A Study of Surgical Management of Abdominal Tuberculosis in Government Rajaji Hospital Madurai

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Department of General Surgery




The Tamilnadu Dr.M.G.R. Medical University




This is to certify that the dissertation entitled A STUDY OF SURGICAL


research work done by Dr. N. Soundharrajan under my guidance ,supervision

and to my satisfaction in the Department of Surgery, Madurai medical college,

Madurai inpartial fulfillment of the requirement for the degree of MS General


Date: Dr.B.Shanthakumar.M.D(F.M)

Place: The Dean,

Madurai Medical College,



This is to certify that the dissertation entitled A STUDY OF SURGICAL


research work done by Dr. N. Soundharrajan under the guidance of Prof Dr.

Nasheer Ahamed Syed M.S, in partial fulfillment of the requirement for the

degree of MS General Surgery

Date : Dr.Shankaramahalingam M.S

Place : Head of department

Department of General Surgery



This is to certify that the dissertation entitledA STUDY OF SURGICAL


research work done by Dr. N. Soundharrajan under my guidance ,supervision and to my satisfaction in partial fulfillment of the requirement for the degree of MS General Surgery

Date : Prof Dr. M.Nasheer Ahamed Syed M.S

Place; Chief of IInd surgery unit

Department of General Surgery



This is to certify that the dissertation entitled A STUDY OF SURGICAL


research work done by me under the guidance of Prof. Dr. M.Nasheer Ahamed

Syed M.S., professor of General Surgery, in partial fulfillment of the

requirement for the degree of MS General Surgery.

Date : Dr. N. Soundharrajan

III yr Post Graduate

Place: M S General Surgery



I express my deep sense of gratitude to my respected Sir and guide, Prof. Dr.

M.Nasheer Ahamed Syed M.S , Chief II Unit , Madurai Medical College,

Madurai , for his valuable guidance and constant encouragement throughout

the course of this study.

I express my heartfelt thanks to Dr .Shankaramahalingam M.S Professor

and Head, Department of General Surgery, Madurai Medical College, Madurai

for his timely advice, guidance and encouragement at every stage in the

conduct of this study.

My sincere gratitude to Dr.Celine Foustina Mary M.S, D.G.O,

Dr.J.Ravisankar M.S, Dr.G.Saravana kumar MS, FAP ,DA Assitant

Professors, Department of Surgery, Madurai Medical College, Madurai for

their constant support of valuable suggestions at every stage of this study.

I also thank my colleagues and fellow postgraduates in the department of

surgery who have been the source and support of companionship throughout

this course and I am indebted to them.



S.No Contents Page No.

1 Introduction

2 Summary of prior publications

3 List of References

4 Research proposal

5 Informed Written consent in Tamil

6 Certificate from the Guide

7 Approval from the Unit Chief

8 Approval from the HOD

9 Name and Designation of Guides

10 National journal Text Reprint

11 International Journal Text Reprint



TB Tuberculosis

LAP Laparoscopy

LR Limited resection

EXR Erect X-ray Abdomen

CXR Chest X-ray

ESR Erythrocyte Sedimentation Rate

i.v. Intravenous

ATT Anti Tuberculous Treatment

LN Lymph Node

RNTCP Revised National Tuberculosis Control Program

DOTS Directly Observed Treatment Shortcourse

RIF Right iliac fossa

MTB Mycobacterium Tuberculosis


Background of the study:

In spite of considerable advances in recent times, tuberculosis, particularly of

theabdomen is the major health problem in India. Several researchershave


needs a fresh look on abdominal tuberculosis. The disease is a diagnostic

enigma and the management is still controversial. Surgical treatments, both

radical and conservative, are being advocated. Approximately one fifth of

patients require surgical intervention. Abdominal tuberculosis (ATB) is the

most important cause of morbidity.

Materials and methods:

The study was done in Govt. Rajaji Hospital and Madurai Medical College

from September 2013 to September 2014. 50 cases have been studied. 49 cases

underwent definitive surgeries. Follow up period ranges from 1 month to 22



The age range of the patients was 16 to 60 years and most commonly involved

agegroup was 20-40 years with Male to female ratio of 1.5: 1. Most of the

patients belonged to low socio-economic group. 12% of the patients had a

positive history of contact. 60% of the patients presented with intestinal

obstruction. The most commonly involved site was the ileocaecal region

(44%). Most common surgical procedure done was Limited (segmental)

resection (46%).All cases were discharged on 6 months ATT.


In the present series the approach to surgery was conservative. Limited

resection waspreferred over Right hemicolectomy. Most of the cases had

uneventful post operativeperiod and showed good response to ATT during the


Key Words:




Sl.no. Tables Page


1. Table1: Age distribution 65

2. Table 2: Sex distribution 66

3. Table 3: Symptoms 69

4. Table 4: Physical signs 71

5. Table 5: Mode of presentation 73

6. Table 6: Surgical options 79

7. Table 7: Histopathological diagnosis 81 8. Table 8: Comparison of age distribution 89 9. Table 9: Comparison of sex incidence 90

10. Table10 : Comparison of symptoms 92



Sl.no. Figure


Page no.

1 Chart 1: Age distribution 65

2 Chart 2: Sex distribution 66

3 Graph 1: Physical signs 71

4 4

Graph 2: Mode of presentation 73 2

5 Graph 3:SurgicalOptions 79

7 6

Graph 5: Histopathological diagnosis



Tuberculosis has been one of the oldest diseases known to mankind.

Even today, every year, 7 million new infections and 2.5 million deaths are

caused by tuberculosis, making it one of the top ten-killer diseases. It forms a

major health hazard in the underdeveloped and developing countries like India

despite the advent of anti tubercular chemotherapeutic drugs and near adequate

control measures. Along with AIDS it has acquired the “Deadly duo” status.

The development of multiple drug resistance is another area of concern.

Tuberculosis is one of the social disease, commonly known as the

barometer of social welfare.

Abdominal tuberculosis is a highly endemic entity. It is most common in

areas where overcrowding and under nutrition predominate.

In our country intestinal tuberculosis is the single largest causes of

intestinal obstruction. The prevalence of abdominal tuberculosis could not been

determined due to lack ofadequate samples fromthe population. Primary

tuberculosis of intestine without antecedent or associated pulmonary

tuberculosis is fairly common.

Abdominal tuberculosis represents the 6th most frequent form of


miliary and meningeal tuberculosis.[7-9]Abdominal tuberculosis involves

gastrointestinal tract, peritoneum, solid viscera like liver, spleen, pancreas,

etc and lymph nodes. The gastrointestinal tract is involved in 65% to 78% of

patients with peritoneal and lymph node involvement. Tuberculous bacteria

will reach the gastrointestinal tract through blood -hematogenous spread,

either ingestion of infected sputum or contiguous spread from adjacent organs.


Perforation is a serious complication of abdominal TB associated with

high morbidity and mortality. [10, 12, 14, 21-23] The low incidence of tuberculous

perforation is due to a reactive fibrosis of the peritoneum. [12, 21, 22, 24-26]

However, in recent years, intestinal perforation, which was relatively rare in

the past, has been reported more frequently. The cause of this remains


This common entity of protean manifestations and presentations with

varied complication poses a challenge to the diagnostic & therapeutic skill and

ingenuity of a surgeon.

