Abdominal Tuberculosis
1
Definition
Abdominal Tuberculosis is a condition in which there
is tuberculous infection of the peritoneum or other
organs in the abdomen.
2
Robert Koch, a German Scientist who found out the
causative organism for consumption and revealed his
invention in1882
3
Gram negative bacillus –
Mycobacterium tuberculosis
4
Pathogenesis
• Mechanisms by which M. tuberculosis reach the
GIT:
▫ Hematogenous spread from primary lung focus
▫ Ingestion of bacilli in sputum from active pulmonary
focus.
▫ Direct spread from adjacent organs.
▫ Via lymph channels from infected LN
• In India, organism from all intestinal lesions –
5
• Most common site - ileocaecal region
▫ Increased physiological stasis
▫ Increased rate of fluid and electrolyte absorption
▫ Minimal digestive activity
▫ Abundance of lymphoid tissue at this site.
6
Distribution of tuberculous lesions
Ileum > caecum > ascending colon > jejunum
>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
• More than one site may be involved
7
• Peritoneal involvement occurs from :
▫ Spread from LN
▫ Intestinal lesions or
▫ Tubercular salpingitis
• Abdominal LN and peritoneal TB may occur
without GIT involvement in ~ 1/3 cases.
8
Ways of presentation:
• Acute tuberculous peritonitis
• Chronic tuberculous peritonitis
• Tuberculous stricture of the intestine (small)
causing subacute intestinal obstruction
• Ileo caecal tuberculosis presenting with a mass
in the right iliac fossa.
9
• The most common site of involvement of the GI
tuberculosis is the ileocaecal region.
• Ileocaecal and small bowel tuberculosis presents
with a palpable mass in the right lower quadrant
and/or complications of obstruction, perforation
or malabsorption especially in the presence of
stricture.
10
Tuberculous ulcers in the intestine
11
11
Symptoms and Presentations
Acute tuberculous peritonitis
• Acute abdomen with severe pain
• Acute inflammation of the peritoneum
• Straw coloured fluid
• Tubercles in the greater omentum and peritoneum
• Tubercles may casseate
12
Chronic tuberculous peritonitis
• The condition presents with abdominal pain
• Fever
• Loss of weight
• Ascites
• Night sweats
• Abdominal mass
13
Gastrointestinal TB: Any site along the GI tract
may become infected. Symptoms are referable to the
site infected, including the following:
• abdominal pain mimicking peptic ulcer disease with
stomach or duodenal infection;
• malabsorption with infection of the small intestine;
• and pain, diarrhea, or hematochezia with infection of
the colon.
14
Rare clinical presentations include :
• dysphagia
• odynophagia
• mid oesophageal ulcer due to esophageal tuberculosis,
• dyspepsia and gastric outlet obstruction due to gastro-
duodenal tuberculosis
15
Origin of infection
• Tuberculous mesenteric lymph nodes.
• Tuberculosis of the ileocaecal region.
• Tuberculous pyosalpinx(pus in uterine tube).
• Blood borne infection from pulmonary tuber-
culosis, usually the ‘miliary’ but occasionally the
cavitating form.
16
Varieties of tuberculous peritonitis
• Ascitic form – peritoneal fluid  distension of
abdomen. Patient comes with the complaint of swelling of
the abdomen. – increased abdominal pressure  umbilical
hernia, inguinal hernia
• Purulent form
Rare – usually secondary to tuberculous salpingitis –
pockets of adherent intestines and omentum containing
tuberculous pus. – cold abscesses
• Encysted form
Inflammation and ascites are confined to one part of the
abdominal cavity
• Fibrous form
Wide spread adhesions  adhesive obstruction
17
Circumferential ulceration is characteristic of intestinal
tuberculosis.   
18
Gastrointestinal Tuberculosis
• This is uncommon today because routine pasteuriz-
ation of milk has eliminated Mycobacterium bovis
infections. However,
• Abdominal tuberculosis is usually secondary to pulm-
onary tuberculosis, radiologic evaluation often shows
no evidence of lung disease
• Ileocecum and Colon,The ileocecal region is the most
common area of involvement in the gastrointestinal
tract due to the abundance of lymphoid tissue.
• The natural course of gastrointestinal tuberculosis
may be ulcerative,hypertrophic or ulcerohypertrophic.
19
Gastrointestinal Tuberculosis
• Barium studies demonstrate spasm and
hypermotility with edema of the ileocecal valve in the
early stages
• Later thickening of the ileocecal valve.
