Man undergoing head-and-neck

workup.
 Additional clinical history: Forty-year-
old man with pain and swelling at right
mandibular angle for 3 months.
 Findings: Mixed solid/cystic lesion seen
adjacent/lateral to right mandibular
angle/right parotid gland. Minimal overlying
fat stranding without associated soft tissue
edema. Solid component enhances
heterogeneously. Cystic component
demonstrates a 3-4 mm thick enhancing
wall, and is crescentic (not round) in shape.
 Differential diagnosis:
Infection with abscess (i.e. parotitis, sialadenitis)
Neoplasm
Benign mixed tumor (parotid)
Squamous cell carcinoma
Warthin's tumor
Adenoid cystic carcinoma
Metastasis
Parotid schwannoma
Diagnosis: Warthins tumor
 Warthin's tumor also called papillary
cystadenoma lymphomatosum,
adenolymphoma, or lymphomatous adenoma
Benign parotid tumor (2nd most common)
Cystic component in 30%, 20% multicentric
Minimal enhancement of solid component
Does not calcify, solid component ("mural
nodule") inhomogeneous
 Standard of care is excision (in this case, close
follow-up and excision by ENT the week of
study). Tumor is benign, but mass effect can
cause great discomfort and damage to sensitive
neurovascular structures.
90% occur in smokers. Mean age = 60 years.
M:F = 3:1. Increase incidence with radiation
exposure
Malignant transformation to carcinoma
exceedingly rare
 Always look closely at ipsilateral "normal"
parotid and contralateral parotid to rule-out
multicentric disease (this patient did have
multiple, smaller nodules in the
contralateral parotid).
Man with gout and elevated
alkaline phosphatase
 Findings: Whole body bone scan with
spot images of the lumbar spine
demonstrate an intense radiotracer uptake
involving the entire L1 and L5 vertebrae.
There is also a linear band of intense
uptake in the mid-portion of the sacral
body.
 Differential diagnosis:
Paget's disease
Bone metastases
Primary bone tumor
Fibrous dysplasia
Diagnosis: Paget's disease
 Paget's disease of the bone: chronic bone disease of
the elderly with abnormal and excessive bone
remodeling, coarse trabeculae, sclerosis, and
expansion of bones
Exact etiology unclear but included in the metabolic
bone disease category
Usually asymptomatic, with elevated serum alkaline
phosphatase and urine/serum hydroxyproline
If symptomatic, patients may present with pain in
extremities, bowing of long bones, and secondary
osteoarthritis
 Abnormal bone is weaker and fracture is common
Malignant degeneration is rare
Bone scans are most sensitive in detecting
Paget's
Intense increased radiotracer activity in all
phases of active disease
Expansile appearance of affected bone
Will see uptake even before radiographic change
 Predominately involves the axial skeleton:
pelvis>vertebra>skull>proximal long
bones; but any bone may be affected
Polyostotic>monostotic
No increased uptake in inactive/quiescent
phase
 If worsening lesion in patient with long-
standing Paget's, or if there are new sites
of increased activity, be concerned for
possibility of superimposed primary tumor
or metastatic disease
Other imaging and/or biopsy correlation
may be necessary to distinguish between
Paget's and metastasis
Young woman with hypercarbia
 Findings: In the region of the epiglottis,
an enhancing mass extends into the
region of the true and false vocal cords.
Mass appears well-encapsulated. No
definite evidence for local invasion
 Differential diagnosis:
Squamous cell carcinoma
Chondrosarcoma
Wegener's granulomatosis
Paraganglioma
Papilloma
Pseudotumor
Schwannoma

 Further chart review from an outside

hospital revealed that the patient had
undergone multiple neurosurgical
debulkings of lumbar spinal cord masses.
 Large laryngeal mass with heterogenous T2
prolongation and heterogenous contrast avidity.
There is a left skull base mass and left axillary and
subclavicular masses with heterogenous signal
and enhancement.

Final pathological diagnosis:

Schwannomatosis. Large laryngeal schwannoma.

 Schwannomas
Usually benign tumors which may occur
sporadically, in patients with neurofibromatosis
type-2 (NF2), or in a recently described entity
called schwannomatosis .
Arise from differentiated Schwann cells from nerve
sheets
Schwannomatosis
Recently recognized as a new category of
neurofibromatosis
 Schwannomatosis
Prevalence = unknown [2]
Incidence = 1/1,700,000 [4]
Peak incidence between 30-60 years of age [2]
No predilection for race or sex [2]
Hallmarks [2]
Multiple schwannomas without vestibular
involvement
1/3 are anatomically located within single limb or
spinal segment
 Accepted diagnostic criteria
Definite
Age > 30 years of age with 2 or more
nonintradermal schwannomas (one must
be biopsy proven), no evidence of
vestibular tumor on MRI, AND no known
constitutional NF2 mutation
ORone biopsy proven schwannoma
with a first degree relative meeting the
above criteria
 Possible
Age < 30 years of age with 2 or more
nonintradermal schwannomas (one must
be biopsy proven), no evidence of
vestibular tumor on MRI, AND no known
constitutional NF2 mutation
ORage > 45 years with 2 or more
nonintradermal schwannomas (one must
be biopsy proven), no symptoms of CN VIII
dysfunction, AND no known constitution
NF2 mutation
 ORradiographic evidence of non-vestibular
schwannoma and first degree relative meeting
criteria for definite schwannomatosis
20 years male
Trufisp-2 chamber
Trufisp-LVOT
DOUBLE INVERSION
RECOVERY
PREFUSION &DELAYED
 CT Findings: The CT shows LV wall
thickening, greatest in the septum.
MRI Findings:
TruFISP two chamber cine in end diastole
and end systole demonstrates asymmetric
left ventricular septal hypertrophy and
hyperdynamic left ventricle (EF 74%):
 Differential diagnosis:
Hypertrophic cardiomyopathy
Aortic coarctation
Aortic stenosis
Restrictive cardiomyopathy
Systemic arterial hypertension
Actual diagnosis: Hypertrophic cardiomyopathy

