Abdominal tuberculosis by dr waseem ashraf skims

MODERN
MANAGEMENT
OF ABDOMINAL
TUBERCULOSIS
DR WASEEM ASHRAF
PG General Surgery
SKIMS-Srinagar
MODERATOR
Dr NATASHA THAKUR
Assistant Professor
Deptt. Of General Surgery

TUBERCULOSIS
 Major health problem
 7-10 million new cases annually
 6% of deaths world wide
 Abdominal tuberculosis is a common extrapulmonary
manifestation of tuberculosis.
 Of non HIV patients 10 – 15 % have extrapulmonary
manifestations of tuberculosis .
 HIV infected patients > 50% have extra pulmonary
manifestations of tuberculosis
There is a resurgence of abdominal tuberculosis due to multidrug resistance
and co existence of HIV – AIDS.

 In India, around 3 – 20 % of all cases of bowel obstruction are
due to tuberculosis.
 Tuberculosis accounts for 5 – 9 % of all small intestinal
perforations in India, second commonest cause after typhoid
fever.
 Abdominal tuberculosis is an important cause of
Malabsorption syndrome in India.

4
Epidemiology:
 Both gender: equally affected
 Most common age: 35-45 years
Risk factors:
 Alcoholic liver disease
 HIV infection
 9% of all new TB cases are related to HIV
 Advanced age
 Low socioeconomic status

Etiology
 Mycobacterium tuberculosis
Pathogen for most cases of abdominal tuberculosis
 Mycobacterium bovis
Cause in small percentage of cases, in developing
countries. Transmitted by unpasteurized diary products.
 Mycobacterium Avium complex
more likely in HIV infected patients

• Tuberculosis in the Globe
•
Pulmonary TB
Extrapulmonary TB
87.5%
10%
2.5%
Abdominal tuberculosis
(~11-16% of extrapulomnary TB)

Mode of infection
Swallowing of
infected sputum
Hematogenous spread
from pulmonary focus
Ingestion of contaminated
milk products
Direct spread from
adjacent organs
Pathogenesis of abdominal TB

Potential fates..Potential fates..
The bacilli have 4 potential fates:
1. They may be killed by the immune
system,
2. They may multiply and cause primary TB,
3. They may become dormant and remain
asymptomatic, or
4. They may proliferate after a latency period
(reactivation disease).
10

Intestinal
49%
Peritoneal
42%
Nodal
4%
Solid visceral
5%
Abdominal tuberculosis
Others
1.3%

1. Intestinal tuberculosis
Ileocaecal
region
Small bowel
& colon

Order of Frequency
Ileum > caecum > ascending colon > jejunum
>appendix > sigmoid > rectum > duodenum
> stomach > oesophagus
• More than one site may be involved

1. Intestinal tuberculosis
Ileocaecal region
Ileal region
• Ulcerative 60%
• Hypertrophic 10%
• Ulcerohypertrophic 30%
• Stricture type

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
Ileocaecal Tuberculosis

A. Ulcerative type (60%)
 Secondary to pulmonary tuberculosis
 Old malnutritioned people
 Virulent organism
 Poor body resistance
 Multiple circumferential transverse ulcers
(Girdle ulcers) with skip leisons
 Commonly in ileum
 Rarely in caecum
Ileocaecal tuberculosis

 Napkin ring strictures in longstanding
ulcers (common in ileum)
 Intestinal nodes involvement with caseation
and abscess
 May present with blood in stools, diarrhoea,
loss of appetite and reduced weight
 Complications:
 Acute: Ulcer perforation
 Chronic: Stricture  Subacute obstruction

B. Hyperplastic Type -10%
 Primary GIT tuberculosis
 Less virulent organism
 Good body resistance
 Chronic granulomatous lesions in ileoceacal region
 Fibroblastic activity in submucosa and subserosa
causes thickening of bowel wall with lymph node
enlargement
 Presenting as Mass in Right Iliac Fossa (Nodular
fixed and firm mass)
 Caseation is very rare
 No primary lesion in the chest

B. Hyperplastic Type -10%

21
 30% of patients
 Inflammatory mass with thickened and
ulcerated mucosa
 Commonly in ileocaecal region
 Cone shaped deformity of caecum
 Shortening of ascending colon
 Thickening of ileocaecal valve
C. Ulcerohypertrophic type-30%

PATHOLOGYPATHOLOGY
Bacilli in depth of mucosal glands
Inflammatory reaction
Phagocytes carry bacilli to Peyers Patches
Formation of tubercle
Tubercles undergo necrosis
Most active inflammation in submucosa.Most active inflammation in submucosa.

