance.

The sclerotic variety is associated with strictures of the intestine (napkin ring strictures) which may be single or multiple. When multiple they occur either in a short segment or over the entire small intestine. Enteroliths can form proximal to the stricture. A combination of all these forms can also occur.

Acute peritonitis due to tuberculosis is very rare and occurs as part of the miliary form of the disease, following perforation of intestinal disease or following dissemination from a ruptured caseating mesenteric lymph node.

The chronic form initially presents as ascites. The fluid which is often straw coloured, but may be sanguinous, presents as a cyst when localized. Flimsy or dense adhesions and miliary nodules also occur. When the nodules increase in size and coalesce, plastic adhesions develop and may completely obliterate the peritoneal cavity, forming an abdominal cocoon encasing the intestine. The omentum thickens to form a transversely placed mass, the so-called ‘rolled up omentum’.

The typical histological feature is caseating granulomas, which may be large and confluent, in the bowel, mesenteric nodes, or both. The granulomas have a peripheral zone of lymphocytes, plasma cells, and Langhans giant cells with a central zone necrosis. Healing of the granulomas is associated with mucosal regeneration.

The clinical features of abdominal tuberculosis are vague and non-specific: this is particularly true of peritoneal tuberculosis. When the intestine is involved the patient may present with gastrointestinal symptoms.

Abdominal tuberculosis is commonly found in patients between the ages of 30 and 50. Females outnumber males by 2:1.

The symptoms of chronic abdominal tuberculosis are insidious, and include fever, which may be present in two-thirds of patients, night sweats, malaise, weakness, anorexia, and weight loss. Abdominal pain is often vague and dull. When colicky it suggests intestinal obstruction. The pain is more often felt in the right lower quadrant of abdomen and is often exacerbated by eating. Diarrhoea and occasionally vomiting tend to relieve the discomfort, which recurs later. The stool is often watery and foul smelling. Other symptoms include flatulence, nausea, altered bowel habits, and borborygmi. Abdominal distension, if present, may be due to ascites or intestinal obstruction. Features which resemble duodenal ulcer may occur when the duodenum is affected. Bleeding from the rectum or haematemesis is rare. Gastrointestinal haemorrhage is occasionally severe and may be life-threatening. Patients with intestinal involvement may also present with acute symptoms due to intestinal obstruction, perforation, or gangrene.

Patients with chronic symptoms are often malnourished, anaemic, and chronically ill. The abdomen usually feels normal or distended, and tenderness is often noted in the right lower quadrant. Peristalsis may be visible and distended loops of intestine are sometimes felt. If rolled up omentum is present it can be felt as a transversely placed mass in the epigastric region. An ileocaecal mass may be palpable high in the right iliac fossa or in the lumber region. Shifting dullness and fluid thrill indicate the presence of ascites, while affected colon feels diffusely thick and tender. Loculated ascites, mesenteric cyst, and mesenteric abscess present as cystic mass. Hepatomegaly is noted in some patients. Rectal examination may reveal anal fistulae, fissures, or stricture.

Intestinal obstruction is common, but perforation and massive gastrointestinal haemorrhage are uncommon. Perforation is usually confined, but free perforation can occur. Fistulae, either internal or external, are relatively rare.

Abdominal tuberculosis is often associated with amoebiasis, helminthiasis, cirrhosis, and sometimes peptic ulcer. These diseases add to the vagaries in presentation, may delay diagnosis, and complicate the effects of the tuberculosis.

Tuberculous lesions of the small bowel must be differentiated from enteric fever, amoebiasis, appendicitis, lymphoma, carcinoma, and malabsorption syndrome. Large bowel tuberculosis must be differentiated from amoebiasis, appendicular mass, carcinoma, ischaemic structure, granulomatous colitis of other causes, and diverticulitis. Malignancy, lymphogranuloma venereum, and mycotic disease are other possible causes of rectal lesions. Miliary peritoneal tuberculosis must be differentiated from carcinomatosis peritonei. Other causes of ascites include cirrhosis and disseminated intra-abdominal malignancy. Abdominal tuberculosis is often associated with alcoholic liver disease. Intestinal tuberculosis resembles Crohn's disease in many ways and distinction is often difficult. The features listed in Table 2 631 may help in the differentiation.

