THE COMPLETE GUIDE

TO
VASCULAR ULTRASOUND

PETER H. ARGER, M.D., SUZANNE DEBARI IYOOB,

F.A.I.U.M., F.A.C.R.
Professor Emeritus
Department of Radiology
University of Pennsylvania Medical Center
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
B.S., R.D.M.S., R.V.T.
Technical Director-Vascular Laboratory
Department of Radiology
University of Pennsylvania Medical Center
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
 THE COMPLETE GUIDE
TO
VASCULAR ULTRASOUND
To Christopher, my parents Susan and Robert, my brother Chris, my grandmother
Edith, and to all the rest of my family and friends (especially Susan Schultz and
Bonnie Brake) for their love, guidance, and support.
S.D.I.

To Afento, Harry, Donald, Anastasia, Eugenia, and Nicholas, to whom I am

immensely grateful, as they have profoundly influenced my whole approach to life.

P.H.A.
 CONTENTS
Preface ix
Acknowledgments xi
1 Blood Vessels: Anatomy and Physiology 1
2 Abdominal Vasculature 6
I. Abdominal Aorta 6
II. Inferior Vena Cava 10
III. Hepatic Veins, Portal Veins, and Hepatic
Arteries 11
IV. Superior Mesenteric Artery 17
V. Renal Arteries and Renal Veins 19
3 Peripheral Arterial Systems 26
I. Lower Extremity Arteries 26
II. Upper Extremity Arteries 41
4 Grafts 45
I. Hemodialysis Grafts 45
II. Bypass Grafts 48
5 Peripheral Venous Systems 55
I. Lower Extremity Veins 55
II. Upper Extremity Veins 69
6 Penile Vessels 75
7 Cerebrovascular System 84
8 Test Validation and Statistics 108
9 A Word About Doppler Controls 109
Appendix 121
I. Review Questions 121
II. Answer Key 129
Subject Index 131
 PREFACE
Vascular ultrasound has expanded to become an inte-
gral component of nearly every aspect of diagnostic ultra-
sound. The complexity of vascular ultrasound has increased
as the technology has increased, along with the ability of
ultrasound equipment to visualize more and more vessels as
well as a wider range of flow variables. The increased capa-
bility and utilization of color, power, and duplex Doppler
are examples of this.
Understanding both the technical and diagnostic
aspects of vascular ultrasound is essential to obtaining the
maximum information that can be acquired and to making
the most cogent and informative diagnosis of a given prob-
lem.
The Complete Guide to Vascular Ultrasound has a differ-
ent approach to vascular ultrasound, that combines the
“technique know-how” and “diagnostic analysis”. This
approach results in a better diagnosis of pathology at mul-
tiple levels. To promote a comprehensive approach to in-
depth knowledge of any given vascular problem, most chap-
ters are divided into a six-part approach:
1. Anatomy. Graphically demonstrates the general anatomy
of the vascular area to be examined as well as the anatomy
of individual vessels.
2. Pathology. Briefly discusses the pathologic processes,
which can affect the vessels being examined. Outlines
important associated pathophysiologic information nec-
essary for good analysis.
3. History/Questions to Ask the Patient. Details symp-
toms associated with potential vascular disease of the
vessels being evaluated.
4. Diagnostic Examinations. Details necessary technical
aspects of the examination tailored to the specific vessel
being evaluated. This may include commonly per-
formed but non-ultrasound tests.
5. Diagnostic Analysis. Includes Doppler waveform images
and illustrations. Discusses in a detailed outline form of
the relevance of various clinical findings.
6. Other Diagnostic Tests related to the clinical problem
including nonultrasound diagnostic tests.
We believe the information in this book speaks to a
wide audience including physicians, i.e., radiologists, vascu-
lar surgeons, and cardiologists, as well as sonographers,
whose work is vital to the field of ultrasound.
Peter H. Arger
Suzanne DeBari Iyoob
 ACKNOWLEDGMENTS

We would like to extend our sincere thanks to Patricia Hartman whose invaluable
help was a key factor in the production of this book. Her computer skills and typing of
the many modifications and re-modifications were a constant source of strength.
We also extend our gratitude to Philips Ultrasound, Scott Leonard, and all of the
sonographers and physicians in the Ultrasound section at the Hospital of the University
of Pennsylvania. We appreciate their help in acquiring the ultrasound images included in
this book. We would also like to thank Steven Horii for sharing his technical expertise.
 1
BLOOD VESSELS:
ANATOMY AND PHYSIOLOGY
I. ANATOMY OF BLOOD VESSELS
A. Three Layers (Tunicae) of Blood Vessels (Fig. 1.1)
1. Tunica interna or intima. This is the innermost
layer and is composed of endothelial cells.
2. Tunica media. This is the middle layer and is com-
posed of smooth muscle and elastic fibers. It is thicker
in arteries, can change the size and shape of arteries,
gives arteries their rigidity and round shape, and is
influenced by hormones and other chemicals.
3. Tunica externa or adventitia. This is the outer layer
and is composed of collagenous and elastic fibers. It
protects and anchors the vessel to surrounding tissues.
B. Circulatory System (Fig. 1.2)
1. Systemic circulation refers to the flow of blood
from the left ventricle of the heart through the body
(except for the lungs) and back to the right atrium of
the heart. The blood carries oxygen and nutrients to
the tissues of the body. It also removes wastes, carbon
dioxide, and heat from the tissues of the body. The
blood leaves the left ventricle of the heart, and goes
through the aorta, arteries, arterioles, venules, veins,
and vena cava to enter the right atrium of the heart:
Heart → Aorta → Arteries → Arterioles →
Capillaries → Venules → Veins →
Vena cava → Heart
2. Pulmonary circulation refers to the flow of blood
from the right ventricle of the heart, through the right
and left pulmonary arteries, to the alveoli (air sacs) in
the lungs, then from the alveoli of the lungs, through
the right and left pulmonary veins, and back to the left
atrium. The blood is deoxygenated when it enters the
alveoli from the right ventricle (as it has already gone
through the rest of the body through the systemic cir-
culation) and is oxygenated when it leaves the alveoli
of the lungs to go into the left atrium.
Heart → Pulmonary arteries → Alveoli →
Pulmonary veins → Heart
C. Types of Blood Vessels
1. Arteries are blood vessels that transport blood
from the heart to the tissues of the body. They contain
all three layers of tunicae. The tunica interna and
media is thicker than in veins. The tunica externa is
thinner than in veins. These divide into smaller and
smaller branches, eventually dividing into arterioles.
2. Arterioles. These small vessels are regulators of
blood flow from the arteries into the capillaries. As
they get closer to the capillaries, the layers of arteriole
decrease to consist only of an endothelial layer sur-
rounded by a few smooth muscle fibers. Vasoconstric-
tion (when the smooth muscle constricts) decreases
blood flow into the capillaries. Vasodilation (when the
smooth muscle relaxes) increases blood flow into the
capillaries. Arterioles have the highest resistance in the
circulatory system. They account for one half of the
total resistance to blood flow.
3. Capillaries. These microscopic vessels only have a
single layer of endothelium and a basement mem-
brane. They allow exchange of nutrients and waste
products between the blood and the cells of tissue.
Capillaries (sometimes extensive networks of capillar-
ies) usually connect arterioles and venules.
4. Venules. These vessels drain blood from the capil-
laries into the veins. Close to the capillaries, venules
may only consist of an endothelial layer surrounded by
the tunica externa. Closer to the veins, venules consist
of all three layers.
5. Veins. Veins are blood vessels that transport blood
from the tissues of the body back to the heart. They
are composed of all three layers of tunicae, although
the tunica intima and tunica media are thinner than in
arteries. The tunica externa is thicker than in arteries.
Veins contain valves to prevent backflow of the blood,
which has lower pressure at this point.
6. Vasa vasorum. This is a network of minute blood
vessels that perfuse the tissues of blood vessels them-
selves.
2 The Complete Guide to Vascular Ultrasound
FIGURE 1.1. Three layers of a vessel wall.
II. PHYSIOLOGY AND CHARACTERISTICS OF
BLOOD FLOW
A. Blood flow is the amount of blood that passes
through a vessel during an episode of time. Blood flows
in a laminar flow pattern in most vessels (Fig. 1.3). A
laminar flow pattern is a stable pattern consisting of
many laminae (layers) that are concentric. Each layer is
thought to flow at a different velocity. The velocity of
each layer increases as they approach the center of the
lumen. The center is where the highest velocity of blood
flow is thought to exist. The two primary factors that
determine blood flow are blood pressure and resistance.
B. Blood pressure. The pressure that the blood exerts
on the vessel walls is considered the blood pressure.
1. Blood pressure is directly proportional to blood
flow. When one increases, so does the other.
2. Blood always flows from areas with higher pressure
to areas with lower pressure.
3. Blood pressure starts off high as the blood leaves
the left ventricle to go into the systemic circulation
(mean pressure of 100 mm Hg) as it progresses down
to 0 mm Hg when the blood returns to the heart in
the right atrium.
4. Principal factors that affect arterial blood pressure:
a. Cardiac output. Cardiac output is determined
by multiplying the stroke volume (which is the
amount of blood ejected from either ventricle in
one systole, typically 70 mL) by the heart rate. This
is 5.25 L/min in a normal, resting adult. Cardiac
output is directly proportional to blood pressure.
When one increases, so does the other. When one
decreases, so does the other.
b. Blood volume. The volume of the blood is also
directly proportional to the blood pressure. When
one increases, so does the other. When one
decreases, so does the other. Normally, the volume
of blood in an adult is about 5 L. Hemorrhage
decreases blood volume and thus the blood pressure
also decreases. High salt intake (water retention)
increases blood volume, and thus the blood pressure
also increases.
c. Peripheral resistance is defined as all the factors
that oppose blood flow in the circulatory system.
Arterioles change their diameters to affect the resis-
tance, which affects blood flow and blood pressure.
As peripheral resistance increases, so does the arter-
ial blood pressure. This is a directly proportional
relationship as well.
5. Resistance. Opposition to blood flow. This occurs
as a result of friction between the blood vessel walls
and the blood. It also occurs due to the viscosity that
is created by the plasma proteins and the red blood
cells. It is directly proportional to blood pressure and
as a result blood flow. An increase in resistance would
result in an increase in both blood flow and blood
pressure.
FIGURE 1.2. Simplified circulatory system.

FIGURE 1.3. Laminar flow.
6. Principal factors that affect resistance to blood
flow:
a. Blood viscosity. The viscosity of the blood is
how “thick” the blood is. It takes more energy to
move blood that is more viscous. The viscosity is
directly proportional to resistance and thus blood
pressure. Dehydration, severe burns, and poly-
cythemia (an increase in the number of red blood
cells) all cause an increase in the viscosity of the
blood, which increases resistance and increases
blood pressure. A condition such as anemia or hem-
orrhage can cause a decrease in the viscosity of the
blood, which decreases the resistance and the blood
pressure.
b. Blood vessel radius. The fourth power of the
radius of a blood vessel is inversely proportional to
the resistance. When the radius decreases, the resis-
tance and blood pressure increase. Smaller vessels
obviously have higher resistances.
c. Blood vessel length. The longer the blood ves-
sel, the higher the resistance. There is a direct pro-
portional relationship.
C. Poiseuille’s Law helps to determine how much fluid
is moving through a vessel. It is an equation that
describes the relationship between resistance, pressure,
and volume flow. It demonstrates that the change in the
diameter of a blood vessel affects resistance the most. As
the radius decreases, the resistance increases. The velocity
of the blood flow then must increase to keep the same
amount of blood moving through the vessel. Therefore,
there is an inversely proportional relationship between
the velocity of a blood vessel and the site of the blood
vessel.
(P 1 − P2) π r4
Poiseuille’s Law = Q = ᎏᎏ
8ηL
Q = volume flow
P1 = pressure at the proximal end of the vessel
P2 = pressure at the distal end of the vessel
r = radius of the vessel
L = length of the vessel
π = 3.1416
η = viscosity of the fluid
1/Blood Vessels: Anatomy and Physiology 3
An abbreviated pressure/volume flow relationship can
also be used:
Q = P/R
Q = volume flow
P = pressure
R = resistance
D. Reynolds Number. As pressure increases, volume flow
increases as well. This occurs only to a point. When the sta-
ble laminar flow becomes disturbed, the smooth stream-
lines break up and form small circular currents called eddy
currents and vortices. Osborne Reynolds discovered that
when the flow pattern changes from smooth to disturbed,
flow volume was no longer increased by increased pressure.
Instead, the flow disturbance increased. Reynolds number
is a “dimensionless” number that reveals at what point flow
becomes turbulent. When the number exceeds 2,000, the
flow becomes turbulent. Other factors such as irregularities
of the vessel wall and plaque, pulsatility of blood flow, and
body movement can cause blood flow to become turbulent
at lower values of the Reynolds number.
Vq2r
Reynolds Number (Re) = Re = ᎏ
η
Re = Reynolds number
V = velocity
q = density of the fluid (since density and viscosity
are usually constant, turbulent flow)
r = radius of the tube (develops mainly as a result of
changes in velocity or radius)
η = viscosity of the fluid
E. The Bernoulli Equation. This demonstrates that
there is an inversely proportional relationship pressure
and velocity. When there is high velocity, there is low
pressure and vice versa. Flow separations are pressure gra-
dients (the difference in pressure from one area of the
vessel to another). These can be caused by a change in
direction of the vessel (curve or bend) or a change in the
geometry of the vessel (due to widening such as in the
carotid bulb or narrowing due to stenosis or plaque) (Fig.
1.4). Velocity decreases in an area of a flow separation,
and the pressure increases. Because blood flows from
high pressure to low pressure, the direction of the blood
flow changes in this area.
4 The Complete Guide to Vascular Ultrasound

FIGURE 1.4. Effects of stenotic plaque on flow pattern, velocity, and pressure.

F. Other Characteristics of Blood Flow
1. Flow that is low-resistance is continuous and
steady throughout systole and diastole. It is usually
found feeding a dilated vascular bed, such as in the
internal carotid, renal, vertebral, hepatic, splenic, and
celiac arteries.
2. Flow that is high resistance is pulsatile (tri- or
biphasic) (Fig. 1.5). It can usually be found in arter-
ies that supply high-resistance peripheral vascular
beds such as the external carotid, aorta, iliac, subcla-
vian, fasting superior mesenteric, and extremity
arteries.
3. Diastolic flow reversal is normally found in arteries
supplying high-resistance peripheral vascular beds.
This flow reversal increases with vasoconstriction and
decreases with vasodilation (which can be produced by
exercise, body heating, and stenosis). For example, a
normally high-resistance arterial Doppler signal
becomes low resistance after exercise. The diastolic
flow reversal portion of the waveform is now seen as a
forward reflection.
4. Diastolic flow reversal disappears distal to a
stenosis.
5. Diastolic flow reversal can also disappear proximal
to a significant stenosis.
6. Vasoconstriction causes an increase in pulsatility in
small and medium-size arteries and a decrease in pul-
satility in minute arteries, arterioles, and capillaries.

FIGURE 1.5. Doppler tracing of the midaorta, demonstrating high-resistance, pulsatile flow.

7. Vasodilation causes a decrease in pulsatility in small
and medium-size arteries and an increase in pulsatility
in minute arteries, arterioles, and capillaries.
8. Total blood flow may be normal in an extremity at
rest even when there is a significant stenosis or occlu-
sion of a vessel. This is due to development of a col-
lateral network.
1/Blood Vessels: Anatomy and Physiology 5
BIBLIOGRAPHY
Rumwell C, McPharlin M. Arterial evaluation in vascular technol-
ogy—an illustrated review Pt. 1, 2nd ed. Pasadena, CA: Davies
Publishing, 2000:1–33.
Tortora GJ, Anagnostakos NP. The cardiovascular system: vessels and
routes. In: Principles of anatomy and physiology, 6th ed. New York:
Harper & Row, 1990: 606–612.
 2
ABDOMINAL VASCULATURE
I. ABDOMINAL AORTA
A. Anatomy (Fig. 2.1)
1. Abdominal aorta extends from the twelfth thoracic
vertebra to the fourth lumbar vertebra.
2. Portions of the Abdominal Aorta (Fig. 2.2):
a. Proximal—superior to or at the level of the celiac
axis, measures 2 to 3 cm
b. Middle—below the celiac axis, above the renal
arteries, measures 1.6 to 2.5 cm
c. Distal—just above the bifurcation, measures 1.1
to 2.0 cm
d. Iliac arteries—measure 0.6 to 1.4 cm
3. Main branches off the aorta:
a. Celiac axis or celiac artery: first branch off the
abdominal aorta, divides into the left gastric
artery, splenic artery, and common hepatic
artery. These feed the stomach, spleen, liver, pan-
creas, and duodenum.
b. The superior mesenteric artery is approxi-
mately 1 cm distal to the celiac axis. This artery
feeds the small intestine, ascending colon, cecum,
and part of the transverse colon.
c. The renal arteries are the next branches. They sup-
ply the kidneys, ureters, and adrenal glands (Fig. 2.3).
d. The inferior mesenteric artery is approximately
3 to 4 cm above the aortic bifurcation. It supplies the
descending, iliac, and sigmoid colon, as well as the left
half of the transverse colon and part of the rectum.
e. The common iliac arteries are the terminal
branches of the abdominal aorta. They divide into the
internal iliac arteries and the external iliac arteries.
4. Other branches off the abdominal aorta but not
commonly seen on ultrasound are:
a. The paired inferior diaphragmatic or inferior
phrenic arteries.
b. The paired middle suprarenal arteries.
c. The paired gonadal arteries.
d. The paired first to fourth lumbar arteries.
e. The middle sacral artery.
5. Above the umbilicus, all paired arteries course pos-
terior to their related vein. Below the umbilicus, all
paired arteries course anterior to their related vein.
B. Pathology
1. Ectasia—when the abdominal aorta does not taper
as it normally does, but is not dilated to the point of
aneurysm.
2. Atherosclerosis or arteriosclerosis—thickening,
hardening, and deposition of plaque in the intimal
wall of arteries, which can cause stenosis.
a. This is associated with smoking, hypertension,
sedentary lifestyle, diabetes mellitus, and increased
levels of low-density lipoprotein (LDL) levels of
cholesterol.
b. Because of its large size and high flow rate, the
abdominal aorta is sensitive to plaque. Two com-
mon sites of plaque formation are the origin of the
renal arteries and the bifurcation into the common
iliac arteries. The most common site is the
infrarenal portion of the aorta.
c. More men than women are affected with ather-
osclerosis, and the incidence increases with age.
d. Atherosclerosis may be associated with
aneurysm and wall weakening.
3. Coarctation is the narrowing of the aorta. There
are two clinical findings associated with this:
a. Hypertension resulting from decreased kidney
perfusion.
b. Manifestation of lower extremity ischemia
decreased lower extremity pulses.
4. Aneurysm—increase in arterial diameter (Fig. 2.4).
a. Types of aneurysms (Fig. 2.5):
(1) Fusiform—symmetric swelling, most com-
mon, usually found below the level of the renal
arteries (90% of all aneurysms) and may extend
into the common iliac arteries. These also may
contain thrombus.
(2) Saccular—focal outpouching, least com-
mon, usually affects the left lateral portion of
the distal abdominal aorta (where the least sup-
port is), causes marked alteration in the pattern
of blood flow. These also may have thrombus or
plaque.
(3) Dissecting—tear in intimal lining of the wall
of the vessel. A false lumen is created between the

FIGURE 2.1. Abdominal vasculature.
intima and the media. These may extend from
the aortic valve to the abdominal aorta. They can
be very dangerous. Blood flow may push the flap
across the lumen and completely (or almost com-
pletely) obstruct flow. Two flow lumens with
markedly different flow characteristics would be
seen. These are most common in the thoracic
aorta (Fig. 2.6).
FIGURE 2.2. Sagittal view of the middle and distal aorta.
2/Abdominal Vasculature 7
(4) Pseudoaneurysms or false aneurysms. Small
pocket of moving blood connected to an artery
through a small opening or neck and may be
partly surrounded by thrombus. These form due
to interventional radiology procedures (e.g., car-
diac catheterization using the common femoral
artery), trauma, surgery, or infection. They can
be felt as a pulsatile mass. A turbulent flow pat-
FIGURE 2.3. Transverse view of the renal arteries coming off the
aorta.
8 The Complete Guide to Vascular Ultrasound
FIGURE 2.4. Abdominal aortic aneurysm. Note the irregular
dilatation of the distal aorta.
tern would be visualized. Compression with a
transducer may clot them off. An alternative
therapy would be thrombin injection.
b. Abdominal aortic aneurysm is considered if the
diameter is greater than 3 cm or greater than 50%
than the original diameter.
c. A true aneurysm contains all the layers of the
artery (fusiform and saccular.) A false aneurysm or
pseudoaneurysm leaks through a hole in the intima
but is contained by the external layer or by the body.
d. There is an increased risk for abdominal aortic
aneurysm in close relatives.
e. The incidence of the disease is highest among
men, particularly those over 65 years of age.
f. The identification of an abdominal aortic
aneurysm increases the risk for aneurysms in the
common iliac arteries, common femoral arteries,
and popliteal arteries.
g. Only 4% of abdominal aortic aneurysms actu-
ally affect flow into the renal arteries. Stenosis of the
renal arteries and hydronephrosis are potential com-
plications of abdominal aortic aneurysms.
FIGURE 2.6. Dissection of the abdominal aorta. There appear to
be parallel hypoechoic lumens within the aorta. The posterior
portion is the false lumen, separated from the true lumen by the
flap (arrow). (Image courtesy of Philips Medical Systems.)
h. Aneurysms over 6 cm in diameter are considered
surgical emergencies, and 60% of all aneurysms
over 7 cm will rupture within 1 year. Abdominal
aortic aneurysms can have small tears and leak into
the body cavity.
i. The main complication of abdominal aortic
aneurysm is rupture; the main complication of
peripheral aneurysm is distal embolization.
j. Atherosclerotic abdominal aortic aneurysms may
become inflammatory, and the wall will become
thickened and surrounded by fibrosis.
k. Marfan syndrome is associated with weakness of
the arterial wall and may result in aneurysm of the
first portion of the aorta leading up to the aortic
valve. This may lead to dissection of this portion of
the aorta.
FIGURE 2.5. Types of aneurysms.

l. To repair an aneurysm, the surgeon may put a
graft in. The native aorta is usually wrapped around
the graft. Fluid can accumulate between the graft and
the vessel wall. Types of aortic grafts are as follows:
(1) Aortic end-to-end graft (wrapped in native
aorta)
(2) Aortoiliac graft
(3) Aorto-bifemoral graft
C. History: Questions to Ask the Patient
1. Do you have abdominal pain? (May be deep and
penetrating, mainly in the back). Aortic rupture causes
severe pain.
2. Do you have a pulsing sensation in your abdomen?
(Most of the time a thoracic aneurysm will not be con-
sidered. However, if this is a consideration or if on early
views of the aorta one sees a suggestion of extension
from the thoracic area, then ask the next question).
3. Do you have high back pain, a cough, wheezing,
hoarseness, or difficulty swallowing?
D. Diagnostic Examination
1. Begin with the patient in the supine position,
although a decubitus position can be helpful to evalu-
ate the bifurcation.
2. Using a 3.5- or 5-MHz curved-array transducer,
place the transducer in a sagittal plane at the midline
of the body, just inferior to the xiphoid process of the
sternum. Slightly move or angle the transducer to the
left and locate the proximal aorta. Slowly move inferi-
orly, using a rock-and-slide motion.
3. Repeat in the transverse plane.
4. Measure anteroposterior and transverse dimensions
of the aorta, outside wall to outside wall.
E. Diagnostic Analysis
Analysis of the abdominal aorta would include the fol-
lowing:
FIGURE 2.7. Sagittal view of a bifurcated endograft (closed
arrows) within dilated aortic lumen (open arrows). (Image cour-
tesy of Philips Medical Systems.)
2/Abdominal Vasculature 9
5. Take sagittal and transverse images of the following
structures with and without calipers:
a. Proximal aorta (inferior to the diaphragm and
superior to the celiac trunk).
b. Mid aorta (inferior to the celiac trunk and along
the length of the superior mesenteric artery).
c. Distal aorta (inferior to the superior mesenteric
artery and superior to the bifurcation).
d. Right and left common iliac arteries.
e. Color images and Doppler waveforms may be
taken if necessary.
f. If evaluating an endovascular stent graft, take
gray-scale images in both planes, and color images
and Doppler waveforms through the native aorta,
entire graft, and outflow iliac vessels. Assess the
entire residual aneurysm sac as well. Evaluate poten-
tial sites for endoleaks, such as the attachment sites
of the graft or branches related to the lumbar artery
and inferior mesenteric artery (Fig. 2.7).
6. Distinguishing the aorta from the inferior vena
cava (IVC) on ultrasound:
a. The aorta never touches the liver; the IVC does.
b. The aorta has thicker walls (thicker tunica media).
c. The aorta has cardiac pulsatility; the IVC
changes with respiration.
d. The aorta tapers from superior to inferior; the
IVC has a “hammock” shape.
e. The aorta and IVC have different Doppler signals.
f. The aorta has multiple anterior branches, while
the only branches from the IVC are the hepatic
veins.
g. The right renal artery is seen posterior to the
IVC; no vessels course posterior to the aorta.
1. The maximum true anteroposterior, length, and
transverse dimensions.
2. Documentation of the location of an aneurysm,
and of whether the renal arteries or iliac arteries are
involved.
3. Notation of wall thickening in terms of what type
and how extensive it is.
4. Evaluation for dissection. This appears as a thin
membrane “fluttering” in the lumen. Doppler shows
different signals in each of the channels.
5. Examination of both kidneys for signs of hydro-
nephrosis or renal artery stenosis.
6. Verification that normal triphasic or biphasic
waveforms that are high resistance are seen with
Doppler.
7. An endoleak associated with an endovascular stent
graft has a distinctly different Doppler signal than
from that of the endograft. There should be no flow
leaking out around the graft, inside or outside of the
residual aneurysm sac.
10 The Complete Guide to Vascular Ultrasound
F. Other Diagnostic Tests
1. Aortic angiography
2. Magnetic resonance angiography (MRA)
3. Computed tomographic angiography (CTA).
II. INFERIOR VENA CAVA
A. Anatomy (Fig. 2.8)
1. Originates from the paired common iliac veins at
fifth lumbar vertebra.
2. Lies to the right of the aorta.
3. The size is generally less than 3.5 cm during full
inspiration.
4. The main branches include the hepatic veins,
renal veins, and the common iliac veins.
5. The right and left renal veins enter the IVC later-
ally, coursing anterior to the renal arteries. The left
renal vein is longer, and courses anterior to the aorta
and posterior to the superior mesenteric artery (SMA).
6. The right gonadal and fourth lumbar vein also enters
the IVC. (The left gonadal vein enters the left renal vein.)
7. The tunica media of the IVC is very thin and elastic.
8. There are no valves in the IVC. There are also no
valves in the external and common iliac veins, hepatic,
renal, lumbar, gonadal, and soleal sinuses.
9. During inspiration, the intrathoracic pressure
decreases and the intraabdominal pressure increases.
Blood moves from the abdomen into the chest with
decreased outflow from the peripheral veins, and flow
in the legs should decrease or stop. Inflow is allowed
from upper extremities. During expiration, vice versa.
Outflow increases from the lower extremity veins.
10. Hydrostatic pressure is pressure due to gravity—
when the patient is supine, hydrostatic pressure is neg-
ligible (0–15 mm Hg). When the patient is erect,
hydrostatic pressure may be 102 mm Hg depending
on his or her height.
B. Pathology
1. Enlargement of the IVC. A faulty tricuspid valve
that allows blood to reflux through the right atrium
FIGURE 2.8. Sagittal view of the inferior vena cava.
into the IVC causes the size of the IVC to be large
(>3.5 cm). Color flow shows reversal—blue then red
then blue again pattern.
2. Thrombus in the IVC may lead to localized
swelling and noncollapse of the IVC during exhalation.
3. Tumors may invade the IVC, especially from the
right kidney through the right renal vein. These metas-
tasize from lymphoma, hepatocellular carcinoma, renal
cell carcinoma, and breast carcinoma. Primary tumors
are rare. Leiomyosarcoma of the IVC wall is the most
common type of mural tumor in the venous system.
4. Budd-Chiari syndrome—thrombus in hepatic
veins prevents blood from draining from the liver to
the IVC.
5. Congenital abnormalities may include the
hepatic veins draining directly into the right atrium.
6. IVC rupture usually occurs after trauma or surgery.
7. Greenfield filter (or other filter) — placed in the
IVC near the confluence of the renal veins or iliac
veins. This keeps the thrombus from coursing through
the IVC, heart, and pulmonary vessels. A surgical clip
can also be placed in the IVC to decrease the risk for
pulmonary embolism.
C. History: Questions to Ask the Patient. Symptoms
may be nonspecific. Primary vena cava tumors are rare,
and symptoms are likely to be due to secondary involve-
ment or compression of the IVC. There may be secondary
renal related symptoms. Ask the following questions:
1. Do you have leg swelling or edema?
2. Do you have any known kidney disease?
D. Diagnostic Examination
1. Begin with the patient in the supine position,
although a slight reverse Trendelenburg position can
pool blood in the IVC. A decubitus position can also
be helpful.
2. Using a 3.5- or 5-MHz curved-array transducer,
place the transducer in the sagittal plane at the midline
of the body, just inferior to the xiphoid process of the
sternum. Slightly move or angle the transducer to the
right and locate the IVC. [See “Distinguishing the
Aorta from the IVC” (Section I.D.2.) for different
sonographic characteristics between the two.] Slowly
move inferiorly, using a rock-and-slide motion.
3. Repeat in the transverse plane.
4. Take sagittal and transverse images of the following
structures:
a. Distal IVC to include the diaphragm and
hepatic veins
b. Mid-IVC at the level of the head of the pancreas
c. Proximal IVC
d. Bifurcation of the right and left common iliac veins
E. Diagnostic Analysis
1. The IVC transmits both respiratory and cardiac pul-
sations, which becomes more noticeable the closer you
are to the heart. The pattern of the Doppler tracing has
been described as a “saw-tooth” tracing (Fig. 2.9).

FIGURE 2.9. Doppler tracing of the inferior vena cava.
2. With deep inspiration, the IVC dilates. With deep
expiration, the IVC diameter decreases. By doing a Val-
salva maneuver, the flow is temporarily suspended.
3. Evaluate the lumen for thrombus, tumor, or slow-
flowing blood. Slow-flowing blood appears more
echogenic and moves in a swirling pattern. Slow-flow-
ing blood is seen with fluid overload, right heart fail-
ure, and inferior to an obstruction.
F. Other Diagnostic Tests
1. Venography
2. MRA
3. CTA
III. HEPATIC VEINS, PORTAL VEINS, AND HEPATIC
ARTERIES
A. Anatomy
1. The portal system delivers approximately 1.2 L of
blood per minute to the liver.
2. The liver receives a double supply of blood. From
the portal vein it receives deoxygenated blood and
from the hepatic artery it receives oxygenated blood.
3. Portal blood carries a significant amount of toxins
and waste products to the liver to be purified.
4. Blood is progressively cleaned and freed of toxins as
it passes through smaller and smaller branches in the
liver. Flow toward the liver is called hepatopetal.
5. The liver breaks down toxins and waste products
into chemicals, which are later removed from the body
in bile.
6. Blood is drained from the liver by three hepatic
veins that enter the IVC just below the diaphragm.
Flow away from the liver is called hepatofugal.
2/Abdominal Vasculature 11
7. The right and left gastric veins enter the main
portal vein and drain the esophagus and stomach.
8. The main portal vein enters the liver and divides
into the right and left portal veins.
9. The splenic vein drains the spleen, liver, and
pancreas.
10. The inferior mesenteric vein drains the distal
colon and rectum and enters the splenic vein.
11. The superior mesenteric vein drains the proxi-
mal colon and small bowel.
12. The hepatic artery arises from the celiac axis
72% of the time. Once in the liver, it branches into
the left and right hepatic arteries.
13. The hepatic artery proper also gives origin to the
gastroduodenal artery (GDA), the supraduodenal
artery, and the right gastric artery.
B. Pathology
1. Budd-Chiari Syndrome
a. This involves thrombus or tumor in the hepatic
veins, obstructing hepatic venous outflow.
b. The most common causes include thrombosis
due to oral contraceptives; invasion of tumor from
hepatocellular carcinoma, renal cell carcinoma, or
adrenal carcinoma; and radiation to the liver, which
can obliterate small hepatic veins.
2. Portal hypertension—an increase in portal
venous pressure. The pressure is normally between 0
and 5 mm Hg. With portal hypertension, it can go up
to 10 to 12 mm Hg.
a. Prehepatic (or infrahepatic)— any increase in
portal blood flow caused by the following:
12 The Complete Guide to Vascular Ultrasound
(1) Congenital atresia of portal veins (increased
pressure below stricture).
(2) Portal vein thrombosis (secondary to tumor
invasion or cirrhosis).
(3) Splenic vein thrombosis.
(4) Compression of portal element (by tumor,
lymph node, or foreign mass).
(5) Splenomegaly (leads to increase in blood
within the portal system).
(6) Arteriovenous (AV) malformation (malfor-
mation between the artery and vein can cause an
increase in portal blood flow).
b. Intrahepatic (or hepatic): decrease in capacity
of liver to transmit portal blood to the IVC caused
by the following:
(1) Cirrhosis
(2) Hepatic schistosomiasis (parasitic infection)
(3) Chronic hepatitis
(4) Fatty liver
(5) Diffuse metastatic disease
c. Suprahepatic (or posthepatic): increased pres-
sure caused by the following:
(1) Cardiac abnormalities (chronic heart failure)
(2) Budd-Chiari syndrome (blocked hepatic veins)
(3) Occlusion of the IVC (tumor, clot, extrinsic
compression)
d. Transjugular intrahepatic portosystemic shunt
(TIPS) procedure. In extreme cases of portal
hypertension, this creates an artificial pathway for
blood to flow from the main portal vein directly to
the hepatic veins, bypassing the venules of the liver.
The TIPS usually extends from the right hepatic
vein through the posterior branch of the right por-
tal vein to the main portal vein.
e. Components involved in and findings associ-
ated with portal hypertension:
(1) Main portal vein and splenic vein: splenic
varices
(2) Intrahepatic portal veins: subcapsular liver
varices
(3) Right and left gastric veins: esophageal
varices
(4) Superior mesenteric vein: hemorrhoids
(5) Main portal vein: patent ligamentum teres
(patent umbilical vein) and caput medusa
(6) Any portion of the portal system with chron-
ically increased pressure: ascites and pleural effu-
sions
3. Portal vein thrombosis
This can be caused by portal hypertension, inflamma-
tory abdominal processes (such as in appendicitis, peri-
tonitis, or pancreatitis), postsurgical complications,
trauma, hypercoagulability states (such as with oral con-
traceptives, pregnancy, thrombocytosis, polycythemia
vera, etc.), abdominal neoplasms, renal transplants, and
benign ulcer disease. This can also be idiopathic.
4. Portal vein aneurysm
This can be caused by congenital malformations, por-
tal hypertension, and weakening of the vessel wall by
pancreatitis. Portal vein aneurysms can lead to portal
hypertension.
5. Hepatic artery aneurysm
a. Hepatic artery aneurysms are mostly extrahep-
atic (75%). When it occurs intrahepatically, it most
often affects the right branch.
b. These are rare and mostly affect males.
c. The most common causes include systemic infec-
tion, trauma, or arteriosclerosis. They may also be con-
genital. Patients with chronic pancreatitis may develop
these. They also occur in the splenic artery, superior
mesenteric artery, or inferior mesenteric artery.
6. Liver transplant
a. Liver transplants are becoming a more common
treatment for patients with end-stage liver disease.
b. Postoperative complications after liver trans-
plants include:
c. Portal vein thrombosis.
d. Pseudoaneurysm formation.
e. IVC thrombosis.
f. Hepatic artery occlusion (leading to hepatic
infarction).
g. Liver transplant rejection.
C. History: Questions to Ask the Patient
1. Have you had or been told you have a large liver or
spleen?
2. Have you had blood tests that were not normal
with regard to liver function?
3. Have you even been jaundiced with yellow skin or
yellow eyes?
4. Have you ever had very dark urine?
5. Have you ever had hepatitis?
6. Have you ever had gallbladder disease?
7. Have you had any of the following:
a. Fatigue?
b. Weakness?
c. Weight loss?
d. Poor appetite?
e. Nausea?
f. Fever?
g. Unusual itching?
h. Blood in your bowels?
i. Coughed up any blood?
j. Abdominal pain?
k. Increase in abdominal girth?
D. Diagnostic Examination
1. Begin with the patient in the supine position,
although a left lateral decubitus position may be help-
ful with some patients.
2. Using a 3.5- or 5-MHz curved-array or phased-
array transducer, place the transducer in the transverse
plane at the midline of the body, just inferior to the
xiphoid process of the sternum, angled slightly to the

patient’s right shoulder. Angle the transducer steeply
superior until the heart is seen then slowly straighten
the transducer into a more perpendicular position
until the liver comes into view. The first vessels that
come into view are the right, middle, and left hepatic
veins draining into the IVC.
3. Slowly straighten the transducer even more per-
pendicular, moving inferior to the left lobe of the liver
slightly. The next vessel that comes into view is the left
portal vein.
4. Slide down the costal margin of the ribs laterally on
the patient’s body while angling superiorly. Intercostal
scanning may be necessary at this point. Just inferior
to the left portal vein, the main portal vein and the
right portal vein come into view. The hepatic arteries
2/Abdominal Vasculature 13
FIGURE 2.10. Color flow image of the
hepatic veins. They flow away from the liver
toward the inferior vena cava; therefore,
they are displayed as blue, or away from the
transducer. (Note the color flow map direc-
tion.)
course along the sides of the portal veins. They are best
visualized with color Doppler.
5. Take color images and Doppler signals with peak
velocity measurements from the following struc-
tures:
a. Right, middle, and left hepatic veins (Fig. 2.10).
b. Right, main, and left portal veins (Figs.
2.11–2.13).
c. Right, proper, and left hepatic arteries. (If
after liver transplantation, document the veloc-
ity along the proper hepatic artery in three
places: the donor artery in the liver, the anasto-
mosis site, and the recipient artery near the
celiac axis. Also evaluate the splenic vein and the
IVC.)
FIGURE 2.11. Color flow image of the right
portal vein. Although both the anterior and
posterior branches flow toward the liver,
the anterior branch is displayed as red
because the flow is toward the transducer,
and the posterior branch is displayed as blue
because the flow is away from the trans-
ducer. (Note the color flow map direction.)
14 The Complete Guide to Vascular Ultrasound

FIGURE 2.12. Color flow image of the main por-

tal vein. It flows toward the liver, and the flow is
displayed as red because it is toward the trans-
ducer. (Note the color flow map direction.)

d. In the case of a TIPS, evaluate the portal venous
end, the middle portion, and the hepatic venous
end of the TIPS. Also evaluate the right, main, and
left portal veins; the IVC; the hepatic vein involved;
and the splenic vein.
E. Diagnostic Analysis
1. Hepatic veins
a. Signs of Budd-Chiari syndrome may include loss
of visualization of the hepatic veins, thrombus or
tumor within the lumen of a vessel, a thick-walled
appearance of the vessels, hypertrophy of the caudate
lobe and the left lateral segment with atrophy of the
right lobe, ascites, splenomegaly, pleural effusions,
hyperechoic areas within the liver, and an hourglass
shape of the IVC.
b. Blood flow in the hepatic veins is normally
hepatofugal, triphasic, and pulsatile (Fig. 2.14). The
pulsatility can appear exaggerated in patients with

FIGURE 2.13. Color flow image of the left portal vein. It flows toward the liver, and the flow is
displayed as red because it is toward the transducer. (Note the color flow map direction.)
 2/Abdominal Vasculature 15

FIGURE 2.14. Normal Doppler tracing of the middle hepatic vein.