The role of surgery in abdominal tuberculosis is:

i. Diagnostic: for Etiopathological, microbiological diagnosis.

ii. Therapeutic: for Complications like intestinal obstruction, perforation and



The aim of this study is to evaluate the surgical management of abdominal


Objectives of the study:

1. To study the various clincopathological manifestations of abdominal


2. To study the various surgical treatment modalities, their complications and



Historical records reveal that tuberculosis had been recognized as a

disease from the earliest time, and Hippocrates in the 4th century BC bestowed

the name phthisis, meaning wasting, upon the disease as it affected the lungs.

In the 5th century BC, Hippocrates recorded that diarrhoea in a person

with phthisis was a mortal symptom. This is probably the first recorded

connection between gastrointestinal symptoms and tuberculosis [1]. In 1643,

probable intestinal tuberculosis was diagnosed in the autopsy of Louis XIII

which showed ulcerative intestinal lesions in association with large pulmonary


John Hunter, described the microscopic tubercle ". . . in the liver, the

spleen, the uterus, the coats of the intestines, the peritoneum . . ." [3]. He

postulated that these tubercles probably arose from the lungs. This was

followed by the description of a tubercle causing an ulcer in the mucous

membrane of the intestine resulting in destruction of the wall and leading to

intestinal phthisis.

During the 18th and 19th centuries, abdominal tuberculosis was

probably as common as pulmonary tuberculosis and other types of the disease.


chronic peritonitis, which is clearly identifiable with tuberculous peritonitis. He

explains the disease as “occurring in young person as an insidious affection of

utmost danger yet extremely obscure in its symptoms”[4]In 1882 Robert Koch

discovered the Tubercle bacilli, in the same year Ziel used carbolic acid to

demonstrate the Acid Fastness of the bacilli. In 1883 Nielson replaced nitric

acid by 25% sulphuric acid.

Even at the beginning of this century, reports of ileocaecal tuberculosis

without lung involvement were common. In 1902 Mayo Robson, a surgeon at

Leeds, presented a paper atthe Clinical Society of London on the surgical

treatment of chronic intestinal tuberculosis. In the 1920's surgeons were

beginning to realise that there were lesions other than abdominal tuberculosis

that could cause thickening and narrowing of the small intestine. Matthew

Stewart commented that 'whether there is such a thing as a hyperplastic

enterocolitis of non-tuberculous origin still remains to be seen.

During the second half of the 19th century, surgeons were beginning to

operate on the abdomen and abdominal tuberculosis. Later on it had become

customary to describe three forms of abdominal tuberculosis:

1) Ulcerative tuberculosis or tuberculous enteritis;

2) Tuberculous peritonitis;


William Boyd [5] in 1925, described the hyperplastic group as being a

separate type occurring in young women under 40 years of age. In 1928, in his

paper on chronic intestinal tuberculosis, Matthew Stewart [6] stated that

tuberculous ulceration of the intestine was present in half the cases of

pulmonary tuberculosis which came to autopsy. He offered the hypothesis that

the hyperplastic type was caused by a bovine strain of mild virulence in a

patient with a high resistance to tubercle, which resulted in marked fibrosis in

the ileocaecal region.

In 1950,Milk pasteurization, using streptomycin and the diagnosis of

Crohn's disease made virtual disappearance of abdominal tuberculosis caused

by human and bovine strains in the western world. It is still a common disease

on the continent of Africa and the subcontinent of India.

In the 1960's and 1970's a new type, mycobacterium tuberculosis

hominis, emerged with many reports in the British literature describing the

disease as it is seen in Britain today where the vast majority of tuberculosis

occurs in immigrants, particularly those from the Indian subcontinent. Post

1985 there was a resurgence of tuberculosis in association with epidemic of

acquired immunodeficiency syndrome (AIDS).


Tuberculosis (TB) is the most important communicable disease


emergency, since it has come back with great vengeance in most developing

countries. TB in all forms is an important cause of morbidity and mortality in

developing countries especially in HIV patients.

TB continues to be prevalent in the underdeveloped and developing Third

world, and although it was on the verge of eradication in the developed world,

its prevalence is increasing there too, due to factors such as transglobal

immigration, ageing populations, alcoholism, socio-economic deprivation, and

more recently, acquired immunodeficiency syndrome (AIDS)[5]. It has been

estimated that nearly half of world's population are infected and about 10

million new cases are noticed every year.

In 2009, “WHO estimated that the largest number of new TB cases

occurred in the South-East Asia, that accounted for 34% of incident cases

globally”. However, the “estimated incidence rate in sub-Saharan Africa is

nearly twice that of the South-East Asia Region with over 350 cases per 100


WHO region

Incidence Prevalence Mortality

N u m b er i n th ou san d s % of gl ob al tot al R at e/ 100 000 p op u lat io n N u m b er i n th ou san d s R at e/ 100 000 p op u lat io n N u m b er i n th ou san d s R at e/ 100000 p op u lat io n

Africa 2 828 30% 351 3 809 473 385 48

The Americas 282 3% 31 221 24 29 3

Eastern Mediterranean 675 7% 115 929 159 115 20

Europe 425 5% 48 322 36 55 6

South-East Asia 3 213 34% 183 3 805 216 477 27

Western Pacific 1 946 21% 109 2 007 112 261 15

Global total 9 369 100 %

139 11 093 164 1 322 20

Table 1: Estimated TB incidence, prevalence and mortality, 2008

Extra pulmonary TB incidence has been increased recently along with

increase in incidence of TB.The presence of abdominal TB is independent of


abdominal TBpatients, the highest incidence was noted in the gastrointestinal

tract and in the peritoneum, followed by the mesenteric lymph nodes.

Ingastrointestinal tract, the ileocaecal area is the most common site of


In young adults Abdominal tuberculosis is predominant. In Nigeria, in

the age group of 21 to 30 years, the peak incidence was 30.1% and 10.5% in

children < 10 yrs[32]. In India, the mean age was about 31 years, with 63% the

male/female ratio of 1:2 with 63% of them between 20 &40yrs of age[33]. In

England the average age was 32 yrs[34].

A steady decrease in notification of tuberculosis noted in united

kingdom and it is gradually increased from 1987 to 1993 (6528).The incidence

rate was increased from 8.6 to 9.4 per lakh population.from 1988 to 1993. The

rate in the white people was reduced from 4.7 to 4.3/lakh, whereas in ISC

people, the incidence rate tends to be 120/lakh[35, 36]

Incidence in India

Before the era of antitubercular drugs,Autopsies were done for the

patients of tuberculosis with pulmonary involvement showed involvement of

intestine in about 55-90% individuals. The frequency of intestinalinvolvement

correlated with pulmonary involvement. A study was done inK.E.M. Hospital,

Mumbai from 1964 to 1970 by Pimparkar,found thatabdominal tuberculosis


With the increase in the incidence of HIV the incidence of abdominal

tuberculosis also invreases.The incidence of coinfection of HIV and TB in

india was about 0.4 million.