PATHOLOGYPATHOLOGY
Submucosal tubercles enlarge
Endarteritis & edema
Sloughing
Ulcer formation
Accumulation of collagenous tissue
Thickening & Stenosis

PATHOLOGYPATHOLOGY
Lymphatic obstruction
of mesentery and bowel
→ Thick fixed mass
Regional lymph nodes
• Hyperplasia
• Caseation necrosis
• Calcification
Bacilli via lymphatics
Inflammatory process in submucosa penetrates to serosa
Tubercles on serosal surface
Bacilli reach lymphatics

Clinical Features
Mainly disease of young adults
~ 2/3 of pt. are 21-40 yr old
Sex incidence equal.
Indian studies → slight female
predominance
Clinical presentation → Acute / Chronic /
Acute on Chronic.

Constitutional symptoms
 fever, night sweats, anorexia, weight loss,
failure to thrive(in children), malaise,
anaemia, lethargy, lassitude
Observed in 30% patients
Atypical symptoms
Lower GI bleed, fistulas, PID like pain,
dysphagia
Pain (80%-95%)
 Colicky (luminal stenosis)
 Continous ( LN involvement)

Diarrhoea (11%-20%)
Constipation
Alternating constipation and diarrhoea
Abdominal mass
 in right iliac fossa (35%)
Hard, nodular, fixed, nontender mass
mimicing ca caecum
Subacute intestinal obstruction (20%)
27

1. Ca Caecum
2. Appendicular mass
3. Lymph node mass
4. Psoas abscess
5. Crohn’s disease
Differential Diagnosis

Diagnosis: intestinal TB
or CD
They can present exactly with same
clinical pictures (same age group,
symptoms and signs)
Same radiological findings and same
endoscopic findings
Mostly with same pathological findings
So how can we make the diagnosis?

Blood tests
No specific diagnostic blood tests available
Common blood parameters:
 Elevated ESR
 Almost always raised but not exceed 60 mm/hr
 Mild anemia
 normochromic/ normocytic
 Mild leukocytosis
 Raised CRP
 Hypoproteinemia
 Hypoalbuminemia

Tuberculin skin test
A +ve tuberculin skin test has been reported in
55 to 100 % pts. with abdominal tuberculosis.
However in areas where TB is highly endemic ,
+ve tst neither confirms the diagnosis of
abdominal TB nor excludes it
31

QUANTI-FERON TB TEST
 Whole blood cytokine assay
 Approved by U.S. food and drug administration
as an aid in the diagnosis of latent TB infection
 Recommended for screening for latent TB
infection in population at low risk of TB.
 The test‘s performance will probably be
enhanced by use of antigen such as ESAT-6 and
CPF-10 that are present in M. tuberculosis but
absent in others.
32

Concomitant PTB
Concomitant PTB
 Present in 15-25% only
Sputum smear and
culture for AFB:
 Low diagnostic yield
Abnormal CXR:
 19-83%
 Average = 38%

34
Thickened bowel wall
Loculated ascites
Interloop ascites-club sandwitch sign
Mesenteric thickening hyperechoic >15mm
Lymph node enlargement
Pulled up caecum (Pseudokidney sign)
USG abdomen

USG abdomen
Ascites Right lower quadrant mass
consisting of matted bowel

COMPUTED TOMOGRAPHY
Abdominal lymphadenopathy
-commonest manifestation
Enlarged lymph nodes
mesenteric,
peri-portal,
peri-pancreatic, and
upper para-aortic groups of nodes.

CECT
The CECT have been described as –
 peripheral rim enhancement,
 non-homogenous enhancement,
 homogenous enhancement and
 homogenous non-enhancement, in that
order of frequency.
Different patterns are seen same nodal
group, possibly related to the different
stages of the pathological process.

CECT
Conglomerate mass
of 6cm.
Enlarged nodes with
hypo enhancing
areas are seen.

CECT
presence of nodal calcification in the
absence of a known primary tumour in
patients from endemic areas suggests a
tubercular aetiology .
CECT imaging criteria differentiating
abdominal lymph node enlargement due to
tuberculosis or lymphoma suggested some
differences in the anatomic distribution and
the CT enhancement patterns

CECT
CECT FINDINGS Tuberculosis lymphoma
Lymph nodes lesser omental,
mesenteric, and upper
para-aortic
lower para-aortic
lymph nodes
Lymphadenopathy features peripheral rim
enhancement,
frequently with a
multilocular appearance
homogenous
attenuation.

