ABDOMEN
(Crohn’s dse,
• Plain films allow one to view the entire
abdomen before proceeding to a more
specific investigation.
Indications:
• Abdominal distention
• Abdominal pain
• Vomiting
• Diarrhea
• Abdominal trauma
*The presence of a palpable abdominal mass
warrants imaging by CT Scan or Ultrasound.
*The plain film is most efficacious when
obtained for patients who have significant
abdominal tenderness or who are strongly
suspected of having bowel obstruction, or
perforation, urinary calculi or ischemia.
*The plain film examination is least effective as
screening study in patients with mild or
nonspecific symptoms.
*The major value of NORMAL findings from a
plain film exam is that they exclude bowel
obstruction or large perforation.
***Films of the abdomen in erect and supine
positions are obtained to complete the
“perforation series.”
NORMAL BOWEL GAS PATTERN
• Intestinal tract of adults - <200ml of gas
• 3 sources of intestinal gas:
a. swallowed air
b. bacterial production
c. diffusion from the blood
• Gas rises and accumulates in the
anteriorly placed segments of intestine,
including the body of the stomach,
transverse colon, and sigmoid colon.
• Gas tends to accumulate in the stomach
and colon bec of the slower exit of fluid
and gas from these structures.
The gas-filled small intestine tends to occupy the
central portion of the abdomen and has a smaller
caliber than the colon.
*Recognition of mucosal features:
- Haustra of the colon = 2-3cm wide,
occur at intervals of 1 cm.-Plicae
circulares of small bowel = 1-2mm
wide, occur at intervals of 1mm.
*however, the differentiation of colon from small
bowel is difficult without a positive contrast
study.*Intestinal gas should be considered a
natural contrast agent in the interpretation of
abdominal plain films.
ABNORMAL BOWEL GAS PATTERNS
• Mechanical Small Intestine Obstruction
• Mechanical Colon Obstruction
• Paralytic (Adynamic) Ileus
• Gastric Outlet Obstruction
Mechanical Small intestinal obstruction
• Abdominal pain, distention, vomiting.
• hx of previous abdl surgery.
• Common Causes in Adults: adhesions,
hernia, malignancy, inflammatory
bowel disease, Misc.
volvulus, appendiceal abscess, and
gallstone ileus)
Radiographic findings:
• w/in 3-5 hrs after the onset of
obstruction, gas and fluid accumulate
proximally.
• In upright film, distended bowel loops
w/ air-fluid levels are present (non-
specific).
• Degree of small bowel dilatation is
greater in pxs w/ true mechanical
obstruction than w/ adynamic ileus.
• As the loops fill w/ air, they may
assume a “STEPLADDER”
configuration.
• Air may be resorbed through the
intestinal wall as fluid accumulates in
the bowel lumen – “GASLESS”
abdomen.
• “STRING OF PEARLS” sign – small
amounts of air trapped bet the plicae
circulares (upright position).
Mechanical colon obstruction
• Usually caused by cancer or
diverticulitis.
• Other causes: volvulus, hernia,
fecal impaction.
• Obstruction usu occurs in the sigmoid
colon (narrower caliber and stool is
more solid).
• Carcinomas of the cecum & ascending
colon are less likely to cause
obstruction bec of wider caliber and
more liquid content of the stool.
Plain film findings:
• Dilated, gas-filled loops of colon
proximal to the site of obstruction and a
paucity or absence of gas in the distal
colon and rectum.
• Competent ileocecal valve – the cecum
may become markedly dilated and little
if any gas may be seen in the small
bowel (risk of perforation).
CLOSED LOOP OBSTRUCTION
• Incompetent ileocecal valve – allows
gas to reflux proximally into the small
bowel, producing plain film findings
that can mimic small bowel obstruction.
Close search for colonic gas is required.
• Sigmoid Volvulus – two parallel gas-
distended colonic loops rising out of the
pelvis (dilated loop of sigmoid colon
that has an inverted U configuration and
absent haustra).
• Cecal Volvulus – dilated, air-filled
cecum in an ectopic location, usu w/ the
cecal apex in the left upper quadrant.
***When plain films suggest colonic
obstruction, it should be confirmed by
endoscopy or barium enema.
PARALYTIC (ADYNAMIC) ILEUS
• Causes: laparotomy and other types of
trauma, sepsis.
 • Other causes: hypothyroidism, drugs
that inhibit intestinal motility,
hypokalemia.
• Plain films usually show a
PROPORTIONATE DISTENTION of
small and large bowel
• Colonic ileus may also result in cecal
perforation, so, cecal diameters in the
range of 12 cm are reason for concern.
GASTRIC OUTLET OBSTRUCTION
• Antrum or pyloric region is the usual
site of GOO
• Most common causes: edema and
spasm resulting from an acute pyloric
channel ulcer and antral scarring caused
by previous ulcers.
• Other causes: scirrhous gastric CA and
scarring from previous ingestion of a
caustic substance.
Plain film: GOO
-dilated air-filled or fluid-filled stomach in the
left upper quadrant with displacement of the
transverse colon inferiorly.-can mimic ascites or
hepatomegaly (but a small amount of air is
almost always present w/in the stomach).-
contrast studies are often performed to confirm
the presence of GOO.
PNEUMOPERITONEUM
• A natural consequence of surgical
exploration of the abdomen.
• Usually indicates bowel perforation.
• Upright plain films or cross-table
decubitus films can detect small
quantities of peritoneal gas.
Radiographic signs:
• Serosal or Rigler’s sign – gas outlining
both sides of the bowel wall; the bowel
wall appears as thin white stripe
(supine).
• Increased lucency in the right upper
quadrant – air accumulating superiorly
in the free space between the anterior
aspect of the liver and the abdominal
wall.
• Visualization of the undersurface of the
diaphragm.
• Air in the Morison’s pouch (posterior
hepatorenal space) – linear or triangular
collection of gas in the right upper
quadrant.
• Outline of the normal peritoneal
ligaments – visualization of the
falciform ligament in the upper
abdomen, the lateral umbilical
ligaments (inverted V sign) in the lower
abdomen and the urachus.
• “FOOTBALL SIGN” – indicates a large
amount of free air filling the oval-
shaped peritoneal cavity, mimicking an
American football (infants).
• Air in the lesser sac of the peritoneal
cavity – ill-defined lucency above the
lesser curvature of the stomach.
Conditions that may mimic pneumoperitoneum
• Chilaiditi syndrome – bowel, usu the
colon becomes interposed bet liver &
diaphragm; common in elderly & pxs
w/ obstructive airway disease.
• Subdiaphragmatic fat – fatty (linear)
lucency lies lateral to the apex of the
hemidiaphragm; occasionally seen in
obese pxs.
• Extraperitoneal gas
• Subphrenic abscess
• Atelectasis of the lower lobes
• Pneumatosis coli – intramural gas
PNEUMOBILIA
• Gas in the bile ducts
• Characterized radiographically by thin,
branched, tubular areas of lucency in
the central portion of the liver.
• Results from some type of
communication between the bile duct
and the intestine.
• Common causes: surgical creation of a
biliary-enteric fistula such as a
choledochoduodenostomy,
choledochojejunostomy, or
cholecystoenterostomy.
• Other causes: (non-surgical)
choledochoduodenal fistula sec to
penetrating duodenal ulcer,
cholecystoduodenal fistula sec to a
gallstone that erodes into the
duodenum.
Rigler’s Triad:
*Air in the biliary tree, small bowel obstruction,
ectopic gallstone (diagnostic of GALLSTONE
ILEUS).
Intramural gas or intestinal wall gas
(pneumatosis)
• Collection of gas in the bowel wall.
• Radiographic patterns: bubbly
appearance
thin, linear streaks
• Can be seen in adult patients w/ bowel
infarction.
ABDOMINAL CALCIFICATIONS
APPENDICITIS
APPENDICOLITH – 10% of pxs w/ acute AP
- round or oval calcified densities, laminated.
- from 1-2cm in size, maybe as large as 4cm.
- located in RLQ, pelvis, RUQ, LUQ
- its presence often indicates appendicitis
complicated by perforation and abscess
formation.
• Abnormal bowel gas pattern – 25% of
pxs
- adynamic ileus, partial or complete SI obstr’n
• Abnormal cecum and ascending colon –
thickening of the cecal wall, widening
of the haustra, air-fluid level in upright
position
• Extraluminal soft tissue mass – found in
up to 1/3 of pxs w/ perforation; may be
caused by a combination of edema,
 fluid, and fluid-filled loops of small
bowel in the RLQ
• Gas in the appendix – has been
described as acute AP but an air-filled
appendix may be a normal finding and
simply reflects the position of the
appendix in relation to the cecum
• Free peritoneal air – may be seen in
ruptured appendix
• Obliteration of normal fat planes –
inflammation and edema may alter the
water content of surrounding fat and
obscure normal fat planes of psoas
muscle or flank stripes
• Scoliosis of the lumbar spine – as a
result of splinting (non-specific and can
be related to positioning)
ORGANOMEGALY IN PLAIN FILM
• Hepatomegaly
• Splenomegaly
• Renal enlargement
HEPATOMEGALY (PLAIN FILM)
• Generalized hepatic enlargement tends
to displace the hepatic flexure and
transverse colon inferiorly and the
stomach to the left
• Other signs:
a. displacement of inferior edge of liver beyond
the right margin of the psoas muscle
b. displacement of the duodenal bulb below the
L2 vertebral body or to the left of the midline
c. inferior displacement of the right kidney
d. enlargement or marked rounding of the
hepatic angle
e. elevation of the right hemidiaphragm with
with decreased motion on normal
respiration
f. inferior displacement of the gastric fundus
away from the diaphragm w/ left lobe
enlargement
g. anterior displacement of the duodenal bulb
on lateral films with caudate lobe
enlargement
splenic flexure usually lies anterior to
the spleen.
• Marked splenomegaly may also
displace the stomach medially.
• Elevation of the left hemidiaphragm
RENAL ENLARGEMENT (PLAIN FILM)
• Bec of surrounding fat, the renal
outlines are visible on the majority of
abdominal films taken in supine
position.
• An enlarged kidney does not displace
intra-abdominal organs bec of its
retroperitoneal location, except in
extreme cases.
ASCITES
• Obliteration of the inferior edge of the
liver
• Widening of the distance between the
flank stripe and the ascending colon –
this distance is normally 2-3mm, but it
may increase as fluid fills the paracolic
gutter.
• Medial displacement of the lateral edge
of the liver (Hellmer’s sign) – more
common w/ malignant ascites than w/
cirrhosis
• Fluid accumulation in the pelvis
• Separation of bowel loops
• •Centrally located bowel loops with
bulging flanks – w/ large amounts of
ascites, the bowel loops may float to the
highest central portion of the
abdomen.Ground-glass appearance – in
large amounts of ascites.

Reidel’s lobe
• downward extension or elongation of
the right lobe of the liver in the absence
of hepatic disease.
• normal variant found in about 4-14% of
population, more common in females
• this lobe may extend caudally below the
iliac crest and does not indicate
hepatomegaly.
• downward extension or elongation of
the right lobe of the liver in the absence
of hepatic disease.
• normal variant found in about 4-14% of
population, more common in females
• this lobe may extend caudally below the
iliac crest and does not indicate
hepatomegaly.