 Hypertrophic cardiomyopathy (HCM) is a

genetic heart muscle disease occurring in 1 of
500 people (0.2%).
HCM is the most common cardiac cause of
sudden death in people under 30 years of age.
The degree of delayed myocardial enhancement
(fibrosis) correlates with risk of sudden cardiac
death. Sudden cardiac death is usually caused
by ventricular fibrillation or tachycardia.
 HCM occurs equally in both sexes and in
many different races.
There is non-dilated hypertrophy and
hyperdynamic left ventricle. The normal
alignment of the muscle fibers is disrupted
(myocardial disarray).
Normal thickness of the LV is 12 mm or less,
while in HCM the LV thickness is usually
greater than 15 mm.
 There is usually asymmetric with greatest
involvement of the intraventricular septum.
The most common location is the basal
septum. Apical hypertrophy is a distinct
subtype more commonly seen in
Japanese and Korean patients.
 LV hypertrophy and systolic anterior motion
of the anterior leaflet of the mitral valve
(SAM) can result in dynamic LVOT
obstruction and mitral regurgitation.
Treatment options include medical
management (beta-blocker or calcium
channel blocker), surgical myectomy,
alcohol septal ablation, ventricular pacing,
and possibly cardiac transplant
Man in car accident referred for
a CT examination
 Findings: Right occipital epidural
haematoma, with the swirl sign, suggesting
active bleeding, with mass effect to the
occipital lobe and cerebellum, surrounded
by narrow oedema; haemorrhagic cortical
occipital and parietal contusions on the
right, with oedema (coup contusions) and
bilateral frontal haemorrhagic cortical
contusions (contre-coup contusions);
 small acute haemorrhagic lesions in the
basal nuclei and internal capsule
(intermediate-coup contusions). The skull
presented occipital fractures, with one
right occipital depressed fracture. A large
fronto-parieto-temporo-occipital scalp
haematoma was present.
 Differential Diagnosis:
Epidural hematoma
Subdural hematoma
Haemorrhagic cortical contusion(s)
In other clinical settings:
Septic emboli
Venous thrombosis
Stroke
Tumor / Metastasis
AVM
Diagnosis: Traumatic head injury with primary associated
lesions.
 The mechanisms responsible for primary
lesions are direct contact between the
skull and the object, and the inertial injury
resulting from the differential accelerations
between white and gray matter, the
biomechanical conditions being extremely
complex
 Contusions occurring at the site of the
impact are called coup contusions
whereas diametrically opposed are called
contre-coup contusions, while those of the
deeper structures are intermediate-coup
contusions.
Three-day-old with abdominal
distention
 Plain radiographs demonstrate multiple air-
distended bowel loops and a round air-filled
structure in the right lower abdomen. There is no
air in the rectum. Findings are compatible with a
distal obstruction. Contrast barium enema was
performed demonstrating a microcolon. Contrast
material could not be refluxed past the mid
transverse colon. An upper GI study was
subsequently performed which was negative for
malrotation or midgut volvulus.
 Differential diagnosis:
Small left colon syndrome
Hirschsprung's disease
Meconium ileus
Colonic atresia
Midgut volvulus
Diagnosis: Colonic atresia
 The colon is the least common site of
atresia in the GI tract.
Patients with colonic atresia or congenital
stenosis may have findings of dilated
bowel loops or polyhydramnios on
prenatal ultrasound
 Failure to completely pass meconium
suggests atresia, whereas delayed
passage of meconium (>24 h) suggests
Hirschsprung's disease. Patients with
colonic atresia may pass meconium
normally because the incident that caused
the atresia may have occurred after the
colon had become filled with meconium
 Colonic atresia has been associated with
abdominal wall defects and abnormalities
of the genitourinary tract.
Radiographs demonstrate findings of distal
obstruction, which is nonspecific, and
necessitates a contrast enema. In colonic
atresia, there is a microcolon with abrupt
termination of retrograde contrast flow.
 Man with groin pain after
angioplasty
seventy-year-old man with right calf
claudication now presents with groin pain
following CO2 angiography, angioplasty,
and stent placement.
 Extremity angiogram- A selective right
lower extremity arteriogram was
performed. Common femoral arteries
patent. Profunda femoral arteries patent.
There is diffuse disease of the SFA with
severe stenosis surrounding an indwelling
SFA stent. Popliteal artery is patent. The
distal SFA was stented using a 6 mm x 15
cm self expanding stent.
 The stent was post dilated using a 5 mm
angioplasty balloon. Post interventional
arteriography demonstrated a good
angiographic result with restoration of
brisk antegrade flow down the SFA. There
is no evidence for distal embolic
complication
 CT abdomen/pelvis- The unenhanced liver
shows evidence of portal venous air. There
is large amount of subcutaneous gas within
the left groin and small amount of fluid.
There is gas within the shaft of the penis as
well as the scrotum and testicles. There is
air within the lumen of the right common
femoral vein. There is also air present within
the bone marrow of the right proximal femur.
 Ultrasound scrotum - Both testicles
demonstrates inhomogeneous echogenicity.
There are hyper echoic foci within the bilateral