CECT
Ascites can be free or loculated.
Characteristically, it is a high density ascites which
could be because of high protein and cellular
contents of the fluid.
Mesenteric involvement and presence of
 macronodules (> 5mm in diameter),
 a thin omental line (fibrous wall covering the infiltrated
omentum),
 peritoneal or extraperitoneal masses with low density
centres and calcification,
 and splenomegaly or splenic calcification have been
more commonly seen with tuberculous peritonitis.

CECT
High density ascitic
fluid
Peritonial and
mesenteric
thickening and
enhancement are
seen.

CECT
The diagnosis of tuberculosis is suggestive
when
 loculated fluid collections are detected in the
presence of omental infiltration,
 peritoneal enhancement,
 transperitoneal reaction, and
 mesenteric or bowel involvement.
 mural thickening affecting the ileocaecal
region.

CECT
Multiple small
hypoenhancing focci
in liver parenchyma.

Computer tomography scan
Gross ascites

46
Thickened omentum

47
Loculated ascites

48
Thickened ileocaecal bowel

49
Enlarged paraaortic LN

50
Tubercles in spleen & liver

Barium study Xray (barium enema or barium follow
through x-ray)
 Pulled up caecum, conical caecum, pulled down
hepatic flexure
 Obtuse ileocaecal angle; straightening (Goose neck)
 Steirlin sign: Hurrying of barium due to rapid flow and
lack of barium in inflamed site
 Fleischner sign (Inverted umbrella sign): Narrow
ileum with thickened ileocaecal valve
 Napkin leisons- ulcers and strictures in the terminal
ileum
 Increased transient time:Hypersegmentation(chicken
intestine)
 Mega Ileum: Dilatation of proximal ileum

Contrast study
Stricture in ileocaecal region Stricture in descending colon
• Good for intestinal tuberculosis affecting small or large bowel

Barium enema:
increased (obtuse)
ileocaecal angle
retracted, fibrosed
caecum (“goose
neck deformity”) ;

Barium
Study
showing
Mega
Ileum

Endoscopy
 Colonoscopy is of value to rule out
malignancy.
 It is easiest and most direct method in
establishing the diagnosis.
 Shows mucosal nodules or ulcers , deformed
ileo caecal valve, mucosal oedema and
pseudopolyps and occasionally diffuse colitis.
Biopsy can be taken to confirm diagnosis.
 Capsule endoscopy is also useful to see small
intestine pathology in difficult cases .
57

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 58

Microbiology and histology exam
Definitive diagnosis:
 Ziehl-Neelsen stain for
AFB
 Tissue culture for
mycobacteria
 Caseating granulomas
on histology

Tissue Biopsy
Peritoneal tapping
Endoscopic biopsy
Laparoscopy
Laparotomy
Histological
exam
Microbiological
Smear & culture

Molecular Methods
Polymerase chain reaction (PCR)
PCR analysis for Mycobacterium
tuberculosis complex in tissues
Reported as 100% sensitivity in some
series

Peritoneal tapping
Ziehl-Neelsen stain: 3% positive
 At least 5000 bacteria/ ml is required
Culture for AFB: 35% positive
 At least 10 bacteria is required
 66-83% positive if 1L of ascitic fluid is cultured after
centrifugation

 Diagnostic laproscopy
 Direct visualization
 Collect acsitic fluid
 Take biopsy from mass, omentum or peritoneum
 is very useful method of investigation .
 Transabdominal peritoneoscopy is
visualization of the peritoneal cavity using
endoscope through small incision in the
abdomen.
 It aids in visualization ,to collect ascitic fluid
for analysis and to biopsy.
Diagnostic laproscopy

1. Obstruction 20%
2. Malabsoprption, blind loop syndrome
3. Dissemination of tuberculosis
4. Cold abscess formation
5. Hemorrhage
6. Perforation
7. Fecal fistula
Complications

TREATMENT
THERE ARE TWO MODILATIES OF
TREATMENT:
1. Medical treatment
2. Surgical treatment
71

72
The cornerstone of antituberculous
therapy is multidrug treatment to
decrease the duration of therapy and
diminish the likelihood that drug-resistant
organisms will develop
Medical treatment