FIGURE 2.15. Normal Doppler tracing of the main portal vein.

16 The Complete Guide to Vascular Ultrasound
right heart failure. A monophasic waveform can be
seen in patients with liver disease such as cirrhosis.
2. Portal veins
a. The size of the main portal vein is usually less
than 1.3 cm. The walls of the portal veins should be
more echogenic than the walls of the hepatic veins.
Evaluate the size of the portal vein and check for
any aneurysms.
b. The flow pattern is normally continuous and
wavy (Fig. 2.15). The flow is normally directed
toward the liver (hepatopetal). Using Doppler, look
for any reversal of blood flow (hepatofugal) (Fig.
2.16), which is a sign of portal hypertension. This
may only be evident upon suspended respiration.
c. Other signs of portal hypertension include a
patent umbilical vein (seen in the falciform liga-
FIGURE 2.16. Main portal vein showing
reversal of flow. Note the color flow map
direction.
ment); esophageal varices; splenic varices (Fig.
2.17); a splenorenal shunt (reversed splenic vein
flow combined with enlargement of the left renal
vein, which indicates blood being shunted to the
left renal vein to relieve pressure); other varices such
as pancreatic, gastrorenal, and duodenal; ascites; an
enlarged spleen; enlarged diameter of the superior
mesenteric and splenic veins; and reversal of flow in
the superior mesenteric vein. It has also been noted
that the blood flow tends to be slower in patients
with portal venous hypertension.
d. Evaluate the portal vein for any signs of
echogenic material (thrombus or tumor) (Fig. 2.18)
or collaterals around the portal vein. With chronic
thrombosis of the portal vein, large collaterals
develop. This is called cavernomatous transforma-
FIGURE 2.17. Color flow image of splenic
varices, which appear as a tangle of multi-
ple, dilated vessels near the splenic hilum.

FIGURE 2.18. Echogenic tumor within the left portal vein.
tion of the portal vein (Fig. 2.19). These look like
multiple, wormlike structures in the area of the por-
tal vein. Absence of flow in the portal vein due to
thrombus is detected by using Doppler.
3. Hepatic arteries
a. Hepatic artery aneurysms appear as anechoic
structures in the liver next to the portal veins. They
may appear complex if thrombus is involved. Tur-
bulent flow is detected with Doppler.
b. Normal flow in the hepatic artery has low resis-
tance (high diastolic velocity) and is pulsatile.
2/Abdominal Vasculature 17
Absent or blunted flow after liver transplantation
indicates obstruction of the hepatic artery.
4. TIPS
a. Following a TIPS procedure, normal flow visual-
ized includes high-velocity and turbulent flow in the
shunt (mean peak systolic velocity of 125 to 200
cm/s) and hepatofugal flow in the left portal vein as
well as the anterior branch of the right portal vein
(flowing toward the TIPS) (Fig. 2.20). An increase in
hepatic artery peak systolic velocity can also be seen.
b. Complications with the TIPS include stent
occlusion, stent stenosis, and hepatic vein stenosis.
c. When the TIPS is occluded or thrombosed,
there will be no evidence of flow within the stent.
d. When there is low-velocity flow (especially at
the portal venous end of the TIPS) that is less than
50 to 60 cm/s, this can suggest stenosis of the stent
beyond that point.
e. Hepatic vein stenosis is suggested by reversal of
flow (away from the IVC) in the hepatic vein
involved with the shunt.
f. Other abnormal findings with a TIPS include
hepatopedal flow (away from the TIPS) in the por-
tal vein branches; a change in the peak stent veloc-
ity of the initial baseline study, with either an
increase or a decrease of 50 cm/s; or secondary signs
such as a reappearance of ascites, varices, and a
recanalized paraumbilical vein.
F. Other Diagnostic Tests
1. Abdominal angiography
2. MRA
IV. SUPERIOR MESENTERIC ARTERY
A. Anatomy
The superior mesenteric artery is approximately 1 cm dis-
tal to the celiac axis. This artery feeds the small intestine,
ascending colon, cecum, and part of the transverse colon.
FIGURE 2.19. Cavernous transfor-
mation of the main portal vein,
showing multiple varied flow direc-
tions and velocities.
18 The Complete Guide to Vascular Ultrasound

FIGURE 2.20. Anterior branch of the right portal vein flowing toward the transjugular intra-
hepatic portosystemic shunt (TIPS). It is displayed as blue, or away from the transducer. (Note the
color flow map direction.) Without a TIPS, the anterior branch of the right portal vein is displayed
as red, or toward the transducer (see Fig. 2.11).

FIGURE 2.21. Although the Doppler tracing of the celiac artery is still low resistance, the
increased velocity and spectral broadening indicate celiac stenosis. (Image courtesy of Philips
Medical Systems.)

B. Pathology
1. Mesenteric ischemia is caused by a deficiency of
blood being sent to the intestines, which results from
significant narrowing or obstruction of the both the
celiac axis and the superior mesenteric artery.
2. Celiac axis compression syndrome (CACS). In this
syndrome, the median arcuate ligament of the diaphragm
compresses the celiac axis. This occurs during exhalation.
C. History: Questions to Ask the Patient
There are a variety of different symptoms for this disease,
consequently it is very difficult to diagnose. You will
need to ask the following questions:
1. Have you had consistent, severe abdominal pain 15
to 20 minutes after eating?
2. Have you had an unexplained weight loss?
D. Diagnostic Examination
1. Begin with the fasting patient in the supine posi-
tion. Using a 3.5- or 5-MHz curved-array transducer,
place the transducer in the sagittal plane at the midline
of the body, just inferior to the xiphoid process of the
sternum.
2. Slightly move or angle the transducer to the left and
locate the proximal aorta. The first branch off the
abdominal aorta is the celiac axis (or celiac trunk). It
quickly branches into the common hepatic artery on the
right and the splenic artery on the left. The next branch
is the superior mesenteric artery, which also takes off
from the anterior wall of the aorta. It runs parallel to the
aorta, coursing distally to infuse the intestine.
3. Doppler signals with peak systolic velocity mea-
surements may be taken from both of these vessels,
both pre- and postprandially.
E. Diagnostic Analysis
1. Normal velocity of the superior mesenteric artery is
less than 200 cm/s. The normal velocity of the celiac
artery is less than 275 cm/s.
2. The normal preprandial (fasting) waveform for the
superior mesenteric artery is high resistance, and the
normal postprandial (after eating a meal) waveform is
low resistance.
3. If there is mesenteric ischemia, the waveform of the
superior mesenteric artery will remain high resistance
postprandially and the velocity will increase.
4. With CACS, the normal low-resistance waveform of
the celiac artery is replaced by a high-resistance wave-
form with increased velocity and turbulence (Fig. 2.21).
There is also a flattened appearance of the celiac artery.
5. Plaque as well as a stenotic narrowing of the vessel
may be seen.
6. Normal flow resistances:
Aorta high
Renal artery low
Celiac artery low
SMA high (prandial) low (post-prandial)
Splenic artery low
2/Abdominal Vasculature 19
V. RENAL ARTERIES AND RENAL VEINS
A. Anatomy
1. The renal arteries arise within 1.5 cm of the ori-
gin of the superior mesenteric artery. They arise from
the lateral sides of the aorta and enter each kidney. The
right renal artery courses behind the IVC to enter the
right kidney.
2. The left renal vein courses from the left kidney
and crosses the anterior aspect of the aorta (but
beneath the superior mesenteric artery) to enter the
lateral aspect of the IVC. The right renal vein arises
from the right kidney and enters the right lateral
aspect of the IVC.
3. Approximately 22% of patients have two renal
arteries. A small percentage have three or more.
B. Pathology
1. Renal artery aneurysm
a. A renal artery aneurysm is a dilatation of the
renal artery. It may be saccular or fusiform.
b. An aneurysm of the renal artery may be congen-
ital or due to trauma, atherosclerosis, inflammation,
or fibromuscular disease.
2. Arteriovenous malformation and fistula
a. These may be congenital or, more commonly,
acquired. Acquired arteriovenous communications
are usually iatrogenic, although some may occur
spontaneously with eroding tumors.
b. Congenital arteriovenous communications usu-
ally consist of a tangle of small vessels, while
acquired lesions usually consist of a single feeding
artery and a single draining vein.
3. Renal artery occlusion and infarction. Occlu-
sion of the renal artery may occur with thrombosis or
due to an embolus. If the main renal artery is
affected, then the entire kidney will be affected. If
smaller intrarenal vessels are affected, there will be an
area of focal infarction.
4. Renal artery stenosis
a. Renal artery stenosis may be caused by athero-
sclerosis or fibromuscular hyperplasia (a rare dis-
ease that can affect young women). Renal artery
stenosis may cause renal hypertension (renal vas-
cular hypertension) by activating the renin-
angiotensin system.
b. Renal artery stenosis can be cured surgically in
some cases by placement of a bypass graft around the
segment that contains the stenotic lesion. The
stenotic segment can also be dilated by balloon
angioplasty. A third way to treat the disease is to
remove the plaque, and then widen the artery with
placement of a vein patch. A fourth and relatively
new treatment is renal artery stenting. The stent may
or may not be echogenic. The distal end of the stent
may cause angulation of the artery that could possi-
bly cause difficulty in achieving a proper Doppler
20 The Complete Guide to Vascular Ultrasound
angle. It is important to look postsurgery for the fol-
lowing complications: renal artery dissection, distal
embolization to the kidney, thrombosis, and incom-
plete deployment of the stent.
5. Enlargement of the renal vein. If the left renal vein
is enlarged, this could be due to splenorenal or gas-
trorenal shunting found in portal hypertension. Other
causes of renal vein enlargement could be tumor
involvement or arteriovenous fistula.
6. Renal vein thrombosis
a. Renal vein thrombosis may occur due to underly-
ing abnormalities of the kidney, hydration status,
coagulation status, tumors of the kidney or adrenal
gland, membranous glomerulonephritis, or extrinsic
compression from tumors, trauma, pancreatitis, or
retroperitoneal fibrosis.
b. Acute thrombosis will result in flank pain and
hematuria. Symptoms are usually insignificant with a
chronic onset due to collateral development.
7. Renal transplants
a. The donor artery is anastomosed to either exter-
nal iliac artery in end-to-side fashion or to the inter-
nal iliac artery in end-to-end fashion. The renal vein
is connected to the external iliac vein in an end-to-
side fashion.
b. Renal transplants are usually located in the right
iliac fossa.
c. Normal intra- and extraparenchymal transplant
arteries are low resistance. Causes of increased renal
transplant arterial resistance include:
(1) Acute rejection.
(2) Renal vein thrombosis.
(3) Infection.
(4) Tubular necrosis.
d. Usually within the first year, 10% of renal trans-
plants will develop renal artery stenosis. This may
occur as a result of rejection, complications of
surgery, or intrinsic vascular disease.
e. Renal artery stenosis occurs in renal transplants in
three locations:
(1) Anastomosis—occurs most frequently in
end-to-end anastomosis
(2) Distal donor artery—occurs most frequently
in end-to-side anastomosis
(3) Recipient artery—occurs equally in both
types of anastomoses and is more rare
f. Renal artery thrombosis usually results in loss of
the renal transplant. The most common cause is
acute and hyperacute rejection. Other causes are
iatrogenic, hypotension, vascular kinking, cyclo-
sporine, end-to-end anastomosis, hypercoagulable
states, atherosclerotic emboli, and with acquired
renal artery stenosis.
g. Renal vein thrombosis and stenosis may be
attributable to compression by fluid collections,
propagation of femoral or iliac deep vein thrombo-
sis, hypovolemia, and surgical or technical difficul-
ties. These are rare.
h. Intrarenal arteriovenous malformations usually
develop as a result of renal transplant biopsy. Most
are small and will resolve spontaneously. Large ones
may be treated by percutaneous embolization. Large
arteriovenous malformations cause a decrease in per-
fusion to the kidney. Symptoms are persistent hema-
turia and high-output cardiac failure.
i. Extrarenal arteriovenous malformations and
pseudoaneurysms are usually iatrogenic in origin.
j. Patients who have renal transplants and who are
immunosuppressed may develop malignancy, includ-
ing Kaposi sarcoma and lymphoma.
C. History: Questions to Ask the Patient
These symptoms generally are related to hypertension. Ask
the following questions:
1. Do you have high blood pressure?
2. Do you have any history of headaches, dizziness,
nosebleeds, or flushed face and tiredness?
3. With chronic hypertension, the possible symptoms
include:
a. Headaches.
b. Fatigue.
c. Nausea.
d. Vomiting.
e. Shortness of breath.
f. Restlessness.
g. Blurred vision.
4. Other questions to be asked include the following:
a. Do you have blood in your urine?
b. Do you have any problems urinating?
c. Do you have any back pain or other abdominal
pain?
D. Diagnostic Examination
1. Begin with the patient in the supine position,
although a right or left lateral decubitus position may
be helpful (especially with the left kidney). Using a
3.5- or 5-MHz curved-array transducer in a sagittal
approach, slide along the most lateral edge of the
costal margin of the ribs.
2. Once the kidney is located, rotate the transducer as
necessary to visualize the long axis of the kidney.
3. For renal artery stenosis studies, take color images
and Doppler signals (maintaining a 60-degree angle of
insonation) from the following vessels:
a. Segmental arteries at the superior, middle, and
inferior poles of the kidney. Using a fast sweep speed
on your Doppler spectrum, obtain acceleration times.
b. Main renal arteries at the hilum of the kidney.
Measure peak systolic velocities (Fig. 2.22).
c. Main renal arteries at their origins off the aorta
(Fig. 2.23). These are best visualized in the trans-
verse plane of the middle aorta, inferior to the
 2/Abdominal Vasculature 21

FIGURE 2.22. Doppler tracing of the right renal artery, taken at the hilum of the kidney.

FIGURE 2.23. Doppler tracing of the left renal artery, taken at its origin off the aorta.
22 The Complete Guide to Vascular Ultrasound

B
FIGURE 2.24. A: Doppler tracing of the left renal artery, taken at its origin off the aorta,
demonstrating a normal velocity value of 88 cm/s. B: Doppler tracing of the right renal artery,
taken at its origin off the aorta, in the same patient as shown in A, demonstrating an abnormally
high velocity value of 286.5 cm/s. This indicates a stenosis.
 2/Abdominal Vasculature 23

The pulsatility index is another formula that indicates

resistance. It is calculated by:
(peak systolic velocity − end diastolic velocity) /
mean velocity.
E. Diagnostic Analysis
1. Renal artery aneurysm
a. Renal artery aneurysms have turbulent flow and
produce a mosaic of color on ultrasound.
b. A renal artery aneurysm appears as a cystic mass
along the renal artery. It can also appear intrarenally.
Thrombus or calcification of the wall may or may
not be present.
c. If the aneurysm is greater than 2.5 cm or is asso-
ciated with pregnancy, treatment is recommended
because the incidence of rupture increases.
2. Arteriovenous malformation and fistula
a. Color and duplex Doppler will show turbulent
FIGURE 2.24. (continued) C: Color flow image in the same site
as in B, demonstrating aliasing in the right renal artery at its ori- flow with a mosaic of color.
gin off the aorta. b. Turbulent diastolic flow and increased flow
velocity is seen in the arterial portion, whereas arte-
rial pulsations are seen in the venous portion. Spec-
tral broadening is also present.
3. Renal artery occlusion and infarction
superior mesenteric artery. The right renal artery
a. Flow to the kidney will not be evident by color
usually takes off at around the 10 o’clock position
or duplex Doppler.
on the aorta, and the left renal artery usually takes
b. The kidney may appear normal in gray scale
off at around the 3 to 4 o’clock position on the
with acute infarction.
aorta.
c. A focal infarction may appear as a hypoechoic,
d. Middle aorta at the level of the renal arteries.
wedge-shaped mass. This is indistinguishable from
Measure peak systolic velocity to obtain the renal-
acute pyelonephritis. As time goes on, this may
to-aortic ratio (RAR), which is calculated by divid-
become echogenic or a scar may form.
ing the peak systolic velocity of the renal artery by
d. A small, scarred kidney will be seen with chronic
the peak systolic velocity of the aorta.
occlusion.
e. Main renal veins may also be evaluated.
4. Renal artery stenosis
4. For renal transplants, begin with the patient in
a. Normal systolic velocity for the renal artery is in
the supine position and use a 5-MHz transducer.
the range of 100 to 200 cm/s.
Measure the transplant in the sagittal and transverse
b. By the University of Washington criteria, peak
planes. Carefully evaluate the parenchyma. Look for
systolic velocities of greater than 180 cm/s indicate
signs of fluid collections (lymphoceles, urinomas,
a greater than 60% diameter reduction, and an
abscesses, hematomas) around the transplant. Look
RAR of greater than 3.5 indicates a greater than
for hydronephrosis.
60% diameter reduction.
5. Using Doppler, assess the donor renal artery, the
c. By the Dean RH, Hansen KJ, Bowman Gray cri-
anastomosis site, and the external or internal iliac
teria, peak systolic velocities of greater than 200
artery for signs of stenosis.
cm/s with poststenotic turbulence indicate a greater
6. Measure the peak systolic and end-diastolic
than 60 % diameter reduction (Fig. 2.24).
velocities and assess whether the flow resistance is
d. The RAR is the ratio of the peak systolic veloc-
normal.
ity of the renal artery by the peak systolic velocity in
7. Measure the resistive index of the arcuate arteries in
the midstream aorta at or near the level of the renal
the upper, middle, and lower pole.
arteries. An RAR of 3.5 or greater indicates a greater
8. Evaluate the donor renal vein. Also evaluate the
than 60% diameter reduction. An RAR of 2 to 3.5
bladder.
is suspicious but not hemodynamically significant.
The resistive index is a formula that indicates resistance.
e. Evaluate the waveform. This is normally low resis-
It is calculated by:
tance. If there is a proximal stenosis, the waveform is
(peak systolic velocity − end-diastolic velocity) / still low resistance but dampened with a prolonged
peak systolic velocity. upslope and downslope. Absence of the notch (at or
 24 The Complete Guide to Vascular Ultrasound

just before peak systole) combined with a dampened
waveform indicates at least 60% stenosis.
f. Evaluate the waveform intrarenally. If the acceler-
ation time (time between beginning of systolic flow
and maximum peak of systole) is 70 msec or more,
this indicates a significant stenosis. The acceleration
index (the slope of the systolic upstroke) may also be
used. A normal acceleration index is 3 m/s2 or greater.
g. A discordance in kidney sizes also indicates a
decrease in blood supply to the smaller of the two.
(Kidney size of <9 cm is suspicious for renal artery
stenosis.)
5. Renal vein thrombosis
a. With acute renal vein thrombosis, the kidney
may appear enlarged, edematous, and hypoechoic
with a loss of the corticomedullary differentiation.
With chronic renal vein thrombosis, the kidney
appears small and echogenic.
b. Thrombus may occasionally be seen within the
renal vein. Acute thrombus may be anechoic and
invisible.
c. Loss of flow on color Doppler may be evident. If
the flow is very low velocity it may be difficult to
detect, however.

A B

C D
FIGURE 2.25. A: Normal renal artery at the donor site of a renal transplant. B: Doppler tracing
of the same site as in A, demonstrating a normal velocity value of 94.7 cm/s. C: Renal artery at
the anastomosis site of a renal transplant. D: Doppler tracing of the same site as in C, demon-
strating an abnormally high velocity of 363 cm/s, indicating stenosis. This is the same patient as
shown in A and B.

d. A secondary sign of renal vein thrombosis may
be absent or reversed end-diastolic flow in the renal
arteries of the parenchyma of the native kidney.
6. Renal transplants
a. Signs of rejection include increased renal trans-
plant size, hypoechoic areas in the parenchyma, and
increased cortical echogenicity. With chronic rejec-
tion, the renal transplant will be small and
echogenic.
b. Arcuate artery resistive indices of 0.6 to 0.8 are
normal, 0.8 to 0.9 are equivocal, and greater than
0.9 indicate increased vascular resistance.
c. Normal peak systolic velocity of the main renal
artery is less than or equal to 180 cm/s.
d. A normal flow pattern in the intra- and extra-
parenchymal arteries is low resistance.
e. Findings of renal artery stenosis include a high-
velocity jet (with aliasing on color Doppler) at the
stenosis with distal turbulent flow. Velocities greater
than 180 cm/s suggest stenosis. A kink in the vessel
may also produce these signs.
f. Flow to the kidney using color or duplex
Doppler will not be detected in the case of com-
plete renal artery thrombosis. A partial thrombosis
may show reversed or decreased diastolic arterial
flow.
g. Other complications of renal transplants to
look for include renal vein thrombosis (absent
renal vein flow on color and duplex Doppler with
reversed diastolic arterial flow), renal vein stenosis
(normal or enlarged hypoechoic kidney and focal
2/Abdominal Vasculature 25
aliasing with increased velocities), intra- or
extrarenal arteriovenous fistula (which appears as
focal areas of color aliasing and Doppler patterns
of turbulent, arterialized venous waveforms),
pseudoaneurysms (cystic area with turbulent pul-
satile flow and swirling colors on color Doppler),
and tumors (Fig. 2.25).
F. Other Diagnostic Tests
1. Renal angiography
2. MRA
3. CTA
4. Nuclear medicine
BIBLIOGRAPHY
Downey DB. The retroperitoneum and great vessels. In: Rumack
CM, Wilson SR, Charboneau JW, eds. Diagnostic ultrasound, 2nd
ed. St. Louis, MO: Mosby Year-Book, 1998:464–486.
Guida JA. Vascular structures. In: Kawamura DM, ed. Abdomen—
diagnostic medical sonography—a guide to clinical practice. Vol. III.
Philadelphia: JB Lippincott, 1992:45–90.
Rumwell C, McPharlin M. Part I. Arterial evaluation. In: Vascular
technology—an illustrated review, 2nd ed. Pasadena, CA: Davies
Publishing, 2000:33–120.
Thurston W, Wilson SR. The urinary tract. In: Rumack CM, Wilson
SR, Charboneau JW, eds. Diagnostic ultrasound, 2nd ed. St. Louis,
MO: Mosby Year-Book, 1998:379-382, 385-391.
Tortora GJ, Anagnostakos NP. The cardiovascular system: vessels and
routes. In: Principles of anatomy and physiology, 6th ed. New York:
Harper & Row, 1990:628–630.
Withers CE, Wilson SR. The liver. In: Rumack CM, Wilson SR,
Charboneau JW, eds. Diagnostic ultrasound, 2nd ed. St. Louis,
MO: Mosby Year-Book, 1998:144–147.
 3
PERIPHERAL ARTERIAL SYSTEMS
I. LOWER EXTREMITY ARTERIES
A. Anatomy (Fig. 3.1)
1. The common iliac arteries divide into the exter-
nal and internal (hypogastric) iliac arteries at the level
of the lumbosacral junction.
2. The internal iliac arteries are 3 to 4 cm in length.
The branches of these arteries supply the pelvic wall,
perineum, pelvic organs, and gluteal region.
3. The external iliac arteries are larger than the
internal iliac arteries in an adult. When it passes
underneath the inguinal ligament, the external iliac
artery becomes the common femoral artery. The two
branches of the external iliac artery are the inferior epi-
gastric artery (supplying the abdominal muscles and
skin) and the deep circumflex artery (supplying the
abdominal muscles.)
4. The common femoral artery (Fig. 3.2) divides
into the superficial femoral artery and the deep
femoral artery (profunda) (Fig. 3.3).
5. The superficial femoral artery (Fig. 3.4) passes
through the adductor canal (Hunter’s canal) and
enters the popliteal fossa. Here it becomes the
popliteal artery.
6. The popliteal artery divides into the anterior tib-
ial artery and the tibioperoneal trunk.
7. The anterior tibial artery is the first branch off
the popliteal artery. It runs along the anterior surface
of the interosseous membrane in the front of the leg.
The anterior tibial artery becomes the dorsalis pedis
artery in the foot.
8. The tibioperoneal trunk is the second branch off
the popliteal artery. It quickly divides into the poste-
rior tibial and peroneal arteries.
9. The posterior tibial artery extends down the
medial and posterior region of the lower leg. It divides
into the medial and lateral plantar arteries in the
foot.
10. The peroneal artery extends down the lateral
and posterior region of the lower leg, along the fibula.
11. The plantar arch consists of the deep plantar
artery (branch of the dorsalis pedis) and the lateral
plantar artery (branch of the posterior tibial artery).
The plantar arch and the dorsal metatarsal arteries
supply the digits.
B. Pathology
1. Arteriovenous fistulas
a. Arteriovenous fistulas can be either congenital or
iatrogenic (caused by surgery and/or procedures
involving puncture into an artery or a vein such as
catheterization.)
b. These are abnormal communications between
an artery and a vein.
2. Pseudoaneurysms
a. A pseudoaneurysm is a small pocket of moving
blood connected to an artery through a small open-
ing (the neck) and may be partly surrounded by
thrombus.
b. These form due to interventional radiology pro-
cedures (e.g., cardiac catheterization using the com-
mon femoral artery), trauma, surgery, or infection.
They can be felt as a pulsatile mass.
c. Compression with a transducer may help to clot
the pseudoaneurysm off. An alternative therapy
would be thrombin injection.
3. Peripheral artery aneurysms
a. Peripheral artery aneurysms develop when the
wall of the artery weakens.
b. These are defined as a bulge or focal enlarge-
ment of 20% of the diameter of the vessel.
c. They are most likely to develop in the distal
superficial femoral artery or the popliteal artery.
d. These may be bilateral and may be asympto-
matic.
e. Thrombus may be present within the
aneurysm.
f. A peripheral artery aneurysm that is 2 cm or
greater in diameter usually requires repair.
4. Entrapment of the popliteal artery by the gas-
trocnemius muscle. This is a rare problem that is due
to an abnormally positioned insertion of the muscle. It
usually occurs in young men. Only a third of cases are
bilateral.
 3/Peripheral Arterial Systems 27

FIGURE 3.3. Sagittal color flow image of the right proximal

superficial femoral artery and the deep femoral artery.

6. Chronic occlusive lower extremity arterial disease

a. Causes:
FIGURE 3.1. Arteries: lower extremity.
5. Compartment syndrome. This is a collection of
symptoms that are produced by an obstruction of a
portion of the blood supply and increased pressure
(often in the calf ). This can be caused by an increase
in blood (deep venous thrombosis, hemorrhage) or
serous fluid (edema, lymph fluid) within the com-
partment. This can occur after revascularization of
the calf artery due to prolonged acute ischemia. The
most effective treatment is surgical opening of com-
partment to relieve pressure. Angiography is often
used.
(1) Atherosclerosis obliterans (ASO). Ninety-
nine percent of all chronic vascular disease in the
United States is caused by ASO. ASO is the accu-
mulation of plaque in the arterial system. Initially
fibrous plaque is deposited under the intima. Fatty
streaks may also appear under the intima. Eventu-
ally, it degenerates and forms complex plaque
(fibrous material, plaque, and calcium). Ulcera-
tions may occur which can hemorrhage.
(2) Thromboangiitis obliterans (TAO), also
known as Buerger disease—A disease that causes
inflammation of the arteries (or veins) preventing
blood flow. Always starts in the plantar or palmar
vessels and proceeds centrally, preventing collat-
erals from forming.

FIGURE 3.2. Sagittal color flow image of the right common femoral artery.
28 The Complete Guide to Vascular Ultrasound
(3) Smoking history, hyperlipidemia, family his-
tory, diabetes, and hypertension—All these are
precursors to peripheral arterial disease.
b. Symptoms:
(1) Claudication—pain produced by exercise
(most common site is the calf ) and relieved by
rest. During exercise, there is an increased
demand for blood to the muscles. Diseased arter-
ies and collaterals cannot deliver the appropriate
amount of blood needed (the arterioles are
already dilated due to their diseased state). Pain
occurs due to oxygen-starved muscles, and is
relieved by rest.
(2) Instep claudication (in the foot)—produced
by TAO. This causes severe pain.
(3) Rest pain is most severe at night, is due to
more advanced disease, and is more commonly
felt in the toes and top of the foot. Limbs must
be lowered so gravity pulls more blood down to
the muscles.
(4) Loss of hair on the lower extremities.
(5) Thickening and color changes of the toe-
nails.
(6) Changes in skin color and appearance (tight,
shiny skin).
(7) Decreased palpable pulses.
(8) Abnormal sensations in the affected limb
(pins/needles, tingling).
(9) Redness of the foot due to dilated arterioles
is present with more advanced disease.
(10) Evidence of a bruit or a thrill (abnormal
noise). In severe stenosis (>90%) the bruit disap-
pears because arterial flow decreases to the point
that there is no longer any tissue vibration.
FIGURE 3.4. Sagittal color flow image of the
right middle superficial femoral artery (SFA, red)
and vein (SFV, blue).
(11) Arterial ulcers—These may become gan-
grenous and are present with more advanced dis-
ease.
7. Acute occlusive lower extremity arterial disease
a. Causes:
(1) Physical compression or obstruction of a
major artery.
(2) Entrapment by the gastrocnemius muscle on
the popliteal artery.
(3) Obstruction caused by emboli—these may
be thrown from a diseased heart valve or an aor-
tic aneurysm.
(4) Hypercoagulation—certain chemotherapies
or malignant diseases can cause this.
(5) Dissection of the intimal lining of a vessel—
the flap may completely occlude blood flow.
(6) Masses or severe hemorrhage following
trauma.
b. Symptoms:
(1) Pain—severe, unilateral claudication during
exercise is a symptom of entrapment by the gas-
trocnemius muscle.
(2) Paralysis.
(3) Paresthesias—abnormal sensations within
the affected limb.
(4) Pallor—pale skin tone, cool to the touch
(hot to the touch may be caused by deep venous
thrombosis).
(5) Absence of a pulse.
(6) Black toes—caused by thrown emboli or
hypercoagulation. “Blue toe syndrome”—emboli
lodged in the digital arteries causes cyanosis.
Arteritis, ulcerated lesions, and sometimes
angiography can cause this.

8. The most frequent sites of claudication and
their indicated levels of disease:
a. Buttocks—this site indicates aortoiliac arterial
disease.
b. Thighs—this site indicates iliac and/or common
femoral artery disease.
c. Calves—this site indicates femoropopliteal arte-
rial disease.
9. Sites of lower extremity occlusive disease and
their effects:
a. The most common site of lower extremity occlu-
sive arterial disease is the distal superficial femoral
artery in the adductor canal. If there is only an iso-
lated site of disease, it rarely produces symptoms of
claudication due to proximity of branches from the
deep femoral artery as well as pelvic and calf arter-
ies that allow blood to flow from the pelvic area or
upper thigh to the calf without using the superficial
femoral artery. Also, the potential for collateraliza-
tion in the thigh to the calf is very great.
b. The second most common site is the aortoiliac
area. If the distal aorta is obstructed, it is possible
for the blood to get to the external iliac arteries by
way of branches given off by the internal iliac
arteries. This would produce reverse flow in one or
both internal iliac arteries. This would produce
symptoms of claudication since the volume flow
capacity of collaterals is much lower than the vol-
ume flow capacity of the aorta. Also, it is possible
for one or both of the common iliac arteries to be
occluded. If one is occluded, collaterals from the
other side may provide blood flow. If both com-
mon iliac arteries were occluded, then the superior
mesenteric artery, inferior mesenteric artery, lum-
bar arteries, or other collaterals would have to be
used. This also produces symptoms of claudica-
tion. Bifurcations are common sites for arterial
disease because of the turbulence that occurs at
these sites.
c. If there is disease in the popliteal artery, collater-
als from the deep femoral artery or genicular artery
may alleviate symptoms of claudication. (The
genicular arteries course from the superficial
femoral arteries, run parallel to the superficial
femoral arteries and the popliteal arteries, and anas-
tomose at several sites along these arteries.)
d. Below the trifurcation (into the posterior tibial,
anterior tibial, and peroneal arteries), single site dis-
ease is rarely significant due to the rich communi-
cations between the calf muscles. Symptoms are
rarely produced.
C. History: Questions to Ask the Patient
1. The vascular laboratory must answer three basic
questions:
3/Peripheral Arterial Systems 29
a. Are the patient’s symptoms due to vascular dis-
ease?
b. How extensive is the vascular disease present?
c. Where is the disease located within the affected
limb?
2. Questions to ask the patient:
a. Do you get pain in either leg upon exercising
and does rest relieve it?
b. How far can you walk before the pain starts?
(Number of blocks.)
c. Where exactly in your leg(s) is the pain present?
(Site of pain is usually distal to the site of the occlu-
sive disease.)
d. Is the pain present in both legs? Is one leg worse
than the other?
e. Do you get pain in your toes, feet, or legs at
night when you rest?
f. How long have you had this sore/ulcer?
g. Do you feel pins/needles or tingling in your
limb?
h. Do you have diabetes? If so, what kind
(non–insulin-dependent diabetes mellitus or
insulin-dependent diabetes mellitus)? The presence
of diabetes increases the chance of peripheral vascu-
lar disease by at least eight times. It is not unusual
for diabetics to have a slow-healing ulcer on the sole
of the foot. A problem with diabetics is neuropa-
thy—neurons are damaged in extremities, causing
pain, and the pain may or may not be related to vas-
cular disease.
i. Do you have hypertension? If yes, are you taking
medication to control your hypertension? Hyper-
tension is a major source of stress to the vascular
system and can accelerate the atherosclerotic
process.
j. Do you have high cholesterol? Is heart disease
present in you or your family? Have you ever had a
stroke?
k. Do you smoke? If so, how many packs per day?
For how many years? The risk for arterial disease
increases dramatically as the number of years smok-
ing and the number of packs per day increase.
Decreased oxygen in the blood may produce symp-
toms of claudication. Nicotine adversely affects the
endothelium and causes vasoconstriction.
3. Physical examination of the patient:
a. Look at the skin for any lesions/ulcers, redness,
pallor, tightness and shininess, loss of hair, thicken-
ing and color changes of the toenails, color changes
in the toes, and whether the skin feels cool, hot, or
warm to the touch.
b. Feel for pulses in the common femoral arteries,
popliteal arteries, posterior tibial arteries and the
dorsalis pedis arteries. Grade the pulses according to
30 The Complete Guide to Vascular Ultrasound
0 for absent; 1 for intermittent or unsure; 2 for
weak; 3 for full and bounding.
c. Feel for lumps (swollen lymph nodes) that sup-
port the diagnosis of cellulitis, which is an infection
of the dermal tissues in the limb and presents with
hot and red tissues often in the shin and the top of
the foot.
d. Feel for thrills or vibrations, which could indi-
cate an aneurysm, pseudoaneurysm, or an arteri-
ovenous fistula.
e. Pseudoaneurysms are often felt as a pulsatile
mass.
4. The severity of symptoms depends on:
a. The degree of arterial obstruction within the
limb.
b. The degree of collateralization. Symptoms in
legs with vascular causes are the result of “regional
hypotension.” Collaterals take time to develop, so
acute disease can be more painful than chronic dis-
ease.
5. Four appropriate places for arterial ausculta-
tion:
a. Carotid artery
b. Abdominal aorta
c. Femoral artery
d. Popliteal artery
6. Three conditions that can produce a palpable
thrill or vibration:
a. A patent hemodialysis graft.
b. Poststenotic turbulence.
c. Arteriovenous fistula. Flow in the proximal
artery greatly increases (especially during diastole)
because the fistula causes a marked decrease in resis-
tance. Flow in the proximal vein also increases and
is more pulsatile.
D. Diagnostic Examinations
1. Duplex Doppler examination:
a. Begin with the patient in the supine position,
with his or her leg bent slightly and relaxed out to
the side. Using a 5.0- or 7.0-MHz linear-array
transducer in a transverse plane, start to image just
above the crease of the groin.
b. Locate the common femoral artery.
c. Slide your transducer down the leg to evaluate
the other vessels. When you get to the popliteal
artery, bring your transducer behind the knee.
This will place the artery posterior to the vein on
the screen since you are now in a posterior
approach.
d. Although few protocols require a detailed look
at the calf arteries, to evaluate the posterior tibial
artery, slide your transducer up the medial aspect of
the calf starting at the ankle.
e. The posterior tibial artery is located (with this
approach) between the tibia and the fibula, just
underneath a fascial plane.
f. The peroneal artery is located posterior to this.
g. The anterior tibial artery is located by placing
the transducer on the anterior surface of the lower
leg midway between the knee and the ankle. It is
seen anterior to the fascial plane between the tibia
and the fibula.
h. Obtain gray-scale images in sagittal and trans-
verse planes, color images, and Doppler signals
(maintaining a 60-degree angle of insonation) with
peak systolic velocity measurements from the fol-
lowing vessels:
(1) Common femoral artery (Fig. 3.5)
(2) Profunda (deep femoral artery)
(3) Proximal, middle, and distal superficial
femoral arteries (Figs. 3.6 and 3.7)
(4) Popliteal artery
(5) Posterior tibial artery, if necessary
(6) Peroneal artery, if necessary
(7) Anterior tibial artery, if necessary
(8) External iliac artery, common iliac artery,
and distal aorta Doppler waveforms may be
obtained if necessary.
2 Segmental pressure examination
(a) Due to the Bernoulli effect, segments of the
limb distal to significant occlusive disease will have
decreased pressures.
(b) The patient must be supine so gravity does not
affect the pressures (hydrostatic pressure artifact).
For every 1 cm the limb is above the heart, the pres-
sure decreases by 0.74 mm Hg.
(c) The width of the cuff should be 20% to 25%
greater than the diameter of the limb, or 40%
greater than the circumference of the limb.
(d) The peak systolic pressure is obtained by plac-
ing a cuff (the widest possible) over the desired seg-
ment of the limb and inflating to a pressure that is
enough to occlude any blood flow through that seg-
ment (at least 20 mm Hg past the disappearance of
a Doppler-detected pulse). Slowly the cuff is
deflated and any portion of the arterial system
below the cuff can be used to determine the pres-
sure of the segment beneath the cuff. (Usually dor-
salis pedis and posterior tibial artery are used.) The
first flow of blood is the peak systolic pressure.
(e) Different patients have different pressures, so
we must normalize the pressure results from the
limb to the patient’s systemic blood pressure. Usu-
ally, peak systolic pressure values from segments are
divided by the higher of the two brachial peak sys-
tolic pressures.
 3/Peripheral Arterial Systems 31

FIGURE 3.5. Doppler tracing of the right common femoral artery.

