nd

2
Sign Tear ACL :
1.Kissing contusion
6.Uncovered posterior horn of latral meniscus
2.Segond fracture
7.Deep lateral femoral notch
3.ACL avulsion fractur
Segond fracture : eliptic fragment of bone
adjacent to the lateral tibial plateu with cortical
irregularity tibal plateau
4.Anterior tibial translation
Distance Postrior cortex tibial plateu with Postrior
cortex lateral fe moral condyle > 7,66 mm
5.Buckling PCL
Posterosuperior border is concave
st
1
Sign Tear ACL :
Sign Tear PCL :
Complete fiber disruption
Complete rupture : continuity
disruption
Abnormal course of cruciate ligament
Incapsular pseudomass in positions of ACL Partial ruptured : Confined areas of
increased signal intensity along course
ligament

clavicle
Coroid process

sub scapularis

seratus anterior

Tendon bicep brachii

Brachii plexus

Coracobrachialis

A/ N Suprascapular

tendon musc biceps brachii

glenohumeral joint
tendon musc biceps brachii

Trapezius

Spne of scapula

inferior glenoid labrum

superior

glenoid labrum
Scapula
acromion
1.
2.
3.
4.
5.
6.

Anterior labrum
Sub scapularis
Infraspinatus
Posterior labrum
Humerus
Glenoid cavity

clavicula

acromion

lig coracoacromialis

Gleno/coracohumeral lig

bicep tendon

A/V anterior circumflex humeral

tricep brachii

coracoid

deltoid

supraspinatus

teres minor

clavicula

teres minor

infraspinatus
latisimus dorsi

Sindrom shoulder impingement :

1. std I : < 25 th, edema & hemorrhage

teres major

2. std II : 25 40 th, tenditis & fibrosis rotator cuff, thickening of sub acromial
bursa
3. Std III : > 40 th, = tear

TUBERCULAR SPONDYLITIS
1.Long standing history of months to years
2.Presence of active pulmonary tuberculosis -60%
3.Most common location thoracic spine followed by thoraco-lumbar
region.
4.> 3 contiguous vertebral body involvement common- 42%.
5.Vertebral collapse - 67%. Bone destruction : 73%
6.Posterior elements involvement common
7.Skip lesions common
8.Disc is involved with less frequency and severity. Disc spared in
central type TB.
9.Paraspinal and epidural abscesses- 60%
10. large involving many contiguous vertebral bodies level.
11. Smooth rim enhancement -74%
PYOGENIC
1. History of days to months.
2. Not present of active pulmonary tuberculosis.
3.Most common location lumbar spine.
4. Vertebral collapse 19% only. Mostly involves 1 spinal segment
2vertebrae & intervening disc.
5.Disc destruction is most often seen in pyogenic osteomyelitis.
6.Heterogenous enhancement. Thick irregular Rim enhancement only 9%
cases.

Central canal and lateral recess narrowing. Axial T2-weighted image shows significant narrowing of the
central canal (arrow head) & lateral recesses which is in part due to ligamentum flavum hypertrophy
(stars) and in part due to facet hypertrophy with additional fluid present in the facets (arrows).

Dr. Rosi
Aneurysmal bone cyst

benign expansile tumour-like bone lesions, 80% occurring in the patients less than 20 years of
age
eccentrically located in the metaphysis of long bones, adjacent to an unfused growth plate.
Although they have been described in most bones, the most common locations are

long bones: 50-60%, metaphysis

o lower limb: 40%

tibia and fibula: 24%, especially proximal tibia

femur: 13%, especially proximally

o upper limb: 20%

spine: 20-30%
o especially posterior elements, with extension into vertebral body in 40% of cases

sacrum

intrinsical
ly have fluid-fluid levels (thus see fluid-fluid level containing bone lesions)

DD GCT

narrow zone of transition: a broader zone of transition is seen in more aggressive

GCTs

no surrounding sclerosis: 80-85%

overlying cortex is thinned, expanded or deficient

periosteal reaction is only seen in 10-30% of cases

soft tissue mass is not infrequent

pathological fracture may be present

no matrix calcification/mineralisation

MRI

T1:
o low to intermediate solid component
o low signal periphery
o solid components enhance, helping distinguish GCT with ABC from pure ABC 3-4
o some enhancement may also be seen in adjacent bone marrow

T2:
o low signal intensity (variable) 9
o if an ABC component present, then fluid-fluid levels can be seen
o high signal in adjacent bone marrow thought to represent inflammatory oedema 4
T1 C+ (Gd): solid components will enhance, helping differentiate from ABCs

