The incidence of tuberculosis of the small intestine is high in developing countries and has increased in developed countries because of the acquired immunodeficiency syndrome. Mycobacterium tuberculosis is the cause of virtually all cases of intestinal tuberculosis. Much of the clinical problem of this condition has been discussed in Section 41.3 126 but special aspects of tuberculosis of the small intestine are worthy of reiteration.

In countries where tuberculosis is common, such as India, the disease affects the young (mean age 26; female:male ratio 2:1), where in the United States of America older people tend to be affected (mean age 44; male:female ratio 3:2). A higher index of suspicion might account for the detection of tuberculosis in the younger age group in developing countries.

In the United States, tuberculosis tends to occur in residents of shelters for the homeless, and nursing homes, and among AIDS patients. About 36 per cent of AIDS patients develop tuberculosis, which is usually extrapulmonary; about 40 per cent of cases are caused by the Mycobacterium avium intracellulare complex. A genetic predisposition to intestinal tuberculosis is present in about 2 per cent of patients.

Intestinal tuberculosis can occur either primarily or secondary to a tuberculous focus at a different site. Primary intestinal tuberculosis caused by the bovine strain has become rare with the widespread pasteurization of milk; secondary intestinal tuberculosis is more common and is usually due to ingestion of infected sputum. The tubercle bacillus is protected against digestion in the stomach by its fatty capsule, and it therefore enters the small bowel, infecting the ileum (ileocaecal area), jejunum, and duodenum, in decreasing order of frequency. The abundance of lymphoid tissue, stasis, and minimal digestion of the bacteria are possible reasons for the higher incidence of tuberculosis in the ileum. Haematogenous spread to the intestine occurs in miliary tuberculosis, and enteric tuberculosis can also be a result of spread from adjacent organs. Quiescent tubercle bacilli can become activated if host immunity decreases.

Thirty per cent of patients suffer from the ulcerative form of the disease, usually occurring in the jejunum. The ulcers are transverse and circumferential, with irregular margins and shaggy bases. The hypertrophic form usually occurs in the ileum and ileocaecal area and accounts for 70 per cent of cases. It is the result of fibroblastic reaction to the tubercle bacilli. The ulcerohypertrophic and annular forms are rare, and the latter mimics carcinoma. The tendency to develop hypertrophic lesions increases with fewer infecting organisms, a low virulence of infecting organisms, and increasing immunity of the host.

Caseation necrosis surrounded by chronic inflammatory tissue is the hallmark of tuberculosis: the presence of caseation differentiates tuberculosis from the granuloma of Crohn's disease. Langerhan's giant cells may also be present. The characteristic histopathology is seen more often in the affected lymph nodes than in the bowel.

The symptoms of intestinal tuberculosis are non-specific, the most common being generalized or localized abdominal pain. Other symptoms include weight loss, night sweats, fever, vomiting, weakness, diarrhoea, constipation or bleeding per rectum. Diarrhoea is more common in the presence of ulcerative lesions. Abdominal cramps with loud borborygmi occur because of partial intestinal obstruction due to strictures. Perforation presents as acute abdominal pain. Duodenal tuberculosis simulates peptic ulcer or presents as gastric outlet obstruction.

Abdominal tenderness is the most frequent sign, affecting 67 per cent of patients and is usually in the right lower quadrant. There is muscle guarding and rebound tenderness if peritonitis is present. A tender fixed mass, formed of hypertrophic tissue, matted nodes, adherent omentum, and brawny mesentery, is palpable in 33 per cent of patients with ileocaecal tuberculosis. Abdominal distension and vigorous intestinal peristalsis are seen in patients with partial intestinal obstruction. Generalized or localized ascites are present in about 50 per cent of patients.

Acute or chronic obstruction from stricture, adhesions, or both is the most common complication, affecting 30 per cent of patients. Perforation with peritonitis develops in 5 per cent of patients, usually in the ileum proximal to a stricture. Perforation often develops when patients are on chemotherapy. Confined perforation with an intra-abdominal abscess is an occasional complication. Fistulae (2 - 20 per cent of patients) between loops of bowel, between the bowel and the skin, and between adjacent organs such as the bladder and female adnexa sometimes occur. Malabsorption from lymphatic obstruction and bacterial overgrowth secondary to stasis is occasionally seen, while intestinal bleeding and traction diverticula are rare.

Anaemia, lymphocytosis, and an elevated erythrocyte sedimentation rate are common in patients with tuberculosis. Although positive tuberculin test indicates infection, it does not establish the pressure of an active process; a negative tuberculin test may occur in infected immunocompromised patients. Stool samples are rarely positive for acid-fast bacilli.

Chest radiography may show evidence of tuberculosis, but a negative chest radiograph does not exclude the diagnosis. An abdominal radiograph may show dilated loops with fluid levels, calcification of mesentric lymph nodes, dilatation of terminal ileum, and ascites.

Barium enema and barium meal examinations help in the diagnosis of ileocaecal lesions and jejunoileal intestinal lesions. The earliest manifestations of intestinal tuberculosis is dysmotility of the small bowel. Later, lack of barium in the diseased segment with columns of barium retained in proximal and distal segments can be seen. Barium retention proximally is a result of obstruction by the diseased segment; hyperirritability causes poor retention of barium retention in the diseased segment. There may be persistent narrowing and irregularity of distal ileum (string sign). This also occurs in Crohn's disease. Distortion of the caecum, with gaping of the ileocaecal valve due to fibrosis, causes a triangular shaped deformity of terminal ileum with its base towards the caecum (Fleischner's sign). This sign is uncommon in Crohn's disease.

