DOPPLER USG

Renal Arteries
Normal, unobstructed renal arteries, the resistance index (Pourcelot index) is roughly the same
on both sides on condition that there is no unilateral damage of the kidney parenchyma, which
would lead to more pulsatile flow and thus affect the Pourcelot index as well. Distal to a high-
grade stenosis, flow is characterized by a delayed systolic increase and lower peak systolic
velocity while diastolic flow is increased, resulting in a lower Pourcelot index. A Pourcelot
index < 0.5 determined in the distal renal artery at the hilum suggests postocclusive
changes due to an upstream flow obstacle. Unilateral reduction of the Pourcelot index by
over 0.05 (or over 10%) compared to the contralateral side as a criterion for 70% renal
artery stenosis has a sensitivity of 82%and a specificity of 92%compared to angiography
(Schwerk et al. 1994).

Different sonographic criteria used for diagnosing renal artery stenosis

Vmax >140 cm/s (Schäberle 1988; duplex scanning) sensitivity 86%, specificity 83%
Vmax >180 cm/s (Karasch1993; color duplex scanning) sensitivity 92%, specificity 90%
Renal-aortic ratio (RAR) >3.5 (Taylor 1988) sensitivity 84%, specificity 97%
Unilateral decrease in RI (Pourcelot) >5–10% (Bönhof 1990; Schwerk 1994)

The resulting renal-aortic ratio (RAR) is normally <3.5, with a ratio >3.5 indicating a
hemodynamically significant renal artery stenosis (60–99%).The RARhas beenfound to have a
surprisingly high sensitivity of 83–100% and a specificity of 73–97% (Frauchinger et al. 1995;
Taylor et al. 1988)

The acceleration time calculated from the poststenotic (damped) waveform at the renal
hilum was proposed as another indirect criterion of stenosis. Using a value of less than 0.07 s as
a criterion yielded sensitivities of 78 to 89%and specificities of 92 to 98% (Martin et al. 1991,
Stavros et al. 1994, Nazzal et al. 1997). The indirect criteria are useful only for stenoses of 70 to
80%and above because lower-grade stenoses do not affect the poststenotic waveform.

Studies investigating the sensitivity and specificity of (color) duplex ultrasound in

identifying hemodynamically significant renal artery stenoses in comparison with
angiography
Duplex scanning Criteria Vmax(cm/sec)
Avasthi 1984 100
Kohler 1986 RAR 3.5
Ferretti 1988 100.
Taylor 1988 RAR 3.5
Strandness 1990 RAR 3.5
Hoffmann 1991 180
Schäberle 1988 140
Color duplex scanning
Breitenseher 1992 120
Karasch 1993 180
Abdominal aorta
Starts at the level of the T12 vertebra and descends in front of or slightly to the left of the
vertebral column. The diameter of the aorta decreases on its downward course from 25 to 20
mm. A diameter of up to 30 mm as a result of age-related dilatation is considered normal.
An abrupt increase in diameter to more than 1.5 times that of the normal proximal segment is
regarded as evidence of an aneurysm. The abdominal aorta divides into the two common iliac
arteries at the level of the L4/5 vertebrae.

Normal parameters of visceral Arteries

Vmax(cm/s) Vdiastole Vmean RI Diameter(mm)

Celiac trunk 100–237 23–58 45–55 0.66–0.82 6–10

Splenic artery 70–110 15–40 4–8

Hepatic artery 70–120 20–40 4–10

Superior m artery* 124–218 5–30 15–35 0.75–0.9 5–8

Carotid bifurcation
is usually situated at the level of the 4th to 5th cervical vertebra, i.e. at about the level of the
thyroid cartilage, but there is wide variation in its location. Typically, the larger internal carotid
artery arises from the posterolateral aspect The external carotid artery arises from the
anteromedial aspect of the internal carotid; in about 10% of cases its site of origin is lateral or
posterolateral. The two vertebral arteries originate from the ipsilateral subclavian arteries at the
level of the 6th cervical vertebra and pass through the transverse foramina of the corresponding
vertebrae, thus taking a partly intraosseous course on their way to the skull base
The vertebral artery is divided into 4 segments:
the V1 segment, which extends from the origin to the site of entry into the transverse foramen of
the 6th cervical vertebra;
the V2 segment, which is the part coursing through the cervical vertebral foramina;
the V3 segment, which takes an arched course around the atlas and is therefore also referred to as
the atlas loop;
the V4 segment, which is the intracranial part of the vertebral artery.

