ABDOMINAL TUBERCULOSIS

Pankaj Rao
Tuberculosis (TB) causes some 3 million (6%) deaths per year world
wide and is increasing in incidence in developed and developing
countries. Approximately one eighth of total TB cases are extra
pulmonary. TB of the gastrointestinal tract is the sixth most frequent
form of extra-pulmonary site, after lymphatic, genitourinary, bone and
joint, miliary and meningeal tuberculosis. In HIV positive patients the
incidence of extra pulmonary TB is up to 50%. TB involves any part of
the gastrointestinal tract from mouth to anus, the peritoneum and the
pancreatobiliary system, presentation, frequently mimicking other
common and rare diseases. [1]
Pathogenesis:
The tubercular bacilli reach the gastrointestinal tract by:
a) Hematogenous spread from the reactivation of primary lung
focus
b) Ingestion of infected sputum from active pulmonary focus
c) Spread from adjacent organs directly
d) Through lymph channels from infected nodes
In India, the organism isolated from all intestinal lesions has been
Mycobacterium tuberculosis and not M.bovis [2].
Pathology:
Tuberculous granulomas are initially formed in the mucosa or the
Peyers patches. Later transverse tubercular ulcers form which are
relatively superficial and usually do not penetrate beyond the
muscularis. Granulomas are often seen just beneath the ulcer bed,
mainly in the submucosal layer.
Cicatrical healing of these
circumferential 'girdle ulcers' results in strictures. Endarteritis with
occlusive arterial changes also occur producing ischemia and
contributing to the development of strictures. Endarteritis also
accounts for the rarity of massive bleeding in cases of intestinal
tuberculosis.
Hoon et al [3] originally classified the gross morphological appearance
of the involved bowel into ulcerative, ulcerohyperplastic and
hyperplastic varieties. Tandon and Prakash [4] described the bowel
lesions as ulcerative and ulcerohypertrophic types. Ulcerative form has
been found more often in malnourished adults, while hypertrophic form
is classically found in relatively well nourished adults [4].
The most common site of involvement is the ileocaecal region, possibly
because of the increased physiological stasis, increased rate of fluid

and electrolyte absorption, minimal digestive activity and an

abundance of lymphoid tissue at this site. The frequency of bowel
involvement declines as one proceeds both proximally and distally
from the ileocaecal region.
Mesenteric lymph nodes involvement may show them to be enlarged
matted and may caseate. Peritoneal involvement may occur from
spread from lymph nodes, intestinal lesions or from tubercular
salpingitis in women .Peritoneal tuberculosis occurs in 3 forms: (a) Wet
type with ascitis; (b) Encysted (loculated) type with a localized
abdominal swelling; and (c) Fibrotic type with abdominal masses
composed of mesenteric and omental thickening, with matted bowel
loops felt as lump(s) in the abdomen. A combination of these types is
also common [5] Hematogenous involvement of liver, spleen and
pancreas may present with solitary or multiple parenchymal abscesses
with organomegaly.
Clinical Features:
Two-thirds of the patients with abdominal tuberculosis are in the 2 nd to
4th decade of life.
Although some Indian studies have suggested a slight female
predominance the sex incidence is equal. The spectrum of disease in
children is different from adults, in whom adhesive peritoneal and
lymph nodal involvement is more common than gastrointestinal
disease. The clinical presentation of abdominal tuberculosis can be
acute, chronic or acute on chronic. Clinical features depend upon the
site, nature and extent of involvement of the gastrointestinal organs.
Most patients have constitutional symptoms of fever (40-70%), pain
(80-95%), diarrhea (11-20%), constipation, alternating constipation and
diarrhea, weight loss (40-90%), anorexia and malaise. Pain can be
either colicky due to luminal compromise, or dull and continuous when
the mesenteric lymph nodes are involved. Rarer presentations include
perianal abscess or fistulae, GI bleed, entrocutaneous fistula and
dysphagia [6].
Diagnosis and Investigations:
Paustian in 1964 stated that one or more of the following four criteria
must be fulfilled to diagnose abdominal tuberculosis: (a) Histological
evidence of tubercles with caseation necrosis; (b) a good typical gross
description of operative findings with biopsy of mesenteric nodes
showing histologic evidence of tuberculosis; (c) animal inoculation or
culture of suspected tissue resulting in growth of M. tuberculosis; and
(d) histological demonstration of acid fast bacilli in a lesion. These
criteria must be kept in mind, and the diagnosis substantiated by

adequate radiological evidence and others like raised ESR, anemia,

and hypoalbuminaemia. Monteux test may be used for screening but
has limited value in endemic areas because of high false positive rates
[5, 6].