• A widely gaping ileocecal valve with narrowing of the
terminal ileum
• A narrowed terminal ileum with rapid emptying of
the diseased segment through a gaping ileocecal
valve into a shortened, rigid, obliterated cecum
• Focal or diffuse aphthous ulcers : tend to be linear or
stellate, following the orientation of lymphoid
follicles (ie, longitudinal in the terminal ileum and
transverse in the colon)
20
Gastrointestinal Tuberculosis
• In advanced cases, symmetric annular stenosis and
obstruction associated with shortening, retraction,
and pouch formation may be seen.
• The cecum becomes conical, shrunken, and retracted
out of the iliac fossa due to fibrosis within the meso-
colon, Ileocecal valve becomes fixed, irregular,
gaping, and incompetent
21
Tuberculosis of esophagus
• Rare ~ 0.2% of total cases
• By extension from adjacent LN
• Low grade fever / Dysphagia / Odynophagia /
Midesophageal ulcer
• Mimics esophageal Ca
22
Gastroduodenal TB
• Stomach and duodenum each ~ 1% of total cases
• Mimics PUD - shorter history, non response to t/t
• Mimics gastric Ca.
• Duodenal obstruction - extrinsic compression by
tuberculous LN
• Hematemesis / Perforation / Fistulae / Obstructive
jaundice
• Cx-Ray usually normal
• Endoscopic picture - non specific
23
Ileocaecal tuberculosis
• Colicky abdominal pain
• ‘Ball of wind’ rolling in abdomen
• Borborygmi
• Right iliac fossa lump - ileocaecal region,
mesenteric fat and LN
24
Obstruction
• Most common complication
Pathogenesis
▫ Hyperplastic caecal TB
▫ Strictures of the small intestine--- commonly multiple
▫ Adhesions
▫ Adjacent LN involvement → traction, narrowing and
fixation of bowel loops.
• In India ~ 3% to 20% of bowel obstruction
25
Perforation
• 5%-9% of SI perforations in India
• 2nd
commonest cause after typhoid
• Usually single and proximal to a stricture
• Clue - TB Chest x-ray, h/o SAIO
• Pneumoperitoneum in ~ 50% cases
26
Malabsorption
• Common
• 2nd only to tropical sprue in India
• Clue----h/o of pain / SAIO
• Pathogenesis
▫ bacterial overgrowth in stagnant loop
▫ bile salt deconjugation
▫ diminished absorptive surface due to ulceration
▫ involvement of lymphatics and LN
27
Segmental / Isolated colonic
tuberculosis
• Involvement of the colon without involvement of
the ileocaecal region
• 9.2% of all cases
• Multifocal involvement in ~ 1/3 (28% to 44%)
28
Investigations
• Blood routine
• Urine routine - to detect diabetes mellitus
• Plain X-ray of the abdomen
• Laparoscopy
• Laparoscopic biopsy of tubercles foun in the
peritoneum or other parts
29
Immunological Tests
• ELISA
• SAFA
• Competitive ELISA
Response to mycobacteria variable &
reproducibility poor
30
Ascitic fluid examination
• Straw coloured
• Protein >3g/dL
• TLC of 150-4000/µl, Lymphocytes >70%
• SAAG < 1.1 g/dL
• ZN stain + in < 3% cases
• + culture in < 20% cases
31
Adenosine Deaminase (ADA)
Aminohydrolase that converts adenosine  inosine
• ADA increased due to stimulation of T-cells by
mycobacterial Ag
▫ Serum ADA > 54 U/L
▫ Ascitic fluid ADA > 36 U/L
▫ Ascitic fluid to serum ADA ratio > 0.985 ( Bhargava et
al)
• Coinfection with HIV → normal or low ADA
32
Colonoscopy
Colonoscopy - 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
33
Laparoscopic Findings
• Thickened peritoneum with tubercles-
▫ Multiple, yellowish white, uniform (~ 4-5mm) tubercles
▫ Peritoneum is thickened & hyperemic
▫ Omentum, liver, spleen also studded with tubercles.
• Thickened peritoneum without tubercles
• Fibro adhesive peritonitis
▫ Markedly thickened peritoneum and multiple thick adhesions
(Bhargava et al)
Caseating granulomas + in 85%-90% of Bx
34
35
Tuberculous
peritonitis –
USGM –
Intestines
floating in
peritoneal
fluid - ascites
36
Treatment
Antituberculous treatment drugs : Akurit – 4
Ripe Kit
• isoniazid
• rifampicin
• pyrazinamide
• ethambutol
• Surgical intervention as and when needed
37

Drugs used to treat TB disease. From left to right isoniazid,
rifampin, pyrazinamide, and ethambutol. Streptomycin (not
shown) is given by injection
38
THANK YOU….. 

Tb

  • 1.
  • 2.
    Definition Abdominal Tuberculosis isa condition in which there is tuberculous infection of the peritoneum or other organs in the abdomen. 2
  • 3.
