Vascular Flashcards
Thoracic Aorta
overview
The thoracic aorta is divided anatomically into four regions; the root, the ascending aorta,
the transverse aorta (arch), and the descending aorta. The “root” is defined as the portion of the aorta
extending from the aortic valve annulus to the sino-tubular junction. The diameter of the thoracic
aorta is largest at the aortic root and gradually decreases (average size is 3.6 cm at the root, 2.4 cm in
the distal descending).
Thoracic Aorta
sinuses of valsalva
There are 3 outpouchings (right,
left, posterior) above the annulus that terminate at the
ST Junction. The right and left coronaries come off the
right and left sinuses. The posterior cusp is sometimes
called the “non-coronary cusp.”
Thoracic Aorta
isthmus
The segment of the aorta between the origin of the left Subclavian and the ligamentum arteriosum.
Thoracic Aorta
ductus bump
Just distal to the isthmus is a contour
bulge along the lesser curvature, which is a normal structure (not a pseudoaneurysm).
Aortic Arch Variants
bovine arch
left common carotid coming off
the brachiocephalic proper
(10%)
Aortic Arch Variants
left CC off brachiocephalic
Bovine Arch
( 15%) - common origin of
brachiocephalic artery and left
common carotid artery
Aortic Arch Variants
separate origins
5% of people
the left vertebral artery
originates separately from the
arch.
Pulmonary Sling
Aberrant Left pulmonary artery coming off the
right pulmonary artery.
-Unique as the only anomaly to create indentations in the posterior
trachea and anterior esophagus.
-Unique as the only anomaly that can cause stridor in a patient with
a normal left sided arch.
Adamkiewicz
The thoracic aorta puts off multiple
important feeders including the great
anterior medullary artery (Artery of
Adamkiewicz) which serves as a dominate feeder of the spinal cord.
This thing usually comes off on the left side (70%) between T9-T12.
“Beware o f the Hairpin Turn”
-The classic angiographic appearance of the artery is the “hairpin turn” as its anastomosis with the anterior spinal artery.
Mesenteric Branches
overview
The anatomy of the SMA and IMA is high yield, and can be shown on a MIP coronal CT, or Angiogram. I think that knowing the inferior pancreaticoduodenal
comes off the SMA first, and that the left colic (from IMA) to the middle colic (from SMA) make up the Arc of Riolan are probably the highest yield facts.
Celiac Branches
The classic branches of the celiac axis are the common hepatic, left gastric, and the splenic arteries.
The “common” hepatic artery becomes the “proper” hepatic artery after the GDA.
This “traditional anatomy” is actually only seen in 55% of people.
V a r ia n t H e p a tic A r te ry A n a tom y
overview
The right hepatic artery and left hepatic arteries
may be “replaced” (originate from a vessel other than the proper hepatic) or duplicated -
which anatomist called “accessory.” This distinction o f “replaced” vs “accessory” would
make a great multiple choice question.
- Replaced = Different Origin, usually off the left gastric or SMA
- Accessory = Duplication o f the Vessel, with the spare coming o ff the left gastric or SMA
V a r ia n t H e p a tic A r te ry A n a tom y
thinkgs to know
• If you see a vessel in the fissure of the Iigamentum venosum (where there is not normally a vessel), it’s probably an accessory or replaced left hepatic artery arising from the left gastric artery. • The proper right hepatic artery is anterior to the right portal vein, whereas the replaced right hepatic artery is posterior to the main portal vein. This positioning o f the replaced right increases the risk o f injury in pancreatic surgeries.
Ilia c A na tom y
The branches o f the internal iliac are high yield, with the most likely
question being “which branches are from the posterior or anterior divisions?” A useful mnemonic is “I Love Sex, ” Illiolumbar, Lateral Sacral, Superior Gluteal, for the posterior
division.
My trick for remembering that the mnemonic is for posterior and not anterior is to think o f
that super religious girl I knew in college — 1 Like Sex in the butt / posterior.
ovarian artery trivia
The ovarian arteries arise from the anterior-medial aorta 80-90% o f time.
Anterior division of internal iliac artery mnemonic
courses posteromedially
I love going places in my very own underwear
iliolumbar -posterior lateral sacral - posterior gluteal (superior and inferior) -posterior pudendal (internal) inferior veiscal (vaginal in females) middle rectal artery vaginal artery obturator umbilical arter and uterine artery (females)
Divisions of the internal iliac superior to inferior
posterior
iliolumbar
lateral sacral
superior gluteal
anterior umbilical (superior vesical comes off) inferior vesicle obturator (runs through obturator foramen) uterine middle rectal internal pudendal inferior gluteal
P e rs is te n t S c ia tic A r te r y
An anatomic variant, which is a continuation o f the
internal iliac. It passes posterior to the femur in the thigh and then will anastomose with the
distal vasculature. Complications worth knowing include aneurysm formation and early
atherosclerosis in the vessel. The classic vascular surgery boards question is “external iliac is
acutely occluded, but there is still a strong pulse in the foot” , the answer is the patient has a
persistent sciatic.
Mesenteric Arterial Collateral Pathways
celiac to SMA
The conventional collateral pathway is Celiac -> Common Hepatic -> GDA -> Superior Pancreatic Duodenal -> Inferior Pancreatic Duodenal -> SMA.
Arc ofBuhler: This is a variant anatomy (seen in like 4% o f people), that represents a collateral pathway from the celiac to the SMA. The arch is independent o f the GDA and inferior pancreatic arteries. This rare collateral can have an even more rare aneurysm, which occurs in association with stenosis o f the celiac axis.
Mesenteric Arterial Collateral Pathways
IMA to llia c s
The conventional collateral pathway is IMA -> Superior Rectal -> Inferior Rectal -> Internal Pudendal -> Anterior branch o f internal iliac
Mesenteric Arterial Collateral Pathways
SMA to IMA
The conventional collateral pathway is SMA -> Middle Colic -> Left Branch o f the Middle Colic -> Arc o f Riolan (as below) -> Left Colic - > IMA.
Arc o f Riolan - Also referred to as the
meandering mesenteric artery. Classically a connection between the middle colic o f the SMA and the left colic o f the IMA.
Marginal Artery’ o f Drummond - This is another SMA to IMA connection. The
anastomosis o f the terminal branches o f the ileocolic, right colic and middle colic arteries o f the SMA, and o f the left colic and sigmoid branches o f the IMA, form a continuous arterial circle or arcade along the inner border o f the colon.
Mesenteric Arterial Collateral Pathways
winslow pathway
This is a collateral pathway that is seen in the setting o f aorto-iliac
occlusive disease. The pathway apparently can be inadvertently cut during transverse
abdominal surgery. The pathway runs from subclavian arteries -> internal thoracic (mammary)
arteries -> superior epigastric arteries -> inferior epigastric arteries -> external iliac arteries.
Mesenteric Arterial Collateral Pathways
corona mortis
Classically described as a vascular connection between the obturator
and external iliac. Some authors describe additional anastomotic pathways, but you should
basically think o f it as any vessel coursing over the superior pubic rim, regardless o f the
anastomotic connection. The “crown o f death” is significant because it can (a) be injured in
pelvic trauma or (b) be injured during surgery - and is notoriously difficult to ligate.
Some authors report that it causes 6-8% o f deaths in pelvic trauma. The last piece o f trivia is
that it could hypothetically cause a type 2 endoleak.
Upper Extremity Anatomy
overview
The scalene muscles make a triangle in the neck. If you have ever had the pleasure of reading a
brachial plexus MRI finding this anatomy in a sagittal plane is the best place to start (in my
opinion). The relationship to notice (because it’s testable) is that the subclavian vein runs anterior to
the triangle, and the subclavian artery runs in the triangle (with the brachial plexus).
Upper Extremity Anatomy
tribia
The subclavian artery runs posterior to the subclavian vein.
The subclavian artery has several major branches
the vertebral, the internal thoracic, the
thyrocervical trunk, the costocervical trunk, and the dorsal scapular
Subclavian name changes
- Axillary Artery: Begins at the first rib
- Brachial Artery: Begins at the lower border of the teres major (major NOT minor!)
