 ABDOMINAL TUBERCULOSIS

INRODUCTION

 It is an endemic disease in developing country.

 Increasing trend in the west due to AIDS.
 TB accounts for 1% of hospital admissions in
INDIA.
 Only 15% of pt.s of abdominal TB have e/o
pulmonary disease . Rest of pt.s have normal
chest radiograph.
 Age 2nd- 4th decade; males > females
PATHOPYSIOLOGY

 Causative organisms
1) Myobacterium tuberculosis hominis.
2) Mycobacterium bovis
3) Atypical mycobacterium –
Mycobacterium avium intracellulare
usually in pt.s sfferrig from AIDS.
 Transmission
1) ingestion of infected milk or cough
droplets,
2) hematogenous spread from distant
source,
3) lymphatic spread,
4) direct extension from adjacent organs.
Types:
 Ulcerative type –
- ingested bacilli resist peptic digestion
- infect submucosal lymphoid tissue to
form epithelioid tubercle.
- mucosal sloughing & ulceration occurs
in 2-4 weeks
ULCERS are multiple small 3-6mm long, irregular
necrotic margins. They progress by granuloma
formation ,caseous necrosis and finally to
cicatization.
 Hypertrophic type- abundant inflammaory
response& reactive tissue to form
mulinodular mucosal pattern or neoplasm
like mass.
 Ulcerohypertrophic type-
combination of above two types.
 Abdominal TB refers to
- Peritoneum & its reflections
-GIT
-Lymphatic system
- Solid organs
TB Peritonitis

 Caused by:
- reactivation of latent TB focus,
-discharge of caseous material from diseased lymph nodes,
- TB salpingitis in females.

Types

Wet ascitic type- seen in 90% , large amount of free or

loculated fluid.
Fibrotic fixed type- mesentric & omental thickening & masses,
matted bowel loops & sometimes loculated ascitis
Dry or plastic type- unusual ,caseous nodules, fibrous peritoneal reaction,
dense adhesions.
Ascitis

 Free or loculated ascitis seen .

USG
- detects even small amount of FF
- shows fine, multiple strands of fibrin, septations & debris.

CT
- high density(25-45HU) due to fibrin & cellular debris.
- water density in initial transudative phase
- Fat-fluid level due to chylous ascitis
- CT cannot show presence of internal septae

MRI - delayed enhancement (15-20 mts) after i.v. contrast

Peritoneum
 USG – peritoneal thickening & tiny
nodules, seen better with ascitis.
CT - smooth peritoneal thickening ,
- shows enhancement,
- ascitis.
Small bowel mesentry
 Commonly involved in pt.s with peritoneal TB.
 shows :
- nodular lesions, solid/cystic forming from lymph node or abscess.
- mesentric thickening( of >15mm for diagnosis). Mesentry appears
echogeic due to fat deposition from obstructed lymphatics.

USG.
Stellate sign- fixed loops of bowel & mesentry standing out as spokes
radiating from root of mesentry.

Club sandwich/ Slice bread sign- focal ascitis between radially

oriented bowel loops due to exudation from inflammed bowel
or ruptered lymph node.
Stellate sign
CT- Stellate sign
Slice bread/Club sandwich sign
 CT shows thickened mesentry with
increased vascularity & tethering of bowel
loop forming an abdominal mass.
-D/D of TB peritonitis
peritoneal carcinmatosis, lymphoma,
peritonitis, mesothelioma.
key point…
- smooth mild peritoneal thickening s/oTB
- nodular & irreular thickening s/o
carcinomatosis.
Omentum
 Omental thickening or caking
 D/D :

TB – thin smooth
omental line.

Peritoneal carcinomatosis –
irregularly thickened
contour

CT is the better modality to

show omental Changes.
TB Lymphadenitis.

 Commonest manifestation of abd. TB.