Radiological studies:
Chest X-ray: Evidence of tuberculosis in a chest X-ray supports the
diagnosis but a normal chest X-ray does not rule it out TB as about 75
per cent cases of abdominal TB do not have evidence of concomitant
pulmonary disease.
Plain X-ray abdomen: Plain X-ray abdomen may show features of
obstruction, evidence of ascitis, perforation and calcified lymph nodes.
Contrast Studies:
Enteroclysis followed by a barium enema may be the best protocol for
evaluation of intestinal tuberculosis.
The features that suggest abdominal TB in contrast studies are:
a) accelerated intestinal transit; b) hypersegmentation of the barium
column (chicken intestine), c) luminal stenosis with smooth but stiff
contours (hour glass stenosis) d)multiple strictures with segmental
dilatation of bowel loops d) thickening of the lips of the ileocaecal valve
in early involvement due to edema and spasm of the terminal ileum
causing wide gaping of the valve with narrowing of the terminal ileum
(Fleischner or inverted umbrella sign e)Conical caecum, shrunken
in size and pulled out of the iliac fossa due to contraction and fibrosis
of the mesocolon f) at a later stage loss of normal ileocaecal angle and
dilated terminal ileum, appearing suspended from a retracted, fibrosed
caecum goose neck deformity. g) Stierlins sign a manifestation of
acute inflammation superimposed on a chronically involved segment
which is characterized by lack of barium in the inflammed segments of
the ileum, caecum and variable length of the ascending colon, with a
normal column of barium on either side [7].
Ultrasonography
Ultrasound is very useful especially for imaging peritoneal tuberculosis.
The following features may be seen, usually in combination [5, 6]:
a) Intra-abdominal fluid which may be free or loculated; and
clear or complex
b) Club sandwich or sliced bread sign due to interloop
ascitis

c) Lymphadenopathy which may be discrete or conglomerated.

Small discrete anechoic areas representing zones of caseation
may be seen within the nodes. Calcification in healing lesions
may also be seen
d) Bowel wall thickening best appreciated in the ileocaecal
region
e) Pseudokidney sign involvement of the ileocaecal region
which is pulled up to a subhepatic position
Computed tomographic (CT) scan
Is a good modality of investigation which can provide vital clue leading
to diagnosis of abdominal TB as it can show intestinal lesions,
lymphnodal lesions, ommental thickening, ascitis and solid organ
involvement.
Endoscopic evaluation:
Endoscopy offers the advantage of being minimally invasive and in
avoiding surgery in certain cases. Upper GI endoscopy for esophageal
and gastric lesions and colonoscopy for rectal, colonic and terminal
ileal lesions. Endoscopic biopsy and brush cytology often clinch the
diagnosis. Capsule endoscopy is useful for lesions not seen by UGI &
LGI scopes however tissue diagnosis is not possible with this modality.
Laparoscopic evaluation:
Laparoscopy a minimally invasive procedure with minimal morbidity is
now considered a very useful adjunct in the diagnosis as it can
visualize the peritoneal cavity in detail and take biopsy from the
suspected lesions.
Ascitic fluid examination:
The ascitic fluid in tuberculosis is straw colored with protein >3g/dl,
and total cell count of 150-4000/ l, consisting predominantly of
lymphocytes (>70%). Serum ascitis albumin gradient is less than 1.1
g/dl. The yield of organisms on smear and culture is low. Adenosine
deaminase (ADA) is an aminohydrolase that converts adenosine to
inosine in the catabolism of purine bases. The enzyme activity is more
in T than in B lymphocytes. ADA is increased in tuberculous ascitic fluid
due to the stimulation of T-cells by mycobacterial antigens. Taking a
cut off level of 33 U/l, the sensitivity, specificity and diagnostic
accuracy were 100, 97 and 98 per cent respectively [5].
Immunological tests:

The value of immunological tests based on detection of specific

antibodies to mycobacterium tuberculosis remains undefined in clinical
practice.
Genetic tests:
TB- nested polymerase chain reaction (PCR) has the ability to detect
mycobacterial DNA from 1-2 bacilli from variety of sources. Restriction
fragment length polymorphism is also a very sensitive and specific test
to diagnose early cases of TB.
Management:
All patients should receive conventional antitubercular therapy, which
is the primary modality of treatment, for at least 6 months, including
initial 2 months of rifampicin, isoniazid, pyrazinamide and ethambutol.
However many physicians extend the treatment duration to 9 to 18
months. Medical therapy shows response in upto 70 % cases. In non
responders drug resistance and associated pathology should be
considered. Surgery is indicated when there is doubt in diagnosis,
mechanical complication, severe GI bleed, perforation or when the
patient presents with acute abdomen. Diagnostic laparoscopy has
resulted in avoiding laparotomy in large number of patients.
Accessible strictures are being treated by balloon dilatation reducing
the need for surgery. The recommended surgical procedures today are
conservative. Stricteroplasty or resection anastomoses for strictures
depends on type and number of stricture. It is advocated to perform
resection anastomoses for perforation than primary closure. Extensive
adhesiolysis should preferably be avoided if one encounters abdominal
cocoon for the risk of causing fistula. Various other surgical procedures
may be required depending on the organ involved [8,9]
Abdominal Tuberculosis We Encountered
At Command Hospital (SC), Pune, over last three years we have
encountered a wide spectrum of presentation of abdominal
tuberculosis. We have a follow-up of all cases which required surgical
procedure including diagnostic laparoscopy. Most of the patients
presented with chronic pain abdomen. Mesenteric lymphnodes
followed by ileocaecal region was most frequently involved sites. We
also operated on two patients with tubercular ileal perforation, both
were HIV positive. Among those with solid organ involvement we
operated on one patient with splenic and other with pancreatic
tuberculosis. Extensive peritoneal involvement was seen in three of our
patients and in one of them the presentation was that of hemorrhagic
ascitis. A rare case came with obscure GI bleed and laparoscopy
showed a small thickened area in ileum. Histopathology of this

resected specimen showed it to be a tubercular ulcer. As per our

existing departmental policy we treat all patients with nine months of
antitubercular drugs. Two months with four drugs followed by seven
months of INH and rifampicin. The good results have deterred us from
shifting to six months regimen.
References:
1. Sheer TA, Coyle WJ. Gastrointestinal tuberculosis. Curr
Gastroenterol Rep 2003; 5: 273-278.
2. 1. Peda Veerraju E. Abdominal tuberculosis. In: Satya Sri S, editor.
Textbook of pulmonary and extrapulmonary tuberculosis. 3rd ed.
New Delhi: Interprint; 1998 p. 250-2.
3. Hoon JR, Dockerty MB, Pemberton J. Ileocaecal tuberculosis
including a comparison of this disease with non-specific regional
enterocolitis and noncaseous tuberculated enterocolitis. Int Abstr
Surg 1950; 91 : 417- 40.
4. Kapoor VK. Abdominal tuberculosis: the Indian contribution.
Indian J Gastroenterol 1998; 17: 141-7.
5. M.P. Sharma & Vikram Bhatia Abdominal tuberculosis. Indian J
Med Res. 2004, 120: 305-315.
6. Sunil Kumar, Hari I Pandey, Prabhjot Saggu. Abdominal
Tuberculosis. Recent advances in Surgery 28.
7. Kapoor VK, Chattopadhyay TK, Sharma LK. Radiology of
abdominal tuberculosis. Australas Radiol 1988; 32 : 365-7.
8. Wadhwa N, Agarwal S, Mishra K. Reappraisal of abdominal
tuberculosis. J Indian Med Assoc 2004; 102 : 31-2.
9. Negi SS, Sachdev AK, Choudhary A, Kumar N, Ranjana. Surgical
management of obstructive tuberculosis. Trop Gastroentrol 2003;
24: 39-41.