INTESTINAL
TUBERCULOSIS
House surgeon
Sadia Shabbir
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
Etiopathogenesis
• Mechanisms by which M. tuberculosis reach the GIT:
By ingestion
– Ingestion of food contaminated with tubercle
bacilli causing Primary Intestinal Tuberculosis
– Ingestion of sputum containing tuberculous
bacteria from primary pulmonary focus -
Secondary Intestinal Tuberculosis
Hematogenous spread from primary lung focus
Direct spread from adjacent organs.
Via lymph channels from infected LN
PATHOGENESIS
Bacilli in the depth of mucosal
glands
Inflammatory Reaction
Phagocytes carry bacilli to Peyer’s
Patches
Formation of tubercle and necrosis
Endarteritis,edema and sloughing
Ulcer formation
Accumulation of collagen-
Thickening and stenosis
Inflammation spreads from
submucosa to serosa
Bacilli via lymphatics – Lympahtic
obstruction and Regional
Lymphadenitis
Ileocaecal Tuberculosis
• Most common site of abdominal tuberculosis
due to:
– Stasis
– Abundant payer’s patches
– Alkaline media
– Bacterial contact time is more
– Minimal digestive activity
– Maximum absorption in the area
Characterisitc lesions
A.Ulcerative :
• Multiple circumferential
transverse ulcers (Girdle ulcers)
with skip leisons
• Napkin ring strictures in
longstanding ulcers (common in
ileum)
• Intestinal nodes involvement
with caseation and abscess
B. Hyperplastic Type
• Chronic granulomatous
lesions in ileoceacal
region
• Fibroblastic activity in
submucosa and
subserosa causes
thickening of bowel
wall with lymph node
enlargement
C. Stricturous type:
• Characterized by strictures – multiple or single
D. Diffuse colitis:
• Rare form, very similar to ulceratice colitis
Distribution of tuberculous lesions
Ileum > caecum > ascending colon > jejunum
>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
• More than one site may be involved
Symptoms
• Local symptoms depending upon site involved
• Constitutional symptoms are:
• Fever
• Malaise
• Anemia
• Night sweats
• Loss of weight
• Pain abdomen: colicky if luminal compromise,
dull and continuous when mesenteric lymph
nodes are involved
• Alteration in bowel habit, diarrhea, constipation
or together, malabsorption, rectal bleeding etc.
Complications
• Intestinal Obstruction:
Most common complication
Mechanism: hyperplastic intestinal lesion,
strictures, adhesion and adjacent lymph node
involvement
• Malabsoprption, blind loop syndrome
• Perforation:
2nd commonest cause of small intestinal
perforation, first being typhoid fever
• Usually single & proximal to a stricture
• Dissemination of tuberculosis Cold abscess
• formation Hemorrhage
• Fecal fistula
• Gastric outlet obstruction
Investigations
• Blood investgations:
Anaemia
Leucopenia with lymphocytosis
Raised ESR
• Mantoux test:
Gives supportive evidence to the diagnosis
Positive in 50 – 70% cases
• Chest Xray: may reveal either healed or active
pulmonary tuberculosis
Plain X ray abdomen:
• Intestinal obstruction
• Calcified lymph nodes
• Hollow viscus perforation
• On Barium
enema
• Loss of normal
ileocaecal angle
and dilated
terminal ileum,
appearing
suspended from
a retracted
fibrosed caecum
– goose neck
deformity
Contrast barium enema
image demonstrates
marked narrowing of the
caecum, ascending colon
and terminal ileum.
Dilatation of the small
intestine proximal to the
narrowed segment of
ileum is also seen.
USG abdomen
Thickened bowel wall
– Loculated ascitis
– Interloop ascitis
– Mesenteric thickening
– Lymph node
enlargement
– Pulled up caecum
(Pseudokidney sign)
Ultrasound image. Multiple enlarged
conglomerate lymphnodes in retroperitoneum
with hypoechoic centers due to caseation
CT Abdomen
• Circumferential wall
thickening of cecum and
terminal ileum
• Asymmetric thickening of
ileoceacal valve and medial
wall of ceacum
• Localized mesenteric
lymphadenopathy with
areas of central low
attenuation
Treatment
• Mediacal management: on same lines as for pulmonary
tuberculosis
• › First line drugs:
 INH
 Rifampicin
Pyrazinamid
 Ethambutol
• › Second line drugs:
Amikacin, kanamycin, PAS, Ciprofloxacin,
Clarithrymycin, Azythromycin, Rifabutin
• › Treatment to be continued for 6 months › Supportive
nutrition
Surgical Management:
• › Indications:
Intestinal obstruction
Severe hemorrhage
Acute abdomen (perforation)
Intra-abdominal abscesses/ fistula formation
Uncertain diagnosis
FOR YOUR KIND LISTENING
THANK YOU….
24

intetinal tuberculosis

  • 1.
  • 2.
    Introduction • TB caninvolve any part of GIT from mouth to anus, peritoneum & pancreatobiliary system. • TB of GIT- 6th most frequent extrapulmonary site.