Infark tromboemboli : Etiologi , patogenesa, prediliksi tempat, gbr MRI ( mgp mbtk
wedge shaped )
-

Ischemia

Stroke hemorhagic

4 major causes of hemorrhagic stroke are hypertension, hemorrhagic infarction,

hypocoagulable state, and amyloid angiopathy

DWI makes use of the variability of Brownian motion of water molecules in brain
tissue. Brownian motion refers to the random movement of molecules
Multipel sclerosis
ovoid lesion perpendicular to ventrikel ( Dawson finger)
Kriteria Mc Donal :

Dissemination in space

Dissemination in time

Periventricular
Simultaneous asimptom contrast enhancing &
Juncta cortical
non enhancing lesion at any time
Infra tentorial
Spinal cord
Dermoid cyst ovarii
MRI : Pelvic cystic structure containing fat

Dr Paulus +/- = Dr Rosi , tambahan :

- Macroadenoma
Rotator cuff tears are one of the most common causes of shoulder pain.
Clinical features

Prevalence of tear increases with age. Most significant findings are impingement and "arc of
pain" sign (pain during descent of abducted arm) 1. Supraspinatus weakness, night pain and
weakness of external rotation (seen in infraspinatus tear) are also seen.
Pathology
Aetiology

Important causes of rotator cuff tear are

trauma (acute, chronic repetitive)

subacromial impingement

tendon degeneration

hypovascularity

Specific sub types

The original Codman classification system published in 1930 was as

full thickness rotator cuff tear (FTRCT)

partial thickness rotator cuff tear (PTRCT)

o

bursal surface tear

articular surface tear (rim rent tear)

intratendinous tear

vertical, with connection from joint to bursa, not involving the whole
breath of tendon

Radiographic features

Exact features depend on the type of tear, general features include

Plain film

may show a decreased acromiohumeral interval

<6mm on true AP shoulder radiograph

<2 mm on an 'active abduction' view

may show decreased supraspinatus opacity and decreased bulk due to

atrophy, may be seen in chronic cases (on an 'outlet view')

humeral subluxation superiorly may be seen in late cases

may show features of acromial impingement -

spur formation on the undersurface of acromioclavicular joint

acromion with an inferolateral tilt (type III acromion) seen on outlet

view i.e. modified 'Y' view

secondary degenerative changes - sclerosis, subchondral cysts, osteolysis,

and notching or pitting of greater tuberosity

Ultrasound

In the hands of good radiologist, ultrasound may have up to 90% sensitivity and specificity. It
can also reveal other mimics like tendinosis, calcific tendinitis, subacromial subdeltoid bursitis,
greater tuberosity fracture and adhesive capsulitis.
Full-thickness tears extend from bursal to articular surface, while partial thickness tears are focal
defects in the tendon that involve either the bursal or articular surface. Full-thickness appear on
ultrasound as hypoechoic/anechoic defects in the tendon. Due to the fluid replacing tendon,
cartilage shadow gets accentuated giving a 'double cortex' or 'cartilage interface sign'. Also, due
to the defect, overlying peribursal fat dips down into the tendon gap, creating a 'sagging
peribursal fat' sign1.
In summary, direct signs are - non-visualization of supraspinatus tendon and hypoechoic
discontinuity in tendon. Indirect signs are - double cortex sign, sagging peribursal fat sign,
compressibility and muscle atrophy.
Secondary associated signs are - cortical irregularity of greater tuberosity, shoulder joint
effusion, fluid along biceps tendon, fluid in axillary pouch and posterior recess.
MRI

Complete tears are easier to diagnose on MRI than full-thickness tear 2 . Hyperintense signal area
within the tendon on T2W, fat-suppressed and GRE sequences, usually corresponding to fluid
signal is seen.

Partial tears are extending to either bursal or articular surface, and sometimes intrasubstance.
Retraction of tendinous fibers from the distal insertion into the greater tuberosity may also be
considered partial tear.
Complete tears extend from articular to bursal surface, most commonly in supraspinatus tendon.
Presence of tendon defect filled with fluid is most direct sign of rotator cuff tear. Tendon
retraction may also be present. Indirect signs on MRI are - subdeltoid bursal effusion, medial
dislocation of biceps, fluid along biceps tendon, and diffuse loss of peribursal fat planes. Muscle
atrophy is seen in chronic cases. Chronic tears have degenerative changes at acromioclavicular
joint, acromioclavicular joint cysts, as well as intramuscular cysts.
MR arthrography may enhance the detection of rotator cuff tears, especially complete tears.