- Brachial Artery: Bifurcates to the ulnar and radial
H o w T o T e ll T h e U ln a r F rom T h e R a d ia l A r t e r y On A n g io g r am O r CTA:
Around the radial head the brachial artery splits into the radial and ulnar arteries. I have three tricks for telling the radial from the ulnar artery apart (in case it’s not obvious).
- The ulnar artery is usually bigger.
- The ulnar artery usually gives o ff the common interosseous
- The ulnar artery supplies the superficial palmar arch (usually), and therefore the radial supplies the deep arch (usually).
Upper Extremity Normal Variants
- Anterior Interosseous Branch (Median Artery) persists and supplies the deep palmar arch o f the hand.
- “High Origin o f the Radial Artery” - Radial artery comes o ff either the axillary or high brachial artery (remember it normally comes off at the level of the radial head).
lower Extremity Anatomy
femoral
The nomenclature pearl for the external iliac is that it becomes the common femoral once it gives off the inferior epigastric (at the inguinal ligament). Once the inferior epigastric comes o ff (level o f the inguinal ligament) you are dealing with the common femoral artery(CFA). The CFA divides into the deep femoral (profunda) and
superficial femoral. The deep femoral courses lateral and posterior. The superficial femoral
passes anterior and medial into the flexor muscle compartment (ADDuctor / Hunter’s Canal).
At the point the vessel emerges from the canal it is then the popliteal artery
lower Extremity Anatomy
popliteal
At the level o f
the distal border o f the popliteus muscle the popliteal artery divides into the anterior tibialis
(the first branch) and the tibioperoneal trunk. The anterior tibialis courses anterior and
lateral, then it transverses the interosseous membrane, running down the front o f the anterior
tibia and terminating as the dorsalis pedis.The tibioperoneal trunk bifurcates into the
posterior tibialis and fibular (peroneal) arteries.
A common quiz is “what is the most medial
artery in the leg?”
with the answer being the posterior tibial (felt at the medial malleolus).
G a s tric V a ric e s
As described in more detail in the GI chapter, portal hypertension
shunts blood away from the liver and into the systemic venous system. Spontaneous portalsystemic
collaterals develop to decompress the system. The thing to know is that most
gastric varices are formed by the left gastric (coronary v e in ) . That is the one they
always show big and dilated on an angiogram. Isolated gastric varices are secondary to
splenic vein thrombosis. Gastric Varices (80-85%) drain into the inferior phrenic and then
into the left renal vein, forming a gastro-renal shunt.
Left Gastric
(Coronary) drains
cardia
Posterior and Short
Gastric
fundus
S p len o re n a l Shunt
Another feature o f portal hypertension, this is an abnormal
collateral between the splenic vein and renal vein. This is actually a desirable shunt because
it is not associated with GI bleeding. However, enlarged shunts are associated with
hepatic encephalopathy (discussed in greater detail in the BRTO section o f the IR chapter).
A common way to show this is an enlarged left renal vein and dilatation o f the inferior vena
cava at the level o f the left renal vein.
L e ft S id ed SVC
overview
- Most commonly associated CHD is the ASD
- Associated with an unroofed coronary sinus
- Nearly always (92% o f the time) it drains into the coronary sinus
L e ft S id ed SVC
trivia
- Most commonly associated CHD is the ASD
- Associated with an unroofed coronary sinus
- Nearly always (92% o f the time) it drains into the coronary sinus
D u p lic a te d SVC
“Left Sided SVC” almost never occurs in
isolation. Instead, there is almost always a “normal” right sided SVC, in addition to the left
sided SVC. It is in this case (which is the majority o f cases o f left sided SVC) that the
terminology “duplicated SVC” is used. It is so common that people will use the terms
duplicated and left sided interchangeably. But, technically to be duplicated you need a right
sided and left sided SVC (even if the right one is a little small - which is often the case in the
setting o f a left SVC).
D u p lic a te d IVC
There are two main points
worth knowing about this: (1) that the appearance
is an Aunt Minnie, and (2) it’s associated with
Renal stuff. Renal associations include
horseshoe and crossed fused ectopic kidneys.
Also these dudes often have circumaortic renal
collars
Duplicated IVC
aunt minnie
(IVCs are the bread, Aorta is the cheese or peanut butter…or bacon)
C irc um a o rtic Venou s C o lla r
Very common variant with an additional left renal
vein that passes posterior to the aorta. It only matters in two situations (a) renal transplant,
(b) IVC filter placement. The classic question is that the anterior limb is superior, and the
posterior limb is inferior.
C irc um a o rtic Venou s C o lla r
superior slice
renal vein is anterior to aorta
C irc um a o rtic Venou s C o lla r
inferior
Renal vein is posterior to aorta
Azygos C o n tin u a tio n
This is also known as absence o f the hepatic segment o f the
IVC. In this case, the hepatic veins drain directly into the right atrium. Often the IVC is
duplicated in these patients, with the left IVC terminating in the left renal vein , which then
crosses over to join the right IVC.
The first thing you should think when I say azygous continuation
is polysplenia (reversed IVC/Aorta is more commonly associated with asplenia).
Azygos Continuation
quick
No IVC in the Liver, Dila ted A z y g o s in the C h e s t
There are 3 “acute aortic syndromes”
aortic dissection,
intramural hematoma, and penetrating ulcer.
3 layers of aorta internal to external
intima
media
externa
Penetrating Ulcer
classification
3 AASs can be classified as type A or B Stanford, based on their locations before (type A) or after the takeoff the o f the left subclavian (type B).
1 risk factor
Penetrating Ulcer
Atherosclerosis
Delicious Burger King and Tasty Cigarettes
Penetrating Ulcer
classic scenario
Elderly patient with hypertension and
atherosclerosis usually involving the descending thoracic aorta
Penetrating Ulcer
genesis
Eating like a pig and smoking results in
atherosclerosis. Nasty atherosclerotic plaque erodes
through the intima. Hematoma forms in the media (intramural
hematoma). With severe disease can eventually
progress to a pseudo aneurysm (and maybe even rupture)
Penetrating Ulcer
pearl
3 AASs can be classified as type A or B Stanford, based on their locations before (type A) or after the takeoff the o f the left subclavian (type B).
Penetrating Ulcer
saccular morphology
These things often result in a saccular morphology around the arch. In general, sac like aneurysm above the diaphragm is related to penetrating ulcer. Sac like aneurysm below the diaphragm is gonna be septic (“mycotic”).
R e la tio n sh ip b e tw e e n P e n e tra tin g U lc e r and D is s e c tio n :
—Controversial (which usually means it won’t he tested) - famous last words
If forced to answer questions on this relationship, 1 would go with the following:
• Penetrating Ulcers are caused by atherosclerosis (this is a fact)
• Penetrating Ulcer can lead to Dissection (this is probably true in some cases)
• Atherosclerosis does NOT cause Dissection (which is confusing, may or may not be true,
and is unlikely to be tested). What is true is that the presence o f dense calcified plaque can
stop extension o f a dissection tear.
• Dissections often occur in the aortic root - where you have the highest flow pressures
• Penetrating Ulcers nearly never occur in the root - as these flow pressures prevent
atherosclerosis (wash those cheeseburger crumbs away).
T re a tm e n t o f P e n e tra tin g U lc e r ?
medical
Similar to Type B Dissections. If they do get treated (grafted e tc …) they tend
to do WORSE than dissections (on average)
T re a tm e n t o f P e n e tra tin g U lc e r ?
when are they surgical
Hemodynamic instability, Pain, Rupture, Distal Emboli, Rapid Enlargement
Dissection
overview
- The most common cause o f acute aortic syndrome (70%)
- Hypertension is the main factor - leads to an intimal tear resulting in two lumens
- Marfans, Turners, and other Connective Tissue Diseases increase risk
Dissection
classic testable scenarios
- Pregnancy — known to increase risk
- Cocaine Use in a young otherwise healthy person
- Patient with “Hypertension” and a sub-sternal “Tearing Sensation.”
