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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5760_Библиотеки_им_академика_М_И_Перельмана.pdf
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Chapter 3 · Extremity Veins
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. Fig. 3.60a–e (Atlas) Asymptomatic venous thrombosis developing in valve pockets.
a Ultrasound has much lower sensitivity in asymptomatic thrombosis than in symptomatic thrombosis. This is due to the fact that thrombus
surrounded by owing blood may be overlooked in calf vein segments notoriously dicult to scan, especially if there is only little dilatation and
partial compressibility, or if clot is conned to valve pockets. The transverse (left) and longitudinal views (right) depict the distal popliteal vein
with a patent lumen (red, ow toward transducer) but with absent color coding at the valve. Color duplex scanning facilitates the identication of
such subtle abnormalities in problematic areas. However, to rule out ow phenomena as a possible cause of the lling defect, the thrombus must
be conrmed by compression ultrasound of this vein segment.
b Duplex scanning performed in a clinically asymptomatic patient prior to stripping of varicose veins demonstrates thrombophlebitis of the
great saphenous vein (V.S.M) with thrombus (TH) protruding into the common femoral vein (V.F). The gray-scale image (left) shows a hyperechoic
structure in a valve (VK) somewhat distal to the saphenofemoral junction. In the color ow image (right), absence of color coding indicates the
thrombus (TH) including its valvular component, which prevents proper opening of the valve (despite ow augmentation by manual thigh compression). Red color in the valve area indicates eddy ow (. Fig.3.12a), particularly in the pocket of the valve (VK) depicted closer to the transducer. To rule out a ow-related cause of this subtle change in the color coding, the thrombus must be conrmed by compression ultrasound.
c The images obtained with compression (transverse view on the left and longitudinal view on the right) show incompressibility of the great
saphenous vein (V.S.M) and incomplete compression of the femoral vein at the level of the thrombotic valve (residual incompressible diameter
of 2mm, see markings). The example illustrates two major sources of thrombosis of the principal deep veins: thrombus development in a valve
pocket (for its pathogenesis see . Fig.3.12a) and extension of thrombi from supercial or muscle veins.
d Thrombus in a venous valve pocket (illustrated for the great saphenous vein in the thigh) can lead to stasis of blood ow and thus become a
nidus for venous thrombosis or thrombophlebitis. Absence of ow signals due to stasis can be dierentiated from true thrombus using compression ultrasound or using color duplex imaging with a very low PRF (aliasing in the vein in left section) during Valsalva’s maneuver or distal compression. In case of thrombosis, the valve leaets (VK) will not move and Valsalva’s maneuver will not elicit ow between the venous wall and the
leaet of the incompetent valve (right section).
e Adequate valve closure. The example shows an incompetent saphenofemoral junction with an incompetent arch vein, while the great saphenous vein valves above the knee are competent. The proximal valves are incompetent, and the image depicts the rst competent valve, indicated
by adequate closure with Valsalva’s maneuver. Retrograde ow causes ow signals extending into the valve pockets during closure (distal point
of insuciency). There is no ow distally, except for a minimal, thin stream coded in red and indicating minimal leakage of the valve; this is no
evidence of relevant valve incompetence (VK=valve leaet)
3.3 · Atlas: Ex tremity Veins
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3
. Fig. 3.61a–d (Atlas) Pelvic vein thrombosis secondary to ascending deep femoral vein thrombosis.
a Compression ultrasound (transverse image on the right) reveals compressibility of the supercial femoral vein (V.F.S), while the deep femoral
vein is not compressible (TH in V.P.F).
b Color ow images (transverse section on the left and longitudinal section on the right) show ow in the supercial femoral vein (red) and no
thrombosis; the deep femoral vein (V.P.F) joins the supercial vein posteriorly. Also depicted are the supercial femoral artery (A.F.S) anterior to
the vein and the profunda femoris artery posteriorly.
c The thrombus (T) extends into the external iliac vein (V.I.E) and is surrounded by owing blood.
d The time-motion display documents oating of a long thrombus tail (T) in the external iliac vein (. Fig.3.13)
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. Fig. 3.62a, b (Atlas) Calf muscle vein thrombosis with thrombus extension into popliteal vein.