testicles right side worse on left which may
represent coarse calcifications or more likely
air. Arterial and venous Doppler waves
demonstrated within the bilateral testicular
parenchyma. However, there is decreased
vascularity in portions of the bilateral testicles.
 Differential diagnosis:
Testicular infarct
Orchitis /epididymitis
Testicular neoplasm
Testicular contusion/rupture
Diagnosis: Bilateral testicular infarcts
following CO2 angiogram
 Acute testicular infarct:
Clinical presentation is typically acute
scrotal/inguinal pain +/- a swollen,
erythematous hemiscrotum. A history of
trauma is usually absent.
CO2 angiography is used in patients that
cannot receive iodinated contrast
secondary to allergy or poor renal function.
 Key point- Absent testicular blood flow on
color Doppler ultrasound with
heterogeneous echotexture. US finding vary
with duration of ischemia. Some findings are
a spiral or whirlpool pattern of the spermatic
cord, enlarged testis with heterogeneous
echotexture, hyper echoic foci representing
hemorrhage, decreased to absent color flow
compared to the contralateral testicle
 Nuclear medicine imaging using Tc-99m
shows absence of radiotracer in the effected
testicle. Increased activity can be seen
around the testicle secondary to hyperemia.
Orchitis /epididymitis also presents with pain
but demonstrates increased not decreased
flow within the affected testicle. Testicular
neoplasms are less likely to be bilateral as
in this case and rarely present with pain.
 Testicular contusion/rupture present with
pain but virtually always have a history of
prior trauma.
Most complications with CO2 angiography
are related to the inadvertent injection of
room air along with the CO2.
Contamination with room air should be
considered when gas persists on imaging
as CO2 is absorbed very quickly.
 Treatment is resection or conservative
therapy with pain management depending
on the amount of testicle affected.
Woman undergoing head and
neck work-up
 Additional history: Patient has history of
ITP and Behcets disease. She presented
with painless palpable nodules below the
left ear
 Findings: Axial CT of the head and neck
with intravenous contrast shows two solid left
parotid nodules, without right-sided nodules.
Follow-up Ultrasound with color-flow Doppler
was performed, showing two hypo echoic
solid nodules, one of which had increased
internal flow. Given the patients ITP, anemia
and bleeding diathesis, US-guided biopsy of
the less vascular nodule was performed.
 Differential diagnosis:
Metastatic disease (Ipsilateral squamous cell
carcinoma or melanoma)
Non-Hodgkin's lymphoma
Benign mixed tumor of the parotid (Most
common benign parotid neoplasm, 80%.
Usually occurs singly, but can have multiple
nodes from surgical resection seeding.)
Warthin tumor (5% of benign parotid tumors)
 Parotid oncocytoma (1% of benign salivary
neoplasms. Usually solid nodules, unilateral or
bilateral.)
Sjogren syndrome (Usually bilateral, cystic and
seen in other salivary glands.)
Benign lymphoepithelial lesions (Bilateral solid and
cystic, HIV, only seen in parotids.)
Parotid sarcoidosis (Bilateral solid nodules, can be
cystic in later stages.)
Diagnosis: Parotid oncocytoma.
 CT of the head and neck is usually the first
diagnostic imaging tool for evaluation of parotid
lesions.
CT can be used to narrow the differential diagnosis
-by evaluating if the masses are single vs. multiple,
unilateral vs. bilateral, and by looking for
lymphadenopathy, masses in other salivary glands,
and intrinsic abnormality of the parotid parenchyma,
which if found is more likely indicative of
inflammatory or infectious etiology of mass lesions.
 However, CT usually cannot accurately
differentiate benign and malignant lesions
based on intrinsic appearance alone.
Therefore, biopsy is often required.
Approximately 25 % of parotid masses are
non-neoplastic (e.g. inflammatory,
infectious).
Of the neoplastic parotid lesions, 70-80%
are benign.
 Except for Warthin tumor, benign parotid
neoplasms are more common in women.
Given that this patient is female, Warthin
tumor was less likely than other benign
tumors in this case.
Parotid oncocytoma is very rare (1% of
salivary gland tumors).
A 40-year-old man with ongoing
lower-extremity complaint
 Additional history: The mass has been slowly
growing for several years. Past biopsies have
been negative.
A three phase bone scan (images not available)
showed increased tracer activity in the left heel
in the flow and blood pool phases. No
involvement of the calcaneus or other osseous
structure was seen in the delayed images. The
study was read as cellulitis without evidence of
osteomyelitis.
 Radiographs show a lobulated soft tissue mass
involving the medial inferolateral aspect of the
left foot. No osseous abnormalities are seen.
MRI shows that the patient's palpable mass
corresponds to a poorly circumscribed,
somewhat cystic enhancing lesion contained in
the subcutaneous tissues of the lateral aspect
or the ankle, and wrapping around the plantar
aspect of the heel on the lateral side.
 Lesion demonstrates heterogeneous
enhancement. Some signal abnormality
within the sinus tarsi, along the flexor
hallucis and flexor digitorum longus, and
within the cuboid bone may be reactive.
 Differential diagnosis:
Mycetoma (Madura Foot)
Foreign body granuloma
Neurofibroma
Abscess
Necrotizing fasciitis
Neuropathic arthropathy
Malignancy
