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ABDOMINAL TUBERCULOSIS
DR SABU AUGUSTINE
ASSOCIATE PROFESSOR
DEPT OF GENERAL MEDICINE
DR S.M C.S.I MEDICAL COLLEGE, KARAKONAM
INTRODUCTION
 Abdominal tuberculosis (TB) includes
involvement of the gastrointestinal tract,
peritoneum, lymph nodes, and/or solid organs.
 Abdominal TB comprises around 5 percent of all
cases of TB worldwide.
RISK FACTORS
 Cirrhosis
 HIV infection,
 Diabetes mellitus,
 Underlying malignancy,
 Malnutrition,
 Treatment with antitumor necrosis factor agents ,
corticosteroids,
 Continuous ambulatory peritoneal dialysis
FORMS OF DISEASE
 Can present with involvement of any of the
following sites:
 Peritoneum,
 Stomach,
 Intestinal tract,
 Hepato-biliary tree,
 Pancreas,
 Perianal region (fistula is common),
 Lymph nodes.
FORMS OF DISEASE
 Most common forms of disease include involvement
of the peritoneum, intestine, and/or lymph nodes
 May occur via
 reactivation of latent TB infection or
 by ingestion of tuberculous mycobacteria (as with
ingestion of unpasteurized milk or undercooked meat).
 In the setting of active pulmonary TB or miliary TB,
abdominal involvement may develop
 via hematogenous spread
 via contiguous spread of TB from adjacent organs (such
as retrograde spread from the fallopian tubes) or
 via spread through lymphatic channels
CLINICAL FEATURES
Depends on the form of disease.
 Fever,
 Weight loss,
 Abdominal pain and/or distension,
 Ascites,
 Hepatomegaly,
 Diarrhea,
 Bowel obstruction, and
 Abdominal mass
PERITONEAL TUBERCULOSIS
 Ascites (93 %), abdominal pain (73 %), and fever
(58 %)
 Visceral & parietal peritoneum become studded
with tubercles.
 Ascites secondary to exudation of proteinaceous
fluid from the tubercles.
PERITONEAL TUBERCULOSIS
 In 10 % patients - a more advanced "dry" phase with
a "doughy" abdomen, which represents a
fibroadhesive form of the disease.
• The absence of signs of chronic liver
disease (such as palmar erythema, spider
angiomata, and dilated abdominal wall
veins) should increase clinical suspicion
for TB peritonitis.
INTESTINAL TUBERCULOSIS
 Most common site of involvement is ileo-cecal
area
 Two types of bowel lesions are seen: ulcerative
(in malnourished) and ulcero-hypertrophic (in
well-nourished).
 Ulcerative and stricturous forms usually in the
small intestine, while colonic and ileocecal
lesions are usually ulcero-hypertrophic.
INTESTINAL TUBERCULOSIS
 Clinical manifestations include intestinal colic,
abdominal distension, chronic diarrhea, nausea,
vomiting, constipation, and Lower GI bleeding.
 In adjacent tissue involvement there will be
ascites, lymph node enlargement, and tubo-
ovarian symptoms.
HEPATIC TUBERCULOSIS
 two presentations
 miliary hepatic disease and
 isolated hepatic disease.
 in 80 % of cases Liver involvement is seen in
disseminated TB.
 In this form TB reaches the liver via the hepatic
artery.
 Isolated hepatic TB occurs in approximately 20 % of
cases where TB reaches the liver from the intestinal
tract via the portal vein or gastrointestinal lymphatics
HEPATIC TUBERCULOSIS
 The most common signs and symptoms of
hepatic TB include hepatomegaly , fever,
respiratory symptoms, abdominal pain , and
weight loss ;
 other signs include splenomegaly , ascites , and
jaundice.
DIAGNOSIS
 Histology and culture of tissue is desirable, but
not always possible.
 Specimens obtained by colonoscopy or
laparoscopy but laparotomy is required in some
cases.
DIAGNOSIS
 Demonstration of M. tuberculosis in peritoneal fluid
(in the setting of ascites) or
 Biopsy specimen of an involved site (such as
peritoneum, intestine, or liver) sent for mycobacterial
culture and/or nucleic acid amplification test (NAAT).
DIAGNOSIS
 Ascitic fluid for routine tests (total & differential
count, albumin and protein, Gram stain).
 As well as adenosine deaminase (ADA) level,
AFB smear, mycobacterial culture, and CbNAAT.
 Straw-colored lymphocytic ascites with serum-
ascites albumin gradient (SAAG) <1.1 g/dL with
an elevated ascites ADA level supports the
diagnosis.
DIAGNOSIS
 Non diagnostic ascitic fluid analysis/in absence
of ascites - peritoneal biopsy can be pursued
according to the clinical suspicion.
 Patients with known or suspected TB warrant
testing for HIV infection.