a The two longitudinal views (leftmost and left center) and the transverse view (right center) show a gap (TH) in the color-coded ow in the popliteal
vein (V.POP). An ascending thrombus (TH) protrudes into the popliteal vein from a thrombosed gastrocnemius vein (V.GC). More cranially, the small
saphenous vein (V.S.P) is depicted with blood ow in blue. The mural thrombosis ascending from the gastrocnemius vein into the popliteal vein ends
at the saphenofemoral junction (leftmost and left center). The gastrocnemius vein thrombosis cannot be traced further distally (rightmost section).
b Muscle vein thrombosis below the knee is suggested by the depiction in the soleus or gastrocnemius muscle of hypoechoic tubular structures
that cannot be compressed. The veins are markedly dilated, making them more conspicuous than normal muscle veins. The distinction between
muscle vein thrombosis and thrombosis of a major calf vein is made sonoanatomically. The major veins run parallel to the lower leg arteries of the
same name. The transverse image (middle section) depicts a hypoechoic structure in the soleus muscle. Noncompressibility of the vein conrms
muscle vein thrombosis (right section). The oblique color duplex image on the left depicts the thrombosed soleus vein (MV, labeled as D2) on its
course from the mid-calf to the knee, where it enters (labeled as D1) the posterior tibial vein. There is appositional thrombus growth into the posterior tibial vein, which is thrombosed up to the tibiobular junction, while it is compressible somewhat distal to the entry site of the muscle vein.
The image on the left was obtained during compression and depicts the hypoechoic, noncompressible posterior tibial veins (labeled as D3 and
D4) to the left and right of the posterior tibial artery (red)
3.3 · Atlas: Ex tremity Veins
237
3
. Fig. 3.63a–c (Atlas) Thrombophlebitis of great saphenous vein with thrombus extension into femoral vein (natural history).
a The proximal extent of thrombophlebitis may be greater than suggested by the clinical ndings. The patient shown presented with reddening
along the course of the great saphenous vein up to the mid-thigh, while color duplex imaging (transverse view on the left and longitudinal view
on the right) demonstrates gaps in the color coding extending up to 1.5cm below the saphenofemoral junction. The longitudinal view depicts
ow in blue along the thrombus. Ultrasound also demonstrates thrombophlebitic involvement of the clinically normal anterior tributary vein (BV).
In this situation, surgical ligation is indicated to prevent further thrombus growth into deep veins.
b Ascending thrombophlebitis can extend into a deep vein in the form of a cone-shaped thrombus. The gray-scale image (left section) already
depicts a slightly more hyperechoic thrombus (TH) protruding into the anechoic lumen of the common femoral vein (V.F.C) from the great saphenous vein (V.S.M). In the color ow image (right), the thrombus (TH) protruding into the common femoral vein is identied by the absence of color
in the blue-coded lumen.
c Based on the duplex ndings, high ligation of the great saphenous vein was indicated but was refused by the patient. In this case, the course of
endogenous thrombolysis under heparin therapy can thus be followed. After 3 weeks, the thrombus in the great saphenous vein has receded to
1cm below the junction. The image on the left demonstrates the thrombus (TH) in the lumen of the great saphenous vein (V.S.M). The color ow
image on the right depicts ow in the great saphenous vein in blue (away from transducer, toward center) and a branch of the deep femoral vein
(V.P.F) coming from posteriorly with ow toward the transducer coded in red
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. Fig. 3.64 (Atlas) Thrombophlebitis of small saphenous vein.
Patients with thrombophlebitis of the small saphenous vein often present with unspecic clinical symptoms that may mimic deep vein thrombosis (DVT). For this reason, diagnostic evaluation of patients for exclusion of DVT must also include the small saphenous vein. The transverse view
on the left depicts the small saphenous vein (V.S.P) as a nonperfused hypoechoic tubular structure posterior to the popliteal vein (V.POP). The
image obtained with compression (middle section) shows incompressibility of the vein. The longitudinal image (right section) depicts the small
saphenous vein (V.S.P) without ow to the level of the saphenopopliteal junction. There is no thrombus extension into the popliteal vein (V.POP),
seen as complete blue color lling of the popliteal vein
. Fig. 3.65 (Atlas) Femoropopliteal vein.