Diagnosis: Madura Foot (mycetoma)
 Madura Foot:
Chronic granulomatous disease affecting the
feet
Most common in Asia
Caused by multiple different fungi and some
bacteria such as Nocardia
Results from post-traumatic invasion of the soft
tissue by organisms living in the soil
Can present with palpable soft tissue mass
 Extensive soft tissue and osseous disruption
with periostitis and sclerosis
Multiple soft tissue granulomas
Surrounding edema and joint effusions are
common
Progressive course with osseous fusion and
multiple sinus tract formation
Eventually can lead to loss of joint definition
and amorphous, fused osseous structures
Woman with discomfort and
abnormal physical exam.
 Additional clinical history: Forty-year-
old woman with complaints of "lump in left
lower quadrant". History of ventral hernia
repair and Caesarian section.
 Findings: Focal soft tissue density mass
in the anterior left lower quadrant
subcutaneous tissues, which abuts the left
abdominal rectus sheath.
 Differential diagnosis for subcutaneous
nodules/mass:
Metastases to skin, via hematogenous spread (e.g.,
malignant melanoma, breast, stomach, ovary, renal,
and lung primaries)
Injection hematomas and granulomas
Sebaceous cysts
Abscess
Endometriomas
Diagnosis: Endometrioma of abdominal wall.
 This patient had an endometrioma, diagnosed
after CT guided biopsy of the soft tissue density
mass. The endometrioma was the result of
implant of endometrium at the site of her
surgical scars from prior surgery (Caesarian
section, as well as prior ventral hernia repair.)
Definition of endometriosis: Presence of
endometrial glands and stroma outside of the
endometrium and myometrium
 Clinical findings: Dysmenorrhea, pain,
dyspareunia, irregular bleeding, +/-cyclical
symptoms and estrogen dependent
Endometrioma: Thick-walled, complex
ovarian cyst with debris (chocolate cyst)
Most common location is ovary, but may
also involve peritoneal sites and more
rarely extraperitoneal sites.
 CT findings will demonstrate nonspecific
soft tissue density mass
Biopsy and/or excision are usually
necessary for diagnosis
On MR, endometriomas will have high
signal intensity on T1W1 due to cystic
contents
Woman brought to ER.
 Findings: An acute transverse odontoid
process fracture is present, with
approximately 7 mm intrapulsion of the C2
vertebral body with respect to the dens tip.
The dens tip remains closely aligned with
the C1 anterior arch.
 Differential diagnosis:
Congenital nonunion of the odontoid tip (os
odontoideum)
3rd occipital condyle (congenital variation)
Rheumatoid arthritis with C1/C2
subluxation
Pathologic C2 fracture
Type I, II or III odontoid process fracture
 Diagnosis: Type 2 odontoid process
fracture
 Three types of dens fractures:
Type 1 is avulsion of the tip. Stable fracture.
Treat with immobilization.
Type 2 (most common) is transverse fracture at
base of the dens at the level of the accessory
ligaments. 30-50% incidence of nonunion.
Frequently minimally displaced. Failure to unite
results in separate fragment called the os
odontoideum, which is unstable. Treat with
primary fusion.
 Type 3 is a fracture extending into the body of
C2. It usually extends between the superior
articular facets with an inferior convexity in
frontal projection, disrupting the axis ring. Often
difficult to recognize on radiograph if minimally
displaced. Treat with traction and bracing.
 Radiograph:
Lateral radiograph shows anterior or posterior
displacement of C1 arch vs C2 and
prevertebral soft tissue swelling.
Open mouth view may show transverse or
oblique fracture line.
 CT:
Axial often does not show the fracture.
Must have sagittal and coronal reformats to see best.
Type 2 odontoid process fracture most common.
Type 2 fracture is fracture through base of dens.
Type 2 and 3 treated surgically.
Best seen on sagittal radiograph or CT.
A teenage girl with abdominal
fullness.
 Findings: Absent left kidney. The right kidney is
prominent with grade 3 hydronephrosis and mild
hydroureter. There is a large fluid-filled mass.
The intensity pattern matches that of the
prominent left uterus and is thought to be filled
with blood products. Signal is bright on T1 and
low signal on T2. There is duplication of the
uterus. The right uterus is grossly unremarkable.
The left uterus is dilated with intermediate
intensity fluid. The left vagina is also dilated.
 Differential diagnosis:
Uterine anomalies:
Didelphys
Bicornuate bicollis uterus
Unicornuate uterus
Complex duplication anomalies
 Abdominal mass considerations
Endometrioma
Lymphangioma
Left ovary hydrosalpinx
Diagnosis: Didelphys with
hematometrocolpos and likely
endometrioma
 Uterus Didelphys:
Majority of cases sporadic, may have
genetic association.
Complete nonfusion of uterovaginal horns
 Other associated abnormalities
Renal anomalies - agenesis, duplex or pelvic
kidney
When hemivagina obstructed RENAL AGENESIS
85-100% CONTRALATERAL RENAL ANOMOLY
50%
Non-obstructed hemivagina - 15% renal agenesis
Increased incidence of RETROGRADE
ENDOMETRIOSIS, especially in obstructed
hemivaginas
 Can be asymptomatic and have second
highest probability of the uterine
anomalies to have successful pregnancy.
 MRI
High T1 - hematometrocolpos (obstruction
caused by transverse vaginal septum)
Variable signal due to age of blood product.
Treatment
Expectant
Metroplasty - unclear benefit
Resection of vaginal septum if obstructed
 A-NORMAL