SPLENOMEGALY(PLAIN FILM)
• Tip of the spleen extends inferiorly
below the 12th rib.
• Displacement of the splenic flexure of
the colon – uncommon finding bec the
GASTROINTESTINAL  SYSTEM CONGENITAL  ANOMALIES
• Defec<ve  dev’t  of  hepa<c  lobe/segment
• Typically  affect  an  en<re  lobe,  rarely  
Liver,  Biliary  Tract,  Pancreas
segmental
o Absence  (agenesis)
To  review  the  gross  anatomy  of  the  liver
o Small  size  with  NORMAL  structure  
To  know  the  segmental  anatomy  of  the  liver
(hypoplasia)
A  basic  imaging  correla<on  of  the  segmental  
o Small  size  with  ABNORMAL  
anatomy  of  the  liver  
structure  (aplasia)
• Must  be  dis<nguished  from  lobar  atrophy  
Surface  anatomy
• Shaped  like  a  wedge secondary  to  vascular/biliary  disease
• Base  against  the  R  abd.  wall  and  <p  poin<ng   LIVER
to  the  spleen • dual  blood  supply
• Extends  from  the  5th  ICS  in  the  MCL  to  the  R   o portal  venous  system  -­‐  75%
costal  margin o hepa<c  artery  -­‐  25%
• 12  to  15  cm  coronally   • hepa<c  vein    ’  inferior  vena  cava
• 15  to  20  cm  transversely   DIFFUSE  HEPATIC  DISEASE
• cirrhosis
• covered  by  a  fibrous  capsule  (of  Glisson)
• hepa<<s
• capsular  peritoneum  reflects  at  the  
• faby  infiltra<on
diaphragm  –  con<nues  as  parietal • Budd-­‐Chiari  Syndrome
• reflec<ons  forms  –  coronary,  R  &  L   • iron  deposi<on
triangular  ligaments,  and  falciform  ligament   FOCAL  LIVER  LESIONS
• round  lig.  –  free  edge  of  falc.  l.  –  obliterated   • hemangioma
umbilical  vein   • hepa<c  cyst
• pyogenic  abscess
• amebic  abscess
Anatomic  variants • echinococcal  disease
• Important  to  recognize  variants  to  avoid   • fungal  abscess
labeling  them  as  pathologies • hepa<c  adenoma
• incomplete  accessory  fissures • focal  nodular  hyperplasia
o invagina<on  of  the  diaphragm • focal  fat  infiltra<on  or  sparing
o one  or  more • hepatocellular  carcinoma
• metasta<c  disease
o common  variant
o commonly  seen  at  the  R  lobe  
superiorly HEMANGIOMA
• LeS  lateral  segment • cavernous  hemangioma  -­‐  most  common  
o leSward  extension  of  and  projects   benign  hepa<c  lesion
posteriorly  to  wrap  around  the   • single  or  mul<ple  (10%)
• 4%  to  20%  of  the  popula<on
spleen
• women  >  men
o may  be  mistaken  for  pathology  of  
• asymptoma<c;  discovered  incidentally
the  stomach/spleen • most  common  in  the  posterior  segment,  
right  lobe
CONGENITAL  ANOMALIES • oSen  subcapsular  or  peripheral
• true  hepa<c  congenital  defects  are  rare • ultrasound  (US)  -­‐  well-­‐defined,  round,  
• either  defec<ve  or  excessive  development homogeneous  hyperechoic  lesion
• large  lesions  -­‐  may  be  heterogeneous  with  
• Riedel’s  lobe  
areas  of  degenera<on
o most  common  anomaly/  more  
• on  noncontrast-­‐enhanced  CT  (NECT)  -­‐  well-­‐
common  in  women circumscribed  and  of  low  density
o due  excessive  dev’t   • on  contrast-­‐enhanced  CT  (CECT)  -­‐  ini<al  
o Sessile  accessory  lobe  extending   peripheral  nodular  enhancement  with  near-­‐
caudally  from  the  inferior  aspect  of   complete  filling-­‐in  on  delayed  images
the  R  lobe   • retain  contrast  for  20  to  30  minutes
• nuclear  single  photon  emission  computed  
oSen  with  bulbous  configura<on
tomography  (SPECT)  -­‐  with  techne<um  

1
 labelled  RBC  -­‐  decreased  ac<vity  in  early   ● liver  is  accessed  by  Entamoeba  histoly/ca  
images  and  increased  ac<vity  on  delayed   via  the  portal  vein
• magne<c  resonance  imaging  (MRI)  -­‐  useful   ● symptoms  similar  to  pyogenic  abscess
for  lesions  <  2  cm.;  well-­‐defined,   ● US  and  CT  appearance  similar  to  pyogenic  
homogeneous  and  markedly  hyperintense   abscess
on  T2-­‐weighted  images;  peripheral  to   ● oSen  located  peripherally
central  enhancement  on  gadolinium-­‐ ● on  aspira<on,  fluid  classically  “anchovy  
contrast paste”
● treatment  -­‐  metronidazole
HEPATIC  CYST ● may  take  months  to  resolve
Ø second  most  common  benign  lesion
Ø single  or  mul<ple ECHINOCOCCAL  DISEASE
Ø 2.5%  to  10%  of  the  popula<on § caused  by  Echinococcus  granulosis
Ø women  >  men § symptoms  similar  to  pyogenic  abscess
Ø usually  asymptoma<c § common  in  the  right  lobe,  may  be  mul<ple,  
Ø seen  in  40%  of  pa<ents  with  polycys<c   and  may  involve  the  chest
kidney  disease;  60%  of  pa<ents  with   § grow  slowly  and  cyst-­‐like  in  appearance
mul<ple  hepa<c  cystc  have  polycys<c   § US  and  CT
kidneys o double  line  sign,  water  lily  sign,  
Ø US  -­‐  anechoic  (no  internal  echoes),  sharp   racemose  cyst  wall
margins,  impercep<ble  wall,  increased   o double-­‐layer  cyst  wall  with  inner  
through  transmission;  US  has  95%  to  99%   germinal  layer  which  gives  rise  to  
accuracy “daughter  cysts”
Ø CT  -­‐  sharply-­‐defined,  water  density  with  no   o daughter  cysts  are  visualized  
percep<ble  wall  and  no  contrast   within  the  parent  cyst  in  70%  of  
enhancement cases
Ø CT  -­‐  delayed  images  show  no  contrast   o 50%  have  shell-­‐like  calcifica<ons
enhancement
Ø MRI  -­‐  homogeneous  low-­‐signal  intensity  on   FUNGAL  ABSCESS
T1-­‐weighted  images  and  high  -­‐signal   1. immunocompromised  pa<ents
intensity  on  T2-­‐weighted  images 2. usually  Candida
3. with  other  organisms  like  Pneumocys/s  
PYOGENIC  ABSCESS carinii,  cytomegalovirus,  mycobacteria
● may  be  bacterial,  parasi<c,  fungal 4. have  concomitant  hepa<c  involvement  with  
● 85%  to  90%  are  bacterial  or  pyogenic Kaposi’s  sarcoma,  lymphoma
● bacteria  access  the  liver  via  the  biliary  tree  
or  portal  vein HEPATIC  ADENOMA
● associated  with  biliary  obstruc<on,   ü seen  exclusively  in  women  of  childbearing  
diver<culi<s,  trauma,  inflammatory  bowel   age  (in  98%)
disease,  iatrogenic ü linked  to  oral  contracep<ves,  anabolic  
● pain,  fever,  diarrhea,  leukocytosis,   steroids,  glycogen  storage  disease
abnormal  liver  func<on  tests ü composed  of  atypical  hepatocytes  and  
● most  commonly  in  the  right  lobe increased  fat  and  glycogen
● US  :  heterogeneous,  round,  hypoechoic   ü usually  asymptoma<c;  pain  if  with  
collec<on  with  irregular  thick  walls hemorrhage
:  internal  echoes,  fluid-­‐fluid  levels,   ü slight  malignant  transforma<on  poten<al
internal  debris ü US  -­‐  well  defined  with  variable  echogenicity;  
:  acous<c  shadowing  indicate  gas   indis<nguishable  from  focal  nodular  
within  the  abscess hyperplasia
● CT  :  heterogeneous  lesion  with  irregular   ü CT:  discrete,  low-­‐density  lesion,  mean  size  
margins of  10  cm.
:  peripheral  contrast  enhancement ü mul<ple  in  30%  of  pa<ents
:  internal  septa<ons  common ü may  have  dense  enhancement
:  20%  may  contain  air ü 50%  heterogeneous  because  of  hemorrhage  
● Differen<al  diagnoses or  necrosis
• cys<c  or  necro<c  metastases MRI  :  inhomogeneous  on  all  pulse  sequences;  
• amebic  abscess increased  signal  on  T1-­‐weighted  images
• hyda<d,  echinococcal  cysts Nuclear  scan  :  cold  lesion  on  sulfur  colloid  scan

AMOEBIC  ABSCESS FOCAL  NODULAR  HYPERPLASIA

2
Ø nonencapsulated Ø CECT  -­‐  enhancement  during  hepa<c  arterial  
Ø common  in  women phase
Ø usually  asymptoma<c Ø MRI  
Ø composed  of  normal  hepatocytes,  Kupffer   o decreased  signal  intensity  on  T1  
cells  and  bile  ducts  in  an  unusual   weighted  images
arrangement o increased  signal  on  T2  weighted  
Ø usually  less  than  5  cm  diameter images
Ø rarely  mul<ple Ø nuclear  scan
Ø common  in  the  periphery  of  the  right  lobe o cold  defect  on  sulfur  colloid  scan
Ø classic  appearance  -­‐  solitary,  well-­‐ o increased  ac<vity  on  gallium  scan
circumscribed  with  central  stellate  scar  of  
fibrosis  (central  scar  seen  in  20%) METASTASIS
Ø US  -­‐  variable  echogenicity   o the  most  common  malignant  lesion  of  the  
Ø CT  -­‐  may  be  seen  only  on  the  hepa<c   liver
arterial  phase  of  enhancement o metastasis  is  20%  more  common  than  
Ø MRI  -­‐  the  central  scar  is  high-­‐signal  intensity   primary  HCC
on  T2-­‐weighted  (versus  low-­‐signal  intensity   o common  primary  source  -­‐  colon,  stomach,  
in  fibrolamellar  carcinoma) lung,  breast,  pancreas
o abnormal  liver  func<on  test,  hepatomegaly  
FOCAL  FAT  INFILTRATION  OR  SPARING o typically  mul<ple,  involve  both  lobes
§ common  in  right  lobe  of  the  liver o solitary  metastasis  in  30%  to  40%
§ associated  with  obesity,  alcohol  abuse,  use   o may  be  calcified
of  steroids,  hyperalimenta<on   o may  be  solid,  necro<c,  cys<c  or  calcified
§ US o can  mimic  any  other  lesion  on  CT  and  MRI
o lobar  or  segmental  distribu<on o should  be  considered  in  pa<ents  >50  years  
o margins  are  angulated old  and  in  those  with  known  primary
o no  mass  effect  on  adjacent  vessels
§ CT LIVER TRAUMA
o patchy  or  focal  area  of  decreased   Ø second  most  frequently  injures  intra-­‐
abenua<on abdominal  organ  aSer  the  spleen
o typically  adjacent  to  the  falciform   Ø commonly  the  posterior  segment  of  the  
ligament  or  gallbladder  fossa   right  lobe
§ sparing  characteris<cally  involve  the   Ø best  evaluated  by  CECT
caudate  lobe,  periportal  region  and   Ø contusions,  lacera<ons,  intrahepa<c  and  
adjacent  to  gallbladder  fossa   subcapsular  hematomas

HEPATOCELLULAR  CARCINOMA  (HCC) BILIARY TRACT

Ø most  common  visceral  malignancy ü abdominal  plain  film  /  radiograph  -­‐  gas  or  
Ø most  common  risk  factor  -­‐  hepa<<s  B  (in   calcium
the  U.S.,  alcoholic  cirrhosis  is  the  most   ü oral  cholecystography  -­‐  not  done  anymore
common  risk  factor) ü ultrasound
Ø other  risk  factors  -­‐  hemochromatosis,   ü hepatobiliary  scan  /  cholescin<graphy  
Wilson’s  disease,  glycogen  storage  disease ü percutaneous  cholangiography  /  ERCP
Ø common  in  men ü opera<ve  cholangiography  
Ø Three  paberns: ü CT,  MRI
o solitary  mass  (50%)
o mul<focal  involvement CHOLELITHIASIS
o diffuse  infiltra<on Ø most  common  disease  of  the  gallbladder
Ø 80%  of  pa<ents  have  underlying  cirrhosis Ø 10%  of  the  popula<on  have  gallstones
Ø invasion  of  portal  vein  seen  in  30%  to  60% Ø most  gallstones  are  cholesterol  stones
Ø increased  alpha  feto  protein,  elevated  liver   Ø 95%  detected  by  US
func<on  tests,  weight  loss,  RUQ  pain,   Ø ultrasound
ascites,  hepatomegaly   o echogenic,  shadowing  foci
Ø poor  prognosis;  average  survival  =  6  months o move  when  pa<ent  changes  
Ø US  -­‐  variable  appearance;  discrete   posi<on
hypoechoic  mass;  or  tumor  may  be   o non-­‐mobile  echoes  may  be  due  to  
undetectable  because  of  diffuse  infiltra<on   bile  sludge,  cholesterol  or  
of  the  parenchyma adenomatous  polyps,  
Ø NECT  -­‐  hypodense  mass  with  areas  of   adenomyomatosis,  gallbladder  
increased  density carcinoma
Ø CT