The femoropopliteal vein (V.FP) passes posteriorly from the small
saphenous vein (V.S.P, dilated by fresh thrombus) just below the
saphenopopliteal junction. Despite thrombophlebitis of the small
saphenous vein distal to the site of entry of the femoropopliteal
vein, proximal compression and release elicits reux at the saphenopopliteal junction due to femoropopliteal valve incompetence
(orthograde venous drainage through the femoropopliteal vein)
3.3 · Atlas: Ex tremity Veins
. Fig. 3.66 (Atlas) Thrombosis arising from thrombophlebitis
extending through perforator.
Extension of thrombophlebitis into the deep venous system can also
occur through a perforating vein. In the case presented, extensive
thrombophlebitis of the great saphenous vein (V.S.M) gives rise to a
thrombus extending through a perforating vein (PV) into the posterior
tibial vein (V.TIB.P), where it causes a circumscribed thrombosis 3cm in
length. Next to the vein, the artery is depicted with ow in red. The great
saphenous, perforating, and posterior tibial veins are markedly dilated
by the thrombus and not compressible (right image). The hyperechoic
reection indicates the site at which the vein pierces the fascia (F)
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3
. Fig. 3.67a–e (Atlas) Monitoring of thrombolytic therapy.
a Marked dilatation of the supercial femoral vein (compared with the accompanying artery) and the hypoechoic, homogeneous thrombus with a
just barely visible hypoechoic halo suggest acute thrombosis. The transverse view depicts a collateral (KOL) with ow in red anterior to the supercial femoral artery (A). The longitudinal view on the left shows a more proximal segment of the supercial femoral vein (V). Proximal to the site of
entry of a collateral vein, the thrombus in the supercial femoral vein is surrounded by residual ow near the walls (blue).
b After three cycles of thrombolytic therapy with streptokinase, there is ow in the center and periphery of the lumen of the supercial femoral
vein (V), indicating beginning recanalization. The image was obtained in the same plane as the transverse image in (a) but with the transducer
angled superiorly. The image on the right shows that ow signals disappear from the collateral vein and the partially recanalized femoral vein
upon compression. The patent lumen collapses and only the thrombosed portion is still visible.
c Complete recanalization of the vein after another three cycles of thrombolytic therapy. The transverse view (left) and the longitudinal view
(right) depict only some residual mural thrombus of low echogenicity around the patent lumen. The collateral (KOL, blue) anterior to the supercial femoral vein (V, blue) is also still present.
d After another cycle of thrombolysis, the residual mural thrombi have almost completely dissolved. Upon compression (right section) of the vein
(V), only a thin, hypoechoic band is depicted posterior to the artery, indicating reactive inammatory wall thickening and intimal edema.
e Despite complete recanalization following streptokinase therapy, Valsalva’s maneuver elicits persistent reux. Valve damage in this patient is due
to the delay of more than 10days between the onset of thrombosis and complete recanalization. The image on the left demonstrates blood ow
in the same direction (coded red) in the vein (V) and the corresponding artery (A). The image on the right shows ow toward the heart (blue) in
the competent collateral vein (KOL) during Valsalva’s maneuver. This forward ow in the competent collateral is induced by the calf muscle pump
because some patients inadvertently also contract their muscles during Valsalva’s maneuver
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. Fig. 3.68a, b (Atlas) Postthrombotic syndrome– valve function.
a The severity of insucient venous drainage depends on the degree of recanalization and the development of postthrombotic valve incompetence of major veins. If there is complete recanalization, the veins may appear perfectly normal on B-mode ultrasound with valve dysfunction
being the only postthrombotic sequela.
b Conversely, there may be normal function of individual venous segments, which will prevent reux, even if B-mode images show vascular wall
changes (sclerosis, thickening). In the example, Valsalva’s maneuver elicits only a short reux before valve closure (Doppler waveform) although
B-mode imaging demonstrates postthrombotic wall thickening
. Fig. 3.69a–e (Atlas) Postthrombotic syndrome– recanalized lumen.