HIV prevalence was noted in 16.6% abdominal tuberculosis patients

when compared to 1.4% in blood donors was found in the study conducted at

mumbai[38]. Extra-pulmonary forms of TB constitutes 10-15% among 50 per

cent of individuals with AIDS.[39]


Tuberculosis is caused byMycobacterium tuberculosis a large, rod

shaped,nonmotile obligate aerobe. Mostof thenon pathogenicmycobacteriums

form a part of normal flora in humans, especially in dry , oily locales. These

rods are about 2-4µm in length and 0.2-0.5 µm width.

In classical case, MTB complexes are almost always found in upper

lobes of lungs which is well-aerated,since Mycobacterium is an obligate

aerobe. Virulence of bacterium is also contributed by the fact that it is a

facultative intracellular parasite, generally of macrophages that has a slow

generation time of 15-20 hours.

Agar based media Middlebrook's medium and egg based medium

-Lowenstein-Jensen medium are the two media used to culture MTB. In both

media MTB colonies appear small, buff colored and inhibitors are used to


Robert Koch was the first to observe ‘Serpentine cords’ - Chains of cells

grown from in vitro colonies and also associated this cord factor with virulent

strains of the bacterium.

MTB stain weakly for Gram-positive or not (cells are called as

"ghosts"). MTB contain only peptidoglycan (murein) in their cell wall and

does not have chemical characteristics of either positive or

negative So, these bacteria can neither be called as positive or


Mycobacterium species and its related genus Nocardia, are classified as

acid-fast bacteria because of their impermeability to certain dyes and stains.

Once stained, acid-fast bacteria will retain dyes when heated and treated with

acidified organic compounds.One common, acid-fast staining method for

Mycobacterium tuberculosis is the Ziehl-Neelsen stain. In this method Smear is

fixed, stained with carbol-fuchsin (a pink dye), and decolorized with

acid-alcohol and then counterstained with methylene-blue or certain other dyes.

Acid-fast bacilli appear pink in contrast background[8, 10, 12, 15].

In order to detect Mycobacterium tuberculosis in a sputum sample,

atleast 10,000 organisms per ml of sputum are needed to visualize the bacilli

with a 100X microscope objective (1000X mag). One acid-fast bacillus per




There are for possible routes of infections involving GIT namely

• Per oral

• Hematogenous

• Lymphatic

• Spread from contiguously involved organ.

MODE OF INFECTION: The Primary Complex:

It is formed by the first exposure of the individual to the agent trough

either droplet or consumption of contaminated food. It spreads to the regional

lymph nodes to form Tubercular Lymphadenitis… the Primary Complex.

Depending on the hosts immunity it either resolves or progresses into Miliary


The Post-Primary Complex:

Unresolved Primary Complex, progress to post-Primary infection, e.g.,

Hyperplastic ileocaecal tuberculosis.

Reinfection or the Secondary Complex:

Reinfection in a patient who has recovered from the Primary disease forms

Secondary Complex, e.g., Ulcero-Constrictive lesions of intestine.


mentioned modes are not uncommon. The bacilli passes unharmed from the

gastric acid barrier because of its resistant fatty coat (mycolic acid).

Ileocaecal region is the common site of involvement because

•pH of chyme in terminal ileum is alkaline favoring the growth of organism.

• The food and sputum are thoroughly digested by the time they reach the

ileum. Hence the bacilli are set free.

• The longer duration of contact of fluid with ileal contents with the mucosa

provides greater chance of implantation.

• The large number of aggregated lymphatic follicles (Peyers patches) acts as

nucleus for its growth.

Typically the organism is trapped in mucosal lymphoid aggregation,

enters the crypts of Leiberkuhn and is carried into sub mucosa by phagocytes

where the characteristic inflammatory change takes place.

Enteritis following the inflammation cuts off the blood supply of the

overlying mucosa, which becomes necrosed and sloughs out to form the

typical ulcer with undermined edges. The inflammation, extends to varying

depth, the base of the ulcer being formed by the sub mucosa, muscular is or

serosa. Because of the slow evolution of the ulcer fibrosis overwhelms it,

adhesions develop early. Since the spread is circumferential, stricture

formation is common. The most active inflammation occurs in the sub mucosa


through lymphatic spread or by direct spread. The infection may then spread

to the mesenteric lymph nodes resulting in caseation and later on calcification.

The type of inflammatory process depends on the immunological reaction

of the host and the virulence of the bacilli so,

• The Hyper plastic type is due to good host immunity and scanty population of

bacteria with low virulence resulting in marked fibrosis and granulomatous


• The Ulcerative type is due to low host immunity and high population of

bacilli with high virulence.



The active lesions are of two types - ulcerative and hypertrophic types.

The ulcerative type

The diseased segment is moderately indurated. Nodules of various sizes are

studded over the circumference of the diseased segment and the mesenteric fat

was found to be increased.Caseated, enlarged Mesenteric nodes are

characteristic. Single or multiple ulcers can be seen, in case of multiple ulcers

varying lengths ofnormal mucosa are foundbetween the diseased part. A

typical ulcer is transversely placed. In a typical case, an Annular ulcer of size


of a segment.The lumen in this region is narrowed forming the characteristic

napkin ring[7, 8, 10, 14, 16, 18].

Ulceration does not penetrate the muscularispropria and is relatively

superficial with varied appearance. The ulcer bed is coarse, granular covered

with a necrotic slough often showing small pseudo polyps.The folds of the

mucosa are scattered with irregular erosions or evened out and may mimic

mamillated surface. In well defined Ulcers, margins are undermined or sloping

or flush with the surface.

In a rare case, the ulcer has stellate appearance with deep excavation

mucosal shelves that are intensely hyperaemic. In this type, the mucosal folds

present nearby converge upon the ulcer and present along the longitudinal

axis. The wall underlying the ulcer bed may be thin or hypertrophic, scarred

with yellowish areas of necrosis i.e., thickness is quite variable.

Hypertrophic type:

Ileocaecal region is commonly affected in hypertrophic type.The mesenteric

fat and lymph nodes with extensive adhesions form a lump –large mass in the

Right iliac fossa with distorted , obtuse ileocaecal angle. The thickness of the

wall is increased up to 3cm resulting in a tubular form.Mucosal changes are

variable with prominent'cobblestoning' or pseudo polyposis or flattened

mucosal folds with irregular furrows on the surface that converge upon


It may be mentioned here that there are no sharp differences between two

varieties and coexistence of these types are seen.[15].


In Hypertrophic type, the mass is due to granulomatous tissue that extends on

to serosa, enlargement of lymphnodes, mesenteric fat, muscularis hypertrophy

and fibrosis. Caeseating granulomas are diagnostic. Granulomas appear first on

the mucosa or peyer patches.

Structure of Granuloma:

Granulomas are large in size but the size may increase progressively

either due to enlargement of initial focus or due to confluence of many satellite

granulomas. Granuloma consists of central and peripheral part. Peripheral part

is infiltrated with plasma cells, giant cells of Langhans type and lymphocytes.

Granulomas are often present in immediate lining of ulcer bed.