FIGURE 3.6. Doppler tracing of the right proximal superficial femoral artery.
32 The Complete Guide to Vascular Ultrasound
FIGURE 3.7. Doppler tracing of the right middle superficial femoral artery.
(f ) The most common index used is the ankle-to-
brachial index (ABI).
(g) Disadvantages of the segmental pressure
examination:
(1) You cannot discriminate between stenosis
and occlusion.
(2) You cannot pinpoint the precise location of
disease.
(3) When the patient is obese, the pressures may
be falsely elevated. When the patient is extremely
thin, the proximal thigh pressure may be falsely
low. This is due to the cuff/limb ratio artifact.
(The width of the cuff should be 20% to 25%
greater than the width of the limb.)
(4) There is difficulty in discriminating between
common femoral artery and external iliac artery
disease.
(5) Calcified vessels yield falsely elevated pres-
sures (seen with diabetics and chronic renal dis-
ease patients). An index of 1.25 or higher indi-
cates falsely elevated pressures. Patients (mostly
diabetic) who are not able to tolerate the
amount of pressure required to “crush” stenotic
arteries must be evaluated with other tech-
niques such as duplex Doppler imaging or arte-
riography. A toe pressure using photoplethys-
mography (PPG) may also be used. Toe pres-
sures are used to confirm abnormally high ABIs
resulting from calcification of vessels. Toe arter-
ies are rarely affected by atherosclerosis or calci-
fication.
(6) Multiple levels of disease make it difficult to
interpret the segmental pressures.
(7) After exercise, patients with uncompensated
congestive heart failure may show decreased
ABIs.
3. Plethysmography–pulse volume recording (PVR)
a. This is also known as pulse plethysmography.
b. Plethysmography is usually combined with
other tests (segmental pressures, duplex Doppler).
c. It is possible to get a normal waveform with an
abnormal Doppler segmental pressure. Plethysmog-
raphy alone cannot evaluate disease when collaterals
are present.
d. Tissues in the limb expand and contract as
blood circulates and each cardiac cycle produces sig-
nificant volume changes within each limb segment.
It is possible to compress away venous input and
record only arterial input.
e. Three methods of plethysmography:
(1) Air cuff. This is the most popular. While it is
not as rapid as using strain gauge plethysmogra-

phy and gives a “softer” appearance to the curve
of the waveform, it is easy to use, doesn’t have to
be continually calibrated, has a low cost, and is
durable.
(2) Strain gauge. This uses a mercury-filled sili-
cone-like tube that has copper electrodes at either
end. It is 1 to 3 cm shorter than the circumfer-
ence of the extremity. The strain gauge is
wrapped around the limb with good contact. As
the limb contracts and expands, the length of the
tube also changes. This has to be calibrated on a
regular basis.
(3) PPG. A photocell is securely attached to the
underside distal portion of the great toe. This
sends infrared light into the tissue with a light-
emitting diode, and the photocell (photodetec-
tor) receives the backscattered infrared light and
measures its reflection.
(4) Water displacement PVR—rarely used
today.
f. Amplitude of the thigh or ankle should be
greater than 15 mm, and amplitude of the calf
should be greater than 20 mm. If the amplitude is
lower, disease probably exists.
g. Three capabilities of plethysmography:
(1) When combined with segmental pressures,
helps differentiate between true arterial claudica-
tion and that resulting from other sources.
(2) Helps locate level of obstruction.
(3) Documents functional aspects of disease.
h. Advantages of PVR:
(1) It is easy to perform, and less technique
dependent.
(2) It can be done in diabetic patients with scle-
rotic arterial walls.
(3) It records all volume expansion of the limb
due to all inflow, including collateral.
i. Disadvantages of PVR:
(1) The accuracy is affected if there is too much
air—sometimes unavoidable in obese patients.
May cause slight loss in amplitude but doesn’t
affect the shape of the wave.
(2) If pressure within the cuff is not 65 mm Hg,
morphology and amplitude may be altered.
(3) Plethysmography cannot evaluate a specific
vessel or differentiate between major arteries and
collaterals.
(4) Plethysmography cannot discriminate
between occlusion and stenosis.
4. PVR/segmental pressure examination
a. First have the patient lie down in the supine
position with the legs at the same level of the
heart for 15 to 20 minutes before you start the
examination. This allows the patient’s blood pres-
3/Peripheral Arterial Systems 33
sure to stabilize from walking. Feel for pulses,
obtain the history, and wrap cuffs with 12 × 40
cm or 10 × 40 cm bladders around the arms,
upper and lower thighs, calves, ankles, and feet.
The cuffs should be wrapped snugly around the
limb. Cuffs that are wrapped too loosely take
longer to inflate and may result in falsely elevated
pressures.
b. Do PVR—first in the upper and lower thighs,
then the calves and the feet. Set the sensitivity
and the gain for the first waveforms and leave
them the same for the rest of the study. Record at
least three waveforms. For toes, use a digital cuff
and PPG with high sensitivity to get the wave-
form.
c. Using a 5- to 8-MHz probe at an angle of 45 to
60 degrees, obtain segmental pressures. Each cuff is
inflated about 20 to 30 mm Hg above the point
that the arterial Doppler signal (or PPG waveform)
is obliterated, and then slowly deflated. When the
audible arterial Doppler signal (or PPG waveform)
returns, that is the systolic pressure. Record the sys-
tolic pressure for the following: arms (using the
brachial artery); upper thighs (using either the dor-
salis pedis or the posterior tibial artery); lower
thighs (using either the dorsalis pedis or the poste-
rior tibial artery); calves (using both the dorsalis
pedis and the posterior tibial artery or just one);
ankles (using both the dorsalis pedis and the poste-
rior tibial artery); and toes (using a PPG and a dig-
ital cuff ).
d. For above-the-knee amputation, get a PPG
recording on the stump. For below-the-knee
amputation, get thigh pressures using the popliteal
artery.
5. Treadmill/reactive hyperemia testing
Occasionally, patients present with classic symp-
toms of claudication but have a normal arterial exam-
ination. If the patient is free of heart problems and
able to tolerate a brief period of exercise, the treadmill
exercise test may be used to determine whether the
patient’s symptoms are due to ischemia from occlusive
arterial disease.
(1) First, do a whole segmental/PVR examina-
tion. Leaving only the ankle and the brachial
cuffs on, the patient walks the treadmill at 1.5
to 2 mph with a 10% to 12% incline for 5 min-
utes or until symptoms appear. The patient lies
down quickly and the ABI is taken within 3
minutes. If the pressures increase or stay nor-
mal, the test is over. If the pressure decreases,
take it again 2 minutes later (at the 5-minute
mark) and repeat every 5 minutes for 20 min-
utes or until normal.
34 The Complete Guide to Vascular Ultrasound
(2) If the ankle pressures decline to a low pres-
sure after exercise but increase rapidly within 2 to
6 minutes to the original levels, a single level of
disease exists.
(3) If the ankle pressure remains low for more
than 10 to 12 minutes, then it is assumed that
several levels of disease are present.
b. Reactive hyperemia testing. This is similar to the
treadmill. This is used when the patient cannot tol-
erate exercise or has heart disease.
(1) Place an occlusive cuff on the upper thigh
(inflated to 20–30 mm Hg above systolic pres-
sure) for 3 to 5 minutes causing severe ischemia
in the lower leg producing claudication.
(2) Deflate the cuff and immediately take the
pressure again, then repeat at 1- to 2-minute
intervals.
(3) Normal: Pressures stay the same or decrease
up to 20%. Abnormal: pressure declines more
than 20%. Whenever possible, the treadmill
should be used since it simulates real life.
6. Transcutaneous oximetry (tcPO2)
a. This helps to determine wound healing and
amputation level.
b. This reflects the tissue oxygen tension, which
depends on the balance between oxygen consump-
tion and oxygen supply.
c. Start with the patient supine, with their head
and torso slightly elevated. Clean the skin site
with alcohol. Make sure that it is dry, and then
place a self-adhesive molded plastic fixation ring
on the skin site. Place a few drops of electrolyte
solution inside the plastic ring. Place the electrode
sensor on the skin and turn it securely into the fix-
ation ring. After the manual calibration, PO2 read-
ings are noted after 15 to 20 minutes of stabiliza-
tion. Take a reference reading in the left upper
chest first, then the other specific sites, such as
near a wound or at the anticipated level of ampu-
tation. Do not place the sensor on edematous
skin, areas of cellulitis, ulcers, or close to bone. If
the PO2 level is below normal, repeat the test with
oxygen challenge. This involves the same test,
only the patient also wears a facemask that deliv-
ers oxygen.
7. Entrapment of the popliteal artery by the gas-
trocnemius muscle. Segmental pressures and PVR
waveforms at the ankle are repeated with the patient
holding the foot in active plantar flexion. Look for dif-
ferences in signals.
E. Diagnostic Analysis
1. Transcutaneous oximetry:
a. Normal PO2 levels are 60 to 80 mm Hg (30–40
mm Hg is normal according to other references).
Oxygen challenge should increase this by 10 to 20
mm Hg.
b. Poor PO2 levels are 10 to 15 mm Hg. Oxygen
challenge would not increase this to normal values.
c. When determining amputation level, move the
electrode proximally until a better reading is
obtained. For example, a poor reading below the
knee compared with a better one above the knee
indicates that an above-the-knee amputation will be
more likely to heal.
d. Use oxygen challenge if the patient’s reading falls
between normal and poor. A reading of 20 mm Hg
could increase to 30 mm Hg with oxygen challenge.
e. Factors that affect the readings include skin
blood flow, capillary temperature under the sensor,
skin thickness, and arterial PO2 .
f. The values at which healing occurs do vary. It
depends on the site and the type of study per-
formed. Healing can occur at levels less than 30 mm
Hg at some sites.
2. Arteriovenous fistulas. The fistula usually can be
visualized as a jet of blood. The draining vein is abnor-
mally distended compared with the other side. The
Doppler signal in the vein shows arterialized venous
flow. The Doppler signal in the jet of blood reveals
high-velocity arterial/venous flow (Fig. 3.8).
3. Pseudoaneurysm. Pseudoaneurysms are visual-
ized on color Doppler as a cystic mass filled with
swirling colors (Fig. 3.9). A small communicating
channel between the cystic mass and the artery can be
seen. This is called the neck. The Doppler signal
within the communicating neck reveals high-velocity,
“to-and-fro” blood flow. Make sure to look for multi-
ple connecting compartments, although most
pseudoaneurysms just have one. A hematoma and a
hyperplastic lymph node can both be mistaken for
pseudoaneurysms. However, neither has a high-veloc-
ity, swirling flow pattern or a communicating channel
to the artery.
4. Peripheral arterial aneurysms. Peripheral arterial
aneurysms can be visualized as an enlargement of the
arterial wall, greater than 20% of the normal vessel
diameter. Thrombus may be seen within the lumen. A
turbulent flow pattern may be evident within the
bulge of the aneurysm.
5. Lower extremity peripheral arterial disease–
duplex scan.
a. As the population ages, the diameter of arteries
increase and peak systolic velocity decreases.
b. A normal lower extremity arterial signal is
triphasic, with no evidence of spectral broaden-
ing.
c. The percentage of stenosis may be calculated
using the measurements of diameter and area:
 3/Peripheral Arterial Systems 35

FIGURE 3.8. Doppler tracing of a jet between the right common femoral artery and the com-
mon femoral vein, revealing an arteriovenous fistula.

FIGURE 3.9. Color flow image of a pseudoaneurysm coming off the right common femoral
artery (CFA). The pseudoaneurysm is connected to the common femoral artery by a communi-
cating channel, or neck.
36 The Complete Guide to Vascular Ultrasound

FIGURE 3.10. Sagittal view of a partially occluded common femoral artery with a small lumen
that can be visualized with color flow Doppler.

(1) % Diameter stenosis = 1 − diameter (resid-
ual)/diameter (original) × 100
(2) % Area of stenosis = 1 − diameter (resid-
ual)/diameter (original) squared × 100
d. Use color to see if there is any “invisible
plaque.” Color Doppler may also help allow very
small but still patent lumens to be seen (the string
sign) (Fig. 3.10). Turbulence distal to a stenosis is
seen on color Doppler as “confetti” or a “color
mosaic.”
e. A tardus parvus waveform is usually seen distal
to the site of a stenosis. This is a low-resistance, low-
velocity signal with a slow upstroke to the peak.
f. High-velocity signals do not always mean steno-
sis. Other situations that can cause a high-velocity
signal are a kink in the vessel, using a steep Doppler
angle, or by sampling a collateral artery by mistake.
g. Large collateral branches seen while using color
Doppler could indicate a more distal occlusion or
high-grade stenosis.
h. When there is a complete occlusion, color flow
is absent (Fig. 3.11).
i. Absence of flow is not always due to occlusion of
the vessel. It is sometimes due to calcification in the
walls of the vessel or poor Doppler sensitivity (due
to the depth of the vessel or poor Doppler settings).

FIGURE 3.11. Complete occlusion of the proximal superficial femoral artery, demonstrated by
the lack of color flow.
 3/Peripheral Arterial Systems 37

TABLE 3.1. LOWER EXTREMITY ARTERIAL

DOPPLER SPECTRAL ANALYSIS
1. Normal
Triphasic waveform
Clear, crisp spectral window
Quick upstroke to systolic peak
2. Mild disease (0%–19%)
Triphasic waveform
Minimal spectral broadening
Quick upstroke to systolic peak
PSV at stenosis/PSV proximal <2
3. Moderate disease (20%–49%)
Biphasic waveform
Spectral window filling, spectral broadening
PSV increases by at least 30% over the proximal PSV
PSV at stenosis/PSV proximal <2
4. Severe disease (50%–99%)
Monophasic waveform
Severe spectral broadening
PSV increases by 100% over proximal PSV FIGURE 3.12. Spectral Doppler waveform in progressive disease
states. (Reproduced from Odwin CS, Dubinsky T, Fleischer AC.
PSV at stenosis/PSV proximal >2
Appleton & Lange’s review for the ultrasonography examina-
PSV >200 cm/s tion, 2nd ed. East Norwalk, CT: Appleton & Lange, 1987, with
5. Occluded artery permission.)
Absence of spectral information
May hear “thump”
6. Flow distal to occluded site (due to collaterals)
Decreased systolic flow
Sluggish upstroke to peak n. Inverse damping factor:
Spectral broadening (1) This is the difference between pulsatility
Monophasic indices—calculated by dividing the distal PI by
Peak Systolic Velocity, (PSV)
the proximal PI.
(2) This indicates the amount of change as
blood has traveled to a particular area.
(3) The inverse damping factor should always be
j. Low-amplitude signals in an occluded vessel close to 1.0 for each segment within the limb.
(“thumps”) may be seen due to transmitted pulsations Note: If the PI is significantly less than 5.0
from another vessel or by sampling a collateral vessel and the inverse damping factor is significantly
running parallel the occluded vessel by mistake. less than 1.0, then significant vascular disease
k. Proximal to a high-grade stenosis, the Doppler is probably present.
waveform can have lower peak systolic velocities, 6. Lower extremity peripheral arterial disease—
with or without change to the shape of the wave- segmental pressure examination:
form (high-resistant, triphasic) (Table 3.1 and Fig. a. If the difference between two adjacent (or right
3.12). to left) segments is greater than 20 mm Hg (15–20
l. Postexercise, Doppler waveforms should be mm Hg for the upper extremity), then disease is
maintained or augmented. In an abnormal case, probably present in the segment with the lower
changes occur in the signal such as a slow upstroke pressure.
with a rounded peak, a slow downstroke, and no (1) If the pressure gradient is from the upper
reverse component. thigh to the arm, this indicates disease in the
m. Pulsatility index (PI): superficial femoral artery or above.
(1) Calculated by dividing the peak-to-peak fre- (2) If the pressure gradient is from the upper to
quency by the mean frequency. the lower thigh, this indicates disease in the
(2) The PI for a triphasic waveform will be superficial femoral artery.
much higher than the PI for a monophasic wave- (3) If the pressure gradient is from the lower
form. thigh to the calf, this indicates disease in the dis-
(3) In a patient without vascular disease, the PI tal superficial femoral artery/popliteal artery.
will increase or stay the same as the measurement (4) If the pressure gradient is from the calf to the
is made in a more peripheral area of the body. ankle, this indicates disease in the tibial arterial.
(4) In general, the PI is over 5.0 in healthy blood b. The pressure in the high thigh should be 30 mm
vessels in the leg. Hg greater than the brachial pressure due to cuff
38 The Complete Guide to Vascular Ultrasound
size artifact. If the pressure in the high thigh is equal
to or less than the brachial pressure, then disease is
probably present at or proximal to the superficial
femoral artery.
c. Any comparison between the right and left
greatly underestimates disease if disease is present
on both sides.
d. If a patient has an ankle pressure less than 55
mm Hg, it is unlikely that a foot ulcer will heal. A
toe pressure (which may be obtained via PPG) can
be used if the patient is diabetic (and has calcified
vessels that do not compress). If the toe pressure is
less than 30 mm Hg, then it is unlikely that the
ulcer will heal. Normal toe pressures are 50 mm Hg
or more than 64% of the brachial pressure,
whichever is higher. Patients with claudication have
a mean toe-to-brachial index of 0.35 ± 0.15.
Patients with rest pain have a mean toe-to-brachial
index of 0.11 ± 0.10.
e. Ankle-to-brachial index ranges:
Normal: > 0.96
Claudication: 0.50–0.95
Rest pain: 0.21–0.49
Ischemia: ≤0.20
FIGURE 3.13. Normal patient with no pressure gradients.
f. Compare the indices with previous studies: if the
difference between the indices is ≥0.15, then this
indicates a significant change (Figs. 3.13–3.16).
7. Lower extremity peripheral arterial disease—
plethysmography:
a. Diagnostic criteria for the shape of PVR
waves:
(1) Normal: sharp systolic peak, prominent
dicrotic notch.
(2) Mildly abnormal: sharp systolic peak, absent
dicrotic notch, downslope bowed away from
baseline.
(3) Moderately abnormal: flattened systolic
peak, upslope and downslope time nearly equal,
dicrotic notch invariably absent.
(4) Severely abnormal: pulse wave of very low
amplitude or entirely absent. If the waveform is
present, it has equal upslope and downslope time
(Fig. 3.17).
b. PVR is usually performed in conjunction with
other tests (segmental pressures, continuous-wave
or duplex Doppler). The amplitude of the PVR
waveform is a less reliable indicator of vascular dis-
ease than the shape of the wave, but it is also used.
 FIGURE 3.14. Patient with left
femoropopliteal and tibial vessel dis-
ease. There is a greater than 30 mm Hg
pressure difference between the left
lower thigh and the calf and the left
calf to the ankle. There is also a greater
than 20 mm Hg pressure difference
between the right leg and left leg at the
calf and ankle levels. This suggests left
femoropopliteal and tibial vessel dis-
ease.

FIGURE 3.15. Patient with aortoiliac dis-

ease. There are reduced pressures at both
high thigh levels without further pressure
gradients. As the calf waveform has normal
amplitude, this indicates only an aortoiliac
obstruction.
40 The Complete Guide to Vascular Ultrasound

FIGURE 3.16. Patient with aortoiliac, femoropopliteal, and tibial vessel disease. There are
reduced pressures at both thigh levels, which correlates with aortoiliac disease. There is also a
greater than 20 mm Hg pressure difference between the low thighs to the calves and the calves
to the ankles. This indicates femoropopliteal and tibial vessel disease.

It is generally reduced in limbs that have advanced 3. Computed tomographic angiography

arterial disease, and unilateral amplitude reduction
is especially meaningful. However, keep in mind
that the amplitude may be influenced by a number
of physiologic variables. A “reference” PVR can be
used from a disease-free segment (the arm), using its
amplitude as a standard against which all others can
be compared. This should compensate for varia-
tions.
F. Other Diagnostic Tests
1. Peripheral angiography
2. Magnetic resonance angiography
II. UPPER EXTREMITY ARTERIES
A. Anatomy (Figs. 3.18 and 3.19)
1. The subclavian artery branches directly off the
aortic arch on the left. On the right, the brachio-
cephalic artery branches directly off the aortic arch
and then turns into the subclavian artery.
2. The subclavian artery turns into the axillary artery
at the level lateral to the first rib (also near the junc-
tion of the cephalic and axillary vein).
3. The axillary artery becomes the brachial artery as
it courses over the proximal humerus. This can be fol-

FIGURE 3.17. Pulse volume recording waveforms.


FIGURE 3.18. Arteries: thoracic vessels.
lowed down the arm to the antecubital fossa, where it
bifurcates into the radial and ulnar branches.
4. The radial and ulnar arteries branch into the
superficial palmar (volar) arch and the deep palmar
(volar) arch. These branch into the digital arteries.
B. Pathology
1. Upper extremity occlusive arterial disease
a. The vascular supply to the arm is more resistant to
atherosclerotic changes than in the lower extremities.
Also, upper extremity vasculature is rich in collateral
pathways. If the subclavian arteries or axillary arteries
are obstructed, other pathways include cranial and
neck arteries, other branches of the subclavian, dorsal
scapular artery, circumflex humeral artery, or sub-
scapular artery. If the brachial artery is obstructed,
FIGURE 3.19. Arteries: upper extremity.
3/Peripheral Arterial Systems 41
branches from the ulnar or radial arteries can act as
collaterals. Also, it is possible to retrograde fill the
brachial artery from branches of the palmar arch.
b. Causes:
(1) Thoracic outlet syndrome. A cervical rib
(an extra rib in the thorax) or scalene muscles
cause extrinsic compression on distal subclavian or
proximal axillary arteries. This is extremely posi-
tion dependent. Symptoms may be due to com-
pression of the nerve instead. It is also possible for
the nerve and artery to be compressed. This is
more common in women 20 to 40 years of age.
(2) Subclavian steal syndrome (also known as
vertebral steal). When significant disease is pre-
sent in the brachiocephalic or proximal subcla-
vian arteries, blood must now course up the con-
tralateral vertebral artery, cross over at the basilar
artery, and course down the vertebral artery of
the affected side to the subclavian artery to per-
fuse the arm. Even at rest, a significant difference
in blood pressure of the affected arm is found
when compared with the unaffected side. The
difference in blood pressure is 15 to 20 mm Hg,
with the side producing the lower pressure being
the affected side. There is increased resistance in
vertebral arterial flow, and reverse flow is seen in
the ipsilateral vertebral artery. A partial vertebral
steal is one that almost meets the circulatory
requirements of the arm and has bidirectional
flow that can be converted to a complete steal by
exercising the arm or by placing a blood pressure
cuff on the arm for a few minutes, then releasing.
(3) Atherosclerosis obliterans can occur in the
upper extremities but is rare. Ninety-nine per-
cent of all chronic vascular disease in the United
States is caused by ASO. ASO is the accumula-
tion of plaque in the arterial system. Initially
42 The Complete Guide to Vascular Ultrasound
fibrous plaque is deposited under the intima.
Fatty streaks may also appear under the intima.
Eventually, it degenerates and forms complex
plaque (fibrous material, plaque, and calcium).
Ulcerations may occur that can hemorrhage.
(4) Thromboangiitis obliterans, also known as
Buerger disease, can occur equally in upper or
lower extremities. This is more common in males
and in smokers. This is a disease that causes
inflammation of the arteries (or veins) preventing
blood flow. It always starts in the plantar or palmar
vessels and proceeds centrally, preventing collater-
als from forming. Feet and hands are reddened.
Rest pain is present in the feet and the hands.
(5) Takayasu arteritis. This is a giant cell arteritis
that affects the aortic arch and larger vessels that
originate from it. It causes narrowing of the artery
due to an inflammatory response of the intimal lin-
ing. This is usually found in females and Asians 15
to 48 years of age. This is rare in the United States
and the cause is unknown. Also known as “pulse-
lessness disease.” If this occurs in the subclavian
artery, it causes decreased blood flow to the arms
and produces pain upon exercise or even rest pain.
(6) Collagen vascular diseases. These involve
production of abnormal collagen within the
arteries. They include scleroderma, lupus erythe-
matosus, rheumatoid arthritis, dermatomyositis,
and fibromuscular dysplasia.
(7) Raynaud syndrome. This syndrome
involves constriction of the blood supply to the
hand, caused by cold temperatures or high emo-
tional conditions. Symptoms are pain and a
change in the color of the hand. The primary
form is usually found in women under 40 years
of age and occurs bilaterally. The waveform has a
slow upstroke, rounded peak. The secondary
form is usually found in men under 40 years of
age, occurs bilaterally or unilaterally, and is often
associated with other vascular problems. Sec-
ondary ischemia is constantly present with fixed
arterial obstruction. This waveform has a slow
upstroke, anacrotic notch, and dicrotic notch
high on the downslope. Treatment includes
avoidance of cold and tobacco, regional sympa-
thectomies and some drug treatments.
(8) Extrinsic tumor or mass. Can interrupt
blood flow.
(9) Embolus. Can interrupt flow.
2. Pseudoaneurysms
a. A pseudoaneurysm is a small pocket of moving
blood connected to an artery through a small open-
ing (the neck) and may be partly surrounded by
thrombus.
b. These form due to interventional radiology pro-
cedures (e.g., cardiac catheterization using the com-
mon femoral artery), trauma, surgery, or infection.
This can be felt as a pulsatile mass.
c. Compression with a transducer may help to clot
the pseudoaneurysm off. An alternative therapy
would be thrombin injection.
3. Peripheral artery aneurysms
a. Peripheral artery aneurysms develop when the
wall of the artery weakens.
b. These are defined as a bulge or focal enlarge-
ment of 20% of the diameter of the vessel.
c. Ulnar aneurysms can form as a result of using
the palm as a hammer.
d. Subclavian aneurysms can be associated with
embolization to the fingers.
e. These may be bilateral and may be asymptomatic.
f. Thrombus may be present within the aneurysm.
g. A peripheral artery aneurysm that is 2 cm or
greater in diameter usually requires repair.
C. History: Questions to Ask the Patient
1. Do you have pain in your arm(s) after exercise or
even at rest?
2. Do you smoke? How many packs per day? For how
long?
3. Any other symptoms such as weakness in the arms
or pins-and-needles tingling in the arms?
4. Any neck pain?
5. Do your hands, arms, or shoulders swell or have a
bluish tinge?
6. Has your doctor performed tests including holding
a deep breath and tipping your head as part of the
examination?
7. Has your doctor told you that you have a differ-
ence of blood pressure between your two arms?
8. Have you had any fever?
9. Have you had numbness or tingling in your hands
or feet?
10. Have you had pain or a change in the color of
your hands?
11. Do you have abdominal pain?
12. Do you have headaches or pain in your scalp?
Take blood pressures in both arms and feel for radial
and ulnar pulses. Evaluate the color of the arms and
hands. Look for excessive redness or loss of color. Feel
for any excessive thrills or bruits.
D. Diagnostic Examinations
1. PVR/segmental pressure examination for upper
extremity arterial disease
a. Have the patient lie down for 15 to 20 minutes
before you start the examination to stabilize the
pressures. Obtain the history and wrap the blood
pressure cuffs on the upper arms, forearms, and fin-
gers. Use cuffs that are 12 × 40 cm for the upper
arms, 10 × 40 cm for the forearms, and the digital
cuffs for the fingers. Make sure the cuffs fit snugly.
b. Do PVR waveforms: upper arms, forearms, and
all 10 fingers.

c. Do segmental pressures: upper arms (using the
brachial arteries), forearms (using the radial and
ulnar arteries), and all 10 fingers (using a PPG).
2. Duplex Doppler examination
a. Have the patient lie supine or with his or her head
and torso slightly elevated. Bring the arm to be imaged
out laterally away from the body with the palm up.
Begin using an 8- to 12-MHz linear-array transducer.
b. For the subclavian artery, a bullet-shaped trans-
ducer with a small footprint works best to get
around the clavicle. For the proximal portion of the
subclavian artery, place the transducer above the
clavicle. The subclavian artery is imaged superficial
to the vein in this location.
c. For the middle and distal subclavian artery, place
the transducer inferior to the clavicle. From this
view, the subclavian artery is seen deep to the sub-
clavian vein.
d. To help image the axillary artery, place the
patient’s arm above his or her head to get into the
axilla.
e. Bring the arm back down into the starting posi-
tion to follow the brachial artery down the arm.
f. Follow the brachial artery as it bifurcates into the
radial and ulnar arteries. The radial artery courses
down the lateral side of the forearm (the thumb
side) and the ulnar artery courses down the medial
side of the forearm (the fifth finger side.)
g. Obtain gray-scale, color, and Doppler images of
the following vessels:
(1) Subclavian artery
(2) Axillary artery
(3) Brachial artery
(4) Radial artery
(5) Ulnar artery
h. Evaluate the vessels for signs of aneurysms and
pseudoaneurysms as well.
3. The Allen test. This test can be used to determine
whether the radial or the ulnar artery is occluded.
Have the patients clench their hand tightly, then pinch
off the radial artery with your thumb and let them
open their hand. If the blood flows back into the hand
(returning it to its red color) the ulnar artery is proba-
bly not occluded. If the hand remains white, the ulnar
artery could be occluded. Repeat the test for the radial
artery by pinching the ulnar artery instead.
4. Examinations for specific vascular disorders
a. Takayasu’s arteritis. Ultrasound may show
thickening of the lining of the subclavian artery and
even the axillary arteries. Segmental pressures may
show decreased brachial systolic pressure. The PVR
waveform may appear abnormal.
b. Buerger disease (TAO). Decreased pressures
are seen in the toes and the fingers. The PVR wave-
form will be abnormal for the fingers, toes, and
metatarsals, with loss of the dicrotic limb.
3/Peripheral Arterial Systems 43
c. Subclavian steal. The affected limb will have
decreased systolic pressure and abnormal PVR
waveforms. If there are segmental pressure differ-
ences between the arms of greater than 15 mm Hg,
then probably significant vascular disease exists.
d. Thoracic outlet syndrome. Symptoms are
pain in the neck, upper extremity pain and weak-
ness, paresthesias, and intermittent weakness during
exercise. There are multiple tests for TOS:
(1) Adson’s test. The patient’s arm is extended
90 degrees and externally rotated. The patient’s
head is turned toward and away from the arm,
with full inspiration. The PVR waveforms are
observed for any changes. Any significant
decrease in brachial systolic pressure or signifi-
cant alteration of wave indicates TOS.
(2) Costoclavicular maneuver. The patient is
placed in an exaggerated military stance with the
shoulders back and chest out. Also, the arm can
be raised 90 degrees, in the same plane as the
torso. Observe PVR waveforms for any signifi-
cant changes.
(3) Hyperabduction maneuver. Examine the
patient while they are fully abducting the arm
with 90-degree extension rotation. Look at the
PVR waveforms for any significant changes.
(4) Other positions. Place the patient with the
arm at rest with the hand in the lap, the arm
raised at 90 degrees in the same plane as the
torso, or the arm raised at 120 degrees in the
same plane as the torso. The “causative” position
is whatever produces symptoms.
e. Raynaud syndrome. This is usually present in
the hands; they turn from white to blue to red. The
PVR waveforms have a characteristic appearance. In
patients with arterial disease, the dicrotic limb is
absent. In patients with Raynaud syndrome, the
dicrotic limb is still present and found very close to
the peak of the waveform. This is very important to
distinguish. This type of waveform is known as a
“peaked pulse” and is also seen in Buerger disease,
frostbite, and different collagen disorders. The test:
Have the patient soak his or her hand in ice for 2 to
5 minutes. Look at the segmental pressures. With
Raynaud syndrome, the pressure in the finger will
decline to unrecordable levels (normally it does
decrease, but only to under 20% of normal pres-
sure). Also, look at PVR waveforms—with Ray-
naud syndrome, they are flattened. Vasoconstriction
is not always induced by this procedure. Signals can
also be measured after the patient does math prob-
lems (high stress). Vasoconstriction also occurs in
some patients when they take a deep breath.
E. Diagnostic analysis
1. Segmental pressures/PVR. Use the same diag-
nostic criteria for evaluating PVR waveforms as for the
44 The Complete Guide to Vascular Ultrasound
lower extremity. Diagnostic criteria for the shape of
PVR waves:
a. Normal—sharp systolic peak, prominent
dicrotic notch.
b. Mildly abnormal—sharp systolic peak, absent
dicrotic notch, downslope bowed away from baseline.
c. Moderately abnormal—flattened systolic peak,
upslope and downslope time nearly equal, dicrotic
notch invariably absent.
d. Severely abnormal—pulse wave of very low
amplitude or is entirely absent. If the waveform is
present, it has equal upslope and downslope time.
e. Loss of the dicrotic limb in the finger waveforms
indicates arterial disease. If the dicrotic limb is still
present but is found close to the peak of the wave-
form (called a “peaked pulse”) this could indicate
Raynaud syndrome.
f. If the difference between two adjacent (or right
to left) segments is greater than 15 to 20 mm Hg,
then disease is probably present in the segment with
the lower pressure.
g. A gradient between upper arm pressures of
greater than 30 mm Hg is consistent with severe
pressure-reducing stenosis (>50% diameter reduc-
ing) or occlusion of the subclavian, axillary, or
brachial arteries. Retake the pressures to rule out
other causes such as sudden systemic pressure
change or cardiac arrhythmia. Consider subclavian
steal syndrome (with possible retrograde vertebral
artery flow) on the low-pressure side.
h. Calculate finger to brachial indices using the
higher of the two arm pressures (normal =
0.88–1.06; occlusion = 0.29–0.83).
2. Duplex Doppler examination:
a. Normal signals are triphasic or multiphasic with
a rapid upstroke to the systolic peak and a clear,
crisp spectral window.
b. Abnormal signals are monophasic, nonpulsatile,
include spectral broadening, or are absent.
c. Look for aliasing on the color Doppler images to
pinpoint a stenosis.
d. With a significant stenosis (≥50%), the peak sys-
tolic velocity in the site of the stenosis increases by
100% over the peak systolic velocity proximal to
the stenosis. The ratio of the peak systolic velocity
to the proximal normal segment is greater than 2
with a stenosis of 50% or greater.
e. Flow distal to an occluded site will be monopha-
sic with a sluggish upstroke to the peak systolic
velocity, will have decreased systolic flow, and will
have spectral broadening. This is often classified as
a tardus parvus waveform.
3. Pseudoaneurysms. Pseudoaneurysms are visual-
ized on color Doppler as a cystic mass filled with
swirling colors. A small communicating channel
between the cystic mass and the artery can be seen.
This is called the neck. The Doppler signal within the
communicating neck reveals high-velocity, to-and-fro
blood flow. Make sure to look for multiple connecting
compartments, although most pseudoaneurysms just
have one. A hematoma and a hyperplastic lymph node
can both be mistaken for pseudoaneurysms. However,
neither has a high-velocity, swirling flow pattern or a
communicating channel to the artery.
4. Peripheral arterial aneurysms. Peripheral arterial
aneurysms can be visualized as an enlargement of the
arterial wall, greater than 20% of the normal vessel
diameter. Thrombus may be seen within the lumen. A
turbulent flow pattern may be evident within the
bulge of the aneurysm.
F. Other Diagnostic Tests
1. Angiography
2. Magnetic resonance angiography
3. Computed tomographic angiography
BIBLIOGRAPHY
Katanick S, Hoffman TG. Sonographic and Doppler investigation of
the peripheral veins and arteries and the cerebrovascular system.
Part I. Peripheral veins and arteries. In: Odwin CS, Dubinsky T,
Fleischer AC, eds. Appleton & Lange’s review for the ultrasonogra-
phy examination, 2nd ed. East Norwalk, CT: Appleton & Lange,
1987:460–462.
Katz ML, Comerota AJ. Noninvasive evaluation of lower extremity
arterial disease. In: Kerstein MD, White JV, eds. Alternatives to
open vascular surgery. Philadelphia: JB Lippincott, 1995:
215–224.
Polak JF. The Peripheral Arteries. In: Rumack CM, Wilson SR, Char-
boneau JW, eds. Diagnostic ultrasound, 2nd ed. St. Louis, MO:
Mosby Year-Book, 1998:921–941.
Rumwell C, McPharlin M. Part I. Arterial evaluation. In: Vascular
technology—an illustrated review, 2nd ed. Pasadena, CA: Davies
Publishing, 2000:33–120.
Tortora GJ, Anagnostakos NP. The cardiovascular system: vessels and
routes. In: Principles of anatomy and physiology, 6th ed. New York:
Harper & Row, 1990:624–633.
 4

GRAFTS

I. HEMODIALYSIS GRAFTS 2. Using a 7.0- or 10.0-MHz linear-array transducer,

A. Anatomy follow the graft from each native vessel and anastomo-
1. Dialysis grafts are placed in the arm to allow easy sis site. Most grafts are fairly easy to scan, as they are
access for dialysis. The types are: usually quite superficial.
a. Brachial artery to axillary vein (most common) 3. Obtain color images and Doppler signals with
b. Brachial artery to antecubital vein (next most peak systolic velocity measurements of the following
common) areas:
c. Radial artery to cephalic vein (Brescia-Cimino a. Native artery
graft) (least common) b. Arterial anastomosis
2. Dialysis grafts may be straight synthetic, looped c. Arterial end of graft
synthetic, or made of autologous vein (Figs. 4.1 and d. Midgraft
4.2). e. Venous end of graft
B. Pathology f. Venous anastomosis
The most common problem with dialysis grafts is that g. Native vein
the venous anastomosis site or outflow vein becomes E. Diagnostic Analysis
stenotic and thrombus forms due to the increased arter- 1. Peak systolic velocities in well-functioning dialysis
ial pressure. Stenosis in the venous side of the graft hap- grafts are typically between 100 and 200 cm/s. The
pens in more than 80% of cases (Figs. 4.3 and 4.4). This velocity tends to be higher in the first 6 months after
can produce endothelial damage or intimal hyperplasia. the placement of the graft (Fig. 4.2).
Other problems with dialysis grafts include pseudoa- 2. High-grade stenosis is probably present with a veloc-
neurysms developing at the dialysis site (Figs. 4.5 and ity elevation of 100% (velocity ratios of 2 or greater).
4.6); the possibility of the arterial anastomosis becoming 3. High-grade stenosis is also consistent with veloci-
stenotic; or hematomas developing since the graft is fre- ties of 50 cm/s or less.
quently pierced. If the arterial flow is greater than 400
cm/s, then the graft most likely has a 75% diameter
reduction. Due to the increased venous return from the
dialysis graft, congestive heart failure can develop.
C. History: Questions to Ask the Patient
Feel for a “thrill” (vibration) and listen for a bruit over
the graft. This is a normal finding for a patent dialysis
graft, but can also be produced by a graft stenosis. Ask:
1. Are you having any pain in your arm over the
graft?
2. Are you having problems with your dialysis
access?
3. Has the “thrill” in your graft disappeared?
D. Diagnostic Examination
1. Begin with the patient in a supine position with
the head and torso slightly raised. Bring the arm out
laterally away from the patient’s body with the palm
facing up. FIGURE 4.1. Types of dialysis grafts.
46 The Complete Guide to Vascular Ultrasound

FIGURE 4.2. Doppler tracing of a normal dialysis graft within the first 6 months of placement.
(Image courtesy of Philips Medical Systems.)