73
Antituberculosis Drugs
Drug/Formulation Adult Dosage (Daily) Main Adverse Effects
First-Line Drugs
Isoniazid (INH)[*]
5 mg/kg (max 300 mg) PO, IM, IV
Hepatic toxicity,
peripheral neuropathy
100, 300 mg tabs
50 mg/5 mL syrup
100 mg/mL injection
Rifampin (Rifadin, Rimactane) 10 mg/kg (max 600 mg) PO, IV Hepatic toxicity,
flulike syndrome,
pruritus
150, 300 mg caps
600 mg injection
powder

74
Pyrazinamide 500 mg tabs 20-25 mg/kg PO Arthralgias, hepatic
toxicity, hyperuricemia,
gastrointestinal upset
Ethambutol[‡]
(Myambutol) 100,
400 mg tabs
15-25 mg/kg PO
Decreased red-green
color discrimination,
decreased visual acuity
Drug/formulation Dosage Adverse effect

75
Drug Dosage Adverse effect
streptomycin 15mg/kg IM Vestibular and auditory
toxicity, renal damage

76
Second-Line Drugs
Capreomycin (Capastat) 15 mg/kg IM (max 1 g) Auditory and vestibular
toxicity, renal damage
Kanamycin (Kantrex and others) 15 mg/kg IM, IV (max 1
g)
Auditory toxicity, renal
damage
Amikacin (Amikin) 15 mg/kg IM, IV (max 1
g)
Auditory toxicity, renal
damage
Cycloserine[¶]
(Seromycin and
others)
10-15 mg/kg in two
doses (max 500 mg bid)
PO
Psychiatric symptoms,
seizures
Ethionamide (Trecator-SC) 15-20 mg/kg in two
doses (max 500 mg bid)
PO
Gastrointestinal and
hepatic toxicity,
hypothyroidism
Ciprofloxacin (Cipro and others) 750-1500 mg PO, IV Nausea, abdominal pain,
restlessness, confusion
Ofloxacin (Floxin) 600-800 mg PO, IV Nausea, abdominal pain,
restlessness, confusion

77
Levofloxacin (Levaquin) 500-1000 mg PO, IV Nausea, abdominal
pain, restlessness,
confusion
Gatifloxacin[¶]
(Tequin) 400 mg PO, IV
Nausea, abdominal
pain, restlessness,
confusion
Moxifloxacin[¶¶]
(Avelox) 400 mg PO, IV
Nausea, abdominal
pain, restlessness,
confusion
Aminosalicylic acid (PAS; Paser) 8-12 g in 2-3 doses PO Gastrointestinal
disturbance

Treatment categories
according to DOTS
strategy:
78
Category of
treatment
Type of patient Regimen
Category I
New sputum smear- positive
- sputum smear negative
- extra-pulmonary
2(HRZE)3
4(HR)3
Category II
- Relapse
- Failure
- Defaulters
2(HRZES)3
1(HRZE)3
5(HRE)3

Surgical Management:
Indications:
 Intestinal obstruction
 Severe hemorrhage
 Acute abdomen (perforation)
 Intra-abdominal abscesses/ fistula formation
 Uncertain diagnosis
Treatment

1. Limited Ileocaecal resection with 5 cm margin
2. Stricturoplasty- single stricture
3. Single strictutre with friable bowel : Resection
4. Multiple Strictures: Resection and anastomosis
5. Multiple strictures with long segment gaps:
Multiple stricturiplasty
Treatment

6. Early perforation: resection and
anastomosis (due to friable bowels)
7. Perforation with severe contamination:
resection with colostomy
8. Adhesiolysis by laproscopy (Very difficult
procedure)
9. Drainage of abscesses and treatment for
fistula in ano
Treatment

It is usually stricture type
May be multiple
Presents with intestinal obstruction
Bowel adhesions, localization, fibrosis,
secondary infection are common
Perforation (5%)
Plain Xray – Multiple air fluid levels
Resection and
anastomosis/stricturoplasty with Anti-
tubercular drugs
Ileal Tuberculosis

Mimics ca rectum
Occurs within 10 cmof anal verge
Presents with tenesmus, diarrhoea and multiple
discahrging fistula in ano
Fistula is painless, not indurated with undermined edges
Shallow bluish ulcers with undermined edges
Investigation:
 Sigmoidoscopy
 USG
 Discharge study
 fistulectomy and biopsy
Treatment: Drugs, fistulectomy or sigmoid resection
Ano-Recto-Sigmoidal
Tuberculosis