3
 o less  sensi<ve  than  US ü increasing  frequency  with  HIV;  
cryptosporidia  and  cytomegalovirus  are  the  
ACUTE  CHOLECYSTITIS pathogens
v most  commonly  due  to  cys<c  duct   ü thickening  of  the  walls  of  the  bile  ducts  and  
obstruc<on  by  cholelithiasis   gallbladder
v 5%  to  10%  are  acalculous   ü intrahepa<c  findings  of  sclerosing  
v US  -­‐  cholelithiasis,  thickening  of  the  GB  wall,   cholangi<s  
Murphy’s  sign ü papillary  stenosis  
v cholescin<graphy  -­‐  non-­‐visualiza<on  of  GB  
by  1  hour  (normally  in  30  minutes) RECURRENT  PYOGENIC  CHOLANGITIS  
(ORIENTAL  CHOLANGIOHEPATITIS)
CHRONIC  CHOLECYSTITIS v endemic  in  Asia
Ø gallbladder  is  oSen  contracted v acute  abdominal  pain,  recurrent  jaundice,  
Ø gallstones,  chronic  inflamma<on,  recurrent   fever,  chills
colic v intra-­‐  and  extrahepa<c  bile  ducst  are  
Ø cholescin<graphy  -­‐  delayed  visualiza<on  in   dilated  and  contain  soS  pigmented  stones  
1-­‐4  hours and  infec<on

BILIARY  DILATATION NEOPLASMS  OF  THE  GALLBLADDER

v not  necessarily  due  to  biliary  obstruc<on ü adenomas,  fibromas,  papillomas,  
v common  bile  duct  >  0.8  cm. cystadenomas  
v gallbladder  diameter  >  4  cm. ü adenocarcinoma  -­‐  oSen  with  gallstones  
v must  determine  presence,  level  and  cause   (70%  to  80%)
of  obstruc<on ü may  be  masked  by  gallstones,  hence  late  
diagnosis
BILIARY  OBSTRUCTION
Ø common  causes CHOLANGIOCARCINOMA
o gallstones § slow  growing  carcinoma  of  the  bile  ducts
o tumor § Klatskin’s  tumor  =  cholangiocarcinoma  at  
o stricture the  junc<on  of  the  right  and  leS  hepa<c  
o pancrea<<s ducts
o Mirizzi’s  syndrome § predisposing  factors:  sclerosing  cholangi<s,  
Ø malignant  cause  of  obstruc<on  produces   hepatolithiasis,  liver  flukes  (Clonorchis  
abrupt  termina<on  of  the  extrahepa<c   sinensis  and  Opistorchis  viverrini;  Caroli’s  
biliary  duct disease,  choledochal  cysts,  familial  
o pancrea<c  carcinoma polyposis  
o ampullary  carcinoma
o cholangiocarcinoma  
PANCREAS
§ Lies  transversely  in  the  upper  abdomen  at  
SCLEROSING  CHOLANGITIS L1-­‐L2  level
Ø primary  sclerosing  cholangi<s  is  associated   § Head  and  body  are  retroperitoneal,  tail  is  
with  ulcera<ve  coli<s  and  Crohn’s  disease intraperitoneal  lying  in  the  splenorenal  lig  
Ø secondary  sclerosing  cholangi<s  are  caused   § Pancrea<c  size  is  variable  but  normal  
by  chronic  low-­‐grade  obstruc<on  or   maximum  adult  AP  measurement  is  3.5  cm  
infec<on for  the  head,  body  and  tail
Ø intermibent  jaundice § Imaging  Modali<es
Ø alterna<ng  areas  of  stricture  and  dilata<on   § plain  abdominal  radiograph  -­‐  pancreas  is  
=  beaded  appearance not  seen;  calcifica<ons  or  gas  within  
Ø complica<ons
pancrea<c  abscesses  only
o cholangiocarcinoma  
§ Chest  film  –  demonstrates  pleural  effusion,  
o cirrhosis  
basal  atelectasis,  elevated  diaphragm
o portal  hypertension
§ Ultrasound  –  homogeneous  echopabern  of  
slightly  higher  echogenicity  than  the  liver
ASCENDING  CHOLANGITIS § US  can  evaluate  pancrea<c  head  and  body
ü acute  infec<on  of  the  biliary  tree § CT  is  best  modality
ü secondary  to  par<al  or  complete   § CT  scan  –  more  helpful  than  ultrasound  in  
obstruc<on assessing  pancrea<c  outline  and  tail,  
ü Escherichia  coli  is  the  frequent  organism  
peripancrea<c  <ssues  and  blood  vessels
responsible § ERCP  (Endoscopic  Retrograde  
Cholangiopancreatography)

4
 o Endoscopic  assessment  of  UGIT   o pancrea<c  pseudocyst  -­‐  
and  ampulla   encapsulated  collec<on  of  fluid  
o Contrast  assessment  of  pancrea<c   and  debris
and  bile  ducts o portal  and  splenic  vein  thrombosis
o Most  effec<ve  method  for  imaging   o pancrea<c  necrosis
pancrea<c  duct
o Therapeu<c  and  diagnos<c   CHRONIC  PANCREATITIS
procedures  may  be  done v repeated  bouts  of  acute  pancrea<<s
§ E.g.  sphincterotomy,   v pancrea<c  calcifica<ons;  irregularity  of  the  
biopsy,  stone  extrac<on,   ducts  with  beading  and  saccular  dilata<on  
balloon  dilata<on,  stent   of  the  branches
inser<on,  cyst  drainage v cause  is  almost  always  alcohol  abuse  or  
§ MRI  specifically  MRCP-­‐  can  demonstrate   gallstones
common,  cys<c  and  pancrea<c  ducts v calcifica<on  suggest  alcohol  abuse
v Plain  film,  barium  studies,  US,  CT  scan,  ERCP
ACUTE  PANCREATITIS
ü alcohol  abuse,  choledocholithiasis;  trauma,   PANCREATIC  ADENOCARCINOMA
drugs  (steroid,  INH,  sulfonamides),  pep<c   v 95%  of  all  malignant  tumors  of  the  pancreas
ulcer  disease,  viruses  (mumps,  coxsackie,   v poor  prognosis
hepa<<s) v hypoechoic/  low-­‐density  mass;  usually  head  
ü diagnosis  is  clinical;  imaging  is  used  for   or  uncinate  process  (60%  to  70%)
prognos<ca<on  and  iden<fy  complica<ons v jaundice
ü Chest  film  changes v atrophy  of  the  distal  gland
o LeS  pleural  effusion,  basal   v smooth  dilata<on  of  the  pancrea<c  duct
atelectasis,  elevated   v dilata<on  of  the  main  pancrea<c  duct  and  
hemidiaphragm   the  bile  duct  (double-­‐duct  sign)
ü Abdominal  film  changes v Barium  studies
o Colon  cut-­‐off  sign  –  transverse   o Widened  duodenal  loop  with  
colon  is  dilated  but  cuts  off   fixa<on
abruptly  at  the  splenic  flexure o Anterior  displacement,  spicula<on  
o Sen<nel  loops   of  medial  mucosal  folds
§ DUODENAL  ILEUS  –  MOST   o Nodular  mucosal  filling  defects
SPECIFIC o Inverted  3  or  Frostberg  sign
o Small  bowel  ileus   v Compression  and  invasion  of  the  second  
o Gasless  abdomen  due  to  persistent   por<on  of  the  duodenum  with  ulcera<on  of  
vomi<ng the  inner  wall
ü Barium  studies v Reverse  3  sign  of  Frostberg  
o Widened  duodenal  loop  or  C-­‐loop   v Ultrasound
with  compressed  medial  border o Posi<ve  findings  in  80-­‐90%  of  cases
o Ampullary  edema § Early  –  focal  bulge  to  
o Thickening  of  gastric  and  duodenal   pancrea<c  outline
folds § Late  –  irregular  lobulated  
ü CT  scan mass  of  low  or  mixed  
o Best  imaging  technique echogenicity  
o pancrea<c  enlargement,  decreased   o Distal  chronic  pancrea<<s
density  due  to  edema,   o Dilated  CBD,  pancrea<c  duct  distal  
intrapancrea<c  fluid  collec<on,   to  tumor
blurring  of  the  gland  margins o Signs  of  spread:  liver  metastasis,  
o Phlegmon  –  low  density  mass portal  and  peripancrea<c  nodes,  
o Hemorrhage  –  high  density  mass invasion  of  retroperioneal  fat,  
o Fluid  collec<ons,  pancrea<c  or   venous  occlusion
peripancrea<c   v CT  scan
o Abscess o Superior  to  ultrasound  in  assessing  
ü Free  peritonel  fluid tumor  invasion  of  peripancrea<c  
ü Complica<ons structures
o phlegmon  -­‐  inflammatory  mass o Preferred  technique  for  assessing  
o hemorrhage  -­‐  from  arterial  injury operability
o abscess  forma<on v CT  findings  indica<ve  of  unresectability  
(Whipple’s  procedure)
o liver  metastasis

5
o ascites  
o local  extension  (except  the  
duodenum)
o arterial  encasement
o venous  occlusion
o lymph  node  enlargement  outside  
the  field

6
ESOPHAGUS, STOMACH. Classification of esophageal motility disorders
DUODENUM l PRIMARY
Methods of Examination of the Upper Gastrointestinal – Achalasia
Tract – Diffuse esophageal spasm
1. Plain film – Intestinal pseudoobstruction
2. Upper GI series – Hypertensive peristalsis
1. Examination with an opaque – Presbyesophagus
contrast medium – Congenital tracheoesophageal
1. Barium sulfate – agent of fistula
choice; inert and isotonic – Chalasia
2. Double contrast method – l SECONDARY
examination with an opaque – Connective tissue
contrast medium plus gas – Chemical or physical
producing medications – Infection
– Metabolic
Rules to follow prior to UGIS – Endocrine
• Free passage through colon must be certain – Neurologic
• Barium studies in a patient with suspected – Muscular
perforation must be approached with – Vascular
caution. Water soluble contrast materials – Neoplasm
are useful on some occasions but these – Pharmacologic
agents are hypertonic and should be used ACHALASIA
with caution in the elderly and dehydrated l Failure of normal lower esophageal
patients sphincter opening produces persistent V
configuration of head of the barium column
ESOPHAGUS above the sphincter
l Straight muscular tube l Impairment or absence of Auerbach’s plexus
l 20-24cm long ganglion cells
l Joins the hypopharynx just above the sternal l Pseudoachalasia-a constricting annular CA
notch,at the level of C5 or C6 and GE jxn at extending from the gastric fundus may cause
the level of T11 motor abnormalities in the esophageal body
l Attaches to the gastric cardia behind the
xiphoid process DIFFUSE ESOPHAGEAL SPASM
l Cricopharyngeus muscle- major element of Clinical syndrome characterized by:
UES 1.symptom of intermittent dysphagia and chest
l LES- 2-4cm with minimal muscle thickening pain
l Divided into proximal,middle and distal 2.forceful,simultaneous repetitive contractions on
l Jxn of proximal and middle 3rd is near the manometry
aortic arch level 3.segmental lumen-obliterating contractions on
l Proximal 3-4cm lies in the lower part of the radiograph
neck, the remainder is intrathoracic behind 4.thickening of the esophageal wall
the heart l Peristalsis may occur in the upper
esophagus
Major impressions: l All nonperistaltic movement are observed in
a. Level of aortic arch the smooth muscle part
b. Left mainstem bronchus
c. Left ventricle TRACHEOESOPHAGEAL FISTULA
Type A =esophageal atresia- NO fistula =10%
Types of examination Type B=esophageal atresia-PROX fistula=1%
l Esophagography Type C=esophageal atresia-DIST fistula=80%
l Flouroscopy Type D=esophageal atresia-PROX + DIST=1%
l Endoscopy Type E=H-type fistula-NO atresia=10%
l Esophageal Manometry
PRESBYESOPHAGUS
Esophagogram/Barium swallow l Curling or corkscrew esophagus
l Ingestion of barium sulfate suspension l Helix configuration suggest possible
l Types: shortening of the spiral esophageal muscle
– Double contrast – demonstrate wall
neoplasm and esophagitis ESOPHAGEAL PERFORATION
– Full column l Nearly all perforations are caused by trauma
– Mucosal relief – esophageal varices l Non-traumatic esophageal perforation is
– Fluoroscopic observation and generally caused by caustic ingestion or
motion recording technique – neoplasm
esophageal motility l The most frequent sites are adjacent to the
cricopharyngeus