Ulcers are lined by inflammatory granulation tissue which is

non-specific and often do not penetrate Musculariswhere as the infiltrated

polymorphs extend on to sub mucosa in the form of Micro abscess. In chronic

longstanding cases, there occurs fibrosis of variable degree in thelesions that

extend into muscularis from the submucosa. Well developed granulomas are

observed in the wall of adjacent areas and the transition was found to be


Well formed lesions show reparative changes.Pyloric gland metaplasia is

most common, extensive and often seen in cases presenting with active




1) Tuberculosis of Peritonium proper

 Wet or Ascitic type- Generalized or local type

 Dry or Fibrous- Adhesive, Plastic,Miliary,Nodulular type

2) Tuberculosis of Peritoneal Folds and their contents:

 Mesenteric Adenitis

 Mesenteric Cysts

 Mesenteric abscess

 Bowel adhesions

 Rolled up Omentum



 Hyperplastic

 Ulcero-Hyperplastic



In Young adults abdominal tuberculosis is common. 2/3rdof patients are

in the age group of 21-40 yrsand there is no gender difference in incidenceof

abdominal TB, but female predominance was seen in few Indian studies. A

study conducted in South Africa, showed that the association of abdominal

with pulmonary Tuberculosis increases (62%) only under low socioeconomic

conditions.[40]Conversely, increased severity of pulmonary tuberculosis

increases the severity of abdominal disease.

Abdominal tuberculosis clinically present either in acute or chronic

form.Common symptoms found are constitutional. Fever in 40-70%, pain

among 80-95%, diarrhoea seen in 11 20%cases, constipation, alternate

constipation and diarrhoea, weight loss in about 40-90% of patients, malaise

and anorexia. Continuous and dull Pain is felt if the mesenteric nodes are

involved and in case of luminal compromise colicky pain is felt. Specific

clinical features are seen depending upon the nature, site and extent of


Table 2: Clinical features

Site Type Clinical features

Small intestine

Ulcerative Diarrhoea,malabsorption

Stricturous Obstruction

Large intestine

Ulcerative,Rectal bleeding Rectal bleeding

Hypertrophic Lump obstruction


Ascitic Pain, distension

Adhesive Obstruction

Bhansali[12]found frank malabsorption in about 21% of patients, while

Tandon et al [41] reported biochemically that 75% of patients with intestinal

obstruction had malabsorptionand 40% without it. Mass in patients with

abdominal tuberculosis is firm, mobile and only slightly tender. Rectal

bleeding has been reported in 4% [42] to 6% [43] of patients; massive lower

gastrointestinal bleeding is rare.[44]

Subacute intestinal obstruction is described as colicky abdominal pain,

distension, vomiting, gurgling, feeling of a ‘ball of wind’ moving in the

abdomen, and visible loops and peristalsis; these symptoms are relieved

spontaneously after passage of flatus. Ano-rectal tuberculosis presents as


are usually multiple; as many as 12 out of 15 multiple flstulae but only four out

of 61 single peri-anal fistulae were tubercular.[49]

Tuberculous Peritonitis:

Tuberculous peritonitis, the common form of abdominal tuberculosis

presenting as ascitic type in about 97% of cases[50, 51].Localised or Generalised

ascites with fine strands of adhesions and filmy membranes are seen. The

tubercles are studded on the peritoneum - on parietal as well as visceral


Remaining 3% of cases are of plastic or fibroadhesivetype,here bowel

loops are matted due to adhesion of masses of tubercles. These matted loops of

bowel are then stuck to the mesentery and to peritoneum so peritoneal space

will be obliterated due to adhesions.[52]Omentummay be palpable, rolled up or

thickened. This illness generally develops slowly over months.

Tuberculosis of oesophagus:

A rare variety, Oesophageal tuberculosis constitutes 0.2 per cent of cases

of abdominal tuberculosis.[39] Patient withOesophageal tuberculosis presents

with difficulty and pain during swallowing, fever – low gradeand an

midoesophagealulcer. This disease can be misdiagnosedas oesophageal

carcinoma and there will be no evidenceforextraoesophageal focus of


Gastroduodenal tuberculosis:

In this type , Stomach and duodenum each contribute for about 1% of cases of

abdominal tuberculosis.Patients presents as peptic ulcer disease of short

duration with decreased or no response to treatment.[54]

Infected sputum, contaminated food, hematogenous spread and direct spread

from adjacent organs result in Tuberculous enteritis. Ulcerative type is the

most common followed by hypertrophic or ulcero-hypertrophic type of

intestinal lesion. Patient complaints are fever, pain abdomen, diarrhea with

weight loss. Rectal bleeding and tenderness over the abdomen are seen. A

palpable mass is seen in 25 to 50% of cases in right lower quadrant.

Common sites involved areileocecal area and jejunoileum.Complications

include obstruction, fistula formation and perforation. Anal fissures, fistulas or

perirectal abscess are the rectal lesions seen in Gastro duodenal tuberculosis.

Hepatic and pancreatic tuberculosis

The liver is frequently affected in association with miliary tuberculosis.

In 41 patients with hepatic tuberculosis from South Africa, the liver was found

to vary in size and consistency. [55]Hepatic involvement tends to be diffuse;

macronodular forms are rare.[56]Pancreatic tuberculosis can mimic pancreatic


occasionally with obstructive jaundice due to a mass at the head of the

pancreas. Tuberculous pancreatic abscess has been reported in patients with


Splenic Involvement:

In abdominal tuberculosis,spleen may be involved that presents as

splenic enlargement–hypersplenism , abscess formation and fever. Along with

medical management Splenectomy is mandatory.HIV – positive drug abusers

presents with multiple abscesses.[58]

Ileocaecal tuberculosis

Typical features of Ileocaecal tuberculosis are abdominal pain –colicky

with borborygmi and vomiting. Abdominal examination may reveal a well

defined, mobile mass, firm in the right lower quadrant. Sometimes examination

reveals no abnormality or a doughy feel. Lymphadenitis may be associated

that present as multiple lumps on palpation. Mobility of the lump also depends

upon the node involved ,if mesenteric nodes are involved the lump is mobile

and para-aortic or iliac nodes are involved the mass is fixed.[59]

Segmental colonic tuberculosis

Segmental also called isolated colonic tuberculosis is the involvement of the

colon without ileocaecal region. This type constitutes 9.2 % of cases of

abdominaltuberculosis. Sigmoid, ascending and transverse colon are


1/3rd of patients presents with hematochezia.[61, 62] Fever, weight loss,

anorexia, change in bowel habits are other features of segmental tuberculosis.

Anorectal lesions

These are rare. Four types have been described: ulcerative being the most

common, varicose (warty-like), lupoid (nodular) and miliary. They are often

confused with rectal carcinoma.[63] Elderly men with anorectal lesions may

present with abscesses and fistulas with concomitant pulmonary disease [64].

Glandular tuberculosis

This affects mesenteric or retroperitoneal nodes as well as nodes in the

neck, axilla and/or groin. It may rarely present with a psoas abscess due to

retroperitoneal lymphadenopathy, in the absence of bony affection [65].

Tuberculosis and HIV Infection


disseminated, bone and joint infections) incidence increases with increase in

incidence HIV infection. There is proportionate increase in extrapulmonary

tuberculosis with increase in HIV infection. The diagnosis of intra abdominal

tuberculosis is difficult, so the contribution of abdominal infection is higher.