 CT in intestinal TB
 concentric mural thickening in the ileocecal
region, with or without proximal intestinal
dilatation
DIAGNOSIS
 CT in peritoneal TB
 ascites, lymph nodes, thickening of the
mesentery, omentum, the peritoneum.
 CT in hepatic TB
 miliary hepatic TB- multiple low-density
micronodules dispersed throughout the liver
 local hepatic TB- large solitary nodule or two
to three low-density nodules with calcification.
DIAGNOSIS
 Ultrasound is useful for detecting
lymphadenopathy, ascites, peritoneal thickening,
omental thickening, and bowel wall thickening.
 Small bowel follow-through or barium enema
may demonstrate mucosal ulcerations and
strictures, a deformed cecum, and/or an
incompetent ileocecal valve
DIAGNOSIS
 Plain radiography may demonstrate air fluid
levels with dilated small bowel levels (suggestive
of intestinal obstruction) or hepatic calcifications.
DIFFERENTIAL DIAGNOSIS
 Differential diagnosis includes Crohn’s disease
and Caecal carcinoma.
 Use of immunosuppressive drugs for a
misdiagnosis of Crohn’s disease may be
associated with clinical deterioration in patents
with TB.
DIFFERENTIAL DIAGNOSIS
 Ascites is uncommon in Crohn’s disease.
 TB granulomas tend to be submucosal, large,
and confluent, often with caseation necrosis.
 In Crohn’s disease granulomas are typically
mucosal, infrequent, small, nonconfluent, and
noncaseating.
DIFFERENTIAL DIAGNOSIS
 Malignancy is distinguished from abdominal TB
by ascitic fluid for cytology, and biopsy for culture
and histopathology.
 Malignant ascites - bloody exudate.
 Serum CA-125 concentrations can be elevated in
peritoneal TB also and so this test cannot be
used to distinguish from malignancy.
MANAGEMENT
 Should be treated with Anti-Tubercular Treatment
same as that for pulmonary TB.
 Fever usually resolves within one week of
commencement.
 Ascites will improve within a few weeks of
initiation in 90 % of cases.
MANAGEMENT
 Generally demonstrate clinical improvement
within two to four weeks on empiric therapy.
 Patients who develop bowel obstruction cannot
ingest medications orally, limiting the choice of
drug therapy to injectable agents.
MANAGEMENT
 If no clinical response to ATT within four to eight
weeks, repeat evaluation for alternative
diagnoses such as Crohn disease, lymphoma, or
malignancy.
 Surgery in complications such as perforation,
abscess, fistula, bleeding, obstruction.
Abdominal Tuberculosis by Dr Sabu Augustine

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Abdominal Tuberculosis by Dr Sabu Augustine

  • 1. ABDOMINAL TUBERCULOSIS DR SABU AUGUSTINE ASSOCIATE PROFESSOR DEPT OF GENERAL MEDICINE DR S.M C.S.I MEDICAL COLLEGE, KARAKONAM
  • 2. INTRODUCTION  Abdominal tuberculosis (TB) includes involvement of the gastrointestinal tract, peritoneum, lymph nodes, and/or solid organs.  Abdominal TB comprises around 5 percent of all cases of TB worldwide.
  • 3. RISK FACTORS  Cirrhosis  HIV infection,  Diabetes mellitus,  Underlying malignancy,  Malnutrition,  Treatment with antitumor necrosis factor agents , corticosteroids,  Continuous ambulatory peritoneal dialysis
  • 4. FORMS OF DISEASE  Can present with involvement of any of the following sites:  Peritoneum,  Stomach,  Intestinal tract,  Hepato-biliary tree,  Pancreas,  Perianal region (fistula is common),  Lymph nodes.
  • 5. FORMS OF DISEASE  Most common forms of disease include involvement of the peritoneum, intestine, and/or lymph nodes  May occur via  reactivation of latent TB infection or  by ingestion of tuberculous mycobacteria (as with ingestion of unpasteurized milk or undercooked meat).  In the setting of active pulmonary TB or miliary TB, abdominal involvement may develop  via hematogenous spread  via contiguous spread of TB from adjacent organs (such as retrograde spread from the fallopian tubes) or  via spread through lymphatic channels
  • 6. CLINICAL FEATURES Depends on the form of disease.  Fever,  Weight loss,  Abdominal pain and/or distension,  Ascites,  Hepatomegaly,  Diarrhea,  Bowel obstruction, and  Abdominal mass
  • 7. PERITONEAL TUBERCULOSIS  Ascites (93 %), abdominal pain (73 %), and fever (58 %)  Visceral & parietal peritoneum become studded with tubercles.  Ascites secondary to exudation of proteinaceous fluid from the tubercles.
  • 8. PERITONEAL TUBERCULOSIS  In 10 % patients - a more advanced "dry" phase with a "doughy" abdomen, which represents a fibroadhesive form of the disease. • The absence of signs of chronic liver disease (such as palmar erythema, spider angiomata, and dilated abdominal wall veins) should increase clinical suspicion for TB peritonitis.