1
 l Abnormal radiographic finding include
pneumomediatinum ,mediastinal widening
and cervical emphysema
CAUSTIC ESOPHAGITIS
l Alkaline-coagulation necrosis in minutes
l Acid-more superficial
l During the 1st 24 hrs,esophagus often
appear normal
l Blurred margin,contour irregularity
l Ulceration
l Thickened folds
HIATAL HERNIA
l Types:
1) Axial
2) Paraesophageal
3) Mixed
l Relevant landmarks:
1) Diaphragmatic hiatus
2) Esophagogastric jxn
3) LES segment
4) Loculus of herniated stomach
SLIDING HIATAL HERNIA
l part of the stomach moves through the
diaphragm so that it is positioned outside of
the abdomen and in the chest.
l lower esophageal sphincter (LES) often
moves up above its normal location in the
opening of the diaphragm.
l Most people have no symptoms, and it is
often diagnosed when a person is being
evaluated for other health concerns.
l If the LES moves above the diaphragm, it
may not close well and stomach acid and
juices may go back into the esophagus (acid
reflux) commonly known as heartburn.
PARAESOPHAGEAL HERNIA
l Stomach bulges up through the opening in
the diaphragm (hiatus) alongside the
esophagus (upside-down stomach).
l LES remains in its normal location inside the
opening of the diaphragm.
l This type of hernia most commonly occurs
when there is a large opening in the
diaphragm next to the esophagus.
l The stomach and, rarely, other abdominal
organs (such as the intestine, spleen, and
colon) may also bulge into the chest
MIXED HERNIA
The LES is above the diaphragm as in a
sliding hiatal hernia, and the stomach is alongside the
esophagus as in a paraesophageal hiatal hernia.
ESOPHAGITIS
l Irregularity of luminal contour
l Granular mucosal pattern
l Discrete ulceration
l Transverse esophageal folds
l Esophageal wall thickening
l Segmental narrowing
l Finding of transverse esophageal ridging or
fold- felinization
2
BARRETT’S ESOPHAGUS
l Partial lining of the esophagus by columnar
type epithelium reflects an adaptive
alteration caused by chronic reflux
esophagitis
l Has a predilection to develop
adenocarcinoma
l Generally older than 40y/o
l Punch-out esophageal ulcer that resembles
gastric ulcer morphology or when an
unexplained stricture of the middle
esophagus is observed
DIVERTICULAR DISEASE
I. Pulsion diverticulum – mucosal herniations thru
muscular wall
- Related to esophageal motility disorders
- Oval or rounded or smooth
a. Zenker’s diverticulum – along the posterior
wall of the upper end of esophagus at its
junction with the pharynx
b. Epinephric – lower third of esophagus just
above the diaphragm
II.Traction – due to extrinsic inflammatory
involvement of esophagus; mid-esophageal
III.Intramural pseudodiverticulosis – multiple small
outpuchings in the wall
FOREIGN BODY
l In the esophagus flat objects such as coins
are oriented in the coronal plane
l In contrast,flat foreign body in the trachea is
oriented in the sagittal plane
ESOPHAGEAL VARICES
l Changeable fold thickening or serpigenous
and polypoid defects in the lower esophagus
l Best shown by mucosal relief technique
ESOPHAGEAL RINGS
l Schatzki’s ring-asymptomatic, mucosal fold
at the esophagogastric jxn
l Exaggeration of the normal transverse
mucosal fold-thickened to 4-5mm in width
causing narrowing of the luminal aperture
l Steak house syndrome
l Rings<12mm always accompanied by
dysphagia
l Rings >12-20mm may or may not cause
symptoms
ESOPHAGEAL STRICTURES
l Any persistent intrinsic esophageal
narrowing > 1cm
l Fibrosis-most common cause
l Benign strictures-”hourglass” appearance
l Malignant strictures-irregular luminal contour
often demonstrating ulceration or tumor
nodules
l Reflux peptic esophagitis-strictures of the
distal 2/3
ESOPHAGEAL CARCINOMA
Polypoid – filling defect in the barium filled lumen
 - Edges of the lesion are sharply demarcated
producing sharp angle or overhanging edges
Infiltrating – annular constricting filling defect or
narrowing of the lumen
- Stenotic area is irregular and mucosal folds
are absent
l About 90%are squamous cell in origin
LEIOMYOMA
l The most common benign tumor of the
esophagus
l 35 y/o-mean age
l Solitary mass in the distal 3rd
l Cxr-soft tissue mediastinal
density,mediastinal widening,or a calcified
mass
l Esophagograms-smooth filling defect
l Seen face on-splitting of barium column,
splaying of longitudinal folds,segmental
widening of esophageal dm
STOMACH
Examination technique using barium sulfate:
1. Single contrast
a. Compression – demonstrate lesions
and structural details including
erosions and area gatrica
b. Mucosal relief – radiographs of the
stomach in prone and supine
position with small amount of
barium
c. Distension with barium suspension
2. Double contrast – provides the greatest
mucosal detail
Anatomically divided into 3 parts:
a. Fundus- lies above the transverse line drawn
thru the EGJ
b. Body- lies between the gastric fundus, and
line transecting the stomach at incisura
angularis
c. Antrum- extends from incisura angularis to
pyloric canal
Rugae – longitudinal folds parallel to long axis of the
stomach
Area gastricae – small tufts of gastric mucosa 1-3mm
in size
CONGENITAL AND DEVELOPMENTAL
ANOMALIES
Gastric diverticulum – located near EGJ
Antral web – diaphragm composed of mucosal and
submucosal tissues
- constriction proximal to pyloric canal
Hypertrophic pyloric stenosis – elongated, narrow
pyloric canal surrounded by muscle mass impinging
on the base of the distal gastric antrum and duodenal
bulb
Duodenal diverticulum – common at the medial
aspect of 2nd portion in proximity to the papilla of
Vater
NORMAL CONFIGURATION
l In infants
– Gas-filled, overdistended and
erroneously suggests obstruction.
3
– Fluid-filled, appears as
pseudotumor
– Mucosal folds are characteristically
absent or sparse, stomach appears
smooth
l In older children, stomach appears same
as in adults.
HYPERTROPHIC PYLORIC STENOSIS
l Precise etiology is unknown
l Hypotheses:
– Nerve cells in the myenteric plexus
of the pylorus are abnormal in
number and function
– Prolonged spasm of the
antropyloric muscle leading to
hypertrophy
l Secondary to hyperacidity
which is common in the
immediate postnatal
period.
UGIS shows contrast material passing through the
mucosal interstices of the canal, forming a “double
track sign.” Mass impression on the gastric antrum
best seen during peristaltic activity is termed “the
shoulder sign”.
l Diagnosis has been relegated to ultrasound
Ultrasound Classic appearance:
l Elongation of the pyloric canal
l Persistent spasm of the pyloric canal with
little, if any, fluid passing into the
duodenum
l Persistent thickening of the circular muscle
in the elongated canal
l Sonolucent donut (thickened muscle) on
cross-section
l Ultrasound
* Muscle thickness of 4 mm or greater
* Length of pyloric canal: 1.2 cm or longer
– “Double Track sign” results from
compressed mucosa showing
numerous linear fluid accumulations
within
Longitudinal sonogram shows anterior thickened
muscle. Double layer of rounded and redundant
mucosa fills the channel and protrudes into fluid filled
antrum. (D) fluid filled duodenal cap.
Cross sectional sonogram shows circumferential
muscular thickening surrounding the central channel
filled with mucosa.
GASTRIC ULCERS
Epidemiology/Pathogenesis
l Helicobacter pylori
l NSAIDs
l Steroids
l Tobacco,alcohol, and coffee
l Stress
l Gastroduodenal reflux of bile and delayed
gastric emptying
l Hereditary factors
Helicobacter pylori
l gram(-), spiral-shaped bacillus
 l responsible for almost all ulcers, 60-80% HYPERPLASTIC
(gastric), 95-100%(duodenal) l up to 90% of all gastric polyps
l increased secretion of gastrin with high l elongated, branching, cystically dilated
basal and peak acid outputs glandular structures
l eradication of H. pylori accelerates ulcer l rare malignant potential
healing and decreases recurrence rate l <1cm,sessile
Radiographic findings l often multiple
l Presence of an ulcer crater or niche ADENOMATOUS
l views obtained en face and in profile l less than 20% of all gastric polyps
l En face: presence of dense ovoid collection l dysplastic epithelium
of barium within the crater l malignant transformation in 50%
l In profile: barium filled projection extending l >1cm, sessile, pedunculated, or lobulated
from the lumen l often solitary
l barium coating the rim of the unfilled ulcer
crater produces the “ring sign” LEIOMYOMA
Complications l 40% of all benign gastric tumors
l gastric outlet obstruction(20%) l consist of intersecting bundles of spindle-
l penetration to contiguous organs shaped cells in a characterisitc whorling
l perforation(7%) pattern
l fistula(duodenum,small bowel,colon) l endogastric(80%), exogastric(15%),
l hemorrhage(20%) “dumbbell”-shaped(5%)
l mostly solitary lesions, <3cm
BENIGN VERSUS MALIGNANT l epigastric pain, UGIB, palpable mass
BENIGN Radiographic findings:
l Project beyond the lumen l discrete submucosal masses
l more likely to be deep l tumors larger than 2 cm frequently contain
l surrounding mucosa is smooth areas of ulceration
l Edematous mound is symmetrical and l may contain calcification
smooth Management:
l radiating folds are smooth and distinct from l small, asymptomatic masses ®follow-up
each other l >2cm ®resected
MALIGNANT
l Extends into the lumen LIPOMA
l more likely to be shallow l 2-3% of benign gastric tumors
l surrounding mucosa has a nodular or l mature fat cells surrounded by a fibrous
irregular component capsule
l Infiltrating tumor is usually asymmetrical and l no malignant potential
maybe distinctly masslike l usually asymptomatic, may cause upper GI
l radiating folds may be irregular, nodular, bleeding or gastric outlet obstuction
variable in thickness, and may merge l solitary lesions, frequently in the antrum
Radiographic findings:
BENIGN TUMORS OF THE STOMACH l CT has proved to be a valuable technique
l 85-90% of all neoplasms in the stomach and ®well-circumscribed areas of uniform fatty
duodenum are benign density with an attenuation of -80 to -120
l 50% mucosal Hounsfield units
l 50% submucosal l soft consistency ®change in size and
MUCOSAL LESIONS shape with peristalsis or palpation at
l Polyps fluoroscopy
(hyperplastic,adenomatous)
l Villous tumors POLYPOSIS SYNDROMES
l Polyposis syndromes l Familial adenomatous polyposis
(familial adenomatous polyposis, Peutz- ® detection of adenomatous polyps in
Jeghers, Cronkhite-Canada) stomach or duodenum is important
SUBMUCOSAL LESIONS ®periodic surveillance of the UGI tract
l Leiomyoma l Peutz-Jeghers syndrome
l Lipoma ®hamartomatous polyps
l Neurofibroma
l Cronkhite-Canada syndrome
®gastrointestinal polyposis with nail and hair
POLYPS (HYERPLASTIC/ADENOMATOUS)
l 50% of all benign gastric tumors changes
l mostly asymptomatic, may cause upper GI ®innumerable benign sessile polyps with
bleeding or gastric outlet obstruction distinctive “whiskering” effect
l some adenomatous polyps undergo
malignant degeneration TUMORS
l need for endoscopic biopsy and removal of l Vast majority are malignant epithelial
polyps is related to size and appearance neoplasm

4
 l Most are detected by direct visual or
endoscopic technique
l Primary radiologic manifestation are –
inraluminal mass and/or deformity caused by
tumor infiltration with loss of normal
distensibility

DUODENUM
- C-shaped curve extending from the pyloric
canal to the junction of the duodenum and
jejunum at the junction of the ligament of
Treitz

- Four segments:
- Duodenal bulb – usually devoid of
mucosal folds
- Descending limb – contains major
and minor papillae
- Transverse limb – extends across
SMA
- Limb ascending to ligament of
Treitz

DUODENAL ATRESIA AND STENOSIS

l Plain Film: Supine frontal radiograph of the
abdomen shows the “Double bubble sign”.
An enlarged stomach and duodenum with
absence of gas in the distal bowel loops.

