Woman with left upper quadrant

pain and emesis

An OctreoScan
 Findings: CT shows 15mm soft tissue
mass within small bowel in the left
midabdomen and a 10 mm mesenteric
node in the right midabdomen.
OctreoScan shows 2 small infrarenal foci
of increased radiotracer uptake in the
midabdomen. The more superior of these
foci is along the midline, just inferior to the
level of the caudal tip of the liver. This
correlates with the retroperitoneal
mesenteric node seen on CT. The second
focus is just inferior to this and slightly to
the left of midline and correlates with the
small bowel mass.
 Differential diagnosis:
Small bowel lymphoma
Small bowel polyp/leiomyoma
Small bowel adenocarcinoma
Kaposi's sarcoma
Carcinoid
Diagnosis: Carcinoid of small bowel.
 Carcinoid tumors are the most common
primary tumors of the small bowel and
appendix and are often malignant
(although low grade) in these locations.
Approximately 80% of tumors greater than
2 cm show local invasion or have
metastasized to the liver
 About 1/3 of patients are symptomatic at
the time of presentation. Symptoms
include abdominal pain, nausea, vomiting
(often due to small bowel obstruction),
weight loss, GI bleeding and a palpable
mass. Less than 10% present with
carcinoid syndrome (diarrhea,
bronchospasm/wheezing, hypotension,
facial flushing
 right sided endocardial fibroelastosis
resulting in tricuspid regurgitation,
pulmonary valve stenosis and right sided
heart failure) secondary to excess
serotonin levels when the metabolic
pathway of 5-HIAA is bypassed (as occurs
in liver metastases or primary pulmonary
carcinoid). Carcinoid syndrome has a
much higher morbidity and mortality than
does the tumor itself.
 Upper GI: smooth submucosal mass;
angulation and kinking of loops of bowel
leading to obstruction (secondary to
desmoplastic response of mesentery).
CT: submucosal vascular lesion; focal
calcified mass surrounded by thick
mesentery; hyper vascular liver mets; low
density LAD.
Nucs: Indium-111 OctreoScan
(somatostatin analogue) or I-123 MIBG will
often be taken up by carcinoid.
 Rule of 1/3s:
1/3 occur in small bowel.
1/3 have mets.
1/3 are multiple.
1/3 have a second malignancy.
Larger tumors are more likely to have
mets (>80% in tumors over 2cm).
Less than 10% will have carcinoid
syndrome (often in pts w/ liver mets or
pulmonary carcinoid).
 The syndrome is secondary to excess
serotonin.
The syndrome causes more morbidity and
mortality than the tumor itself
Male teenager with pain.
 Plain film radiographs of the right knee
reveal a lucent expansile lesion in the
proximal right tibial metaphysis,
eccentrically, with a sclerotic rim and
narrow zone of transition.
Axial CT images from an outside hospital
reveal similar findings. A nondisplaced
proximal tibial fracture is identified near
the posterolateral margin of the lucent
lesion
 MR reveals a 4 cm circumscribed,
eccentric, minimally expansile lesion with
scalloped contours. Lesion is of
decreased signal intensity on both proton
density and inversion recovery
sequences. The nondisplaced proximal
tibial fracture is again identified, with
adjacent bone marrow edema in the
proximal tibia. Post contrast imaging
reveals little enhancement. Adjacent soft
tissues are minimally edematous.
 Differential diagnosis:
Brodie's abscess
Giant cell tumor
Langerhans cell histiocytosis
Osteosarcoma
Fibroxanthoma
Diagnosis: Fibroxanthoma with
pathologic fracture.
 Fibroxanthomas are eccentric
intramedullary lesions extending to the
cortex with a classic superficial scalloping
contour, never abutting the physis.
Histologically they are benign, and contain
spindle shaped fibroblasts oriented in a
cartwheel pattern with scattered giant
cells, foam cells, and collagen
 By definition, these lesions measure
greater than 3 cm. When less than 3 cm,
the lesion is called a fibrous cortical defect
(FCD). Although histologically identical,
FCD lesions are more likely to remain
asymptomatic and resolve spontaneously.
Most commonly occurs between age 10
15, age range 3 20.
Male to female ratio 2
 90 % involve long tubular bones.
Common sites include the distal femur
(38%) and proximal or distal tibial
metaphysis (43%).
Multiple fibroxanthomas / FCD lesions with
caf au lait spots are suggestive of a rare
disorder called Jaffe-Campanacci
syndrome
 Closed reduction is usually sufficient for
pathologic fracture management, as
callous will partially replace the lesion and
provide stability. Curettage with bone graft
provides better prophylaxis against future
fracture.
Pain abdomen
 Findings: There are multiple
homogeneous hypo dense hepatic
masses affecting every segment of the
liver. These range in size from sub
centimeter, to over 3 cm in diameter. For
the most part the masses are
nonenhancing, however some are mildly
enhancing in venous and delayed phase.
Attenuation and enhancement pattern are
uniform. There is no enhancing capsule.
 Differential diagnosis:
Metastases
Multifocal hepatocellular carcinoma
Multiple focal nodular hyperplasia (FNH)
Hepatic adenomatosis
Multiple hepatic abscesses
Multiple hemangiomas
Diagnosis: Hepatic adenomatosis, a rare
condition associated with multiple hepatic
adenomas.
 Hepatic adenomas are uncommon but
benign tumors of the liver which contain
functioning hepatocytes. Histologically, the
adenomas consist of sheets of well-
differentiated hepatocytes. These differ
from normal hepatic architecture, in which
hepatocytes are organized in lobules in a
spoke wheel pattern, centering on the
portal venule
 The hepatocytes contain fat and glycogen
and can produce bile; however, no bile
ducts are present. Most hepatic adenomas
do not contain Kupffer cells. Focal nodular
hyperplasia, by contrast, does contain
functioning Kupffer cells
 As a result, two additional imaging studies
become useful for differentiating the
entities. Sulfur colloid scintigraphy of the
liver will demonstrate photopenic defects
in the areas of hepatic adenomas, where
as focal nodular hyperplasia will be
relatively homogeneous.
 In addition, the MRI contrast agent
gadolinium Dimeglumine (MultiHance) is
secreted by hepatocytes as bile.