B-DIDELPHYS

C Double uterus with single

vagina -

D-Bicornuate uterus

E- Bicornuate uterus
with a rudimentary left horn.

F, Septate uterus

G, Unicornuate uterus
Patient presents with pain.
 Findings: Radiographs reveal no obvious
fracture. Nuclear medicine images
demonstrate abnormal radiotracer uptake
within the sacrum in a pattern known as
the Honda sign.
Diagnosis: Sacral insufficiency fracture
 The sacral stress fracture results from
normal stress on demineralized bone with
decreased inelasticity. Clues to the
diagnosis include: sacral marrow edema
adjacent to the SI joints on MR, sclerotic
bands paralleling the SI joints on CT or
plain film, H shaped or Honda sign on bone
scintigraphy, and additional insufficiency
fractures in the lumbar spine or pelvis.
 Radiographs will be normal in half of
patients at time of presentation. Lucent
fracture lines are rarely seen. The sacral
marrow edema may be unilateral or
bilateral, ill defined, and may be adjacent
to the SI joints but does not involve or
cross them. The marrow edema may
resolve within three months.
 Key negative findings include lack of bony
expansion, absent soft tissue mass, intact
SI joints. Sacral metastatic disease is
more discrete and random in distribution.
There may be invasion of adjacent soft
tissue and/or neural foramina.
 A primary sacral neoplasm may be
associated with bony expansion and will
likely by large and solitary. Sacral
osteomyelitis will often have coexisting
soft tissue abnormalities and the marrow
edema will be contiguous with the soft
tissue edema and may extend across the
SI joints.
Woman with history of asthma
presents to ER.
 Follow-up information: After initial
workup and initiation of systemic
corticosteroid therapy, the patients
condition improved both radiologically and
clinically.
 CXR reveals patchy multilobar hazy
alveolointerstitial opacities, principally
localized the peripheral lung zones. CT
shows patchy nonsegmental geographic
areas of intermixed lobular ground-glass
superimposed upon a smooth reticular
latticework, largely confined to the
subpleural periphery (best illustrated on
high-resolution images).
 Several regions exhibit an apparent
crazy-paving architectural pattern. There
are rare foci of randomly occurring
airspace consolidation. Mild basilar
bronchiectatic airways changes in lung
bases.
 Additional follow-up information: During
workup, transbronchial biopsy and
bronchoalveolar lavage samples returned were
nondiagnostic. No infectious organism was
isolated. As stated, patients condition improved
both radiologically and clinically with systemic
corticosteroid therapy.
Diagnosis: Steroid-responsive
pneumonopathy
 Differential diagnosis for inflammatory
(non-infectious) peripheral lung opacities:
Chronic eosinophilic pneumonia
Idiopathic intra-alveolar inflammatory cellular
infiltrate, largely composed of eosinophils
Common in asthmatics
Hallmark imaging findings of bilateral
nonsegmental upper peripheral lobe airspace
disease (photographic negative of pulmonary
edema)

