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DR MASOODTAREEN
RESIDENTGASTRO
LNH KHI
ABDOMINAL TUBERCULOSIS
INTRODUCTION
 Tuberculosis, MTB, in the past also called phthisis, phthisis
pulmonalis or consumption caused by various strains of
mycobacteria usually Mycobacterium tuberculosis.
 Until mid 1800s, many believed TB was hereditary .
 1865 Jean Antoine-Villemin proved TB was contagious
 Robert Koch discovered M. tuberculosis, the bacterium that
causes TB in 1882.
INTRODUCTION
TB can involve any part of GIT from mouth to
anus, peritoneum & pancreatobiliary system
TB of GIT- 6th most frequent extrapulmonary
site
Mycobacterium tuberculosis is the pathogen in
most cases.
Mycobacterium bovis in some parts of the world
Mycobacterium avium intracellulare has become
a major pathogen in HIV patients.
ETIOPATHOGENESIS
 Ingestion of milk or infected food
 Swallowing of sputum in active PTB
 Hematogenous spread from active pulmonary lesion, miliary
tuberculosis
 Contiguous spread from infected foci like
 fallopian tubes, mesenteric lymph node
 Very rarely as a consequence of peritoneal
 dialYSIS
CLASSIFICATION OF ABDOMINAL
TB
 Gastrointestinal Tuberculosis
 Tuberculosis OfThe SolidViscera
 PeritonealTuberculosis
 Tuberculosis OfThe Mesentery And Its Contents
GASTROINTESTINALTUBERCULOSIS
 Ulcerative
 Hypertrophic
 Sclerotic or fibrous
 Diffuse colitis
Peritoneal tuberculosis
 -Acute
 -Chronic
o Ascitic form
o Encysted form
o Fibrous form
Tuberculosis of the solid viscera
 Liver ,BILLIARYTRACT
 Pancreas
 Spleen
 Tuberculosis of the mesentery and its contents
o Mesentric adenitis
o Mesentric abscess
o Bowel adhesions
MISCELLANOUS
 Retroperitoneal lymph node tuberculosis
G I TUBERCULOSIS
 Constitutes 70 to80% of abdominal tuberculosis.
 Ileoceacal area most commonly affected.
 It can be of ulcerative, hypertrophic, diffuse
colitis, ulcerohypertrophic, and sclerotic forms.
 Luminal narrowing is often caused by adjacent
lymphadenitis which results in traction diverticula
formation, narrowing and sinus tract formation.
G I Tuberculosis
 Ulcerative form
Usually occurs in adult patients who
are malnourished
Ulcers lie transverse “girdle ulcers”
Areas of the normal appearing mucosa
may be found
Healing and fibrosis results in stricture
Hypertrophic form Commonly occurs in young
patients who are relatively well nourished.
Characterized by extensive inflammation and
fibrosis which often results in adherence of bowel,
mesentery and lymph nodes
CLINICAL FEATURES
 20 to 40 yrs age group most often affected
 Most common symptom is;
 abdominal pain
 others include abdominal distention, witless anorexia,
fever, diarrhea or constipation bleeding per rectum.
 Signs include
 Anemia, malnutrition, abdominal tenderness, as cites,
mass in the right iliac fossa And features of intestinal
obstruction.
Peritoneal Tuberculosis
sis
 Acute tuberculous peritonitis
 Chronic tuberculous peritonitis
A. Ascitic form
o Insidious in onset, abdominal pain usually absent, rolled up
omentum infiltrated with tubercle may felt as a transverse
solid mass
B. Encysted (loculated) form
C. Fibrous form
o Wide spread adhesions may cause coils of intestine matted
together and distended, they may act as blind loop
HEPATOBILARY TB
 In a patient with PUO, marked elevation of serum alkaline
phosphatase(3 to 6 times) with mild elevation of s.transaminases,
normal PT, s.albumin and a slight increase in bilirubin, hepatic
tuberculosis should be suspected
 CLINICAL SYNDROMES OF HEPATOBILIARY
TUBERCULOSIS
 Congenital tuberculosis
 Primary hepatic tuberculosis
 Disseminated/miliary tuberculosis
 Tuberculoma
 Tuberculosis of biliary tract
 Hepatic failure
 Granulomatous hepatitis
INVESTIGATIONS
 Hematology &serum biochemistry
 Anemia, raised ESR, hypoalbumenemia,
leucopenia
 with relative lymphocytosis, normal serum
 transminase level, raised serum ALP
ASCITIC FLUID EXAMINATION
 Exudative, fluid protein>3gm%, SAAG<1.1
 Ascitic/blood glucose ratio<0.96,
 WBC count usually 140 to 4000cells/mm³
consist of lymphocytes predominantly,
AFB(+<3%),
 culture(+<20%), IFN-γ increased
 ADA((98%sensitivity&95%specificityat cut
off value 32 IU/L), PCR
 Monteux test (positive in 50 to 100%)
INVESTIGATIONS
 CUlture medium
 Lowenstein-Jensen
 Liquid medium
 QuantiFERON-TB test(QFT)
 BACTEC radiometric system
 Mycobacterial Growth indicator tubes
 Animal pathogenicity
 PCR assay
 Ligase chain reaction
Illeoceacal TB (80-90%)
PLAIN XRAY
May show calcified lymph nodes or granulomas in
the liver, spleen, pancreas. Other features include
dilated loops with fluid levels, dilatation of
terminal ileum and ascites .