Therefore, since hepatic adenomas
contain functioning hepatocytes but not
bile ducts, there will be delayed
enhancement due to MultiHance secretion
and retention. This phenomenon can also
be demonstrated on HIDA scanning, in
which hepatic adenomas will fill in with
radiotracer, but FNH will be photopenic.
 Hepatic adenomas are usually found in
young woman who are taking oral
contraceptives, man receiving anabolic
steroids, or patients with Type 1a glycogen
storage disease (von Gierke's disease).
Adenomas have also been associated with
hereditary hemochromatosis. Hepatic
adenomas are solitary and most cases.
However, sporadic instances of 2 to 3
adenomas have been reported
 Hepatic adenomatosis, defined as the
presence of multiple (arbitrarily, greater
than 10) adenomas, is a rare disorder. As
with solitary hepatic adenomas,
spontaneous hemorrhage or malignant
transformation is a concern. In one series
of 15 patients with hepatic adenomatosis,
there were 2 cases of hepatocellular
cancer, and one death from widespread
malignant disease. In these cases,
management remains controversial,
however liver transplantation is becoming
more common
 Findings: Diffusely thickened and
irregular distal stomach extending to the
pylorus and duodenal cap; decreased
distensibility and motility of gastric
emptying. CT confirms tumor emanating
from the greater curvature of the stomach
at the gastric antrum with evidence of
peritoneal carcinomatosis and metastatic
disease of the regional nodes, as well as
periaortic and portocaval regions.
 Differential diagnosis for fold
thickening:
Gastric carcinoma
Gastritis
Gastric varices
Gastric ulcer
Eosinophilic gastritis
Diagnosis: Gastric carcinoma
 Gastric carcinoma:
Middle aged men
Symptoms: weight loss, anorexia, pain
Risk factors: H. pylori, atrophic gastritis,
pernicious anemia, foods high in
nitrates/nitrites, or poorly preserved foods
 Imaging appearance:
CT: Gastric wall mass or nodular thickening +
lymphadenopathy and omental metastases
Double contrast barium upper GI: Polypoid mass
lesion, sometimes with ulceration, infiltrative type is
5-15%; may cause gastric outlet obstruction
 Differential diagnoses include gastric
metastases (breast cancer is the most
common, although melanoma, colon, lung are
possible), lymphoma (non-Hodgkin's B cell
type), Mntrier's disease (usually spares the
antrum)
Boards pearls: Look for metastases in the left
supraclavicular region ("Virchow's node"),
rectal shelf, or to the ovary ("Krukenberg"
tumor)
 The fluoroscopic findings are classic for
linitis plastica, which literally means limited
distensibility. Linitis plastica is seen most
commonly in gastric carcinoma, gastric
metastases and lymphomatous infiltration
either from primary gastric lymphoma (less
common) or lymphoma metastases (more
common). Linitis plastica is less commonly
seen with gastritis, caustic gastric injury, or
peritoneal metastases
right-sided hip pain after tripping
and falling on the sidewalk
 Findings: There is no evidence of
fracture, dislocation or acute osseous
abnormality. There is demonstration of
shallow acetabulum and deformity
bilaterally in the hips as well as bilateral
subluxation, right greater than left, without
evidence of displacement.

Diagnosis: Hip dysplasia.

 The Center-Edge angle of Wiberg: After
four years of age, the capital femoral
epiphysis has typically achieved full
ossification, making the diagnosis of gross
hip displacement less difficult. More
subtle displacements or subluxations can
be evaluated by the Center-Edge angle of
Wiberg, which is a parameter of the
relationship of the femoral head to the
acetabulum
 It is obtained by first drawing a baseline
connecting the two centers of the femoral
heads. The Center-Edge angle itself is
formed by two lines originating from the
center of the femoral head. One is drawn
perpendicular to the baseline straight up
into the acetabulum. The other connects
the center of the femoral head with the lip
of the superior acetabulum. In a patient
this age, a Center-Edge angle below 25
degrees can indicate the presence of hip
dysplasia. In this patient the Center-Edge
angles on both sides are below this level
 Developmental dysplasia of the hip (DDH),
also known as congenital dislocation of the
hip, occurs in approximately 1 in 1000
births and affects girls more often than
boys. The etiology is unclear but is most
likely multifactorial, with genetic
predisposition and intrauterine positioning
playing likely roles. It is typically found
during the examination of the newborn and
treated with a Pavlik harness.
 A history of prior developmental dysplasia
of the hip often results in several
abnormalities. One is the aforementioned
decreased C-E angle of Wiberg. Other
characteristics typically include a shallow
acetabulum and decreased lateral and
anterior coverage of the femoral head by
the acetabulum
Teenager with pain
 Findings: Nuclear medicine three phase
bone scan demonstrates increased blood
pool activity of radiotracer in the bilateral
pedicles at L3-L4 consistent with an acute
stress reaction. SPECT imaging confirms
this finding. Noncontrast CT images of the
lumbar spine in bone windows
demonstrate linear lucency or defect
extending through the pars interarticularis
bilaterally at L3 without spondylolisthesis.
Diagnosis: Bilateral L3 pars defects
 Increased blood pool activity on three
phase bone scans is indicative of
nonspecific stress reaction, and can be
seen in the presence of stress
injuries/fractures, reactive bone turnover in
osteomyelitis, primary and secondary
bone tumors/metastatic disease, and
postoperatively. However, the CT findings
in this case or classic for bilateral pars
interarticularis defects.
 Spondylolysis is believed to be caused by
repeated microtrauma, resulting in stress
fracture of the pars interarticularis.
Heredity also is believed to be a factor.
Patients with spina bifida occulta have an
increased risk for spondylolysis.
Approximately 95% of cases of
spondylolysis occur at the L5 level. Lyses
can occur much less commonly at other
lumbar or the thoracic levels. Involvement
of multiple levels is rare. The process may
be unilateral or bilateral
 Approximately 3-7% of the general
population (14 million people) have
spondylolysis. In certain athletes, the
incidence increases to 23-62%.
Spondylolysis is 2-4 times more common
in men than in women.
Woman with cranial nerve
abnormality.