Dissection
chicken vs egg
Some people say that hypertensive pressures kill the vasa vasorum (the
little vessels inside the vessel walls) leading to development o f intramural hematoma which
then ruptures into the intima. This is the “inside out” thinking. Other people think the
hypertensive forces tear the inner layer directly (“outside in” thinking).
Honestly… who gives a shit? Not even sure why I mentioned that.
Dissection
classifications
1) Time: Acute (< 2 weeks), or Chronic
(2) Location:
• Stanford A: Account for 75% of dissections and involves the ascending aorta and arch proximal
to the take-off of the left subclavian. These guys need to be treated surgically.
• Stanford B: Occur distal to the take-off of the left subclavian and arc treated medically unless
there are complications (organ ischemia etc…)
Dissection
true lumen
Continuity with
undissected portion of
aorta
Smaller cross sectional
areas (with higher velocity
blood)
Surrounded by
calcifications (if present)
Usually contains the origin
of celiac trunk, SMA, and
RIGHT renal artery
Dissection
false lumen
“CobWeb Sign” - slender
linear areas of low
attenuation
Larger cross section area
(slower more turbulent
flow)
Beak Sign - acute angle at
edge of lumen - seen on
axial plane
Usually contains the origin
of LEFT renal artery
Surrounds true lumen in
Type A Dissection
Dissection
floating viscera sign
This is a classic angiographic sign of abdominal aortic dissection.
It is shown as opacification of abdominal aortic branch vessels during aortography (catheter placed in the aortic true lumen), with the branch vessels— ( celiac axis, superior mesenteric artery, and right renal artery) arising out of nowhere.
They appear to be floating, with little or no antegrade opacification of the aortic true lumen.
Dissection Flap in the Abdomen - Vocab Trivia:
Static = dissection flap in the feeding artery (usually treated by stenting)
Dynamic = dissection flap dangling in front of ostium (usually treated with fenestration).
It can be hard to tell these apart. I f a sk ed I ‘d expect them to ju s t use the vocab words.
THIS vs THAT: Aneurysm with Mural Thrombus VS Thrombosed Dissection
- The dissection should spiral, the thrombus tends to drop straight down
- Intimal Calcs - the dissection will displace them.
THIS vs THAT: Aneurysm with Mural Thrombus VS Thrombosed Dissection
- The dissection should spiral, the thrombus tends to drop straight down
- Intimal Calcs - the dissection will displace them.
Intramural hematoma
htn
blasted vaso vasorum > intramural hematoma > intima tears > dissection
blasted vaso vasorum > intramural hematoma >serosal rupture > psuedoaneurysm
Intramural hematoma
atherosclerosis
focal plaque ruptures > focal intramural hematoma > dissection
focal plaque ruptures > focal intramural hematoma > serosal rupture > pseudoaneurysm
IMH
mechanism flow
can occur as
- primary event secondary to htn
- seconary event usually from atherosclerosis, but also as a focal hematoma on the road to dissection
for multible choice the cause is htn
IMH imaging findings
crescent sign
hyperdense on noncon
contrast CT difficult to distinguish from plaque
T1 bright crescent
IMH
treatment
Also uses the Stanford A vs B idea
Some people will say Type A = Surgery, Type B medical
• This is controversial and unlikely to be tested
IMH predictors of outcome
- Most o f these will spontaneously regress. These are the things that make that less likely:
- Hematoma Thickness Greater than 2 cm
- Association with aneurysmal dilation o f the aorta - 5 cm or more
- Progression to dissection or penetrating ulcer
- IMH + Penetrating Ulcer has a worse outcome compared to IMH + Dissection
THIS vs THAT: A n eu ry sm v s P s eu d o -a n e u r y sm -
The distinction between a true
and false aneurysm lends itself well to multiple choice testing. A true aneurysm is an
enlargement o f the lumen o f the vessel to 1.5 times its normal diameter. True = 3 layers are
intact. In a false (pseudo) aneurysm all 3 layers are NOT intact, and it is essentially a
contained rupture. The risk o f actual rupture is obviously higher with false aneurysm. It
can sometimes be difficult to tell, but as a general rule fusiform aneurysms are true, and
saccular aneurysms might be false. Classic causes o f pseudoaneurysm include trauma,
cardiologists (groin sticks), infection (mycotic), pancreatitis, and some vasculitides. On
ultrasound they could show you the classic yin/yang sign, with “to and fro” flow on pulsed
Doppler. The yin/yang sign can be seen in saccular true aneurysms, so you shouldn’t call it
on that alone (unless th at’s all they give you). To and Fro flow within the aneurysm neck +
clinical history is the best way to tell them apart.
SVC S y n d rom e
Occurs secondary to complete or near complete obstruction o f flow
in the SVC from external compression (lymphoma, lung cancer) or intravascular
obstruction (Central venous catheter, or pacemaker wire with thrombus). A less common
but testable cause is fibrosing mediastinitis (just think histoplasmosis). The dude is gonna
have face, neck, and bilateral arm swelling.
Traum a tic P s e u d o a n e u r y sm
Again a pseudoaneurysm is basically a
contained rupture. The most common place
to see this (in a living patient) is the aortic
isthmus (90%). This is supposedly the
result o f tethering from the ligamentum
arteriosum. The second and third most
common sites are the ascending aorta and
diaphragmatic hiatus - respectively.
Ascending aortic injury is actually probably
number one, it ju st kills them in the field so
you do n ’t see it. They could show you a
CXR with a wide mediastinum, deviation
o f the NG Tube to the right, depressed left
main bronchus, or left apical cap and want
you to suspect acute injury.
Asc end ing A o r tic C a lc ific a tio n s
There are only a few causes o f ascending aortic
calcifications, as atherosclerosis typically spares the ascending aorta. Takayasu and
Syphilis should come to mind. The real-life significance is the clamping o f the aorta may
be difficult during CABG.
A n eu ry sm
Defined as enlargement o f the artery to 1.5 times its expected diameter
(> 4 cm Ascending and Transverse, > 3.5 cm Descending, > 3.0 cm Abdominal).
Atherosclerosis is the most common overall cause. Medial degeneration is the most
common cause in the ascending aorta. Patients with connective tissue (Marfans, Ehlers
Danlos) diseases tend to involve the aortic root. When I say cystic medial necrosis you
should think Marfans. Aneurysms may develop in any segment o f the aorta, but most
involve the infra-renal abdominal aorta. This varies based on risk factors, rate o f growth,
e tc … but a general rule is surgical repair for aneurysms at 6cm in the chest (5.5 cm with
collagen vascular disease) and 5 cm in the abdomen.
Sinus o f V a ls a lv a A n eu ry sm
Aneurysms o f the valsalva sinus (aortic sinus) are
rare in real life, but have been known to show up on multiple choice tests. Factoids worth
knowing are that they are more common in Asian Men, and typically involve the right
sinus. They can be congenital or acquired (infectious). VSD is the most common associated
cardiac anomaly. Rupture can lead to cardiac tamponade. Surgical repair with Bentall
procedure.
R upture / Im p en d in g R u p tu re
Peri-aortic stranding, rapid enlargement (10 mm or
more per year), or pain are warning signs o f impending rupture. A retroperitoneal hematoma
adjacent to an AAA is the most common imaging finding o f actual rupture. The most
common indicator for elective repair is the maximum diameter o f the aneurysm , “Sac Size
Matters,” with treatment usually around 6 cm (5.5 cm in patients with collagen vascular
disease). A thick, circumferential mural thrombus is thought to be protective against rupture.
Enlargement o f the patent lumen can indicate lysis o f thrombus and predispose to rupture.
Findings of impending rupture
Draped Aorta Sign
Posterior wall of the aorta drapes over the vertebral column.
Increased Aneurysm Size
10 mm or more increased per year
Focal Discontinuity in Circumferential Wall Calcifications
Hyperdense Crescent Sign
Well-defined peripheral crescent of increased attenuation. One of the most specific manifestations of impending rupture.
M y c o tic A n eu ry sm
These are most often saccular and most often pseudoaneurysms. They are prone to rupture. They most often occur via hematogenous seeding in the setting o f septicemia (endocarditis). They can occur from direct seeding via a psoas abscess or vertebral osteomyelitis (but this is less common). Most occur in the thoracic or supra-renal aorta (most atherosclerotic aortic aneurysms are infra-renal).