BRUNNER’S GLAND ADENOMA

l Small protuberant lesions covered by
duodenal mucosa
l Smoothly demarcated filling defects with a
dm varying from several mm to
approximately 1cm
l If multiple lesions occur this is generally
called hyperplasia of Brunner’s gland

ADENOCARCINOMA OF THE DUODENUM,

POLYPOID FORM
l Barium study. a. Overview of the duodenum,
and (b) spot view of the lower part. There are
multiple rounded and oval sharply delineated
filling defects in the second and third portion
of the duodenum revealing polypoid surface
of the tumour.
l Most common malignant duodenal tumor

LEIOMYOSARCOMA OF THE DUODENUM

l Second most common malignant duodenal
tumor
l May mimic polypoid adenocarcinoma
l The presence of a sinus or fistula suggest
leiomyosarcoma
l Thickened folds or constrictive lesion

5

SMALL AND LARGE INTESTINES
Indications for the examination of the
small intestines
1. presence of an abdominal
mass
2. suspicion of small bowel
obstruction
3. unexplained diarrhea
4. malabsorption
5. unexplained intestinal
bleeding
6. abdominal pain or tenderness
Basic anatomy
- duodenum is fixed
- jejunum and ileum are not fixed =
mesenteric small intestine
- mucosal folds (valvulae conniventes)
normally 1-2 mm in width and are
regularly spaced
- jejunum may be 3 cm in diameter
- ileum may be 2.5 cm in diameter
Basic physiology
- digestion and absorption
- reabsorption of bile salts and
water - ileum
- motility = quiescent and active
phase
- active phase = churning phase and
propulsive phase
- contractile activity = myogenic,
neural, and biochemical controls
Methods of examination
1. plain film of the abdomen -
supine and upright views
2. upper gastrointestinal series
(UGIS)
3. enteroclysis
4. peroral small bowel
examination with
pneumocolon
5. water-soluble contrast
studies
Congenital anomalies
1. tubulation defects - atresia
and stenosis
2. rotation anomalies -
nonrotation, midgut volvulus
3. duplication cysts and
diverticula - Meckel’s
diverticulum
ABNORMALITIES OF THE SMALL
BOWEL
1. Meconium Ileus
• Obstruction results from
impaction of thick,
1
tenacious meconium in
the distal small bowel
• Complications:
• Ischemia-induced
ileal atresia or
stenosis
• Ileoperforation
• Meconium
peritonitis (most
common)
• S/S:
• vomiting (bile
stained)
• Abdominal
distention
• Failure to pass
meconium
Plain Film:
• Low small bowel
obstruction with
numerous air-filled loops
of small bowel
• Air fluid levels usually are
absent
• Absence of gas in the
rectal vault
• “Soap bubble effect” of
gas mixed with meconium
Ultrasound shows dilated intestinal
loops containing echogenic material
representing calcified meconium.
Contrast Enema
- Aqueous contrast ( hyperosmolar)
agents diluted 3:1 with normal saline
- When contrast is refluxed into the
small intestine, the enema becomes
diagnostic and at the same time
therapeutic
- Filling of the terminal colon should be
attempted in all cases, even though
occasional perforation can occur.
STAGES OF INTESTINAL ROTATION
A. The duodenum has rotated 90
counterclockwise to lie to the
right of the SMA The distal large
bowel also rotates 90
counterclockwise.
B. The duodenum has rotated
another 90 counterclockwise.
C. The duodenum has rotated to its
final 90 counterclockwise with
the duodenojejunal flexure lying
to the left of midline. The cecum
continues to rotate.
D. The normal rotated bowel is
depicted.

ROTATIONAL ABNORMALITIES AND
MIDGUT VOLVULUS
Types of Rotational abnormalities
1. Non-rotation
2. Malrotation
3. Reversed rotation
NON-ROTATION
1. Usually asymptomatic
2. Small bowel lies on the right and
colon on the left
3. Bowel is not mobile
4. Volvulus is not common
UGIS shows the small intestine on the
right side of the abdomen.
UGIS of the same patient shows the
colon and cecum on the left side of the
abdomen. The ileum is seen crossing
the midline from right to left.
Small intestine on the right side of the
abdomen; colon on the left
MALROTATION
• Final positioning is
somewhere between the
normal and complete non-
rotation
• Cecum and terminal ileum are
displaced upward and
medially
• Hypermobile cecum
• Small bowel mesenteric
attachment is lost
• Poorly fixed small bowel is
floppy and predominantly lies
on the right
• Duodenal bands (Ladd’s
band) and absence of the
ligament of treitz are
common
• Volvulus is common.
On BE, the intestine occupies an
intermediate position between that of
non rotation and the normal post natal
position. The cecum and terminal ileum
are displaced upward and medially.
REVERSED ROTATION
• Hepatic flexure and left
transverse colon lie
behind the descending
duodenum and SMA.
• Cecum is malrotated and
medially placed
• Small bowel is more on
the right side.
2
If duodenal bands and midgut volvulus
are present:
A. Beaked deformity of
the obstructed
duodenum and
spiraling of the
small intestine
B. Obstructed
duodenum ends at
a point medial to
the left vertebral
bony pedicle
MIDGUT VOLVULUS
UGIS demonstratres the “corkscrew
appearance” of the proximal small
bowel as it twist around the SMA
INTUSSUSCEPTION
• Common between the ages of 6
months and 4 years
• Neonatal intussusception is rare.
• Associated with lead points:
o Meckel’s diverticula,
polyps, lymphoma,
appendix
• S/S:
o Crampy abdominal pain
o Vomiting
o Bloody (currant jelly) stool
o Palpable abdominal mass
• Types:
o Ileocolic (most common)
o Ileo-ileo
o Ileo-ileocolic
Plain Film:
- depends on the duration of symptoms
and presence or absence of
complications
1. Normal abdominal gas pattern
2. Small bowel obstruction with paucity
of gas in the right.
3. Soft tissue mass within the right side
of the colon
4. “Target Sign” (Ring like area of
lucency within the mass
5. “Interrupted air column sign”
The mass causes cut off of the air
column in the transverse colon
6. “Meniscus sign”
- Rounded soft tissue mass
(intussusceptum) protruding into the
gas-filled transverse colon
ULTRASOUND - sensitivity of 100% and
specificity of 88%
Axial UTZ shows the “Doughnut Sign”.

- Hyperechoic outer ring
represents the intussuscipiens
- Hypoechoic outer ring formed by
the everted limb of the
intussusceptum
- Center varies with the section
level, represents the central limb
of the intussusceptum
UTZ obtained at the base of the
intussusceptum shows the “ Crescent-
in-doughnut sign”.
-a hyperechoic, crescent shape center
-occurs when the mesentery encloses
the central limb of the intussusceptum.
Longitudinal Scan shows the “Sandwich
Sign”.
-Outer hypoechoic bands represents
the everted limb of the intussusceptum
beside the intussuscipiens.
-Two hyperechoic bands represent the
mesentery
-Central hypoechoic band represents
the central limb of the intussusceptum
Reduction:
• Barium reduction:
• 40-45% Success
rate
• Air contrast (Enema and
ultrasound) and
Ultrasound-guided
reduction (air or aqueous
contrast)
• 80-90% success
rate
• Three or four tries
• If no progression of
reduction occurs within 4
to 5 minutes at any one
location, reduction is less
likely to occur.
• Air reduction:
• Pressures of at least
60 mmHg
• Pressure beyond
120 mmHg should
be avoided
• Barium reduction:
• Elevate the
reservoir to 3.5 feet
• Diluted aqueous contrast
agents
• Elevate the
reservoir to 5 feet
MECKEL’S DIVERTICULUM
• Persistence of the
omphalomesenteric duct
3
• May be a site of volvulus or
intussusception with resultant
SBO
• •May contain acid-secreting cells
that may cause ulceration of the
sensitive ileal mucosa and
subsequent
hemorrhageEnteroclysis;
Technetium studies are helpful in
patients who are bleeding and
have ectopic gastric mucosa in
the diverticulum
SMALL INTESTINES INFECTIONS/
INFESTATION
● Tuberculosis- commonly at
ileocecal area
● Yersinia enterocolitica
● parasites - ascaris, tapeworms.
Campylobacter and Giardia,
Strongyloides
TUBERCULOSIS
-coning of cecum with mucosal
ulcerations and stricture of ileum
ASCARIASIS – worms
GIARDIASIS
- jejunal folds are thick and irregular
SMALL INTESTINES: PARALYTIC ILEUS
- most common motility disorder
- small bowel and colon dilate with
gas, and transport is inhibited
- equal distension of small bowel
and colon
- air-fluid level occur only if the
process persists 5-7 days
- usually self limited
SMALL INTESTINES: HERNIA
● greater tendency for right than
left inguinal herniation
● diaphragmatic hernia
● internal hernia
ADHESIONS
• most common cause of small
bowel obstruction in the adult
• following laparotomy g
intraperitoneal fixed adhesions
vs. mobile bowel
• small bowel is distended
• air-fluid levels seen proximal to
the site
• usually little or no gas in the
colon
•
COLON

Indications for the examination of the
colon
• carcinoma - hematochezia or
occult blood in stool
• inflammatory bowel disease -
diarrhea
• other symptoms - change in
caliber of stool, constipation,
weight loss, anemia,
abdominal distension, mass,
tenderness, other GU
malignancies
Basic anatomy
1. transverse and sigmoid - mobile
2. cecum may be mobile if with
long mesentery
3. rest of colon has short
mesentery, relatively fixed
4. rectum - extraperitoneal
5. appendix- variable in position
6. generalized redundancy
particularly the sigmoid flexure
7. less prominent haustral folds
Basic physiology
● storage and transport of feces
● water absorption in the right
hemicolon
● motility not studied
Methods of examination
1. plain film of the abdomen -
supine and upright views
2. barium enema
3. ultrasound - to determine bowel
wall thickening; abscesses
4. computed tomography -
including extracolonic extent
ABNORMALITIES OF THE COLON
Hirschprung’s Disease (Aganglionosis
of the colon)
• Precise etiology is not
known
• Absence of ganglion cells
in the myenteric plexus
due to failure of migration
of neuroblasts.
• Commonly involves the
distal colon, specifically
the rectal and
rectosigmoid regions.
Plain Film
• Dilatation of the air-filled
colon and or small bowel
• Rectal gas is absent
Contrast Enema
• Demonstration of the
transition zone (point at
4
which the colon becomes
dilated)
• Rectosigmoid index of less
than 1:1
- transverse
measurement of the
rectum compared with
that of the sigmoid
colon
Contrast Enema
• Aganglionic segment may
show abnormal
contractions manifesting
in spastic corrugation or
serration.
• 24-hour delayed films- to
judge the degree of colon
emptying
● Definitive Diagnosis:
• Rectal Biopsy
Frontal and lateral BE images show the
proximal sigmoid colon and descending
colon greatly dilated as compared with
the distal sigmoid and rectum.
FUNCTIONAL MEGACOLON
- Result of intense anorectal spasm
secondary to anal fissures
- Barium Enema
• Fecal filled rectum with
pronounced posterior
indentation on the lower
rectum (due to
hypertrophied
puborectalis muscle or
sling)
- Difficult to differentiate from
extremely low, short segment
Hirschprung’s disease.
ANORECTAL ANOMALIES
(IMPERFORATE ANUS, ECTOPIC ANUS)
Gans Classification:
1. Ectopic anus
The hindgut opens ectopically at an
abnormally high location (perineum,
vestibule, urethra, bladder, vagina,
cloaca). There is failure of normal
descent of the hindgut.
2. Imperforate Anus
The terminal bowel ends
blindly and there is no
opening or fistula.
Types:
a. Membranous
imperforate anus
b. Anorectal or anal
atresia