 The head CT (bone windows)
demonstrates a region of bony destruction
extending from the right petro-occipital
fissure into the carotid canal. The axial T2
images demonstrate a hyper intense,
extra-axial, right petrous apex mass that
extends from the petro-occipital fissure to
the cavernous sinus. The margins of the
mass are lobulated, and it encases the
cavernous internal carotid artery. The axial
T1 contrast-enhanced images
demonstrate intense enhancement of the
mass.
 differential diagnosis for a bony lesion
in the region of the petrous apex:
Metastatic tumor
Chondrosarcoma
Plasmacytoma
Nasopharyngeal cancer
Chordoma
Cholesteatoma
Calcified meningioma
Chondromyxoid fibroma
 Diagnosis: Petrous apex
chondrosarcoma
 Classic MR imaging appearance of
petrous apex chondrosarcoma is a mass
located at the petro-occipital fissure with
high T2 signal intensity that
heterogeneously enhances.
The CT shows chondroid mineralization in
50%.
Invasive bone changes at the petro-
occipital fissure strongly favors the
diagnosis. Greater than 50% will have
associated bone destruction
 2/3 located at the petro-occipital fissure,
1/3 located at the anterior basis sphenoid
Usually has lobulated margins
High T2 signal, low to intermediate T1
signal
Heterogeneous enhancement with
contrast; whorls of enhancement within
tumor matrix are often seen
 Often displaces or encases the ICA
Classic presentation is a CN 6 nerve
palsy. Other CN palsies can occur less
commonly (3, 5, 7, 83, 4, and 6 are
possible with cavernous sinus invasion
 Distinguishing characteristics from other
entities in the differential:
Chondromyxoid fibroma - Similar MR
appearance to chondrosarcoma; areas of
ground glass density can be seen on CT
Chordoma - Similar appearance to
chondrosarcoma but often see tumor "thumb"
indenting the anterior pons; often midline
 Calcified meningioma Not typically
destructive; low to intermediate T2 signal
Plasmacytoma - Usually intermediate T1 and
T2 signal; usually more midline
Cholesteatoma - Does not enhance but has
an otherwise similar appearance
Metastatic tumor Can have a similar
appearance; breast cancer and prostate
cancer are two of the most common tumors to
metastasize to the petrous apex
newborn
 Findings: On the ultrasound, there is a
round mass within the right lobe of the
liver. The mass has heterogeneous
echogenicity, and demonstrates flow on
color-Doppler imaging. In particular, neo-
vascularity is noted about the periphery of
the tumor. On the CT, there is a round
mass occupying the majority of the right
lobe of the liver. This mass is
predominantly hypo-attenuating to the liver
on arterial, portal venous, and delayed
imaging. There is heterogeneous
enhancement within the mass. A few non-
enhancing areas are noted.
 Differential diagnosis for neonatal
hepatic masses:
Hepatoblastoma
Hemangioendothelioma
Mesenchymal hamartoma
Embryonal sarcoma of the liver
Hemangioma
Diagnosis: Hepatoblastoma
 Hepatoblastoma has an incidence of
approximately 1 case per million, per year
in children in western countries.
Hepatoblastoma is the most common
primary hepatic malignancy in childhood.
On ultrasound, hepatoblastoma often has
heterogeneous echogenicity, with areas
both hyper echoic and hypo echoic to the
normal hepatic parenchyma
 On color-Doppler ultrasound,
neovascularity may be detected at the
periphery of the tumor.
On non-contrast CT, hepatoblastoma is
typically hypo-attenuating to the normal
hepatic parenchyma. Depending on the
sub-type, it may be homogeneous or
heterogeneous in appearance.
Calcifications may be present
 Typically, the tumor enhances less than
the hepatic parenchyma on all phases.
The serum alpha-fetoprotein is often
markedly elevated in hepatoblastoma.
This is useful in the clinical determination
between hepatoblastoma and
hemangioendothelioma. It may also be
useful as a marker for response to therapy
and disease progression.
Complete surgical resection is required for
cure. Adjuvant chemotherapy may convert
a non-resectable tumor into a resectable
lesion.
Patient with left eye pain and
decreased vision
 Findings: Gyriform calcifications are
observed over the left occipital lobe in the
CT exam. The MRI demonstrates atrophy
of the left cerebral hemisphere. There is
enlargement of the left choroid plexus
which demonstrates homogeneous
enhancement post contrast. There is also
gyriform enhancement post contrast most
significantly on the left occipital lobe.
There is diffuse enhancement of the
subcutaneous tissues over the left eye
 Skin discoloration over the left eye since
birth

Diagnosis: Sturge-Weber syndrome

 Classically the patients have a facial port-
wine stain, ipsilateral intracranial
abnormalities, contralateral hemiparesis,
hemiatrophy, mental retardation, and
homonymous hemianopia. The severity of
these features varies widely patient to
patient. Commonly the patients will have
glaucoma on the affected side. Seizures
are also very common.
 Only 8% of patients with port-wine stains
have Sturge-Weber Syndrome. 13% of
Sturge-Weber syndrome patients do not
have a facial angioma.
There is no clear genetic link at this time.
There is no sex or race predilection and it
is very seldom seen more than once in the
same family. Several different
chromosomal abnormalities have been
implicated
 Radiographically one can see "tram track
calcifications" which are leptomeningeal
calcifications like those seen on the CT
image.
MRI can demonstrate the angiomatous
abnormalities. In this case the cutaneous
capillary angioma (port-wine stain) is well
demonstrated as is the meningeal
angiomatosis over the left occipital lobe.
Cerebral hemiatrophy is well
demonstrated by MRI as is the choroidal
angiomatosis.
 Multiple therapies are employed in these
patients. The port-wine stains can be
"removed" with laser treatments. Seizures
can be treated with anticonvulsants.
Refractory seizures can be treated
surgically. The surgeries can be as
extensive as a hemispherectomy.
Man with increased bilirubin.
 Findings: CT shows hyperdense portal
vein and splenic vein on NONcontrasted
imaging compatible with thrombus clot. US
shows confirmatory evidence of occlusive
clot within portal vein with possible portal
venous collaterization/cavernous
transformation
 Differential diagnosis:
Essentially none. Potentially could
represent malignant thrombus versus
bland thrombus
General differential diagnosis for PV
thrombus:
Streaming artifact/"pseudo thrombus"
Extrinsic compression by enlarged lymph
nodes, primary tumor, hematoma, etc.