FIGURE 4.3. Doppler tracing of a dialysis graft, demonstrating a stenosis by the abnormally high
velocity values. Aliasing is also seen in the color flow image. (Image courtesy of Philips Medical
Systems.)
 4/Grafts 47

FIGURE 4.4. Gray-scale image of a

thrombosed dialysis graft. (Image cour-
tesy of Philips Medical Systems.)

FIGURE 4.5. Color flow image of a dialysis graft with a pseudoaneurysm (arrow). (Image cour-
tesy of Philips Medical Systems.)

FIGURE 4.6. Color flow image of a dialysis graft with a large

pseudoaneurysm. (Image courtesy of Philips Medical Systems.)
48 The Complete Guide to Vascular Ultrasound

c. Femoropopliteal
d. Axillofemoral
e. Axillofemoral/femorofemoral
f. Femorotibial
g. Femorofemoral
3. What grafts are made of:
a. Synthetic grafts (Gore-Tex) (Fig. 4.8)
b. Synthetic grafts (Dacron)—generally used if the
bypass graft involves the aorta. It has a corregated
outline on ultrasound and is more echogenic than
Gore-Tex (Fig. 4.9).
c. Autologous vein grafts:
(1) Reversed vein grafts (or harvesting vein
graft). After surgical removal of the saphenous
vein and ligation of all its branches, the vein is
reversed and anastomosed to the artery. The
small end of the vein is connected to the prox-
imal segment of the artery, and the larger end
of the vein is connected to the distal end of the
artery. The venous valves are not disrupted
because the arterial flow forces them to stay
open. This must be mapped before surgery.
(2) In situ vein grafts. The greater saphenous vein
is left in place with the proximal and distal ends
anastomosed to the artery. The valves of the saphe-
nous vein are surgically removed with a valvotome
and the branches are ligated (Fig. 4.10).
(3) Other types of vein used for a graft are the
umbilical vein and the lesser saphenous vein.
FIGURE 4.7. Types of bypass grafts.
These may be used when the native greater
saphenous vein is not available and the graft
must cross the knee. Synthetic material does
II. BYPASS GRAFTS not tolerate continual bending of the knee
A. Anatomy well.
1. When arterial disease is extremely severe, only sur- B. Pathology
gical intervention can save the limb. 1. Acute failure of a graft can be due to a pseudoa-
2. Types of arterial bypass grafts (Fig. 4.7): neurysm at the anastomosis site, initial surgical dissec-
a. Aorto-bifemoral tion of the intima of the vessel at anastomosis site, or
b. Aortofemoral a retained valve.

FIGURE 4.8. Gray-scale image of a Gore-Tex

graft. (Image courtesy of Philips Medical Sys-
tems.)
 4/Grafts 49

an arteriovenous fistula exists. This decreases the

amount of blood to available to the lower limb. There
is tremendous turbulence at the site.
5. Pseudoaneurysms may develop.
6. Arteriovenous fistulas can open in the first few
weeks after surgery. This is more likely to occur with
the in situ graft.
C. History: Questions to Ask the Patient
1. Questions to ask the patient:
a. Do you get pain in either leg upon exercising
and does rest relieve it?
b. How far can you walk before the pain starts?
(Number of blocks.)
c. Where exactly in your leg(s) is the pain present?
(Site of pain is usually distal to the site of the occlu-
sive disease.) Is one leg worse than the other?
d. Do you get pain in your toes, feet, or legs at
night when you rest?
e. How long have you had this sore/ulcer?
f. Do you feel pins/needles or tingling in your
limb?
g. Do you have diabetes? If so, what kind?
FIGURE 4.9. Gray-scale image of a Dacron graft. (Image cour- (Non–insulin-dependent diabetes mellitus or
tesy of Philips Medical Systems.) insulin-dependent diabetes mellitus?) The presence
of diabetes increases the chance of peripheral vascu-
lar disease by at least eight times. It is not unusual
for diabetics to have a slow-healing ulcer on the sole
2. Long-term failure (>2 years) of a graft is usually of the foot. A problem with diabetics is neuropathy:
due to the progression of atherosclerotic disease within neurons are damaged in extremities causing pain
the artery supplying or supplied by the graft. and the pain may or may not be related to vascular
3. Failure 1 to 2 years after surgery may be due to disease.
fibrous constriction of the graft. Deposits of scar tissue h. Do you have hypertension? If yes, are you taking
may compress the graft and occlude the flow. medication to control your hypertension? Hyperten-
4. If the graft has less than expected perfusion, the sion is a major source of stress to the vascular system
surgeon could have missed a perforating vein, and thus and can accelerate the atherosclerotic process.

FIGURE 4.10. Color flow image of an in situ vein graft. (Image courtesy of Philips Medical Sys-
tems.)
50 The Complete Guide to Vascular Ultrasound
i. Do you have high cholesterol? Is heart disease
present in you or your family? Have you ever had a
stroke?
j. Do you smoke? If so, how many packs per day?
For how many years? The risk for arterial disease
increases dramatically as the number of years smok-
ing and the number of packs per day increase.
Decreased oxygen in the blood may produce symp-
toms of claudication. Nicotine adversely affects the
endothelium and causes vasoconstriction.
2. Physical examination of the patient:
a. Look at the skin for any lesions/ulcers, redness,
pallor, tightness and shininess, loss of hair, thicken-
ing and color changes of the toenails, color changes
in the toes, and whether the skin feels cool, hot, or
warm to the touch.
b. Feel for pulses in the common femoral arteries,
popliteal arteries, posterior tibial arteries, and dor-
salis pedis arteries. Grade the pulses according to 0
for absent; 1 for intermittent or unsure; 2 for weak;
3 for full and bounding.
c. Feel for lumps (swollen lymph nodes) that sup-
port the diagnosis of cellulitis, which is an infection
of the dermal tissues in the limb and presents with
hot and red tissues often in the shin and the top of
the foot.
d. Feel for thrills or vibrations, which could indi-
cate an aneurysm, pseudoaneurysm, or an arteri-
ovenous fistula.
e. Pseudoaneurysms are often felt as a pulsatile
mass.
D. Diagnostic Examinations
1. Duplex Doppler examination
a. Begin with the patient in a supine position.
Using a 7.0- or 10-MHz linear-array transducer,
follow the graft from each native vessel and anasto-
mosis site. Most grafts are fairly easy to scan; they
are usually quite superficial.
b. Obtain color images and Doppler signals with
peak systolic velocity measurements of the follow-
ing areas (NOTE: With aorto-bifemoral grafts and
axillofemoral with femorofemoral grafts, don’t for-
get you are evaluating two grafts.):
(1) Native vessel (depending on type of graft)
(2) Proximal anastomosis
(3) High graft
(4) Midgraft
(5) Low graft
(6) Distal anastomosis
(7) Native vessel (depending on type of graft)
2. Pulse volume recording (PVR)/segmental pres-
sure examination
a. First have the patient lie down in the supine
position with the legs at the same level as the heart
for 15 to 20 minutes before you start the examina-
tion. This allows the patient’s blood pressure to sta-
bilize from walking. Feel for pulses, obtain the his-
tory, and wrap cuffs with 12 × 40 cm or 10 × 40 cm
bladders around the arms, upper and lower thighs,
calves, ankles, and feet. The cuffs should be
wrapped snugly around the limb. Cuffs that are
wrapped too loosely take longer to inflate and may
result in falsely elevated pressures.
b. Do pulse volume recording, first in the upper
and lower thighs, then the calves and the feet. Set
the sensitivity and the gain for the first waveforms
and leave them the same for the rest of the study.
Record at least three waveforms. For toes, use a dig-
ital cuff and photoplethysmography (PPG) with
high sensitivity to get the waveform.
c. Using a 5- to 8-MHz probe at an angle of 45 to
60 degrees, obtain segmental pressures. Each cuff is
inflated about 20 to 30 mm Hg above the point
that the arterial Doppler signal (or PPG waveform)
is obliterated, and then slowly deflated. When the
audible arterial Doppler signal (or PPG waveform)
returns, that is the systolic pressure.
d. Record the systolic pressure for the following:
(1) Arms (using the brachial artery)
(2) Upper thighs (using either the dorsalis pedis
or the posterior tibial artery)
(3) Lower thighs (using either the dorsalis pedis
or the posterior tibial artery)
(4) Calves (using both the dorsalis pedis and the
posterior tibial artery or just one)
(5) Ankles (using both the dorsalis pedis and the
posterior tibial artery)
(6) Toes (using a PPG and a digital cuff )
E. Diagnostic Analysis
1. Duplex Doppler examination
a. The velocities are measured at the anastomosis
site of the inflow (proximal) end and 2 to 4 cm
above the anastomosis. Also, measure graft veloci-
ties every 4 to 5 cm, the outflow (distal) anastomo-
sis, and 2 to 4 cm below the distal anastomosis
(Figs. 4.11 and 4.12).
b. If the ratio between two measurements is less
than 2, then it is free of disease. If it is greater than
2, there is a 50% to 75% stenosis. If it is greater
than 3, then there is at least a 75% stenosis (Fig.
4.13 and 4.14).
c. If the overall graft velocity is less than 40 cm/s,
then there is a high suspicion for thrombosis (Fig.
4.15). If the velocity measures 40 cm/s in a single
segment, it depends on the size of the segment. If it
is a large segment, then it is not necessarily abnor-
mal. If it is a small segment, then a velocity of 40 to
45 cm/s is abnormal (remember the Poiseville Law
which states that decreased diameter causes
increased velocity).

FIGURE 4.11. Color flow image of an arterial graft anastomosis. (Image courtesy of Philips Med-
ical Systems.)
d. Normal regions of increased velocity in in situ
and reversed vein grafts. With in situ grafts, the
proximal segment has a larger diameter and
decreased velocity and the distal segment has a
smaller diameter with increased velocity. In a
reversed graft, it is vice versa.
e. In the distal anastomosis of a bypass graft, it is
not unusual to see retrograde flow in the proximal
direction in the native arterial segment. This is
caused by low pressure in the diseased native vessel
and the fact that blood flows from high- to low-
pressure areas. The segment of native artery distal to
the anastomosis carries flow in the normal direction
toward the feet.
f. During insertion of a vein graft, intraoperative
monitoring is useful to check the patency of anas-
4/Grafts 51
tomotic sites and to evaluate suspicious stenotic or
turbulent areas (such as valve cusp sites or suspected
branch sites).
g. In comparing two graft studies (one performed
on a previous date), the examiner should ask the fol-
lowing:
(1) Has flow in any segment decreased by at
least 30 cm/s since the last study?
(2) Has the Doppler signal quality changed
from tri- to biphasic?
(3) Has the ankle-to-brachial index decreased by
more than 0.15?
(4) Has the Doppler peak systolic velocity
decreased to less than 45 cm/s in the smallest
diameter when it was previously less than 45
cm/s?
FIGURE 4.12. Color flow image of an arterial Dacron
graft anastomosis. (Image courtesy of Philips Medical
Systems.)
 FIGURE 4.13. Doppler tracing in an arterial graft, demonstrating stenosis with an abnormally
high velocity value. (Image courtesy of Philips Medical Systems.)

h. For summary analysis of the above, see Table
4.1.
2. Segmental pressure examination
a. If the difference between two adjacent (or right
to left) segments is greater than 20 mm Hg (15–20
mm Hg for the upper extremity), then disease is
probably present in the segment with the lower
pressure.
(1) If the pressure gradient is from the upper
thigh to the arm, this indicates disease in the
superficial femoral artery or above.
(2) If the pressure gradient is from the upper to
the lower thigh, this indicates disease in the
superficial femoral artery.
(3) If the pressure gradient is from the lower
thigh to the calf, this indicates disease in the dis-
tal superficial femoral artery/popliteal artery.
(4) If the pressure gradient is from the calf to the
ankle, this indicates disease in the tibial artery.
b. The pressure in the high thigh should be 30 mm
Hg greater than the brachial pressure due to cuff
size artifact. If the pressure in the high thigh is equal

FIGURE 4.14. Color flow image of an arterial graft stenosis. Note the aliasing within the graft.
(Image courtesy of Philips Medical Systems.)
 4/Grafts 53

FIGURE 4.15. Gray-scale image of an arterial Gore-Tex graft that is thrombosed. (Image courtesy
of Philips Medical Systems.)

to or less than the brachial pressure, then disease is used if the patient is diabetic (and has calcified ves-
probably present at or proximal to the superficial sels that do not compress). If the toe pressure is less
femoral artery. than 30 mm Hg, then it is unlikely that the ulcer
c. Any comparison between the right and left will heal. Normal toe pressures are 50 mm Hg or
greatly underestimates disease if disease is present more than 64% of the brachial pressure, whichever
on both sides. is higher. Patients with claudication have a mean
d. If a patient has an ankle pressure less than 55 toe-to-brachial index of 0.35 ± 0.15. Patients with
mm Hg, it is unlikely that a foot ulcer will heal. A rest pain have a mean toe-to-brachial index of 0.11
toe pressure (may be obtained with PPG) can be ± 0.10.
e. Ankle-to-brachial index ranges:
Normal: >0.96
TABLE 4.1. ARTERIAL GRAFT ASSESSMENT Claudication: 0.50–0.95
Rest pain: 0.21–0.49
1. Normal
No spectral broadening Ischemia: ≤0.20
No PSV increase >30% relative to proximal site f. Compare indices to previous studies: if the dif-
PSV >45 cm/s ference between the indices is greater than or
2. <20% equal to 0.15, then this indicates a significant
Minimal spectral broadening in decrease phase of systole
change.
No focal increase in PSV
PSV >45 cm/s 3. Plethysmography
3. 21%–49% a. Diagnostic criteria for the shape of PVR
>30% increase in PSV relative to proximal site waves:
Increased spectral broadening throughout systole and (1) Normal—sharp systolic peak, prominent
diastole
dicrotic notch.
4. 50%–75%
>100% increase in PSV relative to proximal site (2) Mildly abnormal—sharp systolic peak,
Spectral broadening (systole and diastole) absent dicrotic notch, downslope bowed away
Ratio (of PSV/PSV proximal) = 2–3 from baseline.
5. >75% (3) Moderately abnormal—flattened systolic
Same as 50%–75% but PDV >100 cm/s
peak, upslope and downslope time nearly equal,
Loss of reverse flow component in diastole
Ratio (of PSV/PSV proximal) >3 dicrotic notch invariably absent.
6. Occluded (4) Severely abnormal—pulse wave of very low
No audible Doppler signal amplitude or is entirely absent. If the waveform
High-resistance wave proximal to site is present, it has equal upslope and downslope
Monophasic waveform distal to site with decreased
time.
velocities
b. PVR is usually performed in conjunction with
(PDV), Peak Diastolic Velocity other tests (e.g., segmental pressures, or continuous-
54 The Complete Guide to Vascular Ultrasound
wave or duplex Doppler). The amplitude of the PVR
waveform is a less reliable indicator of vascular dis-
ease than the shape of the wave, but it is also used. It
is generally reduced in limbs that have advanced arte-
rial disease, and unilateral amplitude reduction is
especially meaningful. However, keep in mind that
the amplitude may be influenced by a number of
physiologic variables. A “reference” PVR can be used
from a disease-free segment (the arm) and its ampli-
tude used as a standard against which all others can
be compared. This should compensate for variations.
4. Arteriovenous fistulas. The fistula can usually be
visualized as a jet of blood. The draining vein is abnor-
mally distended compared with the other side. The
Doppler signal in the vein shows arterialized venous
flow. The Doppler signal in the jet of blood reveals
high-velocity arterial/venous flow.
5. Pseudoaneurysm. Pseudoaneurysms are visualized
on color Doppler as a cystic mass filled with swirling
colors. A small communicating channel between the
cystic mass and the artery can be seen. This is called
the neck. The Doppler signal within the communicat-
ing neck reveals high-velocity, “to-and-fro” blood flow.
Make sure to look for multiple connecting compart-
ments, although most pseudoaneurysms just have one.
A hematoma and a hyperplastic lymph node can both
be mistaken for pseudoaneurysms. However, neither
has a high-velocity, swirling flow pattern or a commu-
nicating channel to the artery.
BIBLIOGRAPHY
Katanick S, Hoffman TG. Sonographic and Doppler investigation of
the peripheral veins and arteries and the cerebrovascular system.
Part I. Peripheral veins and arteries. In: Odwin CS, Dubinsky T,
Fleischer AC, eds. Appleton & Lange’s review for the ultrasonogra-
phy examination, 2nd ed. East Norwalk, CT: Appleton & Lange,
1987:460–462.
Katz ML, Comerota AJ. Noninvasive evaluation of lower extremity
arterial disease. In: Kerstein MD, White JV, eds. Alternatives to
open vascular surgery. Philadelphia: JB Lippincott, 1995:215–224.
Polak JF. The peripheral arteries. In: Rumack CM, Wilson SR, Char-
boneau JW, eds. Diagnostic ultrasound, 2nd ed. St. Louis: Mosby
Year-Book, 1998:921–941.
Ridgway DP. Lower extremity arterial scanning. In: Introduction to
vascular scanning—a guide for the complete beginner, 2nd ed.
Pasadena, CA: Davies Publishing, 2001:159–161.
Rumwell C, McPharlin M. Part I. Arterial evaluation. In: Vascular
technology—an illustrated review, 2nd ed. Pasadena, CA: Davies
Publishing, 2000:33–120
 5
PERIPHERAL VENOUS SYSTEMS
I. LOWER EXTREMITY VEINS
A. Anatomy
1. During inspiration, intrathoracic pressure
decreases, intraabdominal pressure increases, outflow
from the peripheral veins decrease, and blood moves
from the abdomen to the chest. During expiration,
intrathoracic pressure increases, intraabdominal pres-
sure decreases, and outflow from the peripheral veins
increases (Fig. 5.1). Several factors determine the rate
of blood that returns to the heart, including the fol-
lowing:
a. The calf muscle pump
b. Venous valves
c. Respiratory related pressures in the thorax
d. Venous pressure
e. Cardiac factors
2. The venous system in the lower extremity is com-
posed of a deep venous system and a superficial venous
system. In the lower extremity, blood flows from the
superficial system to the deep system. The reverse is
true for the upper extremity.
3. The superficial system in the lower extremity is
composed of the greater and lesser saphenous veins
and their branches. The greater saphenous vein
extends into the subcutaneous tissues from the
medial aspect of the common femoral vein (at the
level of the proximal thigh) to the level of the foot.
The normal diameter of the greater saphenous vein is
3 to 5 mm at the level of the saphenofemoral junc-
tion and 1 to 3 mm at the level of the ankle. The
lesser saphenous vein extends into the subcutaneous
tissues from the posterior aspect of the popliteal vein
to the level of the ankle. The diameter of the lesser
saphenous vein is normally 2 to 4 mm at the level of
the saphenopopliteal junction and 1 to 2 mm at the
level of the ankle.
4. The deep system in the lower extremity is com-
posed of the common femoral vein, the superficial
femoral vein, the deep femoral vein, the popliteal vein,
the posterior tibial veins, the anterior tibial veins, and
the peroneal veins.
5. The external iliac vein continues into the com-
mon femoral vein at the level of the inguinal liga-
ment. The common femoral vein lies just medial
and slightly deep to the common femoral artery.
Several centimeters distal to the bifurcation of the
common femoral artery and 6 to 8 cm distal to the
level of the inguinal ligament, the common femoral
vein bifurcates into the superficial and deep femoral
veins.
6. The deep femoral vein (also known as the pro-
funda) lies medial to the deep femoral artery and
extends deep and laterally. Usually only the proximal
portion can be seen.
7. The superficial femoral vein lies medial and
slightly deep to the superficial femoral artery. It is deep
and just posterior to the superficial femoral artery as
the vein proceeds down the medial thigh into the
adductor canal. The adductor canal is formed by a sep-
aration in the tendinous insertion of the adductor
magnus muscle. Since the canal is deep in the medial
thigh and consists of dense tissue, it is often difficult
to visualize the distal superficial femoral vein in larger
patients.
8. The distal superficial vein turns into the
popliteal vein as it enters the popliteal space behind
the knee. The popliteal vein lies anterior to the
popliteal artery.
9. The first deep branches of the popliteal vein are the
anterior tibial veins. These veins are paired and travel
with the anterior tibial artery along the anterior sur-
face of the interosseous membrane in the front of the
leg to the dorsal aspect of the foot.
10. The next branch of the popliteal vein is the
tibioperoneal trunk, which quickly divides into the
posterior tibial veins and the peroneal veins.
11. The posterior tibial veins are paired and
travel with the posterior tibial artery along the
medial and posterior area of the lower leg, posterior
to the tibia.
12. The peroneal veins are paired and travel with the
peroneal artery along the lateral and posterior region
56 The Complete Guide to Vascular Ultrasound
FIGURE 5.1. Anatomy of lower extremity veins.
of the lower leg, medial to the posterior aspect of the
fibula.
13. The gastrocnemial veins and soleal veins (or
sinuses) are deep veins that drain the gastrocnemius
muscle and the soleal muscle. The gastrocnemius veins
are paired with an artery and they drain into the
popliteal vein. The soleal sinuses do not have arteries
that accompany them and vary in size and extent.
They drain into the posterior tibial veins and the per-
oneal veins. Venous sinuses act as a reservoir for
venous blood and are an important part of the calf
muscle pump.
14. The perforators (or communicating veins) con-
nect the deep and superficial veins. The majority of
perforating veins can be seen passing through the
subcutaneous tissues to the deep tissues of the medial
calf. Normal perforating veins are difficult to visual-
ize due to their small size. Insufficient perforating
veins can be visualized with the patient in the upright
position.
15. There are 100 to 200 valves in each leg. The soleal
sinuses do not have valves.
B. Pathology
1. Deep venous thrombosis (DVT)
a. Millions of individuals are affected each year in
the United States with DVT. Up to 50% will
develop a pulmonary embolism. It is the third lead-
ing cause of death in the United States, with over 1
million deaths attributed to it each year. It is esti-
mated that approximately 90% of all pulmonary
emboli originate in the leg or pelvis.
b. Major risk factors for developing DVT are the
Virchow triad:
(1) Stasis
(2) Trauma
(3) Hypercoagulability (can be due to preg-
nancy, cancer, estrogen intake/birth control pills,
or myeloproliferative disorders)
c. Those with increased risk for DVT include the
elderly, postsurgical patients, cancer patients, and
posttraumatic patients.
d. Valvular incompetence and pulmonary emboli
are the most frequent complications of DVT.
e. As the risk for DVT increases, so does the risk
for pulmonary emboli. Pulmonary emboli are rare
in healthy ambulatory patients and when DVT
exists below the knee. Some cases of DVT origi-
nate below the knee and progress to higher regions
of the leg. Once thrombus is found above the
knee, the risk for pulmonary embolism increases
significantly.
f. The major symptoms of DVT are leg swelling
(edema), often seen in venous disease due to
increased capillary pressure; pain and redness; and
superficial varicose veins.
g. The Homans sign is the presence of calf pain
when the foot is dorsiflexed. However, this is not a
reliable symptom for DVT. The clinical symptoms
alone are not enough to diagnose DVT.
h. For every 100 patients with symptoms of
DVT, there are 15 to 35 patients who do not have
DVT but some other vascular disorder or nonva-
scular problem. In diagnosing DVT, the clinical
findings are about 50% accurate. Other causes of
redness, pain, and swelling of the lower extremi-
ties can include: a muscle strain or tear, a direct
injury of the leg, a Baker cyst, cellulitis, lym-
phangiitis, congestive heart failure, extrinsic com-
pression, and complications of chronic venous
insufficiency.
i. Patients who are short of breath, have severe
chest pain, and low pulse-oximetry values are sus-
pected of having a pulmonary embolus; then the
clinician should check for DVT.
j. Anticoagulation is the number one way to treat
DVT. Types of anticoagulants are heparin and
coumadin. Thrombolytic therapy, which includes
streptokinase and urokinase, is another treatment
method used to dissolve the clot. A thrombectomy
can be performed only when anticoagulation and
thrombolytic agents don’t work and there’s a clot in
the iliofemoral area or impending limb loss (as with
phlegmasia cerulea dolens). A Greenfield filter may
also be placed in the inferior vena cava to decrease

the risk for pulmonary embolism in a patient that
has DVT and cannot be anticoagulated.
k. Some unusual forms of DVT:
(1) Phlegmasia alba dolens. Consistent with a
painful, swollen white leg (“milk leg”),
iliofemoral thrombosis, there is increased fre-
quency of this in the postpartum period.
(2) Phlegmasia cerulea dolens. Consistent
with a painful, swollen cyanotic (blue) leg,
iliofemoral and greater saphenous vein thrombo-
sis is the most severe form of limb thrombosis.
(3) May-Thurner syndrome. When the left
common iliac vein courses posterior to the right
common iliac artery, DVT more often occurs on
the left side.
(4) Klippel-Trenaunay-Weber syndrome is the
congenital absence or atresia of the deep veins.
Some deep venous segments may be grossly
enlarged.
2. Venous insufficiency
a. In many patients, venous insufficiency is
caused by damage to the valves from DVT. It
develops in approximately half of the patients with
acute DVT.
b. With venous insufficiency, the valves fail to
function properly, and blood is allowed to flow in
the incorrect direction (reflux).
c. When there is valvular incompetence, the hydro-
static pressure is sufficient enough to distend the
veins (which are highly elastic) and the blood is
allowed to pool.
d. Chronic stasis causes the veins to become
inflamed. Expansion of the veins exerts pressure on
the surrounding tissues causing pain. The constant
pooling of the blood and the increased hydrostatic
pressure causes fluid to leak out into the tissues
(edema).
e. Symptoms of venous insufficiency:
(1) Deep vein incompetence is associated with
pain or swelling or both.
(2) Perforator incompetence is associated with
swelling and skin changes in the gaitor zone
(the medial ankle can be red to purple or
brown).
TABLE 5.1. THE DIFFERENCE BETWEEN ARTERIAL AND VENOUS ULCERS
Variable Venous ulcers
Location Near medial malleolus
Discomfort Mid
Appearance Shallow, regular
Bleeding Venous ooze
Other findings Brawny discoloration, varicosities
5/Peripheral Venous Systems 57
(3) Superficial incompetence is associated with
varicose veins.
(4) Venous stasis ulcers may form near the
medial malleolus (Table 5.1).
(5) It is important to determine whether a per-
son has primary or secondary varicose veins:
(a) Primary varicose veins are due to heredi-
tary weakness or absence of valves and can be
aggravated by pregnancy and obesity.
(b) Secondary varicose veins are due to dis-
ease in the deep system.
(6) Venous insufficiency can be treated med-
ically or surgically. If there is only superficial
incompetence, varicose veins can be removed by
sclerosing or vein stripping. Compression cuffs
on the legs (which mimic the muscle pump) or
elastic support stockings can be used.
f. Causes of venous insufficiency:
(1) Occasionally the calf muscle pump itself
may not produce enough energy to give adequate
venous return. This happens with patients who
are paraplegic, inactive, or sitting for long periods
of time. They become prone to phlebitis and
eventually DVT.
(2) A congenital defect of the valve cusps not
opposing each other when they are closed causes
reflux down the superficial veins. If the patient
has increased venous pressure due to heart or pul-
monary hypertension or congestive heart failure,
reflux is increased and produces symptoms.
(3) A previous DVT episode causes the veins to
enlarge so that the valve cusps no longer coapt.
This leads to valve incompetency. Also, the valves
may become thickened and small bits of chronic
DVT adhere to the valves, preventing closure.
When deep vein valves are destroyed, the calf
pump enlarges, causing increased intravenous
pressure, the perforator valves become nonfunc-
tional due to increased pressure, then the super-
ficial venous system becomes incompetent as the
increased pressure and volume is transferred.
3. Lymphedema. Lymphedema is painless, firm
swelling that progresses over time. The patient may
develop recurrent bouts of cellulitis. Primary lym-
Arterial ulcers
Tibial area, toes, bony prominences
Severe
Deep, irregular
Little bleeding
Shiny skin, hair loss, thickened toenails
58 The Complete Guide to Vascular Ultrasound
phedema is idiopathic and/or congenital. Secondary
lymphedema is due to an obstruction or inflamma-
tion.
4. Cellulitis. Cellulitis is an infection of the dermal
tissues of the limb. It results in increased blood flow to
the leg. It presents with hot and red tissues, often in
the shin and top of the foot.
C. History: Questions to Ask the Patient
1. About half of the people with DVT have no symp-
toms at all. Pulmonary embolism may be the first indi-
cation that something is wrong. Ask:
a. Have you had any pain in your legs?
b. Have you had any swelling in either leg? If you
have, is it worse late in the day?
c. Have you ever had any blood clots in your legs?
d. Have you had any recent surgery?
e. Have you taken any long trips?
f. Have you recently given birth?
g. Do you take birth control pills or hormone
replacement therapy?
h. Have you ever had any skin discolorations or an
ulcer on either leg?
i. Does either leg feel hot to the touch?
j. Do you have cancer?
k. Do you have any myeloproliferative disorders?
2. Evaluate the patient’s legs for any swelling, discol-
orations (may be brown in color), lesions, ulcers, red-
ness (or other color changes such as blue or white),
whether they feel hot to the touch, and superficial
varicose veins. Have the patient dorsiflex the foot to
see if he or she develops pain in the calf (Homans
sign). Feel for any lumps—swollen lymph nodes sup-
port the diagnosis of cellulitis. Feel for any palpable
“cords,” which is actually a thrombosed superficial
vein.
D. Diagnostic Examinations
1. Duplex Doppler examination
a. Begin with the patient in the supine or in the
reverse Trendelenberg position, with the leg bent
slightly and relaxed out to the side.
b. Using a 5.0- to 7.0-MHz transducer in the
transverse plane, start to image just above the crease
of the groin.
c. Locate the common femoral vein. Evaluate the
vein by compressing it until it is collapsed completely.
d. Continue in this fashion down the leg, evaluat-
ing the other vessels, compressing every 2 to 3 cm
(Fig. 5.2).
e. When you get to the popliteal vein, slide your
transducer behind the patient’s knee. This posterior
approach will place the vein anterior to the artery
on the screen.
f. The posterior tibial and peroneal veins may be
evaluated by placing the transducer on the medial
surface of the lower leg and sliding up from the
ankle. With this approach, these veins are located
between the tibia and the fibula. The posterior tib-
ial veins are more anterior and just beneath a fascial
plane connecting the tibia and the fibula. The per-
oneal veins are more posterior and just anterior and
medial to the fibula.
g. You may also follow the calf veins in a posterior
approach as they split off the popliteal vein. The
anterior tibial vein may be found by placing the
transducer on the anterior surface of the lower leg.
They are located between the tibia and fibula, just
anterior to the fascial plane between the two
bones. They resemble “ants on a bridge.” Check
for masses pressing on the veins (Baker cysts or
lymph nodes.)
h. Obtain compression/noncompression gray scale
images, color images, and duplex Doppler signals
with augmentation (squeezing of the distal body
part to cause a sudden rush of flow) of the follow-
ing vessels:
(1) Common femoral vein with the origin of the
greater saphenous vein (Fig. 5.3)
(2) Proximal superficial femoral vein with deep
femoral vein (Fig. 5.4)
(3) Middle superficial femoral vein (Fig. 5.5)
(4) Distal superficial femoral vein (Fig. 5.6)
(5) Popliteal vein (Fig. 5.7)
(6) Posterior tibial veins (Fig. 5.8)
(7) Peroneal veins
(8) Anterior tibial veins, if necessary (Fig. 5.9)
i. In addition, the common femoral vein may be
interrogated with Doppler while the patient per-
forms the Valsalva maneuver. This indirectly evalu-
ates for obstruction in the pelvic veins.
j. The calf is not always evaluated in some medical
centers since it is rare for DVT in the calf to cause
pulmonary emboli. However, in other places it is
evaluated routinely due to the 20% incidence of the
clot traveling further up the leg, as well as the
increased incidence of significant venous insuffi-
ciency after untreated calf DVT.
2. Continuous - wave Doppler. Continuous-wave
Doppler is an indirect and noninvasive test often used
in conjunction with other indirect tests. It is “blind”—
you don’t always know if you’re on the right vessel. Use
a 5-MHz probe. The basic principles and signal
changes that would be expected for a continuous-wave
examination are the same as for a duplex Doppler
examination.
3. Phleborheography. This is a type of plethysmog-
raphy. Cuffs are placed around the thorax, thighs,
lower thighs, calves, ankles and feet. It is rarely used
today. This is an indirect and noninvasive test. Fluctu-
ations in respiration seen at the thorax should be seen
in all tracings.

FIGURE 5.2. Cross-sectional view of the right lower extremity. Red, arteries; blue, veins.
4. Impedance plethysmography (IPG)
a. This is the most common indirect and noninva-
sive test. It measures the rate at which blood leaves
the leg via the venous system.
b. The patient’s leg is elevated above their heart,
and a thigh cuff is inflated to 50 mm Hg (which
occludes venous flow but still allows arterial flow).
There are four electrodes on the patient’s calf—the
two outer ones receive electric current, the two
inner ones record the change in voltage that occurs.
c. Because outflow is obstructed and inflow contin-
ues, the calf swells with the increased volume of
blood. As the volume increases, the voltage decreases
dramatically. (This is plotted as inverted on a strip
chart recorder, so it looks like the voltage is increased.)
5/Peripheral Venous Systems 59
d. After 30 to 45 seconds, the calf is filled com-
pletely and strip chart has leveled off. At this point,
the cuff is released. As blood flows back to the heart,
the recorder pen falls rapidly.
e. The amount of change in voltage that occurs dur-
ing the 3-second period following the cuff release is
known as the maximum venous outflow (MVO).
The MVO is the number related to how much blood
is allowed to leave the calf in 3 seconds and thus
relates to how open the venous system is. The higher
the MVO, the less likely that DVT exists.
f. The segmental venous capacitance (SVC) is the
distance in height (in millimeters) between the
position of the recorder pen before inflation of the
thigh cuff and after the thigh cuff inflation. This
60 The Complete Guide to Vascular Ultrasound

B
FIGURE 5.3. A: Transverse gray-scale image of the left common femoral vein with the greater
saphenous vein, without and with compression. B: Color image and Doppler tracing of the left
common femoral vein, with augmentation.
 FIGURE 5.4. Gray-scale image of the left prox-
imal superficial femoral vein, without and with
compression.

FIGURE 5.5. Gray-scale image of the left middle

superficial femoral vein, without and with com-
pression.