Calcific tendinitis

Greater tuberosity fracture

Adhesive capsulitis

Konventional Chief Tigor

HPS, Symphysiolisis, Pneumothorax,Fraktur pada anak, ileus, OA( gbr &
alasan ), Pneumoperitoneum, Jenis meta ke paru, TB .. schwatrze ( alasan
terjadi ), GCT

Dr Wati :
1. EDH ,SDH
2. Stroke emboli -> teritory apa beda patofisiologi ACA & MCA dengan infark emboli
penyumbatan mendadak -> lebih buruk infark -> di distal, masih bisa bikin collateral, Tx :
thrombolitic, perlu angiografi ? ya
3. Diaphragmatic hernias
are defined as congenital or acquired defect in the diaphragm.
a. Morgagni hernias are one of the congenital diaphragmatic hernias. It is
characterised by herniation through the foramen of Morgagni which is located
immediately adjacent to the xiphoid process. As compared to the Bochdalek hernia, the

Morgagni hernia is:rare, small, anterior, at low risk of prolapse

b. Bochdalek hernia is a form of congenital diaphragmatic hernia. They occur
posteriorly and are due to a defect in the posterior attachment of the diaphragm
when there is a failure of pleuroperitoneal membrane closure in utero.
Retroperitoneal structures may prolapse through the defect,

2.groin herniation:
o

direct inguinal hernia

indirect inguinal hernia: indirect five times commoner than direct

femoral hernia

obturator hernia

3.lumbar herniation: superior and inferior

4.internal herniation: an uncommon cause of bowel obstruction

the foramen of Winslow

a hole in the mesentery

a hole in the transverse mesocolon

a defect in the broad ligament

the left paraduodenal fossa (Landzerd)

the right duodenojejunal fossa (Waldyer)

the superior ileocaecal fossa

the inferior ileocaecal fossa

the retrocaecal fossa

lesser sac hernia

anterior abdominal wall herniation:

o

Spigelian hernia

parastomal hernia

umbilical hernia

paraumbilical hernia

incisional hernia

epigastic hernia

Richter hernia: a hernia containing only one wall of a bowel loop and
therefore causing no obstruction

Littre hernia: a hernia containing a Meckel diverticulum

indirect inguinal hernia

bilateral direct inguinal H

femoral H

obturator hernia

Spigelian hernia

incisional H : on ulltrasound

incisional hernia

umbilical H : on ultrasound

Richter hernia

sliding hiatal H

hiatal and morgagni H

para-oesophageal hiatal H

Invaginasi :
Plain radiographic (supine and upright) may be unremarkable. Findings
suggestive of intussus ception include dilated loops of small bowel with or
without air-fluid levels, an airless or opaci fied right lower quadrant (see the
image below), or both. Occasionally, the intussusceptum is apparent on plain
abdominal radiography.

corcade structure (target-ring form), mostly in the right lower/midgut area. In

this case, representation of of a short segment in the right midgut, distal to
the ileocecal pole. The outer ring is a representation of the edematously
changed colon, within it the invagination from the terminal ileum with
mesenterium and a small lymph node. Proof of minimal free fluid
intraabdominally.

a. Target sign (arrow) in cross-section. b. Dilated proximal bowel and target sign (arrow).

Burst
fractures are a specific type of spine fracture in which the body of a given vertebrae breaks
into pieces. By definition a burst fracture involves the entire vertebral body (see image below).
The image below is an example of a normal lumbar spine with the vertebral bodies outlined.
Burst fractures most commonly occur at the junction between the thoracic and lumbar spine. This
junction is an area where the rigid thoracic spine gives way to the more mobile lumbar spine, and

hence is an intrinsic point of weakness. This is why most burst fractures occur between the T10
through L2 vertebrae.

Axial loading of the spine is what causes burst fractures. They typically occur after a traumatic
event involving high impact events such as car accidents or falls from significant heights. Elderly
individuals, and those with poor bone quality may suffer burst fractures after minor trauma such
as falling from a chair.
Signs and Symptoms
Burst fractures invariably present with back pain at the site of the fracture. Depending on the
exact location signs and symptoms of nerve root compression or lower spinal cord injury may
occur. If the nerves that dangle in the lumbar spine (aka: the cauda equina) get compressed by the
fragments of bone then weakness, numbness, tingling, and even bowel and bladder problems
may occur.Burst fractures between T10 and L1 can cause damage to the end of the spinal cord
(the spinal cord ends at L1 or L2 in most individuals), which can lead to lower extremity
weakness, or even paralysis, as well as bowel and bladder dysfunction.
Criteria should be strongly considered for surgical correction:

Greater than 50% vertebral body height loss.