  • 3.
    • Mycobacterium tuberculosisis the pathogen in most cases. • Mycobacterium bovis in some parts of the world
  • 4.
    Etiopathogenesis • Mechanisms bywhich M. tuberculosis reach the GIT: By ingestion – Ingestion of food contaminated with tubercle bacilli causing Primary Intestinal Tuberculosis – Ingestion of sputum containing tuberculous bacteria from primary pulmonary focus - Secondary Intestinal Tuberculosis Hematogenous spread from primary lung focus Direct spread from adjacent organs. Via lymph channels from infected LN
  • 5.
  • 6.
    Bacilli in thedepth of mucosal glands Inflammatory Reaction Phagocytes carry bacilli to Peyer’s Patches Formation of tubercle and necrosis Endarteritis,edema and sloughing
  • 7.
    Ulcer formation Accumulation ofcollagen- Thickening and stenosis Inflammation spreads from submucosa to serosa Bacilli via lymphatics – Lympahtic obstruction and Regional Lymphadenitis
  • 8.
    Ileocaecal Tuberculosis • Mostcommon site of abdominal tuberculosis due to: – Stasis – Abundant payer’s patches – Alkaline media – Bacterial contact time is more – Minimal digestive activity – Maximum absorption in the area
  • 9.
    Characterisitc lesions A.Ulcerative : •Multiple circumferential transverse ulcers (Girdle ulcers) with skip leisons • Napkin ring strictures in longstanding ulcers (common in ileum) • Intestinal nodes involvement with caseation and abscess
  • 10.
    B. Hyperplastic Type •Chronic granulomatous lesions in ileoceacal region • Fibroblastic activity in submucosa and subserosa causes thickening of bowel wall with lymph node enlargement
  • 11.
    C. Stricturous type: •Characterized by strictures – multiple or single D. Diffuse colitis: • Rare form, very similar to ulceratice colitis
  • 12.
    Distribution of tuberculouslesions Ileum > caecum > ascending colon > jejunum >appendix > sigmoid > rectum > duodenum > stomach > oesophagus • More than one site may be involved
  • 13.
    Symptoms • Local symptomsdepending upon site involved • Constitutional symptoms are: • Fever • Malaise • Anemia • Night sweats • Loss of weight • Pain abdomen: colicky if luminal compromise, dull and continuous when mesenteric lymph nodes are involved • Alteration in bowel habit, diarrhea, constipation or together, malabsorption, rectal bleeding etc.
  • 14.
    Complications • Intestinal Obstruction: Mostcommon complication Mechanism: hyperplastic intestinal lesion, strictures, adhesion and adjacent lymph node involvement • Malabsoprption, blind loop syndrome • Perforation: 2nd commonest cause of small intestinal perforation, first being typhoid fever • Usually single & proximal to a stricture
  • 15.
    • Dissemination oftuberculosis Cold abscess • formation Hemorrhage • Fecal fistula • Gastric outlet obstruction
  • 16.
    Investigations • Blood investgations: Anaemia Leucopeniawith lymphocytosis Raised ESR • Mantoux test: Gives supportive evidence to the diagnosis Positive in 50 – 70% cases • Chest Xray: may reveal either healed or active pulmonary tuberculosis
  • 17.
    Plain X rayabdomen: • Intestinal obstruction • Calcified lymph nodes • Hollow viscus perforation
  • 18.
    • On Barium enema •Loss of normal ileocaecal angle and dilated terminal ileum, appearing suspended from a retracted fibrosed caecum – goose neck deformity
  • 19.
    Contrast barium enema imagedemonstrates marked narrowing of the caecum, ascending colon and terminal ileum. Dilatation of the small intestine proximal to the narrowed segment of ileum is also seen.
  • 20.
    USG abdomen Thickened bowelwall – Loculated ascitis – Interloop ascitis – Mesenteric thickening – Lymph node enlargement – Pulled up caecum (Pseudokidney sign) Ultrasound image. Multiple enlarged conglomerate lymphnodes in retroperitoneum with hypoechoic centers due to caseation
  • 21.
    CT Abdomen • Circumferentialwall thickening of cecum and terminal ileum • Asymmetric thickening of ileoceacal valve and medial wall of ceacum • Localized mesenteric lymphadenopathy with areas of central low attenuation
  • 22.
    Treatment • Mediacal management:on same lines as for pulmonary tuberculosis • › First line drugs:  INH  Rifampicin Pyrazinamid  Ethambutol • › Second line drugs: Amikacin, kanamycin, PAS, Ciprofloxacin, Clarithrymycin, Azythromycin, Rifabutin • › Treatment to be continued for 6 months › Supportive nutrition
  • 23.
    Surgical Management: • ›Indications: Intestinal obstruction Severe hemorrhage Acute abdomen (perforation) Intra-abdominal abscesses/ fistula formation Uncertain diagnosis
  • 24.
    FOR YOUR KINDLISTENING THANK YOU…. 24