Typical findings include saccular shape, lobular contours, peri-aortic inflammation, abscess, and peri-aortic gas. They tend to expand faster than atherosclerotic aneurysms. In general small, asymptomatic, and unruptured.
M y c o tic A n eu ry sm
gamesmanship
If you see a saccular aneurysm o f the aorta (especially the I f abdominal aorta) you have to lead with infection.
NF 1
One o f the more common neurological genetic disorders, which you usually think about causing all the skin stuff (Cafe au lait spots and freckling), and bilateral optic gliomas. Although uncommon, vascular findings also occur in this disorder. Aneurysms and stenoses
are sometimes seen in the aorta and larger arteries, while dysplastic features are found in smaller vessels. Renal artery stenosis can occur, leading to renovascular hypertension (found in 5% o f children with NF). The classic look is orificial renal artery stenosis presenting with hypertension in a teenager or child. The mechanism is actually Dysplasia o f the arterial wall itself (less common from peri-arterial neurofibroma).
Marfan Syndrome
overview
Genetic disorder caused by mutations of the fibrillin gene (step 1 question). There are lots o f systemic manifestations including ectopic lens, being tall, pectus
deformity, scoliosis, long fingers etc… Vascular findings can be grouped into aneurysm, dissection, and pulmonary artery dilation:
Marfan Syndrome
aneurysm
Dilation with Marfans is classically described as “Annuloaortic ectasia”,
with dilatation o f the aortic root. The dilation usually begins with the aortic sinuses, and then progresses into the sinotubular junction, ultimately involving the aortic annulus. Dilatation of the aortic root leads to aortic valve insufficiency. Severe aortic regurgitation occurs that may progress to aortic root dissection or rupture. The mechanism for all this nonsense is that disruption o f the media elastic fibers causes aortic stiffening, and predisposes to aneurysm and dissection. The buzzword for the Marfans ascending aneurysm is “tulip bulb. They are usually repaired earlier than normal aneurysm (typically around 5.5 cm).
Marfan Syndrome
dissection
Recurrent dissections are common, and even “triple barreled dissection” can be seen (dissections on both sides o f a true channel).
Marfan Syndrome
pulmonary artery enlargement
Just like dilation o f the aorta, pulmonary artery enlargement favors the root.
Marfans quick
Annuloaortic extasia with dilationof the aortic root
Loeys Dietz Syndrome
overview
Despite the name, this is actually not a Puerto Rican DJ. Instead think o f this as the really shitty version o f Marfans. They have a terrible prognosis, and rupture their aortas all the time. Vessels are very tortuous (twisty). They also have crazy wide eyes (hypertelorism).
Loeys Dietz Syndrome
classic triad
- Hypertelorism (frog eyes),
- Bifid uvula or cleft palate
- Aortic aneurysm with tortuosity
Loeys Ditz classic look
Crazy twisty vertebral arteries
Ehlers -D an los
This one is a disorder in collagen, with lots o f different subtypes. They have the stretchy skin, hypermobile joints, blood vessel fragility with bleeding diatheses.
Invasive diagnostic studies such as conventional angiography and other percutaneous procedures should be avoided because o f the excessive risk o f arterial dissection. Imaging characteristics o f aortic aneurysms in Ehlers-Danlos syndrome resemble those in Marfan syndrome, often involving the aortic root. Aneurysms o f the abdominal visceral arteries are common as well.
S y p h ilitic (L u e tic ) A n eu ry sm
This is super rare and only seen in patients with untreated tertiary syphilis. There is classically a saccular appearance and it involves the ascending aorta as well as the aortic arch. Classic description “saccular asymmetric aortic aneurysm with involvement o f the aortic root branches. ” Often heavily calcified “tree bark” intimal calcifications. Coronary artery narrowing (at the ostium) is seen 30% o f the time. Aortic valve insufficiency is also common.
A o r to e n te ric F is tu la
primary
Very, very, very rare. Refers to an A-E fistula without history o f instrumentation. They are only seen in the setting o f aneurysm and atherosclerosis.
A o r to e n te ric F is tu la
secondary
Much more common. They are seen after surgery with or without stent
graft placement.
Aortenteric fistula
The question is usually what part o f the bowel is involved, and the answer is 3 rd and 4th portions of the duodenum. The second most likely question is A-E fistula vs perigraft infection (without fistula)? The answer to that is unless you see contrast from the aorta into the bowel lumen (usually duodenum), you c an ’t tell. Both o f them have ectopic perigraft gas > 4 weeks post repair, both have perigraft fluid and edema, both lose the fat place between the bowel and aorta (tethering o f the duodenum to the anterior wall o f the aorta), both can have pseudoaneurysm formation.
In flamm atory Aneurysms
Most are symptomatic, more common in young men, and associated with increased risk o f rupture regardless o f their size. Unlike patients with atherosclerotic AAA, most with the inflammatory variant have an elevated ESR. Their etiology is not well understood but may be related to periaortic retroperitoneal fibrosis or other autoimmune disorders (SLE, Giant Cell, RA). Smoking is apparently a strong risk factor, and smoking cessation is the first step in medical therapy. In 1/3 of cases hydronephrosis or renal failure is present at the time o f diagnosis because the inflammatory process usually involves the ureters. Imaging findings include a thickened wall and inflammatory or fibrotic changes in the periaortic regions. Often there is asymmetrical thickening o f the aorta with sparing o f the posterior wall (helps differentiate it from vasculitis).
Leriche Syndrome
overview
Refers to complete occlusion o f the aorta distal to the renal arteries (most
often at the aortic bifurcation). It is often secondary to bad atherosclerosis. There can be
large collaterals.
Leriche Syndrome
triad
. Limp Dick (impotence)
• Ass claudication
• Absence femoral pulses
Mid Aortic Syndrome (C oarcta tion of
the Abdominal Aorta)
Refers to progressive narrowing of the abdominal aorta and its major branches. Compared to Leriche, this is higher, and
longer in segment. It’s also a total freaking zebra. It tends to affect children / young adults. This thing is characterized by progressive narrowing of the aorta. It is NOT secondary to arteritis or atherosclerosis but instead the result o f some intrauterine insult (maybe) with fragmentation o f the elastic media.
Mid A ortic Syndrome (C oarcta tion of
the Abdominal Aorta)
triad
- HTN (most common presenting symptom) - this is the most common cause o f death i f not treated
- Weak or Absent Femoral Pulses
- Claudication
- Renal failure
mid aortic syndrome quick
narrow aorta without arteritis or atherosclerosis
Aortic Coarctation
overview
- There are two subtypes
- Strong Association with Turners Syndrome (15-20%).
- Bicuspid Aortic valve is the most common associated defect (80%).
- They have more berry aneurysms.
- Figure 3 sign (appearance o f CXR).
• Rib Notching: most often involves 4th - 8th ribs. It does NOT involve the l sl and
2nd because those are fed by the costocervical trunk.
Aortic Coarctation
infantile
Presents with heart failure within the first week of life.
Pre-Ductal (Before the left Subclavian A.)
Aortic Arch = Hypoplastic
Aortic Coarctation
adult
Leg Claudication BP differences between arms and legs.
Post-Ductal (Distal to left Subclavian A.)
Aortic Arch = Normal Diameter
Collateral Formation is More Likely
Pseudocoarctation
This is a favorite o f multiple choice writers. You will have elongation with narrowing and kinking o f the aorta. It really looks like a coarctation, BUT
there is NO pressure gradient, collateral formation, or rib notching - that is the most likely question. The second most likely question is the area o f aneurysmal dilation may occur distal to the areas o f narrowing in pseudocoarctation, and they may become progressively dilated and should therefore be followed.
Tho ra c ic Outlet Syndrome
Congenital or acquired compression o f the Subclavian vessels (artery and vein), and brachial plexus nerves as they pass through the thoracic inlet. It is a spectrum: Nerve (95%) » » » Subclavian Vein » Subclavian Artery. With
symptoms varying depending on what is compressed. Compression by the anterior scalene muscle is the most common cause. However, cervical rib, muscular hypertrophy, fibrous bands, Pagets, tumor e tc … can all cause symptoms. Treatment is usually surgical
removal o f the rib / muscle. The classic way to show this is arms up and arms down angiography (occlusion occurs with arms up).