Lymphangiography will disclose involvement of mesentric lymph nodes, while angiography shows hyperaemic nodes adjacent to diseased intestine; this picture is not found in Crohn's disease.

Sonography may disclose ascites and multiple interlacing septations, while CT scanning has been used to detect thickening of ileum, caecum, mesentry, and peritoneum; enlarged nodes with central low density as a result of caseation; omental masses; and high density ascites. CT can be helpful in ruling out the presence of a neoplasm and in observing resolution of disease during chemotherapy.

Gallium citrate scans detect serosal inflammation and peritonitis while colonoscopy may reveal nodular lesions in the ileocaecal area.

Laparoscopy may disclose numerous tubercles studding on the peritoneal surface. Tissue for histopathological and bacteriological study can be obtained by percutaneous, laparoscopic, colonoscopic, or open peritoneal biopsy.

An ascitic fluid tap shows clear straw-coloured or turbid or haemorrhagic fluid with a specific gravity usually above 1.016, lymphocytes above 1000/ml, protein above 25 g/l with a serum: ascites albumin ratio less than 1.1, increased adenosine deaminase (mean 112 U/l) and an ascites: blood glucose ratio less than 0.96.

Serum antibodies can be detected by the enzyme linked immunosorbent assay or by the soluble antigen fluorescent antibody test.

The differential diagnosis includes inflammatory diseases such as Crohn's disease, and appendicular abscess, infections including Yersinia enterocolitis, herpes, cytomegalovirus, amoebiasis, actinomycosis, and histoplasmosis, and neoplasms such as adenocarcinoma, carcinoid, and lymphoma.

The definite diagnosis of tuberculosis can be made by demonstration of M. tuberculosis in the lesion, growth of tubercle bacilli in culture or animal inoculation, or the presence of typical histopathological findings.

Enteric tuberculosis is treated medically; surgery is reserved for complications.

Isoniazid (300 mg) and rifampin (600 mg) daily for 18 to 24 months is the regimen of choice. When the sputum reveals large numbers of acid-fast bacilli, streptomycin 1 g/day for 2 to 3 months is recommended. In patients with tuberculous peritonitis, the addition of steroids to the antituberculosis regimen may help prevent adhesions.

Acute intestinal obstruction, perforation, and peritonitis are treated conservatively, if possible. Operations undertaken during the acute stage carry a high mortality rate.

When the diagnosis of tuberculous enteritis is confirmed preoperatively, optimum treatment consists of preoperative chemotherapy (isoniazid, rifampin, and ethambutol) for 4 to 6 weeks followed by surgery. Postoperative chemotherapy (isoniazid and rifampin) is given for 18 months.

Bypass (enteroenterostomy, ileotransverse colostomy) is not recommended, as it results in the formation of blind loops leading to obstruction, malabsorption, or both. Strictureplasty is recommended for partial intestinal strictures, but if the stricture is complete, or if multiple strictures are present in a short segment, resection of the segment with anastomosis is recommended.

Hypertrophic ileocaecal tuberculosis requires either a limited ileocaecal resection with a 5-cm margin or a right hemicolectomy and anastomosis, while perforating ulcers are treated by excision of the perforated segment with primary anastomosis.

When massive small bowel resection is undertaken intravenous rifampin (18 months) and total parenteral nutrition are needed.

Anand SS. Hypertrophic ileo-caecal tuberculosis in India with a record of fifty hemicolectomies. Ann R Coll Surg Engl 1956; 19: 205 - 22.

Bhansali SK. Abdominal tuberculosis. Experiences with 300 cases. Am J Gastroenterol 1977; 67: 324 - 7.

Chawla TC, Sharma A, Kiran U, Bhargava DK, Tandon BN. Serodiagnosis of intestinal tuberculosis by enzyme immunoassay and soluble antigen fluorescent antibody tests using a saline extracted antigen. Tubercle 1986; 67: 55 - 60.

Epstein BM, Mann JH. CT of abdominal tuberculosis. Am J Roentgenol 1982; 139: 861 - 6.

Gleason T, Prinz RA, Kirsch EP, Jablokow V, Greenlee HB. Tuberculosis of duodenum. Am J Gastroenterol 1979; 72: 36 - 40.

Haddad FS, Ghossain A, Sawaya E, Nelson AR. Abdominal tuberculosis. Dis Colon Rect 1987; 30: 724 - 35.

Kapoor VK, Sharma LK. Abdominal tuberculosis. Br J Surg 1988; 75: 2 - 3.

Paustian FF, Marshall JB. Intestinal tuberculosis. In: Berk EJ, ed. Bockus Gastroenterology. Philadelphia: WB Saunders, 1985: 2018 - 36.

Vanderpool DM, O'Leary PJ. Primary tuberculous enterocolitis. Surg Gynecol Obstet 1988; 167: 167 - 73.

Voight MD, Kalvaria I, Trey C, Berman P, Lombard C, Kirsch RE. Diagnostic value of ascites adenosine deaminase in tuberculous peritonitis. Lancet 1989; i: 751 - 4.