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Abdominal TB is a great mimicker of other diseases

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Abdominal TB is a great mimicker of other diseases

Nonspecific features of the abdominal tuberculosis result in difficulty in establishing a diagnosis. After a diagnosis has been established, prompt initiation of treatment helps prevent morbidity and mortality as it is a treatable disease.

Abdominal TB is a great mimicker of other diseases

Specialist’s Corner

Dr  Deepak Agarwal

The writer is senior consultant  gasteroenterologist, hepatologist & endoscopist and is running a successful medical centre in Lucknow

Tuberculosis (TB) is a life threatening disease which can virtually affect any organ system. Global burden of tuberculosis is nearly 12 million. India has the world’s largest tuberculosis cases which is around 26% of the world TB cases, followed by China and South Africa. Tuberculosis has become a resurgent global problem with increasing numbers of immunocompromised patients, largely related to the global acquired immunodeficiency syndrome pandemic. The spread of the disease is further aided by poverty, overcrowding, and drug resistance. Abdominal tuberculosis rates are rising, consistent with the overall trend. Nonspecific features of the abdominal tuberculosis result in difficulty in establishing a diagnosis. This condition is regarded as a great mimicker of other abdominal pathology. After a diagnosis has been established, prompt initiation of treatment helps prevent morbidity and mortality as it is a treatable disease.

The primary site of TB is usually lung, from which it can get disseminated into other parts of the body. The abdominal TB, which is not so commonly seen as pulmonary TB, can be a source of significant morbidity and mortality and is usually diagnosed late due to its nonspecific clinical presentation. The abdominal TB usually occurs in four forms: tuberculous lymphadenopathy, peritoneal tuberculosis, gastrointestinal (GI) tuberculosis and visceral tuberculosis involving the solid organs. Usually a combination of these findings occurs in any individual patient. Generally, computed tomography (CT) appears to be the imaging modality of choice in the detection and assessment of abdominal TB, other than gastrointestinal TB. Barium studies remain superior for demonstrating intestinal mucosal lesions.

There are several ways by which tuberculosis can involve abdomen. Firstly, the tubercle bacilli may enter the intestinal tract through the ingestion of infected milk or sputum. The mucosal layer of the GI tract can be infected with the bacilli with formation of epithelioid tubercles in the lymphoid tissue of the submucosa. After 2-4 weeks, caseous necrosis of the tubercles leads to ulceration of the overlying mucosa which can later spread into the deeper layers and into the adjacent lymphnodes and into peritoneum. Rarely, these bacilli can enter into the portal circulation or into hepatic artery to involve solid organs like liver, pancreas and spleen. The second pathway is hematogenous spread from tubercular focus from elsewhere in the body to abdominal solid organs, kidneys, lymphnodes and peritoneum. The third pathway includes direct spread to the peritoneum from infected adjacent foci, including the fallopian tubes or adnexa, or psoas abscess, secondary to tuberculous spondylitis. Lastly it can spread through lymphatic channels from infected nodes.

Although neither clinical signs, laboratory, endoscopic findings and radiological signs nor the bacteriological and histopathological findings are gold standard for the diagnosis of abdominal TB, the diagnosis of abdominal TB is usually made by adequate radiological and histopathological studies. The methods of biopsy include endoscopic GI mucosal biopsy, image-guided percutanous biopsy, endoscopic ultrasound guided biopsy, and surgical (open or laparoscopic) biopsy. The caseation necrosis in granulomas is the histologic hallmark of TB. In intestinal tuberculosis the granulomas are multiple, larger (more than 200 μm) and coalescent in mucosa and submucosa. Hematologic findings are nonspecific and include raised erythrocyte sedimentation rate, anaemia and hypoalbuminemia. The tubercular ascitic fluid has protein more than 3 g/dL, with a total cell count of 150-4000/μL and consists predominantly of lymphocytes. The ascitic fluid to blood glucose ratio is less than 0.96 and serum ascitic albumin gradient is less than 1.1 g/dL. The yield of organisms on smear and culture is low. Staining for acid fast bacilli is positive in less than 3% of cases and a positive culture is seen in only 20% of cases. Ascitic fluid adenosine deaminase (ADA) levels are elevated in tubercular ascites. Serum ADA level above 54 U/L, ascitic fluid ADA level above 36 U/L and an ascitic fluid to serum ADA ratio more than 0.98 are suggestive of tuberculosis. However, in cases of co-infection with HIV, ascitic ADA levels can be normal or low. The various radiological studies are used for the diagnosis of abdominal TB include ultrasonography (USG), CT, barium studies and magnetic resonance imaging (MRI). Ultrasound is an initial modality of choice which is useful in picking up lymphadenopathy, tubercular ascites, peritoneal thickening, omental thickening and bowel wall thickening in some cases. Plain radiographs may show enteroliths, perforation and features of intestinal obstruction. Barium studies are still gold standard in diagnosing strictures, fistulae, erosions, etc. Contrast enhanced CT and CT enterography provide adequate cross sectional imaging in depicting various forms of abdominal TB.