a In about 10% of cases, thrombosis leads to permanent damage of the vein (see . Fig.3.51 (Atlas)), depicted sonographically as a hypoechoic, tubular
strand with a thin caliber adjacent to the artery. In most cases, however, there is postthrombotic recanalization but often with a smaller lumen. In the
example shown, the supercial femoral vein is patent 4months after thrombosis, but only trickling ow is present. Hypoechoic thrombotic wall deposits and sclerotic wall lesions persist. Aliasing in the supercial femoral artery closer to the transducer conrms the PRF to be adequate for the detection
of slow venous ow. There is continuous venous ow due to loss of respiratory phasicity, indicating persistent ow obstruction in the recanalized vein.
b Flow in the supercial femoral vein (V.F.S) during Valsalva’s maneuver is coded in blue (away from transducer), and the Doppler waveform shows
reversed ow.
c–e Postthrombotic syndrome– paradoxical ow during Valsalva’s maneuver.
c When Valsalva’ maneuver elicits increased ow rather than ow reversal in a recanalized vein (here the supercial femoral vein), this indicates
ow through dilated collaterals. In the example, Valsalva’s maneuver induces blood ow from the incompetent great saphenous vein into the femoral vein via incompetent perforating veins. The resulting ow increase in the supercial femoral vein (Doppler waveform) indicates poor recanalization of the femoral vein and above all of the popliteal vein (see d) and persistent severe obstruction of peripheral venous drainage. While the
paradoxical ow pattern indicates pathology in the case presented here, the examiner must be aware that such a pattern may also occur because
some patients inadvertently also contract their leg and in particular their calf muscles when performing Valsalva’s maneuver.
d In more distal, partially recanalized vein segments such as the popliteal vein (distal to the Dodd perforators, through which the blood enters the deep
system), Valsalva’s maneuver induces typical to-and-fro ow with ow reversal (spontaneous ow in the left image, augmented ow in the right image).
e Valsalva’s maneuver reveals severe terminal valve incompetence of the great saphenous vein (reux in the Doppler waveform)
3.3 · Atlas: Ex tremity Veins
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. Fig. 3.70a–e (Atlas) Postthrombotic recanalization with arteriovenous stula.
a Patient with venous thrombosis of the thigh showing the typical signs of early recanalization (color duplex) after 4months: meandering ow
and ow signals mostly conned to the center of the vein. The Doppler waveform obtained from the partially recanalized vein shows retrograde
pulsatile ow. A possible cause is an arteriovenous (AV) stula; in this patient, retrograde ow is due to occlusive thrombosis proximally.
b In the distal femoral vein, color duplex ultrasound also shows signs of recanalization with residual mural thrombus, with the Doppler waveform
demonstrating high-frequency ow toward the periphery.
c To search for the AV stula, the length of the femoral artery is scanned from proximal to distal with continuous Doppler recording. A sudden
change to more pulsatile ow indicates the site where to look for the AV stula. The Doppler waveform on the left was obtained in the femoral
artery, upstream of the AV stula, and the one on the right downstream of the stula.
d Transverse image of the AV stula between the supercial femoral artery (A) and the femoral vein (V). The sample volume is placed in the stula,
and the Doppler waveform shows the typical pulsatile ow pattern of a stula; however, the frequency is lower than expected. The femoral vein is
still largely thrombosed, but some ow is present, suggesting recanalization (next to the “V”). The communication between the AV stula and the
recanalized venous lumen is not visualized because it does not lie in the scan plane.
e Angiogram simultaneously depicts the artery and a thin stream in the vein with ow directed toward the periphery. The preceding color duplex
examination provides the explanation for this phenomenon
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. Fig. 3.71a, b (Atlas) Chronic venous insuciency.
a Primary chronic venous insuciency of the deep leg veins diers from the postthrombotic syndrome in that valve failure is due to venous dilatation. The delicate venous walls are free of deposits and therefore easy to compress. In the example shown, valve incompetence of the proximal
posterior tibial vein is associated with persistent reux during Valsalva’s maneuver, indicated by the color change from red to blue. In patients with
severe dysfunction of all venous valves proximal to the transducer, even deep abdominal inspiration can induce reversed ow, and normal rhythmical inspiration and expiration may induce to-and-fro ow.