  • 9. INTESTINAL TUBERCULOSIS  Most common site of involvement is ileo-cecal area  Two types of bowel lesions are seen: ulcerative (in malnourished) and ulcero-hypertrophic (in well-nourished).  Ulcerative and stricturous forms usually in the small intestine, while colonic and ileocecal lesions are usually ulcero-hypertrophic.
  • 10. INTESTINAL TUBERCULOSIS  Clinical manifestations include intestinal colic, abdominal distension, chronic diarrhea, nausea, vomiting, constipation, and Lower GI bleeding.  In adjacent tissue involvement there will be ascites, lymph node enlargement, and tubo- ovarian symptoms.
  • 11. HEPATIC TUBERCULOSIS  two presentations  miliary hepatic disease and  isolated hepatic disease.  in 80 % of cases Liver involvement is seen in disseminated TB.  In this form TB reaches the liver via the hepatic artery.  Isolated hepatic TB occurs in approximately 20 % of cases where TB reaches the liver from the intestinal tract via the portal vein or gastrointestinal lymphatics
  • 12. HEPATIC TUBERCULOSIS  The most common signs and symptoms of hepatic TB include hepatomegaly , fever, respiratory symptoms, abdominal pain , and weight loss ;  other signs include splenomegaly , ascites , and jaundice.
  • 13. DIAGNOSIS  Histology and culture of tissue is desirable, but not always possible.  Specimens obtained by colonoscopy or laparoscopy but laparotomy is required in some cases.
  • 14. DIAGNOSIS  Demonstration of M. tuberculosis in peritoneal fluid (in the setting of ascites) or  Biopsy specimen of an involved site (such as peritoneum, intestine, or liver) sent for mycobacterial culture and/or nucleic acid amplification test (NAAT).
  • 15. DIAGNOSIS  Ascitic fluid for routine tests (total & differential count, albumin and protein, Gram stain).  As well as adenosine deaminase (ADA) level, AFB smear, mycobacterial culture, and CbNAAT.  Straw-colored lymphocytic ascites with serum- ascites albumin gradient (SAAG) <1.1 g/dL with an elevated ascites ADA level supports the diagnosis.
  • 16. DIAGNOSIS  Non diagnostic ascitic fluid analysis/in absence of ascites - peritoneal biopsy can be pursued according to the clinical suspicion.  Patients with known or suspected TB warrant testing for HIV infection.  CT in intestinal TB  concentric mural thickening in the ileocecal region, with or without proximal intestinal dilatation
  • 17. DIAGNOSIS  CT in peritoneal TB  ascites, lymph nodes, thickening of the mesentery, omentum, the peritoneum.  CT in hepatic TB  miliary hepatic TB- multiple low-density micronodules dispersed throughout the liver  local hepatic TB- large solitary nodule or two to three low-density nodules with calcification.
  • 18. DIAGNOSIS  Ultrasound is useful for detecting lymphadenopathy, ascites, peritoneal thickening, omental thickening, and bowel wall thickening.  Small bowel follow-through or barium enema may demonstrate mucosal ulcerations and strictures, a deformed cecum, and/or an incompetent ileocecal valve
  • 19. DIAGNOSIS  Plain radiography may demonstrate air fluid levels with dilated small bowel levels (suggestive of intestinal obstruction) or hepatic calcifications.
  • 20. DIFFERENTIAL DIAGNOSIS  Differential diagnosis includes Crohn’s disease and Caecal carcinoma.  Use of immunosuppressive drugs for a misdiagnosis of Crohn’s disease may be associated with clinical deterioration in patents with TB.
  • 21. DIFFERENTIAL DIAGNOSIS  Ascites is uncommon in Crohn’s disease.  TB granulomas tend to be submucosal, large, and confluent, often with caseation necrosis.  In Crohn’s disease granulomas are typically mucosal, infrequent, small, nonconfluent, and noncaseating.
  • 22. DIFFERENTIAL DIAGNOSIS  Malignancy is distinguished from abdominal TB by ascitic fluid for cytology, and biopsy for culture and histopathology.  Malignant ascites - bloody exudate.  Serum CA-125 concentrations can be elevated in peritoneal TB also and so this test cannot be used to distinguish from malignancy.
  • 23. MANAGEMENT  Should be treated with Anti-Tubercular Treatment same as that for pulmonary TB.  Fever usually resolves within one week of commencement.  Ascites will improve within a few weeks of initiation in 90 % of cases.
  • 24. MANAGEMENT  Generally demonstrate clinical improvement within two to four weeks on empiric therapy.  Patients who develop bowel obstruction cannot ingest medications orally, limiting the choice of drug therapy to injectable agents.
  • 25. MANAGEMENT  If no clinical response to ATT within four to eight weeks, repeat evaluation for alternative diagnoses such as Crohn disease, lymphoma, or malignancy.  Surgery in complications such as perforation, abscess, fistula, bleeding, obstruction.