5. 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
6. • 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
7. Distribution of tuberculous lesions
Ileum > caecum > ascending colon > jejunum
>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
• More than one site may be involved
7
8. • 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
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 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
12. 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
13. Chronic tuberculous peritonitis
• The condition presents with abdominal pain
• Fever
• Loss of weight
• Ascites
• Night sweats
• Abdominal mass
13
14. 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
15. Rare clinical presentations include :
• 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 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
19. 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
20. 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
21. 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
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
• 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
24. Ileocaecal tuberculosis
• Colicky abdominal pain
• ‘Ball of wind’ rolling in abdomen
• Borborygmi
• Right iliac fossa lump - ileocaecal region,
mesenteric fat and LN
24
25. 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
26. 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
27. 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
28. 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
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
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)
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
33. 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
34. 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
37. Treatment
Antituberculous treatment drugs : Akurit – 4
Ripe Kit
• isoniazid
• rifampicin
• pyrazinamide
• ethambutol
• Surgical intervention as and when needed
37
38. Drugs used to treat TB disease. From left to right isoniazid,
rifampin, pyrazinamide, and ethambutol. Streptomycin (not
shown) is given by injection
38
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