Budd-Chiari syndrome
Diagnosis: Portal vein/splenic vein
thrombosis
 Hyper dense thrombus reflects recent clot
formation (<1 month)
In contrast to bland thrombus, malignant
thrombus tends to distend vein + exhibit
pulsatile flow
May demonstrate compensatory
decreased resistive index/elevated
velocities in hepatic arteries
Can develop collateralization/cavernous
transformation
 Distension of portal vein more likely in
acute thrombus.
Etiology: Most often associated with
chronic pancreatitis, cirrhosis. Other
causes include malignancy, trauma, and
hypercoagulable states (e.g.: pregnancy).
Seeding of portal vein with infected
material may be inciting event (acute
appendicitis/diverticulitis/inflammatory
bowel disease).
Head ache
 Findings: Lateral ventricles and third
ventricle are dilated. A mildly
heterogeneous low density mass involves
the dorsal aspect of the midbrain near the
anticipated position of the pineal gland and
cerebral aqueduct
 MR confirms a mass in the region of the
cerebral aqueduct extending into the
fourth ventricle inferiorly and superiorly
into the region of the posterior third
ventricle. Closely following CSF, the mass
demonstrates decreased T1 signal and
increased T2 signal. There is restricted
diffusion. There is no associated abnormal
enhancement on the C+ sagittal images
 Intracranial epidermoid represents up to
1.8% of all primary intracranial tumors.
They are the most common congenital
intracranial tumor. They represent the third
most common CPA/IAC mass after
schwannoma and meningioma.
 They most commonly present with
headaches and possibly with cranial nerve
palsies, typically of the 5th, 7th, and 8th
nerves. They may remain clinically silent
for many years. There is no gender
predilection. Their presentation peaks at
age 40 and has a range of 20 60 years
of age.
 As the have epithelia components they
grow slowly. They can cause chemical
meningitis if they leak and rarely have
been reported to undergo malignant
transformation to squamous cell
carcinoma
 Epidermoid typically follow CSF density
and may encase surrounding structures.
Most commonly they are found in the CP
angle (40-50%). They can also commonly
be found in the fourth ventricle and middle
cranial fossa, typically para-sellar.
Occasionally they can be found within the
skull and spine
 CT findings: Most are hypo dense,
although 10-25% will have calcifications.
They typically do not show post contrast
enhancement however may have minimal
enhancement at the margin. There is a
rare variant which may be dense
secondary to hemorrhage or high protein
 MRI findings: Again they are similar to
CSF on T1 and T2 pulse sequences. On
T1 they are slightly hyper intense to CSF
and on T2 they are isointense to slightly
hyper intense to CSF. Intensity will be
altered depending on the cyst contents.
Minimal enhancement can be seen at the
margins. They key distinguishing feature is
the appearance on diffusion weighted
images which is markedly intense, "light
bulb bright". On ADC mapping they are
isointense to brain parenchyma
 The differential diagnosis includes
arachnoid cyst, which follow CSF signal on
all sequences and does not show
restricted diffusion. Arachnoid cysts
typically displace adjacent structures
whereas epidermoid lesions encase them.
Cystic neoplasm's often enhance and do
not follow CSF signal. Dermoid cysts are
typically heterogeneous on MR and more
closely follow fat signal characteristics.
Additionally dermoid are typically midline.
Inflammatory cysts typically enhance and
have surrounding edema and/or gliosis
2 months old,jaundice
 Findings: Ultrasound shows a
homogenous liver with no focal
parenchymal abnormalities; normal caliber
of intrahepatic biliary ducts; lack of
gallbladder visualization. HIDA scan
shows preserved hepatic uptake and
radiotracer extraction from blood pool, with
no small bowel radiotracer activity at 4
hour and 24 hour delayed imaging. Again,
no gallbladder visualization.
 Differential diagnosis:
Biliary atresia
Neonatal hepatitis
Choledochal malformation
Stone disease
Alagille syndrome
Bile plug
Diagnosis: Biliary atresia
 Biliary atresia:
Background:
Due to absent or severely deficient
extrahepatic biliary tree.
Affects 1 in 10,000-13,000 newborn infants.
10-25% have coexisting congenital
anomalies.
Prompt diagnosis is crucial to surgical
success.
 Classification:
Type I: Common bile duct atresia, proximal ducts
are patent.
Type II: Common hepatic duct atresia.
Type III: (>90% cases) Right and left hepatic duct
atresia
 Nuclear Medicine hepatobiliary scan.
Tc-99m diosgenin (DISIDA) and mebrofenin
(BRIDA) have highest hepatic extraction rate and
shortest transit time of hepatobiliary radiotracers.
Pretreatment with oral Phenobarbital for 5 days
improves accuracy by inducing hepatic micro
enzymes and biliary extraction.
Lack of radiotracer excretion into the intestines at
24 hour imaging.
Initially hepatocyte function and extraction of
radiotracer from blood pool is preserved the first 2-
3 months, but decreases as symptoms prolong.
Excretion of radiotracer into intestines excludes
biliary atresia.
 Echogenic triangular cord sign: focal
area of increased echogenicity in the
region of the porta hepatis (usually
anterior and slightly caudal to the
hepatic artery and portal vein); it
forms secondary to luminal
obstruction of the extrahepatic bile
duct with a fibrous ductal remnant.
Normal liver echotexture, but may be
enlarged.
25% of time gallbladder is visualized;
it may have an irregular shape and
wall thickness.
 Gallbladder ghost triad:
Gallbladder < 19 mm in length.
Irregular wall.
Indistinct mucosal lining.
Common bile duct never visualized.
Can obtain biopsy at same time; pathology shows
absent extrahepatic ducts and cirrhosis if diagnosis
delayed.
 Color Doppler.
Search for associated anomalies: preduodenal
portal vein, transverse liver (showing continuity of
portal veins in leftward hepatic tissue), interrupted
inferior vena cava, and cardiac anomalies
 CT (seldom used when biliary atresia
suspected):
Variable liver density.
No dilated biliary ducts.
Useful in excluding obstructive causes of jaundice:
choledochal malformation, stone disease, masses,
dilated biliary tree.