FIGURE 5.6. Gray-scale image of the left distal superficial

femoral vein, without and with compression.
62 The Complete Guide to Vascular Ultrasound
should be at least 75 impedance units (IU) or
greater. If it is decreased, this means the calf is
already filled with thrombus.
g. The MVO for 3 seconds should be equal to at
least 50% of the SVC (at least half of the blood that
has accumulated in the calf should leave in the first
3 seconds).
5. Venous pulse volume recording (PVR) test
a. A calf cuff, inflated to 5 to 10 mm Hg to ensure
a snug fit, replaces IPG electrodes.
b. The patient’s leg is elevated above the heart, and
a thigh cuff is also inflated to 50 mm Hg. The
increase in calf volume causes displacement of air in
the calf cuff.
c. Once plateau is reached, the thigh cuff is
released.
d. The strip chart looks like an IPG examination.
The MVO and the SVC are calculated from the
curve. The only difference from an IPG examina-
tion is that the MVO is determined from 1 second
of outflow rather than 3 seconds. This test is more
rapid than the IPG. This is due to the total volume
of calf being measured by airflow as opposed to the
IPG measuring electrical conductivity, which
depends not only on calf volume but also on the
amount of blood in venules in the skin. Minute
veins empty more slowly than larger veins. The
SVC should be equal to 30 mm of deflection. The
venous PVR test uses different units than the IPG
technique since it is a volume measurement and not
an electrical measurement.
e. A tracing with DVT has a “humped” slope, and
the difference between the starting plateau and the
postocclusion plateau is much less than for a nor-
mal tracing.
FIGURE 5.7. Gray-scale image of the left
popliteal vein, without (left) and with (right)
compression.
f. A strain gauge may also be used to determine the
change in calf size during and after thigh occlusion.
Results are similar to the air cuff technique.
g. Calf cuffs can be used without a thigh cuff to
determine whether basic changes are occurring with
respiration.
h. If a patient has DVT, it is virtually impossible to
obtain a normal IPG or air cuff test result (false neg-
ative).
i. False-positive results (an abnormal test in a nor-
mal patient) can be obtained if the patient’s deep
system is compressed in some way by positioning or
tight clothing. Also, obesity may compress the groin
and outflow rate (the patient may have to lie on a
slight angle). It is also important for the patient to
relax (if they are tense, Valsalva decreases the out-
flow rate). Cold decreases the outflow rate as well.
Chronic phlebitis and sclerotic therapy also
decrease the outflow rate.
j. SVC values may be higher than normal in
cases of venous malformation or severe varicosi-
ties.
6. Duplex Doppler examination for venous insuf-
ficiency. Place the patient in a standing position,
bearing their weight on the leg that is not being
examined and the leg in question dangling. (A step
stool may have to be used.) The patient may also be
supine on a stretcher in a severely reversed Trende-
lenburg position with their feet well below the level
of their heart. Either position provides increased
hydrostatic pressure, which causes veins with incom-
petent valves to dilate. Examine the common femoral
vein, saphenofemoral junction, mid superficial
femoral vein, saphenopopliteal junction, and
popliteal vein. Use proximal compression or the Val-
 5/Peripheral Venous Systems 63

B
FIGURE 5.8. A: Transverse gray-scale image of the left posterior tibial and peroneal veins. B:
Color image and Doppler tracing of the left posterior tibial vein, with augmentation.
64 The Complete Guide to Vascular Ultrasound
FIGURE 5.9. Gray-scale image of the left anterior tibial veins.
salva maneuver while interrogating these vessels with
Doppler. If there are incompetent valves, there will
be prolonged reverse flow (reflux) upon the release of
the proximal augmentation of the Valsalva maneuver.
Reverse color flow also can be seen. Varicose veins
may be seen as “snakes” with changing flow direc-
tions on color (Doppler Imaging).
7. Photoplethysmography (PPG) examination for
venous insufficiency
a. PPG can detect the amount of blood contained
just under the skin. (The technique uses an infrared
transducer that transmits, receives, and quantitates
light). If it is Direct Current (DC) coupled it can be
used to evaluate reflux in small venules just under
the skin. The more blood that is there, the more
that gets absorbed, and causes less reflectivity.
b. Place the PPG sensor a few centimeters above
the medial malleolus. Adjust the electrical signal so
that the baseline is at the top of the strip chart or
monitor.
c. Place the patient sitting with both feet on the
floor; have them raise the heel of the foot quickly
while keeping the toes on the floor for five cycles.
This causes the muscle pump to effectively empty
much of the venous blood from the limb. If the
patient has normal values, the blood goes through
the artery, capillary beds, then venules, with the
refill time taking 20 or more seconds. If the patient
has incompetent valves, blood may fall directly
down the veins of the limbs to the venules beneath
the sensor. Repeat the test three times for accuracy.
d. The PPG reflux test is repeated using tourni-
quets placed at different locations on the leg. This
can determine which segment is incompetent.
When no tourniquet is used and the test result is
abnormal, use an ankle tourniquet. If the refill time
is less than 20 seconds, this signals that there is deep
insufficiency, with possible superficial or perforator
insufficiency as well. If the refill time is greater than
20 seconds (normal), move the tourniquet from the
ankle to just below the knee level. If this result is
normal (>20 seconds), then there is only superficial
insufficiency. If the result is less than 20 seconds
(abnormal), this signals perforator insufficiency.
When the result is normal, move the tourniquet
from below the knee to just above the knee level. If
the results are normal (>20 seconds), this signals
greater saphenous vein insufficiency only. If the
results are abnormal (<20 seconds), this implies
lesser saphenous vein and/or greater saphenous vein
insufficiency.
8. Vein mapping
a. The greater saphenous vein can be used as a
graft—that is, as an in situ or reversed vein graft, or
for bypassing the coronary artery. The lesser saphe-
nous vein may also be used. First, perform a duplex
Doppler examination to make sure that the superfi-
cial system is not needed for an occluded deep sys-
tem, if there is DVT.
b. Place the patient supine on a stretcher in the
reverse Trendelenberg position. Use a 7.0-MHz lin-
ear transducer. Be careful to not exert too much
pressure and collapse the vessels. Begin in the trans-
verse plane at the level of the greater saphenous
vein’s confluence with the common femoral vein
(the saphenofemoral junction).
c. Mark the course of the greater saphenous vein on
the patient’s skin with a surgical marking pen. Any
visible branches or perforators should be drawn in
also. Trace the greater saphenous vein to the end at
the level just anterior to the medial malleolus. Trace
the branches as well.
d. Indicate the size of the greater saphenous vein in
several positions on the leg. A vein greater than or
equal to 3 mm is useful knowledge to the surgeon.
e. The lesser saphenous vein can be mapped in a
similar fashion.
E. Diagnostic Analysis
1. Duplex Doppler examination for DVT
a. Types of thrombus:
(1) Acute thrombus has low-level echoes, the
affected veins are dilated, there can be a free-
floating appearance of the thrombus, it is soft
and compliant when compressed, there is lack of
collateralization, it results in abnormal venous
Doppler signals, and it appears as a filling defect
on color Doppler images.
(2) Chronic thrombus has hyperechoic or
very bright echoes, the affected veins are con-
tracted, there is a firm attachment of the tip of

the thrombus to the venous wall, there is firm-
ness and noncompliance when compressed,
there is evidence of collateralization, it appears
as a filling defect on color Doppler images, and
it results in normal or abnormal Doppler sig-
nals depending on the extent of recanalization
(pathways open in the old thrombus and are
now only partially obstructed instead of com-
pletely).
b. Doppler signals:
(1) Spontaneity of flow. A loss of the sponta-
neous signal may indicate obstruction at the site
by thrombus.
(2) Phasicity of flow. Normal phasicity is
when inspiration decreases or stops the flow
and expiration resumes or increases the flow
(Fig. 5.10). A loss of phasicity may indicate
obstruction superior to the site being exam-
ined. A continuous signal is also seen with cel-
lulitis or compression of the vein by an extrin-
sic mass. Collaterals that form in response to
DVT have a continuous signal. Sluggish blood
flow may be seen real-time with gray-scale
imaging because red blood cell rouleaux
becomes echogenic.
(3) Augmentation. Compression of the venous
segment inferior to the site being examined will
enhance the flow on spectral display (Fig. 5.11).
FIGURE 5.10. Color image and Doppler tracing of the right common femoral vein, demonstrat-
ing the phasicity of normal flow.
5/Peripheral Venous Systems 65
If this does not occur, it may indicate an obstruc-
tion from the site of compression to the Doppler
site. If the flow increases only slightly with infe-
rior compression, then there is partially occlusive
thrombus.
(4) Valsalva. The Valsalva maneuver should slow
or stop blood flow in the femoral vein and the
greater saphenous vein. On release, there should
be a brief increase in flow (Figs. 5.12 and 5.13). If
a prolonged flow reversal occurs (reflux), this is
due to incompetent venous valves (Fig. 5.14),
Patients with complete obstruction of the external
or common iliac vein will have loss of phasicity or
absent flow in the common femoral vein, and this
will not change with the Valsalva maneuver. The
Valsalva maneuver provides indirect evidence that
the pelvic vessels are patent. However, if there is
only partial thrombus that does not completely
occlude the vessel or if the patient has many pelvic
collaterals, the Valsalva maneuver will be normal.
(5) Proximal compression. This has the same
effect as the Valsalva maneuver but works for the
lower femoral vein, popliteal vein, and calf. There
should be no flow reversal.
(6) Pulsatile venous flow. This may occur due
to congestive heart failure and pulmonary hyper-
tension (due to an enlarged right heart and tri-
cuspid regurgitation) (Fig. 5.15).
66 The Complete Guide to Vascular Ultrasound

FIGURE 5.11. Color image and Doppler tracing of the right common femoral vein, demonstrat-
ing normal augmentation of venous flow.

2. Impedance plethysmography. The amount of
change in voltage that occurs during the 3-second
period following the cuff release is known as the MVO.
The MVO is the number related to how much blood is
allowed to leave the calf in 3 seconds and thus relates to
how open the venous system is. The higher the MVO,
the less likely that DVT. The SVC is the distance in
height (in millimeters) between the position of the
recorder pen before inflation of the thigh cuff and after
the thigh cuff inflation. This should be at least 75 IU or
greater. If it is decreased, this means the calf is already
filled with thrombus. The MVO for 3 seconds should

FIGURE 5.12. Respiratory changes in vein diameter. (Reproduced from

Odwin CS, Dubinsky T, Fleischer AC. Appleton & Lange’s review for the
ultrasonography examination, 2nd ed. East Norwalk, CT: Appleton &
Lange, 1987, with permission.)
 5/Peripheral Venous Systems 67

FIGURE 5.13. Color image and Doppler tracing of the right common femoral vein, demonstrat-
ing the effect of the Valsalva maneuver on normal venous flow.

FIGURE. 5.14. Doppler tracing of the left greater saphenous vein, demonstrating reflux due to
incompetent venous valves.
68 The Complete Guide to Vascular Ultrasound
FIGURE 5.15. Color image and Doppler tracing of the right common femoral vein, demonstrat-
ing pulsatile venous flow.
be equal to at least 50% of the SVC (at least half of the
blood that has accumulated in the calf should leave in
the first 3 seconds). (Figs. 5.16 and 5.17).
3. Venous PVR test. The SVC should be equal to 30
mm of deflection. The venous PVR test uses different
units than the IPG technique since it is a volume mea-
surement and not an electrical measurement. A tracing
with DVT has a humped slope, and the difference
between the starting plateau and the postocclusion plateau
is much less than for a normal tracing. A strain gauge may
also be used to determine the change in calf size during
and after thigh occlusion. Results are similar to the air cuff
technique. Calf cuffs can be used without a thigh cuff to
determine whether basic changes are occurring with respi-
ration. If a patient has DVT, it is virtually impossible to
obtain a normal IPG or air cuff test result (false negative).
False positive results (an abnormal test in a normal
FIGURE 5.16. Venous outflow plethysmography with normal
results.
patient) can be obtained if the patient’s deep system is
compressed in some way by positioning or tight clothing.
Also, obesity may compress the groin and outflow rate
(the patient may have to lie on a slight angle). It is also
important for the patient to relax (if the patient is tense,
Valsalva decreases the outflow rate). Cold decreases the
outflow rate as well, as do chronic phlebitis and sclerotic
therapy. SVC values may be higher than normal in cases
of venous malformation or severe varicosities.
4. Duplex Doppler for venous insufficiency. If there
are incompetent valves, there will be prolonged reverse
flow (reflux) on the Doppler signal upon the release of
the Valsalva maneuver or proximal compression.
Reverse color flow also can be seen. Varicose veins may
be seen “snakes” with changing flow direction on color.
FIGURE 5.17. Venous outflow plethysmography with abnormal
results (patient has deep venous thrombosis).
 5/Peripheral Venous Systems 69

5. PPG for venous insufficiency. The PPG reflux

test is repeated using tourniquets placed at different
locations on the leg. This can determine which seg-
ment is incompetent. When no tourniquet is used and
the test result is abnormal, use an ankle tourniquet. If
the refill time is less than 20 seconds, this signals that
there is deep insufficiency, with possible superficial or
perforator insufficiency as well. If the refill time is
greater than 20 seconds (normal), move the tourni-
quet from the ankle to just below the knee level. If this
result is normal (>20 seconds), then there is only
superficial insufficiency. If the result is less than 20
seconds (abnormal), this signals perforator insuffi-
ciency. When the result is normal, move the tourni-
quet from below the knee to just above the knee level.
If the results are normal (>20 seconds), this signals
greater saphenous vein insufficiency only. If the results
are abnormal (<20 seconds), this implies lesser saphe-
nous vein and/or greater saphenous vein insufficiency.
F. Other Diagnostic Tests
1. Contrast venography. Contrast venography is the
gold standard. It involves the injection of contrast into
veins and is extremely accurate. However, it is limited
by the high technical level to perform and interpret
the test, is more expensive, is uncomfortable for the
patient, and may cause an allergic reaction to or
extravasation of the contrast media.
FIGURE 5.18. Upper extremity veins.
2. Isotope venography. This uses iodine-labeled fib-
rinogen. It can simultaneously evaluate peripheral and
pulmonary veins, is highly sensitive to active throm-
bosis, and is extremely accurate in detecting isolated 5. The basilic vein travels in the subcutaneous tissues
calf clot. However, the limitations are its inability to of the medial aspect of the arm. It joins with the paired
detect established clots, sensitivity to even clinically brachial veins.
insignificant clots, and difficulty documenting throm- 6. The radial and ulnar veins are paired and travel
bosis in the pelvis and upper thigh. with their respective artery on the lateral and medial
3. Lung perfusion scan or ventilation quotient side of the forearm. They join with the brachial veins.
(VQ scan). This is a screening test used to detect per- 7. The brachial veins are paired and travel with the
fusion defects of the lungs commonly caused by pul- brachial artery in the upper arm. They join the basilic
monary emboli. This test is limited by the fact that vein at the level of the teres major muscle to become
defects can also be due to emphysema, asthma, pneu- the lateral aspect of the axillary vein.
monia, bronchial cancer, congestive heart failure, liver 8. The axillary vein travels adjacent to the axillary
cirrhosis, radiotherapy, multiple blood transfusions, or artery. As it crosses the first rib, it becomes the subcla-
postoperative status. vian vein.
II. UPPER EXTREMITY VEINS 9. The subclavian vein is inferior and anterior to the
A. Anatomy (Figs. 5.18 and 5.19). subclavian artery. It travels medially toward the base of
1. In the upper extremity, the venous system is also the neck.
divided into a superficial system and a deep system. 10. The internal jugular vein extends from the jugu-
2. In the upper extremity, the superficial system is the lar foramen in the base of the skull down the lateral
primary means for returning blood. The blood flows aspect of the neck, anterior and lateral to the carotid
from the deep system to the superficial system. artery, to join the subclavian vein (near the base of the
3. The main portions of the superficial system are neck) to form the brachiocephalic vein. It drains the
composed of the cephalic vein and the basilic vein. interior of the skull and portions of the face and neck.
4. The cephalic vein travels in the subcutaneous tis- 11. The external jugular vein courses laterally to the
sues of the lateral aspect of the arm. It joins the distal internal jugular vein and is smaller. It drains into the sub-
portion of the subclavian vein or superior axillary vein. clavian vein. It drains the superficial head, neck, and face.
70 The Complete Guide to Vascular Ultrasound
FIGURE 5.19. Veins: thoracic vessels.
12. The brachiocephalic veins join to form the
superior vena cava.
13. The vertebral veins course through the vertebral
foramina and drain into the brachiocephalic veins.
They drain the posterior portions of the skull and
some upper neck muscles.
B. Pathology
1. DVT
a. Injury of the intima poses an increased risk for
thrombus formation (iatrogenic injury) that may be
caused by percutaneous intravenous central catheter
(PICC) lines (which are central venous catheters
usually inserted into the basilic vein), a central
venous catheter in the internal jugular vein for
chemotherapy or hyperalimentation (patients
receiving these lines are often at increased risk for
DVT to begin with), as well as pacemaker wires or
Swan-Ganz catheters through jugular or subclavian
veins. Duplex Doppler is an excellent method for
determining whether DVT is present. (Venography
increases the risk for intimal injury.)
b. Although the majority are asymptomatic, 26%
to 67% of patients with central venous catheters
develop thrombosis.
c. Causes of venous obstruction in the arm and
thorax include radiation therapy, malignant
obstruction, and effort-induced thrombosis.
d. Only 10% to 20% of patients with upper
extremity thrombosis actually develop pulmonary
emboli.
e. Since the upper extremity veins are not exposed
to the high hydrostatic pressure that lower extrem-
ity veins are, the upper extremity differs from the
lower extremity when it comes to the severity of the
symptoms and after-effects of an episode of DVT.
The fact that multiple extensive collaterals develop
in the arm and upper thorax after an episode of
DVT also helps.
f. The development of venous insufficiency (post-
DVT), with symptoms such as chronic arm
swelling, nonhealing venous ulcers, and skin
changes, is rare in the arm.
2. Lymphedema. Lymphedema is painless, firm
swelling that progresses over time. The patient may
develop recurrent bouts of cellulitis. Primary lym-
phedema is idiopathic and/or congenital. Secondary
lymphedema is due to an obstruction or inflamma-
tion. This can be due to a radical axillary lymph node
dissection in a patient with breast cancer.
C. History: Questions to Ask the Patient
1. Do you have any pain in either arm?
2. Do you have any swelling in either arm?
3. Do you have cancer?
4. Is either arm red or hot to the touch?
5. Do you have any shortness of breath or pain in the
chest?
6. Do you have any myeloproliferative disorders?
7. Have you recently given birth?
8. Have you recently had surgery?
9. Have you had a mastectomy? Did they remove any
lymph nodes as well?
10. Have you been taking estrogen such as in birth
control pills or hormone replacement therapy?
11. Have you had an indwelling catheter for access to
your veins?
12. Have you had chemotherapy or radiation therapy
in the past?
Evaluate the patient for any skin color changes, ulcers, or
swelling in either arm. Look for any central venous
catheters, PICC lines, or a pacemaker.
D. Diagnostic Examination
1. Duplex Doppler examination
a. Begin with the patient in the supine position
with the head and torso slightly raised. Bring the
arm out laterally away from the patient’s body with
the palm up.

b. Using a 7.0- or 10.0-MHz transducer, start at
the anterolateral side of the neck to image the inter-
nal jugular vein. The superior vena cava and most of
the brachiocephalic veins cannot be imaged due to
superimposition of bony structures.
c. To image the subclavian vein, superior brachio-
cephalic vein, and inferior internal jugular vein, a
bullet-shaped probe with a small footprint works
best to get around the clavicles.
d. To image the axillary vein, position the patient
with the arm above the head (if possible) to get into
the axilla.
e. Bring the arm back down into the starting position
to follow the brachial veins, cephalic vein, basilic vein,
and forearm veins. Many protocols do not require
images of the forearm veins. The radial veins course
laterally and the ulnar veins course medially. You
should also remember that the basilic vein courses
medial to and empties into the brachial veins. The
cephalic vein courses anterolateral to the brachial
B with compression (right).
5/Peripheral Venous Systems 71
veins and joins up with the axillary vein. Since these
two veins are superficial, be careful to maintain very
light pressure while imaging them or you may col-
lapse the vessels. If there is a venous catheter present,
look carefully around the catheter for any thrombus.
f. Obtain compression/noncompression gray-scale
images, color images, and Doppler signals of the
following vessels:
(1) Internal jugular vein (Fig. 5.20)
(2) Subclavian vein (Fig. 5.21)
(3) Axillary vein
(4) Brachial veins
(5) Cephalic vein (Fig. 5.22)
(6) Basilic vein
(7) Radial and ulnar veins, if necessary
g. While interrogating the internal jugular vein and
the subclavian vein, you may also have the patient
execute the Valsalva maneuver or take a deep inspira-
tory sniff. This helps to evaluate the patency of the
central brachiocephalic vein and superior vena cava.
FIGURE 5.20. A: Color image of the left inter-
nal jugular vein. B: Gray-scale image of the
left internal jugular vein, without (left) and
72 The Complete Guide to Vascular Ultrasound

B
FIGURE 5.21. A: Color image and Doppler tracing of the right subclavian vein, demonstrating
normal venous flow. B: Transverse gray-scale image of the right subclavian vein, without and
with compression.

E. Diagnostic Analysis ization, it results in abnormal venous Doppler sig-

1. Types of thrombus
a. Acute thrombus has low-level echoes, the
affected veins are dilated, there can be a free-float-
ing appearance of the thrombus, it is soft and com-
pliant when compressed, there is lack of collateral-
nals, and it appears as a filling defect on color
Doppler images (Fig. 5.23 and Fig. 5.24).
b. Chronic thrombus has hyperechoic or very
bright echoes, the affected veins are contracted,
there is a firm attachment of the tip of the throm-
 FIGURE 5.22. Transverse gray-scale image of
the right cephalic vein, without and with com-
pression. Notice the superficial location of the
cephalic vein, and that it is not paired with an
artery (in contrast to the deep veins, which are
paired with artieries). The basilic vein is also a
superficial vein, and shares these characteris-
tics as well.

B
FIGURE 5.23. A: Transverse gray-scale image of the left middle subclavian vein with a percuta-
neous intravenous central catheter (arrows), without and with compression. Notice how the vein
is dilated, filled with echogenic thrombus, and does not compress. B: Sagittal color image of the
same site as in A. Notice the absence of color flow.
74 The Complete Guide to Vascular Ultrasound
bus to the venous wall, there is firmness and non-
compliance when compressed, there is evidence of
collateralization, it appears as a filling defect on
color Doppler images, and it results in normal or
abnormal Doppler signals depending on the extent
of recanalization (pathways open in the old throm-
bus and are now only partially obstructed instead of
completely).
2. Doppler signals
a. Spontaneity of flow. A loss of the spontaneous
signal may indicate obstruction at the site by
thrombus.
b. Phasicity of flow. Since intraabdominal pres-
sure and intrathoracic pressure are inversely related,
the phasic quality of the upper extremity contrasts
with the lower extremity. In the upper extremities,
the phasic quality of the Doppler signal increases
with inspiration and decreases with expiration.
Normal phasicity in the lower extremities occurs
when inspiration decreases or stops the flow and
expiration resumes or increases the flow. A loss of
phasicity may indicate obstruction superior to the
site being examined. A continuous signal is also
seen with cellulitis or compression of the vein by an
extrinsic mass. Collaterals that form in response to
DVT have a continuous signal. Sluggish blood flow
may be seen real-time with gray-scale imaging
because red blood cell rouleaux becomes echogenic.
c. Pulsatility of flow. The subclavian vein and
inferior internal jugular vein signals may be pul-
satile since they are close to the heart and augmen-
tation during distal compression may be reduced. A
more central venous obstruction may result in loss
of this pulsatility. It is helpful to compare the
Doppler waveforms of each arm.
FIGURE 5.24. Transverse gray-scale
image of the left axillary vein in the
same patient as in Fig. 5.23, without
and with compression. Notice how the
vein is filled with echogenic thrombus
and does not compress.
d. Valsalva maneuver. If you have the patient
sniff or execute the Valsalva maneuver while inter-
rogating the subclavian vein and internal jugular
vein, the response should be an increase in velocity
on the Doppler spectral waveform and an increase
in the diameter of the vessel. This will not occur if
a patient has brachiocephalic vein or superior vena
cava obstruction.
e. Augmentation is often not done. This is due to
the fact that the volume of blood is smaller than in
the arms; therefore, when one augments the arms
there is not as much of a change in the Doppler sig-
nal as with the legs.
BIBLIOGRAPHY
Katanick S, Hoffman TG. Sonographic and Doppler investigation of
the peripheral veins and arteries and the cerebrovascular system.
Part I. Peripheral veins and arteries. In: Odwin CS, Dubinsky T,
Fleischer AC, eds. Appleton & Lange’s review for the ultrasonography
examination, 2nd ed. East Norwalk, CT: Appleton & Lange,
1987:455–459.
Lewis BD. The peripheral veins. In: Rumack CM, Wilson SR, Char-
boneau JW, eds. Diagnostic ultrasound, 2nd ed. St. Louis, MO:
Mosby Year-Book, 1998:943–958.
Rumwell C, McPharlin M. Part III. Venous evaluation. In: Vascular
technology—an illustrated review, 2nd ed. Pasadena, CA: Davies
Publishing, 2000:169–214.
Semrow CM, Rollins DL. Sonographic and Doppler investigation of
the peripheral veins and arteries and the cerebrovascular system.
Part II. Diagnosis of venous disease. In: Odwin CS, Dubinsky T,
Fleischer AC, eds. Appleton & Lange’s review for the ultrasonography
examination, 2nd ed. East Norwalk, CT: Appleton & Lange,
1987:495–506.
Tortora GJ, Anagnostakos NP. The cardiovascular system: vessels and
routes. In: Principles of anatomy and physiology, 6th ed. New York:
Harper & Row, 1990:633–642.
 6
PENILE VESSELS
I. ANATOMY (Figs. 6.1 and 6.2)
A. The internal iliac arteries give rise to the internal
pudendal arteries. Each internal pudendal artery gives
off the urethral artery, the bulbar artery, and a perineal
branch before it becomes the penile artery. Each penile
artery divides into the right and left cavernosal arteries
and the right and left dorsal arteries.
B. The cavernosal arteries supply the corpora cavernosa
and communicate directly with the sinusoidal spaces
(small spaces that occupy the corpora cavernosa and the
corpus spongiosum that fill with blood during an erec-
tion).
C. The dorsal arteries supply the skin of the penis and
glands.
D. The urethral artery supplies the corpus spongio-
sum and urethral tissue.
E. The bulbar artery supplies the urethral bulb and the
bulbourethral gland.
F. The emissary veins drain into the circumflex veins
(both drain the corpus cavernosum) that then empty into
the deep dorsal vein, which empties into the internal
pudendal vein.
G. The crural veins also drain the corpus cavernosum.
H. The urethral veins drain the corpus spongiosum,
and empty into the internal pudendal vein.
I. The superficial dorsal vein drains the skin and sub-
cutaneous tissue.
II. PATHOLOGY
A. Erectile Dysfunction
1. An erection is produced when the arterial beds
relax, allowing blood to fill the sinusoids and causing
an increase in blood flow and pressure, which causes
mechanical pressure on the veins that prevents or
decreases venous drainage from the penis.
2. Failure to achieve an erection can be due to:
a. Arterial occlusive disease in the right and/or left
cavernosal arteries, the penile artery, and the inter-
nal pudendal artery. This may be due to atheroscle-
rosis or trauma. Cigarette smoking, high choles-
terol, and hypertension are associated with
atherosclerosis.
b. Veins that drain the penis may not become suf-
ficiently compressed during an erection and thus
arterial blood escapes. This may be due to degener-
ative changes (from old age, diabetes, or Peyronie
disease) or trauma resulting in penile fracture. Pey-
ronie disease is a condition in which a focal
“plaque” or scar develops on the tunica albuginea
(the thick fascial outer layer that surrounds the cor-
pora cavernosa and the corpus spongiosum) of the
corpora cavernosa. During an erection, this causes
the penis to have a curvature or bend in that area.
c. Insufficient smooth muscle relaxation, which
does not allow enough blood to fill the sinusoids
and compress the veins.
d. An arteriovenous malformation allows blood to
leave the corpus cavernosum before a sufficient
blood pressure is achieved.
e. Other nonvascular causes of erectile dysfunc-
tion may include any disease or problem affecting
the brain, spinal cord, cavernous nerves, pudendal
nerves, or receptors in the cavernous smooth mus-
cles and terminal arterioles; endocrine disorders
such as hyperthyroidism, hypopituitarism, and
several types of pituitary tumors; as well as drugs
(such as nicotine with cigarette smoking) that
interfere with local neurovascular or central neu-
roendocrine control of the smooth muscle of the
penis.
B. Varicoceles
1. This is another vascular problem in which the veins
of the pampiniform plexus or cremasteric plexus
become greatly enlarged.
2. This occurs more often on the left side due to the
higher pressures from the left hemiscrotum draining
into the left renal vein. The presence of a varicocele on
the right may indicate a mass pressing somewhere on
the venous pathway.
3. The presence of a varicocele increases the tempera-
ture in the scrotum and lowers the sperm count.
4. It may produce pain and swelling and may be pal-
pated.
76 The Complete Guide to Vascular Ultrasound

H. Do you have high blood pressure?

I. Do you have high cholesterol?
J. Have you had any trauma to your penis?
IV. DIAGNOSTIC EXAMINATIONS
A. Duplex Doppler Examination for Erectile Dys-
function
1. Using an 8.0- to 10.0-MHz transducer (may be
linear-array or curved-array), obtain gray-scale
images of the flaccid penis in sagittal and transverse
orientations. Each cavernosal artery should be exam-
FIGURE 6.1. Cross-sectional vascular anatomy of the penis.
ined for evidence of visible plaque or narrowing of
the lumen. For your baseline, take color images and
Doppler spectral waveforms (with a 60-degree or
5. The varicocele may be removed by ligating the- less sample angle) of the right and left cavernosal
large draining vein, thus allowing the dilated venous arteries, the right and left dorsal arteries, and the
tissue to die and become absorbed by the body. deep dorsal vein. Measure the peak systolic and end-
III. HISTORY: QUESTIONS TO ASK THE PATIENT diastolic velocities. The diameter of the cavernosal
A. Have you had any difficulty with achieving an erec- arteries may also be measured. Use color Doppler
tion? imaging to look for any branches from one vessel to
B. Have you noticed any curvature to your penis? another.
C. Are you having fertility problems? 2. Prostaglandin E1 (6 μg if under 50 years of age;
D. Are you having any pain or swelling? 10 μg if greater than or equal to 50 years of age) is
E. Have you noticed any lumps, or feel a structure that injected directly into the corpus cavernosum. (This
feels like a “bag of worms” in your scrotum? has been shown to be more effective than direct
F. Do you smoke? injection into the urethra.) Papaverine can also be
G. Do you have diabetes? used instead of prostaglandin E1, although the latter

FIGURE 6.2. Color image of the normal vasculature of the penis.


is generally preferred due to the lower incidence of
priapism and its efficacy. Ten minutes postinjection,
the erection may be graded: 1, no erection; 2, slight
erection; 3, full erection without rigidity; 4, suffi-
cient for intercourse but still not complete rigidity;
5, full erection with rigidity. Once again, obtain
color images and Doppler spectral waveforms (mea-
suring peak systolic and end-diastolic velocities) of
the right and left cavernosal arteries, the right and
left dorsal arteries, and the deep dorsal vein. The
diameter of the cavernosal arteries may also be mea-
sured. If a full erection has not been achieved at this
point, the measurements are repeated after giving
the patient 5 minutes to enhance his erection by self-
stimulation.
3. Protocols vary with different medical centers.
Another protocol involves taking the Doppler spectral
waveforms every 5 minutes post injection, until the
peak systolic velocity has leveled off. It is important to
instruct the patient to contact his urologist or go to
the emergency room immediately if the erection has
not worn off 1 hour postinjection.
B. Segmental Pressure Examination for Erectile Dys-
function
1. Before obtaining the penile data, first calculate an
ankle-to-brachial index (PBI) to determine whether
inflow into the lower extremities is normal. The
patient could have aortoiliac disease that extends into
the internal iliac arteries. Use a toe cuff at the base of
the penis and measure the blood pressure using first
the right and then the left cavernosal arteries as the
flow sensor. Continuous-wave Doppler, photoplethys-
mography (PPG), strain gauge, or pulse volume
plethysmography may be used. Obtain bilateral
brachial pressures. Use the higher of the two to calcu-
late the PBI. Pulse volume plethysmography wave-
forms may be obtained as well.
2. The PBI is not a reliable indicator of vasculogenic
impotence due to many factors. The continuous-wave
probe is blind and may pick up the dorsal arteries
instead of the cavernosal arteries. The measurements
taken while the penis is in a flaccid state differ from
the measurements taken while the penis is in an erect
state. If the cuff does not fit the penis properly, errors
may occur.
C. Duplex Doppler Examination for Varicocele
Using a 10.0- to 12.0-MHz linear array transducer,
obtain gray-scale and color images around the testicles.
Varicoceles will appear as dilated, tubelike structures.
They are usually located lateral and posterior to the testi-
cles. Have the patient execute the Valsalva maneuver
while using color Doppler. You may also take a Doppler
spectral waveform while the patient performs the Valsalva
maneuver.
6/Penile Vessels 77
FIGURE 6.3. Hyperechoic area with very echogenic calcification,
indicating Peyronie plaque (arrows) on this sagittal view of the
penis.
V. DIAGNOSTIC ANALYSIS
A. Duplex Doppler Examination for Erectile Dys-
function
1. The echogenicity of the corpora cavernosa should
remain homogeneous throughout the study. An area
of increased echogenicity may indicate an area of
fibrosis or a Peyronie plaque (Fig. 6.3).
2. Preinjection, while the penis is flaccid, a peak sys-
tolic velocity of less than 10 cm/s has been shown to
be a predictor of arterial insufficiency.
3. A few minutes after injection of papaverine or
prostaglandin E1, the diameter of the cavernosal arter-
ies should increase by greater than 75%. The peak sys-
tolic velocity also increases.
4. Preinjection, the arterial flow in the penis has a
high-resistance quality. Postinjection, the arterial flow
becomes more low resistance as the diastolic flow
increases while the erection is developing. Once the
erection has developed, the diastolic flow decreases
and may become reversed. When the higher diastolic
flow persists, this indicates a significant venous leak-
age. The end-diastolic velocity should be less than 5
cm/s. If it is greater than that, the probability of a
venous leak or an arteriovenous malformation is
markedly increased (Fig. 6.4). There should also be no
dilated veins postinjection. If there are, then this also
raises the suspicion for a venous leak or an arteriove-
nous malformation.
5. Other data (which may vary among published ref-
erences) conclude that a normal peak systolic velocity
78 The Complete Guide to Vascular Ultrasound

B
FIGURE 6.4. A: Pre-stimulation right cavernosal artery (RCA). B: Pre-stimulation left cavernosal
artery (LCA).
 6/Penile Vessels 79

D
FIGURE 6.4. (continued) C: Post-stimulation, RCA. D: Post-stimulation, LCA. Note the high end-
diastolic flow of the cavernosal arteries in this patient, both pre- and post stimulation, indicating
a venous leak.

postinjection should be equal to or greater than 25
cm/s. A peak systolic velocity of 25 to 34 cm/s demon-
strates some level of compromise. Peak systolic veloci-
ties of 35 cm/s and above are normal. Significant arte-
rial insufficiency is indicated by peak velocities that are
less than 25 cm/s (Fig. 6.5).
6. Postinjection, the deep dorsal vein flow persists but
should not increase in velocity. It has been noted that an
increase to greater than 4 cm/s may indicate a venous leak.
7. Dorsal to cavernous and cavernous to cavernous col-
lateral arterial vessels are normally common (Fig. 6.6).
B. Segmental Pressure Examination for Erectile Dys-
function
1. The PBI is calculated by dividing the penile sys-
tolic pressure by the brachial systolic pressure. The PBI
should be greater than 0.65 to 0.70. If it is less than
0.65, then this is consistent with vasculogenic impo-
tence. If it is greater than 0.75, it is normal. A mar-
80 The Complete Guide to Vascular Ultrasound

B
FIGURE 6.5. A: Pre-stimulation RCA. B: Pre-stimulation LCA.
 6/Penile Vessels 81

D
FIGURE 6.5. (continued) C: Post-stimulation RCA. D: Post-stimulation LCA. Note the low peak
systolic velocities of the cavernosal arteries in this patient, both pre- and post stimulation, indi-
cating arterial insufficiency.
82 The Complete Guide to Vascular Ultrasound

FIGURE 6.6. Color image of the penis demonstrating a normal (arrow) collateral between the
left and right cavernosal arteries.

ginal recording is between 0.65 and 0.74. The penile-
to-brachial segmental gradient may also be used. If the
difference between the penile and brachial pressures is
greater than or equal to 60 mm Hg, then the test is
suspicious for vasculogenic impotence. If the differ-
ence between the two pressure is less than or equal to
20 mm Hg, then the test is normal. Between 20 and
60 mm Hg may be considered a borderline result.
2. Pulse volume recording waveform interpretation
a. Normal: A sharp waveform with a prominent
dicrotic notch.
b. Mildly abnormal: A sharp peak to the wave-
form with an absent dicrotic notch and bowed away
from the baseline.
c. Moderately abnormal: A flattened systolic peak,
the upslope and downslope time are nearly equal and
decreased, and the dicrotic notch is absent.
d. Severely abnormal: The pulse wave has low
amplitude with equal upslope and downslope times,
or may be absent.
C. Duplex Doppler for Varicocele
1. Varicoceles light up extensively with color Doppler
while the patient performs the Valsalva maneuver (Fig.
6.7). With this maneuver, the veins increase in size,
and the Doppler spectral waveform augments with
prolonged reverse flow.
2. Occasionally, severe epididymitis increases the size
of the ducts within this organ and mimics a varicocele.