Lateral Voiding Cystogram
demonstrates an air filled distal rectal
pouch ending blindly below the “M” line
of Cremin, a finding indicative of a low
lesion.
There is no fistula opening in the
terminal bowel.
3. Rectal Atresia:
• The anus is present and
open, but a variable
segment of rectum is
atretic. No fistula is
present.
4. Anal and rectal stenosis
• Incomplete atresia of
either structure
ECTOPIC ANUS
• Often also referred to as
imperforate anus
• Most common anorectal anomaly
encountered in neonatal infants
• Failure of the descent of hindgut
through the puborectalis sling
• Hindgut fails to reach the anal
dimple
• In females, it opens through a
fistula into the perineum, vagina,
urethra, bladder.
• In males, it opens into the
bladder, urethra, or perineum.
Radiographic findings:
• Colonic Obstruction
• In males, air bubbles can
be seen in the bladder
• “Cross table prone” or
“Butt-up” views
1.Pubococcygeal line
- drawn approximately
from the sacrococcygeal junction to the
midpubic bone.
2. “M” line of Cremin
- runs horizontally
through the junction of the lower and
upper two thirds of the ischia.
- currently being used
- corresponds more
closely to the level of the puborectalis
muscle.
Lateral radiograph shows an
imperforate anus below the “M” line of
Cremin.
- Line drawn through the junction of
the upper two thirds and lower one
- closed loop of the volved
thirds of the ischium.
- beak deformity of the twisted
Interpretation:
5
High – if air filled hindgut falls above
this line
Low – if air filled hindgut falls below
this line
Further delineation of the fistula
• Injection of contrast
material into the bladder,
male urethra, or female
genital tract.
• After colostomy, pressure
injection into the distal
portion of the colon
NECROTIZING ENTEROCOLITIS
- Most commonly affects premature
infants
- Can be seen in older infants and
children due to hypoperfusion of the
bowel secondary to dehydration
Etiology:
1. Intestinal ischemia or
hypoperfusion leading to altered
mucosal integrity
2. Bacterial overgrowth with gas
formation in the bowel wall
3. Continued irritation of the bowel
by continued feedings.
Radiographic Findings:
1. Generalized intestinal
distention resulting from
paralytic ileus
2. Pneumatosis cystoides
intestinalis-linear,
curvilinear, bubbly, or
foamy collections of gas
best visualized in the
colon but can occur
anywhere from the
stomach to the colon.
3. Portal vein gas-seen in
advanced disease
4. Pneumoperitoneum
5. Peritonitis / Ascites-
Abdomen becomes
opaque; thickened loops
of bowel
6. Disappearing intestinal
gas-indicates presence of
necrotic bowel
VOLVULUS
Usually involves the sigmoid colon in
children
Radiographic findings:
1. Cecal volvulus
cecum comes to lie in the LUQ
cecum
 6

● from few polyps to hundreds or

CT scan shows engorged mesenteric
vessels and collapsed distal ileum,
constitutes the “Whirl Sign”
2. Sigmoid volvulus
Plain film:
- twisted loop of sigmoid
colon tends to point to the RUQ
- beak deformity of the
twisted colon.
Barium Enema:
- Thumbprinting and colonic
spasm of the colonic segment.
Plain abdomen shows the characteristic
“Coffee Bean Sign”.
-formed by grossly dilated and closely
apposed closed loop obstruction of the
sigmoid colon.
-Air-fluid levels are present in each
segment.
-Central cleft of the coffee bean.
BE in supine patient demonstrates the
typical “Bird’s Beak” at the point of twist
of the sigmoid colon.
thousands
● rectal bleeding and diarrhea in
75%
● family history = screened with
colonoscopy and barium enema
before age 10
● total colectomy because of
development of adenocarcinoma
● Peutz-Jegher’s syndrome -
hamartomas, small bowel polyps
• circumoral melanin
pigmentation
● Cronkhite-Canada syndrome -
juvenile polyp histology
• alopecia
• skin pigmentation
• atrophy of fingernails and
toenails
ADENOCARCINOMA
● polyp with carcinoma g spreads
at the base g ulcerate g surround
the bowel g obstruct
● barium enema; CT detects spread
to the lymph nodes and liver

APPENDICITIS
● obstruction at the appendix g
inflammation g perforation g
abscess formation
● rarely requires imaging
● plain film may be normal, partial
or complete obstruction pattern,
RLQ mass, pneumoperitoneum;
calcification/ appendicolith
● ultrasound may demonstrate
thickened appendix wall

DIVERTICULOSIS/DIVERTICULITIS
● due to low residue diet
● incidence of 10-20%
● infection of an obstructed
diverticulum g diverticulitis
● usual site - sigmoid
● ddx- annular carcinoma

POLYPOSIS SYNDROMES
● familial adenomatous polyposis
syndromes (FAPS)
• familial polyposis coli
• Gardner’s syndrome -
epidermoid cysts,
craniofacial osteomas,
neurofibromas, soft tissue
fibromas
• Turcot’s syndrome -
intracerebral gliomas
● polyps may be 5 mm or less
 magnetic resonance imaging
Genito-urinary Tract ●
● renal scintigraphy
● retrograde pyelography
KIDNEYS ● renal angiography
Paired, retroperitoneal, bean-shaped organs ● percutaneous antegrade pyelography/
Upper border of T11 & lower border of L3 nephrostomy
R kidney is ~2cm lower than the L ● voiding cystography/ cystourethrography
Normal length: ● cystography
Adult: 11-15cm
3.7+/-0.37x ht of L2 PLAIN FILM X-RAY
Children: length of L1-L4 including the 3 ● kidneys- bean-shaped, T11 to L3 level
intervening disc spaces +1cm ● right kidney lower than the left
● kidneys descends 2-3 cm in the upright
3 ANATOMIC SPACES position
A. Perirenal ● left kidney may have fetal lobulation;
B. Anterior pararenal dromedary hump
C. Posterior pararenal
EXCRETORY UROGRAPHY/INTRAVENOUS
The kidneys are usually visible on a standard PYELOGRAPHY/INTRAVENOUS
anteroposterior radiograph of the abdomen because UROGRAPHY(EXU/IVP/IVU)
the PERIRENAL FAT surrounding the kidneys ● renal pelvis - triangular or conical, variable
produces a transradiant line. ● major and minor calyces
The calyces, pelvis, and ureter can only be ● ureters with three normal narrowings
demonstrated by the use of Radioopaque compounds ● bladder - transversely round or oval above
in IVP or Retrograde pyelography. the symphysis pubis
● rounded dome in male; flat or concave dome
HILUS in females
Medial border ● relatively larger in children
Orifice of renal sinus
Renal Sinus: CONGENITAL ANOMALIES OF THE KIDNEYS
1. Renal pelvis and calyces ANOMALIES IN NUMBER
2. Branches of renal artery and tributeries of renal vein A. Supernumerary Kidneys
3. Lymph vessels and nerves - more than 2 separate kidneys
4. Small amount of fat - extremely seldom/ rare
- Independent kidney with its own vascular supply,
URETER a capsule and its own urinary tract but is usually
5mm in diameter, 25 cm in length hypoplastic and rudimentary
2 portions: Superior abdominal portion ● Cause: very early division of the ureter
Inferior pelvic portion anlage before the invasion into the
metanephric blastema
3 AREAS OF NORMAL NARROWING ● Diagnosis
1. Ureteropelvic junction (UPJ)/Superior isthmus - demonstration of presence of separate pelvis,
2. Ureterovesical junction(UVJ)/Intramural constriction ureter, and blood supply is necessary to make the
3. Bifurcation of iliac vessels/Inferior isthmus diagnosis
- anomalous kidney is small and rudimentary and
Renal pelvis – funnel-shaped expanded upper end of other kidney of same side is smaller than normal on
the ureter. opposite side
- lies within the hilus of the kidney and
receives the major calyces B.RENAL AGENESIS
— Kidney is either absent or
BLOOD SUPPLY undeveloped including its vessels
Renal Artery – branch of the aorta; divides into 2 main and ureters
branches: POSTERIOR and ANTERIOR branches ● Cause: Failure of the ureteric bud to contact
Interlobar Arteries the metanephric blastema
Arcuate Arteries ● Incidence of 1/1000, often in males
Interlobular Arteries — Virtually always unilateral; majority
are on the left side
Renal Vein emerges from the hilus in front of the renal ● often go unnoticed because they are
artery and drains into the IVC compatible with normal life
● compensatory hypertrophy of the normal
kidney (> as 10% of the normal renal volume)
METHODS OF EXAMINATION OF THE GENITO- Radiographic features:
URINARY TRACT ● Absence of renal shadow on one side
● plain film x-ray ● Unusually large kidney on the other side
● excretory urography ● Trigone is usually deformed with ureteral
● ultrasonography
orifice missing on involved side
● computed tomography
 ● Angiography: absence of renal artery ANOMALIES IN POSITION
Ectopic kidney:
RENAL HYPOPLASIA A. Simple ectopy: the kidney does not ascend
1. reduction in the number of nephrons. properly and is found in the pelvis or over the
2. kidneys are small (< 3 percentile) with a brim.
normal parenchymal structure • Prone to obstruction and infection
3. appear as one small kidney with the other B. Crossed ectopy without fusion: The kidney
one larger than normal. then lies on the opposite side and is not attached
4. Functions normally to the normally placed kidney
5. Small kidneys also have small arteries and • Crossed renal ectopia may be
are associated with hypertension requiring associated with VUR.
nephrectomy.
RENAL ANOMALIES
RENAL DYSPLASIA AND MULTICYSTIC KIDNEY CROSSED ECTOPY- fusion of the kidneys on the
- seen in only one kidney as irregularly lobulated mass same side
of cysts and usually absent or atretic ureter (in • lower one is ectopic; ureter crosses
newborn). the midline to enter the bladder on
- associated with contralateral abnormalities, especially the opposite side
ureteropelvic junction obstruction. • Both kidneys are lower in position
- Dysplasia of the renal parenchyma is seen with • associated with rotation anomalies
urethral obstruction or reflux present early in pregnancy • associated with partial obstruction
or obstructed ureter.
- Cause: atresia of the renal pelvis and ureter during ANOMALIES IN FORM
embryonic development of the kidney. HORSHOE KIDNEY
1. Most common type of renal fusion.
MULTICYSTIC DYSPLASTIC KIDNEY 2. Both lower poles connect across the
1. Disorganized, dysplastic kidney with midline by an isthmus lying next to the
essentially no function. aorta and inferior vena cava.
2. The MCDK is typically unilateral 3. Usually supplied by multiple arteries
(bilateral MCDK would result in stillbirth 4. Hydronephrosis can be associated
or fetal demise). when ureteropelvic junction obstruction
3. Developmental abnormality unrelated to is caused by high ureteral insertion or
polycystic kidney disease and other anomalous vessels.
hereditary forms of cystic renal Radiographic features
dysplasia ● Alteration in the axis of kidneys
● Mass observed connecting lower poles
ANOMALIES IN ROTATION
A. Nonrotation Urography
- renal pelvis anterior to kidney lie 90º from - Malrotation with pelvis anterior or
horizontal (lie ventral) anterolateral in position
- Nephrographic demonstration of
B. Incomplete Rotation parenchymal isthmus connecting lower poles
- pelvis lies between 30º and 90º from horizontal - Varying dilatation of collecting system
(lies ventromedial) - Possible non function of one kidney because
of massive obstructive hydronephrosis
C. Reverse rotation - Upper ureteral displacement
- pelvis lies lateral to kidney; vessels are twisted
around anterior surface of kidney (lies lateral; Abdominal sonography of the abdomen in this patient
vessels run ventral to hilum) revealed: a) kidneys located at a lower level than
normal b) the lower poles of both kidneys pointing
D. Excessive Rotation medially, c) a bridge of renal tissue or isthmus
- renal vessels are twisted around posterior connecting the two kidneys. This isthmus is seen
surface of kidney (renal pelvis lies dorsal to passing anterior to the abdominal aorta. These
lateral, vessels run dorsal from kidneys to hilum ultrasound images are diagnostic of horseshoe kidney.