    Robert Koch, aGerman Scientist who found out the causative organism for consumption and revealed his invention in1882 3
  • 4.
    Gram negative bacillus– Mycobacterium tuberculosis 4
  • 5.
    Pathogenesis • Mechanisms bywhich M. tuberculosis reach the GIT: ▫ Hematogenous spread from primary lung focus ▫ Ingestion of bacilli in sputum from active pulmonary focus. ▫ Direct spread from adjacent organs. ▫ Via lymph channels from infected LN • In India, organism from all intestinal lesions – 5
  • 6.
    • Most commonsite - ileocaecal region ▫ Increased physiological stasis ▫ Increased rate of fluid and electrolyte absorption ▫ Minimal digestive activity ▫ Abundance of lymphoid tissue at this site. 6
  • 7.
    Distribution of tuberculouslesions Ileum > caecum > ascending colon > jejunum >appendix > sigmoid > rectum > duodenum > stomach > oesophagus • More than one site may be involved 7
  • 8.
    • Peritoneal involvementoccurs from : ▫ Spread from LN ▫ Intestinal lesions or ▫ Tubercular salpingitis • Abdominal LN and peritoneal TB may occur without GIT involvement in ~ 1/3 cases. 8
  • 9.
    Ways of presentation: •Acute tuberculous peritonitis • Chronic tuberculous peritonitis • Tuberculous stricture of the intestine (small) causing subacute intestinal obstruction • Ileo caecal tuberculosis presenting with a mass in the right iliac fossa. 9
  • 10.
    • The mostcommon site of involvement of the GI tuberculosis is the ileocaecal region. • Ileocaecal and small bowel tuberculosis presents with a palpable mass in the right lower quadrant and/or complications of obstruction, perforation or malabsorption especially in the presence of stricture. 10
  • 11.
    Tuberculous ulcers inthe intestine 11 11
  • 12.
    Symptoms and Presentations Acutetuberculous peritonitis • Acute abdomen with severe pain • Acute inflammation of the peritoneum • Straw coloured fluid • Tubercles in the greater omentum and peritoneum • Tubercles may casseate 12
  • 13.
    Chronic tuberculous peritonitis •The condition presents with abdominal pain • Fever • Loss of weight • Ascites • Night sweats • Abdominal mass 13
  • 14.
    Gastrointestinal TB: Anysite along the GI tract may become infected. Symptoms are referable to the site infected, including the following: • abdominal pain mimicking peptic ulcer disease with stomach or duodenal infection; • malabsorption with infection of the small intestine; • and pain, diarrhea, or hematochezia with infection of the colon. 14
  • 15.
    Rare clinical presentationsinclude : • dysphagia • odynophagia • mid oesophageal ulcer due to esophageal tuberculosis, • dyspepsia and gastric outlet obstruction due to gastro- duodenal tuberculosis 15
  • 16.
    Origin of infection •Tuberculous mesenteric lymph nodes. • Tuberculosis of the ileocaecal region. • Tuberculous pyosalpinx(pus in uterine tube). • Blood borne infection from pulmonary tuber- culosis, usually the ‘miliary’ but occasionally the cavitating form. 16
  • 17.
    Varieties of tuberculousperitonitis • Ascitic form – peritoneal fluid  distension of abdomen. Patient comes with the complaint of swelling of the abdomen. – increased abdominal pressure  umbilical hernia, inguinal hernia • Purulent form Rare – usually secondary to tuberculous salpingitis – pockets of adherent intestines and omentum containing tuberculous pus. – cold abscesses • Encysted form Inflammation and ascites are confined to one part of the abdominal cavity • Fibrous form Wide spread adhesions  adhesive obstruction 17
  • 18.
    Circumferential ulceration ischaracteristic of intestinal tuberculosis.    18
  • 19.
    Gastrointestinal Tuberculosis • Thisis uncommon today because routine pasteuriz- ation of milk has eliminated Mycobacterium bovis infections. However, • Abdominal tuberculosis is usually secondary to pulm- onary tuberculosis, radiologic evaluation often shows no evidence of lung disease • Ileocecum and Colon,The ileocecal region is the most common area of involvement in the gastrointestinal tract due to the abundance of lymphoid tissue. • The natural course of gastrointestinal tuberculosis may be ulcerative,hypertrophic or ulcerohypertrophic. 19
  • 20.
    Gastrointestinal Tuberculosis • Bariumstudies demonstrate spasm and hypermotility with edema of the ileocecal valve in the early stages • Later thickening of the ileocecal valve. • A widely gaping ileocecal valve with narrowing of the terminal ileum • A narrowed terminal ileum with rapid emptying of the diseased segment through a gaping ileocecal valve into a shortened, rigid, obliterated cecum • Focal or diffuse aphthous ulcers : tend to be linear or stellate, following the orientation of lymphoid follicles (ie, longitudinal in the terminal ileum and transverse in the colon) 20
  • 21.