FIGURE 6.7. Color image of the scrotum, demonstrating the multiple wormlike veins of a varic-
ocele dilating with color upon the Valsalva maneuver.
 6/Penile Vessels 83

It does not increase in size during the Valsalva maneu- intracorporeal injection of prostaglandin E1. J Clin Ultrasound
ver and has no flow. 2001;29(5):273–278.
King BF. The penis. In: Rumack CM, Wilson SR, Charboneau JW,
VI. OTHER DIAGNOSTIC TESTS eds. Diagnostic ultrasound, 2nd ed. St. Louis, MO: Mosby Year-
A. Arteriography Book, 1998:823–838.
B. Cavernosography Nisenbaum HL, Broderick GA. The Evaluation of erectile dysfunc-
C. Radioisotopic Penography tion. In: Bluth EI, Arger PH, Benson CB, et al., eds. Ultrasound—
D. Magnetic Resonance Imaging a practical approach to clinical problems. New York: Thieme Med-
ical, 2000:164–185.
Roy C, Saussine C, Tuchmann C, et al. Duplex Doppler sonography of
the flaccid penis: potential role in the evaluation of impotence. J
BIBLIOGRAPHY Clin Ultrasound 2000;28(6):290–294.
Rumwell C, McPharlin M. Part I. Arterial evaluation. In: Vascular
Kim JM, Joh YD, Huh JD, et al. Doppler sonography of the penile technology—an illustrated review, 2nd ed. Pasadena, CA: Davies
cavernosal artery: comparison of intraurethral instillation and Publishing, 2000:65–70.
 7
CEREBROVASCULAR SYSTEM
I. ANATOMY (Figs. 7.1–7.3)
A. The common carotid artery (CCA) is 5 to 6 mm
in size. The right CCA originates from the brachio-
cephalic artery, and the left CCA originates from the
aortic arch. The CCA bifurcates into the internal and
the external carotid arteries (Fig. 7.4). The carotid
bulb is the enlarged portion of the distal CCA (or it
can be part of the proximal internal carotid artery).
This has baroreceptors that sense and regulate blood
pressure.
B. The internal carotid artery (ICA) is approximately
4 mm in size. It is usually located posterior and lateral
to the external carotid artery (ECA), although 15% of
the time this is reversed. This artery supplies the ante-
rior brain, eyes, forehead, and nose. It enters the skull
through the carotid canal. After passing into the skull,
it gives off its first branch, the ophthalmic artery.
After this branch, the ICA joins the circle of Willis,
where it gives off the anterior choroidal and posterior
communicating arteries before it finally divides into
the anterior cerebral artery (ACA) and middle cerebral
artery (MCA). The portions of the ICA are divided as
follows:
1. Cervical—the longest portion
2. Petrous
3. Cavernous (“siphon”)—S-shaped, from whence
the ophthalmic artery branches
4. Supraclinoid
C. The ophthalmic artery is the first branch off the
ICA. It has several branches:
1. Central retinal artery. This artery supplies the
eye.
2. Supraorbital artery. This artery courses anterior
and superior until it reaches the globe, then joins the
ECA via the superficial temporal artery.
3. Frontal artery. This artery exits the orbit medially
to supply the midportion of the forehead. It joins the
ECA via the superficial temporal artery as well.
4. Nasal artery/angular artery. This artery branches
off the frontal artery to supply the nose. As the angu-
lar artery, it courses down the lateral border of the
nose. It joins the ECA via the facial artery.
D. The external carotid artery is approximately 3 mm
in size. It is usually located anterior and medial to the
ICA. Unlike the ICA, it gives off branches right away.
It has eight branches that supply the face, neck, tongue,
thyroid gland, ear, scalp, and dura mater. The branches
include: the ascending pharyngeal artery, superior
thyroidal artery, lingual artery, posterior auricular
artery, internal maxillary artery, superficial temporal
artery, transverse facial artery, and the occipital
artery.
E. The vertebral artery originates from the subclavian
arteries (Fig. 7.5). They are usually asymmetric in size,
with the right usually being smaller than the left. They
enter the vertebral space at the level of C6 and course
through the foramina. They exit the vertebral foramina
at the level of C1 and enter the skull through the fora-
men magnum to join together to form the basilar
artery.
F. The circle of Willis (Fig. 7.6) is a circle of vessels that
lie at the base of the brain connecting the anterior and
posterior circulatory systems. There is a “normal” circle
of Willis only 18% to 20% of the time. The most com-
mon variant is a hypoplastic ACA. The circle of Willis
provides an important collateral pathway in cases of
stenosis or occlusion. The circle of Willis is made up of:
1. Anterior cerebral artery —this artery carries 20%
to 30% of the blood to the brain.
2. Middle cerebral artery—this artery carries 70%
to 80% of the blood to the brain.
3. Posterior cerebral artery (PCA)
4. Basilar artery—this artery is formed by the verte-
bral arteries, and supplies blood to the posterior struc-
tures of the cranial cavity.
5. Distal ICA
6. Anterior communicating artery (ACA)
7. Posterior communicating artery (PCA)
G. Nearly one sixth of the cardiac output is sent through
the CCAs and the vertebral arteries. Approximately 75%
of blood going to the brain is sent through the ICAs
(each delivers 300–400 mL per minute). The other 25%
of the blood going to the brain is sent through the verte-
bral arteries (each delivers 100 mL per minute).
 7/Cerebrovascular System 85

FIGURE 7.3. The circle of Willis.

I. The major collateral pathways available for transfu-

sion are:
1. Circle of Willis pathways include:
a. External to internal collateral via the ophthalmic
artery (supraorbital artery to superficial temporal
artery, frontal artery to superficial temporal artery,
FIGURE 7.1. Blood supply to the brain. (Reproduced from
Odwin CS, Dubinsky T, Fleischer AC. Appleton and Lange’s review angular artery to transverse facial artery).
for the ultrasonography examination, 2nd ed. East Norwalk, CT: b. Crossover collateral via the ACA.
Appleton & Lange, 1987, with permission.) c. Posterior to anterior collateral via the PCA.
2. Intracranial to extracranial anastomoses include:
a. Connections via the ophthalmic and orbital
arteries, the meningohypophyseal branches, and the
H. The brain’s blood supply is divided into two systems: carotid-tympanic branches.
1. Anterior circulatory system. This system is made b. Connections via the occipital branch of the ECA
up of the carotid arteries and their branches. and the atlantic portion of the vertebral artery.
2. Posterior circulatory system. This system is c. The ECA’s connections across the midline.
made up of the vertebrobasilar arteries and their d. The deep cervical and ascending cervical branches
branches. of the subclavian artery to the branches of the lower

FIGURE 7.2. Portions of the internal carotid artery.

 FIGURE 7.4. Sagittal color image of the internal
(ICA) and external carotid arteries (ECA). (Image
courtesy of Philips Medical Systems.)

FIGURE 7.5. Sagittal color image of the left vertebral artery.

FIGURE 7.6. Color image of the circle of Willis using contrast enhancement. (Image courtesy of
Philips Medical Systems.)
 7/Cerebrovascular System 87

FIGURE 7.8. Sagittal gray-scale image of the carotid bulb with

homogeneous fibrous plaque (arrow). (Image courtesy of Philips
Medical Systems.)

FIGURE 7.7. Sagittal gray-scale image of the common carotid

artery with homogeneous fibrous plaque. (Image courtesy of
Philips Medical Systems.)
vertebral artery, the atlantic portion of the vertebral
artery, and the occipital branch of the ECA.
3. Small intraarterial communications.
II. PATHOLOGY
A. Arteriosclerosis
Arteriosclerosis is a number of pathologic conditions in
which there is thickening, hardening, and loss of elasticity
of the walls of the arteries.
B. Atherosclerosis
1. Atherosclerosis is a form of arteriosclerosis that is
characterized by a variable combination of changes in
the intima of the arteries. These changes include focal
accumulation of: lipids or a lipid containing material
(atheroma), complex carbohydrates, blood and by-
products, fibrous tissue, calcium deposits, smooth
muscle cells, collagen, fibrin, and platelets. This is
associated with changes in the media of the arteries.
2. Types of atherosclerotic plaque:
a. Fatty streak. A fatty streak is a thin layer of
lipid material on the intima of the artery. It has low-
level echoes and is homogeneous.
b. Fibrous plaque. Fibrous plaque is an accumu-
lation of lipids, covered by additional lipid deposits,
collagen, and elastic fibers. It has low- to medium-
level echoes and is homogeneous (Figs. 7.7 and
7.8).

FIGURE 7.9. Sagittal gray-scale image of the internal

carotid artery with heterogeneous complicated plaque
(arrows). (Image courtesy of Philips Medical Systems.)
88 The Complete Guide to Vascular Ultrasound
C. Mechanisms Involved in Cerebrovascular Disease:
FIGURE 7.10. Sagittal gray-scale image of the internal carotid
artery with heterogeneous complicated plaque (arrows). (Image
courtesy of Philips Medical Systems.)
c. Complicated lesion. This is fibrous plaque that
has progressed to include fibrous tissue and addi-
tional collagen, as well as calcium and cellular
debris. It is heterogeneous in appearance, and the
calcium deposits have bright echoes with shadowing
(Figs. 7.9 and 7.10).
d. Ulcerative lesion. This type of lesion occurs
when the normally smooth surface of the fibrous
cap has undergone deterioration. These may result
in distal embolization. A focal indentation (possibly
U shaped) or a break in the plaque’s surface is seen.
There may be eddies of color within the plaque.
Between 50% and 70% of patients with this type of
plaque have hemispheric symptoms. All ulcerated
lesions are associated with Intraplaque hemorrhage.
e. Intraplaque hemorrhage. This is seen as a
sonolucent area within the plaque. There can be
multiple sonolucent areas, giving a “Swiss cheese”
appearance.
1. Stenosis. This is a narrowing in the blood vessel
caused by the processes of atherosclerosis.
2. Thrombosis. This is the formation of a blood clot.
This is one of the most common causes of a stroke.
3. Embolism. This is a foreign substance or piece of
thrombus (may be solid, liquid, or gas) that moves
through the circulatory system until it becomes lodged
in a distant blood vessel. This results in complete or
partial obstruction of that vessel. The most frequent
type of embolus is atherosclerotic plaque that breaks
loose. A stenosis, thrombus, and embolus may all exist
at the same time.
4. Aneurysm. This is an abnormal dilatation of the
wall of a vessel. They rarely occur in the cervical
carotid artery. They are due to congenital defects, or
weakness of the wall from trauma, atherosclerosis, or
infection.
5. Nonatherosclerotic disease. This includes:
a. Dissection of the intima can be caused by
trauma. It may also occur spontaneously in a
patient with atherosclerotic disease. This shows up
as a mobile or fixed echogenic flap. It may or may
not have thrombus formation. It may cause occlu-
sion (Fig. 7.11).
b. Fibromuscular dysplasia, which is an over-
growth of collagen (dysplasia of the media of the
arteries). This is more common in young females.
This condition shows up on angiography like a
“string of beads.” Many patients have nonspecific or
no obvious ultrasound abnormalities.
c. Carotid body tumor. This is a highly vascular
tumor that arises between the external and internal
carotid arteries. It may occur bilaterally (Fig. 7.12).
d. Extravascular masses, such as lymph nodes,
abscesses, or hematomas, can compress or displace
the carotid arteries.
e. Posttraumatic pseudoaneurysms can occur
after trauma or surgery, such as endarterectomy.
This appears as a swirling pocket of blood attached
FIGURE 7.11. Sagittal color image of the carotid
artery demonstrating a dissection. There appear to
be two lumens separated by a flap. (Image courtesy
of Philips Medical Systems.)
 7/Cerebrovascular System 89

FIGURE 7.12. Sagittal color image of a carotid

body tumor. (Image courtesy of Philips Medical
Systems.)

to the artery by a “neck.” On color Doppler, there
is a swirling pattern of blood often with a “yin-
yang” appearance (Fig. 7.13).
f. Aneurysm appears as an abnormal bulge in the
vessel.
g. Collagen vascular connective tissue disorders.
h. Arteritis resulting from autoimmune diseases
such as Takayasu arteritis, temporal arteritis, or
radiation changes. This causes diffuse concentric
thickening of the carotid walls, frequently involving
the CCA.
6. The two most common causes for brain ischemia
are embolization and hypoperfusion. These are most
often caused by stenosis, thrombosis, and embolism.
7. Plaque in the carotid arteries may be removed sur-
gically, a procedure that is called an endarterectomy.
Two clinical trials recently established the therapeutic
benefit of endarterectomy in asymptomatic patients

A B
FIGURE 7.13. Color images of a pseudoaneurysm extending off the distal common carotid
artery. This occurred postendarterectomy. (Image courtesy of Northeast Philadelphia Vascular
Surgeons, P.C.). A: Sagittal view of the distal common carotid artery. B: Transverse view of the
distal common carotid artery.
90 The Complete Guide to Vascular Ultrasound
FIGURE 7.14. Sagittal gray-scale image of a carotid artery stent.
(Image courtesy of Philips Medical Systems.)
with greater than 60% diameter reduction of the ICA
(the Asymptomatic Carotid Atherosclerosis Study, or
ACAS), and for symptomatic patients with greater
than 70% stenosis of the ICA (the North American
Symptomatic Carotid Endarterectomy Trial, or
NASCET).
8. Although unusual, a potential complication fol-
lowing carotid endarterectomy is pseudoaneurysm.
This may present as a painful and pulsatile mass fol-
lowing surgery.
9. Although endarterectomy is considered the stan-
dard for treatment of atherosclerotic carotid arterial
occlusive disease, carotid angioplasty with stent
placement has emerged recently as a potential alter-
native (Fig. 7.14). Some medical centers may also use
patch angioplasty following endarterectomy. This
may be done with a synthetic or a vein (usually
FIGURE 7.15. Gray-scale image of a vein patch in the carotid
artery. (Image courtesy of Philips Medical Systems.)
saphenous) patch (Fig. 7.15). Vein patching may
help reduce early or late restenosis after a carotid
endarterectomy. A potential complication of saphe-
nous vein patching is that it can cause the carotid
artery to become dilated, risking rupture and throm-
bosis.
10. A bypass graft may be used for occlusion of the
proximal common carotid, subclavian, or brachio-
cephalic arteries.
D. Subclavian steal syndrome (also known as verte-
bral steal). When significant disease is present in the
brachiocephalic or proximal subclavian arteries, blood
must now course up the contralateral vertebral artery,
cross over at the basilar artery, and course down the
vertebral artery of the affected side to the subclavian
artery to perfuse the arm. Even at rest, a significant dif-
ference in blood pressure of the affected arm is found
when compared with the unaffected side. The differ-
ence in blood pressure is 15 to 20 mm Hg, with the
side producing the lower pressure being the affected
side. There is increased resistance in vertebral arterial
flow, and reverse flow is seen in the ipsilateral vertebral
artery. A partial vertebral steal is one that almost meets
the circulatory requirements of the arm, and has bidi-
rectional flow that can be converted to a complete steal
by exercising the arm or by placing a blood pressure
cuff on the arm for a few minutes, then releasing. Sur-
gical treatment may include endarterectomy or a bypass
graft.
III. HISTORY: QUESTIONS TO ASK THE PATIENT
A. Have you ever had a cerebrovascular accident (CVA)?
[A cerebrovascular accident is otherwise known as a
stroke. It produces permanent neurologic deficits. Stroke
is the third leading cause of death in the United States.
Strokes are either ischemic (due to a decreased blood sup-
ply) or hemorrhagic (due to a blood vessel that bursts.)
Approximately 80% of strokes are due to ischemia from
thromboemboli. In the United States, a large portion of
thromboemboli are due to atherosclerotic disease of the
carotids. The plaque breaks off and interrupts blood flow
to the brain. It is estimated that one third of patients who
have had a transient ischemic attack (TIA) will have a
CVA within 5 years.]
B. Have you ever had a TIA? [A transient ischemic
attack is a neurologic event that reverses within 24
hours or less. It usually reverses within 30 minutes.
These are usually caused by embolization from the
heart or the carotid arteries. Symptoms may include
dysfunction of an arm or leg, speech problems, and
visual disturbances.]
C. Have you ever had a reversible ischemic neurologic
deficit (RIND)? [A reversible ischemic neurologic
deficit is a TIA that lasts longer than 24 hours but less
than 72 hours.]

D. Have you ever had any of the following symptoms:
1. Hemispheric symptoms:
a. Amaurosis fugax. This is transient unilateral
blindness that is caused by emboli from a more cen-
tral source. If this is from carotid plaque it will
occur in the ipsilateral eye.
b. Hemiparesis/hemiplegia. This is paralysis or
weakness on one side of the body (arm or leg or
both.) If this is from carotid plaque it will occur on
the contralateral side. It may be accompanied by:
c. Paresthesia or anesthesia. This is numbness or
tingling on one side of the body.
d. Aphasia or dysphasia. This is a language
deficit. The patient has a problem with understand-
ing or finding words. The causal lesion would be in
the carotid artery supplying the dominant hemi-
sphere (which is the left for most patients).
e. Behavioral abnormalities.
f. Hemianopsia. This is blindness in one half of
the visual field.
2. Vertebrobasilar symptoms:
a. Vertigo. This is the difficulty in maintaining
equilibrium, the feeling that you are moving around
in space or having objects move around you in space.
b. Ataxia. This is the failure of muscle coordina-
tion, gait disturbance, or imbalance.
c. Dysphagia. This is pain or difficulty with swal-
lowing.
d. Dysphonia. This is impairment of the voice.
e. Dysarthria. This is abnormal articulation or
pronunciation.
f. Paresthesia or anesthesia. This involves numb-
ness and tingling on both sides of the body.
g. Diplopia. This is double vision.
h. Nystagmus. This is rapid involuntary move-
ment of the eyeball.
i. Horner syndrome. This is ptosis (drooping) of
the upper eyelid, with sinking in of the orbit and
constriction of the pupil.
j. Drowsiness, stupor, or altered consciousness.
k. Motor and sensory deficits of the face. This
includes a facial droop and perioral numbness. This
can be unilateral, bilateral, or alternating.
l. Motor and sensory deficits of the body. This
can be unilateral, bilateral, or alternating.
3. Nonlocalizing symptoms:
a. Dizziness or lightheadedness
b. Syncope—This is a transient loss of conscious-
ness.
c. Headache, nausea, vomiting
d. Confusion
4. The MCA is the most commonly affected artery
for a stroke. The symptoms that correlate with specific
arteries include:
7/Cerebrovascular System 91
a. Internal carotid artery. Frequently seen symp-
toms are contralateral weakness, paralysis, numb-
ness, and/or sensory changes; ipsilateral amaurosis
fugax, and/or a bruit; possibly aphasia or altered
level of consciousness.
b. Middle cerebral artery. Frequently seen symp-
toms are aphasia or dysphasia, severe contralateral
hemiparesis or hemiplegia, dysarthria, behavioral
changes, confused state, possibly agitated delirium.
c. Anterior cerebral artery. Frequently seen
symptoms are contralateral hemiparesis, loss of con-
sciousness, impaired motor and sensory functions,
loss of coordination.
d. Vertebrobasilar. Frequently seen symptoms are
vertigo, ataxia, diplopia, amnesia, dysphagia, loss of
coordination, perioral numbness.
e. Posterior cerebral artery. Frequently seen
symptoms are dyslexia and coma.
E. Do you have hypertension?
F. Do you have diabetes?
G. Do you have high cholesterol?
H. Do you smoke? How many packs per day? For how
long have you smoked?
I. Do you have congestive heart failure?
J. Have you ever had a heart attack?
K. Do you have atrial fibrillation?
L. Do you exercise?
M. Do you take birth control pills?
N. Do you take any weight loss products containing
ephedra?
O. Have you ever had an endarterectomy? (Surgical
removal of the plaque—the recurrence rate for plaque is
5%–10% in the first year.) Do you have any pain in your
neck following the surgery?
P. Note whether the patient is obese. Listen with a
stethoscope for a bruit. A bruit is an abnormal sound
that is produced by turbulent blood flow. Carotid bruits
are a nonspecific sign of significant carotid artery disease.
This is due to the fact that a carotid bruit can be pro-
duced by another type of lesion, or by a tortuosity in the
vessel, and may be absent upon severe stenosis or occlu-
sion. Listen for the CCA in the low to middle neck, the
bifurcation in the middle to high neck, and the subcla-
vian artery just above and/or below the clavicle. Feel for
any pulsatile masses in the neck if the patient is status
post endarterectomy surgery. Take bilateral brachial
artery pressures. A difference of pressure greater than 30
mm Hg suggests stenosis of greater than 50% of the sub-
clavian or axillary artery.
IV. DIAGNOSTIC TECHNICAL
EXAMINATIONS
A. Oculopneumoplethysmography (OPG-Gee)
1. This is an indirect test. It provides information
about hemodynamically significant lesions in the
92 The Complete Guide to Vascular Ultrasound
ICA, as well as indirect information about the devel-
opment of collateral channels that provide blood to
the brain.
2. The limitations of this test are as follows:
a. This test cannot determine the exact location of
a stenosis.
b. It cannot differentiate between a tight stenosis
and an occlusion.
c. It is nondiagnostic when evaluating well-collat-
eralized lesions or lesions that are not hemodynam-
ically significant.
d. It is not useful for documentation of the pro-
gression of disease.
e. It may not be diagnostic in patients with severe
hypertension.
3. The contraindications of this test are as follows:
a. Patients with glaucoma.
b. Patients with allergies to local anesthetics.
c. Patients with a history of or have potential for
retinal detachment.
d. Patients who have had eye surgery within the
preceding 6 months.
e. Patients who have acute or chronic conjunctivitis.
f. Patients who cannot hold their eyes open.
4. Side effects that occur after this test include sub-
junctival edema (redness and tearing that usually dis-
appears within 30 minutes), as well as severe redness of
the sclera. Patients should not rub their eyes for a
while after the study.
5. The patient is positioned supine, with his or her
head on a pillow. The head of the bed may be elevated
slightly. Bilateral brachial pressures are taken. If the
patient has a systemic blood pressure of less than 140
mm Hg, then a vacuum of 300 mm Hg may be used.
If the patient has a systemic blood pressure of greater
than 140 mm Hg, then 500 mm Hg may be needed
to obliterate the arterial inflow. A local anesthetic is
applied to the eyes. Eye cups are placed on the lateral
sclera (white of the eye). A vacuum (300 or 500 mm
Hg) is applied to the cups, deforming the shape of the
globe, and increasing intraocular pressure. Strip chart
recordings are made as the pressure increases to a point
where it obliterates arterial inflow and the waveforms
disappear. The patient may experience a temporary
loss of vision. As the vacuum is slowly released, the
pulse waveform reappears when the ophthalmic arter-
ial pressure exceeds the intraocular pressure. This pres-
sure in the ophthalmic artery reflects the pressure in
the distal ICA.
6. To determine information about the collateral
pathways to the brain, carotid compression maneu-
vers may be used while administering the OPG-Gee
test. It is very important to never compress both
carotid arteries at the same time. It is also important
to not compress the region of the carotid sinus
(bulb) in order to not disturb the heart rate or
rhythm, decrease cerebral perfusion, or cause distal
embolization from dislodged plaque. The first part
of this test is to compress the carotid artery for 3 to
5 seconds while the OPG maintains an intraocular
pressure of 60 mm Hg. The second part, performed
only if pulsations are noted during the first part,
consists of a less than or equal to 15 second com-
pression while the OPG decreases the intraocular
pressure from 110 mm Hg to the level at which the
pulsations reappear.
7. Carotid compression should be released gradually
to prevent the sudden return of blood flow.
B. Periorbital Doppler
1. This test is an indirect test that can evaluate the
flow in the terminal branches of the ICA around the
eye.
2. The limitations of this test are as follows:
a. It cannot differentiate between a tight stenosis
and an occlusion.
b. It is not diagnostic when there is a lesion that is
not hemodynamically significant (<50%).
c. It requires considerable skill to perform.
3. The patient is positioned supine, with his or her
head on a pillow. The head of the bed can be elevated
slightly. Using an 8- to 10-MHz transducer, locate the
frontal artery at the inner canthus of the eye. Flow in
the frontal artery should be antegrade, toward the
transducer. A series of compression maneuvers are per-
formed both ipsilaterally and contralaterally to the fol-
lowing arteries:
a. Facial artery
b. Superficial temporal artery
c. Infraorbital artery
d. CCA (do not press the region of the carotid
bulb)
4. This test may be repeated using the supraorbital
artery, located superior to the eye, as well as the frontal
artery (Fig. 7.16).
FIGURE 7.16. Periorbital Doppler.
 7/Cerebrovascular System 93

C. Continuous-Wave Doppler carefully for any plaque (soft plaque has very low-level
1. Although this test can directly interrogate the carotid echoes and can be missed). Note the characteristics of
arteries, it is generally not the preferred test, as opposed the plaque (smooth, irregular, homogeneous, heteroge-
to duplex Doppler imaging. It has many limitations: neous, or calcified.) Look for aneurysms, pseudoa-
a. It is “blind”—there is a possibility that the vessel neurysms, signs of dissection, or extravascular masses.
desired to be interrogated is not actually the one With the color Doppler on, take pulsed Doppler wave-
being sampled. forms and measure the peak systolic and end-diastolic
b. It provides only physiologic information, since velocities in the following vessels (Fig. 7.17):
there is no imaging of the vessels. a. Proximal CCA
c. It is unable to differentiate between a tight b. Mid-CCA (Fig. 7.18)
stenosis and an occlusion. c. Distal CCA
d. Information may be obtained from more than d. Proximal ICA (Fig. 7.19)
one vessel along the path of the beam. e. Mid-ICA
e. A collateralized ECA may be mistaken for an f. Distal ICA
ICA when it is actually occluded. g. ECA (any portion) (Fig. 7.20)
f. It requires considerable skill to perform. h. Vertebral artery. The transducer must be
2. Place the patient in the supine position. Pointing angled out laterally to evaluate this artery. It is
the continuous-wave probe slightly cephalad, main- deeper than the others, and will be seen as it goes
tain a 45- to 60-degree angle of insonation and place through the vertebral bodies. Some medical cen-
the probe just above the clavicle to one side of the tra- ters try to evaluate the origin of the vertebral
chea. This evaluates the CCA. Slide the probe cepha- artery as well (Fig. 7.21). It is important to main-
lad to evaluate the bifurcation, sliding medial for the tain an angle of 45 to 60 degrees. The optimal
ECA and lateral for the ICA. angle is 60 degrees. The only time the angle may
D. Duplex Doppler Examination be changed is when the vessel dives straight down,
1. This is a direct test with many advantages. It can and then an angle of 0 degrees may be used. Use
localize the presence of disease in the carotid arteries. the color Doppler to look for areas of turbulence
It can differentiate a tight stenosis from an occlusion. or high velocity. Take pulsed Doppler waveforms
It is capable of following the progression of arterial at those areas.
disease. It can provide information about the charac-
teristics of the plaque. It can be used to evaluate pul-
satile masses in the carotid or subclavian areas.
2. The limitations of the test are as follows:
a. It may be limited by the presence of dressings,
staples, or sutures.
b. It may be limited by the depth of the artery, or
if there is a high bifurcation.
c. It may be limited by the patient’s movement,
rapid breathing, or size of their neck.
d. Shadowing from calcification may block infor-
mation in that area.
e. Tortuosity of a vessel, collateralizing for disease
(ipsilateral or contralateral), or a hypoplastic vessel
may mimic stenosis by producing high velocities at
that area.
3. The patient should be in a supine position or the
head of the bed may be slightly elevated. His or her head
should be slightly hyperextended and should be turned
away from the side to be evaluated. Using a 7.0-, 5.0-,
or 10.0-MHz linear array transducer, begin in the trans-
verse plane just lateral to the trachea and just above the
clavicle to evaluate the CCA. Slide the transducer cepha-
lad to evaluate the bifurcation. Next do the same in the FIGURE 7.17. Cerebrovascular recording sites. (Reproduced
from Philips Medical Systems. Vascular ultrasound protocol
sagittal plane. Take transverse and sagittal gray-scale and guides—expanding your clinical experience. Bothell, WA: Philips
color images of the CCA, the ICA, and the ECA. Look Ultrasound, 2002:2, with permission.)
94 The Complete Guide to Vascular Ultrasound

FIGURE 7.18. Color image and Doppler tracing of the right common carotid artery.

FIGURE 7.19. Color image and Doppler tracing of the right internal carotid artery.
 7/Cerebrovascular System 95

FIGURE 7.20. Color image and Doppler tracing of the right external carotid artery.

FIGURE 7.21. Color image and Doppler tracing of the left vertebral artery.
96 The Complete Guide to Vascular Ultrasound
4. In addition to peak systolic velocity and end-dias-
tolic velocity, other measurements may be obtained.
a. The ratio of the peak systolic velocity of the
proximal ICA divided by the peak systolic velocity
of the distal CCA may be calculated.
b. The percentage of stenosis may be calculated
using the measurements of diameter and area.
(1) % Diameter stenosis = 1 − diameter (resid-
ual)/diameter (original) × 100
(2) % Area of stenosis = 1 − diameter (resid-
ual)/diameter (original) squared × 100
5. The examination may be performed intraopera-
tively during carotid endarterectomy to identify resid-
ual plaque, stricture of the suture line, intimal flaps, or
areas of platelet aggregation. After placing the trans-
ducer in a sterile sleeve (gel should be placed inside the
tip of the sleeve), the wound is filled with sterile saline
and the examination may proceed.
E. Transcranial Doppler
1. Transcranial Doppler (TCD) has many uses:
a. TCD can detect intracranial stenoses and occlu-
sions, as well as aneurysms.
b. It can be used to monitor vasospasm—vessels
narrow usually 3 days after a bleed. The velocity
FIGURE 7.22. Transcranial Doppler windows. (Reproduced from Philips Medical Systems. Vascu-
lar ultrasound protocol guides—expanding your clinical experience. Bothell, WA: Philips Ultra-
sound, 2002:2, with permission.)
increases as the vessels narrow. A velocity of greater
than 200 cm/s indicates severe vasospasm.
c. It can be used to confirm brain deaths.
d. It can be used during intraoperative monitoring
while a carotid endarterectomy is being performed. It
can determine whether the MCA declines to a dan-
gerous level when the carotid artery is cross-clamped.
Usually collateral flow will maintain a reasonable
amount to the MCA. If it does decrease, the surgeon
can place a shunt around the surgical site to maintain
blood flow. Once surgery is complete, the MCA
needs to be monitored to make sure that there is not
too much flow (hyperperfusion.) Blood pressure
medication may be needed to prevent damage.
e. It can evaluate arteriovenous malformations.
f. It can evaluate collateralization in known cases of
severe carotid stenosis or occlusion.
2. Place the patient in a supine position. A rolled towel
may be placed beneath his or her neck for support. A 2-
to 2.5-MHz probe is used that transmits a much higher
energy than regular transducers. The probe also con-
tains special filters to remove reflective signals from
bone. A 0-degree angle of insonation is assumed. There
are four windows that may be used (Fig. 7.22):
 7/Cerebrovascular System 97

3. A routine study begins using the transtemporal

window to identify the MCA, ACA, PCA, and ICA
(Fig. 7.23). The transtemporal approach is performed
on both sides of the head.
a. The first step is to use a sample volume depth of
50 to 60 mm. Once a Doppler signal from an
intracranial artery is identified, increase the sample
volume depth to 60 to 70 mm. This is usually
FIGURE 7.23. Ultrasound view from the transtemporal window.
where the internal carotid bifurcation into the
MCA and ACA is found. The Doppler waveform
a. Transtemporal—just anterior and slightly supe- should show flow above the baseline or toward the
rior to the ear. In approximately 10% of patients, transducer (MCA) and below the baseline or away
one may not be able to penetrate this window due from the transducer (ACA) (Fig. 7.24).This may be
to hyperostosis of the temporal bone. This condi- used as the reference signal.
tion is more commonly found in the elderly, b. The MCA is then evaluated by reducing the
females, and blacks. sample volume depth in increments while angling
b. Transorbital—over the closed eye. This window the transducer to achieve the best signal. The MCA
may not be used if the patient has recently under- can usually be examined at a depth of 30 to 60 mm
gone eye surgery. (Fig. 7.25).
c. Subocciptal or transforaminal—midposterior c. Return to the ICA bifurcation signal and increase
portion of the skull. the depth of the sample volume (to 60–80 mm) while
d. Submandibular—the fourth window beyond angling the transducer slightly anterior and superior
the angle of the jaw, not usually used, is for cervical from the initial reference signal to then examine the
ICA only. ACA. The ACA is smaller and more tortuous, so it is

FIGURE 7.24. Color image and Doppler tracing of the bifurcation of the middle and anterior
cerebral arteries. (Image courtesy of Philips Medical Systems.)
98 The Complete Guide to Vascular Ultrasound

FIGURE 7.25. Color image and Doppler tracing of the middle cerebral artery. (Image courtesy of
Philips Medical Systems.)

sometimes more difficult to evaluate. As the ACA is rior from the reference signal. The anterior com-
“traced” to the midline, another bidirectional signal municating and the PCA are evaluated only if they
appears. This signal represents both anterior cerebral are involved as a collateral pathway.
arteries. Flow in the ipsilateral MCA is away from the 4. The transorbital window is then used to identify
transducer, while flow in the contralateral MCA is the carotid siphon and the ophthalmic artery (Fig.
toward the transducer. The ACA joins the two ACA 7.26). This approach is also repeated on the other
segments at the midline. This is usually seen at 75 to side. While using the transorbital window, it is rec-
80 mm of depth, and the direction of flow will be ommended to decrease the output or intensity level
away from the transducer. Normally the ACA signal of the equipment to reduce ultrasound exposure to
is turbulent and has high velocity.
d. The terminal ICA may be examined by angling
the transducer slightly inferior to the reference
bifurcation signal, while using a depth of 55 to 65
mm. Only a short segment of the ICA may be eval-
uated from this approach. The Doppler waveform is
toward the transducer and low velocity from this
angle.
e. The PCA is found by angling the transducer
posterior and inferior while increasing the sample
volume depth to 60 to 70 mm. The Doppler signal
is toward the transducer. Again, when sampling the
PCA near the midline, the flow becomes bidirec-
tional due to flow from the opposite side. The ipsi-
lateral PCA is toward the transducer, while the con-
tralateral PCA is away from the transducer. The
PCA joins the two PCA segments at the midline
and is found by angling posterior and slightly infe- FIGURE 7.26. Ultrasound view from the transorbital window.
 7/Cerebrovascular System 99

the eye. Place the transducer gently on the closed

eyelid. Make sure the patient is not wearing contacts
or has had recent eye surgery. Angle the transducer
slightly medially and use a depth of 40 to 60 mm to
localize the ophthalmic artery. The Doppler signal
should be toward the transducer. Increase the depth
to 60 to 80 mm to locate the carotid siphon. The seg-
ments of the carotid siphon may be identified by
their direction of flow. The Doppler waveform from
the genu will be bidirectional. Angle inferiorly, and
the parasellar segment flow will be toward the trans-
ducer. Angle superiorly, and the supraclinoid (distal
segment) of the siphon is found with flow away from
the transducer.
5. The transforaminal window is next used to evaluate
the intracranial vertebral and basilar arteries (Figs.
7.27 and 7.28). The patient should be positioned on
his or her side with the head tucked in toward the
chest. Place the transducer at the nape of the neck and
angle toward the patient’s eyes. Start with a sample
volume depth of 60 to 90 mm. The vertebral arteries
may be located by aiming the transducer slightly away
from the midline toward either side. The Doppler FIGURE 7.28. Color image of the vertebrobasilar arteries.
waveform should show flow away from the transducer (Image courtesy of Philips Medical Systems.)
in this approach (toward the brain). Follow the verte-
bral arteries distally while increasing the sample vol-
ume depth to 80 to 120 mm. The vertebral arteries release the pressure after two to four cardiac cycles.
join to form the basilar artery. The Doppler signal is Note changes to the flow. Instead of slow steady pres-
away from the transducer. sure, a series of short, rapid compressions may be per-
6. The submandibular window is not usually used. By formed on the CCA. This is the oscillation technique.
placing the probe beneath the mandible, the retro- Note any changes to the flow.
mandibular and proximal intracranial ICA may be 8. The Stroke Prevention Trial in Sickle Cell Ane-
visualized. The ICA Doppler signal is away from the mia (STOP) developed a specific protocol for chil-
transducer with this approach. dren with sickle cell anemia. The trial demonstrated
7. Before carotid compression maneuvers are per- that TCD could reliably indicate which children
formed, a duplex scan of the carotid arteries should be with sickle cell anemia were at higher risk for stroke
performed. This portion of the test is contraindicated due to stenosis. The STOP protocol proceeds as fol-
in patients with ICA occlusion, ICA high-grade steno- lows:
sis, and the presence of complicated plaque. While a. Before beginning the examination, the child’s
interrogating an artery with pulsed Doppler, palpate bitemporal diameter (BTD) should be measured
the CCA and apply slow downward pressure. Slowly with calipers to calculate the midline (BTD/2) and
expected depth of intracranial structures. The child
should also be advised to attempt to stay awake dur-
ing the procedure. A false-positive result could
occur due to falsely elevated velocities (as CO2 lev-
els increase if a patient gets sleepy).
b. The patient should be placed in the supine posi-
tion with a rolled towel under his or her neck for
support. Using a 2- to 2.5-MHz transducer, start at
the transtemporal window with the sample volume
depth set at 50 mm. Locate the strongest MCA sig-
nal and record it at a depth of 36 to 38 mm. Flow
direction should be toward the transducer. Label
FIGURE 7.27. Ultrasound view from the transforaminal win- this “M-1.”
dow.
100 The Complete Guide to Vascular Ultrasound

c. Trace the course of the MCA by increasing the
sample volume depth, recording the signal every 2
mm.
d. Trace the MCA to the bifurcation between the
MCA and the ACA. The signal will be bidirec-
tional. Record the optimum signal here.
e. Trace the ACA (flow will be away from the trans-
ducer) 4 mm deeper than the bifurcation. Record
this signal.
f. Decrease the depth of the sample volume back to
the bifurcation level, angle the transducer inferiorly,
and increase the sample volume by 4 mm. Record
the signal here at the distal ICA. The flow is usually
turbulent and harsh, due to the angle of insonation
and flow dynamics.
g. Return to the bifurcation and angle posteri-
orly/inferiorly to locate the PCA. The flow will be
toward the transducer in the PCA1 segment. Trace
the PCA to the midline, where the PCAs originate
from the basilar artery. Record this signal as “TOB”
(top of basilar). The flow will be bidirectional.
h. After repeating the protocol on the other side,
turn the patient on his or her side, chin to chest,
and place the transducer on the base of the skull.
Angle the transducer toward the bridge of the nose,
and set the sample volume at 74 mm. Record the
basilar artery (BA) signal here. The flow should be
toward the transducer. Record a waveform every 2
mm for three to four waveforms.
V. DIAGNOSTIC ANALYSIS
A. Transcranial Doppler Examination
1. Table 7.1 identifies location and characteristics of
intracranial arteries.
2. Collateralization:
a. Antegrade flow in the ipsilateral ACA indicates
crossover collateralization. This occurs due to
flow from the contralateral ACA through the aca.
Increased flow velocities (>150%) in the contralat-
eral ACA are also evident. An additional finding
with crossover collateralization is the decreasing or
obliterating of flow in the ipsilateral MCA when the
contralateral CCA is compressed. A fourth finding
is a positive response to contralateral CCA oscilla-
tion maneuvers.
b. When there is retrograde flow in the ipsilateral
ophthalmic artery, this indicates external-to-inter-
nal collateralization. This is due to flow from the
external carotid branches. With compression of the
ipsilateral ECA branches, ophthalmic artery flow
will decrease, be obliterated, or reverse. The ipsilat-
eral ophthalmic artery will also have decreased pul-
satility and increased velocity.
c. When flow velocities in the ipsilateral PCA
exceed those of the ipsilateral MCA (e.g., >125%),
this indicates posterior-to-anterior collateraliza-
tion. An additional finding is increased flow veloc-
ity in the ipsilateral PCA with ipsilateral compres-
sion of the CCA.
3. Occlusion:
a. The criteria for occlusion are similar to those
used in evaluation of occlusion of other vessels:
absence of the Doppler waveform, a low diastolic
component in the arterial segment just proximal
to the occlusion, and evidence of collateraliza-
tion.
b. This is often difficult to diagnose due to the
technical limitations of the study. Suspected inter-
nal carotid and MCA occlusions are most accurately
diagnosed.
4. Stenosis:
a. The criteria for stenosis are similar to those used
in evaluation of stenosis of other vessels: increased
velocity with spectral broadening at the stenotic
site, decreased diastolic flow proximal to the