In the recent years various molecular and immunological techniques are used as a new approach for the rapid diagnosis of abdominal TB. The clinical samples can be ascitic fluid, lymphnode, thickened omentum or mesentery. Abdominal lymphadenopathy is the most common manifestation of the abdominal TB. It usually follows the drainage of the affected organs, though it can affect any lymphnode in abdomen. The most commonly involved lymphnodes are the mesenteric nodes, omental nodes, those at porta hepatis, along the celiac axis and in peripancreatic location. The commonest route of transmission is usually secondary to ingestion of the infected material along with associated intestinal TB. Hematogenous route of transmission and contiguous spread from adjacent affected abdominal organ can also occur. On imaging, the appearance of affected lymphnodes can vary from increase in the number of the normal sized nodes to increase in the size of the nodes to formation of large conglomerate lymphnodal masses. However, the most common presentation is presence of multiple mildly enlarged nodes in clusters which are circular or ovoid. They usually have central areas of caseous necrosis with peripheral enhancement.

Traditionally the peritoneal TB is divided into three types: (1) The wet ascitic type is more common and is associated with large amounts of free or loculated fluid in abdomen; the ascites is usually of high density due to increased protein content of the inflammatory exudate. Associated peritoneal enhancement is usually present; the fixed fibrotic type is relatively less common and is characterized by involvement of omentum and mesentery and is characterized by presence of matted bowel loops on imaging. Loculated ascites can be occasionally present; and (3) The dry plastic type is characterized by fibrous peritoneal reaction, peritoneal nodules and presence of adhesions. However, this classification is usually not adequate and a combination of features is usually noted. The most common clinical features are abdominal pain followed by loss of weight and appetite and altered bowel habits. During colonoscopy, the most common finding of colorectal TB is presence of ulcers, which are linear/fissured, transverse or circumferential and are covered with dull white or yellow exudates. These ulcers can be differentiated from those of CD by presence of abnormal mucosa surrounding these ulcers which show features like erythema, edema, mucosal irregularity and nodularity. In contrast, the ulcers in the CD are usually surrounded by normal appearing mucosa.

Abdominal TB is generally responsive to medical treatment alone, so early diagnosis can prevent unnecessary surgical intervention. In general, with advent of antituberculous therapy, surgery is usually reserved for those cases where it is absolutely indicated as in cases of non-resolving intestinal obstruction, perforation and abscess or fistula formation. Even in cases of tuberculous strictures medical management with antituberculous drugs will result in significant resolution of symptoms in most of patients. Endoscopic balloon dilation offers an alternative to the surgical management of GI strictures. All the diagnosed cases of gastrointestinal TB should receive at least six months of antituberculous therapy which includes initial two months of therapy with isoniazid, rifampicin, pyrazinamide and ethambutol thrice weekly. Although six month treatment regimen is recommended as per the revised national tuberculosis program guidelines, many clinicians extend the treatment regimen to 9 or 12 months.

The surgeries performed in the gastrointestinal TB are of three types. The first type is the surgery which is done to bypass the involved segments of bowel as in case of an enteroenterostomy or an ileotransverse colostomy. These surgeries are usually complicated by blind loop syndrome, fistula formation and recurrent disease in the remaining segments and hence usually not performed routinely. The second type of surgeries are those involving the radical resection like a right hemicolectomy which are feasible with the advent of effective antituberculous drugs so as to eradicate the disease completely. However, these surgeries are also hindered by malnourished status of the most of the patients which make them poor surgical candidates. Also the lesions can be widely placed and radical resection may not be possible in all the cases. The third type of surgeries is usually conservative like a strictureplasty in those strictures which cause more than 50% luminal compromise. These kinds of conservative surgeries are usually preferred nowadays. The tuberculous bowel perforations are usually treated with resection of involved segments with primary anastomosis.

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