BARIUM ENEMA
 Irregular thickened nodular folds in the
terminal illeum
 ‘Stierlin sign’: on ba enema -rapid emptying
of narrowed terminal illeum into the cecum
which is shortened and rigidThickened
illeoceacal valve
Enema Shows Wide Gaping Of Ileocecal
Valve With Thickkening Of Valve
Barium Meal Follow Through
Highly s/o intestinalTB if one or more of the
following features are present.
a. Deformed ileocaecal valve with dilatation of
terminal ileum.
b. Contracted cecum with an abnormal ileocaecal
valve and/or terminal ileum
c. Stricture of the ascending colon with
shortening of and involvement of ileocaecal region
ULTRASOUND
 ‘Fleischner sign’: Inverted umbrella defect:-
wide gaping patulous IC valve associated with
narrowing of the immediately adjacent
terminal illeum
 Deep fissures and large shallow linear/stellate
ulcers with elevated margins Sinus tracts and
fistulas
 Symmetric annular ‘napkin ring ‘ stenosis
ABDOMINAL CT
 CT is better than USG in detecting high dense ascites
 Abdominal lymphadenopathy is the commonest
manifestation of tuberculosis on CT
 Retroperitoneal, peripancreatic, porta hepatis, and
mesenteric/omental lymph node enlargement may
be evident.
 Caseous necrosing lymph node appears as low
attenuating, necrotic centers and thick, enhancing
inflammatory rim.
 Preferential thickening of the medial caecal wall with
an exophytic mass engulfing the terminal ileum
associated with massive lymphadenopathy is
characteristic of tuberculosis
ENDOSCOPY
 Colonoscopy:- Ulceration is the most common
finding.
 Ileocaecal valve may edematous or deformed.
Nodules, ulcers, pseudopolyps may be seen. A
combination of histology and culture can
establish diagnosis in 80% of cases.
 Fine needle aspiration cytology
 Peritoneal biopsy
COLONOSCOPY
 COLONOSCOPYY - mucosal nodules & ulcers Nodules;
Variable sizes (2 to 6mm)
 Non friable
 Most common in caecum especially near IC valve.
TUBERCULAR ULCERS;
 Large (10 to 20mm) or small (3 to 5mm)
 Located between the nodules
 Single or multiple
 Transversely oriented / circumferential contrast to Crohns
 Healing of these ‘girdle ulcers’→ strictures
 Deformed and edematous ileocaecal valve
COLONOSCOPIC DIAGNOSIS
 8 –10 Bx from ulcer edge
 Low yield on histopath as mainly submucosal
disease
 Granulomas in 8%-48%
 Caseation in ~ 1/3 (33%-38%) of + cases
 AFB stains – variable
 Culture positivity in 40%
 Combination of histology & culture ⇒
diagnosis in 60%
LAPROSCOPY
 Most Effective Method. 80 to 95% diagnostic
accuracy. Characteristic finding include multiple,
yellowish-white miliary nodules over
peritoneum, erythematous, thickened and
hyperemic peritoneum
TREATMENT
 MedicalTreatment
 standard 12 month regimen
 Corticosteroids-role not well established
 A six month short-courseATT is as effective
 SurgicalTreatment
 To manage complication such as obstruction,
perforation and massive hemorrhage
 Strictures by stricturoplasty or resection
 Perforation by resection and anastomosis
 Bypass surgery not indicated
 Surgery followed by full course of ATT
DRUG INDUCED HEPATITIS
 Once the diagnosis of DIH is established;
 first stop all potentially hepatotoxic drugs .
 In the interim period, at least three non-hepatotoxic drugs
such as ethambutol, streptomycin and quinolones such as
levofloxacin or ofloxacin or ciprofloxacin can be used
 . After complete resolution of transaminitis, most
antituberculosis drugs can be safely restarted in a phased
manner.
 The BTS suggested that the first-line drugs can be
reintroduced sequentially in the order isoniazid, rifampicin
and pyrazinamide.
 Abdominal tuberculosis, a frequently recognized form
extrapulmonary tuberculosis is increasing with increasing
frequency of HIV infection.
