“
A STUDY OF SURGICAL MANAGEMENT OF
ABDOMINAL TUBERCULOSIS IN
GOVERNMENT RAJAJI HOSPITAL,MADURAI”
M.S. DEGREE EXAMINATION
BRANCH I - GENERAL SURGERY
Department of General Surgery
MADURAI MEDICAL COLLEGE AND GOVT RAJAJI HOSPITAL
Madurai
–
20
The Tamilnadu Dr.M.G.R. Medical University
Chennai,India
CERTIFICATE
This is to certify that the dissertation entitled “A STUDY OF SURGICAL
MANAGEMENT OF ABDOMINAL TUBERCULOSIS” is a bonafide
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
Surgery
Date: Dr.B.Shanthakumar.M.D(F.M)
Place: The Dean,
Madurai Medical College,
ENDORSEMENT BY THE HEAD OF THE DEPARTMENT
This is to certify that the dissertation entitled “A STUDY OF SURGICAL
MANAGEMENT OF ABDOMINAL TUBERCULOSIS” is a bonafide
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
CERTIFICATE BY THE GUIDE
This is to certify that the dissertation entitled“A STUDY OF SURGICAL
MANAGEMENT OF ABDOMINAL TUBERCULOSIS” is a bonafide
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
DECLARATION BY THE CANDIDATE
This is to certify that the dissertation entitled “A STUDY OF SURGICAL
MANAGEMENT OF ABDOMINAL TUBERCULOSIS” is a bonafide
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
ACKNOWLEDGEMENT
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.
TABLE CONTENTS
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
LIST OF ABBREVIATIONS USED
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
ABSTRACT
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
months.
Results:
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.
Conclusion:
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:
The key words are ABDOMINAL TUBERCULOSIS; SURGERY;
LISTOF TABLES
Sl.no. Tables Page
no.
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
LISTOF CHARTSANDGRAPHS
Sl.no. Figure
s
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
INTRODUCTION
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.
[7-15]
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
unknown.
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
AIM AND OBJECTIVES Aim :
The aim of this study is to evaluate the surgical management of abdominal
tuberculosis.
Objectives of the study:
1. To study the various clincopathological manifestations of abdominal
tuberculosis.
2. To study the various surgical treatment modalities, their complications and
REVIEW OF LITERATURE
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
cavity[2].
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).
EPIDEMIOLOGY OF TUBERCULOSIS:
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 %
[image:20.595.110.541.198.604.2]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
involvement.
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]
AETIOLOGY:
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
Gram-negative.
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
PATHOGENESIS:
ROUTE OF INFECTION
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
Tuberculosis.
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
reaction.
• The Ulcerative type is due to low host immunity and high population of
bacilli with high virulence.
PATHOLOGY
MACROSCOPIC CHANGES
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].
MICROSCOPIC CHANGES:
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
inflammation.[12],[15]
CLASSIFICATION OF ABDOMINAL TUBERCULOSIS:
PERITONEAL TUBERCULOSIS–Acute or Chronic
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
GASTROINTESTINAL
TUBERCULOSIS- Ulcerative
Hyperplastic
Ulcero-Hyperplastic
CLINICAL MANIFESTATIONS:
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
Peritoneal
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
peritoneum.
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
AIDS[57].
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
Extrapulmonary-tuberculosis(pericardial,pleural,meningeal,lymphadenopathic,
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
mortality.[114]
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
patients.[68]
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:
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
(53%).
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
obstruction.[75]
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
1964:
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
Figure1(a):AbdomenX-ray(erectfilm)
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
[image:45.595.87.487.67.319.2]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
deformity”).
“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
[image:47.595.122.502.322.494.2]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
[image:48.595.103.532.326.744.2]malignancy.[84]
Table 3: Findings of barium meal followthrough study in intestinal tuberculosis
Group I
Highly suggestive
of
intestinaltuberculosi
s if one or more of
thefollowing
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
Non-specificchanges
Ultrasonography
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
[image:50.595.88.521.231.364.2]ulceration in terminal ileum, in association with narrowing and proximal
dilatation.
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.
[image:51.595.89.511.427.637.2]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
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]
MANAGEMENT Medical
Treatment:
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.
STANDARDIZED TREATMENT REGIMENS
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
CATEGORYWISE TREATMENT REGIMENS FOR TUBERCULOSIS CATEGORY INTENSIVE PHASE CONTINUATION PHASE DURA TION (months) COMMENTS I NEW PATIENT
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 )
MDR–regimen
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
of MDR–TB
( 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
tuberculosis[101]
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