TABLE 7.1. TRANSCRANIAL DOPPLER GUIDELINES FOR INTRACRANIAL ARTERIES

Depth Velocity
Vessel Window (mm) (cm/s) Direction of Flow Angle

MCA Transtemporal 30–60 55 ± 12 Toward transducer Anterior and superior

ACA Transtemporal 60–80 50 ± 11 Away from transducer Anterior and superior
PCA (P1) Transtemporal 60–70 39 ± 10 Toward transducer Posterior
PCA (P2) Transtemporal 60–70 39 ± 10 Away from transducer Posterior
Terminal ICA Transtemporal 55–65 55 ± 12 Bidirectional Anterior and superior
ICA Transorbital 60–80 47 ± 14 Parasellar—toward transducer Varies
Supraclinoid—away from transducer
Genu—bidirectional
Ophthalmic artery Transorbital 40–60 21 ± 5 Toward transducer Medial
Vertebral artery Transforaminal 60–90 38 ± 10 Away from transducer Right and left of midline
Basilar artery Transforaminal 80–120 41 ± 10 Away from transducer Midline

ACA, anterior cerebral artery; ICA, internal carotid artery; MCA, middle cerebral artery; PCA, posterior
cerebral artery.

stenotic site, and decreased flow velocity with tur-
bulence distal to the stenotic site. Diagnosis of
stenosis using TCD is mainly based on increased
flow velocities in one vessel compared with the con-
tralateral vessel at the same location.
b. TCD is most accurate in identifying stenosis of
the MCA.
c. As the patient ages, flow velocities decrease. Flow
velocities are increased in anemic patients. These
should be taken into consideration.
5. Sickle cell anemia
a. Since children with sickle cell anemia are often
anemic, their mean flow velocities are normally
higher than in patients with normal hematocrits.
b. The STOP protocol diagnostic analysis refers to
the intracranial ICA and MCA:
Normal: <170 cm/s
Conditional: 170 to 199 cm/s
Abnormal: >200 cm/s (Fig. 7.29)
c. Children with a normal result should have an
annual follow-up. Children with a conditional
result should be reevaluated in 6 months to deter-
mine if there has been any progression. Children
FIGURE 7.29. Color image and Doppler tracing of the middle cerebral artery in a patient with
sickle cell anemia. Notice the abnormally high peak systolic velocity value of 283 cm/s. (Image
courtesy of Philips Medical Systems.)
7/Cerebrovascular System 101
with an abnormal result should be reevaluated
within 2 to 4 weeks to confirm the abnormal find-
ing. Children with two abnormal studies may be
eligible for transfusion therapy, depending on local
policy.
6. Arteriovenous malformation:
a. The arteries supplying the malformation have
increased peak systolic and end-diastolic velocities.
The pulsatility indices are low.
b. Flow in the adjacent arteries usually is reduced.
7. Vasospasm:
a. This diagnosis is most accurate in the MCA.
b. The normal velocity of the MCA is less than 120
cm/s. The normal MCA/ICA ratio (hemispheric
ratio) is less than 3.
c. A series of Doppler waveforms are necessary to
document the increased velocity associated with
vasospasm.
d. A velocity of greater than 200 cm/s usually indi-
cates severe vasospasm.
8. Brain death:
a. The MCA may be used. Initially the diastolic
flow decreases and the pulsatility index increases.
102 The Complete Guide to Vascular Ultrasound
FIGURE 7.30. Normal OPG-Gee tracings. Both sides appear to have the same ocular systolic pres-
sure.
b. The end-diastolic velocity reaches zero, then
reverses.
c. Reverberatory flow appears, followed by a low-
velocity systolic waveform that is spiked.
d. The final stage is absence of flow.
9. Intraoperative monitoring:
a. TCD can be used to monitor the MCA during
many cerebrovascular and cardiovascular surgeries
(such as carotid endarterectomy and cardiopul-
monary bypass.)
b. Abnormalities in the flow may cause changes in
surgical technique. A significant increase in MCA
flow during the cross-clamping portion of carotid
endarterectomy indicates the need for shunting.
The surgical technique may also be altered due to
auditory signals from microemboli. These signals
will be evident as high-amplitude “spikes” on the
waveform.
FIGURE 7.31. Abnormal OPG-Gee tracings. There is a pressure difference of greater than 5 mm
Hg between the right side and the left side.
c. The transtemporal window is not in the sterile
field; therefore, a sterile probe cover is not necessary.
TCD probes are mounted in a headpiece that is
placed on the patient’s head for continuous MCA
monitoring.
B. Oculopneumoplethysmography (OPG-Gee)
1. The ophthalmic systolic pressures should not differ
by 5 mm Hg or more. If the difference is above 5 mm
Hg, then there is likely arterial disease on the side with
the lower pressure (Figs. 7.30 and 7.31).
2. If the ophthalmic systolic pressures are greater
than 140 mm Hg, the amplitude of the first pulse
should be measured. It should be less than or equal
to 2 mm.
3. A normal ratio of ophthalmic systolic pressure
(OSP) to brachial systolic pressure (BSP) should exist:
OSP − 39 ÷ BSP ≥ 0.430

FIGURE 7.32. Ratio scoring grid for OPG-Gee.
This ratio appears as a line on a scoring grid. Values
above the line are normal and values below the line are
abnormal (Fig. 7.32).
C. Periorbital Doppler
1. Flow in the frontal artery should be antegrade,
toward the transducer. If the flow is reversed, then that
signals a hemodynamically significant lesion in the
ipsilateral ICA.
2. If the flow is diminished or reversed during the
compression maneuvers, then the frontal artery is
being supplied by collateral flow from the artery that
is being compressed. This is secondary to a hemody-
namically significant lesion in the ICA.
3. Ipsilateral compression of the CCA should nor-
mally diminish flow in the frontal artery, as it
decreases flow to the brain. Depending on the degree
of collateralization, reversed flow may also be evi-
dent.
FIGURE 7.33. Gray-scale image of the right common carotid artery demonstrating the normal
smooth walls of the intima (arrows).
7/Cerebrovascular System 103
4. This test may be repeated using the supraorbital
artery, located superior to the eye, as well as the frontal
artery.
D. Continuous-Wave Doppler
1. The diagnostic criteria are the same as for duplex
Doppler imaging below.
2. The only difference is that the waveforms for con-
tinuous-wave Doppler have more spectral broadening
than waveforms for pulsed Doppler. This is because
the sample size or depth cannot be regulated with con-
tinuous-wave Doppler; therefore, all the velocities
(even the slower ones from the edges of the vessel) are
included.
E. Duplex Doppler Examination
1. Gray-scale evaluation of the vessels should nor-
mally show smooth vessel walls with two nearly paral-
lel echogenic lines, separated by a thin hypoechoic or
anechoic area. This represents the lumen-intima inter-
face, the media, and the media-adventitia interface.
Together it is called the intima-media complex (or I-
M complex.) This thickness should not exceed 0.8
mm (Fig. 7.33).
2. Areas of turbulence or high-velocity flow show
up as a mosaic-like pattern with swirling colors on
color Doppler imaging. It is important to sample
along this area, looking for the highest peak systolic
velocity.
3. Sonographic characteristics that differentiate the
ICA from the ECA:
a. The ICA is usually larger than the ECA,
although not always.
104 The Complete Guide to Vascular Ultrasound
b. The ICA is usually located lateral and posterior,
while the ECA is usually located anterior and
medial, although not always.
c. The ECA has branches visible, while the ICA
does not.
d. The ICA normally has low-resistance flow with
a wide systolic peak and high diastolic flow.
e. The ECA normally has high-resistance flow with
a sharp increase and decrease of systolic velocities
and a relatively small amount of diastolic flow.
f. The ECA responds to a “temporal artery tap,”
while the ICA does not. To do a temporal artery
tap, just tap the temple of the patient. The Doppler
signal will jump up and down.
4. Occlusion of the ICA is evident when there is an
absence of color and plaque fills the lumen. Often this
finding may be seen with the initial gray-scale image
(Fig. 7.34). If an ICA appears occluded, look carefully
with color or power Doppler for a “string sign.” This
is a narrow string of color through the plaque, show-
ing a very small amount of flow.
5. When the ICA appears occluded, the ipsilateral
CCA may show decreased or absent diastolic flow, and
the ECA may appear “internalized” with higher dias-
tolic flow. When there is an occlusion on one side, the
other side’s velocities increase.
6. Be sure to characterize the type and extent of
plaque formation. Types of plaque are listed above
under “Pathology” (Section II.B.2.).
7. Proximal to a stenosis, a more resistive flow pattern
may be seen with lower diastolic flow. The velocities
are within normal limits.
8. At the stenosis, the peak systolic velocity increases,
the end-diastolic velocity increases, and spectral broad-
FIGURE 7.34. Sagittal gray-scale image of the internal carotid artery. Notice the complete oblit-
eration of the lumen by plaque (arrows). (Image courtesy of Philips Medical Systems.)
ening is present (Fig. 7.35). Spectral broadening is
when the spectral line becomes wider, filling in the nor-
mal black spectral window. This is due to the red blood
cells moving with a wider range of velocities, as their
normal flow pattern is disturbed by the presence of
plaque extending into the lumen of the vessel. “Pseu-
dospectral broadening” can be caused by too high of a
gain setting, as well as vessel wall motion when the
Doppler sample volume is too large or placed too close
to a vessel wall. Spectral broadening may normally be
seen in tortuous vessels, as well as the carotid bulb as it
divides into the ECA and ICA. Spectral broadening
may also be seen for months postendarterectomy, possi-
bly due to changes in wall compliance.
9. Other causes of spectral broadening and increased
velocity include arteriovenous malformations,
aneurysms, arterial wall dissections, and fibromuscular
dysplasia.
10. A “tardus parvus” waveform is usually seen distal
to the site of a stenosis. This is a low-resistance, low-
velocity signal with a slow upstroke to the peak. Distal
to a stenosis, turbulent flow may also be noted.
11. Aliasing is the misrepresentation of the Doppler
signal that occurs because the flow information is
greater than one half of the Nyquist limit (pulse repe-
tition frequency, or PRF). The way to fix this is to
increase the PRF, alter the angle of insonation to
decrease the depth of the vessel, or use a continuous-
wave probe. It appears as though the signal is “wrap-
ping around” and displayed as coming up below the
baseline. On color Doppler it appears as an area of
swirling, mixed colors (Fig. 7.36).
12. Mirror image artifact is a common artifact that
occurs by an overly high gain setting or is produced by
 7/Cerebrovascular System 105

FIGURE 7.35. Color image and Doppler tracing of the internal carotid artery. Notice the elevated
peak systolic velocity of 205 cm/s and the presence of spectral broadening. (Image courtesy of
Philips Medical Systems.)

FIGURE 7.36. Sagittal color image of the internal carotid artery. Notice the mixed colors within the
lumen representing aliasing. (Image courtesy of Philips Medical Systems.)
106 The Complete Guide to Vascular Ultrasound

TABLE 7.2. DOPPLER CRITERIA OF STENOSIS

% Diameter Reduction Doppler Clinically

Normal PSV <1.25 m/s Normal

No spectral broadening
Clear window
1%–15% PSV <1.25 m/s Minimal disease
Minimal spectral broadening
in decreased phase of systole
Clear window at systole
16%–49% PSV <1.25 m/s Moderate disease
Spectral broadening
No window
50%–79% PSV >1.25 m/s Moderately severe (hemodynamically significant)
↑ Diastolic flow seen
Marked spectral broadening
80%–99% PSV >1.25 m/s Severe disease (hemodynamically significant)
EDV >1.40 m/s
Marked spectral broadening

End Diastolic Velocity, (EDV)

strong reflectors. Normal flow can also look this way if
it is traveling in a helical or spiral pattern as opposed
to parallel to the vessel walls. You can try turning
down the gain.
13. Table 7.2 demonstrates Doppler criteria of
stenosis.
14. The velocity measurements may be less reliable
when there are variations in cardiovascular physiology.
Hypertensive patients have higher velocities at the site
of a narrowing than nonhypertensive patients with a
similar narrowing. Both peak systolic and end-dias-
tolic velocities will be diminished in patients with a
reduction in cardiac output. Cardiac arrhythmias,
severe cardiomyopathies, bradycardia, severe or critical
aortic stenosis, an aortic balloon pump, and aortic
valvular lesions may also affect systolic velocities, dias-
tolic velocities, and the shape of the waveform. When
there is an occlusion or critical stenosis on one side,
the velocities may be affected on the contralateral side
(particularly in areas of stenosis). When there is a
proximal CCA or brachiocephalic artery stenosis, this
may reduce flow.

FIGURE 7.37. Spectral Doppler waveform in progressive disease states in the internal carotid
artery. (Reproduced from Odwin CS, Dubinsky T, Fleischer AC. Appleton & Lange’s review for the
ultrasonography examination, 2nd ed. East Norwalk, CT: Appleton & Lange, 1987, with permis-
sion.)

15. The following two trials recently established ther-
apeutic benefit of carotid endarterectomy in asympto-
matic patients with greater than 60% stenosis and in
symptomatic patients with greater than 70% stenosis:
a. The NASCET criteria: A PSV of ICA/PSV of
CCA ratio of greater than or equal to 4.0 is consis-
tent with a greater than or equal to 70% diameter
reduction of the ICA.
b. The ACAS criteria: A PSV of greater than or
equal to 290 cm/s and EDV of greater than or equal
to 80 cm/s are consistent with a greater than or
equal to 60% diameter reduction of the ICA.
16. The vertebral arteries should demonstrate flow
toward the brain. If the flow is reversed, this indicates
subclavian steal syndrome. If the flow is bidirectional,
this indicates a partial steal. This may be changed to a
complete steal by having the patient exercise the arm
of the affected side or by placing a blood pressure cuff
on the arm for a few minutes and then releasing.
17. A summary of spectral Doppler waveforms in pro-
gressive disease states in the ICA is provided in Fig. 7.37.
VI. OTHER DIAGNOSTIC TESTS
A. Magnetic resonance angiography
B. Angiography—this test is considered to be the gold
standard
C. Computed tomographic angiography
7/Cerebrovascular System 107
BIBLIOGRAPHY
Archie JP Jr. A fifteen-year experience with carotid endarterectomy
after a formal operative protocol requiring highly frequent patch
angioplasty. J Vasc Surg 2000;31(4):724–735.
Freed KS, Brown LK, Carroll BA. The extracranial cerebral vessels.
In: Rumack CM, Wilson SR, Charboneau JW, eds. Diagnostic
ultrasound, 2nd ed. St. Louis, MO: Mosby Year-Book, 1998:
885–919.
Jones A. Transcranial Doppler in the evaluation of pediatric patients
with sickle cell anemia: the STOP protocol. In: Vascular ultra-
sound protocol guides—expanding your clinical experience. Bothell,
WA USA: Philips Ultrasound, 2002:22–23.
Katanick S, Hoffman TG. Sonographic and Doppler investigation of
the peripheral veins and arteries and the cerebrovascular system.
Part I. Peripheral veins and arteries. In: Odwin CS, Dubinsky T,
Fleischer AC, eds. Appleton & Lange’s Review for the Ultrasonogra-
phy Examination, 2nd ed. East Norwalk, CT: Appleton & Lange,
1987:463–472.
Katz ML, Comerota AJ. Transcranial Doppler: a review of technique,
interpretation, and clinical applications. Ultrasound Q 1991;
8:241–265.
Rumwell C, McPharlin M. Part II. Cerebrovascular evaluation. In:
Vascular technology—an illustrated review, 2nd ed. Pasadena, CA:
Davies Publishing, 2000:121–168.
Tortora GJ, Anagnostakos NP. The cardiovascular system: vessels and
routes. In: Principles of anatomy and physiology, 6th ed. New York:
Harper & Row, 1990:623–627.
Wheeler JM, Wright I, Pugh N, et al. Is there carotid artery aneurysm
formation following saphenous vein patch endarterectomy? Car-
diovasc Surg 2000;8(1):47–50
 8

TEST VALIDATION AND STATISTICS

I. THE GOLD STANDARD abnormality. It reveals how meaningful a positive result

This is the reference test that is assumed to be “the actually is. It is calculated using the following formula:
truth.” It is important to determine validity of noninva-
True positives/(true positives + false positives)
sive studies by comparing them to the gold standard. By
comparing studies to the gold standard, limitations of D. Negative Predictive Value. This indicates the per-
the test can be identified or a level of confidence in the centage of noninvasive test results that accurately predict
test may be established. Ideally, results will match 100% normality. It reveals how meaningful a negative result
of the time. Realistically, results that match 90% of the actually is. It is calculated using the following formula:
time are considered good.
True negatives/(true negatives + false negatives)
II. FIVE MEASURES BY WHICH COMPARISONS
TO THE GOLD STANDARD ARE EVALUATED E. Accuracy. This is the percentage of correct noninva-
A. Specificity. This is the ability of a test to document a sive test diagnoses. It is calculated by:
normal study when the gold standard also documents a
The total number of correct tests/the total number of all
normal study. It can be calculated using the following
studies
formula:
III. DEFINING RESULTS
True negatives/(true negatives + false positives)
A. True Positive. The vascular laboratory reports that
B. Sensitivity. This is the ability of the test to detect dis- disease is present and the gold standard agrees.
ease, confirmed by an abnormal result with the gold stan- B. True Negative. The vascular laboratory reports that
dard. It can be calculated using the following formula: there is no disease present and the gold standard agrees.
C. False Positive. The vascular laboratory reports that
True positives/(true positives + false negatives)
disease is present and the gold standard disagrees.
C. Positive Predictive Value. This indicates the per- D. False Negative. The vascular laboratory reports that
centage of noninvasive test results that accurately predict there is no disease present and the gold standard dis-
agrees.
IV. USING THE 2 × 2 FACTORIAL TABLE
A well-accepted method of calculation statistics is illus-
trated in Figure 8.1. The five measures by which compar-
isons to the gold standard are calculated are:
A. Specificity = D/(B + D)
B. Sensitivity = A/(A + C)
C. Positive Predictive Value = A/(A + B)
D. Negative Predictive Value = D/(C + D)
E. Accuracy = A + D/A + B + C + D

BIBLIOGRAPHY

Rumwell C, McPharlin M. Part IV. Test validation and statistics. In:

vascular technology—an illustrated review, 2nd ed. Pasadena, CA:
FIGURE 8.1. 2 × 2 factorial table. Davies Publishing, 2000:215–221.
 9
A WORD ABOUT DOPPLER CONTROLS
On every ultrasound machine, there are several controls
that are always the same (although they may not be
arranged in the same way). It is important to understand
these controls in order to optimize your image and to not
create pathology when there is none. Although we will be
focusing on the basic Doppler controls, there are also some
gray-scale controls that are important as well. Please note
that this book does not cover all the controls available on
ultrasound machines and is not intended to cover ultra-
sound physics.
I. BASIC GRAY-SCALE CONTROLS
A. Overall Gain and Time-Gain Compensation
(TGC). These are found on the machine as a round
knob and usually a series of sliding switches, respec-
tively. They control the gray-scale gain, or the strength
of the signal (the TGC controls the gain at different lev-
els of the image). They control the “brightness” of the
image. It is important to maintain the proper gain
throughout the image and to not have it be too bright
in some areas and not in others. When you have an
image that is too bright in the near field and too dark
in the far field, this is the time to use your TGC (Fig.
9.1). Adjust the slides until your image is more homo-
geneous (Fig. 9.2). When the image is too dark or too
light overall, this is the time to use your overall gain
(Figs. 9.3 and 9.4).
B. Depth. This is a switch that sets the depth of the
image. It is important to adjust this according to which
body part you are evaluating. A vein in a leg, for exam-
ple, needs a greater depth than a carotid artery. Adjust
your depth so that you have a clear image in the center
of the screen. When looking at a superficial structure,
decrease the depth to eliminate all of the useless infor-
mation posterior to that structure (Fig. 9.5).
C. Focus. This is an important switch that is often
overlooked. It is important to place the level of the focus
(often displayed as an arrow or a triangle on the right
hand side of the screen) at the level of the structure you
are looking at. This not only optimizes your gray-scale
image by providing a clearer image, but it optimizes your
color image as well (Fig. 9.6).
II. BASIC COLOR CONTROLS
A. Steer. This is a switch that steers the direction of the
color box. It is important to steer the box along the direc-
tion of the vessel to achieve a good Doppler angle. Most
ultrasound machines allow you to steer the box to the
right, to the left, and center or straight down. If the ves-
sel is sloped down to the right side of the screen, then the
box should be angled along with it (Fig. 9.7). If the box
is not properly steered, color will not fill the lumen of the
vessel properly and could be mistaken for occlusion,
plaque, or thrombus by an untrained eye (Fig. 9.8). If the
vessel already dives at a sharp angle, then the center posi-
tion may be used. Another way to adjust this is to “heel-
toe” or rock the transducer to angle the vessel in the
plane that fits the color box. This is important to do
when a vessel is perpendicular to the beam and runs hor-
izontal across the screen. With a 90-degree angle to flow,
there is no frequency shift and therefore there will be lit-
tle or no color in the center of the box. On one side there
might be some degree of shift giving you one color, and
on the other side the same with the opposite color. (On
one side, flow is moving toward the transducer, and on
the other side it is moving away from the transducer.)
B. Size. This adjusts the size of the color box. The
largest box that is appropriate for the area being exam-
ined should be used. The larger the box, the slower the
frame rate, so if the frame rate seems slow, try decreasing
the size of the box to cover just the area being examined.
It is important to cover the whole area that you are eval-
uating (e.g., you don’t want to cut off half of the
pseudoaneurysm that you are trying to evaluate). It is
also important not to use a box that is too big that con-
tains a lot of useless confusing information that could
cause artifact. For example, when evaluating the left por-
tal vein, narrow the box to include only the left portal
vein. Opening the box wide often includes part of the
heart, causing flash artifact. The box will change shape
depending on which transducer you are using (linear- vs.
curved-array).
C. Invert. This is a switch that flips the color on the
color map. The color map is the bar in the upper right
FIGURE 9.1. The image demonstrates that it is too bright in the
near field and too dark in the far field, thus the TGC needs to be
adjusted.

FIGURE 9.4. The overall gain in this image is darker than it

should be.

FIGURE 9.2. The time-gain compensation in the image in Fig.

9.1 has been adjusted, and the image is now more homoge-
neous.

FIGURE 9.5. The depth in this image needs to be decreased,

which will center the object of interest in the middle of the
screen.

FIGURE 9.3. The overall gain in this image is too high (the
image is too bright).

FIGURE 9.6. The focus in this image is set incorrectly. It needs to

be moved up to the level of the object of interest, which is the
carotid artery in this case.
 9/A Word about Doppler Controls 111

FIGURE 9.7. This image demonstrates the proper technique of steering the color box along with
the vessel of interest.

FIGURE 9.8. The color box is not properly steered with the slope of the vessel. This results in sub-
optimal color visualization.
112 The Complete Guide to Vascular Ultrasound
hand corner of the color image that displays red and
blue (in varying shades) one on top of the other.
Whichever color is on top is the color that is displayed
toward the transducer. The color on bottom is away
from the transducer. Often this is red displayed as
towards the transducer, while blue is away from the
transducer. The invert feature allows you to flip the
map so that you may assign specific colors to specific
vessels, such as blue to veins and red to arteries. It is
important to know what the proper flow direction
is and make sure that is the case before you change
it. If you are scanning in a plane where you know that
the portal vein flow should be toward the transducer
and should be red as assigned by the color map and it
is displayed as blue, this indicates that the flow is
reversed (see Fig. 2.16). Remember that flow direction
changes in response to the angle with the beam. If you
rock the transducer to display the popliteal vein angled
down to the right, the flow is toward the transducer
and is displayed as red. If you rock the transducer to
display the popliteal vein angled down to the left, the
flow is away from the transducer and is displayed in
blue.
D. Baseline. On the color map, there is a zero velocity
baseline in the middle between the two colors. Most
machines default to the middle setting, but you may
adjust it. Adjusting the baseline down will widen the
range for red velocities and narrow the range for blue
velocities, for example. This will allow more high red
velocities and may reduce aliasing.
E. Color Gain. This is a round knob that controls the
overall color gain, or the strength of the color signal dis-
played. It is usually located near the overall gray-scale
gain. The gain should be set at the proper level to
FIGURE 9.9. The color gain is set too high in this image.
achieve an optimal image. This is different for different
structures. If the gain is set too high, speckles of color
fill the entire color box and obliterate the image (Fig.
9.9). If the gain is set too low, not enough color fills the
structure and could mimic plaque or thrombus (Fig.
9.10). If the gain is set too low, structures that have
lower flow will not be picked up. A good way to find
the proper gain setting is to turn it high enough so that
the speckled artifact fills the screen, then back it down
until the color just fills the walls of the lumen and the
artifact is gone.
F. Pulse Repetition Frequency (PRF) or Scale. This is
a switch that controls the PRF or the velocity limits.
Higher-velocity flow (such as arterial) needs higher PRF
settings, and lower-velocity flow (such as some venous
flow) needs lower PRF settings. If the PRF is set too
high, color will not fill the vessel lumen and will appear
occluded to the untrained eye (Fig. 9.11). Start with the
settings provided in the settings package, which the ultra-
sound company should have set up for you. (For exam-
ple, use the peripheral venous setting when scanning
veins.) Then adjust your PRF accordingly if needed (Fig.
9.12). When trying to pick up low flow (such as a “string
sign” in an almost occluded carotid artery), decrease the
PRF until you see flow, not artifact. Decreasing it too low
can cause artifact. At our facility, we generally use a PRF
of 500 to 700 Hz when trying to locate extremely low
flow. Remember, not all machines display PRF the same
way.
G. Wall Filter. This is a switch that adjusts the filter
on low-frequency signals. The low-frequency signals are
often “noise” and do not represent blood flow. The wall
filter should be set to low, however, when trying to
locate low-flow structures such as some veins, low-flow
 9/A Word about Doppler Controls 113

FIGURE 9.10. The color gain is set too low, resulting in not enough color filling the vessel. This
could mimic disease.

FIGURE 9.11. The pulse repetition frequency is set too high for this vessel, resulting in a similar
effect as in Fig. 9.10.
114 The Complete Guide to Vascular Ultrasound

FIGURE 9.12. This image demonstrates proper pulse repetition frequency settings for this vessel.

vessels in the abdomen due to disease, flow in the testi-
cles or ovaries, or a string of flow through an almost
occluded artery. The wall filter should be set to medium
or high when evaluating high-flow structures such as
arteries or when evaluating vessels in the abdomen
(where there is a lot of background noise). If the wall
filter is set too high for lower-flow vessels, color will not
fill the vessel lumen and will give the appearance of
plaque, thrombus, or occlusion to the untrained eye
(Fig. 9.13).
H. Priority or Write Priority. This switch is dis-
played in the upper right corner of the color image

FIGURE 9.13. The wall filter is set too high for the flow in this vessel. This results in a similar
effect to Figs. 9.10 and 9.11.
 9/A Word about Doppler Controls 115

FIGURE 9.14. The priority bar (arrow) is set at the darkest range of the gray scale, resulting in
poor color visualization.

FIGURE 9.15. The priority bar (arrow) is set at a lighter range of the gray scale, resulting in more
color filling the vessel. However, one should be careful not to set it too high, which causes color
to “bleed” out of the vessel as an artifact.
116 The Complete Guide to Vascular Ultrasound
next to the color map. It is shown as a small usually
green line present within a bar of varying shades of
gray. Adjusting this switch adjusts the way the color is
displayed against darker or lighter shades of gray. If
the priority is set too much in the darker shades of
gray, then color will be displayed only in areas where
the actual gray-scale shade is the same (Fig. 9.14). If
there is flow present in the areas with the lighter
shades of gray, the color will not be displayed in this
case. This gives too much gray-scale and not enough
color information. A way to fix this is to raise the pri-
ority into the lighter shades (Fig. 9.15) so that color is
displayed in all the gray-scale areas at the level of the
bar and below. Another way to fix this is to lower the
overall gray-scale gain to give the color more priority.
We do not recommend doing this, because lowering
your gray-scale gain unnecessarily reduces the quality
of the gray-scale image. If the priority is set too high,
color will be falsely displayed as “bleeding” out of
everywhere. This gives too much color and not enough
gray-scale information. Usually at our facility we set
the priority bar in the lower upper half of the bar (Fig.
9.12).
III. BASIC DOPPLER CONTROLS
A. Steer. This switch steers not only the color box but
also the Doppler beam line when the Doppler is turned
on. This also must be angled with the vessel. See “Steer”
above (Section II.A.) under “Basic Color Controls.” It is
FIGURE 9.16. The Doppler gain is set too low, making the signal barely visible.
important to be angled with the vessel in order to get an
optimal Doppler spectral waveform.
B. Sample Volume Size. This switch controls the size
of the sample volume, which is usually represented as
two parallel lines on the Doppler beam line. When you
use angle correct, the angle line is shown within the
sample volume. The sample volume represents the area
of flow assessed with the Doppler. Using a smaller sam-
ple volume will sample a narrow portion of the vessel,
versus opening up the sample volume wider to sample
the wider range of velocities throughout the vessel.
Usually it is best to use a sample volume about one
third or less the diameter of the vessel. At times you
have to search for small amounts of flow or patient
motion causes the vessel to move, making it difficult to
keep the sample volume in the vessel. In these cases a
larger sample volume is warranted. When sampling a
normal vessel, it is best to keep the sample volume in
the middle of the vessel. When there is a stenosis pre-
sent, it is best to “walk” the sample volume through the
vessel, to obtain the highest velocity.
C. Angle Correct. This switch controls the angle of the
sample volume. It is important to use angle correct
whenever you are taking a spectral waveform for mea-
surement, specifically. The only time angle correct is not
used is when the vessel is completely parallel with the
beam and the angle is 0 degrees. However, this does not
often occur in vascular scanning. Generally, optimal

angles are between 45 and 60 degrees for vascular scan-
ning. Anything above 60 degrees results in significant
errors in velocity measurements. Many centers feel that it
is important to use 60 degrees exactly, since that is what
studies defining velocity measurement criteria have used.
Make sure that the vessel walls are parallel with the angle
correct line. (You may rock the transducer as needed to
adjust the dive of the vessel.)
D. Invert. This switch inverts the Doppler signal from
above the baseline to below the baseline and vice versa. It
is important to know what the proper flow direction
is and make sure that is the case before you change it.
E. Baseline. This switch controls the level of the base-
line on the spectral Doppler display. If the waveform is
too large for the display and is aliasing, you may lower
the baseline (or raise it if the waveform is displayed below
the baseline) to adjust for this. This allows for a wider
range of velocities to be displayed in that area above the
baseline.
F. Doppler Gain. This is a round knob that usually
resides close to the color gain and overall gray-scale gain
controls. This controls the strength of the Doppler sig-
nal displayed. Different structures require different
amounts of Doppler gain. Usually a high-velocity
superficial vessel such as a carotid needs less Doppler
FIGURE 9.17. The Doppler gain is set too high, creating artifact and noise.
9/A Word about Doppler Controls 117
gain than a calf vein. The Doppler gain may need to be
turned up in the cases of deep vessels or vessels that are
almost occluded. When the gain is set too low, the sig-
nal is barely visible (Fig. 9.16). When the Doppler gain
is set too high, artifact fills the waveform and sur-
rounding area (Fig. 9.17). It is important not to mimic
spectral broadening this way.
G. PRF or Scale. This switch controls the PRF. A ves-
sel that has higher velocity needs a higher PRF, and a ves-
sel that has lower velocity needs a lower PRF. When the
PRF is set too low for a vessel’s velocity, aliasing occurs.
The Doppler waveform signal is displayed as “wrapping
around” the baseline (Fig. 9.18). The PRF must be
increased. If the PRF is set too high for a vessel’s velocity,
the Doppler waveform signal is displayed as a tiny signal
that makes it difficult to assess correctly (especially if you
are trying to evaluate the signal for spectral broadening)
(Fig. 9.19). A proper PRF setting displays the waveform
filling up the spectral display appropriately (Fig. 9.20).
H. Wall Filter. This is a switch that adjusts the filter on
low-frequency signals. The low-frequency signals are
often “noise” and do not represent blood flow. A low wall
filter allows low-frequency signals to be displayed. A high
wall filter removes the most low-frequency information
(Fig. 9.21). This is often used when there is a lot of noise
118 The Complete Guide to Vascular Ultrasound

FIGURE 9.18. The pulse repetition frequency is set too low for this Doppler signal, resulting in
aliasing.

FIGURE 9.19. The pulse repetition frequency is set too high for this Doppler signal. This makes
the signal too small and difficult to assess.
 9/A Word about Doppler Controls 119

FIGURE 9.20. This Doppler spectral waveform has a proper pulse repetition frequency setting.

FIGURE 9.21. This Doppler spectral waveform demonstrates the difference between a low,
medium, and high wall filter setting.
120 The Complete Guide to Vascular Ultrasound

in the background, such as in abdominal aorta scanning.
A low wall filter is used for lower-velocity vessels such as
calf veins.
I. Sweep Speed. This toggle changes the speed of the
Doppler spectral display. Typically it may be changed
from slow to medium to fast. Usually a medium sweep
speed is used. However, in certain cases such as renal
artery stenosis studies, a fast sweep speed might be help-
ful. The waveform appears slightly “stretched” out,
which makes it easier to determine where the first peak
is, so the acceleration time may be measured.
BIBLIOGRAPHY
Ridgeway DP. Color flow scanning. In: Introduction to vascular scan-
ning: a guide for the complete beginner, 2nd ed. Pasadena, CA:
Davies Publishing, 2001:194–200.
 APPENDIX

REVIEW QUESTIONS

1. The name of the outer layer of a blood vessel wall that is
composed of collagenous and elastic fibers is the:
a. Tunica intima.
b. Tunica adventitia.
c. Tunica interna.
d. Tunica media.
2. Which part of the circulatory system has the highest
resistance to blood flow?
a. Venules
b. Capillaries
c. Vasa vasorum
d. Arterioles
3. Which of the following statements is NOT TRUE
about veins?
a. Veins contain valves to prevent the backflow of blood.
b. The tunica intima of veins is thinner than in arteries.
c. The tunica externa of veins is thicker than in arteries.
d. The tunica media of veins is thicker than in arteries.
4. The two primary factors that determine blood flow are:
a. Capillaries and the vasa vasorum.
b. Blood viscosity and blood vessel length.
c. Blood pressure and resistance.
d. Resistance and cardiac output.
5. What is the cardiac output in a normal, resting adult?
a. 5.25 L/min
b. 5.75 L/min
c. 7.85 L/min
d. 7.25 L/min
6. What is the definition of stroke volume?
a. The velocity of blood in the center of the stream
b. The “thickness” of the blood
c. The amount of blood ejected from either ventricle in
one systole
d. The volume of blood in the left ventricle
7. Which of the following does NOT have a directly pro-
portional relationship with blood pressure:
a. Cardiac output
b. Blood vessel radius
c. Blood volume
d. Peripheral resistance
8. Which of the following does NOT cause an increase in
blood viscosity?
a. Dehydration
b. Severe burns
c. Polycythemia
d. Anemia
9. Which of the following increases resistance?
a. An increase in blood vessel radius
b. A decrease in blood viscosity
c. A decrease in blood vessel radius
d. A decrease in blood vessel length
10. What is Poiseuille’s Law?
a. It is a “dimensionless” number that reveals at what
point the flow becomes turbulent.
b. It is an equation that describes the relationship
between resistance, pressure, and volume flow.
c. It is an equation that demonstrates that there is an
inversely proportional relationship between pressure and
velocity.
d. It is an equation that reveals the highest velocity in
the center of the stream.
11. When the Reynolds number exceeds ____, the flow
becomes turbulent.
a. 2,000
b. 3,000
c. 5,000
d. 8,000
12. What does the Bernoulli Equation describe?
a. When velocity increases, so does pressure.
b. When radius increases, pressure decreases.
c. When velocity increases, so does viscosity.
d. When velocity increases, pressure decreases.
13. Low-resistance flow is found in everything below
EXCEPT the:
a. Internal carotid artery.
b. Renal artery.
c. Iliac artery.
d. Hepatic artery.
122 The Complete Guide to Vascular Ultrasound

14. High-resistance flow is found in everything EXCEPT 22. Signs of Budd-Chiari syndrome on ultrasound include
the: all of the following EXCEPT:
a. Aorta. a. Hypertrophy of the caudate lobe.
b. Fasting superior mesenteric artery. b. Loss of visualization of the hepatic veins.
c. External carotid artery. c. Thrombus or tumor within the lumen of a hepatic
d. Vertebral artery. vein.
d. Increased visualization of the hepatic veins.
15. What is atherosclerosis?
a. A bulging in the arterial wall 23. What is cavernomatous transformation of the portal
b. A high flow state due to patient nervousness vein?
c. Thickening, hardening, and deposition of plaque in a. Large collaterals develop in response to chronic portal
the intimal wall of arteries, which can cause stenosis vein thrombosis.
d. Narrowing of the aorta b. The portal vein enlarges with multiple cystic spaces
16. Types of aneurysms include everything EXCEPT: called caverns.
a. Coarctation. c. The portal vein shrinks and disappears in response to
b. Fusiform. chronic portal vein thrombosis.
c. Saccular. d. The umbilical vein becomes patent and takes over the
d. Pseudoaneurysm. portal vein in the case of portal vein thrombosis.