 A high index clinical suspicion, appropriate and timely
I Investigations, early diagnosis and treatment can
considerably reduce the morbidity and mortality from
this curable but potentially lethal disease.
THANK YOU

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Abdominal tb (dr masood tareen)

  • 1.
  • 3. INTRODUCTION  Tuberculosis, MTB, in the past also called phthisis, phthisis pulmonalis or consumption caused by various strains of mycobacteria usually Mycobacterium tuberculosis.  Until mid 1800s, many believed TB was hereditary .  1865 Jean Antoine-Villemin proved TB was contagious  Robert Koch discovered M. tuberculosis, the bacterium that causes TB in 1882.
  • 4. INTRODUCTION TB can involve any part of GIT from mouth to anus, peritoneum & pancreatobiliary system TB of GIT- 6th most frequent extrapulmonary site
  • 5. Mycobacterium tuberculosis is the pathogen in most cases. Mycobacterium bovis in some parts of the world Mycobacterium avium intracellulare has become a major pathogen in HIV patients.
  • 6. ETIOPATHOGENESIS  Ingestion of milk or infected food  Swallowing of sputum in active PTB  Hematogenous spread from active pulmonary lesion, miliary tuberculosis  Contiguous spread from infected foci like  fallopian tubes, mesenteric lymph node  Very rarely as a consequence of peritoneal  dialYSIS
  • 7. CLASSIFICATION OF ABDOMINAL TB  Gastrointestinal Tuberculosis  Tuberculosis OfThe SolidViscera  PeritonealTuberculosis  Tuberculosis OfThe Mesentery And Its Contents
  • 8. GASTROINTESTINALTUBERCULOSIS  Ulcerative  Hypertrophic  Sclerotic or fibrous  Diffuse colitis
  • 9. Peritoneal tuberculosis  -Acute  -Chronic o Ascitic form o Encysted form o Fibrous form
  • 10. Tuberculosis of the solid viscera  Liver ,BILLIARYTRACT  Pancreas  Spleen
  • 11.  Tuberculosis of the mesentery and its contents o Mesentric adenitis o Mesentric abscess o Bowel adhesions
  • 13. G I TUBERCULOSIS  Constitutes 70 to80% of abdominal tuberculosis.  Ileoceacal area most commonly affected.  It can be of ulcerative, hypertrophic, diffuse colitis, ulcerohypertrophic, and sclerotic forms.  Luminal narrowing is often caused by adjacent lymphadenitis which results in traction diverticula formation, narrowing and sinus tract formation.
  • 14. G I Tuberculosis  Ulcerative form Usually occurs in adult patients who are malnourished Ulcers lie transverse “girdle ulcers” Areas of the normal appearing mucosa may be found Healing and fibrosis results in stricture
  • 15. Hypertrophic form Commonly occurs in young patients who are relatively well nourished. Characterized by extensive inflammation and fibrosis which often results in adherence of bowel, mesentery and lymph nodes
  • 16. CLINICAL FEATURES  20 to 40 yrs age group most often affected  Most common symptom is;  abdominal pain  others include abdominal distention, witless anorexia, fever, diarrhea or constipation bleeding per rectum.  Signs include  Anemia, malnutrition, abdominal tenderness, as cites, mass in the right iliac fossa And features of intestinal obstruction.
  • 17. Peritoneal Tuberculosis sis  Acute tuberculous peritonitis  Chronic tuberculous peritonitis A. Ascitic form o Insidious in onset, abdominal pain usually absent, rolled up omentum infiltrated with tubercle may felt as a transverse solid mass B. Encysted (loculated) form C. Fibrous form o Wide spread adhesions may cause coils of intestine matted together and distended, they may act as blind loop
  • 18. HEPATOBILARY TB  In a patient with PUO, marked elevation of serum alkaline phosphatase(3 to 6 times) with mild elevation of s.transaminases, normal PT, s.albumin and a slight increase in bilirubin, hepatic tuberculosis should be suspected  CLINICAL SYNDROMES OF HEPATOBILIARY TUBERCULOSIS  Congenital tuberculosis  Primary hepatic tuberculosis  Disseminated/miliary tuberculosis  Tuberculoma  Tuberculosis of biliary tract  Hepatic failure  Granulomatous hepatitis
  • 19. INVESTIGATIONS  Hematology &serum biochemistry  Anemia, raised ESR, hypoalbumenemia, leucopenia  with relative lymphocytosis, normal serum  transminase level, raised serum ALP
  • 20. ASCITIC FLUID EXAMINATION  Exudative, fluid protein>3gm%, SAAG<1.1  Ascitic/blood glucose ratio<0.96,  WBC count usually 140 to 4000cells/mm³ consist of lymphocytes predominantly, AFB(+<3%),  culture(+<20%), IFN-γ increased  ADA((98%sensitivity&95%specificityat cut off value 32 IU/L), PCR  Monteux test (positive in 50 to 100%)
  • 21. INVESTIGATIONS  CUlture medium  Lowenstein-Jensen  Liquid medium  QuantiFERON-TB test(QFT)  BACTEC radiometric system  Mycobacterial Growth indicator tubes  Animal pathogenicity  PCR assay  Ligase chain reaction
  • 22. Illeoceacal TB (80-90%) PLAIN XRAY May show calcified lymph nodes or granulomas in the liver, spleen, pancreas. Other features include dilated loops with fluid levels, dilatation of terminal ileum and ascites .