E. Transverse Rotation ABNORMALITIES IN NUMBER

- calyces point superiorly or inferiorly A. Ureteral atresia:
• The ureter may be absent or fails to
MALROTATION extend to the bladder and therefore
v relatively frequent. blind ending.
v The kidney and urinary tract are • It is associated with ipsilateral
anatomically and histologically normal. absent or multicystic kidney.
v Can occur uni- or bilaterally and be • Bilateral atresia is incompatible
associated with an ectopia or fusion of the with life.
two kidneys .

  -­‐  2  -­‐
 • Unilateral atresia is usually hypothesis as to why congenital UPJ
asymptomatic but may cause obstruction occurs
hypertension.
B. Duplex ureter Anteroposterior IVP in the excretory phase. Contrast
a. consequence of the development material fills the dilated calyces and pelvis of the right
of two ureteric buds in the kidney. No contrast enhancement is seen in the right
mesonephric duct. ureter suggesting ureteropelvic junction obstruction.
b. The ureter draining the lower The right kidney demonstrates relatively increased
segment migrate more cephalad renal length in comparison with the left kidney; this is
and lateral than the ureter draining consistent with obstruction
the upper segment. (Weigert Meyer
Rule) Megaureter and vesicoureteral reflux. Postvoid image
c. There is often reflux to the ureter of from a voiding cystourethrogram (VCUG) shows
the lower collecting system. Upper bilateral vesicoureteral reflux and bilateral
pole ureter is prone to ureteral ureterovesical junction obstruction caused by stenosis
ectopia and obstruction. of the distal ureters
d. More common in females and is
often bilateral 21-year-old man with left megaureter. Coronal
e. Often asymptomatic but commonly maximum-intensity-projection excretory MR urogram
presents with persistent or reveals markedly dilated distal ureter, less dilated
recurrent urinary tract infections upper ureter, normal-sized pelvis, and minimally
rounded renal calices.
DOUBLE COLLECTING SYSTEM
● Renal units containing 2 pyelocalyceal Vesico-ureteral Reflux Grading
systems
● Two ureters empty separately into the CONGENITAL ANOMALIES OF THE URINARY
bladder or fuse to form a single ureteral BLADDER
orifice ● Develops from the urogenital sinus and the
Associated with congenital genitourinary tract surrounding splanchnic mesenchyme
abnormalities ● The urogenital sinus is comprised of 3
regions:
COMPLETE DUPLICATION OF URETER a. The cranial or vesical region which will form the
- second ureteral bud bladder and which is attached to the allantois.
arising from b. The middle or pelvic region.
mesonephric duct c. and the caudal or phallic region.
- ureters develop from
separate ureteric buds ANOMALIES IN NUMBER
originating from a single wolffian duct A. Agenesis
- Rare
ANOMALIES IN POSITION AND FORM - No bladder is present
Ureterocele: - Urethra and penis are absent in male
A sacculation of the bladder end of the ureter that can - Generally stillborn but all surviving infants are
occur either in the bladder or ectopically. female
Girls > boys. - Complaint: persistent incontinence
Bilateral in 10%
Asymptomatic or cause obstruction/ incontinence/ Agenesis of the bladder in a 5-day-old girl with wetting.
infection. Image from bilateral ureterography performed with
catheters placed in ectopic ureteral orifices shows
Simple ureterocele. (a) IVU image shows the typical dilated and tortuous ureters (u) with dilatation of the
cobra head appearance at the end of both ureters renal pelves and calices. Intrarenal reflux is also noted.
(arrowheads). ★ = bladder. (b) IVU image shows the IVU showed poorly functioning hydronephrotic kidneys.
contrast material-filled bladder (★) with a negative
B. DUPLICATION
filling defect (arrowheads) that represents a a. Complete Duplication
ureterocele. (c) Transverse US image of the bladder ● Involves 2 completely separate bladder, each
(B) demonstrates a sonolucent cystic structure with an with its own wall of muscle and mucosa
echogenic wall (U) that projects into the bladder, a separated by peritoneal fold
finding that represents a simple ureterocele ● Right and left kidney drain into left and right
bladder via single ureter
URETEROPELVIC JUNCTION (UPJ) OBSTRUCTION ● 2 urethras are present
● Cause: Intrinsic narrowing of the junction of ● Male: 2 penises or one penis with 2 urethras;
the renal pelvis and ureter scrotum is bifid
● Result of a patent but aperistaltic segment at ● Female: 2 urethra, 2 vagina, 2 uterus with
the UPJ one horn and FT
● Abnormal recanalization of the ureter during b. Incomplete Duplication
embryologic development is the favored ● Septum partially divides the bladder

  -­‐  3  -­‐
 ● Partial horizontal septa à hourglass ● pyelectasis, caliectasis, ureterectasis,
appearance of bladder hydroureter

Mutiple Septa or Multiseptate Bladder NON-OBSTRUCTIVE HYDRONEPHROSIS

Fibromuscular septa divide bladder into 4 unequal
● diabetes insipidus - large volume of
parts
Only one segment opens into urethra; other segments hypotonic urine
and bladder segments are obstructed ● UTI - segmental or generalized dilatation,
Remaining kidney and entire opposite are with poor or reversed peristalsis
hydronephrotic and dysplastic ● intra-abdominal inflammatory disease
IV Urogram: one pole of one kidney draining into a tiny ● overhydration
deformed chamber

Complete duplication of the bladder and urethra in the OBSTRUCTIVE UROPATHY

coronal plane. (a) Lateral retrograde cystourethrogram ● tumors
through both separate urethral openings shows two ● calculi
bladders, one (a) anterior to the other (b). (b) ● strictures
Transverse US image also shows the two bladders (a, ● radiation therapy
b), one lying in front of the other and each with its own ● operative procedures
muscular wall.
● prostatic enlargement
ANOMALIES IN SIZE ● 3rd trimester pregnancy R>L
a. Hypoplasia
- Small/ tiny bladder and is usually seen in infants HYDRONEPHROSIS
with sacral agenesis Flattening of the normal concavity of the calyx and
b. Megacystis blunting of the sharp peripheral angle of the papilla
- Large bladder
- earliest urographic change in
- Common cause in congenital bladder outlet
obstruction/ areflexia secondary to spinal dysraphism hydronephrosis
Congenital Megacystis (Vesical Gigantism) Later changes:
- Congenitally huge unobstructed bladder § Pelvis enlarges gradually with increasing and
- Large residual volume following voiding prolonged obstruction
§ Next calyceal change is “clubbing” in which
BLADDER DIVERTICULUM the concavity produced by the papillae is
● Localized bladder wall weakness leads to
reversed
bulging of all wall layers
● Sites: hiatus uretericus, bladder lateral wall, Calyces gradually enlarge with progressive destruction
area of torus interuretericus of the parenchyma and enlargement of the collecting
● Diverticula - >2cm on post void film system of the kidney until it becomes a non-functoning
● Saccules - <2cm hydronephrotic sac
- Both are hernias of the bladder through detrussor
muscle RENAL CALCULI
- Diverticula usually in male
- Bladder base; usually in the region of ureteral hiatus originate as Randall’s plaques deep in the lining of the
(Hutch’s diverticula) collecting ducts of the renal papillae
urinary stasis and infection are factors promoting
Bladder diverticula: VCUG is the best imaging modality. formation of calculi
Bladder ultrasonography may also be used to detect opacity overlying the urinary tract
bladder diverticula but does not provide the same excretory urography - for calculi localization and
anatomic definition as the VCUG. determine condition/function of calyceal system
ultrasound, CT may be necessary to find radiolucent
ANOMALIES IN FORM low-density calculi
● Bladder exstrophy: with renal or ureteral colic g delayed excretion by
• Absence of the anterior wall of the involved kidney
bladder, with ureters delivering dilatation of drainage structures
urine into the lower abdomen. CT stonogram using helical CT
• Square appearance of pelvis
• Requires surgical reconstruction. CHEMICAL COMPOSITION
HYDRONEPHROSIS ● calcium phosphate, calcium oxalate,
● “obstructive uropathy” magnesium ammonium phosphate (struvite)
● dilatation of the calyces and pelvis with ● diammonium calcium phosphate, magnesium
potential progressive destruction of renal phosphate
parenchyma ● cystine, urate and xanthine
PREDISPOSING FACTORS

  -­‐  4  -­‐
 ● matrix calculi - mucoprotein and ● wall is very thin
mucopolysaccharide; Proteus infection ● mass is quite radiolucent and sharply
● hyperparathyroidism - hypercalcemia demarcated from renal parenchyma
● osteolytic metastasis, leukemia, multiple ● beak-like deformity - “claw sign”
myeloma, sarcoidosis
● gout/ hyperuricemia; hyperoxaluria ACQUIRED RENAL CYSTIC DISEASE
● develops during dialysis treatment
RENAL TUBERCULOSIS ● large number of cysts, less than 3 cm
● Infection is hematogeneous ● cortical and medullary
● Early lesions are multiple involving the renal ● develop renal cell carcinoma in 7%
papillae ● complication: retroperitoneal hemorrhage
● As disease progresses, involvement of the
adjacent infundibula often leads to VON HIPPEL LINDAU DISEASE
obstruction ● autosomal dominant phakomatosis
● May lead to stricture formation if there is ● retinal angiomatosis, CNS
ureteral involvement hemangioblastomas, pheochromocytoma
● If destruction continues, irregular cavities are ● multiple simple renal cysts; one third have
found adjacent to the calyces which leads to renal cell carcinomas
virtual destruction of the entire kidney
● Demonstration of tubercle bacilli in the urine AUTOSOMAL RECESSIVE PKD
● Alteration in kidney size ● grossly elongated, dilated collecting ducts
● Calcification throughout the renal parenchyma
● Multiple ureteral stricture formation ● both kidneys symmetrically and uniformly
enlarged
ULTRASOUND FINDINGS OF ACUTE ● associated hepatic cysts
PYELONEPHRITIS
Normal AUTOSOMAL DOMINANT PKD
Renal enlargement ● spherical fluid-filled cysts, 1-3 cm in size
Compression of the renal throughout
sinus ● may have curvilinear wall or intrarenal
Abnormal echotexture punctate calcifications
Hypoechoic (edema) ● knobby appearance of kidney surface
Hyperechoic (hemorrhage) ● kidneys are greatly enlarged
Loss of corticomedullary ● associated hepatic cysts; also in the
differentiation pancreas, spleen, lungs and ovaries
Poorly marginated mass ● associated with 10% rupture of berry
Gas within the renal parenchyma aneurysm of the arteries at the base of the
Decreased blood flow in power brain

RENAL CYSTIC DISEASE CLASSIFICATION RENAL CARCINOMA

simple renal cyst ● hypernephroma, adenocarcinoma
renal cysts with multiple renal neoplasm ● men > women; 40-60 years
• acquired cystic kidney disease ● weight loss, flank pain, palpable mass,
• vonHipple-Lindau disease hematuria
• tuberous sclerosis ● metastasize to lungs, liver, lymph nodes,
polycystic kidney disease renal vein and inferior vena cava
• autosomal dominant ● kidneys enlarged, may be irregular
• autosomal recessive ● may have calcification - irregularly scattered
or curvilinear
cysts of the renal medulla ● renal displacement, tilting of axis
• medullary sponge kidney
• medullary cystic disease
RENAL CYST VERSUS CARCINOMA
multicystic kidney
Bosniak classification
cysts of the renal sinus
• Type 1 - simple renal cyst
miscellaneous cystic disease
• Type 2 - minimally complicated
cyst; increased attenuation values,
SIMPLE RENAL CYSTS
● lesion is peripheral, bulges out of the kidney thin calcifications, thin septation