Three standardized approaches for longitudinal imaging are distinguished:

positioning of the transducer between the larynx and sternocleidomastoid muscle for .....sagittal
anteroposterior sections .
…..lateral approach through the sternocleidomastoid muscle;
….posterolateral approach with the transducer behind the sternocleidomastoid muscle.

Criteria for differentiating the internal and external carotid arteries…

Internal carotid artery lies posterolateral to external carotid.
Medial course of the internal carotid.
Less pulsatile flow (large diastolic flow component) in internal carotid compared to external
carotid.
Larger lumen of internal carotid artery, especially of bulb
Doppler waveform of external carotid artery shows pulsation transmitted upon intermittent
tapping of temporal artery
External carotid gives off arterial branches (1st branch: superior thyroid artery) and internal
carotid does not.

Carotid Arteries
The common carotid artery has a constant luminal diameter of about 7mm to the level of the
bulb. Flow is pulsatile with a large diastolic component. Peak systolic flow velocity ranges
from 60 to 100 cm/s.
The normal thickness of the intima-media complex measured in the B-mode (from the lumen-
intima interface, the first hyperechoic line, to the media-adventitia interface, the second
hyperechoic line) is 0.5–0.6 mm and increases somewhat with age.

Vertebral Arteries
The flow velocity in the vertebral artery reported in different studies varies widely from 19 to 98
cm/s in systole and from 6 to 30 cm/s at end-diastole. The resistance index ranges from 0.62
to 0.75.
The normal diameter of the vertebral artery is 3 to 5 mm but there may be asymmetry with
hypoplasia on one side and compensatory hyperplasia of the contralateral artery, resulting in
right-left diameter differences of over 2 mm.

Plaque Evaluation and Morphology

Plaques and stenoses mainly affect the bifurcation and the first 2 cm of the internal and external
carotid arteries.
The morphologic description of a plaque comprises the following features:
Localization:
– anterior/posterior wall,
– proximal/distal;
Extension:
– circular/semicircular,
– plaque diameter;
Plaque surface:
– clearly delineated/moderately delineated/not delineated,
– smooth/irregular (0.4–2.0 mm deep craters)/ulcer
( 2.0 mm deep);
Internal structure:
– homogeneous/inhomogeneous;
Echogenicity:
– hyperechoic (with or without acoustic shadowing)/
hypoechoic/not visualized.
The thickness of the intima-media complex is measured at the site of maximum thickening in
the wall away from the transducer. Thickening above 1 mm is considered abnormal and
thickening above 2 mm is assumed to indicate a plaque. Plaques
mainly occur in the carotid bifurcation and along the first 2–3 cm of the internal carotid artery.
Progressive lumininal narrowing due to plaque thickening leads to higher flow velocities in the
stenotic area ( >350 cm/s), which is associated with an increased risk of
ulceration.

Based on these criteria and the descriptions of plaques classified as follows:

Type I: hyperechoic and homogeneous plaque with a clearly delineated surface;
Type II: plaque of mixed echogenicity with a predominance of hyperechoic portions and with a
moderately delineated surface;
Type III: very hypoechoic or markedly heterogeneous plaque with a poorly delineated surface;
Type IV: plaque not visualized or suggested only by isolated echogenic spots in an otherwise
anechoic lumen. Plaque extent visualized only in the color flow mode (flow in patent residual
lumen).
Duplex ultrasound criteria for classifying internal carotid artery stenoses.
Local d redn% CSA redn % Distal d redn % PSFV cm/s PDFVcm/s ICA/CCA vel ratio waveform, duplex
llo
0–49 0–74 0–15 <110 <40 <1 Normal
to disturbed flow
50–59 75–82 16–32 110–139 40–50 1.0–1.8 Spectral broadening,
increasing fill-in of spectral window
60–69 83–90 33–49 140–199 >50 1.8–2.5 Turbulence,
poststenotic flow separation,
70–79 91–95 50–65 200–250 >70 2.5–3.8 and flow
jet……….do……
80–95 96–99 66–99 >250 > 100 >3.8 Pronounced turbulence,
reduced Postste
Subtotalocclusion 250–500 variable notic flow velocity, and eddy
currents…do..