Consolidation with admixed ground-glass (may
have "crazy-paving" appearance)
Less likely nodular opacities and interlobular septal
thickening
Evolutionary course may reveal linear peripheral
band-like opacities paralleling chest wall
Migratory opacities (waxing and waning in different
lung zones)
Rapid corticosteroid response
 Cryptogenic organizing pneumonia
Consolidation with ground-glass, primarily juxtapleural
and bronchoarterial distribution within mid to lower lung
zones
Bronchoarterial bundle thickening, nodules, non-septal
linear opacities, reticulation, solitary mass like opacities,
reverse halo sign (consolidation encircling focus of
ground-glass), and bronchiectasis are less common
findings
Peri-lobular pattern
Intra-alveolar granulation tissue plugs with small
airways extension
 Nonspecific interstitial pneumonitis
Inflammatory or fibrotic homogenous alveolar wall thickening
Two types: Cellular (15%) and fibrosing (85%); worse prognosis
with fibrosis
Reticulation and ground-glass (ground-glass > reticular
opacities)
Cicatricial bronchiectasis, bronchial dilatation out of proportion to
reticulation
Consolidation, peribronchovascular thickening, and
honeycombing are rare findings
Lower lung zones, mostly diffuse
Adenopathy in majority of cases
May have "crazy-paving" pattern
 Desquamative interstitial pneumonitis
Smoker's disease: Continuum of smoking-related
disease: RB ? RB-ILD ? DIP
Intra-alveolar macrophage accumulation
Basilar peripheral predominance
Ground-glass and reticulation
Honeycombing, usually mild
May have small thin-walled cysts
 Lymphoid interstitial pneumonia
Lymphocytic alveolar septal infiltration
Ground-glass opacities, perilymphatic nodules,
patchy consolidation, and thin-walled cysts
Basal interstitial thickening (classically associated
with Sjgren's syndrome)
Fibrosis/honeycombing rare
May evolve into B-cell lymphoma
Six-day-old girl undergoing
ultrasound evaluation.
 Findings: Grayscale images demonstrate
distended hepatic veins globally. An
abnormal connection is noted between
what appears to be a portal vein branch
and the IVC with internal nonocclusive
clot.
Diagnosis: Patent ductus venosus
 Ductus is fetal vascular connection between PV
and IVC
Usually open at time of birth
Should normally auto occlude by 3 days - 1
week in term infants
Remnant is ligamentum venosum
Failure to close results in portosystemic shunt
Overall very rare, has been associated with
liver masses
Teenage girl with an ankle
injury.
 Findings: There is a complex fracture in
the distal tibia and metaphysis that
extends through the transverse (growth
plate), sagittal (epiphysis), and coronal
(obliquely through the distal tibial
metaphysis) planes
 Differential diagnosis:
Triplane fracture
Pilon fracture
Tilleaux fracture
Diagnosis: Triplane fracture; Salter-
Harris IV
 The classic triplane fracture is multiplanar,
extending through the transverse (growth
plate), sagittal (epiphysis), and coronal
(distal tibial metaphysis) anatomic planes.
The fracture disrupts the tibial plafond
intra-articularly, and results in classically
described fragments.
 Peak incidence for any type of ankle
fracture is in the spring and autumn. It
appears in boys more often than girls.
Most common mechanism is a short fall
(i.e., skateboards, scooters). Triplane
injures are 5-10% of pediatric intra-
articular ankle fractures.
 The triplane fracture is a result of several factors.
Tibial growth plate takes 18 months to fuse. For the
majority of adolescents this occurs between the ages
of 12-15. The fusion progresses from medial to lateral.
Hence, the tibial growth plate during this time is
weakest laterally.
External rotation puts stress on the lateral growth
plate causing its disruption in the transverse plane.
Axial loading and various degrees of flexion cause
fractures in the sagittal and coronal planes.
 Delineating the exact fracture lines and
planes is relatively simple with CT and
MRI.
The term "triplane fracture" was first
coined in the 1970s by Lynn. There are
two classically described types: Two-part
triplane fracture, and three-part triplane
fracture.
 Two-part triplane fracture:
One "part" = distal tibia with anteromedial
corner of the epiphysis attached
Second "part" = a fragment containing the
lateral and posteromedial epiphysis attached
to a posterior metaphyseal spike
 Three-part triplane fracture:
Overall same fracture planes as in the two part
triplane, except the fracture line in the coronal
plane completely extends through the epiphysis
First "part" = distal tibia with anteromedial corner
of the epiphysis attached
Second "part" = anterolateral corner of the
epiphysis on its own
Third "part" = remaining posterior epiphysis with
posterior metaphyseal spike
Women with palpable
abnormality
 Findings: There are scattered fibroglandular
tissues. Cleavage view of the breasts
demonstrates a 6 mm x 12 mm asymmetry,
posterior third, adjacent to the medial aspect of
the right silicone implant. Limited ultrasound of
the medial aspect of the right breast
demonstrates a 14 mm x 16 mm x 27 mm mass
with "snowstorm appearance and dirty posterior
acoustic shadowing."
 Differential diagnosis:
Extracapsular silicone implant rupture
Breast cancer
Hematoma
Abscess
Cyst
Diagnosis: Right breast extracapsular
silicone implant rupture.
 Silicone implant is actually envelope
containing silicone gel. Capsule is the
fibrous tissue that forms around the
implant.
Standard screening includes routine and
ID (implant displaced) views.
Gold standard for evaluation of rupture -->
MRI
 Contracture = hardening of the capsule
which can cause pain.
Siliconoma = foreign body reaction to
silicone gel beyond the capsule
Intracapsular rupture - gel contained in
capsule.
Extracapsular - gel outside formed
capsule
 MRI findings include "keyhole", "teardrop", or
"noose" sign of uncollapsed rupture.
Linguine sign - collapse of elastomer shell into
gel.
Silicone can be seen in breast tissue or lymph
nodes after extracapsular rupture.
Classic US finding of extracapsular rupture is
"snowstorm" appearance of echogenic scatter
in the tissue adjacent to implant.
 Silicone can be seen in breast tissue or lymph
nodes after extracapsular rupture.
Classic US finding of extracapsular rupture is
"snowstorm" appearance of echogenic scatter in
the tissue adjacent to implant.
Silicone only sequence, STIR with water
suppression - good for localizing extracapsular
silicone
Median time to rupture is 8-11 years. Patient is
often asymptomatic.
Football player in emergency
room.
 Findings: CR: The lateral masses of C1
are displaced laterally by approximately 5
- 6 mm on each side in relation to the
lateral masses of C2 consistent with
history of Jefferson fracture. There is also
significant prevertebral soft tissue
swelling.
 MR: A hematoma is present in the
prevertebral space . The tectorial membrane
is intact. The anterior alanto-occipital ligament
is disrupted. The anterior atlantoaxial ligament