 Differential:
Neonatal hepatitis.
Self limited medical disease often confused with
biliary atresia.
Will see extraction of radiotracer into intestinal tract
on HIDA imaging.
Causes: Hep A, Hep B, CMV, Rubella,
Toxoplasmosis, alpha-1-antitrypsin deficiency,
familial recurrent cholestasis, other metabolic
disorders
 Bile plug syndrome.
Causes: cystic fibrosis, dehydration, sepsis,
hemolytic disorders, total parenteral nutrition.
Biliary hypoplasia or Alagille syndrome.
Paucity of intrahepatic ducts and arteriohepatic
dysplasia.
Choledochal malformation.
Five subtypes of localized dilation of extrahepatic
biliary tree
 Treatment:
Surgical: Kasai portoenterostomy (intestinal
loop is anastomosed to dissected surface of
porta hepatic).
Young man in motor vehicle
accident
 Findings: Markedly narrowed of the
celiac artery origin with poststenotic
dilatation and upward hooking of the
celiac artery. No hematoma or wall
irregularity.
 Differential diagnosis:
Traumatic celiac artery transection
Compression by median arcuate ligament
Fibromuscular dysplasia
Atherosclerosis
Diagnosis: Compression of celiac axis by
median arcuate ligament
 The median arcuate ligament is a band of
connective tissue connecting the right and
left crura of the diaphragm at the anterior
aspect of the diaphragmatic hiatus. This
band can in a small percentage of people
be positioned/shaped so as to compress
the celiac artery from its superior aspect,
typically best seen during end inspiration.
 Patients can experience symptoms of
ischemia as a result of this compression,
including postprandial or end-inspiratory
abdominal pain, vomiting, gastric
dysrhythmias and weight loss. Treatment
of the variant, if symptoms warrant,
include excision of the ligament, bypass
surgery, or ganglion blockage. The entity
is more common in thin women. Its
incidence is low, but ultimately unknown.
 Conventional or CT angiography will
demonstrate the entity of median arcuate
ligament syndrome as a focal narrowing of
the celiac artery at its origin, often with
poststenotic dilatation. There is a
characteristic upward hooking of the celiac
artery. The artery is most often narrowed
at its superior aspect, at the expected
location of the median arcuate ligament
 MRA may also demonstrate these
findings, and may also demonstrate the
actual ligament as intermediate to low
signal. Images should be obtained in end-
inspiration to better demonstrate
compression. Secondary radiographic
signs of celiac axis ischemia are not
commonly identified. Nuclear medicine
gastric emptying studies may demonstrate
delayed emptying.
Failure to pass meconium-
normal anus
 Findings:
KUB: Diffuse gas distention of bowel
loops throughout the abdomen; multiple
air/fluid levels. no definite rectal gas. No
free air. Bubbly lucencies in the right
lower quadrant represent stool rather than
pneumatosis.
Contrast enema: Left colon is small to
the level of the splenic flexure. normal
distention of the ascending and transverse
colon. multiple filling defects throughout
the colon
 Differential diagnosis:Classic
differential diagnosis of term neonate
with distal obstruction (provided the
child has an anus!)
Small left colon syndrome (meconium
plug)
Meconium ileus
Hirschsprung's
Ileal atresia
Diagnosis: Small left colon / meconium
plug syndrome.
 Dilated terminal ileum, multiple filling
defects: meconium ileus.
CF, can be complicated by perforation, intra-
abdominal calcifications.
Collapsed terminal ileum, dilated loops
more proximally: ileal atresia.
Small left colon with multiple filling defects:
meconium plug.
 Most common diagnosis in this presentation,
increased in diabetic mom's, enema is
therapeutic.
Considered a transient functional immaturity
in the myenteric plexus.
Occasionally falsely diagnosed as meconium
plug when true underlying diagnosis is
Hirschsprung's.
 Abnormal rectosigmoid ratio;
Hirschsprung's.
The most distal bowel should be the largest
diameter in normal examin Hirschsprung's'
this is reversed.
Boys>girls, down's association, biopsy to
prove, can have varying lengths of
involvement.
 Distal colonic air/fluid levels may lean
differential towards Hirschsprung's.
Right colonic stool may lean the leading
differential consideration towards
meconium ileus.
Our case has both..needs an enema
study regardless.
Per Donnelly, midgut volvulus could be
entertained initially, as it is an emergent
cause of multiple dilated bowel loops;
however, the child would be expected to
be rather ill at presentation
 Man with smoking history and
recent dyspnea with chest wall
pain.
 Findings: There is a large, solid right
perihilar upper lobe lung mass, which
extends from the pleural surface to the
hilum. The mass measures 9.2 x 6.6 cm.
The central airways remain patent, as do
the passing vessels. The mass is greater
than 2 cm from the carina. There is early
sub-adjacent desmoplastic reaction of the
parenchyma. There is no mediastinal or
axillary lymphadenopathy.
 this lesion is NOT:
Squamous cell carcinoma
Bronchoalveolar carcinoma
Adenocarcinoma
Large cell carcinoma
Small cell carcinoma
Fibrous tumor of the pleura
Metastasis
 Diagnosis: Adenomyoepithelioma
 Adenomyoepithelioma is a very rare
pulmonary tumor which is composed of
outer myoepithelial cells and inner
epithelial cells. Not much discussion of this
tumor in the literature exists as relating to
a primary lung tumor, but case reports
have described a typically well-
circumscribed, solid neoplasm with the
potential for very rapid growth
 When viewed as a pathology specimen,
typically present will be solid, glandular
and papillary growth patterns. Case
reports exist of the inner epithelial cells
staining positive for carcinoembryonic
antigen and the outer myoepithelial cells
staining positive for S-100 protein.
 Extremely rare pulmonary tumor
Tumor of epithelial inner cell and
myoepithelial outer cell differentiation
thought to be of bronchial minor salivary
gland origin
Tumors usually well-circumscribed
Solid, glandular and papillary growth
patterns typically noted on pathology
Inner cells may stain positive for
carcinoembryonic antigen
Potential for very rapid growth
Anemia and abdominal pain
tagged RBC images-one
frame every 5 minutes
100 minutes
 Findings: CT scan demonstrates wall
thickening, mesenteric stranding and
question of mass at splenic flexure in the
colon. Tagged RBC scan shows positive
radiotracer uptake at 1 hour 40 minutes at
the splenic flexure. Mesenteric angiogram
showed blush of contrast at the splenic
flexure in a distal SMA branch with
puddling of contrast which persists
 Embolized utilizing Gelfoam slurry and
0.018 Renegade microcatheter. Post
embolization angiogram showed normal
contrast enhancement without blush or
persistent contrast puddling.