Valve incompetence of calf veins.
b Determination of the duration of reux from the Doppler waveform enables dierentiation of short physiologic reux prior to valve closure from
persistent reux due to incompetent valves. Blue indicates reux in the posterior tibial vein away from the transducer. Repeated and somewhat
longer manual compression and release of the distal calf lead to alternating ow toward the transducer during compression (KOMP) and away
during release (DEKOMP)
. Fig. 3.72 (Atlas) Dilated muscle veins.
Patient with crural ulcer but without signs of insuciency of the great
saphenous vein in the thigh. There is valve incompetence of the supercial femoral vein and the proximal popliteal vein with good valve
closure in the major veins distally. Valsalva’s maneuver reveals valve
incompetence with persistent reux (Doppler waveform) in a dilated
gastrocnemius vein (V.GC). The color duplex image (left) shows no
ow in the popliteal vein (V.POP) with Valsalva’s maneuver, indicating
competent valves. The crural ulcer in this patient was caused by incompetent indirect perforating veins (not shown) and healed after elimination of the incompetent perforators identied by ultrasound (several
weeks of prior compression therapy had no eect). Such dilated gastrocnemius and soleus veins can cause stasis of blood ow, giving rise
to calf thrombosis with extension into the popliteal vein
3.3 · Atlas: Ex tremity Veins
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3
. Fig. 3.73a–g (Atlas) Postthrombotic syndrome– residual lesions/synechia.
a Patient with severe postthrombotic syndrome. Incomplete compressibility (right image) of postthrombotic veins may be due to residual thrombus or synechia. The image obtained without compression (left) depicts hyperechoic thread-like structures in the partially recanalized (more
hypoechoic) lumen. These structures, which may occasionally have a honeycomb appearance, are sclerotic strands persisting after thrombosis.
The image on the right shows these structures in longitudinal orientation.
b The transverse and longitudinal gray-scale images (left) show the recanalized popliteal vein (V.POP) with postthrombotic wall sclerosis and
synechia (S). The longitudinal color ow images (right) reveal postthrombotic reux in the recanalized popliteal vein (V.POP). The rst color ow
image (without Valsalva’s maneuver) shows the blood in the popliteal vein (blue) draining between the strands (S). They appear as membraneous
structures within the lumen and are identied by the absence of color-coded ow. During Valsalva’s maneuver (second color ow image), the ow
direction in the vein is the same as in the adjacent popliteal artery (from the center toward the periphery, displayed in red).
c Recanalized postthrombotic vein with severe wall sclerosis and postthrombotic strands.
d Intraluminal synechia (S) extend to the proximal supercial femoral vein (V.FS). The left color ow image shows the recanalized supercial femo-
ral vein with blood ow toward the heart (red). The right color ow image shows reversed ow (blue) along the strands (S) toward the periphery
with Valsalva’s maneuver. There is normal valve closure in the deep femoral veins (V.PF) without reux (A.FS=supercial femoral artery). The grayscale image depicts synechia in the recanalized lumen, and the Doppler waveform shows slow ow due to obstruction by the strands and marked
reux elicited by Valsalva’s maneuver (ow away from transducer, toward the periphery).
e–g Postthrombotic residues– wall sclerosis.
e The popliteal vein is completely patent, but there is postthrombotic wall sclerosis depicted as hyperechoic thickening of the wall (SKL, longitu-
dinal view on the right). The transverse image on the left also depicts more hypoechoic areas in the lumen, corresponding to residual thrombotic
deposits on the wall or wall thickening. These abnormalities appear to the left of the recanalized patent lumen (with owing blood displayed in
red) and farther away from the transducer. The more supercial small saphenous vein appears normal shortly before it joins the popliteal vein.
f Postthrombotic wall lesions can lead to wall sclerosis and calcications with acoustic shadowing on ultrasound. The Doppler waveform shows
reux due to incompetent valves.
g Vasosclerotic changes with wall thickening and calcication may also occur after thrombophlebitis. In the example, the longitudinal view on the
right shows the hyperechoic sclerotic wall lesions with intraluminal deposits in the small saphenous vein. There is posterior acoustic shadowing
(SS) due to partial calcication. The longitudinal image in the middle and the transverse image on the left depict ow (blue) in the thin recanalized lumen of the postthrombophlebitic small saphenous vein