Peak systolic flow velocity: The highest flow velocity derived from the angle-corrected Doppler
tracing obtained by continuous scanning of the stenotic area. A hemodynamically significant
stenosis ( >50%stenosis) is assumed at peak systolic flow velocities >120 cm/s and intermediate-
to high-grade stenosis ( >70–80% stenosis) at 180– 240 cm/s. Recent studies of color duplex
ultrasound demonstrated sensitivities of 90–96% and specificities of 86–93% (Faught et al. 1994;
Grant et al. 2000; Neale et al.
1994; Moneta et al. 1993; Polak et al. 1992).
Minimum end-diastolic flow velocity: This parameter likewise increases with the stenosis grade
for stenoses with a diameter reduction of at least 50%. In stenoses greater than 50%, end-
diastolic flow velocity is increased to >40 cm/s. Velocities of over 80–100 cm/s suggest a
highgrade stenosis. This parameter is especially useful for
quantifying subtotal occlusion, in which peak systolic velocity is more difficult to determine.
Internal carotid artery to common carotid artery velocity ratio: Absolute flow velocities are
influenced by physiologic and abnormal systemic factors (hypertension, aortic valve stenosis,
medial sclerosis, contralateral occlusion). The effect of these factors can be reduced by
calculating the ratio of peak systolic velocity in front of and within the stenosis (Moneta et al.
1993; Ranke et al. 1999). However, as the external carotid artery also arises from the common
carotid, the ratio is altered if the external carotid is stenosed or acts as a collateral in the presence
of an internal carotid artery stenosis.

Cutoff for discriminating between low-grade and hemodynamically significant ( 50%) stenoses
must be increased to a peak systolic velocity of 140 –150 cm/s (modified according to
AbuRahma et al.

D stenosis PX stenosis occln flap aneurysm

PERIPHERAL ARTERIES
Normal diameters (D) and peak systolic velocities (Vmax and standard deviation) of the pelvic
and leg arteries determined in 30 healthy subjects
Diameter(cm) PSV(Vmax)cm/s
External iliac artery 0.85+/- 0.11 116+/- 29.7
Common femoral artery 0.81+/- 0.17 112.2+/- 22.7
Prox sup femoral artery 0.65+/- 0.14 93.95+/- 15.9
Profunda femoris artery 0.55+/- 0.14 95.1+/- 21.5
Popliteal artery 0.58+/- 0.12 71.6+/- 12.4

Duplex ultrasound of peripheral arteries – stenosis criteria

Direct stenosis criteria
Turbulent flow
Flow acceleration
Vmax180 cm/s
Abrupt doubling of Vmax
Perivascular vibration
Indirect stenosis criteria
Flow profile: Damping (triphasic/monophasic)
Delayed systolic rise

Stenotic grade duplex duplex just waveF far distal WaveFprox intra/pre
intrastenotic distal PSV ratio
No stenosis Triphasic Clear spectral Unchanged Unchanged <1.5
waveform window
Markedly pulsatile
(Vmax <150 flow
cm/s) Steep systolic
upslope
20–50% Increase in Vmax Only mild Same as prestenotic Normal 1.5–2
Low-grade (150–200 cm/s) turbulence
stenosis Moderate spectral
broadening
may occur

51–75% Further increase in Eddy currents Slightly reduced Normal 2–4

Intermediategrade Vmax (200–380 Possibly slight pulsatility
stenosis cm/s) turbulence
Slight reduction in Partial filling-in of
pulsatility systolic
window
76–95% Very pronounced Considerable Lengthened systolic Amplitude normal or slightly >4
High-grade increased in Vmax turbulence acceleration time reduced (compared to other
stenosis ( >380 cm/s) Complete filling-in Reduced pulsatility side)
Reduction in of systolic Pulsatility may be reduced
pulsatility window before sites of origins of
collaterals

95% Nearly complete Pronounced Flattened systolic Reduced amplitude >4

Subtotal loss turbulence peak Increased pulsatility immediately
occlusion of pulsatility Completely filled-in Considerably before stenosis
Marked increase in systolic reduced pulsatility Normal prestenotic pulsatility
peak systolic and window but reduced before sites of
end-diastolic flow origins of collaterals
velocity

Occlusion No flow signal Very reduced flow Very flat systolic Low amplitude
detectable in distal peak Blunt waveform immediately
segment before occlusion: increased
Marked damping of pulsatility, small complex with
waveform large negative component
Decreased pulsatility before
sites of origins of collaterals