Haematological investigations disclose varying degrees of anaemia, leucopenia with relative lymphocytosis, and a raised ESR. The Mantoux test is usually strongly positive. Intestinal involvement may result inthe passage of occult blood. Evidence of tuberculosis is seen on chest radiographs in one-third of patients. Plain radiograph of the abdomen may show calcified nodes or multiple fluid levels.

Barium meal series, barium enema, and small bowel enemata (enteroclysis) are useful investigative procedures in the diagnosis of gastrointestinal tuberculosis. Barium swallow may show compression of the oesophagus by a mediastinal node, and ulceration. Altered motility and irritability of the small intestine are amongst the earliest signs.

Localized areas of irregular, thick, distorted, and angulated folds, filling defects, and dilated loops and areas of stenosis may be seen in small bowel disease. Internal or external fistulae are less common.

The caecum and ascending colon are contracted and irregular, and straightening of the ileocaecal junction occurs in ileocaecal tuberculosis. A cocoon may form, and barium enema may show colonic or rectal stricture. Rapid transit and lack of barium retention in an inflamed segment of small bowel (Sherlin's sign) may accompany ulcerative lesions of the intestine. A thin linear barium streak (string sign) may be a sign of small bowel stenosis. Small bowel biopsy is sometimes useful. Samples for bacteriological and histological examination can be obtained from the large bowel and upper gastrointestinal tract by endoscopy. Colonoscopy may reveal ulcerating lesions in the caecum and ascending colon and constricting lesions of the colon; these may resemble malignancy of the colon. Biopsy of these lesions may reveal caseating granulomas and tubercle bacilli. It is important to realize that malignancy may coexist with tuberculosis.

Ultrasonography or CT scan may disclose either generalized or loculated ascites, mesenteric or intestinal mass, thickening of the ileum, caecum, or colon, or dilated loops of intestine. Analysis and culture of ascitic fluid and guinea-pig inoculation will establish the diagnosis. The protein content of ascitic fluid is usually more than 3 g/dl unless cirrhosis is present, and lymphocytosis is present. The tubercle bacillus is seldom found on staining. Needle biopsy specimens of the peritoneum may be useful.

This is very useful in the diagnosis of abdominal tuberculosis. It allows typical miliary nodules to be visualized, and enables material to be collected for histopathological examination. Involvement of the intestine, liver, omentum, and other abdominal organs can be assessed. This procedure may be hazardous when dense adhesions are present.

Antituberculous chemotherapy should be instituted in all cases of abdominal tuberculosis. The drugs most often used are isonicotinic acid hydrazide, streptomycin, ethambutol, pyrazinamide, and rifampicin. The standard regimen is streptomycin (15 - 20 mg/kg intramuscularly daily for 2 months), ethambutol (25 mg/kg for 2 weeks followed by 15 mg/kg for 12 - 18 months orally), and isoniazid (7 - 10 mg/kg for 12 - 18 months orally).

Short-term chemotherapy with rifampicin (10 mg/kg daily), isoniazid ((INH) 7 - 10 mg/kg), and pyrazinamide (30 mg/kg) daily for 2 months orally followed by rifampicin and isoniazid daily for a further 4 months is currently being evaluated. At present the antituberculosis regimen recommended by the World Health Organization and the International Union against Tuberculosis and Lung Diseases is isoniazid (300 mg daily), rifampicin (450 mg daily) pyrazinamide (1.5 g daily orally), and streptomycin (0.75 g intramuscularly daily) or ethambutol (25 mg/kg daily orally) for 2 months followed by isoniazid (600 mg) and rifampicin (600 mg) twice weekly orally for 4 months for an individual of weight 40 - 60 kg (Table 3) 632. The patient is monitered periodically, especially for hepatotoxicity. Pyridoxine hydrochloride (5 - 10 mg/day) must be given along with isoniazid to prevent peripheral neuropathy.

General management includes rest, a high protein diet, parenteral nutrition in selected malnourished patients, and other symptomatic therapy. When obstruction or perforation is present release of adhesions or resection and anastomosis of damaged bowel is warranted.

Surgery is reserved for complications and for those in whom medical treatment fails. Indications for surgery include intestinal obstruction due to single or multiple strictures, adhesions, mass, or rarely due to cocoon formation; intra-abdominal abscess due to confined perforation or mesenteric abscess; internal or external enteric fistulae (leading to malnutrition); free perforation of tuberculous ulcer; and massive haemorrhage. Surgery may also be appropriate when the diagnosis cannot be confirmed with reasonable accuracy or when malignancy could not be ruled out or may coexist.