 Vary from increased no. of normal size LN to massive
conglomerate/matted nodes due to periadenitis.
Sites involved due to:
-lymphatic drainage from bowel: mesentric
periportal, ant. Pararenal, upper para-
aortic & lesser omental regions.
- hemaogenous spread : mesentric, lesser omental,
ant. Pararenal , uper & lower para- aortic.
- direct spread : from adjacent organs .
 LNDpathy

USG :- discrete/conglomerate masses

-central hypoechoic/ heterogeneous
-areas of caseation form collection
-adhere to surrounding vessels
- fibrous reaction around nodes can
increase backround echogenicity.
-macrocalcification-
peripheral/central
- may show transient increase in size for
3-4 weeks after the onset of treatment.
Discrete & conglomerate type
 CT reveals multiple site involvement with relative sparing of
retroperitoneum.
 Noncontrast CT show nodes with low density(<30HU) or with
soft tissue density similar to muscle.
 Contrast CT- 4 patterns of enhancement
1)peripheral enhancement- most common.
s/o central liquefaction / caseous necrosis & perinodal
inflammation.
D/D mets from testicular tumors
head & neck Sq. cell C.A,
lymphoma
whipple’s & crohn’s disease.
2) Inhomogeneous enhancement due to intranodular
granulomas & relatively less necrosis.
3) Homogeneous enhancement –uncommon,
seen in AIDS pt. on infection with mycobacterium avium
intracellulare.
D/D untreated lymphoma.
4) Nonenhancing low density nodes , seen in AIDS.

Mixed pattern of enhancement can be seen in a single nodal

group due to nodes in different stages of pathological
process.
1) peripheral
enhancement.

2) Soft tissue density

nodes
1) Necrotic nodes in
retroperitoneum &
soft tissue density
nodes in mesentry.

2) Nodes with
heterogeneous
density in mesentry.
MR
majority- hypo on T1w & hyper on T2w & show
peripheral rim hypo on T1 & hyper on T2.
show peripheral enhancement on dynamic
contrast study.
MR useful – to show relationship of nodes to
vessels & ducts & to differentiate necrotic
peripancreatic nodes from CA head of pancreas.
 Key points-
-heterogeneity of echopattern in nodes of
single anatomic group prior to treatment
strongly s/o TB.
-caseation & calcification strongly s/o TB
-homogeneously hypoehoic group of nodes
….. Suspect lymphoma as D/D
GIT

 GIT involvement is influenced by

1) abundance of lymphoid tissue
2) increased physiological stasis
3) increased rate of elecrolyte & water
reabsorption
4) greater contact time of bacilli with mucosa

sites in decreasing order

ileocecal region > colon > jejunum > rectum
> duodenum.
 Symptoms :
- diarrhoea, pain, distension,
anorexia, Wt loss,
complications:
obstruction, perforation, fistula formation,
haemorrhage, enterolithiasis due to
stricture formation.
ILEOCECAL REGION

Most commonly affected region.

Types
1) Hyperplastic – with long segments of narrowing & rigidity , seen
as “ pipe-stem” colon.

2) Ulcerative
3) Ulcerohyperplastic
4) Carcinoma type with short annular defects & overhanging edges.