Paget Schroetter
This is essentially thoracic outlet syndrome, with development of a venous thrombus in the Subclavian vein. It’s sometimes called “effort thrombosis’’
because it’s associated with athletes (pitchers, weightlifters) who are raising their arms a lot. They will use catheter directed lysis on these dudes, and surgical release o f the offending agent as above. Stenting isn’t usually done (and can only be done after surgery to avoid getting the stent crushed).
Pulmonary Artery Aneurysm/Pseudoaneurysm
Think about three things for
multiple choice; (1) Iatrogenic from Swan Ganz catheter *most common (2) Behcets, (3)
Chronic PE. When they want to lead Swan Ganz they may say something like “patient in the 1CU.”
The buzzwords for Behcets are: “Turkish descent”, and “mouth and genital ulcers.”
Pulmonary Artery Aneurysm/Pseudoaneurysm
hughes-stovin syndrome
This is a zebra cause of pulmonary artery aneurysm that is similar
(and maybe the same thing) as Behcets. It is characterized by recurrent thrombophlebitis and
pulmonary artery aneurysm formation and rupture.
Pulmonary Artery Aneurysm/Pseudoaneurysm
rasmussen aneurysm
This has a cool name, which instantly makes it high yield for testing.
This is a pulmonary artery pseudoaneurysm secondary to pulmonary TB. It usually involves
the upper lobes in the setting of reactivation TB.
Pulmonary Artery Aneurysm/Pseudoaneurysm
tetralogy of fallot repair gone south
So another possible testable scenario is the patch aneurysm, from the RVOT repair.
Splenic Artery Aneurysm
epidemiology
The most common visceral arterial aneurysm (3rd most common abdominal - behind aorta and iliac).
Splenic Artery Aneurysm
etiology
Etiology of these things depends on who you ask. Some source will say arteriosclerosis is the most important cause. However, it seems that most sources will say that arteriosclerosis less
important and things like portal hypertension and a history of
multiple pregnancy are more important. More common in pregnancy, and more likely to rupture in pregnancy.
Splenic Artery Aneurysm
high risk for rupture
- Liver Transplantation
- Portal Hypertension
- Pregnancy
- Connective Tissue Disorders
- Alpha 1 Antitrypsin Def
Splenic Artery Aneurysm
location
Most are located in the distal artery. False aneurysms are associated with pancreatitis.
Splenic Artery Aneurysm
mimic
An important mimic is the islet cell pancreatic tumor (which is hypervascular). Don’t be a dumb
ass and try to biopsy the aneurysm. If you are forced to choose which ones to treat I guess I’d go
with: anything over 2 cm, any pseudoaneurysm, and any in a women planning on getting pregnant.
SMA Aneurysm
All SMA aneurysms should be treated - as there is a high rate of rupture and
association with mesenteric ischemia.
Hepatic Artery Aneurysm:
Treated if the patient is symptomatic or size exceeds 2cm (just
like the spleen). In patients with FMD or polyarteritis nodosa - typically they are treated regardless
of size.
Median Arcuate Ligament Syndrome (Dunbar Syndrome)
This is compression of the celiac artery by the median arcuate ligament (fibrous band that connects the diaphragm). Most people actually have some degree of
compression, but it’s not a syndrome until there are symptoms (abdominal pain, weight loss). Typical age is 20-40 years old. The buzzword is “hooked appearance.” It’s classically shown
on angiography and they will want you to know that it gets worse with expiration. It can actually lead to the development
of pancreaticoduodenal collaterals and aneurysm formation. It’s
treated surgically.
M e s e n t e r i c Is c h e m i a
chronic
Significant Stenosis o f 2 out o f 3 main mesenteric vessels + symptoms (“ food
fear” ) , LUQ pain after eating, pain out o f proportion to exam). Some practical pearls are
that you can have bad disease and no symptoms if you have good collaterals. Alternatively
if you have bad one-vessel disease you can have symptoms if you have crappy collaterals.
Remember that the splenic fle xu re (“Griffith s Point ”) is the most common because it’s the
watershed o f the SMA and IMA.
M e s e n t e r i c Is c h e m i a
acute types
Arterial, Venous, Non-occlussive, and Strangulation.
M e s e n t e r i c Is c h e m i a
acute arterial
Occlusive emboli (usually more distal, at branch points), or Thrombus
(usually closer to the ostium). Vasculitis can also cause it. The SMA is most
commonly affected. Bowel typically has a thinner wall (no arterial inflow), and is
NOT typically dilated. After reperfusion the bowel wall will become thick, with a
target appearance.
M e s e n t e r i c Is c h e m i a
acute venous
Dilation with wall thickening (8-9mm, with < 5mm being normal) is
more common. Fat stranding and ascites are especially common findings in venous
occlusion.
M e s e n t e r i c Is c h e m i a
acute non-occlusive
Seen in patients in shock or on pressors. This is the most difficult
to diagnose on CT. The involved bowel segments are often thickened.
Enhancement is variable. Look fo r delayed filling o f the porta! vein at 70 seconds.
M e s e n t e r i c Is c h e m i a
acute tstrangulation
This is almost always secondary to a closed loop obstruction. This
is basically a mixed arterial and venous picture, with congested dilated bowel.
Hemorrhage may be seen in the bowel wall. The lumen is often fluid-filled.
mesenteric ischemia trivia
Trivia: Mesenteric Ischemia has a described association with SMA Aneurysm.
M e s e n te r ic Is c h em ia
arterial imaging findings
thin bowel wall (thick after reperfusion)
diminished enhancement
bowel not dilated
mesentery not hazy (until it infarcts)
M e s e n te r ic Is c h em ia
venous imaging findings
thick bowel wall
variable
moderate dilation
hazy with ascites
M e s e n te r ic Is c h em ia
strangulation imaging findings
thick bowel wall
variable
sever dilation (and fluid filled)
hazy with ascites and whirl sign with closed loop
M e s e n te r ic Is c h em ia
non0occlusive imaging findings
thck bowel wall
variable
bowel not dilated
mesentery not hazy (until it infarcts)
Griffith’s Point
• SMA-IMA - Watershed • “Most Common Location for Ischemia”
splenic flexure
Sudeck’s Point
• IMA - Iliac Watershed
• Highly Susceptible to
Ischemia
sigmoid
angry (thick walled) bowel algorithm
Colitis/Enteritis> infection diffuse or TI
Colitis/Enteritis > inflammatory (TI)
Colitis/Enteritis> ischemic > arterial > occlusive > embolic (branch points)
Colitis/Enteritis> ischemic > arterial > occlusive > Thrombotic (closer to ostium)
Colitis/Enteritis> ischemic > arterial > non- occlusive > (think hypotension watershed)
Colitis/Enteritis> ischemic > venous
Colonic A n g io d y sp la s ia
This is the second most common cause o f colonic arterial
bleeding (diverticulosis being number one). This is primarily right sided with angiography
demonstrating a cluster o f small arteries during the arterial phase (along the antimesenteric
border o f the colon), with early opacification o f dilated draining veins that persists late into
the venous phase. There is an association with aortic stenosis which carries the eponym
Heyde Syndrome (which instantly makes it high yield for multiple choice).
Osier W ebe r Rendu (H e re d ita ry H em o rrh ag ic T e la n g ie c ta s ia )
overview
This is an AD multi-system disorder characterized by multiple AVMs. On step 1 they used to show you
the tongue / mouth with the telangiectasis and a history o f recurrent bloody nose. Now, they
will likely show multiple hepatic AVMs or multiple pulmonary AVMs. Extensive shunting in
the liver can actually cause biliary necrosis and bile leak. They can have high output cardiac
failure.
Osier W ebe r Rendu (H e re d ita ry H em o rrh ag ic T e la n g ie c ta s ia )
most die from
Most die from stroke or brain abscess.