2. Peritoneal Tuberculosis
Acute form Chronic form
Ascitic
Clear straw-coloured ascitic fluid
Fibrous
Intestines and viscera matted
together causing obstruction
Encysted
Matted intestines enclosing a
loculation of serous fluid
Purulent
Purulent ascitic fluid
Tuberculous peritonitis
• Acute abdomen
• Exploratory laparotomy
 ascitic fluid
 thickened omentum
 scattered tubercles

It is post primary
Becoming more common
Activation of long standing latent foci
Blood spread
Can develop from diseased mesenteric
lymph nodes, intestines or fallopian
tubes
Peritoneal Tuberculosis

Pathogenesis
Peritoneal seeding by tuberculosis bacilli
Granulomatous multiple whitish nodules(<5 mm) over
visceral and parietal peritoneum
>95% of patients develop exudative free/ loculated ascitis
Small group of patients … dry fibroadhesive (plastic)
Adhesions/ matting of bowel loops
Adenopathy, mesenteric omental thickening
(omental cake)
Purulent peritonitis
Secondary to tuberculous salpingitis
Abscess formation … lymph node, mesentery , omentum
Fistula formation…. Cutaneous/ enteric

Basic pathology
Enormous thickening of the parietal
peritoneum
Multiple tiny yellowish tubercles
Dense adhesions in peritoneum and
omentum with small intestines
May precipitate obstruction
Thickening of bowel wall

Abdominal Cocoon Syndrome
Dense adhesions in peritoneum and
omentum with contents inside as small
bowel causing intestinal obstruction

90
Ascitic fluid analysis
-exudate with protein level >3gm/dl
-SAAG <1.1
-lymphocyte predominant cells with cell count
as high as 4000 / mm3
-AFB +ve seen only < 3%
-specific gravity > 1.016
-glucose < 30mg
-LDH > 90 units/lit
-ADA activity>33U/L in ascitic fluid

A. Acute type –mimics acute abdomen
 Rare
 On-table diagnosis
 Features of peritonitis
 Due to perforation or rupture of mesenteric lymph nodes
 Exploratory laparotomy reveals straw coloured fluid with
tubercles in the peritoneum, greater omentum and bowel
wall
 Fluid evacuated and sent for culture and AFB study
 Biopsy taken from omentum
 To be closed without drains
 ATD is started

A. Chronic
 Presents as
 Abdominal pain
 Fever
 Ascites
 Loss of appetite and weight
 Abdominal mass
 Doughy abdomen (10%)
 Types
a) Ascitic form
b) Encysted form
c) Plastic form
d) Purulent form

a) Ascitic peritoneal tuberculosis:
 Intense exudate caused ascitis
 Common in children and young adults
 Enormous abdominal distension
 May cause congenital hydrdocele,
umbilical hernia, shifting dullness, fluid
thrill and mass per abdomen
 Rolled up omentum and nodular due to
extensive fibrosis

a) Ascitic peritoneal tuberculosis:
 Asitic tap reveals straw coloured fluid from
which AFB can be isolated (<3%). Fluid is
pale yellow, clear, rich in lymphocytes with
high specific gravity
 Anti-tubercular drugs for one year
 Repeated tapping may be required initially
as a part of treatment

b) Encysted (Loculated) peritoneal tuberculosis
 Exudation with minimal fibroblastic reaction
 Ascites gets loculated due to fibrinous deposition
 Non shifting Dullness is the typical feature
 May present as intra-abdominal mass mimicing
ovorain cyst, mesenteric cyst
 USG guided aspiration and antitubercular drugs
to be given

c) Plastic Peritoneal Tuberculosis
 Extensive fibroblastic reaction
 Widespread adhesions
 Between coils of intestine (matted intestines),
abdominal wall, omentum
 Obstruction  Distension of abdomen
 Colicky abdominal pain (recurrent)
 Diarrhoea, loss of weight, mass per abdomen
 Doughy abdomen

c) Plastic Peritoneal Tuberculosis
 Open or laproscopic biopsy (to rule out
peritoneal carcinomatosis)
 Anti-tubercular drugs
 Surgery to relieve obstruction by
adhesolysis

d) Purulent peritoneal tuberculosis
 Direct spread from tuberculous salpingitis
 Mass per abdomen containing pus,
omentum, fallopian tubes, small and large
bowel
 Cold abscess may get adherant to umbilicus
 May cause umbilical discharge
 Genitourinary tuberculosis usually present
 Anti-tubercular drugs with exporation of
umbilical fistula

