Deb, Prabal MD*; Chander, Yogesh MD*; Banerjee, Jayanta K. MS†
Departments of *Pathology, and †Gastrointestinal Surgery, Command Hospital (Northern Command), Udhampur, Jammu and Kashmir, India.
Address correspondence and reprint requests to Prabal Deb, MD, Department of Pathology, Command Hospital (Northern Command), Udhampur, Jammu and Kashmir, India. E-mail: email@example.com.
Intestinal tuberculosis is a major concern in many regions of the world. Currently, with the advent of acquired immunodeficiency syndrome pandemic, and immigration from endemic regions, its incidence is rising even in the Western countries.1,2
Although tuberculosis is known to affect all segments of the gastrointestinal tract, isolated primary tuberculosis of the large bowel is uncommon, and that presenting with perforation of viscus is exceptional.3
We report this extremely rare manifestation of abdominal tuberculosis in a 39-year-old human immunodeficiency virus-negative man, who presented with clinical features of perforating peritonitis with septicemia.
A 39-year-old man presented with fever with generalized dull aching abdominal pain of days' duration. This was associated with, nausea, vomiting, and abdominal distention. There was no history of altered bowel habit, abdominal trauma, or fever and no history of Koch or contact with tuberculosis patient.
On admission, he had fever with mild tachycardia. There was abdominal distention with guarding rigidity and tenderness over right pelvic region without any associated rebound tenderness or free fluids. Bowel sounds were increased.
Laboratory investigations showed polymorphonuclear leukocytosis, with raised erythrocyte sedimentation rate (40 mm/h), blood glucose, and serum amylase levels. All investigations including serum electrolytes, liver and renal function tests, and chest radiograph were normal. Clinically, rupture of hollow viscus was suspected, although repeated radiograph did not reveal free gas in abdomen (Fig. 1A). Differential diagnosis of acute pancreatitis was considered, and he was started on conservative management with broad-spectrum antibiotics.
Condition of the patient deteriorated the next day, when he became hypotensive and developed ascites with absent bowel sounds. Peritoneal fluid aspirate was purulent and contaminated with fecal matter, confirming intestinal perforation with fecal peritonitis. Contrast-enhanced computed tomography (Fig. 1B) showed ascites and intra-abdominal air-fluid level, indicating a perforation and warranting an urgent exploratory laparotomy. However, pancreas seemed normal.
Emergency laparotomy showed transverse colon stenosis with an exophytic growth simulating malignancy. This was associated with gangrenous rupture of cecum and fecal peritonitis. Extended right hemicolectomy with ileostomy and mucous fistula was done, along with thorough peritoneal toilet.
Condition of patient deteriorated with development of renal failure. Subsequently, on the second postoperative day, he died because of the effects of septicemia.
We received extended right hemicolectomy specimen measuring 35 cm in length, consisting of terminal ileum, cecum, ascending colon, right flexure, and transverse colon. Cecal wall seemed thinned out and atrophic, with loss of mucosal rugosities, and perforation measuring 1 cm in diameter, with congested edges but no induration. At 3 cm from the distal cut margin, mucosal surface of transverse colon showed an exophytic growth measuring 4 × 2 cm, cut surfaces of which yielded caseous material (Fig. 2). Intestinal wall at this part seemed thickened, without any ulceration or perforation. Remaining mucosal and serosal areas were congested. Extensive search over the serosal surface did not yield any lymph nodes.
Specimen was fixed in 10% neutral buffered formalin, routinely processed and paraffin embedded. Five-micron-thick sections were stained by hematoxylin and eosin stain. Ziehl-Neelsen (ZN) stain for acid-fast bacilli was done.
Sections from the transverse colon showed multiple transmural granulomatous inflammation with central caseation necrosis, rimmed by lymphocytes, plasma cells, epithelioid cells, and Langhans-type giant cells (Fig. 3). The ZN stain revealed acid-fast bacilli, confirming tuberculous etiology (Fig. 3 inset).
Sections from the cecal perforation showed mucosal ulceration, along with mixed polymorphonuclear leukocytic and lymphocytic infiltrates, extending into the serosa and fibroadipose tissue. Adjacent mucosa did not show any distortion of crypt architecture. There were no granulomas, and ZN stain was negative for acid-fast bacilli.
Generally, most cases of intestinal tuberculosis have simultaneous small bowel involvement along with a pulmonary or extrapulmonary focus. Colorectal tuberculosis is an uncommon condition, with incidence ranging between 3%4 and 10.8%5 of all abdominal cases. Although ileocecal affection is a very common entity,4 involvement of transverse colon is relatively rare, isolated primary colonic tuberculosis being exceptional.6 Deodhar et al6 noted a case with extensive disease having multiple strictured lesions involving descending, transverse, and ascending colon. In contrast, tubercular focus in the present case was confined only to transverse colon, without any associated intestinal or extraintestinal focus.
Colonic tuberculosis is known to present variably as inflammatory strictures, hypertrophic lesions resembling polyps or tumors, segmental ulcers and colitis, and rarely as diffuse tubercular colitis or coexistent lesion with carcinoma. Perforation, noted in 19% of cases,5 is rare and generally a manifestation of complication, although this, being a presenting feature, is exceptional.3 Although the present case also had transverse colon tuberculosis, it presented with gangrenous perforation of cecum (ie, at a site different from that of obstruction) unlike the case of Gonzalez Martin et al.3
Although colorectal tuberculosis is apparently more common in the immunocompromised population,7 the present case was immunocompetent.
Intestinal tuberculosis bears close resemblance to Crohn disease, in the form of patchy ulcerations, strictures, and fistulae.8 However, unlike longitudinal ulcers of Crohn disease, tuberculous ulcers are transverse. Biopsy generally reveals acute and chronic inflammation with granulomas; in the absence of caseation necrosis and acid-fast bacilli, differentiation is often difficult.2,9 However, absence of severe crypt distortion and extensive chronic inflammation in the lamina propria in mucosa away from the ulcerated foci suggests tubercular etiology, especially in endemic regions. In such cases, confirmation may be obtained by polymerase chain reaction for mycobacterium tuberculosis/bovis.10 In our case, diagnosis was confirmed by multiple caseating transmural epithelioid granulomas and Langhans-type giant cells, with presence of acid-fast bacilli.
Isolated colonic tuberculosis presenting with cecal perforation is one of the rarest manifestations of tuberculosis and often poses great difficulty in diagnosis. Definitive confirmation of such rare lesions rests on high index of suspicion, supplemented by radiological investigation, exploratory laparotomy, and histopathology of biopsy tissue.
To conclude, we report this extremely rare presentation of abdominal tuberculosis to sensitize the medical fraternity to its varied presentation, which will be of paramount importance owing to its increasing incidence all over the world.
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