Osier W ebe r Rendu (H e re d ita ry H em o rrh ag ic T e la n g ie c ta s ia )
gamesmanship
If the syndrome is suspected, these guys need CT o f the
Lung & Liver (with contrast), plus a Brain MR / MRA
Renal A rte ry Stenosis
Narrowing o f the renal artery most commonly occurs secondary to atherosclerosis (75%). This type o f narrowing is usually near the ostium, and can be stented. EMD is the second most common cause and typically has a beaded appearance
sparing the ostium (should not be stented). Additional more rare causes include PAN,
Takayasu, NL-1, and Radiation.
FMD (Fib rom u s cu la r Dysplasia) -
overview
A non-atherosclerotic vascular disease, primarily affecting the renal arteries o f young white women.
FMD (Fib rom u s cu la r Dysplasia) -
things to know
- Renovascular HTN in Young Women = LMD
- Renal arteries are the most commonly involved (carotid #2, iliac #3)
- There are 3 types, but just remember medial is the most common (95%)
- They are predisposed to spontaneous dissection
FMD (Fib rom u s cu la r Dysplasia) -
buzzword
String of beads
FMD (Fib rom u s cu la r Dysplasia) -
treatment
Angioplasty WITHOUT stenting. Eating walnuts helps (seriously, there is a
paper on it). Eating cashews does not help (same paper), which is too bad because
cashews are delicious… and walnuts taste like shit.
N u tc ra c k e r S yndrom e
Usually a healthy female 30s-40s. The left renal vein gets smashed as it slides under the SMA, with resulting abdominal pain (left flank) and hematuria. The left renal vein gets smashed a lot, but it’s not a syndrome without symptoms. Since the left gonadal vein drains into the left renal vein, it can also cause left testicle pain in men, and LLQ pain in women.
N u tc ra c k e r S yndrom e
gold standard
Retrograde venography with renal / caval pressure measurements
N u tc ra c k e r S yndrom e quick
Renal Vein, Smashed by SMA. Note the prominent venous collateral (arrow)
SAM (S e gm e n ta l A r te r ia l M e d io ly s is )
disease hallmark
multiple abdominal splanchnic artery saccular aneurysms, dissections, and occlusion - Can also be shown as spontaneous intra-abdominal hemorrhage.
WTF is a splanchnic artery
Typically the splanchnic circulation o f the GI tract refers to the Celiac, SMA, and IMA.
P e lv ic C on g e s tio n S yn d rom e
This is a controversial entity, sometimes grouped
in the fibromyalgia spectrum. Patients often have “chronic abdominal pain.” They also
often wear a lot o f rings and drink orange soda. The classic demographic is a depressed,
multiparous, pre-menopausal women with chronic pelvic pain. Venous obstruction at the left
renal vein (nutcracker compression) or incompetent ovarian vein valves leads to multiple
dilated parauterine veins. This very “real” diagnosis can be treated by your local
Interventional Radiologist via ovarian vein embolization.
T e s tic u la r V a r ic o c e le
Abnormal dilation o f veins in the pampiniform plexus. Most
cases are idiopathic and most (98%) are found on the left side (left vein is longer, and
drains into renal vein at right angle). They can also occur on the left, secondary to the
above mentioned “nutcracker syndrome.” They can cause infertility. “Nondecompressible”
is a buzzword for badness. Some sources state that neoplasm is actually the
most likely cause o f non-decompressible varicocele in men over 40 years o f age; (left renal
malignancy invading the renal vein). Right-sided varicocele can be a sign o f malignancy as
well. When it’s new, and on the right side (in an adult), you should raise concern for a pelvic
or abdominal malignancy. New right-sided varicocele in an adult should make you think
renal cell carcinoma, retroperitoneal fibrosis, or adhesions.
Testicular varicocle
non-decompressible
Bad
Get an ABD CT (or MR, or US)
Testicular varicocle
right
Bad
Get an ABD CT (or MR, or US)
Testicular varicocle
left
ok
Might need treatment if infertile etc.., but doesn’t need additional cancer hunting imaging.
Testicular varicocle
bilateral
ok probably
Might need treatment if infertile etc.., but doesn’t
need additional cancer hunting imaging.
Testicular varicocle
gamesmanship
This diagnosis is the classic next step question o f all next step
questions because you need to recognize when this common diagnosis is associated with something bad.
Testicular varicocle
gamesmanship
This diagnosis is the classic next step question o f all next step
questions because you need to recognize when this common diagnosis is associated with something bad.
U te r in e AVM
This can present with life threatening massive genital bleeding. Rarely they can present with CHF. They come in two flavors (a) Congenital, and (b) Acquired.
Acquired occurs after D&C, abortion, or multiple pregnancies. They are most likely to show this on color Doppler with serpiginous structures in the myometrium with low resistance high velocity patterns. This one needs embolization. Could look similar to retained products o f conception (clinical history will be different, and RPOC is usually centered in the endometrium rather than the myometrium).
Pop lite a l Aneurysm
This is the most common peripheral arterial aneurysm (2nd most
common overall, to the aorta). The main issue with these things is distal thromboembolism,
which can be limb threatening. There is a strong and frequently tested association with AAA.
* 30-50% o f patients with popliteal aneurysms have a AAA
* 10% o f patients with AAA have popliteal aneurysms
* 50-70% o f popliteal aneurysms are bilateral
most dreaded complication of a popliteal artery aneurysm
an acute limb from thrombosis and distal embolization o f thrombus pooling in the aneurysm.
H yp o th en a r H am m e r -
Caused by blunt trauma (history o f working with a jackhammer)
to the ulnar artery and superficial palmar arch. The impact occurs against the hook o f the hamate. Arterial wall damage leads to aneurysm formation with or without thrombosis of the vessel. Emboli may form, causing distal obstruction o f digits (this can cause confusion with the main DDx Buergers). Look for corkscrew configuration of the superficial palmar arch, occlusion of the ulnar artery, or pseudoaneurysm of the ulnar artery.
Venous T h romb oemb olism (VTE)
term used to refer to PE and DVT (PE
and DVT are both forms o f VTE).
Venous T h romb oemb olism (VTE)
trivia
You are more likely to develop VTE if you are paraplegic vs tetraplegic.
Venous T h romb oemb olism (VTE)
motor complete
VTE is more likely in “motor complete” AIS A patients (those that have lost motor and sensory) vs motor incomplete AIS B,C,D (those with some residual sensory or motor function) -- which is more intuitive. Quad being worse than tetra for VTE risk makes zero sense (and therefore makes a good trivia question).
Venous T h romb oemb olism (VTE)
motor complete
VTE is more likely in “motor complete” AIS A patients (those that have lost motor and sensory) vs motor incomplete AIS B,C,D (those with some residual sensory or motor function) -- which is more intuitive. Quad being worse than tetra for VTE risk makes zero sense (and therefore makes a good trivia question).
P e rip h e ra l V a s c u la r M a lfo rm a tio n s
About 40% o f vascular malformations
involve the extremities (the other 40% are head and neck, and 20% is thorax). Different than
hemangiomas, vascular malformations generally increase proportionally as the child grows.
This dude Jackson classified vascular malformation as either low flow or high flow. Low
flow would include venous, lymphatic, capillary, and mixes o f the like. High flow has an
arterial component. Treatment is basically determined by high or low flow.
K lip p e l-T re n a u n a y S yn d rom e (K TS )
overview
This is often combined with Parkes-
Weber which is a true high flow AV malformation. KTS has a triad o f port wine nevi,
bony or soft tissue hypertrophy (localized gigantism), and a venous malformation. A
persistent sciatic vein is often associated. The marginal vein o f Servelle (some superficial
vein in the lateral c a lf and thigh) is pathognomonic (it’s basically a great saphenous on the
wrong side).
K lip p e l-T re n a u n a y S yn d rom e (K TS )
trivia
20% have GI involvement and can bleed, if the system is big enough it can
eat your platelets (Kasabach Merritt). Basically, if you see a MRA/MRV o f the leg with a
bunch o f superficial vessels (and no deep drainage) you should think about this thing.