  • 23. BARIUM ENEMA  Irregular thickened nodular folds in the terminal illeum  ‘Stierlin sign’: on ba enema -rapid emptying of narrowed terminal illeum into the cecum which is shortened and rigidThickened illeoceacal valve
  • 24. Enema Shows Wide Gaping Of Ileocecal Valve With Thickkening Of Valve
  • 25. Barium Meal Follow Through Highly s/o intestinalTB if one or more of the following features are present. a. Deformed ileocaecal valve with dilatation of terminal ileum. b. Contracted cecum with an abnormal ileocaecal valve and/or terminal ileum c. Stricture of the ascending colon with shortening of and involvement of ileocaecal region
  • 26. ULTRASOUND  ‘Fleischner sign’: Inverted umbrella defect:- wide gaping patulous IC valve associated with narrowing of the immediately adjacent terminal illeum  Deep fissures and large shallow linear/stellate ulcers with elevated margins Sinus tracts and fistulas  Symmetric annular ‘napkin ring ‘ stenosis
  • 27. ABDOMINAL CT  CT is better than USG in detecting high dense ascites  Abdominal lymphadenopathy is the commonest manifestation of tuberculosis on CT  Retroperitoneal, peripancreatic, porta hepatis, and mesenteric/omental lymph node enlargement may be evident.  Caseous necrosing lymph node appears as low attenuating, necrotic centers and thick, enhancing inflammatory rim.  Preferential thickening of the medial caecal wall with an exophytic mass engulfing the terminal ileum associated with massive lymphadenopathy is characteristic of tuberculosis
  • 28.
  • 29. ENDOSCOPY  Colonoscopy:- Ulceration is the most common finding.  Ileocaecal valve may edematous or deformed. Nodules, ulcers, pseudopolyps may be seen. A combination of histology and culture can establish diagnosis in 80% of cases.  Fine needle aspiration cytology  Peritoneal biopsy
  • 30. COLONOSCOPY  COLONOSCOPYY - mucosal nodules & ulcers Nodules; Variable sizes (2 to 6mm)  Non friable  Most common in caecum especially near IC valve. TUBERCULAR ULCERS;  Large (10 to 20mm) or small (3 to 5mm)  Located between the nodules  Single or multiple  Transversely oriented / circumferential contrast to Crohns  Healing of these ‘girdle ulcers’→ strictures  Deformed and edematous ileocaecal valve
  • 31. COLONOSCOPIC DIAGNOSIS  8 –10 Bx from ulcer edge  Low yield on histopath as mainly submucosal disease  Granulomas in 8%-48%  Caseation in ~ 1/3 (33%-38%) of + cases  AFB stains – variable  Culture positivity in 40%  Combination of histology & culture ⇒ diagnosis in 60%
  • 32.
  • 33. LAPROSCOPY  Most Effective Method. 80 to 95% diagnostic accuracy. Characteristic finding include multiple, yellowish-white miliary nodules over peritoneum, erythematous, thickened and hyperemic peritoneum
  • 34.
  • 35. TREATMENT  MedicalTreatment  standard 12 month regimen  Corticosteroids-role not well established  A six month short-courseATT is as effective  SurgicalTreatment  To manage complication such as obstruction, perforation and massive hemorrhage  Strictures by stricturoplasty or resection  Perforation by resection and anastomosis  Bypass surgery not indicated  Surgery followed by full course of ATT
  • 36. DRUG INDUCED HEPATITIS  Once the diagnosis of DIH is established;  first stop all potentially hepatotoxic drugs .  In the interim period, at least three non-hepatotoxic drugs such as ethambutol, streptomycin and quinolones such as levofloxacin or ofloxacin or ciprofloxacin can be used  . After complete resolution of transaminitis, most antituberculosis drugs can be safely restarted in a phased manner.  The BTS suggested that the first-line drugs can be reintroduced sequentially in the order isoniazid, rifampicin and pyrazinamide.
  • 37.  Abdominal tuberculosis, a frequently recognized form extrapulmonary tuberculosis is increasing with increasing frequency of HIV infection.  A high index clinical suspicion, appropriate and timely I Investigations, early diagnosis and treatment can considerably reduce the morbidity and mortality from this curable but potentially lethal disease.