    Gastrointestinal Tuberculosis • Inadvanced cases, symmetric annular stenosis and obstruction associated with shortening, retraction, and pouch formation may be seen. • The cecum becomes conical, shrunken, and retracted out of the iliac fossa due to fibrosis within the meso- colon, Ileocecal valve becomes fixed, irregular, gaping, and incompetent 21
  • 22.
    Tuberculosis of esophagus •Rare ~ 0.2% of total cases • By extension from adjacent LN • Low grade fever / Dysphagia / Odynophagia / Midesophageal ulcer • Mimics esophageal Ca 22
  • 23.
    Gastroduodenal TB • Stomachand duodenum each ~ 1% of total cases • Mimics PUD - shorter history, non response to t/t • Mimics gastric Ca. • Duodenal obstruction - extrinsic compression by tuberculous LN • Hematemesis / Perforation / Fistulae / Obstructive jaundice • Cx-Ray usually normal • Endoscopic picture - non specific 23
  • 24.
    Ileocaecal tuberculosis • Colickyabdominal pain • ‘Ball of wind’ rolling in abdomen • Borborygmi • Right iliac fossa lump - ileocaecal region, mesenteric fat and LN 24
  • 25.
    Obstruction • Most commoncomplication Pathogenesis ▫ Hyperplastic caecal TB ▫ Strictures of the small intestine--- commonly multiple ▫ Adhesions ▫ Adjacent LN involvement → traction, narrowing and fixation of bowel loops. • In India ~ 3% to 20% of bowel obstruction 25
  • 26.
    Perforation • 5%-9% ofSI perforations in India • 2nd commonest cause after typhoid • Usually single and proximal to a stricture • Clue - TB Chest x-ray, h/o SAIO • Pneumoperitoneum in ~ 50% cases 26
  • 27.
    Malabsorption • Common • 2ndonly to tropical sprue in India • Clue----h/o of pain / SAIO • Pathogenesis ▫ bacterial overgrowth in stagnant loop ▫ bile salt deconjugation ▫ diminished absorptive surface due to ulceration ▫ involvement of lymphatics and LN 27
  • 28.
    Segmental / Isolatedcolonic tuberculosis • Involvement of the colon without involvement of the ileocaecal region • 9.2% of all cases • Multifocal involvement in ~ 1/3 (28% to 44%) 28
  • 29.
    Investigations • Blood routine •Urine routine - to detect diabetes mellitus • Plain X-ray of the abdomen • Laparoscopy • Laparoscopic biopsy of tubercles foun in the peritoneum or other parts 29
  • 30.
    Immunological Tests • ELISA •SAFA • Competitive ELISA Response to mycobacteria variable & reproducibility poor 30
  • 31.
    Ascitic fluid examination •Straw coloured • Protein >3g/dL • TLC of 150-4000/µl, Lymphocytes >70% • SAAG < 1.1 g/dL • ZN stain + in < 3% cases • + culture in < 20% cases 31
  • 32.
    Adenosine Deaminase (ADA) Aminohydrolasethat converts adenosine  inosine • ADA increased due to stimulation of T-cells by mycobacterial Ag ▫ Serum ADA > 54 U/L ▫ Ascitic fluid ADA > 36 U/L ▫ Ascitic fluid to serum ADA ratio > 0.985 ( Bhargava et al) • Coinfection with HIV → normal or low ADA 32
  • 33.
    Colonoscopy Colonoscopy - mucosalnodules & 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 33
  • 34.
    Laparoscopic Findings • Thickenedperitoneum with tubercles- ▫ Multiple, yellowish white, uniform (~ 4-5mm) tubercles ▫ Peritoneum is thickened & hyperemic ▫ Omentum, liver, spleen also studded with tubercles. • Thickened peritoneum without tubercles • Fibro adhesive peritonitis ▫ Markedly thickened peritoneum and multiple thick adhesions (Bhargava et al) Caseating granulomas + in 85%-90% of Bx 34
  • 35.
  • 36.
  • 37.
    Treatment Antituberculous treatment drugs: Akurit – 4 Ripe Kit • isoniazid • rifampicin • pyrazinamide • ethambutol • Surgical intervention as and when needed 37 
  • 38.
    Drugs used totreat TB disease. From left to right isoniazid, rifampin, pyrazinamide, and ethambutol. Streptomycin (not shown) is given by injection 38 THANK YOU….. 

Editor's Notes

  • #4 Consumption = TB