K lip p e l-T re n a u n a y S yn d rom e (K TS )
KTS
Low Flow (venous)
K lip p e l-T re n a u n a y S yn d rom e (K TS )
Parkes weber
High Flow (arterial)
K lip p e l-T re n a u n a y S yn d rom e (K TS )
Klippel Trenaunay weber
Something people say when they (a) do n ’t know what they
are talking about, or (b) do n ’t know what kind o f malformation it is and want to use a
blanket term.
A BIs
ovverview
So basic familiarity with the so called “Ankle to Brachial Index” can occasionally
come in handy, with regard to peripheral arterial disease. This is basically a ratio o f systolic
pressure in the leg over systolic blood pressure in the arm. Diabetics can sometimes have
unreliable numbers (usually high), because dense vascular calcifications won’t let the vessels
compress.
A BIs
cutoff numbers
Opinions vary on what the various cut o ff numbers mean. Most people will agree that you
can safely deploy the phrase “peripheral arterial disease” if the resting ABI is less than 0.90
You can also deploy the following generalizations: 0.5-0.3 = claudication, < 0.3 = rest pain
In tim a l H y p e rp la s ia
“The bane o f endovascular intervention.” This is not a true
disease but a response to blood vessel wall damage. Basically this is an exuberant healing
response that leads to intimal thickening which can lead to stenosis. You hear it talked
about the most in IR after they have revascularized a limb. Re-Stenosis that occurs 3-12
months after angioplasty is probably from intimal hyperplasia. It’s sneaky to treat and
often resists balloon dilation and/
or reoccurs. If you put a bare
stent in place it may grow through
the cracks and happen anyway. If
you put a covered stent in, it may
still occur at the edges o f the
stent. The take home point is that
it’s a pain in the ass, and if they
show an angiogram with a stent
in place, that now appears to be Intimal Hyperplasia
losing flow, this is probably the
answer.
In tim a l H y p e rp la s ia
with stent
-dark stuff growing along the inside of the stent walls
C y s tic A d v e n titia l D is e a s e
This uncommon disorder classically affects the
popliteal artery, of young men. Basically you have one or multiple mucoid-filled cysts
developing in the outer media and adventitia. As the cysts grow, they compress the artery.This uncommon disorder classically affects the
popliteal artery, of young men. Basically you have one or multiple mucoid-filled cysts
developing in the outer media and adventitia. As the cysts grow, they compress the artery.
V a s c u l i t i s
overview
Basically all vasculitis looks the same, with wall thickening, occlusions, dilations, and
aneurysm formation. The trick to telling them apart is the age o f the patient, the gender /
race, and the vessels affected. Classically, they are broken up into large vessel, medium
vessel, small vessel ANCA +, and small vessel ANCA negative.
Large vessel vasculitis
Takayasu
GCA
Cpgan
T a k a y a s u
overview
“The pulseless disease.” This vasculitis loves young Asian girls (usually
15-30 years old). If they mention the word “Asian,” this is likely to be the answer. Also, if
they show you a vasculitis involving the aorta this is likely the answer. In the acute phase
there will be both wall thickening and wall enhancement. There can be occlusion o f the
major aortic branches, or dilation o f the aorta and its branches. The aortic valve is often
involved (can cause stenosis or AI). In the late phase there is classically diffuse narrowing
distally. The pulmonary arteries are commonly involved, with the typical appearance o f
peripheral pruning.
T a k a y a s u
types
If anyone was a big enough jerk to ask, there are 5 types with variable involvement o f the
aorta and its branches. Which type is which is beyond the scope o f the exam, ju st know type
3 is most common - involves arch and abdominal aorta.
Takayasu quick
wall thickening involving the aorta
G ian t C e ll (GCA)
overview
The most common primary system vasculitis. This vasculitis loves
old men (usually 70-80)** although there are a few papers that will say this is slightly more
common in women. This vasculitis involves the aorta and its major branches particularly
those o f the external carotid (temporal artery). This can be shown in two ways: (1) an
ultrasound o f the temporal artery, demonstrating wall thickening, or (2) CTA / MRA or even
angiogram o f the armpit area (Subclavian/ Axillary/ Brachial), demonstrating wall
thickening, occlusions, dilations, and aneurysm. Think about it as the part o f the body that
would be compressed by crutches (old men need crutches).
G ian t C e ll (GCA)
trivia
• ESR and CRP are markedly elevated,
• Disease responds to steroids.
• “Gold Standard” for diagnosis is temporal artery biopsy (although it’s often negative).
• Clinical connection between GCA and polymyalgia rheumatica. (they might be different
phases o f the same disease). History might be “morning stillness in shoulders and hips.”
Cogan S yn d rom e
Total Zebra probably not even worth
mentioning. It is a large vessel vasculitis that targets children and young
adults. It likes the eyes and ears causing optic neuritis, uveitis, and
audiovestibular symptoms resembling Menieres. They can also get
aortitis, and those that do have a worse prognosis.
Basically, kid with eye and ear symptoms + or - aortitis.
Medium vasculitis list
PAN
Kawasaki disease
PAN (P o ly a r te ritis N odosa )
overview
This is one o f two vasculitides (the other being Buergers) that is more common in men. PAN is more common in a MAN. This can effect a lot o f places with the big 3 being Renal (90%), Cardiac (70%), and GI (50-70%). Typically we are talking about microaneurysm formation, primarily at branch points, followed by infarction. I would expect this to be shown either as a CTA or angiogram o f the kidneys with microaneurysms, or a kidney with areas o f infarct (multiple wedge shaped areas).
PAN (P o ly a r te ritis N odosa )
trivia
association with Hep B.
PAN (P o ly a r te ritis N odosa )
random trivia
micro-aneurysm formation in the kidney can also be seen in patients who abuse Crystal Meth (sometimes called a “speed kidney”).
K aw a s a k i D is e a s e
overview
Probably the most common vasculitis in children (HSP also common). Think about this as a cause o f coronary vessel aneurysm. A calcified coronary artery aneurysm shown on CXR is a very rare aunt Minnie.
K aw a s a k i D is e a s e
clinical trivia
“Fever for 5 Days” • Strawberry Tongue • Neck Lymph Nodes • Rash of Palms of Hands / Soles of Feet • Sore Throat Diarrhea • “Etiology Unknown”
K aw a s a k i D is e a s e
coronary artery
- Coronary Artery Aneurysms > 8mm are “Giant” and prone to badness including Ml
- Coronary Artery Aneurysms < 8mm may regress
Small Vessel Disease (ANCA +)
list
Wegeners
churg strauss
miscroscopic polyangiitis
W e g e n e rs
1 think about upper respiratory tract
(sinuses), lower respiratory tract (lungs), and
kidneys. cANCA is (+) 90% o f the time. Ways this
is shown are the nasal perforation (like a cocaine
addict) and the cavitary lung lesions.
Churg S tra u s s
This is a necrotizing
pulmonary vasculitis which is in the spectrum o f
Eosinophilic lung disease. They always have asthma
and eosinophilia. Transient peripheral lung
consolidation or ground glass regions is the most
frequent feature. Cavitation is rare (this should make
you think Wegeners instead). They are pANCA (+)
75% if the time.
M ic ro s c o p ic P o ly a n g iitis
Affe c ts the kidneys and lungs. Diffuse pulmonary hemorrhage
is seen in about 1/3 o f the cases. It is pANCA (+)
80% o f the time.
Small Vessel Disease (ANCA -) list
HSP (henoch schonlein purpura)
behcets
buergers
HSP (H en o ch -S ch o n le in P u rp u ra )
The most common vasculitis in children
(usually age 4-11). Although it is a systemic disease, G1 symptoms are most common
(painful bloody diarrhea). It is a common lead point for intussusception. They could show this two classic ways: (1) ultrasound with a doughnut sign for intussusception, or (2) as a ultrasound o f the scrotum showing massive skin edema. A less likely (but also possible) way to show this case would be multi-focal bowel wall thickening, or a plain film with
thumbprinting.
B e h c e ts
Classic history is mouth ulcers and genital ulcers in someone with Turkish
descent. It can cause thickening o f the aorta, but for the purpose o f multiple choice test I expect the question will be pulmonary artery aneurysm.