Manifestation of abdominal infection is altered by HIV infection but the extent

is unknown. A study relates this to Immunosupression. Thus, in HIV infected


common and CT findings suggests visceral lesions. In HIV negative

individuals ascites and Jaundice are seenand CT scan commonly reveal ascitis

and omental thickening in these patients.Aspirates from abdominal lymph

nodes revealedrapid diagnosis in 8 HIV-infected patients showing acid-fast

bacilli in the smear.

93% of HIVinfected patients, showed disseminated tuberculosis whereas

only 31% of HIV negative cases had disseminated TB .Tuberculosis caused

death in HIV-infected patients (23%) and about 31% in patients without HIV

infection. Thus, in HIV-infected patients, abdominal tuberculosis is a

manifestation of disseminated disease and therefore results in significant


Tuberculosis is one of the common ‘HIV-related opportunistic infection

in India’, patients with both diseases should be cared properly which is a

major public health challenge. In India, annually about 1.8 million new cases

of tuberculosis are reported, that accounts for a fifth of new cases in the world.

Patients with latent Mycobacterium tuberculosis infection are at higher risk for

progression if they are coinfected with HIV. The response to treatment in HIV

patients is similar when compared with Patients without HIV infection but HIV

patients have higher risks of recurrence and death. The influence of


A study conducted in Malawi reported that 74.6% of patients with

tuberculosis are HIVpositive.[66] 6% of patients with acquired

immunodeficiency syndrome (AIDS) had tuberculosis in London.[67]

Tuberculosis infection in AIDS patients increases the mortality in HIV


Cryptic Miliary Tuberculosis

This type is common in Elderly people. So occult malignancy, should be

ruled out while diagnosing Cryptic miliary tuberculosis. It occurs due to

decreased immunity which may be related to reactivation of previous

disease.[69]patient presents with features like: malaise, weight loss, fever, an

raised erythrocyte sedimentation rate (ESR) andwith normal chest X ray.


Complications include

Obstruction (acute or subacute)

Perforation (generalized or localized)

Abscess formation and GI bleeding.

Most of the bleeding arenot life threatening, but ulceration inthe transverse

colon results in lower abdominal bleeding.

Hassan retrospectivelyanalysed 18 patients, who were treated for abdominal

tuberculosis in United States. These patients were diagnosed as abdominal


suggesting abdominal tuberculosis are mesenteric/omental stranding in 50% of

cases, ascites in about 37% and retroperitoneal lymphadenopathy among 31%

of patients. [70]

Tananalysed the abdominal TB cases retrospectively in 57 patients of which

37 are men diagnosed as abdominal TB, in the age group of 47 (range 14-74)

yrs. Here 27 patients – 47% had active pulmonary TB . 30% withPositive

HIV status whereas 58% were untested. Findings that reveal abdominal TB

are thickening of bowel, ascites,lymphadenopathy, abscess and free gas

suggestive of perforation.[71]

33 patients showed bowel involvement, 24 had mesenteric

lymphadenopathy, In 13 patients, peritoneum was involved and seven patients

had splenic involvement, pancreas showed signs in two, anus in two & the liver

is involved in two patients.There was Disseminated (including pulmonary) TB

in 27 patients - 47% and isolated intra-abdominal TB seen in 30 patients


Uzunkoyrecorded 11 individuals diagnosed with abdominal tuberculosis

in Turkey. Ascites was observed in all cases. Other common findings were

weight loss and weakness in 81% of patients, abdominal mass with painin

about 72%, abdominal distension among 63%, anorexia in 45% of cases and

night sweat in about 36%. 8.2 g/dl was the average hemoglobin found and ESR


elevated cancer antigen CA-125. In all patients Abdominal ultrasound showed

abnormalities: ascites was seen in all patients , five of them had

tuboovarianmass, 3 cases showed omental thickening and only two patients

presented with lymph nodes enlargement (mesenteric, paraaortic).

CT scans revealed ascites in all patients, 5 cases showed pelvic mass, 4

cases had retroperitoneal lymphadenopathy, 4 of them showed mesenteric

stranding and 3 patients had omental stranding , bowel wall thickening in

2cases and mesenteric lymphadenopathy again in 2 patients.[72]

Chen reviewed “the patients with abdominal TB at a major hospital in southeastern Taiwan from January 1987 to December 2006. Common

presenting features included abdominal pain (18/21, 85.7%), fever (16/21,

76.2%), ascites (13/21, 61.9%), and weight loss (12/21, 57.3%). The mean

time to reach a diagnosis was 48 +/- 10 days. Tuberculous peritonitis was

noted in 11 patients, with a high correlation with liver cirrhosis. The other

patients were diagnosed with TB of the gastrointestinal tract (n = 6), urinary

tract (n = 2), and pelvis (n = 2).”[73]

Aggarwal retrospectively reviewed 50 paediatric cases admitted to

tertiary hospital in Mumbai. Out of 50 cases admitted, ‘definite surgery was

done in 31 (62%) cases for complications or emergencies arising out of

abdominal tuberculosis and the rest 19 (38%) cases were subjected to medical


USG guided biopsy’. The commonest mode of presentation was Acute

intestinal obstruction in about 62%. Indicator used to assess prognosis was

ESR since it is elevated in most cases in about 88%. In about 50% patients

there was Coexistent pulmonary tuberculosis.[74]

Negiretrospectively reviewed 17 patients who were managed surgically

for gastroduodenal obstruction caused by tuberculosis. Author observed the

site of obstruction was ‘the pyloroduodenal canal in 53% of patients, second

part of the duodenum in 24%, third part of the duodenum in 12% and

duodenojejunal flexure in 12%.’Fibrotic stricture results in obstruction in about

59% and in 41% compression by lymph node mass was main cause of


Sheikh studies 26 cases of abdominal tuberculosis prospectively. Author

found mean age of 10 male and 16 female patients was 33 years (range 14-66

years).Varied presentation of abdominal tuberculosis included pain in abdomen

(88.46%), fever (84.6%), weight loss (69.2%), mass in abdomen (46.1%) and

abdominal distention Ascites) (26.9%).[76]

Diagnosis and investigations

Paustian[39]putforthfour criteria to diagnose abdominal tuberculosis in



2. Gross typical operative findings along with histologic evidence of

tuberculosis in biopsy specimen of mesenteric nodes.

3. M. tuberculosis must grow either on animal inoculation or in culture of

suspected tissue and

4. Acid-fast bacilli must be demonstrated in a lesion.

Laboratory Investigations: SPUTUM:

Sputum is collected from suspected patients of tuberculosis .Early morning

sputum is collected on 2 consecutive days and sent for culture. In patients

admitted in the hospital, 8 hrly sputum sample can be collected. Sputum

induction can be done with hypertonic saline in patients without spontaneous

sputum production. In case of children, gastric aspirate is a better specimen and

done in Early morning or transbroncial biopsy with bronchial washings taken

using fiber optic bronchoscope for sputum collection.

Bone marrow, liver biopsies or blood cultures are occasionally

done.Growth of mycobacterial cultures takes some weeks for identification.