Barium studies include BaMFT/enteroclysis & enema in colonic

involvement.
Ba meal evaluates motility& organic lesions in small bowel
Per oral pneumocolon & enema best evaluate caecum & IC jn.
 Early involvement of IC region manifests as spasm &
hypermotility with edema of the valve.
 Double contrast barium study in early stage shows
mucosal ulcerations in early stage which are-
shallow , with elevated mrgins, linear or stellate in
configuration & are longitudinally oriented in terminal
ileum & transversly in colon
 Fleischner/inverted umbrella sign:
- characteristic of TB
- thickening of IC valve lips & or wide
gaping of valve with narrowing of
terminal ileum.
 Inverted umbrella
appearance due to
spasm of valve
 Also complete
obliteration of cecum
is seen.
 Advanced disease show :
 Napkin ring stenosis & conical cecum:
symmetric, annular narrowing with
obstruction, shortening, retraction & pouch
formation.
subhepatic cecum :”pseudokidney” sign on
USG where cecum becomes conical,
shrunken,& is retracted out of iliac fossa.
Conical Cecum
 Goose neck deformity :
loss of normal IC angle & dialated
terminal ileum appear hanging from conical
retracted & shortened cecum.
Goose neck geformity.
 Purse string stenosis :
localised partial stenosis opposite the IC valve with a rouded
off smooth cecum & dialated terminal ileum resemble purse
string stenosis.
In later stages IC valve becomes fixed,irregular, gaping &
incompetent. Terminal ileum is narrowed due to stricture
formation.

- Stierlin sign : narrowing of terminal ileum may occur due to

irritability with rapid emptying through a gaping IC valve with
shortened rigid or obliterated cecum. This sign is s/o acute on
chronic inflammation of ileum, cecum & asc colon with a
normal column of barium on either side.
stierlin’s sign
 Cecum is fibrotic &
Contracted, IC valve
Is irregular , gaping &
Incompetent & terminal
Ileum appears to
Empty directly into
Asc. colon
 Club sign
 Hypoechoic mural
thickening of cecum
& terminal ileum
corresponding to head
& stalk of a club.
 String sign :persistent
narrrow stream of
bariumin bowel
indicates stenosis
 Both stierlin & string
sign are seen in
crohn’s disease also.
 Findings of barium study are grouped as:
1) Highly suggestive: when one or more of
following features are seen

a) Deformed IC valve with dialated terminal ileum

b) Contracted cecum with an abnormal IC valve &
or terminal ileum.
c) Stricture of asc. Colon with shortening &
involvement of IC region.
2) Suggestive :if any of following is seen
a) Contracted cecum
b) Ulcerations or narrowing of terminal ileum
c) Stricture of asc. Colon
d) Multiple areas of dialation , narrowing
& matting of small bowel loops.
3) Nonspecific : features of matting, dialation
or mucosal thickening of small bowel loops.
4) Normal study.
 CT scan of IC region shows
 Circumferential symmetric or asymmetric bowel
wall thickening, may have homogeneous or
inhomogeneous appearance.
 Adjacent mesentric adenopathy,
 Minimal stranding is seen in pericecal or
mesentric fat,
 Distal small bowel obstruction may be seen
 D/D lymphoma & crohn’s disease.
Various findings in CT
- exophytic soft tissue mass around
constricted & ulcerated lumen
- minimal but asymmetric bowel wall
thickening with spiky or tethered mucosal
outline
- minimal symmetric wall thickening or
absence of wall thickening.
- mucosal stratification is not seen.
IC thickening
 Key points for D/D
1)Crohn’s – uniform pattern of wall
thickening usually concentric or
symmetrical(0.6-1.7cm)
- few show mucosal straification
2) Amoebiasis – may show contracted cecum
but small bowel involvment is rare.
3) cecal malignancy as always limited by IC valve.
TB Enterits.
 Ulcerative TB is most common in small bowel. Ulcers are
perpendicular to the long axis of intestine.
 Stages of disease
First stage :

1) Accelerated intestinal transit,

2) Chicken intestine : disturbance in tone & peristaltic contractions
causing hypersegmentation of barium column,
3) Disturbnce in secretion resulting in precipitation, flocculation or
dilution of barium suspension.
4) Changes in intestinal contour which are iregular, crenated &
interrupted by spiculae.
5) Altered mucosal pattern seen as softened & thickened folds.
Second stage

Here in addition to above ulcerations are seen as barium fleck

surrounded by either a thickened wall or by converging folds.

Third stage

- Sclerosis,hypertrophy & stenosis.

