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Extrapulmonary tuberculosis, part 3: Abdominal involvement

Extrapulmonary tuberculosis, part 3: Abdominal involvement

Abdominal tuberculosis is one of the most common forms of extrapulmonary tuberculosis. It includes tuberculous infection of the GI tract; peritoneum; omentum; mesentery and its nodes; and other solid intra-abdominal organs, such as the liver, spleen, and pancreas.

This infection is typically caused by Mycobacterium tuberculosis. Abdominal infection caused by Mycobacterium bovis is rarely seen in the present era because of stringent pasteurization of milk and control of tuberculosis on dairy farms.

In the August and September 2005 issues of The Journal of Respiratory Diseases, we reviewed pleural and lymph node involvement and CNS involvement, respectively. In this article, we will focus on the presentation of abdominal manifestations of tuberculosis.


Tuberculous peritonitis constitutes 4% to 10% of all cases of extrapulmonary tuberculosis.1 The reactivation of long-standing latent tuberculous infection of the peritoneum or hematogenous spread of bacilli from an active pulmonary lesion results in peritonitis. The contiguous spread of infection from an intestinal lesion or fallopian tube is relatively infrequent.

Acute tuberculous peritonitis has an onset resembling that of acute abdomen. Laparotomy may reveal straw-colored fluid, with tubercles scattered over the peritoneum and greater omentum.1 Chronic peritonitis occurs in patients in the third to fifth decade of life, with a slight preponderance in women. In addition to constitutional features (fever, weight loss, and night sweats), abdominal pain and swelling are the most common presenting symptoms.

There are 3 forms of chronic tuberculous peritonitis: ascitic, encysted (loculated), and fibrous. The ascitic form often has an insidious onset, with constitutional features and abdominal distention. Abdominal pain is usually absent. The rolled-up greater omentum infiltrated with tubercles may be felt as a transverse solid mass in the patient's abdomen.

The clinical presentation of the encysted form of chronic peritonitis resembles that of the ascitic form. Patients often present with localized abdominal swelling.

In the fibrous form, widespread adhesions may cause the intestine (especially in the ileal region) to be matted together and distended. The disease frequently presents as acute or subacute intestinal obstruction, especially in developing countries such as India.

The matted intestine may also act as a "blind loop" leading to the development of steatorrhea, malabsorption syndrome, and abdominal pain. On physical examination, the adherent loops of intestine and the thickened mesentery may be felt as a lump in the abdomen.1


Although GI tuberculosis is rare in industrialized countries, it is common in developing countries. In India, tuberculosis has been reported to be the cause of intestinal obstruction in 3% to 20% of patients. About 5% to 7% of all GI perforations (excluding appendiceal perforations) are caused by tuberculosis.2

Pathogenesis and pathology

M tuberculosis often reaches the abdomen as a result of a person's swallowing sputum containing the bacilli or by hematogenous dissemination from active pulmonary tuberculosis or miliary tuberculosis or by local spread from infected adjacent viscera. Any region of the GI tract, from oral cavity to anus, can be affected.

The striking predilection for the ileocecal region is the result of the abundance of lymphoid tissue (Peyer patches) there. In the ileocecal region, there generally is increased physiologic stasis, increased rate of fluid and electrolyte absorption, and minimal digestive activity. The greater contact time between the organism and the mucosal surface renders the area more vulnerable to the development of intestinal tuberculosis.

GI tuberculosis can manifest as ulcerative, hypertrophic, ulcerohypertrophic, or diffuse colitis.2 The ulcerative form usually occurs in malnourished persons. Tuberculous ulcers may be solitary or multiple and usually lie transverse to the long axis of the gut ("girdle ulcers"). The healing and fibrosis result in stricture formation ("napkin ringstrictures"), which leads to obstructive symptoms.

"Skip lesions"of normal mucosa are also observed in the diseased segment. Adhesions between the bowel loops prevent free perforation but promote formation of intestinal fistulae.

Unlike the ulcerative form, hypertrophic intestinal tuberculosis commonly occurs in relatively well-nourished patients. The cecum is the most commonly affected site. The hypertrophic form is caused by infection with a less virulent organism in a host with good resistance and wound-healing capacity.

Caseation is often seen in the mesenteric lymph nodes but is occasionally absent in tuberculous granulomas. These noncaseating granulomas may be difficult to distinguish from the findings in Crohn disease. The important findings supporting the diagnosis are confluence of the granulomas, relative absence of fissures, and submucosal edema.

Diffuse colitis is a rare form of intestinal tuberculosis that cannot be easily distinguished from ulcerative colitis on the basis of mucosal appearance on endoscopy.


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