Buergers
This vasculitis is strongly associated with smokers. It affects both small and
medium vessels in the arms and legs (more common in legs). Although it is more commonly
seen in the legs, it is more commonly tested with a hand angiogram. The characteristic
features are extensive arterial occlusive disease with the development o f corkscrew collateral
vessels. It usually affects more than one limb.
Burgers buzzword
autoamputation
If they are showing you a hand angiogram
Buuergers or hypothenar hammer syndrome
Gamesmanship Hand Angiograms
(1) Ulnar artery involved = HHS. The most helpful finding is a pseudo-aneurysm off the ulnar artery - this is a slam dunk for HHS.
(2) Ulnar artery looks ok - then look at the fingers - if they are out, go with Buergers. It sure would be nice to see some “corkscrew collaterals” - to make it a sure thing.
Be careful, because the fingers can be out with HHS as well (distal emboli), but the ulnar
artery should be fucked. Look at that ulnar artery first.
Vasculitis central
Think Takayasu
Vasculiti mid clavicle
Think Thoracic Syndrome
Vasculiti armpit
Think Giant Cell
Takayasu quick
Young Asian Female - thickened aneurysmal aorta
giant cell quick
Old Person with involvement o f the “crutches” / armpit region
(Subclavian, axillary, brachial).
cogan syndrome quick
Kid with eye and ear symptoms + Aortitis
pan quick
PAN is more common in a MAN (M > F). Renal Microaneurysm
(similar to speed kidney). Associated with Hep B.
kawasaki quick
Coronary Artery Aneurysm
wegeners quick
Nasal Septum Erosions, Cavitary Lung Lesions
churg strauss quick
Transient peripheral lung consolidations.
microscopic polyangiitis quick
Diffuse pulmonary hemorrhage
hsp quick
Kids. Intussusception. Massive scrotal edema.
behcets quick
Pulmonary artery aneurysm
buergers quick
Male smoker. Hand angiogram shows finger occlusions.
General Vascular Ultrasound Concepts — Stenosis
overview
The waveform will go through changes before entering a stenosis, within the stenosis, and after exiting the stenosis.
General Vascular Ultrasound Concepts — Stenosis
porximal upstream findings
Waveform can be normal,
monophasic decreased
peak systolic velocity, or
loss of diastolic flow.
Diastolic flow is reduced in
proportion to the severity
of the stenosis.
General Vascular Ultrasound Concepts — Stenosis
stenosis findings
Waveform usually has a
high velocity jet -might
see aliasing.
High velocity = low
pressure (Bernouli’s effect
mother fuckers)
General Vascular Ultrasound Concepts — Stenosis
distal downstream findings
Waveform can be Tardus Parvus (prolonged “slow” systolic acceleration / upstroke, and small systolic peak - “rounding of the peak”)
General Vascular Ultrasound Concepts — Stenosis
stuff with words
It would be correct to say that Tardus Parvus is found downstream from a
stenosis. It would also be correct to say that Tardus Parvus is the result of upstream stenosis. See what I did right there? I’m not the only one who can pull some shit like th at…
High Yield Topics of Carotid Doppler
subclavian steal
This is discussed in greater detail in the cardiac chapter, but this time lets
show it on ultrasound. As a refresher, we are talking about stenosis and/or occlusion of the proximal subclavian artery with retrograde flow in the ipsilateral vertebral artery.
subclavian steal who will they show it
They are going to show two things: (1) Retrograde flow in the left vertebral, and (2) a stenosis of the subclavian artery with a high velocity
subclavian steal
how they can get really sneaky
They can show this thing called “early steal.” Steal is apparently a spectrum, which starts with midsystolic
deceleration with antegrade latesystolic
velocities. Some people think the
“early steal” waveform looks like a rabbit.
subclavian steal
how they can get really sneaky
They can show this thing called “early steal.” Steal is apparently a spectrum, which starts with midsystolic
deceleration with antegrade latesystolic
velocities. Some people think the
“early steal” waveform looks like a rabbit.
THIS vs THAT: G am e sm a n sh ip Inte rn a l Carotid vs E x te rn a l Carotid
This really lends itself well to multiple choice test questions. The big point to
understand is that the brain is always on. You need blood flow to the brain all the time, which means diastolic flow needs to be present all the time, and thus continuous color flow throughout the cardiac cycle. The external carotid feeds face muscles… they only need to be on when you eat and talk.
Internal carotid US findings
low resistance
low systolic velocity
diastolic velocity does not return to baseline
continuous color flow is seen throughout the cardiac cycle
External carotid us findings
high resistance
high systolic velocity
diastolic velocity approaches zero baseline
color flow is intermittent during the cardiac cycle
Temporal Tap
It is a technique Sonographers use to tell the external carotid from the internal carotid. You tap the temporal artery on the forehead and look for ripples in the
spectrum. The tech will usually write “TT” on the strip - when they do this.
A o rtic R eg u rg ita tio n
Just like aortic stenosis they are going to show you bilateral CCAs. In this case you are going to get reversal o f diastolic flow.
Brain D e a th
Apparently in the ever-feuding monarchies o f Europe, ultrasound can be used for brain death studies. A loss o f diastolic flow suggests cessation o f cerebral blood flow.
A n eu ry sm s
In case someone asks you, distal formation o f an aneurysm (such as one in the skull) cannot be detected by ultrasound, because proximal flow remains normal.
In tra -A o r tic Balloon Pump
Remember these guys are positioned so that the
superior balloon is 2 cm distal to the take o ff o f the left subclavian artery, and the inferior
aspect o f the balloon is ju st above the renals (you d o n ’t want it occluding importing stuff
when it inflates). When the balloon does inflate it will displace the blood in this segment o f
the aorta - smashing it superior and inferior to the balloon. The balloon will inflate during
early diastole (right after the aortic valve closes) because this is when the maximum amount
o f blood is available for displacement.
In tra -A o r tic Balloon Pump
What does this do to the internal carotid (ICA) waveform
You are going to see an extra
bump or “augmentation” as the balloon inflates and displaces blood superior.
In tra -A o r tic Balloon Pump
which wave should you measure to evlauate velocity
The first one (the one that is not assisted).
In tra -A o r tic Balloon Pump
which wave should you measure to evlauate velocity
The first one (the one that is not assisted).
Bro… WTF is a “LVAD” ?
The Left Ventricular A ssist Device is a surgically
implanted device that helps pump blood from the left
ventricle to the aorta. It’s done in the setting o f severe
heart failure, typically as a bridge to cardiac
transplantation, or in those who are simply too evil to die
o f natural causes (Dick Cheney) and require an
intermediate step while the Darth Vader suit is prepped.
LVAD
testable doppler changes
LVAD Waveforms will lose the normal high resistance spiked look o f the ICA, CCA,
Vertebral Arteries. Instead they are mostly flat, with a tardus parvus look. The flow is
continuous through systole and diastole. The little spikes you see during systole are from
the small amount o f residual LV function.
LVAD
testable doppler changes
LVAD Waveforms will lose the normal high resistance spiked look o f the ICA, CCA, Vertebral Arteries. Instead they are mostly flat, with a tardus parvus look. The flow is continuous through systole and diastole. The little spikes you see during systole are from the small amount o f residual LV function.
Normal CCA us waves
Normal Peak Velocity 60-100cm/s
Continuous Diastolic Flow
Normal ICA us waves
Lower Peak Velocity
High Velocity Continuous Diastolic Flow
Normal ECA us waves
Higher Peak Velocity
Less Diastolic Flow
ICA Occlusion us waves
-The CCA looks like the E C A , with a highresistance waveform, and loss of diastolic flow
Aortic Regurgitation classic us
- With Classic Reversal of Diastolic Flow
- Most Likely Shown Bilaterally
Aortic Regurgitation other us
-This time showing the “Pulsus Bisferiens” or double systolic peak. This is also seen in hypertrophic obstructive cardiomyopathy.
Aortic Stenosis us
- Characteristic Tardus Parvus waveform
- This will be shown BILATERAL - to prove it’s the aortic valve. Unilateral will be a more central vascular stenosis.