Greater than 25 to 40 degrees of kyphosis.

Greater than 50% spinal canal compromise.

Significant posterior ligamentous injury.

Any neurological signs or symptoms referable to the injury.

If the patient fails conservative therapy with a brace.

Fahr disease, also known as familial cerebral ferrocalcinosis, is a congenital

disorder characterized by abnormal calcium deposition with subsequent atrophy

involving the basal ganglia, cerebral and cerebellar cortical regions. Both autosomal
dominant and autosomal recessive inheritance patterns have been proposed. There
is variable expressivity.
Pathology

Characterised by deposition of calcium in the walls of the capillaries and larger arteries and
veins. Other compounds, such as mucopolysaccharides, and elements, including magnesium,
zinc, aluminum, and iron have also been found deposited in the vessels.
Calcification can be found in the globus pallidus, putamen, caudate, thalamus, cerebellum
(especially dentate nucleus), corona radiata, and subcortical white matter. There is no
abnormality in calcium or phosphate metabolism.
CT

Calcification is extensive and has a fairly typical distribution 3:

basal ganglia and thalami

o

symmetric involvement of caudate, lentiform nucleus, thalamus, and

dentate nuclei

globus pallidus affected first

subcortical white matter

Bilateral calcification of the basal ganglia on neuroimaging or other brain regions, although in
isolated cases patients from families with FIBGC may not present such findings;
MRI

Depending on the degree of calcification and the stage of the disease.

T1: contrary to expectation, the calcified areas are of high signal, attributed
to the surface area of calcium crystals 4.

T2

calcified areas demonstrate low to isointense signal

high signal regions may be identified in the basal ganglia, white matter
and internal capsule which are not in the areas of calcification

CMV ventriculoencephalitis is a rare but serious potential complication of CMV

infection in immunocom promised patients. Characteristic DWI can be helpful for
the diagnosis of CMV ventriculitis, as in this case report. CMV can provoke
opportunistic
infection
and
be
fatal
in
immunocompromised
patient
Ventriculoencephalitis is the main CNS pathology because CMV tends to localise
to ependymal and subependymal regions. On MRI, it can show subependymal
signal changes along the lateral ventricles, septum pellucidum, corpus callosum and
fornices owing to the necrotic changes of ventriculitis. However, the subependymal
signal changes are hard to see on conventional T1 and T2 weighted images even
with contrast enhancement. On T1 and T2,
multiple high-signal intensity
nodular lesions in both subcortical and periventricular deep white matter,
both basal ganglia and both medial temporal lobes (Figure 1a,b). Also,
curvilinear high signal changes were detected along both lateral ventricular walls on
fluid attenuated inversion recovery (FLAIR)

Axial (a) T1 and (b) T2: mild ventricular dilatation and multiple tiny nodular T2 high-signal
intensity lesions in basal ganglia and right frontal subcortical white matter without definite
periventricular signal change. (c) Axial fluid attenuated inversion recovery image shows thin
curvilinear high-signal intensities along the walls of both lateral ventricles and multifocal faint
high-signal intensities at right frontal and basal ganglia regions. (d) Axial contrast enhanced T1 :
subtle subependymal enhancement (arrow). (e,f) DWI: striking curvilinear high-signal intensities
along the ventricular wall with a subtle low apparent diffusion coefficient value (arrow).
Balthazar score is used in CT severity index (CTSI) for grading of acute pancreatitis. CTSI
includes grading of pancreatitis (A-E) and the extent of pancreatic necrosis.
Grading of pancreatitis

A: normal pancreas: 0

B: enlargement of pancreas: 1

C: inflammatory changes in pancreas and peripancreatic fat: 2

D: ill defined single fluid collection: 3

E: two or more poorly defined fluid collections: 4

Pancreatic necrosis

none: 0

less than/equal to 30%: 2

>30-50%: 4

>50%: 6

The maximum score that can be obtained is 10.