 Differential diagnosis:
Colitis
Large colon ulceration.
Colonic neoplasm-Adenocarcinoma
Bleeding polyp
Infectious hemorrhagic enterocolitis- E
Coli, Salmonella, Shigella
Diagnosis: Bleeding splenic flexure ulcer.
Successful embolization. Pathologic
correlation: Colon splenic flexure biopsy
showed fibropurulent exudates consistent
with ulcer.
 60% of lower GI bleeds occur from SMA
territory/left upper quadrant.
Acute lower gastrointestinal (GI)
hemorrhage accounts for approximately
20% of all cases of GI hemorrhage.
Mortality rates are reportedly 10-20%
Localization of hemorrhage relative to the
Ligamentum Treitz directs the initial
evaluation and resuscitation.

 Lower GI hemorrhage can be due to

numerous conditions, including
diverticulosis, anorectal diseases,
carcinomas, inflammatory bowel disease
(IBD), and angiodysplasias.
 NM tagged RBC pitfalls/advantages:
Poor radiolabelling or dissociation of label
in vivo.
Focal activity in the GU system can be
misinterpreted as a bleed, and
visualization of peristalsis is necessary.
False positives: abdominal varices,
hemangioma, accessory spleen, arterial
grafts, aneurysms.
Bleeding rate sensitivity: 0.1 ml/minute
versus 1 ml/minute via conventional
angiogram
 Definitive criteria to localize GI bleed:
Focal activity appears.
Activity increases over time.
Activity movement conforms to intestinal
anatomy.
Movement may be antegrade or
retrograde.
Frequent image acquisition important for
localizing bleeding.
Imaging for 90-120 minutes is essential
 Mesenteric Angiogram
Early arterial blush may be seen with any
inflammatory response or reason for
increased arterial flow, such as
angioneogenesis in neoplastic processes.
 Differential includes:
Ulceration/colitis (our patient)
Mass/Neoplasm (most commonly colonic
neoplasm such as adenocarcinoma)
Angiodysplasia (seen commonly in elderly)
 Treatment options:
Gelfoam slurry embolization (eventually
absorbs)
Embolization PVA 150-500 microns.
Go as far distally with microcatheter to
avoid devascularization of large amounts
of colonic tissue.
Sensitivity and specificity of NM scan is
ten fold greater than sensitivity and
specificity of angiogram
 Findings: At first glance, there is
apparent diffusion restriction in the left
cerebellar hemisphere on DWI and ADC
map images. Another image pair though
the occipital and temporal lobes
demonstrates that in fact the L side is the
normal side. There is increased signal in
the right cerebellar hemisphere on T2
weighted images. On FLAIR images, there
is decreased signal arising from the right
cerebellar hemisphere secondary to fluid
attenuation
 Diagnosis: Right cerebellar
encephalomalacia
 Encephalomalacia is usually a
consequence of aging and/or brain insult,
and in this case, the patient had a prior
right cerebellar infarct. The brain
parenchyma becomes atrophic and
becomes replaced by CSF.
Encephalomalacia usually does not cause
acute symptoms and was likely not the
cause of this patient's symptoms.
 In this patient, there was a sequence of
DWI images that demonstrated increased
signal in the left cerebellar hemisphere.
However, on ADC map images, there was
no associated loss of signal. The adjacent
right cerebellar encephalomalacia (and
bright signal due to the high extracellular
water e.g. CSF), gave the illusion of signal
loss in the left cerebellar hemisphere
 On T2 and FLAIR images, acute ischemia
shows up as increased signal. In this case,
there was no increased T2 signal
throughout the brain parenchyma. The
encephalomalacia in the right cerebellar
hemisphere shows up bright on T2
weighted images due to CSF replacement
of brain parenchyma.
 Acute ischemia causes cellular swelling
and decreased movement of water.
Decreased mobility of cellular water
manifests as bright signal on DWI. Other
entities that increase extracellular water
also lead to increased signal on DWI.
ADC map images track decreases in water
diffusion coefficients, with decreases
indicated by decreased signal.
Acute ischemic stroke is demonstrated by
increased signal on DWI with
accompanying dark signal on ADC map.
Changes are seen as early as 30 minutes
 Findings: Multiple large esophageal
varices are identified, some measuring 2.5
cm in diameter. No significant biliary
dilatation or overt hepatic lesion. A couple
of tiny low attenuation foci in the right
hepatic lobe may represent cysts. The
spleen is massively enlarged with
peripheral low attenuation area suggesting
infarcts. There is diffuse haziness in the
omentum with large omental varices.
 Differential diagnosis:
Cirrhosis
Splenic vein occlusion
Right heart failure
Hepatoma
Budd-Chiari syndrome
Schistosomiasis
Diagnosis: Portal hypertension
 Classification:
Prehepatic
Intrahepatic, acute, chronic liver diseases
Posthepatic
 Characteristics:
Elevated pressure (>10mmHg ) in the portal
venous system
Increased resistance to blood into the liver
Reversal of flow in the portal vein
Dilation of the portal vein, splenic and
mesenteric veins
Porto-systemic collaterals
Splenomegaly
 US for primary diagnosis of portal
hypertension, portal vein occlusion
CT/MR if US technically impaired, and pre-
transplantation evaluation
Pathology
Most commonly caused by hepatic cirrhosis
 Prehepatic
Portal vein thrombosis
Portal compression or occlusion by biliary and
pancreatic neoplasms and metastases
Intrahepatic
Acute, chronic liver diseases
Presinusoidal resistance: schistosomiasis
Sinusoidal: liver fibrosis, usually cirrhosis
Hepatoportal fibrosis
Nodular regenerative hyperplasia
 Posthepatic
Thrombosis of posthepatic hepatic veins (Budd-
Chiari), posthepatic portion of IVC, congestive
heart failure, constrictive pericarditis
Increased portal flow
AV fistula
Hepatoma with arterioportal shunt
Massive splenomegaly
 Imaging findings
Reversal of flow in the portal vein
Dilation of the portal vein, splenic and
mesenteric veins
Porto-systemic collaterals
Splenomegaly
Irregular and lobulated hepatic contour
 CT
Dilated portal vein >17mm with deep
inspiration
Porto systemic collaterals
Gastroesophageal
Coronary vein-left gastric
Right gastric, splenogastric
Perisplenic
Retro gastric
 Spontaneous splenorenal shunt entering and
enlarging the left renal vein
Hepatic cirrhosis
Splenomegaly
Ascites
Decreased liver volume
Increased size and prominence of intrahepatic
fissures
Caudate: right lobe ratio
Normal C:RL 0.47
Cirrhotic C:RL 1.00
Man with HIV and non-small cell
lung cancer.