- Hour glass stenosis,formed by penetrating ulcers and walls
have smooth & stiff contours
- Multiple strictures
- Fixity of loops, spiculation, matting & signs of malabsorbtion
 USG shows thickened bowel loops, sometimes
deep ulcerations can be seen,
later short segment strictures & partial intestinal
obstruction can be seen.
Enterolithiasis- intralumial calculi formed above
the level of stricture. calculi high up in bowel are
non opaque due to choleic acid & those lower
down are opaque due to calcium
Colonic TB
 Large bowel is involved in 9% of cases without small bowel
involvement.
 Show
- segmental (long/ short) involvement
- spiculation, spasm, rigidity & ulceration,
- inflammatory polyps, perforation & fistulae,
& pericolic abscess.
D/D UC , crohn’s , amoebic colitis, ischemic, &
pseudmembranous enterocolitis & malignancy.
Crohn’s – anal involvement & internal fistulae are more
common, & ulcers are along the mesentric border.
TB- shows circumferential ulcers,
Stricture in transverse colon
Anorectal TB
 Rare .fistulae, strictures, & chronic
ischiorectal abscess
 D/D LGV ,
amoebiasis
acinomycosis
schistosomiasis.
Oesophageal TB
 Rare , usually secondary to advanced pulmonary &
mediastinal TB
 Sources
- TB laryngitis
- Caseating lymph nodes
- Vertebral body
- lymphatics/hematogenous route.
Barium study shows extrinsic compression by enlarged nodes,
ulcerations, smooth strictures, mucosal irregularity , traction
diverticuli & fistulae
CT assists in knowing the mediastinal extent of the disease.
Gastric TB
 Rare
 secondary spread from adjacent nodes or hemaogenous route.
Types:
1) Ulcerative – commonest , along lesser
curvature & pylorous
2) Hypertrophic,
3) Miliary tubercles,
4) Tuberculous pyloric stenosis
5) Solitary tuberculoma
6) Tubercular lymhadenitis.
findings vary from benign ulcer in ulcerative type to malignant ulcer in
hypertrophic type. Gastric outlet obstruction can b seen due to
fibrosis or enlarged lymph nodes.
Duodenal TB
 2% of intesinal TB.
 Affected by extrinsic or intrinsic process,
more commonly by extrinsic lymph nodes.
Barium study shows
-widening/ impressions on medial aspect of C loop.
- Intrinsic type show ulcerative or hyperplastic type.
- Incompetence of sphincter of oddi leads to air in the biliary tract,
- Perforation & fistula formation can occur,
- Healing leads to stenosis & duodenal obstruction
Endoscopic biopsy are often –ve due to submucosal nature of disease.
D/D lymphoma , CA pancreas , atypical peptic ulcer disease.
Duodenal narrowing
Liver & Spleen
 Common in miliary TB, or through portal V in GI lesions. Types:

1)micronodular – seen in miliary TB.

USG shows bright liver & spleen

on CT small nodules are not well seen, hepatosplenomegaly is seen & can be
homogeneous & heterogeneous.

2) macronodular. rare. Infection spread by portal V , hepatic A, para aortic/portal nodes.

USG- hypoechoic lesions, sometimes

hyperechoic lesion with or without calcificaion uncommonly a septated honeycomb like
lesion is seen.

CT shows low density lesion ( 15-45HU), shows minimal central enhancement & moderate
periphral enhancement.
Healed granulomas
MRI shows hypointense lesion on T1w with a
hypointense rim & iso to hyper intense
lesion on T2w with less intense rim.
Spleen is involved more in HIV positive pt.s.
D/D abscess, mets ,HCC , parasitic disease
histoplasmosis.
Assosiated peritoneal, nodal & intestinal
involvement suggest TB.
TB pancreas
 Rare ,seen in miliary TB.
 Usually located in the head of pancreas.
 USG – well defined hpoechoic lesion
 CT – hypodense lesion with irregular
margin with/without pancreatic
enlargement .
- peripancreatic nodes
D/D abscess, malignancy ,chronic pancreatitis.
Pancreatic TB
Urinary tract TB
 Introduction
- GU Koch’s is not uncommon in india.
- Increasing concern world over due to AIDS & multi drug
resistant strains.
- TB occurs in about 10% of pt.s of AIDS & involves atleast one
extrapulmonary site in 50% of pt.s with kidneys being the
most common genitourinary site.
- diagnostic problem because of nonspecifc
symptoms & imaging features which resemble other lesions.
- if undiagnosed & untreated it progresses to renal failure.
Pathology