Stratification of pancreatitis severity

mild pancreatitis (interstitial pancreatitis): Balthazar B or C , without

pancreatic or extrapancreatic necrosis

intermediate (exudative pancreatitis): Balthazar D or E, without pancreatic

necrosis; peripancreatic collections are due to extrapancreatic necrosis

severe pancreatitis (necrotising): with pancreatic necrosis

Necrosis of the pancreas, visualised best on contrast enhanced CT as non-enhancing areas, is

considered to represent severe pancreatitis.
Major risk factors for development of chronic pancreatitis may be categorised according to
the TIGAR-O system 9:

T: toxic-metabolic (e.g. alcohol)

I: idiopathic

G: genetic

A: autoimmune

R: recurrent

O: obstructive (e.g. choledocholithiasis, pancreatic head tumour)

CT features of chronic pancreatitis include:

dilatation of the main pancreatic duct

pancreatic calcification

changes in pancreatic size (i.e. atrophy), shape, and contour

pancreatic pseudocysts

Features of chronic pancreatitis can be divided into early and late findings:

early findings
o

low-signal-intensity pancreas on T1-weighted fat-suppressed images

decreased and delayed enhancement after IV contrast administration

dilated side branches

late findings
o

parenchymal atrophy or enlargement

pseudocyst formation

dilatation and beading of the pancreatic duct often with intraductal

calcifications

Ultrasound

The pancreas might appear atrophic, calcified or fibrotic. Findings that may be present on
ultrasound include:

hyperechogenicity (often diffuse) often indicates fibrotic changes

pseudocysts

pseudoaneurysms

presence of ascites

the pancreas is enlarged (either focally or diffusely) in the autoimmune type

calcifications are visible in acquired types

ERCP images, left: stones in CBD and right:

stone in cystic duct

Prof Tri :
Virchow described the classic triad of predisposing factors for DVT, namely, venous stasis,
injury of the vascular wall, and a hypercoagulable state.[6] Events or conditions that alter the equi
librium of one or more of these factors may produce DVT. Over a few months, most acute DVTs
evolve to complete or partial recanalization, and collaterals develop (see the Images below).

Lower-extremity venogram shows outlining of an acute deep venous thrombosis in the popliteal
vein with contrast enhancement.

Lower-extremity venogram shows a nonocclusive chronic thrombus. The superficial femoral

vein (lateral vein) has the appearance of 2 parallel veins, when in fact, it is 1 lumen containing a
chronic linear thrombus. Although the chronic clot is not obstructive after it recanalizes, it
effectively causes the venous valves to adhere in an open position, predisposing the patient to
reflux in the involved segment.
Takayasu arteritis is also known as "aortic arch syndrome", "nonspecific aortoarteritis" and the
"pulseless disease"[1]:841) is a form of large vessel granulomatous vasculitis[2] with massive intimal
fibrosis and vascular narrowing, affecting often young or middle-aged women of Asian descent.
It mainly affects the aorta (the main blood vessel leaving the heart) and its branches, as well as
the pulmonary arteries
a rare, systemic, inflammatory large-vessel vasculitis of unknown etiology that most commonly
affects women of childbearing age. It is defined as "granulomatous inflammation of the aorta and
its major branches" by the Chapel Hill Consensus Conference on the Nomenclature of Systemic
Vasculitis.[1] See the image below. (See Etiology and Epidemiology.)

Complete occlusion of the left common carotid artery in a 48-year-old woman with
Takayasu disease. Also note narrowing of the origin of the right subclavian artery
and a narrowed small vessel with subsequent aneurysmal dilatation on the right
side. Image courtesy of Robert Cirillo, MD.

Takayasu arteritis commonly occurs in woman younger than age 50 years and can manifest as
isolated, atypical, and/or catastrophic disease. It can involve any or all of the major organ
systems. The disease has been reported in all parts of the world, although it appears to be more
prevalent in Asians.

Pathophysiology
Takayasu arteritis is an inflammatory disease of large- and medium-sized arteries, with a
predilection for the aorta and its branches. Advanced lesions demonstrate a panarteritis with
intimal proliferation.
Lesions produced by the inflammatory process can be stenotic, occlusive, or aneurysmal. All
aneurysmal lesions may have areas of arterial narrowing. Vascular changes lead to the main
complications, including hypertension, most often due to renal artery stenosis or, more rarely,
stenosis of the suprarenal aorta; aortic insufficiency due to aortic valve involvement; pulmonary
hypertension; and aortic or arterial aneurysm.
Congestive heart failure is a common finding, much more so than dilated cardiomyopathy,
myocarditis, and pericarditis, which also have been reported. In patients in whom the pulmonary
artery is involved, the right artery appears to be affected more than the left, with patients
developing pneumonia, interstitial pulmonary fibrosis, and alveolar damage.
Other pathophysiologic consequences include hypotensive ischemic retinopathy, vertebrobasilar
ischemia, microaneurysms, carotid stenosis, hypertensive encephalopathy, and inflammatory
bowel disease. Rarely, Takayasu arteritis has also been associated with glomerulonephritis,
systemic lupus, polymyositis, polymyalgia rheumatica, rheumatoid arthritis, Still disease, and
ankylosing spondylitis.