 Additional clinical history: Resection of
left upper lobe and involved chest wall.
Also intervention for recurrent L pleural
effusion
 Findings: On PET, there is increased L
pleural FDG uptake in a nodular pattern.
The CT image demonstrates nodularity
and thickening of the posterolateral left
pleura. Some of the nodular pleural
thickening demonstrates high density foci
(e.g., on lowest CT cut shown
 Differential diagnosis:
Recurrent non-small cell lung cancer or
other neoplastic process
Inflammatory changes from talc
pleurodesis
Pleural fibrosis
Diagnosis: Talc pleurodesis inflammatory
changes.
 In the setting of recurrent pneumothorax or
persistent pleural effusion, often a
pleurodesis is performed to maintain the
expansion of the affected lung. Perhaps
the most commonly used agent is talc,
which causes a granulomatous reaction at
the pleural interspace
 effectively binding the visceral to the
parietal pleura. The reaction is persistent,
and can cause markedly increased FDG
uptake on PET scans. If the uptake is
marked and in a distribution concerning for
neoplasm,
 comparison with CT should be performed
to evaluate for radio dense talc in the
same distribution. Because talc
pleurodesis is often performed in the
setting of nonresolving malignant pleural
effusion, care should be taken to
distinguish this benign process from
recurrent malignancy with the above PET
findings.
 Talc pleurodesis can mimic pleural
malignancy on PET.
Talc pleurodesis is often performed in the
setting of recurrent malignant pleural
effusion.
The therapeutic granulomatous reaction
with talc causes the pleura to be FDG-
avid.
Correlation with radio dense talc on CT is
advised with large FDG-avid foci
Altercation. Now has
headaches.
 Findings: CT: Expansile, lytic lesion of
the clivus is present without cortical
disruption. The lesion has a ground-glass
appearance. It is lytic centrally and
sclerotic peripherally. Bilateral jugular
tubercle and right occipital condyle
involvement also present. MRI:
Heterogenous (T2 hyper intense and T1
hypo intense) expansile clival lesion. The
majority of the lesion demonstrates avid
contrast enhancement. The brain
parenchyma is normal.
 Differential diagnosis:
Fibrous dysplasia
Chordoma
Chondrosarcoma
Plasmocytoma
Metastasis
Lymphoma
Diagnosis: Monostotic clival fibrous
dysplasia
 Monostotic clival fibrous dysplasia is a rare
entity (According to Sirvanci et al., only 3
cases were reported in the literature by
2002). Overall, craniofacial fibrous
dysplasia represents three percent of bone
tumors. Fibrous dysplasia is a
developmental disorder felt to be
secondary to a genetic mutation. It is not
hereditary. It results in abnormal fibroblast
proliferation with replacement of normal
medullary bone. This causes expansion
and structural integrity compromise.
 Fibrous dysplasia can be classified as
monostotic and polyostotic. The
polyostotic form represents 30% of cases
and can present as part of Albright-
McCune-Sternberg syndrome. The initial
presentation in the majority of cases is in
the first two decades of life. No racial or
gender predilection has been described.
Besides craniofacial involvement, other
commonly involved areas include the ribs,
femurs, tibias, and the pelvis.
 MRI and CT are the best imaging
modalities for clival evaluation. On MRI,
fibrous dysplasia appears as hypo intense
on T1 weighted images. The imaging
characteristics on T2 weighted images are
variable from hypo intense to isointense to
hyper intense. The variability on T2
weighted images is attributed to several
factors including (but not limited to)
cellularity, cyst formation, and presence of
collagen. Avid enhancement after
gadolinium administration is typically
present.
 On CT, a ground glass appearance is
associated with fibrous dysplasia.
Additionally, a sclerotic border is also
present. Smaller cystic, circumscribed
areas are present within the lesion.
Overall, CT is superior to evaluate for
subtle change and internal lesion
structure. If nuclear scintigraphy is
performed (not necessary), mild,
nonspecific activity is usually present in
the clivus
 Management is almost always
conservative with followup imaging to
evaluate for stability if warranted (typically
CT). Surgical treatment may be warranted
if neurological compromise or significant
pain develops. Rarely (.05% of monostotic
craniofacial lesions), malignant
transformation may occur.
Woman with seizure
 CT head: Multiple areas of intracranial
hemorrhage in the left hemisphere. There
is thrombosis of the superior sagittal sinus
and a left cortical vein. Two focal hyper
dense masses are seen in the left occipital
lobe and the medial left temporal lobe
 Cerebral angiogram: No evidence of
aneurysm or AVM. There is a large left
venous angioma draining the entire left
hemisphere into the internal cerebral vein
then to the vein of Galen. Left cortical vein
thrombosis, nonocclusive posterior
superior sagittal sinus thrombus, and
absence of the anterior superior sagittal
sinus.
 MRI and MRV brain: Multiple intraaxial
masses in the left cerebral hemisphere
seen in the temporal lobe, basal ganglia,
occipital lobe, and genu of the corpus
callosum which show blooming artifact on
gradient echo images, and a hypo intense
rim on T2-weighted images. There is a
large left hemispheric venous angioma
with dilated medullary veins which drain to
the internal cerebral vein best seen on
post contrast images. The anterior
superior sagittal sinus is hypoplastic or
stenotic.