Ribosomal RNA probes or DNA polymerase chain reaction, newer

technologies that allow identification in 24 hours. The DNA probes can be

tested either on smear-positive or smear-negative sputum. However, sensitivity


Laboratory tests:

The laboratory tests done are

 CBC count

 Alanine aminotransferase (ALT) &Aspartateaminotransferase(AST)

was done.

 Alkaline phosphatase

 Bilirubin–Direct and Indirect

 Creatinine

 Uric acid

Mantoux test:

The Mantoux test (also known as the Mantoux screening test, Tuberculin

Sensitivity Test, Pirquet test, or PPD test for Purified Protein Derivative) is a

diagnostic tool for tuberculosis.

Mantoux technique:

A standard dose of 5 Tuberculin units (0.1 ml) is injected intradermally

(between the layers of dermis) and read 48 to 72 hours later. A person already

exposed to bacteria produces an immune response in the skin containing the

bacterial proteins.

The reaction is noted by measuring diameter of induration across the

forearm (Perpendicular to long axis) in millimeters. No induration, the result is


Tuberculin test is indicated if the person hashistory of a positive tuberculin

skin test or a recent negative tuberculin skin test (within one year).

Induration 5 mm or more is seen in

 HIV infected patients

 Recent contact with TB case

 Personswith old healed TB and changes on chest X ray such as nodular

or fibrotic changes

 ImmunosupressedPatients and patients with organ transplants .

Induration of 10 mm or more is positive in

 Recent arrivals (less than 5 years) from high-prevalence countries

 Injection drug users

 Residents and employees of high-risk congregate settings (e.g., prisons, nursing homes, hospitals, homeless shelters, etc.)

 Mycobacteriology lab personnel

 Persons with clinical conditions that place them at high risk (e.g.,

diabetes, prolonged corticosteroid therapy, leukemia, end-stage renal

disease, chronic malabsorption syndromes, low body weight, etc.)

 Children less than 4 years of age, or children and adolescents exposed to

adults in high-risk categories

15 mm or more is positive in


Radiological studies Chest X-ray:

Chest X ray may show signs of tuberculosis but in most of the cases it is

normal so chest X ray was taken just to support the diagnosis. In a study

conducted by Sharma et al [77] reported active / healed lesions in 46% of cases

out of 70 patients with abdominal tuberculosis. He also found that X- rays are

positive in patients presenting with acute complications in about 80%.[77]

Prakash in a study with 300 patients, reported that none had active pulmonary

TB but 40% showed healed lesions.[78]

Tandon et al [79]in his study reportedthat only 25 % of patients had positive

X-ray findings. So, it can be concluded that concomitant pulmonary disease will

not be evident in 75 per cent cases.

Plain X-ray abdomen:

Enteroliths, obstruction features like dilated bowel loops, multiple air

fluid levels, perforation, ascites and intussusceptions are major findings in

plain X- ray abdomen. Calcified nodes, hepatomegaly with spleenomegaly and



showingmultipleairfluidlevelsinsubacute intestinal obstruction; (b)

Abdominal X ray showing calcified mesenteric lymph nodes.

Radiological investigations play a major role in the diagnosis of

abdominal tuberculosis.[80]Homan et al [81] in his study observed that a normal

X-ray chest excludes abdominal tuberculosis diagnosis but 25% of patients

show positive finding in X-ray - chest.[42, 43] X- ray findings like active or

healed tuberculosis just support the diagnosis in case of abdominal

tuberculosis howevera normal chest X-ray does not rule it out.

Small bowel barium meal:

Small bowel barium meal shows “chicken intestine” – hypersegmented


are thick and stiffened ; lumen is stenosed with stiff contours called “hour

glass stenosis”, bowel loops show multiple strictures andsegmental dilatation

along with matting of bowel loops.

Barium enema:

The features [77]seen are:

 Spasm and edema of the ileocaecal valve are the early findings in

ileocaecal region. Ileocaecal valve margins are thickened with wide

gaping in the valve along with narrowed terminal ileum. (“Fleischner or

inverted umbrella sign”) is typical finding.

 Double contrast study shows fold thickening and contour irregularity in

terminal ileum.

 “Conical caecum”, here contraction, fibrosis of mesocolon causes

caecum to shrunken and get pulled out from the iliac fossa. In Some

cases hepatic flexure also pulled down.

 Ileocaecal angle is lost with dilation of terminal ileum, that appears as if

the ileum is suspending from fibrosedand retracted caecum (“goose neck


 “Purse string stenosis”– this stenosis is localized characterized by

smooth caecum ,dilated terminal ileum opposite to ileocaecal valve.

 “Stierlin’s sign”: Stierlin sign is due to presence of narrowed terminal


caecum. Inflamed segments of ileum, caecum and ascending colon do

not retain barium which is characteristic with normal barium column on

either side.This sign is typically seen when acute inflammation

superimposes on chronic diseased segment.

 “String sign” – persistent narrow barium column that indicate stenosis.

“Stierlin and String signs” are also seen in Crohn's disease

hencenotdiagnostic of tuberculosis. “Enteroclysis followed by a barium

enema may be the best protocol for evaluation of intestinal tuberculosis”

Figure 2(a): Barium meal follow through showing distal ileal stricture. (b): Bariumenema showing terminal ileal stricture with proximal dilatation.

Double-contrast barium enema:

Ileocaecal tuberculosis presents with shortened ascending colon, caecum

irregular, shortened, narrowed i.e.,deformed,ileocaecal valve incompetent

anddeformed with dilated ileum and distorted ileocaecal junction there is

obtuse increasedileocaecal angle .[77]Barium studies are sensitive for ileocaecal


extra-intestinal lesions (peritoneal and lymph nodes) may be misinterpreted as

intestinal strictures or vice versa. [82, 83]Tandon et al [79] reported that about 25%

of patients showed false-negative results inbarium studies. Radiological studies

may not always differentiate tuberculosis from Crohn's disease and


Table 3: Findings of barium meal followthrough study in intestinal tuberculosis

Group I

Highly suggestive



s if one or more of


features are present.

• Deformed ileocaecal valve

with dilated ileum

• Contracted caecumwith

abnormal ileocaecalvalve or terminal ileum

• Stricture of ascending colon with shortening or involvement of ileocaecal region

Group II

SuggestiveofIntestin altuberculosis if one of the following is present:

• Contracted caecum

• Ulceration or narrowing

of terminal ileum

• Stricture ofascendingcolon

• Multiple sites ofnarrowing and dilatation leading to

formation of small bowel loops

Group III




Barium studies cannot diagnose peritoneal lesions but they are accurate

for lesions inside the bowel. So,for imaging and to diagnose peritoneal

tuberculosis,Ultrasound is necessary. Features that reveal peritoneal

tuberculosis are[85]

Intra-abdominal fluid appear free, clear or complex, loculatedwith debri

and septae. Pelvis contain fluid collectionsand have thick septa which mimican

ovarian cyst.

“Club sandwich or sliced bread sign’: Localized fluidcollection

seen(exudation from the inflamed bowel) between radially oriented

bowel loops (interloopascitis)

 Tuberculouslymphadenopathy have an heterogenous echo texture when

compared to homogenous echos in case of lymphoma. Nodes appear in

discrete or conglomerated (matted) form.Some anechoic discrete small

zones are seen which represent areas of caseation present in the nodes.