17. An abdominal aortic aneurysm is considered if the 24. Which of the following is TRUE about the superior
diameter is greater than ___ cm. mesenteric artery (SMA)?
a. 5 a. The SMA is located 3 cm distal to the celiac axis.
b. 4 b. The normal preprandial waveform for the SMA is low
c. 3 resistance, and the normal postprandial waveform is high
d. 2 resistance.
c. With mesenteric ischemia, the waveform of the SMA
18. An abdominal aneurysm over ____ cm is considered a will remain high resistance postprandial and the velocity
surgical emergency. will decrease.
a. 2 d. The normal preprandial waveform for the SMA is
b. 6 high resistance, and the normal postprandial waveform is
c. 4 low resistance.
d. 3
25. With renal artery stenosis, all of the following is true
19. On an ultrasound image, the inferior vena cava (IVC) EXCEPT:
is distinguished from the aorta according to everything a. Renal artery stenosis may be caused by arteriosclerosis
below EXCEPT: or fibromuscular hyperplasia.
a. The aorta never touches the liver while the IVC does. b. Peak systolic velocities of greater than 180 cm/s and a
b. The aorta tapers from superior to inferior, the IVC renal-to-aortic ratio of greater than 3.5 indicate a greater
has a “hammock” shape. than 60% diameter reduction according to the Univer-
c. The aorta has thicker walls. sity of Washington criteria.
d. The IVC has more branches visible than the aorta. c. Peak systolic velocities of greater than 150 cm/s and a
20. What is Budd-Chiari syndrome? renal-to-aortic ratio of greater than 2.5 indicate a greater
a. A tumor in the aorta than 60% diameter reduction according to the Univer-
b. Enlargement of the interior vena cava sity of Washington criteria.
c. Thrombus in the hepatic veins preventing blood from d. Absence of the notch (or at just before peak systole)
draining from the liver to the interior vena cava combined with a dampened waveform indicates at least
d. A congenital abnormality in which the hepatic veins 60% stenosis.
drain directly into the right atrium
26. Signs of renal transplant rejection on ultrasound
21. Portal hypertension can be caused by all of the follow- include all of the following EXCEPT:
ing EXCEPT: a. Increased renal transplant size.
a. Thrombus in the aorta. b. Hyperechoic areas in the parenchyma.
b. Portal vein thrombosis. c. Increased cortical echogenicity.
c. Cirrhosis. d. Decreased renal transplant size with chronic rejec-
d. Budd-Chiari syndrome. tion.
 Appendix 123

27. In the case of evaluating a renal transplant, arcuate 34. Claudication in the calves indicates _________ arter-
artery resistive indices from ____ to ____ are normal. ial disease.
a. 0.7 to 0.9 a. Common femoral
b. 0.2 to 0.3 b. Femoropopliteal
c. 0.5 to 0.7 c. Aortoiliac
d. 0.6 to 0.8. d. Plantar

28. The common femoral artery divides into the
_________ and the _________.
a. Internal iliac artery, external iliac artery
b. Superficial femoral artery, profunda artery
c. Superficial femoral artery, popliteal artery
d. Peroneal artery, deep femoral artery
29. What does the term iatrogenic mean?
a. An event caused by surgery and/or procedures involv-
ing puncture into an artery or a vein
b. A small pocket of moving blood connected to an
artery through a small opening
c. A bulge in the arterial wall
d. An abnormally positioned insertion of the muscle
30. A peripheral artery aneurysm usually requires repair if
it is ____ cm or greater.
a. 5
b. 4
c. 3
d. 2
31. A disease that causes inflammation of the arteries (or
veins), preventing blood flow, is called ______. It always
starts in the plantar or palmar vessels and proceeds centrally,
preventing collateralization.
a. Entrapment syndrome
b. Compartment syndrome
c. Thromboangiitis obliterans
d. Raynaud disease
35. The width of the cuff used in the segmental pressure
examination should be _____% greater than the diameter
of the limb, or _______% greater than the circumference of
the limb.
a. 20–25, 40
b. 30–35, 50
c. 10–20, 30
d. 40–45, 40
36. Segmental pressures may be falsely elevated when:
a. The patient is very thin.
b. The patient is lying supine.
c. The cuff width is 20% to 25% greater than the diam-
eter of the limb.
d. The patient’s vessels are calcified.
37. What is transcutaneous oximetry used for?
a. To determine the location of disease in a limb
b. To determine the diameter of the vessel
c. To determine wound healing and amputation level of
a limb
d. To determine how long patients can walk before they
develop claudication
38. All of the following are signs of arterial stenosis
EXCEPT:
a. Spectral broadening.
b. An increase in peak systolic velocity.
c. Monophasic waveform.
d. Clear, crisp spectral window with triphasic waveform.

32. Symptoms commonly associated with chronic lower 39. If the difference between two adjacent segments is
extremity arterial disease include: greater than ____ mm Hg in a lower extremity segmental
a. Claudication, chest pain, and tingling in the scalp. pressure examination, then disease is probably present in
b. Jaundice, rest pain, and thickening of the toenails. the segment with the lower pressure.
c. Swollen, red, hot to the touch leg; ulcers; and dizzi- a. 40
ness. b. 50
d. Claudication, rest pain, and decreased or absent pal- c. 30
pable pulses. d. 20

33. A cause of acute lower extremity arterial disease may 40. Causes of upper extremity occlusive arterial disease
be: include all of the following EXCEPT:
a. Raynaud syndrome. a. Thoracic outlet syndrome.
b. Smoking. b. Deep venous thrombosis.
c. Chemotherapy. c. Subclavian steal syndrome.
d. Buerger disease. d. Thromboangiitis obliterans.
124 The Complete Guide to Vascular Ultrasound

41. An important finding in an upper extremity pulse vol- 49. If the overall graft velocity is less than ___ cm/s, then
ume recording waveform that indicates Raynaud syndrome is: there is a high suspicion for thrombosis.
a. The dicrotic limb is absent. a. 40
b. The waveform is triphasic. b. 50
c. The dicrotic limb is found very close to the peak of c. 60
the waveform. d. 70
d. The dicrotic limb is found far from the peak of the
50. With in situ grafts, the proximal segment has a _____
waveform.
diameter and the distal segment has a ______ diameter.
42. Types of dialysis grafts include all of the following a. Large, large
EXCEPT: b. Larger, smaller
a. Brachiocephalic artery to axillary vein. c. Smaller, larger
b. Brachial artery to antecubital vein. d. Small, small
c. Radial artery to cephalic vein.
51. If a patient has an ankle pressure that is less than ____
d. Brachial artery to axillary vein.
mm Hg, then it is unlikely that a foot ulcer will heal.
43. The most common problem with dialysis grafts is: a. 65
a. The venous anastomosis site becomes stenotic. b. 75
b. The arterial anastomosis site becomes stenotic. c. 80
c. The entire graft thromboses. d. 55
d. The middle of the graft becomes stenotic.
52. A patient with claudication should have an ankle-to-
44. If the arterial inflow is greater than ____ cm/s, then a brachial index in the range of:
dialysis graft most likely has a greater than 75% diameter a. Greater than 0.96.
reduction. b. Less than or equal to 0.20.
a. 200 c. 0.50–0.95.
b. 300 d. 0.21–0.49.
c. 400
53. A patient with claudication should have a mean toe-to-
d. 500
brachial index of:
45. Types of arterial bypass grafts include all of the follow- a. 0.35 ± 0.15.
ing EXCEPT: b. 0.45 ± 0.15.
a. Aorto-bifemoral. c. 0.55 ± 0.15.
b. Femoroperoneal. d. 0.75 ± 0.15.
c. Femoropopliteal.
54. The segmental pressure in the high thigh should be
d. Axillofemoral.
greater than ____ mm Hg than the brachial pressure due to
46. A ________ arterial bypass graft has a corregated, cuff size artifact.
echogenic outline on ultrasound. a. 40
a. Gore-Tex b. 30
b. Reversed vein graft c. 50
c. Dacron d. 60
d. In situ vein graft
55. On color Doppler ultrasound, a cystic mass filled with
47. Acute failure of an arterial bypass graft can be due to all swirling colors with a communicating neck to an artery is
of the following EXCEPT: visualized. This is a:
a. A retained valve. a. Hematoma.
b. A pseudoaneurysm at the anastomosis site. b. Lymph node.
c. Atherosclerotic disease. c. Arteriovenous fistula.
d. Surgical dissection of the intima of the vessel at the d. Pseudoaneurysm.
anastomosis site.
56. Several factors that determine the rate of blood that
48. If the ratio between two velocity measurements is returns to the heart include all of the following
greater than 2, then there is a _____ stenosis. EXCEPT:
a. 75% or greater a. The calf muscle pump.
b. 0% b. Venous valves.
c. 20%–40% c. Claudication.
d. 50%–75% d. Venous pressure.
 Appendix 125

57. In the lower extremity, blood flows from the _____ sys- 65. What is cellulitis?
tem to the _____ system. a. A painful swollen white leg that is due to iliofemoral
a. Deep, superficial thrombosis
b. Superficial, deep b. An infection of the dermal tissues of the limb pre-
c. Deep, gastric senting with red, hot tissues often in the shin and top of
d. Superficial, arterial the foot
c. A congenital defect in which the valve cusps do not
58. What are the perforators?
oppose each other when they are closed
a. Veins that connect the deep and superficial veins
d. A serious case of varicose veins from a prior episode of
b. Veins that are sinuses and act as a reservoir for venous
deep venous thrombosis.
blood
c. Arteries that connect capillaries and arterioles 66. During an impedance plethysmography test the seg-
d. Another name for venous valves mental venous capacitance should be _______ impedance
59. Major risk factors for developing deep venous throm- units or greater.
bosis include all of the following EXCEPT: a. 25
a. Stasis. b. 50
b. Atherosclerosis. c. 60
c. Trauma. d. 75
d. Hypercoagulability. 67. The major difference between the impedance plethys-
60. What is phlegmasia alba dolens? mography (IPG) test and the venous pulse volume record-
a. Congenital absence of the deep veins ing (PVR) test is that:
b. When the left common iliac vein courses posterior to a. The maximum venous outflow is determined from
the right common iliac artery one second of outflow rather than three seconds.
c. A painful, swollen blue leg due to iliofemoral and b. The maximum venous outflow is determined from 3
greater saphenous vein thrombosis seconds of outflow rather than 1 second.
d. A painful, swollen white leg due to iliofemoral throm- c. The IPG test is more rapid.
bosis with increased frequency in the postpartum period d. The segmental venous capacitance is the only value
calculated in the PVR test.
61. The most frequent complications of deep venous
thrombosis include: 68. Deep venous thrombosis may be indicated in all of the
a. Pain in the calves upon walking, dizziness. following EXCEPT:
b. Edema and rest pain. a. Loss of spontaneous flow.
c. Pulmonary emboli and valvular incompetence. b. Lack of augmentation.
d. Pulmonary emboli and swelling. c. Pulsatile venous flow.
d. Continuous venous flow instead of phasic venous flow.
62. The number one way to treat deep venous thrombosis is:
a. Surgery. 69. The basilic vein joins with the:
b. Anticoagulation. a. Cephalic vein.
c. A Greenfield filter. b. Brachial veins.
d. Thrombectomy. c. Internal jugular vein.
d. Subclavian vein.
63. What is venous insufficiency?
a. A condition when the venous valves fail to function 70. All of the following pose an increased risk for deep
properly and blood is allowed to flow in the incorrect venous thrombosis in the upper extremity EXCEPT:
direction a. A peripherally inserted central catheter.
b. A condition when the veins are congenitally absent b. Excessive motion of the upper extremity.
c. A condition when the veins are abnormally small c. A central venous catheter.
d. A condition when the left common iliac vein courses d. Chemotherapy.
posterior to the right common iliac artery
71. If a vein affected with deep venous thrombosis appears
64. Symptoms of venous insufficiency include all of the dilated with hypoechoic thrombus, this is more likely
following EXCEPT: ______ thrombus.
a. Pain. a. Acute
b. Swelling. b. Chronic
c. Thickened toenails. c. Recanalized
d. Varicose veins. d. Dissected
126 The Complete Guide to Vascular Ultrasound

72. The _________ arteries supply the skin of the penis 79. A penile-to-brachial index of 0.85 is measured in a
and the glans. patient during a segmental pressure examination for erectile
a. Cavernosal dysfunction. What does this indicate?
b. Urethral a. This is a normal value.
c. Dorsal b. This indicates arterial insufficiency.
d. Bulbar c. This indicates chronic venous occlusive disease.
d. This indicates vasculogenic impotence.
73. A condition in which a focal “plaque” or scar devel-
ops on the tunica albuginea of the corpora cavernosa is 80. During a segmental pressure examination for erectile
called: dysfunction, a patient’s brachial segmental pressure mea-
a. Diabetes. sured 120 mm Hg and penile segmental pressure measured
b. Priapism. 180 mm Hg. What does this indicate?
c. Arterial insufficiency. a. This is a borderline test result.
d. Peyronie disease. b. This indicates vasculogenic impotence.
c. This indicates that the patient has diabetes.
74. Causes of erectile dysfunction include all of the follow-
d. This is a normal test result.
ing EXCEPT:
a. Arterial occlusive disease. 81. During a duplex Doppler examination for erectile dys-
b. An arteriovenous malformation. function, the velocity of the deep dorsal vein increases to 10
c. The presence of a varicocele. cm/s postinjection. What could this indicate?
d. Insufficient smooth muscle relaxation. a. The possibility of arterial insufficiency
75. A condition in which the veins of the pampiniform b. The possibility of Peyronie disease
plexus or cremasteric plexus become greatly enlarged is c. The possibility of a venous leak
called: d. This is a normal value
a. An arteriovenous malformation.
b. A varicocele. 82. The left common carotid artery originates from the:
c. Peyronie disease. a. Brachiocephalic artery.
d. Priapism. b. Vertebral artery.
c. Subclavian artery.
76. During a Duplex Doppler examination for erectile d. Aortic arch.
dysfunction, _____μg of prostaglandin E1 is usually
used in a patient that is greater than or equal to 50 years 83. The first branch of the internal carotid artery is the:
old. a. Internal maxillary artery.
a. 10 b. Posterior auricular artery.
b. 5 c. Ophthalmic artery.
c. 6 d. Superficial temporal artery.
d. 20
84. The most common variant in a circle of Willis is:
77. While performing a duplex Doppler examination for a. A hypoplastic middle cerebral artery.
erectile dysfunction, the peak systolic velocities of the cav- b. A hypoplastic anterior cerebral artery.
ernosal arteries in your patient are measuring 12 and 15 c. An enlarged basilar artery.
cm/s. What does this indicate? d. An enlarged middle cerebral artery.
a. Nothing is indicated, the test is normal.
b. Chronic venous occlusive disease. 85. Approximately 75% of blood going to the brain is sent
c. Peyronie disease. through the:
d. Arterial insufficiency. a. Internal carotid arteries.
b. External carotid arteries.
78. While performing a duplex Doppler examination for c. Vertebral arteries.
erectile dysfunction, the end-diastolic velocities of the cav- d. Circle of Willis.
ernosal arteries are measuring 10 and 15 cm/s. What does
this indicate? 86. The anterior circulatory system is made up of:
a. Nothing is indicated, the test is normal. a. The vertebrobasilar arteries and their branches.
b. Chronic venous occlusive disease. b. The brachiocephalic arteries and their branches.
c. Peyronie disease. c. The circle of Willis and the vertebral arteries.
d. Arterial insufficiency. d. The carotid arteries and their branches.
 Appendix 127

87. A thin layer of lipid material on the intima of the artery 94. According to the North American Symptomatic
is described as: Carotid Endarterectomy Trial criteria, a ratio between the
a. A fibrous plaque. PSV of the internal carotid artery and the PSV of the com-
b. A fatty streak. mon carotid artery of greater than or equal to ___ is con-
c. An intraplaque hemorrhage. sistent with a ____% diameter reduction.
d. A complicated lesion. a. 8, 60
b. 10, 75
88. The Asymptomatic Carotid Atherosclerosis Study
c. 4, 70
determined the therapeutic benefit of endarterectomy in
d. 5, 80
asymptomatic patients with greater than ___% diameter
reduction of the internal carotid artery. 95. The ability of a test to document a normal study
a. 80 when the gold standard also documents a normal study is
b. 70 called:
c. 50 a. Specificity.
d. 60 b. Sensitivity.
c. Positive predictive value.
89. When significant disease is present in the brachio-
d. Negative predictive value.
cephalic or proximal subclavian arteries, blood must now
course up the contralateral vertebral artery, cross over at the 96. The sensitivity of a test is calculated by:
basilar artery, and course down the vertebral artery of the a. True negatives / (true negatives + false positives).
affected side to the subclavian artery to perfuse the arm. b. True positives / (true positives + false positives).
This is called: c. True negatives / (true negatives + false negatives).
a. Fibromuscular dysplasia. d. True positives / (true positives + false negatives).
b. A carotid body tumor.
97. The total number of correct tests divided by the total
c. Vertebral steal syndrome.
number of all studies is known as:
d. Amaurosis fugax.
a. Accuracy.
90. When using transcranial Doppler, the middle cerebral b. The gold standard.
artery is best located using the ________ window. c. Positive predictive value.
a. Transtemporal d. Sensitivity.
b. Transforamenal
98. The positive predictive value of a test is calculated by:
c. Transorbital
a. True negatives / (true negatives + false positives).
d. Submandibular
b. The total number of correct tests / the total number
91. During a transcranial Doppler study, external-to-inter- of all studies.
nal collateralization is indicated by: c. True positives / (true positives + false positives).
a. Antegrade flow in the ipsilateral medial collateral d. True positives / (true positives + false negatives).
artery.
99. The __________ indicates the percentage of noninva-
b. Retrograde flow in the ipsilateral anterior collateral
sive test results that accurately predict normality.
artery.
a. Positive predictive value
c. Retrograde flow in the ipsilateral ophthalmic artery.
b. Negative predictive value
d. Retrograde flow in the ipsilateral vertebral artery.
c. Specificity
92. The ophthalmic systolic pressures in an oculopneumo- d. Sensitivity
plethysmography-Gee test should not differ by ____ mm
100. One hundred patients [200 internal carotid arteries
Hg or more.
(ICAs)] were examined in a vascular laboratory by carotid
a. 3
duplex ultrasound and cerebral angiography. Out of these
b. 5
patients, 50 ICAs were correctly found to have hemody-
c. 4
namically significant stenoses, 120 ICAs were correctly
d. 2
found to be within normal limits, 23 ICAs were incorrectly
93. During a carotid duplex Doppler examination, a considered to have hemodynamically significant stenoses,
patient’s proximal internal carotid artery measures and 7 ICAs were incorrectly considered to be within normal
1.54/0.89 m/s. What does this indicate? limits. How is the overall accuracy calculated?
a. A diameter reduction of 1%–15%. a. 120/143
b. A diameter reduction of 50%–79%. b. 170/193
c. This is a normal value. c. 120/127
d. A diameter reduction of 16%–49%. d. 170/200
128 The Complete Guide to Vascular Ultrasound
101. You are evaluating the calf veins of a patient and are
not seeing them fill in with color. What do you do?
a. End the study, because the calf veins must have
thrombus in them.
b. Check to make sure that the wall filter is turned to
high.
c. Check to make sure that the color gain is turned down
lower.
d. Check to make sure that the pulse repetition fre-
quency is not set too high.
102. You are evaluating the internal carotid artery of a
patient and the signal is displayed as “wrapping around” the
baseline. What would you do to fix this?
a. Increase the pulse repetition frequency.
b. Decrease the pulse repetition frequency.
c. Change the wall filter to “high.”
d. Increase the Doppler gain.
103. You are evaluating the superficial femoral vein of a
patient with color Doppler. The color Doppler box on the
screen shows one side of the vessel as blue, one side as red,
and the middle of the vessel is absent of color. What can
you do to fix this?
a. Change the wall filter to “low.”
b. Increase the pulse repetition frequency.
c. Steer the box along with the vessel or heel-toe the
transducer to angle the vessel.
d. Increase the color gain.
104. When using Doppler to interrogate a vessel and it is
necessary to use angle correct, an angle of ____ degrees is
usually preferred to obtain accurate velocity measurements.
a. 65
b. 75
c. 30
d. 60
 APPENDIX

ANSWER KEY

1. b 36. d 71. a
2. d 37. c 72. c
3. d 38. d 73. d
4. c 39. d 74. c
5. a 40. b 75. b
6. c 41. c 76. a
7. b 42. a 77. d
8. d 43. a 78. b
9. c 44. c 79. a
10. b 45. b 80. b
11. a 46. c 81. c
12. d 47. c 82. d
13. c 48. d 83. c
14. d 49. a 84. b
15. c 50. b 85. a
16. a 51. d 86. d
17. c 52. c 87. b
18. b 53. a 88. d
19. d 54. b 89. c
20. c 55. d 90. a
21. a 56. c 91. c
22. d 57. b 92. b
23. a 58. a 93. b
24. d 59. b 94. c
25. c 60. d 95. a
26. b 61. c 96. d
27. d 62. b 97. a
28. b 63. a 98. c
29. a 64. c 99. b
30. d 65. b 100. d
31. c 66. d 101. d
32. d 67. a 102. a
33. c 68. c 103. c
34. b 69. b 104. d
35. a 70. b
 SUBJECT INDEX

Page numbers followed by F refer to figures; page numbers followed by t refer to tables

A jugular vein, 69–70 definition, 87

Abdominal aorta lower extremity arteries, 26, 27f See also Atherosclerosis
anatomy, 6, 7f lower extremity veins, 55–56, 59f Arteriovenous malformation
aneurysm, 6–9, 8f ophthalmic artery, 84 cerebrovascular, 101
arteriosclerosis, 6 penile artery, 75 renal artery, 19, 23
atherosclerosis, 6 penis, 75, 76f Arteritis, cerebrovascular, 89
coarctation, 6 peroneal veins, 55–56 Ataxia, 91
diagnostic evaluation, 9–10 popliteal artery, 26 Atherosclerosis
ectasia, 6 popliteal vein, 55 abdominal aorta, 6
grafts, 9, 9f portal veins, 11 carotid artery, 87f, 88f, 89–90
normal flow resistances, 19 pudendal artery, 75 definition, 87
pathology, 6–9 pudendal vein, 75 types of plaques, 87–88
sagittal view, 7f radial vein, 69 Atherosclerosis obliterans, lower extremity, 27
vs. inferior vena cava, 9 renal arteries, 19 Auricular artery, 84
Abdominal vascular anatomy, 7f. See also renal veins, 19 Axillary artery, 39
specific vessel soleal veins, 56 Axillary vein, 69, 74f
Acceleration time, 24 subclavian vein, 69
Adson’s test, 43 tibial artery, 26 B
Aliasing effects, 104 tibial veins, 55 Basilar artery, 84, 99
Allen test, 43 ulnar vein, 69 Basilic vein, 69
Amaurosis fugax, 91 upper extremity arteries, 41, 41f Bernoulli Equation, 3
Anatomy upper extremity veins, 69–70, 69f Blood flow
abdominal aorta, 6 urethral artery, 75 Doppler imaging, 112–114, 117
abdominal vasculature, 7f vertebral artery, 84 hepatic, 11, 13f, 14–16, 14f, 16f
axillary vein, 69 vertebral veins, 70 physiology, 2–5
basilic vein, 69 Anemia, blood viscosity in, 3 reversal, 4
blood vessels, 1 Aneurysm Blood pressure
brachial veins, 69 abdominal aorta, 6–9, 8f bypass graft evaluation, 50, 51, 52–53
brachiocephalic veins, 70 cerebrovascular, 88, 89 definition, 2
bulbar artery, 75 hepatic artery, 12, 17 erectile dysfunction evaluation, 77,
carotid artery, 84 peripheral artery, 26, 34, 42, 44 82–83
cavernosal artery, 75 portal vein, 12 lower extremity examination, 30–32,
cephalic vein, 69 renal artery, 19, 23 37–38
cerebrovascular, 84–87, 85f types of, 6–8, 8f physiology, 2–3
circle of Willis, 84, 85, 85f Angioplasty, carotid artery, 90 upper extremity examination, 42, 43–44
circumflex veins, 75 Angle correct, 116–117 Blood vessel anatomy, 1, 2f
crural veins, 75 Anticoagulant therapy, deep venous Blood vessel types, 1
dorsal arteries, 75 thrombosis, 56–57 Brachial artery, 39
dorsal vein, 75 Aphasia, 91 Brachial veins, 69
emissary veins, 75 Arteries Brachiocephalic artery, 39
femoral arteries, 26 anatomy, 1 Brachiocephalic veins, 70
femoral vein, 55 definition and function, 1 Brain death, 101–102
gastrocnemial veins, 56 See also specific artery Brain ischemia, 89
hepatic arteries, 11 Arterioles Bruit, 91
hepatic veins, 11 anatomy, 1 Budd-Chiari syndrome, 10, 11, 14
iliac arteries, 26, 75 definition and function, 1 Buerger disease, 43
iliac vein, 6, 55 Arteriosclerosis Bulbar artery, 75
inferior vena cava, 10 abdominal aorta, 6 Burns, blood viscosity response, 3
132 Subject Index

C D anatomy, 55
Capillaries Dacron graft, 48, 49f, 51f Fibromuscular dysplasia, cerebrovascular,
anatomy, 1 Deep venous thrombosis 88
definition and function, 1 lower extremity, 56–57, 64–68 Fibromuscular hyperplasia, renal artery
Cardiac output, 2 upper extremity, 70 stenosis in, 19
Carotid arteries, 84, 86f, 87f Dehydration, blood viscosity in, 3 Fistula
anatomy, 84 Depth of image, 109, 110f bypass graft complication, 54
diagnostic evaluation, 91–92 Diabetes, graft complications in, 49 lower extremity arteriovenous, 26, 30, 34,
dissection, 88f Dialysis graft, 45, 45f, 46f, 47f 35f
duplex Doppler examination, 93, 94f, Diaphragmatic arteries, 6 renal artery, 19, 23
95f, 96, 103–107, 103f, 104f, 105f, Diastolic flow reversal, 4 Flow separations, 3
106f Digital arteries, 39 Focus controls, 109, 110f
endarterectomy, 89–90, 107 Diplopia, 91 Frontal artery, 84
intima imaging, 103f Doppler controls
stroke, 91 angle correct, 116–117 G
transcranial Doppler imaging, 97, 98, 99 baseline, 112, 117 Gain
tumors, 88, 89f color, 109–116 color, 112, 112f, 113f
Catheterization gain, 109, 110f, 112, 112f, 113f, 117, Doppler, 117, 117f
deep venous thrombosis related to, 70, 117f gray-scale, 109, 110f
73f gray-scale, 109, 110f, 114–116, 115f Gastric artery, 6
Cavernomatous transformation of portal invert, 109–112, 117 Gastric vein, 11
vein, 16–17, 17f pulse repetition frequency, 112, 113f, Gastrocnemial veins, 56
Cavernosal arteries, 75, 78–82ff 114f, 117, 118f, 119f Gastroduodenal artery, 11
Celiac artery, 6 sample volume size, 116 Gold standard, 108
Doppler tracing, 18f steer, 109, 116 Gonadal arteries, 6
normal flow resistance, 19 sweep speed, 120 Gore-tex graft, 48, 48f
Celiac axis compression syndrome, 19 wall filter, 112–113, 114f, 117–120, 119f Graft
Cellulitis, 58 Dorsal arteries, 75 abdominal aorta aneurysm repair, 9, 9f
Cephalic vein, 69, 73f Dorsal vein, 75 assessment, 49–54, 53t
Cerebral arteries, 84 Dorsalis pedis artery, 26 composition, 48
color imaging, 97f, 98f, 101f Duplex Doppler examination Dacron, 48, 49f, 51f
Doppler tracing, 97f, 98f, 101f cerebrovascular system, 93–96, 94f, dialysis, 45, 45f, 46f, 47f
in patient with sickle cell anemia, 101f 103–107 Gore-tex, 48, 48f
stroke, 91 lower extremity arteries, 30, 34–37, 37f, pathologies of, 45, 48–49
transcranial Doppler imaging, 96–102 37t in situ vein, 48, 49f, 51
Cerebrovascular system lower extremity veins, 58, 62–65, 68 types, 45, 48
anatomy and function, 84–87, 85f Dysarthria, 91 Gray-scale controls, 109, 110f, 114–116,
pathology, 87–90 Dysphagia, 91 115f
patient evaluation, 90–107 Dysphasia, 91
Circle of Willis, 84, 85, 85f, 86f Dysphonia, 91 H
Circulatory system anatomy, 1, 2f Hemianopsia, 91
Circumflex veins, 75 E Hemiparesis, 91
Coarctation, abdominal aorta, 6 Ectasia, abdominal aorta, 6 Hemiplegia, 91
Cognitive deficits, 91 Embolism Hepatic artery
Collagen vascular disease, 42 cerebrovascular, 88 anatomy, 6, 11
cerebrovascular, 89 pulmonary, 56, 70 aneurysm, 12, 17
Collateralization, intracranial, 100 renal artery, 19 diagnostic evaluation, 12–14, 17
Color controls Emissary veins, 75 Hepatic veins
baseline, 112 Endarterectomy, 89–90, 96 anatomy, 10, 11
gain, 112, 112f, 113f indications, 107 blood flow, 13f
invert, 109–112 Erectile dysfunction, 75, 76–82 diagnostic evaluation, 12–16
priority settings, 114–116 Doppler tracing, 15f
pulse repetition frequency, 112, 113f, F pathology, 11–12
114f Facial artery, 84 Homans sign, 56, 58
size, 109 Factorial table, 108 Horner syndrome, 91
steer, 109, 111f False negative, 108 Hyperabduction maneuver, 43
wall filter, 112–113, 114f False positive, 108 Hyperemia testing
Communicating arteries, 84 Femoral arteries lower extremity arteries, 33–34
Compartment syndrome, lower extremity anatomy, 26 Hypertension
arteries, 27 aneurysm, 26 graft complications, 49
Continuous-wave Doppler imaging, 93, 103 Doppler tracing, 31f, 32f portal vein, 11–12, 16
Contrast venography, 69 fistula, 35f renal artery, 19, 20
Controls, Doppler. See Doppler controls occlusive disease, 29, 36f
Corpus spongiosum, 75 pseudoaneurysm, 35f I
Costoclavicular maneuver, 43 sagittal color flow, 27f, 28f Iliac arteries
Crural veins, 75 Femoral vein, 60f, 61f, 65f, 66f, 67f, 68f anatomy, 6, 26, 75
 Subject Index 133

occlusive disease, 29 Lymphedema Popliteal artery

Iliac veins, 10, 55 lower extremity, 57–58 anatomy, 26
Infarction, renal artery, 19, 23 upper extremity, 70 aneurysm, 26
Inferior vena cava entrapment by gastrocnemius muscle, 26,
anatomy, 10 M 34
diagnostic evaluation, 10–11 Marfan syndrome, 8 Popliteal vein, 62f
Doppler tracing, 10, 11f Maxillary artery, 84 anatomy, 55
pathology, 10 Maximum venous outflow, 59, 62 Portal veins
sagittal view, 10f May-Thurner syndrome, 57 anatomy, 11
vs. abdominal aorta, 9 Mesenteric artery, inferior, 6 blood flow, 13f, 14f, 16f
Isotope venography, 69 Mesenteric artery, superior cavernomatous transformation, 16–17,
anatomy, 6, 17 17f
J diagnostic evaluation, 19 diagnostic evaluation, 12–14, 16–17
Jugular vein, 69–70, 71f normal flow resistance, 19 Doppler tracing, 15f
pathology, 19 pathology, 11–12
K Mesenteric vein, 11 with transjugular intrahepatic
Kidney transplants, 20, 23, 24f, 25 Metatarsal arteries, 26 portosystemic shunt, 18f
Klippel-Trenaunay-Weber syndrome, 57 Mirror image artifact, 104–106 Positive predictive value, 108
Predictive value of tests, 108
L N Prostaglandin E, 76–77
Laminar flow pattern, 2, 3f Nasal artery, 84 Pseudoaneurysm
Length of blood vessels, 3 Negative predictive value, 108 abdominal aorta, 7–8
Lingual artery, 84 Nystagmus, 91 bypass graft complication, 48, 54
Liver transplants, 12 cerebrovascular, 88–89, 90
Lower extremity arteries O graft complication, 45, 47f
acute occlusive disease, 28–29 Obese patient evaluation, 91 peripheral artery, 26, 30, 34, 35f
anatomy, 26, 27f Occipital artery, 84 upper extremity arteries, 42, 44
aneurysm, 34 Oculopneumoplethysmography, 91–92, Pudendal artery, 75
arteriovenous malformation, 26 102–103, 102f Pudendal vein, 75
chronic occlusive disease, 27–28, 29 Ophthalmic artery, 84 Pulmonary circulation, 1
compartment syndrome, 27 Oxygenation of blood, 1 Pulsatility index, 23
diagnostic history taking, 29 Pulse repetition frequency, 112, 113f, 114f,
diagnostic objectives, 29 P 117, 118f, 119f
duplex Doppler examination, 30, 34–37, Papaverine, 76–77 Pulse volume recording
37f, 37t Penile artery, 75 bypass graft evaluation, 50, 53–54
physical examination, 29–30 Penis lower extremity arteries, 32–33, 38–41,
plethysmography–pulse volume anatomy, 75, 76f 38f, 39f, 40f
recording, 32–33, 38–41, 38f, 39f, Doppler examination, 76–82 lower extremity veins, 62, 66–68
40f erectile dysfunction, 75, 76–82 upper extremity arteries, 42, 43–44
pseudoaneurysm, 26, 34, 35f segmental pressure examination, 82–83
pulse volume recording/segmental varicocele, 75–76, 77, 82f, 83 R
pressure examination, 33 vascular anatomy, 75 Radial artery, 39
segmental pressure examination, 30–32, Percutaneous intravenous central Radial vein, 69
37–38 catheterization, 70, 73f Radius of blood vessels, 3
transcutaneous oximetry, 34 Perforating veins, 56 Raynaud syndrome, 42, 43, 44
treadmill/reactive hyperemia testing, Periorbital Doppler imaging, 92, 92f, 103 Renal arteries, 6
33–34 Peripheral resistance, 2 anatomy, 19
See also specific artery Peroneal artery, 26 aneurysm, 19, 23
Lower extremity veins Peroneal veins, 55–56, 63f arteriovenous malformation, 19, 23
anatomy and function, 55–56, 56f, 59f Peyronie disease, 75 diagnostic evaluation, 20–24
continuous-wave Doppler, 58 Pharyngeal artery, 84 Doppler tracing, 21f, 22f, 23f
contrast venography, 69 Phleborheography, lower extremity, 58 fistula, 19, 23
duplex Doppler examination, 58, 62–65, Phlegmasia alba dolens, 57 normal flow resistance, 19
68 Phlegmasia cerulea dolens, 57 occlusion, 19, 23
isotope venography, 69 Photoplethysmography, lower extremity, 64, stenosis, 19–20, 23–24
lung perfusion scan evaluation, 69 68–69 thrombosis, 19, 20
pathologies, 56–58 Phrenic arteries, 6 transverse view, 7f
patient history taking in evaluation of, 58 Plantar arteries, 26 Renal-to-aortic ratio, 23
phleborheography, 58 Plethysmography Renal veins, 10
photoplethysmography, 64, 68–69 bypass graft, 53–54 anatomy, 19
physical examination, 58 lower extremity arteries, 32–33, 38–41, diagnostic evaluation, 20, 24–25
plethysmography, 59–62, 66, 68f 38f, 39f, 40f enlarged, 20
pulse volume recording, 62, 66–68 lower extremity veins, 59–62, 66, 68f thrombosis, 20, 24–25
See also specific vein See also Photoplethysmography Resistance to blood flow, 2–3
Lumbar arteries, 6 Poiseuille’s Law, 3 high-resistance, 4, 4f
Lung perfusion scan, 69 Polycythemia, blood viscosity in, 3 low-resistance, 4
134 Subject Index

Resistive index, 23 Temporal artery, 84 anatomy, 41, 41f

Retinal artery, 84 Test validation, 108 diagnostic evaluation, 42–44
Reversible ischemic neurologic deficit, 90 Thoracic outlet syndrome, 43 pathologies, 41–42
Reynold’s Number, 3 Thromboangiitis obliterans, lower extremity, Upper extremity veins
27–28 anatomy and function, 69–70, 69f
S Thrombus/thrombosis deep venous thrombosis, 70
Sacral artery, 6 bypass graft complication, 51, 53f Doppler examination, 70–71, 74
Sample volume size, 116 cerebrovascular, 88 lymphedema, 70
Saphenous vein, 64, 67f deep venous, 56–57, 64–69, 70 patient history taking in evaluation of, 70
anatomy, 55 dialysis graft complication, 45, 47f thrombus evaluation, 71–74
Segmental venous capacitance, 59–62 inferior vena cava, 10 Urethral artery, 75
Sensitivity, test, 108 portal vein, 12, 16–17
Sickle cell anemia, 99–100, 101, 101f renal artery, 19, 20 V
Soleal veins, 56 renal veins, 20, 24–25 Varicocele, penile, 75–76, 77, 82f, 83
Specificity, test, 108 upper extremity, 71–74 Varicose veins, 57
Spectral broadening, 104, 105f Thyroidal artery, 84 Vas vasorum, 1
Splenic artery, 6 Tibial artery, 26 Vasoconstriction, 1
normal flow resistance, 19 Tibial veins, 63f, 64f pulsatile flow effects of, 4
Splenic varices, 16, 16f anatomy, 55 Vasodilation, 1
Splenic vein, 11 Time-gain compensation, 109, 110f pulsatile flow effects of, 5
Steer controls, 109, 111f, 116 Tobacco use, 50, 75 Vasospasm, 96, 101
Stenosis Transcranial Doppler imaging, 96–102, 96f, Vein mapping, 64
blood flow patterns, 3, 4f 100t Vein patch, carotid artery, 90f
bypass graft, 50, 52f Transcutaneous oximetry, lower extremity, Veins
cerebrovascular, 88, 100–101, 106–107, 34 anatomy, 1
106t Transforaminal window, 99, 99f definition and function, 1
dialysis graft, 45, 46f Transient ischemic attack, 90 See also specific vessel
diastolic flow reversal related to, 4 Transjugular intrahepatic portosystemic Velocity, blood flow, 2, 3
renal artery, 19–20, 23–24 shunt (TIPS), 12, 18f bypass graft evaluation, 50–51
Stent evaluation, 14, 17, 18f Doppler imaging, 112
carotid artery, 90, 90f Transorbital window, 98–99, 98f Venous insufficiency, 57–58, 62–64,
renal artery, 19–20 Transtemporal window, 97, 97f 68–69
Stroke, cerebrovascular, 90, 91 Treadmill testing, 33–34 Ventilation quotient, 69
risk in child with sickle cell anemia, True negative, 108 Venules
99–100 True positive, 108 anatomy, 1
Stroke volume, 2 Tumors definition and function, 1
Subclavian artery, 41 carotid body, 88, 89f Vertebral artery, 84, 86f
Subclavian steal syndrome, 43, 44, 90, 107 inferior vena cava, 10 duplex Doppler examination, 93, 95f
Subclavian vein, 69, 72f, 73f portal vein, 16–17, 17f subclavian steal syndrome, 90, 107
Supraduodenal artery, 11 Tunica externa (adventitia), 1 Vertebral veins, 70
Supraorbital artery, 84 Tunica interna (intima), 1 Vertebrobasilar artery, 91, 99f
Suprarenal arteries, 6 Tunica media, 1 Vertigo, 91
Sweep speed, 120 Virchow triad, 56
Syncope, 91 U Viscosity of blood, 3
Systemic circulation, 1 Ulcers, arterial/venous, 57t Volume of blood, 2
Ulnar artery, 39
T Ulnar vein, 69 W
Takayasu arteritis, 42, 43 Upper extremity arteries Wall filter, 112–113, 114f, 117–120, 119f