Ex : unknown of Takayasu arteritis. The underlying pathologic process is inflammatory, with

several etiologic factors having been proposed, including spirochetes, Mycobacterium
tuberculosis, streptococcal organisms, and circulating antibodies due to an autoimmune process.
Genetic factors may play a role in the pathogenesis.
Takayasu arteritis is estimated to affect 2.6 persons per million annually. The prevalence is 2.66.4 persons per million population. Any discrepancy in terms of pinpointing the prevalence is
attributed to genetic factors and difficulty in diagnosis.
Angiography-based categories
Takayasu arteritis can be divided into the following six types based on angiographic involvement
(see Workup)[2] :

Type I - Branches of the aortic arch

Type IIa - Ascending aorta, aortic arch, and its branches

Type IIb - Type IIa region plus thoracic descending aorta

Type III - Thoracic descending aorta, abdominal aorta, renal arteries, or a

combination

Type IV - Abdominal aorta, renal arteries, or both

Type V - Entire aorta and its branches

Angiograms :Takayasu aortitis demonstrating long, smooth stenotic lesions of the left
subclavian artery and involvement of other branches of the aortic arch vessels.

A venogram is a procedure that provides X-ray visualization of the

veins, particularly in the lower extremities (legs). Contrast material,
also known as X-ray dye, is injected that is visible on X-ray. The
contrast dye allows the doctor to evaluate the size and condition of the
veins. A venogram may be used for diagnosing deep vein thrombosis
(DVT), although ultrasound is usually used for this. Venography can
also be used to diagnose other abnormalities.
Depending on the reason for the procedure, several methods can be used to examine the veins
with venography:

Ascending venography. Identifies the presence and location of DVT.

Descending venography. Assesses the function of the deep vein valves.

Venography of the upper extremities. Assesses blockage, lesions, or thrombosis in the

veins of the neck and axillary (armpit) region.

Venacavography. Evaluates the inferior vena cava, the vein that brings bloods to the
heart, for obstruction and malformation.

What is an X-ray?
X-rays use invisible electromagnetic energy beams to produce images of internal tissues, bones,
and organs on film. X-rays are made by using external radiation to produce images of the body,
its organs, and other internal structures for diagnostic purposes. X-rays pass through body
structures onto specially-treated plates (similar to camera film) and a "negative" type picture is
made (the more solid a structure is, the whiter it appears on the film).
Other related procedures that may be used to diagnose problems of the veins include vascular
studies and renal venogram. Please see these procedures for additional information.

Reasons for the procedure

A venogram is used to confirm a diagnosis of DVT and to distinguish clot formation from other
venous obstructions. It can also be used to evaluate congenital (present at birth) venous
malformations or to locate a vein for arterial bypass graft surgery. It may be used to determine
the cause of swelling or pain in the extremity and also to determine the source of pulmonary
emboli (blood clots that have traveled to the lung).

Risks of the procedure

You may want to ask your doctor about the amount of radiation used during the procedure and
the risks related to your particular situation. It is a good idea to keep a record of your past history
of radiation exposure, such as previous scans and other types of X-rays, so that you can inform
your doctor. Risks associated with radiation exposure may be related to the cumulative number
of X-ray examinations and/or treatments over a long period of time.
If you are pregnant or suspect that you may be pregnant, you should notify your health care
provider. Radiation exposure during pregnancy may lead to birth defects.
Because contrast is used, there is a risk for allergic reaction to the dye. Patients who are allergic
to or sensitive to medications, contrast dye, or iodine should notify their doctor.
Patients with kidney failure or other kidney problems should notify their doctor. In some cases,
the contrast dye can cause kidney failure, and it is especially important to let your doctor know if
you are taking Glucophage (a diabetic medication).
Notify your doctor if you have a history of bleeding disorders or if you are taking any
anticoagulant (blood-thinning) medications, aspirin, or other medications that affect blood
clotting.
For certain individuals, a venogram may be contraindicated. These include persons with a known
allergy to contrast dye, severe congestive heart failure, and severe pulmonary hypertension.

There may be other risks depending on your specific medical condition. Be sure to discuss any
concerns with your doctor prior to the procedure.
Certain factors or conditions may interfere with the accuracy of a venogram. These factors
include, but are not limited to, the following:

Ability of the patient to remain still during the procedure

Extreme obesity

Severe swelling in the legs

Before the procedure

Your doctor will explain the procedure to you and offer you the opportunity to ask any
questions that you might have about the procedure.

You will be asked to sign a consent form that gives your permission to do the test. Read
the form carefully and ask questions if something is not clear.