is intact. The left transverse ligament has
separated from the medial lateral mass of C1
corresponding to the donor site in the medial
lateral mass of C1 and small avulsion fracture
on the comparison CT scan
 The alar ligaments are intact. The
posterior atlantooccipital ligament is intact.
The anterior longitudinal ligament and
poster longitudinal ligament are intact. The
ligamentum flavum is intact.
 Differential diagnosis:
Jefferson fracture (Compression C1 arch
fracture)
Congenital variants, malformations
Rotational malalignment of atlas
Pseudospread of the axis in children
Diagnosis: Jefferson fracture (Compression
C1 arch fracture)
 The most common presentation is a
patient with upper neck pain after axial
loading. The axial loading transmits the
force through the occipital condyles into
the C1 lateral masses acting like a wedge
and causes the bone fragments to burst
away from the cord, making neurologic
signs rather uncommon
 Neurologic symptoms are much more likely to
be present in patients who have concomitant
instability due to ligamentous injury. Greater
than 9mm of offset of the atlas on the axis is a
sign of transverse ligamentous injury, making
the fracture unstable. The fracture is also
considered unstable if the arch is comminuted
or the posterior longitudinal ligaments are
disrupted.
 Often secondary fractures are noted at lower
levels which may or may not cause
neurologic deficits. C1 fractures make up 6%
of all vertebral injuries. It is uncommon in
children due to an incompletely ossified atlas
allowing for more elasticity. For example the
predental space (between C1 and the
odontoid) is considered normal if less than
5mm in children but only 3mm in adults.
 PLAIN FILM
On the open mouth view there is offset of the
C1 lateral masses compared to those of C2.
Pitfall is that normal rotation may make the
lateral masses appear offset.
Separation between the dens and the C1 anterior
arch greater than 3mm in adults or 5mm in
children is abnormal
Prevertebral soft tissue swelling at the C1 level
Subluxation is possible with unstable fractures
The fracture can be missed on plain film,
particularly if the transverse ligament is intact.
 CT:
Disrupted ring of the C1 arch are usually best
visible in the axial plane. Single rupture is
rare, "ring phenomenon."
Double fracture usually includes either the
anterior or posterior arch and a lateral mass.
Avulsion off the inner lateral mass at the site
of the transverse ligament indicates instability.
 MR:
T1- Soft tissue swelling anterior to C1
T2- signal intensity within the cord indicated cord contusion
Where possible assess the stability of the following ligaments
Transverse ligament
Alar ligament
Apical ligament
Anterior and posterior longitudinal ligaments
Anterior and posterior atlanto-occipital ligaments
Tectorial membrane
 Key points:
Caused by axial load injury splitting the C1 ring
Unstable fracture if transverse ligament is
disrupted
Can be missed on plain film
Offset of the atlas on the axis, or >3mm
separation between the dens and C1 is diagnostic
CT is standard imaging protocol
MR is required for ligamentous assessment
Man with hematuria
 Findings: On the noncontrast images,
there is a hypo dense mass in the inferior
pole of the right kidney. Post contrast
delayed images demonstrate pooling of
contrast within the dependent aspect of
this mass. The rest of the mass remains
hypo dense without significant contrast
enhancement.
 Differential diagnosis:
The imaging findings are pathognomonic
of a calyceal diverticulum
Other "cystic" renal lesions:
Renal cyst
Abscess
Renal tumor
Diagnosis: Calyceal diverticulum
 Calyceal diverticulum is a focal eventration
(outpouching) of the renal calyx into the
renal parenchyma.
It is usually an incidental finding and
typically asymptomatic. Rarely, it may
cause flank pain, fever, pyuria or hematuria.
Urinary stasis within this diverticulum is the
cause of infection or stone formation
 On non-contrasted CT, it mimics a simple renal
cyst. It appears as a well circumscribed, low
density lesion with average HU < 10. It is usually
located at the corticomedullary junction.
Post contrast delayed images (15 to 30 minutes
delayed imaging) are the key to distinguishing
this entity from any other. It classically displays
layering/pooling of contrast medium on delayed
images. This finding is pathognomonic of a
calyceal diverticulum.
 A simple renal cyst would not have any
contrast layering on delayed images.
An abscess is a rim-enhancing lesion
without delayed opacification.
The main reason to be able to identify this
lesion appropriately is to recognize that it
is totally benign and does not need any
intervention.
 Rarely, drainage of this lesion is
performed in case it becomes infected.
Otherwise, it is an incidental finding and
requires no specific treatment.
Man with worsening joint pain.
 Ankle radiographs demonstrate severe cartilage loss
with sclerosis and subchondral cystic change.
Bilateral ankle involvement is considerably worse
than in the feet. Knee radiographs demonstrate joint
space narrowing and osteophyte formation
predominantly in the patellofemoral compartment.
Hand radiographs demonstrate cartilage loss and
hook osteophytes at the 2nd and 3rd
metacarpophalangeal joints of both hands as well as
radiocarpal joint narrowing and sclerosis on the left.
 Differential diagnosis:
Osteoarthritis
Calcium pyrophosphate deposition disease
Rheumatoid arthritis
Wilson's disease
Hemochromatosis
Diagnosis: Calcium pyrophosphate deposition
disease (CPPD)
 Calcium pyrophosphate deposition disease:
Most common in the elderly population. Rare below age
30.
Thought to be a result of enzyme mutation which regulates
pyrophosphate. Aging cartilage predisposes to deposition
due to matrix changes.-Also known as pseudogout
Often associated with chondrocalcinosis of the hyaline or
fibrocartilage
Calcification components include pyrophosphate, calcium
hydroxyapatite, or dicalcium phosphate dihydrate crystals
 Imaging findings:
Usually symmetric
Cartilage narrowing, sclerosis, subchondral
cysts, normal bone density
Chondrocalcinosis of the knee menisci,
symphysis pubis, and carpal triangular
fibrocartilage seen often but not required
 Knee:
Triangular shape in menisci
Patellofemoral compartment predominant
narrowing and osteophytes
Hand and wrist:
Triangular or amorphous shape in TFCC
(triangular fibrocartilage complex)
Hook-like osteophytes are the metacarpal heads
2nd and 3rd metacarpal predominant
Scapholunate advanced collapse is common
 Other joints far less common; however,
disease will be symmetric within the joint as
well as across the body.
CPPD can be superimposed on other
processes such as osteoarthritis.
Elderly man with failure to
thrive.
 Findings: Concentric mural thickening of
a long segment of distal sigmoid and
proximal rectum with surrounding soft
tissue stranding and lymph nodes.
Multiple hypoattenuating liver masses.