 Hematogenous spread of infection from primary source

elsewhere,most commonly past or present pulmonary infection,
followed by bone or joint TB.
 Initially both the kidneys may be involved.
1) Organisms are lodged in the glomerular & peritubular capillary
network.
2) Most of initial lesions heal without sequelae only few progress to
clinical & adiological abnormality.
3) Bacilli erode out of their vascular location & spill into tubules
which results in granuloma formation along the nephron.
4) Granuloma , caseation , cavitation are furher stages.
5) Cavity communicates with the pcs and infection spreads to ureter
& bladder to cause mucosal ulceration , dialatation & later
healing by fibrosis & calcification.
Pathology
 Symptoms : frequency, burning ,urgency hematuria,
renal pain , wt. Loss, fatigue, fever

Diagnosis: conventional procedures still remain

the procedure of choice.

IVP : best for detection of early findings,

USG & CT : for evaluation of late changes &
evaluation of kidney not visualised on
IVP.
 Plain X ray:
-calcification – amorphous granular seen with
granulomatous masses, or dense punctate type
representing healed tuberculoma.
-If hydronephrotic kidney becomes nonfunctioning then
extensive dystrophic putty like calcification may form a
cast of kidney & is known as Auto-nephrectomy.
-Calcification in ureter & bladder are not common.
-Primary source of infection can be seen in hip Jt.
SI joint, spine or in chest X ray.
-Active pulmonary TB is seen in only 5-10 % pt.s.
Extensive calcification
 IVP: In 70% of cases disease progression
& radiological abnormality are unilateral.
 IVP can be normal in initial phase when
bacilli are lodged in glomerular &
peritubular capillaries.
 IVP picks up the lesion only when it
ulcerates into the calyx.
 Early IVP findings.
 Earliest abnormality:
- loss of definition of minor calyx producing
an indistinct feathery outline , irregularity of
one or more papillae or calyces.
- renal size & contour can be normal
Early findings In IVP
 Irregular & moth eaten
appearance of upper
pole calyx.
Early findings in IVP
 Irregular margins
of calyces with
papillary cavities,
simulating papillary
necrosis.
 Progressive involvement
1) Coalescence of granulomas leading to uni
or multi focal mass lesions. Kidney may
enlarge in length & thickness & can cause
diaplacement of adjacent collecting system.
Mass lesions
Caliectasis with irreglarity of contour indicating erosion of
pyramids & cortical necrosis.
Necrotic area in the cortex erodes forming a cavity
which communicates with a deformed calyx.
Papillary necrosis & cavity
Parenchymal surface scarring over retracted papilla &
dialated calyces.Impaird excretion of contrast is seen.
Autonephrectomy
1) caseocavernous type: enlarged sac filled
with caseous material with or without
calcifaction.
2) calcified shrunken non functioning kidney
Autonephrectomy
Lobar calcification
 Following drainage of cavity into collecting
system there is stimulation of scirrhous
reaction causing stenosis & obstruction of
parts of collecting system.
 common sites of stricture are
neck of calyx
PUJ
lower end of ureter.
Infundibular narrowing & pelvic contraction
 Phantom calyx: completely stenosed
infundibulum or calyx leads to failure of
contrast excretion by overlying renal
parenchyma.
 Amputated calyx: a tiny infundibular stump
is seen in such cases
Phantom calyx
Amputated infundibulum
 Renal pelvis
1) May show filling defects due to caseous debris.
2) Hiked up pelvis: inferior margin of renal pelvis is
involved with resultant cephalic retraction.
3) Kerr’s kink : deformity of the pcs may be caused