Notify your doctor if you have ever had a reaction to any contrast.

Notify your doctor if you are sensitive to or are allergic to any medications, latex, tape,
and anesthetic agents (local and general).

You may be asked to stop eating and/or drinking for at least four hours before the
procedure.

Notify your doctor if you are pregnant or suspect you may be pregnant.

Notify your doctor of all medications (prescribed and over-the-counter) and herbal
supplements that you are taking.

Notify your doctor if you have a history of bleeding disorders or if you are taking any
anticoagulant (blood-thinning) medications, aspirin, or other medications that affect
blood clotting. It may be necessary for you to stop these medications prior to the
procedure.

If a sedative is given before or during the procedure, you may need to have someone
drive you home afterwards.

Based on your medical condition, your doctor may request other specific preparation.

During the procedure

A venogram may be performed on an outpatient basis or as part of your stay in a hospital.
Procedures may vary depending on your condition and your doctor's practices.
Generally, the venogram follows this process:
1. You will be asked to remove your jewelry or other objects that interfere with the
procedure.
2. You will be asked to remove clothing and will be given a gown to wear.
3. A pen may be used to mark various sites of pulses on the leg before the procedure. This
will allow easier monitoring of the pulses after the procedure.
4. You will lie on your back on the X-ray table.
5. After cleansing the area, an intravenous (IV) line will be inserted into a vein in your foot.
6. An injection of contrast dye will be given. You may feel some effects when the dye is
injected into the IV line. These effects include a flushing sensation, a brief headache, or
nausea and/or vomiting. These effects usually last for a few moments. Also, let the doctor
know if you are having difficulty breathing, itching of the skin, or hives.
7. X-rays will be taken at timed intervals as the dye travels through the lower extremities.
8. A tourniquet may be placed on the extremity to control the speed of blood flow.
9. The intravenous site will be flushed with heparin/saline solution, and the needle will be
removed from the vein.
10. A pressure dressing will be placed over the puncture site.

After the procedure

Following the procedure, your vital signs (heart rate, breathing rate, and blood pressure) will be
monitored frequently and then at intervals determined by your doctor. The peripheral pulses in
your feet, as well as the temperature, color, and sensation in your legs will be checked. The
injection site will also be monitored for redness, warmth, swelling, and tenderness.
Normal activities and diet can be resumed after the procedure as directed by your doctor.
Drink plenty of fluids to prevent dehydration and to help pass the contrast dye.
Notify your doctor to report any of the following:

Fever or chills

Increased pain, redness, swelling, or bleeding or other drainage from the injection site

Your doctor may give you additional or alternate instructions after the procedure, depending on
your particular situation.
Renal angiomyolipomas (AMLs) are a type of benign renal neoplasm and are composed of
vascular, smooth muscle and fat elements. They can spontaneously haemorrhage, which can be
fatal. AMLs usually have characteristic radiographic appearances.
Epidemiology

The majority of angiomyolipomas are sporadic (80%) and are typically identified in adults (mean
age of presentation 43 years), with a strong female predilection (F:M of 4:1) 7,9.
The remaining 20% are seen in association with phakomatoses, the vast majority in the setting of
tuberous sclerosis, although they have also been described in setting of Von Hippel-Lindau
syndrome (VHL) and neurofibromatosis type 1 (NF1) 5,7. In these cases they present earlier
(usually identified by the age of 10 years), are larger, and are far more numerous. They are more
likely to be fat-poor which accounts for their earlier presentation 2,6-7.
Clinical presentation

Angiomyolipomas are often found incidentally when the kidneys are imaged for other reasons, or
as part of screening in patients with tuberous sclerosis.
Symptomatic presentation is most frequently with spontaneous retroperitoneal haemorrhage;
the risk of bleeding being proportional to the size of the lesion (>4 cm diameter). Shock due to
severe haemorrhage from rupture is described as Wunderlich syndrome 4-5,7.
Patients may present with numerous other symptoms and signs 2, e.g. palpable
mass, flank pain, urinary tract infections, haematuria, renal failure, or hypertension 3.
Pathology

Angiomyolipomas are members of the perivascular epithelioid cells tumour group (PEComas)
and are composed of variable amounts of three components; blood vessels (-angio), plump
spindle cells (-myo) and adipose tissue (-lipo). Almost all classic angiomyolipomas are benign
but they do have the risk of rupture with bleeding or secondary damage/destruction of
surrounding structures as they grow.
Variants

There is a special variant called an epithelioid angiomyolipoma, composed of more plump,

epithelial looking cells, often with nuclear atypia, that have a described risk of malignant
behaviour. This variant, unlike conventional AMLs, may mimic renal cell carcinoma. 10
Metastases have also been described 9.