 Differential diagnosis:
Colon cancer with liver metastases
Colitis (infectious, inflammatory)
Diverticulitis
Nondistended colon
Diagnosis: Colorectal cancer with liver
metastases
 Colon cancer is the most common
malignancy of the GI tract and 2nd most
common cancer mortality. There are
approximately 147,000 new cases of colon
cancer diagnosed each year in the U.S., of
which around 106,000 are colon and the
remainder rectal. Approximately 50,000
Americans die each year of colorectal
cancer.
 Many patients are asymptomatic at
presentation. Symptoms in order of
frequency are: change in bowel habit,
abdominal pain, hematochezia or melena,
weakness, anemia, weight loss. 20% of
patients have distant metastatic disease at
presentation. Synchronous cancer is seen
in 2-5% of patients.
 Risk factors include: low fiber/high fat and
animal protein diet, history of colon
cancer, benign polyps over 1cm, IBD,
family history, colon cancer in first-degree
relative (increases risk 2-3 fold), FAP,
Gardners, HNPCC
 Greater than 95% are adenocarcinoma.
Benign adenoma takes 7-10 years to
become malignant.
IBD inflammation can lead to dysplasia
and malignancy.
HNPCC is AD with high penetrance.
Lynch syndrome- (HNPCC or Hereditary
nonpolyposis colorectal cancer )
 Spread by lymphatic or hematogeneous
route or contiguous spread. First site of
metastases usually the liver because
venous drainage of GI tract to portal system,
then lungs, bone, and even brain. Distal
rectal cancer can go to lungs first because
the inferior rectal vein drains to the IVC.
Synchronous colorectal cancer in 2-5% of
patients
 Screening for average risk patient starts at
age 50:
Colonoscopy every 10 years
Computed tomographic colonography every
five years
Flexible sigmoidoscopy (FS) every five years
Double contrast BE every five years
 People who have one first-degree relative
with colorectal cancer or adenomatous
polyps at a young age (before the age of 60
years), or two first-degree relatives
diagnosed at any age, should begin
screening for colon cancer earlier, typically at
age 40, or 10 years younger than the earliest
diagnosis in their family, whichever comes
first. Screening repeated every five years.
 If find polyp, recommendations for surveillance,
depend on pathology of the polyp. Polyps >6mm
should be biopsied
Surgical resection is treatment of choice for
localized disease.
Select cases require pre and post-op
chemotherapy.
CT: Follow-up 3-4 months after surgery, then every
6 months for 2-3 years, then annually for 5 years
 CEA titer: If elevated, CT is indicated
PET-CT is best for recurrence and
surveillance
Metachronous tumors arise in 1.5-3% in
first 5 years post-op and in 9% within
several decades.
 CT colonography:
Technique: Requires same bowel prep as use for
BE or colonoscopy. Requires hand pumping air
into the colon or using a machine to pump CO2
into the colon. Scan patients prone without
contrast and then supine with IV contrast.
Sagittal and coronal reformats.
Utility is being debated. Some insurance
companies will reimburse.
Can detect polyp size greater than 6-10mm
 Benefits:
In 5% of patients can't pass colonoscope through bowel.
Colonoscopy fails to reach full length of colon in 10% of
patients.
Lower risk of perforating the colon than conventional
colonoscopy.
Most of those examined do not have polyps, and can be
spared having to undergo a full colonoscopy.
Alternative for patients who have clinical factors that increase
the risk of complications from colonoscopy.
Sedation and pain-relievers are not needed, so there is no
recovery period.
Less costly than colonoscopy.
 Local expertise varies.
Sensitivity has been variable
The methods of performing and interpreting virtual
colonoscopy have not been standardized.
The size of a polyp found on CT colonoscopy that
should prompt colonoscopy is unclear. Some use 6
mm as cutoff. If have positive result, may have to
undergo two bowel preparations and two procedures.
Potential to uncover unexpected findings outside of
the colon, potentially leading to unnecessary
evaluation of incidental findings
 CT:
Short segment asymmetric mural thickening
and irregular surface.
Wall thickness >6mm (3-6mm indeterminate).
Tumor seen in lumen.
Extra colonic tumor extension.
Loss of fat planes between colon and
surrounding muscles.
Metastatic disease to nodes, liver, etc.
 Advanced cancer may have annular,
semiannular, polypoid or carpet appearance.
Use in staging cancer and follow-up. If CEA
level elevated post-op, need CT. Follow-up CT
3-4 months after surgery and then every 6
months for 2-3 years, then annually for 5 years.
Location: Cecum (10%); ascending colon
(15%); transverse colon (15%); descending
colon (5%); sigmoid colon (25%); rectosigmoid
colon (10%); rectum (20%)
 "Apple core" lesion highly concerning for
colon cancer.
CT colonography as surveillance tool is
debatable but becoming more utilized and
now reimbursed by several insurance
companies. Most useful in patients with
failed colonoscopy or who have
contraindications for colonoscopy.
20% of patients have distant metastases
 First site of metastases usually the liver
because venous drainage of GI tract to
portal system, then lungs, bone, and even
brain. Distal rectal cancer can go to lungs
first because the inferior rectal vein drains to
the IVC.
Up to 5% of patients have synchronous
tumors.
Sigmoid colon most common location
Teenage male with enlarging left
groin mass.
 Findings: Ultrasound demonstrates a
large mass with a heterogenous smaller
solid component and larger cystic
component. CT localizer demonstrates
large heterogeneous mass within the left
scrotum. There is a highly vascular
enhancing solid component. Left periaortic
retroperitoneal adenopathy.
 Differential diagnosis:
Sarcoma
Paratesticular embryonal rhabdomyosarcoma
Other sarcoma (leiomyosarcoma or liposarcoma)
Adenomatoid tumor of epididymis
Lymphoma
Diagnosis: Paratesticular embryonal
rhabdomyosarcoma
 The prevalence of scrotal tumors is estimated at
0.5-2.0 cases per 100,000 boys.
Ultrasound is the first line test of evaluating with
excellent sensitivity. It is also able to characterize
tissues and location.
CT is reserved for staging and studying spread of
disease.
MR can be helpful for further tissue
characterization and better delineation of the
borders of extratesticular masses.
 Levels of alpha fetoprotein and human
chorionic gonadotropin should also be
obtained for more precision in diagnosis.
Paratesticular refers to a group of
extratesticular tumors that are not easily
identified as originating from a particular
tissue
 The most frequent extratesticular tumor is
paratesticular embryonal rhabdomyosarcoma.
This mass originates in the spermatic cord or
scrotal tunics.
The majority occurs in the first two decades of life.
US usually demonstrates a hypo or hyper echoic
solid mass that may invade the adjacent
epididymis and testis. Hypervascularity is also
usually present