by traction from a strictured infndibulum or
parenchymal fibrosis kinking the pelvis.
4) Occassionaly obstruction may be of high grade
to cause gross hydronephrosis.
Hiked up pelvis: narrowing & contraction of upper calyseal
infundibulum &dialation of lower pole calyx.
Gross HN
Extensive destruction
 Ureter :
- in early stages there is dialation resulting from atony &
prolonged bacilluria
- with progress of disease irregular sgments of ureter are seen
due to mucosal ulceration.
- necrosis followed by fibrosis leads to stricture formation
producing “beaded” appearance or “cork screw” appaerance.
- terminal portion of ureter is most comonly involved.
-late stages severe thickening of the wall occurs leading to
rigid shortened ureter with narow lumen known as
“pipe stem” ureter.
Beaded ureter .
Ureteric Stricture
 U . Bladder: involved in 1/3 cases of urinary tract
TB.
 Tubercular cystitis leads to edema of mucosa.
Tuberculomas in the bladder wall if large can be
seen as filing defects .
 Thimble bladder : seen in late stages , irregular
contracture with thick walls & reduction of
capacity
 VUR : due to fibrosis in region of trigone causing
gaping of VUJ leading to VUR.
Thimble bladder
U bladder: focal irregularity & wall thickening seen
shows reduced capacity
VUR
 Urethral TB :uncommon
 Assosiated with prostatic abscess ,
periurethral abscess or fistula formation.
 Stricture formation : usually at
bulbomembranous urethra.
Urethra
Role of USG
 It is not used as primary inv for diagnosis as it is
unable to show early calyceal changes
 It do not provides information about renal function.
 USG picks up morphological abnormalities
 Can be used to provide guidance for per
cutaneous nephrostomy or drainage of
perinephric abscess.
 Renal papillary lesions seen as
- Areas of hypoechogenicity or
- Areas of hypoecho… with echogenic walls
- Or echogenic non shadowing lesions.
- Sloughed calyx is seen as echogenic flap
separated from the calycel wall
- Focal lesion in the kidney is the most
common finding.
 Large liquefying conglomerate cavities or dialated calyces
formed as a result of infundibular stricture appear as
hypoechoic nodules or masses.
 Sometimes a communicating track can be seen between a
cavity & a calyx.
 Heterogeneous echo of parenchyma : these pt have poor
contrast excretion
 Others: caliectasis, HN , parenchymal calcification .
 Scar
 Complications: perinephritis, perinephric abscess , fistulae &
psoas abscess..
Role of CT
 CT is indicated in pt with normal or
equivocal findings on IVP & USG .
 Features
- Multiple small poorly enhancing nodules,
- Uneven caliectasis & calcification pattern
- In poorly functioning kidneys nephrogram
effects are bettr sen in CT than IVP.
- retroperitoneum
 Thickening of ureter or renal pelvis is better
seen in CT
 CT Shows wall calcification in UB better
than USG.
HIV & abdominal TB
 MAI commonly affects when CD 4 counts are 50-
100 , however both are seen frequently.
 Infection is acquired by primary infection rather
than reactivation.
 MAI incite less inflammatory response & less
caseation necrosis in lymph nodes.
 Focal lesions in liver & spleen are seen more with
M TB.
 proximal bowel is affected more with MAI
simulating whipple’s disease both radiologically
&histologically.
 Tuberculosis can affect virtually any organ syste
in the body .
 Tuberculosis has a variety of radiologic
appearances and can mimic numerous other
disease & malignancies.
 A high degree of clinical suspicion and familiarity
with the various radiologic manifestations of
tuberculosis allow early diagnosis and timely
initiation of appropriate therapy, thereby reducing
patient morbidity.