 Differential diagnosis:
Multiple arteriovenous malformations
Multiple cavernous malformations with
large venous angioma and sagittal sinus
stenosis and partial thrombosis
Multiple cavernous malformations with
venous stasis due to sinus stenosis and
partial thrombosis
 Multiple hemorrhagic metastases with
leptomeningeal enhancement
Multiple calcified metastases and
leptomeningeal enhancement
Sturge Weber with arteriovenous
malformations
Diagnosis: Multiple cavernous
malformations (AKA cavernomas) with
associated large hemispheric
developmental venous anomaly (AKA
DVA or venous angioma
 The diagnosis is favored over cavernomas
with venous stasis because:
There is a known association between
cavernous malformations and developmental
venous anomalies.
The cerebral angiogram shows an
embryologic drainage pattern
 Cavernous malformations
Cerebral angiography: Most common
angiographically occult vascular malformation, i.e.
not detectable. May be associated with a venous
angioma
MRI: Popcorn ball appearance; mixed signal
intensity core with a hypo intense hemosiderin rim;
prominent susceptibility artifact ("blooming").
Diffusion usually normal
CT: Negative in 30-50%; may appear as an ovoid
hyper dense lesion. 40-60% have Ca2+
 Developmental venous anomaly (AKA
venous angioma):
Prevalence: 2.5-9% of MRI scans
Contain normal intervening brain
Dilated medullary veins have the "medusa head"
or umbrella-like appearance; located often at the
angle of the ventricle; stellate, tubular vessels
converse on a collector vein which drains into a
dural sinus/ependymal vein
 Differential diagnosis includes dural sinus
occlusion with venous stasis and collateral
drainage.
Cerebral angiography: Most common
angiographically occult vascular malformation, i.e.
not detectable; may be associated with a venous
anomaly
MRI:
 MRI:
T1 and T2 weighted images: Can be normal if small, or
see flow void if large enough
T1+C: Stellate pattern of tubular vessels of strong
enhancement draining to a collector vein to a dural
sinus/ependymal vein
MRV: Demonstrates medusa head and drainage pattern
CT: Usually normal. Parenchymal hemorrhage if
draining vein occluded
ASCITES,H/O LIVER BIOPSY
 Findings: US liver with Doppler shows
saccular lesion adjacent to right hepatic
artery with circular / turbulent flow (Yin-
yang sign). Low velocity / hepatofugal
flow within in the main and right portal
veins, with the suggestion of mild
pulsatility of the RPV waveform).
Hepatopetal flow in left portal vein.
 Angiography shows selective
catheterization and angiography of the
common hepatic artery shows abnormal,
early (retrograde) filling of the right portal
vein. This is confirmed by super selective
angiography in a right hepatic artery
branch. Coil embolization of distal right
hepatic arterial branch. Post-embolization
arteriogram shows no filling of the portal
venous system.
 Diagnosis: Hepatic arterial-portal fistula
(due to percutaneous liver biopsy)
 US shows classically, pulsatility and
reversal of flow within the portal vein
Doppler waveforms. Turbulent flow seen
at the hepatic artery near the fistula.
CT w/ contrast (dual phase) shows large,
high flow APFs show early filling of portal
veins in hepatic arterial phase of imaging
(same density as aorta). Small APFs are
usually peripheral, wedge-shaped lesions
which are hyper attenuating to liver on
arterial phase and no seen on portal
venous phase of imaging.
 Hepatic arterial-portal fistula can be
congenital (Osler-Weber-Rendu disease)
or acquired.
Acquired A-P fistulas can be iatrogenic,
post-traumatic, cirrhosis, or HCC.
Iatrogenic A-P fistulas could be seen post
TIPS, percutaneous biliary drainage, or
liver biopsy (as in our patient).
 Small A-P fistulas are rarely symptomatic,
frequently close spontaneously. Large /
high-flow A-P fistulas are associated with
rapid development of portal hypertension
(weeks to months) with GI bleeding,
ascites, and sometimes high-output
cardiac failure
 Hepatic arteriography shows early filling of
portal vein branch in a retrograde fashion.
Treatment is percutaneous transarterial
coil embolization.
Patient with episodic abdominal
pain
 Findings: There is gallbladder wall
thickening with comet tail artifacts in the
anterior wall. The gallbladder has an
hourglass configuration
 Differential diagnosis:
Adenomyomatosis
Strawberry gallbladder
Gallbladder polyp
Gallbladder carcinoma
Chronic cholecystitis
Sonographic
diagnosis: Adenomyomatosis of the
gallbladder
 Adenomyomatosis is a benign condition
characterized by hyperplastic changes of
the gallbladder wall and mucosa. This
results in thickening of the muscular wall,
and exaggeration of normal mucosal folds
termed Rokitansky-Aschoff sinuses
creating sinus tracts or diverticula. The
Rokitansky-Aschoff sinuses can fill will
cholesterol and may contain matrix
calcifications
 Adenomyomatosis may occur in a focal,
segmental, or diffuse form. This is
pathologically (although not always
radiographically) distinct from
cholesterolosis. This term refers to both
large accumulations of cholesterol in the
lamina propria causing cholesterol polyps
or numerous small cholesterol deposits
(so called "strawberry gallbladder"). Both
diseases, adenomyomatosis and
cholesterolosis, are included in the
umbrella term: hyperplastic cholecystosis.
 Females are affected more often and there
is no racial predilection. Patients are
usually older than 35 years of age. There
is an association with vague abdominal
pain although many patients are
asymptomatic. There is no treatment
necessary if asymptomatic and
cholecystectomy can be considered if
symptomatic.
 Gallbladder wall thickening in diffuse,
midbody, or fundal portions of the
gallbladder. US shows high amplitude
intramural echoes. Reverberation artifact
("comet tail") may be present. CECT
shows an enhancing gallbladder wall with
visualization of cystic structures in the
gallbladder wall. MRI shows nonenhancing
cystic spaces in the gallbladder wall.
 Adenomyomatosis is causes by
exaggeration of the normal Rokitansky-
Aschoff sinuses which develop into
diverticula and fill with cholesterol.
There is no malignant potential and
treatment is indicated only if symptomatic.
Distribution may involve the entire
gallbladder, a segment of the midbody, or
the fundus.
Ultrasound is often diagnostic showing
thickening of the wall and comet tail