Aftertreatment when the patients are followed, the nodes initiallyshowed

an increasein size for 3-4 wksthen reduced in size gradually.

Calcification appear in the form of discrete lines that are reflective in

healing lesions. caseation and calcification are suggestive of tubercular


 Bowel wall thickening is concentric and uniform as compared to

eccentric in Crohn‘s disease and irregular in malingnancy. Bowel

thickening are commonly seen inileocaecal region..

 Pseudokidney sign – ileocaecal region is involved and is pulled up to

subhepatic position.

Figure:3 (a) Abdominal ultrasonography showing enlarged mesentericlymph nodes (Note the hypoechoic centers due to caseation) (b) Echogenic

mesenteric thickening (within calipers) and small round lymph nodes interspersed within the mesentery

Computed tomographic (CT) scan

Ileocaecal tuberculosis commonly presents in hyperplastic type and is

well evaluated on CT scan. Circumferential and symmetric caecal and terminal

ileal thickening are seen in early stage, then in later stage the thickening

becomes asymmetrical. In further advanced stage there is gross wall

thickening, loops become adherent, nodes become thickened along with soft


ulceration in terminal ileum, in association with narrowing and proximal


Circumferential wall thickening, narrowed lumen with ulceration are

findings seen in other areas of bowel involvement. Hepatic flexure is also

involved if the colon is infected.Complications such as perforation, abscess,

and obstruction are seen. In CT Scan , Mesenteric disease appear as patchy

or diffuse stellate lesion with increase in density and strands are also seen in

mesentery. Nodes appear interspersed. Thickening of omentumoften resemble

‘omental cake appearance’. Fibrouswall over the omentum is called omental

line, developed due to long standing inflammation. This omental line is less

common in malignant infiltration.[87]

Figure: 4 (a) CT scan at the level of porta showing multiple hypodense nodes showing peripheral rim enhancement in tuberculous lymphadenitis.


Caseated nodes are seen that have centers which are hypodenseand

enchancement in peripheral rim. These findings with calcification are highly

diagnostic of tuberculosis. In tuberculosis The mesentery, mesenteric root,peri

pancreatic nodes, celiac and porta hepatis are typically involved in

tuberculosis. The retroperitoneal nodes (i.e., the periaortic and pericaval) are

spared and are never seen in alone, unlike in lymphoma.[86]


Colonoscopy is better procedure for diagnosing colonic and terminal

ileal involvement but it is underutilised. Nodules in mucosa are of sizes2 to 6

mm and ulcers in a colonic segment, of 4 to 8 cm in length are pathognomic.

Caecum contains many nodules with pink surface near the ileocaecalvalve.

Large of size 10 to 20 mm or small in the range of 3 to 5 mm ulcers can be

located in between nodules. The mucosa in between the ulcers are hyperemic

or normal.[88]

Strictures with nodular and ulcerated mucosa are seen. Often up to 8-10

colonoscopic biopsies from the edge of the ulcersare taken for histopathology

and culture. However, there is only a low yield on histopathology because of

predominant involvement of sub mucosa. Granulomas are reported in 8-48 per

cent of patients and caseation in a third (33-38%) of positive cases.[89] The

yield of acid fast bacilli stains are variable in studies. Culture positivity is not


cultures in 40 per cent of patients and concluded that routine culture of biopsy

tissue increases the diagnostic yield. A combination of histology and culture of

the biopsy material establishes the diagnosis in about 60 % patients.

Ascitic fluid examination

The ascitic fluid is straw coloured with protein >3g/dl, total cell count

150-4000/ μl, predominantly lymphocytes (>70%) are seen. ‘The ascites to blood

glucose ratio is less than 0.9650 and serum ascitis albumingradient is less than

1.1 g/dl’. The identification of organisms is difficult on smear and culture

.‘Staining for acid fast bacilli is positive in less than 3 per cent of cases. A

positive culture is obtained in less than 20 per cent of cases and it takes 6-8

wks for the mycobacterial colonies to appear’. However Singh et al, ‘in his

study cultured 1 litre of ascitic fluid after centrifugation and reported 83 per

cent culture positivity’.

‘Adenosine deaminase (ADA)’ is an aminohydrolase that converts

adenosine to inosine is involved in thecatabolism of purine bases. Enzyme

‘sactivity is more in T than in B lymphocytes and is proportional to the degree

of T cell differentiation. ADA is increased in tuberculousascitic fluid due to the

stimulation of T-cells by mycobacterial antigens. Dwivedi et al.[90]measured

‘ADA levels in the ascitic fluid of 49 patients, the levels in tuberculousascitis


off level of 33 U/l, the sensitivity, specificity and diagnostic accuracy were

100, 97 and 98 per cent respectively’.[90]

In the study by Bhargava et al.,[91]‘serum ADA level above 54U/l, ascitic fluid

ADA level above 36 U/l and a ascitic fluid to serum ADA ratio >0.985 were

found suggestive of tuberculosis. [92] In coinfection with HIV the ADA values

can be normal or low. Falsely high values are found in malignant ascitis. High

interferon-g levels in tubercular ascitis have been reported to be useful

diagnostically’.[93]Estimating both ADA and interferon can further increase the

sensitivity and specificity.

Laparoscopic findings

Bhargava et al[94] in his study‘with 87 patients reportedthat ascetic fluid

contain high protein out of 87, 38 patients are diagnosed as tuberculosis.

Reported that visual appearances are more helpful (95% accurate) than

histology, culture or guinea pig innoculation(82, 3 and 37.5% sensitivity

respectively). Caseating granulomas are found in 85-90 per cent of the

biopsies’. The laparoscopic findings in peritoneal tuberculosis can be grouped

into 3 categories:

I. Peritoneum was thickened with multiple, same sized uniform ,yellowish

tubercles distributed entirely on the parietal peritoneum.. Omentum,


II. Peritoneum thickened but without tubercles.

III. Thickened peritoneum with fibro adhesive peritonitis along with

multiple thick adhesions are seen that fixes viscera.

Operative findings in abdominal tuberculosis include ascites, small white-to

yellow nodules over the visceral and parietal peritoneum (tubercles),

adhesionsbetween intestinal loops and to the parietes, calcified or enlarged

mesenteric lymph nodes (figures 5 and 6) which may show caseation on

bisection, infiltrated thickened and rolled up omentum, increased mesenteric

fat wrapping the bowel, short and fibrotic strictures (figure 6), and soft to firm

hypertrophic lesions (figure 7(a)). The opened specimen shows thickened

folds, nodularity, ulceration and fibrosis (figures 7(b),(c)). In many patients it

may not be possible to differentiate tuberculosis from malignancy and Crohn's

disease, even at laparotomy. Algorithmic approach to diagnosis of abdominal


Figure: 8 Algorithmic approaches to diagnosis of abdominal tuberculosis

Uzunkoystudied in11 patients diagnosed as abdominal tuberculosis. 8.2

g/dl is the average hemoglobin and ESRrange was in range of 30-125 with an

average50 mm/h. four patients showed elevated Cancer antigen CA-125.