Radiographic features

The cornerstone of diagnosis on all modalities is the demonstration of macroscopic fat, however
in the setting of haemorrhage, or when lesions happen to contain little fat, it may be difficult to
distinguish an AML from a renal cell carcinoma.
Ultrasound

tend to appear as hyperechoic lesions on ultrasound, located in the cortex

and with posterior acoustic shadowing

in the setting of tuberous sclerosis, they may be so numerous that the entire
kidney is affected, appearing echogenic with loss of normal cortico-medullary
differentiation 7

contrast-enhanced ultrasound

12

tend to enhance peripherally

decreased central enhancement, compared with normal cortex

CT

Most lesions involve the cortex and demonstrate macroscopic fat (less than -20 HU). When
small, volume averaging may make differentiation from a small cyst difficult.
It is important to realise that a proportion of angiomyolipomas are fat-poor. This is especially the
case in the setting of tuberous sclerosis, where up to a third do not demonstrate macroscopic fat
on CT 6. Calcification is rare.

Angiomyolipoma

Angiomyolipoma in both kidneys (arrows) in

computer tomography. The tumours are hypodense
(dark) due to fat content

MRI

MRI is excellent at evaluating fat containing lesions, and two main set of sequences are
employed. Firstly, and traditionally if you will, fat saturated techniques demonstrate high signal
intensity on non-fat saturated sequences, and loss of signal following fat saturation.
The second method is to use in and out of phase imaging which generates India ink artifact at the
interface between fat and non-fat components. This can occur either at the interface between the
angiomyolipoma and surrounding kidney or between fat and non-fat components of the mass 8.
It is essential to remember that rarely renal cell carcinomas may have macroscopic fat
components and as such the presence of fat is strongly indicative of an angiomyolipoma, but not
pathognomonic. Since macroscopic fat in RCC almost always occurs in the presence of
ossification/calcification, absence of ossification/calcification on imaging is in favour of AML.
DSA - angiography

Angiomyolipomas are hypervascular lesions demonstrating often characteristic features:

micro- or macro-aneurysms

sharply marginated

dense early arterial network

late whorled appearance

absent AV shunting

Treatment and prognosis

Angiomyolipomas found incidentally usually require no therapy (when small), although followup is recommended to assess for growth. Small solitary AMLs (< 20 mm) probably do not
require follow-up due to their slow growth 13.
Larger AMLs, or those that have been symptomatic, can be electively embolised and/or resected
with a partial nephrectomy.
Lesions that present with retroperitoneal haemorrhage often requires emergency embolisation as
a life saving measure.
Differential diagnosis

retroperitoneal liposarcoma invading the kidney

adrenal myelolipoma

renal cell carcinoma (RCC)

may contain fat: lipid necrosis or osseous metaplasia

oncocytoma: may contain fat

Wilms tumour: may contain fat

perirenal fat entrapment / renal junctional parenchymal defect

11

Chief Dr Sugeng
USG : deskripsi per organ yg perlu dilaporkan( upper/ lower abdomen/
small part / mamma/ kepala bayi
X Ray : CIL : colitis , massa colon
HSG : deskripsi apa saja
Tumor tulang : gambarannya
Pembagian lung edema & gambarannya
CT : Tumor otak/ KNF / Tumor usus

MRI : Tumor otak jinak & ganas , Infeksi otak, HNP, Tumor tulang

Chief Dr Leni
Thorax & CT : Achalasia
Richetsia ( konventional )
CIL : naphkin ring di rectumTumor rectum
Round pneumonia ( thorax anakpatofisiologi )
Hernia DD eventerasio ( thorax )
MRI
MRCP : atresia bilier
Sturge weber, Atrophy brain,MRA : anatomi, Cholangio Ca , Ca caput
pancreas, Lipocele di spine , ICH, IVH, Macroadenoma
CT : Pankreatitis ( balthazar )
Chief Dr Pri
Konventional : Pneumomediastinum, TB, Pneumoperitoneum,
Volvulus ( & KONTRAS) Hirsprung , MAR ( knee projection ), ,
Ct : HPS, Colitis, Chron disease, SDH, ICH, LNH ( lihat sekitar

pancreas ), Intususepsi & massa di colon desceneden, massa colon

descendend, Apendisitis , hypofise macroadenoma, Trauma ginjal
(AST ), AVF pada a. renalis ( & tindakannnya), Meta di tulang