Limited right hemicolectomy with ileocolic anastomosis is the procedure of choice for ileocaecal tuberculosis. Ileal or jejunal disease is treated by limited segmental resection with end-to-end anastomosis. A short segment containing multiple structures should be resected; stricturoplasty is ideal for the treatment of supple strictures of the small bowel, especially when multiple strictures are present. Extensive resection will result in the short bowel syndrome. Ileocaecoplasty and coloplasty are also advocated for ileocaecal and colonic strictures, respectively.

Bypassing the obstruction by ileotransverse anastomosis has almost no place in tuberculosis, as it causes blind loop syndrome and worsens the condition. This may, however, be performed as a life-saving measure in a patient in poor general condition who develops acute intestinal obstruction. Recurrent adhesive obstructions and enterocutaneous fistula are treated by release of adhesions, drainage of abscess, resection of the fistulous site, and intestinal anastomosis. Small bowel stenting and laparotomy are required if florid sepsis is present; this is followed by closure of the abdomen later. These measures may help prevent recurrent adhesions and reduce postoperative morbidity and mortality.

When intestinal obstruction is due to cocoon formation, release of the intestine by removing the membrane is curative. This must be performed with great care, and limited resection of the small bowel may be needed if release of adhesions is not possible. In plastic forms of the disease, even entry into the peritoneal cavity may become impossible. ‘Second-look surgery’ may be needed after antituberculous therapy.

An incidence of 0.1 to 3 per cent has been reported for tuberculosis of the appendix. Isolated tuberculosis of the appendix is rare; appendicectomy followed by antituberculosis chemotherapy is the treatment of choice.

Limited surgical resection of the involved segment is the treatment of choice. When malignancy cannot be ruled out, resection should be performed as for malignancy.

In the patient with anal canal tuberculosis who presents with multiple fistulae, fissure, or perineal abscesses, simple surgical procedures such as drainage of the abscess should be combined with antituberculosis chemotherapy.

Involvement of the stomach by tuberculosis is rare, occurring in about 0.3 to 2.3 per cent of patients with pulmonary tuberculosis. The rarity is probably due to the resistance of the gastric mucosa, lack of lymphoid tissue in the stomach, and the constant movement of chyme in the stomach. Tuberculous lesions in stomach may assume an ulcerative, granulomatous, or fibrosing form. The last two types may present with gastric outlet obstruction. Endoscopic biopsy confirms the diagnosis, although it is often mistaken for peptic ulcer disease or gastric carcinoma. Carcinoma may coexist.

Antituberculous treatment and surgical intervention in the form of limited resection, when gastric outlet obstruction is present or when malignancy cannot be excluded, produces excellent results in gastric tuberculosis.

Hepatic tuberculosis is very rare, but may be detected during autopsy, laparoscopy, or abdominal exploration in patients with tuberculosis of the abdomen. The lesions produced are granulomas, large caseating lesion, a calcified mass, or biliary strictures. A tuberculous periportal lymph node can cause obstructive jaundice by compressing the bile duct. The patient usually presents with hepatomegaly, with or without jaundice. Symptoms due to abdominal tuberculosis may overshadow those due to the liver disease. Liver function tests, particularly alkaline phosphatase levels, may be abnormal. The condition must be differentiated from many other conditions which can cause non-caseating hepatic granulomas, including leprosy, sarcoidosis, Hodgkin's disease, brucellosis, infectious mononucleosis, inflammatory bowel disease, drug-induced liver damage, and syphilis. Chronic active hepatitis can also mimic tuberculosis of the liver. Splenic tuberculosis is rare and may present as hypersplenism or splenic abscess. It is usually diagnosed on histopathological examination of a spleen excised for abscess.

The treatment relies on chemotherapy; however most antituberculous drugs (except ethambutol) are hepatotoxic and may induce liver damage and jaundice. The response and toxicity must therefore be assessed carefully during therapy.

The prognosis of uncomplicated abdominal tuberculosis is good. Most patients who undergo effective surgical management of complications respond well. Obstruction or perforation associated with plastic adhesions and development of enterocutaneous fistulae with intra-abdominal abscesses are associated with morbidity and poor prognosis.

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