Ultrasound abdomen showed changes in all the cases: ‘all cases had ascites,

tuboovarian mass in five, omental thickening in 3, and enlarged lymph nodes

(mesenteric, paraaortic) in 2. CT scans showed ascites in all, pelvic mass in 5,

retroperitoneal lymphadenopathy in 4, mesenteric stranding in 4, omental

stranding in 3, bowel wall thickening seen in 2 cases and 2 patients showed

mesenteric lymphadenopathy.’[72]

In a study by Chen, abdominal sonography and abdominal computed


patients showed Pulmonary involvement. Mostpatients (16/21,

76.2%)improved well with anti-tuberculosis treatment and about five patients

were dead from sepsis and respiratory failure. [73]

In a study by Negi, Endoscopic biopsy was found to be diagnostic in

only 29% of the patients in whom it was performed. So overall, a pre-operative

diagnosis of gastroduodenal tuberculosis was suspected in only 35% of

patients”. In all patients diagnosis was done by histopathology and laparotomy

and surgical drainage procedures are done.[75]



Antituberculous Drugs

Antituberculous drugs for 6 months with isoniazid and rifampicin, along

with pyrazinamide added for the first 2 months, usually cures tuberculosis at

any site (except the Central nervous system) provided the bacilli are fully

sensitive.[67, 95-99]A 4th drug, ethambutol or a 5th drug streptomycin, should be

included in intensive phase if drug resistance is suspected .[98, 99,100] There are

about 20 antituberculous drug combination treatments are used.[100]

“ RNTCP or the Revised National Tuberculosis Control Program” - The


has the principles of Directly observed treatment-Shortcourse (DOTS) –which

is the global TB control strategy of the World Health Organization. It is given

at free of cost all over the country through primary health centers and also

through private sector - DOTS providers.


 One of the pillars of DOTS strategy

 Based on the Nature/severity of disease and the Patients' exposure to

previous anti-tubercular treatments

RNTCP classifies tuberculosis patients into 3 Treatment Categories. The

Directly observed treatment Short-course DOTS strategy along with the other

ingredients of STOP TB Partnership are also implemented as a

comprehensive package for TB control.

The five principal components of DOTS are

1. Political and administrative commitment

2. Case detection - Sputum Smear Microscopy

3. Continuous supply of good quality anti-TB drugs

4. Standardized treatment regimens with directly observed treatment for at

least during first two months of treatment



2 $ HRZE daily

2 HRZE daily

2 HRZE thrice weekly

4 s HR daily

4 HR thrice weekly 4 HR thrice weekly 6$ 6 6 Optimal Acceptable if DOT ensured. Acceptable if DOT ensured, and no HIV coinfection or its risk. II Previously treated patients pending DST result

2 HRZES daily +

1 HRZE daily

Empirical (standardized )


5 HRE daily

Empirical (standardized) MDR - regimen

8 18- 24 Or Till DST result For patient with low/medium risk of MDR-TB(failure,defa ult,etc)

For patient with high risk


( failure,2nd default,contact of MDR-TB, etc.)

DST–Drug sensitivity testing ; DOT–Directly Observed therapy , H, R,Z,E,S -Standard codes for isoniazid, rifampicin, pyrazinamide, ethambutol and


Longer course of treatment have been recommended for abdominal


There is no clear evidence that abdominal tuberculosis requires longer

treatment, but the numbers of patients in the reported series are too small for

clinical trials. One study showed only 53% of patients were being treated as

recommended. [102]Compliance with treatment is the major problem which is

the main determinant of treatment outcome.[95]The levels of some acute phase

proteins (C-reactive protein, ceruloplasmin, haptoglobulin, and α1-acid

glyco-protein) usuallyfalls after successful treatment which may be useful for

monitoring .[103] Complications reported other than drug toxicity following

treatment. A distal common bile duct stricture producing Jaundice was

observed following treatment of duodenal tuberculosis.[104]Small-bowel

perforation isalso reported.[105]

India's national tuberculosis-control program provides care, diagnosis,

and treatment on a large scale.When patients with HIV infection are treated at

the same facility like with tuberculosis, effective infection-control measures

are essential due to high risk of nosocomial transmission of tuberculosis.

Incoinfectedpatients,care must be taken in relation to the


 Timing of treatment

 Choice of drugs

 drug interactions

 side effects

 Drug resistance

 Potential reinfection with other mycobacterium strains.

Antiretroviral therapy is essential for reducing the number of deaths from

Tuberculosis that are related to HIV infection.

In India, tuberculosis and HIV care are increasingly being coordinated,

but the full benefits are yet to be realized. An example of successful

coordination is the referral of people with suspected TB from voluntary

counseling & testing centers for HIV to tuberculosis-control facilities. Between

January& September 2006, about 15,000 patients with suspected tuberculosis

who wereHIVpositiveand 16,420 who were HIV-negative were referred by

centers in the six Indian states with the highest HIV prevalence (Andhra

Pradesh, Karnataka, Maharashtra, Manipur, Nagaland, and Tamil Nadu);

tuberculosis was diagnosed in 22.3% and 23.9% of patients in these groups,

respectively. DOTS were begun in mostof these patients. The control of both

Tuberculosis and HIV is likely to be most successful if programs collaborate


Table 1: Estimated TB incidence, prevalence and mortality, 2008

Table 1:

Estimated TB incidence, prevalence and mortality, 2008 p.20
Table 2: Clinical features

Table 2:

Clinical features p.31
Figure1(a):AbdomenX-ray(erectfilm) p.45
Figure 2(a): Barium meal follow through showing distal ileal stricture. (b):Bariumenema showing terminal ileal stricture with proximal dilatation.

Figure 2(a):

Barium meal follow through showing distal ileal stricture. (b):Bariumenema showing terminal ileal stricture with proximal dilatation. p.47
Table 3: Findings of barium meal followthrough study in intestinaltuberculosis

Table 3:

Findings of barium meal followthrough study in intestinaltuberculosis p.48
Figure:3 (a) Abdominal ultrasonography showing enlarged mesentericlymph
Figure:3 (a) Abdominal ultrasonography showing enlarged mesentericlymph p.50
Figure: 4 (a) CT scan at the level of porta showing multiple hypodense nodes
Figure: 4 (a) CT scan at the level of porta showing multiple hypodense nodes p.51
Figure: 8 Algorithmic approaches to diagnosis of abdominal tuberculosis
Figure: 8 Algorithmic approaches to diagnosis of abdominal tuberculosis p.56
Table No. 1 Age distribution

Table No.

1 Age distribution p.72
Table No.  2   Sex distribution

Table No.

2 Sex distribution p.73
Table No. 3

Table No.

3 p.77
Table No. 4 :  Physical Findings

Table No.

4 : Physical Findings p.79
Table No. 5: Mode of Presentation

Table No.

5: Mode of Presentation p.81
Table Number 6: Surgical options

Table Number

6: Surgical options p.86
Table 7: Histopathological diagnosis

Table 7:

Histopathological diagnosis p.89
Table Number: 8

Table Number:

8 p.97
Table Number: 9

Table Number:

9 p.98
Table Number:12

Table Number:12