3. Nodal/ Glandular tuberculosis
A. Calcified lesion
B. Acute Mesenteric lymphadenitis
C. Pseudo-mesenteric cyst
D. Tabes mesenterica
E. Chronic Lymphadenitis
Complications
 Abscess formation

1. Calcified lesion:
 Along the line of the mesentery a single or
multiple calcified lesions
 Payer’s patches involved
 No active infection
 May be on right or left side (R>L)
 Antitubercular drugs
Tuberculous Mesenteric
Lymphadenitis

2. Acute mesenteric lymphadenits
 Common in children
 Mimics acute appendicitis
 Tender mass of lymph node palpapble in
Right iliac fossa which are matted and non-
mobile
 Intestines adherant to caseating lymph nodes
obstruction
 Surgery for appendicitis or obstruction with
lymph node biopsy
 Antitubercular drugs
Lymphadenitis

3. Pseudo-mesenteric cyst
 Caseating material collected between the layers of
mesentery
 Forms cold abscess
 Mimicking a mesenteric cyst
4. Tabes mesenterica
 Massive enlargement of mesenteric lymph nodes due to
tuberculosis
5. Chronic Lyphadenitis
 Children
 Failure to thrive
 Protuberant abdomen and emaciation
 Lymph node on deep palpation in right iliac fossa
Lymphadenitis

4. Solid visceral tuberculosis
Intraabdominal viscera:
Liver‘
Spleen
Pancreas

the portal of entry :hematogenous
dissemination
miliary tuberculosis :hepatic artery
focal liver tuberculosis :portal vein.
HEPATIC TB

three forms
diffuse hepatic involvement- most
common
granulomatous hepatitis
focal/local tuberculoma or abscess- rare

INVESTIGATIONS
Percutaneous liver biopsy.
laparoscopy liver biopsy- cheesy white
irregular nodules.
 CT SCAN.

CT abdomen
 miliary micronodular with miliary
calcifications
Multiloculated cystic mass(cluster sign)

MILIARY TB
 lesions are small 1 to 2 mm epitheloid
granulomas.
TUBERCULOMA
Masses larger than 2mm in diameter

• It can occur due to disseminated or miliary form of
the disease
• Most commonly encountered in HIV pt(developed
countries)
• Fever, weight loss, diarrhea, left upper abdominal
pain, splenomegaly
• Investigations
• Image-guided percutaneous needle biopsy is the
gold standard for diagnosis.
CECT-abdomen-multiple hypo echoic foci(<2cm)
SPLENIC
TUBERCULOSIS

Gross pathology of resected spleen showing innumerable caseating granulomas consistent
with splenic tuberculosis.
Mackowiak P A et al. Clin Infect Dis. 2011;52:418-420
The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases
Society of America. All rights reserved. For Permissions, please e-mail:
journals.permissions@oup.com.

Computed tomograph scan of the abdomen showing a spleen diffusely infiltrated by small,
hypodense lesions consistent with splenic granulomas.
Mackowiak P A et al. Clin Infect Dis. 2011;52:418-420
The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases
Society of America. All rights reserved. For Permissions, please e-mail:
journals.permissions@oup.com.

It is rare
Often associated with miliary TB &
immunocompromised pt
Result from lymphohaematogenous
dissemimation after pulmonary exposure
Anorexia,malaise fever,weight loss,mass
Investication: FNAC & BIOPSY (CT
guided)
PANCREATIC TB

A. Oesophageal (0.2% of abdominal)
B. Gastroduodenal(1%)
C. Retroperitoneal tuberculosis
5. Rare types

Esophageal Tuberculosis
Extension of the disease from mediastinal lymph nodes or from pulmonary focus.
Rarely without a primary contiguous focus.
Ulceration, nodularity, stricture, sinus track formation, and fistulae with trachea or
bronchus.
Dysphagia, odynophagia, choking, and aspiration due to tracheoesophageal or
bronchoesophageal fistula and upper GI bleeding. Massive bleed from
aortoesophageal fistula has been reported.
CXR and CT scan …. Active pulmonary lesions and mediastinal masses.
Barium swallow …. Ulcerations, strictures, pseudotomor masses, fistulae, sinuses,
and traction diverticula.
Upper GI Endoscopy with biopsy is the diagnostic procedure of choice.

Abdominal tuberculosis by dr waseem ashraf skims

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Abdominal tuberculosis by dr waseem ashraf skims

Editor's Notes