  -­‐  5  -­‐
 •Type 3 - with thick septation or ● usually transitional cell; squamous cell and
chunky calcifications, uniform thick adenocarcinoma are rare
wall or non-enhancing nodules ● irregular filling defect, usually at the base,
• Type 4 - thick walls, enhancing resulting in ureteral obstruction
components and solid enhancing ● appearance vary depending on whether
nodules sessile or polypoid
BOSNIAK CLASSIFICATION ● MRI used in staging diagnosed bladder
• Type 1 = no chance of malignancy malignancy
• Type 2 = may have chance of
malignancy POSTERIOR URETHRAL VALVES
• Type 3 = 57% probability of ● causes obstruction leading to infection,
malignancy vesicoureteral reflux, hydronephrosis, and
• Type 4 = 100% malignant eventually renal damage
● almost exclusively in males, often in children
RENAL CELL CARCINOMA ● enuresis; bladder distension, dribbling, poor
● solid, with or without cystic component stream, failure to thrive
● tumor enhancement on contrast infusion ● in newborn - flank mass caused by urinary
● areas of necrosis or hemorrhage do not ascites, respiratory distress
enhance ● voiding cystourethrography
● perihilar lymphadenopathy, direct tumor ● thin membrane arising from the
invasion of adjacent organs veromontanum which partially obstructs the
urethra during voiding
WILM’S TUMOR
● nephroblastoma
● most common abdominal neoplasm in
infancy and childhood
● arise from embryonic renal tissue
● tends to become very large
● x-ray - large intrarenal tumor with distortion of
calyces and pelvis
● impaired renal function
● ultrasound - homogeneous echogenic renal
mass
● CT show no vessel encasement

NEUROBLASTOMA VERSUS WILM’S TUMOR

● present at birth
● contains calcification in 50% of cases
● less calyceal distortion, arising adjacent to
the kidney and displaces it
● vessel encasement and retrocrural
adenopathy are seen on CT

URINARY BLADDER
● smooth-walled, round or oval
● 5 to 10 mm above the symphysis pubis
● floor parallels the superior aspect of the pubic
rami
● dome is round in males, flat or slightly
concave in females
VESICAL CALCULI
● obstruction & infection are the chief causes
● half are radioopaque, visible in plain x-ray
● common in males
● usually midline, unless within a bladder
diverticulum

CARCINOMA OF THE URINARY BLADDER

  -­‐
 6
 -­‐
Male and Female Genito-urinary Tract
Prostate
• inner gland (transition zone -
periurethral)
• outer gland (central and peripheral
zone)
1. transition zone
o site of benign prostatic
hyperplasia
o can occlude urethra when
severe
2. peripheral and central zones
a. lie posterior and lateral to the
transition zone
b. primary tumor site in 70-80%
of cases
Modalities:
ultrasound and MRI
transrectal ultrasound - introduced in the 70’s by
Watanabe
Prostatic CA
Ø primarily hypoechoic
Ø most originate in the peripheral zone
Ø as tumors enlarged, histology become
more infiltrative
Ø transrectal ultrasound-guided biopsies
Ø very high prevalence
Ø affects up to 30% of patients who died
of other causes
Ø which of these patients have clinically
significant tumors?
Ø tumor volume predicts tumor behavior
Ø tumors 3cc or more - likely to have
extracapsular spread and aggressive
histology
Ø screening with prostate specific antigen
(PSA) & ultrasound
Scrotum
§ contains the testis, epididymis,
spermatic cord
§ testicle is covered by fibrous sheath -
tunica albuginea, and surrounded by
tunica vaginalis
§ epididymal head - superior to testis;
epididymal body and tail - posterior and
inferior to testis
§ blood supply to testicle from the
spermatic cord which contains the
testicular artery
§ imaging by ultrasound and nuclear
scintigraphy
§ high resolution, linear array ultrasound;
with Doppler imaging
Testicular Torsion
ü testicular pain in newborn or adolescent
male
ü twisting of spermatic cord causing
compromise of venous and arterial flow
ü diagnosis should be prompt, within 6
hours, to ensure testicular viability
ü nuclear scintigraphy, doppler ultrasound
ü Doppler ultrasound
o presence of arterial signal from
the central portion of the
testicle excludes torsion
o confirm normal flow in the
contralateral testis
Epididymitis
Ø associated with infection of other parts
of the GU tract
Ø ultrasound - enlarged, heterogeneous
appearing epididymis with increased
flow by Doppler
Ø orchitis usually present
Testicular Tumor
● painless scrotal mass - from the testicle
or elsewhere?
● common between 25 to 35 years
● seminoma, choriocarcinoma, embryonal
carcinoma, teratoma/ teratocarcinoma
● lymphoma, leukemia, metastasis
● varied appearance on ultrasound; does
not correlate with histology
● must do CT of retroperitoneum for
nodal spread
● ddx: testicular hematoma from trauma
Hydrocele
Ø fluid collection between the layers of
the tunica vaginalis
Ø often idiopathic
Ø may be secondary to trauma, infection
or tumor
Varicocele
● abnormal collection of dilated veins in
the spermatic cord
● due to abnormal venous valvular
mechanism or obstruction to blood
return
● 90% of idiopathic varicocele occur in
the left - due to more obtuse union of
left spermatic vein to the left renal vein
(right spermatic vein joins the IVC at
acute angle)
● ultrasound evaluation, with valsalva
maneuver and upright position
● may cause male infertility because of
increased scrotal temperature
● surgical repair
Spermatocele
• dilatation of efferent ductules
• usually in the head of epididymis
• generally symptomatic
• must be differentiated from varicocele
OB-GYNE RADIOLOGY
o anatomy of the gravid and nongravid
female pelvis
o no ionizing radiation
o assess thermal index and mechanical
index
o magnetic resonance imaging
First trimester
• 0-12th menstrual week
• fertilization occurs at day 14 or week 2
menstrual age
• gestational age = menstrual age
• earliest sonographic finding of an
intrauterine pregnancy = intradecidual
sign
• intradecidual sign - echogenic mass in a
subendometrial location; seen at 3.5 to 4
weeks
• gestational sac - can be identified at
4.5 weeks by endovaginal ultrasound;
well-defined, thick, echogenic rim;
surrounded by thick echogenic
endometrium
• gestational sac measures approximately
1 cm at 5.5 weeks
 • estimate of gestational age using mean
sac diameter (MSD)
• yolk sac - seen at 6 weeks; well-defined
echogenic ring
• absence of yolk sac by the time MSD is
8mm, consider failed pregnancy
• embryo - seen at 6.5 weeks ; lies
adjacent to the yolk sac; fetal cardiac
activity visible
• placenta should be easily visible by 9
weeks
Threatened Abortion
Ø vaginal bleeding in the first 20 weeks =
threatened abortion
Ø may be associated with mild cramping
Ø closed cervical os
Ø occurs in 25% of clinically apparent
pregnancies
Ø about 50% subsequently abort
Blighted Ovum
● early pregnancy failure
● crown-rump length (CRL) of > 5mm
but with no cardiac activity
● GS > 16mm but with no embryo
● GS > 8mm but with no yolk saac
● rescan pregnancy after 1 week
Ectopic pregnancy
ü abdominal pain and vaginal bleeding
ü endovaginal and transabdominal
scanning
ü transabdominal scanning - locate large
mass or free fluid
ü pathognomonic finding = identification
of an extrauterine gestational sac that
contains a live embryo (seen in 30% of
cases)
ü other findings - empty uterus, decidual
cyst, adnexal mass, particulate fluid in
cul de sac, pseudogestational sac in the
endometrial cavity
ü decidual cyst - 2- to 5-mm cyst near
endomyometrial junction
ü tubal ring = echogenic ring of early
gestational sac with positive pregnancy
test and empty uterus; seen in 50% of
ectopic pregnancy
ü adnexal mass - complex or echogenic
solid in appearance
ü echogenic fluid in the posterior cul-de-
sac
ü quantitative serum ß-hCG determination
- lower than normal pregnancy and
plateaus rather than rise with time
Estimating Gestational Age
● gestational sac
● crown rump length
● biparietal diameter
● head circumference
● abdominal circumference
● femur length
Fetal death
● absent fetal cardiac activity
● absent extremity motion
● fetal stimulation - ballottement of
anterior abdominal wall
● within days of fetal death, fetal skin
become edematous and alterations in
the fetal anatomy
PLACENTA
Ø thickening in the decidual reaction
identified by 7 to 8 weeks
Ø placenta clearly defined by end of 1st
trimester
Ø smoothly marginated structure with
homogeneous fine echopattern
Ø later, the fetal surface develops
undulations and the internal echopattern
become heterogeneous
Ø calcium deposition in the basal plate,
increasing after 29 weeks
Placenta Previa
● most common cause of vaginal bleeding
in 2nd and 3rd trimester
● relationship of placenta to internal
cervical os identified through a
distended maternal urinary bladder
● “placental migration” - represents
differential growth rate of the lower
uterine segment
Abruptio placenta
● painful vaginal bleeding
● retroplacental lucency representing
blood clot between the placenta and
myometrium
UTERUS
● elongated, pear-shaped, hollow,
muscular organ
● usually midline and anteverted
● myometrium - homogeneous
echopattern, with a linear central bright
echo representing the endometrial
cavity
CERVIX
● contiguous with the vagina
● vagina - midline bright linear echo
representing the collapsed vaginal canal
OVARIES
● lateral to the uterus
● increasing volume during puberty;
decreasing volume after menopause
● average volume = 24 cc; longest
dimension can reach 5 cm
● small cystic structures represent
developing follicles
LEIOMYOMA
§ uterine fibroid
§ most common benign neoplasm of the
uterus
§ commonly asymptomatic
§ may be multiple
§ uterine fibroid
§ most common benign neoplasm of the
uterus
§ commonly asymptomatic
§ may be multiple
§ may contain “popcorn” configuration
calcification
§ US = well-defined hypoechoic,
isoechoic or hyperechoic mass
§ with thin hypoechoic border or
pseudocapsule
§ degree of deformity of uterine contour
depends on location and size
§ subserosal leiomyomas may be
pedunculated; exophytic
§ intramural leiomyomas are more
common
§ influenced by estrogen; tend to grow
during pregnancy

ADENOMYOSIS
ü deposits of endometrial glands within
the myometrium
ü pain, uterine tenderness, menorrhagia,
metrorrhagia, intermenstrual bleeding
ü can be focal or diffuse
ü US - mixed echogenicity with no well-
defined margins
ü cysts within the myometrium are almost
exclusively a feature of adenomyosis
ü cysts are dilated, fluid-fileld
endometrial glands that become
noticeable during the secretory phase of
the cycle
ENDOMETRIAL CARCINOMA
• most common malignant neoplasm of
the uterine body
• abnormal postmenopausal bleeding
• diagnosed by direct examination of
endometrial tissue obtained by
endometrial biopsy
• US
o enlarged uterus with distorted
endometrial echoes
o inhomogeneous, hypoechoic
myometrium
o hypoechoic ring surrounded by
a widened endometrial cavity
o widened fluid-filled
endometrial cavity due to
hematometra
• increased serum ß-hCG level
• clinical hallmark = vaginal bleeding in
1st trimester or early 2nd trimester
• uterus may be appropriate, large or
small for dates
• may exhibit symptoms of hyperemesis
gravidarum or pre-eclamptic toxemia
• complete or classic h. mole - no fetal
tissue or amniotic membranes; 46,XX
genotype
• partial h. mole - contain fetal tissue or
amniotic membranes; polyploidy
genotype
• US
o echogenic solid appearing
mass that completely fills the
endometrial cavity
o small vesicles in the 1st
trimester, becoming more
complex and may reach 2 cm
o larger hypoechoic areas
represent hemorrhage

CERVICAL CARCINOMA
v second most common uterine neoplasm
v diagnosed by direct observation of the
cervix and sampling of the cervical
epithelium
v imaging of the pelvis is helpful in
staging of cervical ca

OVARIAN MASSES
Ø ultrasound as a screening examination
o palpable mass
o unexplained pelvic pain
o endocrine disorders
Ø cystic masses - fluid-filled, no internal
echoes, have smooth walls, with
posterior enhancement
Ø complex masses - exhibit cystic and
solid characteristics
Ø solid masses - varying degrees of
internal echoes in homogeneous or
heterogeneous pattern
Ø cystic masses are generally benign
Ø solid tissue, heterogeneous appearance,
thick irregular septa increases the
probability of malignancy
Ø cysts with papillary projections =
papillary cystadenocarcinoma
Ø ascites - more common in malignant

GESTATIONAL TROPHOBLASTIC
DISEASE
• complete or classic hydatidiform mole
• partial hydatidiform mole
• hydatidiform mole with coexistent live
fetus
• invasive mole
• metastatic gestational trophoblastic
disease (choriocarcinoma)