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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5760_Библиотеки_им_академика_М_И_Перельмана.pdf
254
ab
Chapter 3 · Extremity Veins
3
d
c
e
. Fig. 3.94a–f (Atlas) Edema of various etiologies, lymphoma, lymphedema, lipedema.
a Apart from thrombosis, leg swelling can be caused by cardiac, inammatory, or lymphogenic edema with epifascial uid collections in fatty
or connective tissue clefts. Edema causes scattering and thus impairs evaluation of deeper subfascial areas and detection of venous thrombosis
below the knee. In the case shown, there is edematous subcutaneous thickening (indicated by calipers, 12mm). The small saphenous vein (V.S.P)
and a gastrocnemius vein (MV) are seen in transverse orientation. Inammatory edema is associated with reactively enlarged lymph nodes in the
groin. They are depicted as hypoechoic, inhomogeneous structures that can be dierentiated from thrombophlebitis by gray-scale ultrasound
in two planes (round shape). Color duplex imaging with a low PRF depicts the supply and perfusion of the lymph node. Atherosclerosis with wall
irregularities and calcied plaque (P) with acoustic shadowing (SS) is seen as an accessory nding.
b Patient presenting with swelling of the calf and thigh as in 4-level thrombosis. Color duplex imaging demonstrates patent deep leg veins. The
images show the patent femoral vein with red-coded ow (V). In this patient, leg swelling was due to obstructed lymphatic drainage caused by
lymph node metastases from prostate cancer in the true pelvis and groin. Seen here are metastatic lymph nodes (L) in the groin, which are characterized by loss of internal structure, an irregular contour, and low echogenicity.
Calf swelling caused by edema.
c Channel-like structures in the subcutaneous fatty connective tissue (which tend to be near fasciae) on gray-scale images are pathognomonic of
lymphedema. For reliable dierentiation from edema due to other causes, the dilated lymphatics must be visualized as tubular structures on longitudinal (left) and transverse scans (right). A thin, wall-like structure is occasionally identied by its higher echogenicity between the lumen and
connective tissue (left image, adjacent to calipers). Diameter of 2–3mm.
d Transverse and longitudinal images of lymphedema with markedly dilated lymphatic vessels.
e Edema due to other causes (cardiac, secondary to chronic venous incompetence) has a honeycomb-like appearance on both longitudinal and
transverse images, indicating uid collections in connective tissue clefts of the subcutaneous fatty tissue (F=fascia, underlying muscle tissue
without uid collection).
f Transverse image (left) and longitudinal image (right) showing lipedema (echogenic) in a patient with phlebitis of the small saphenous vein. Like
the great saphenous vein, the small saphenous vein courses in a fascial compartment (Cleopatra’s eye)
f
3.3 · Atlas: Ex tremity Veins
255
. Fig. 3.95 (Atlas) Vein compression by Baker’s cyst.
a Patient with calf swelling caused by a large Baker’s cyst compressing the vein. The lumen of the vein is still patent but reduced. Pressure applied
with the transducer causes complete collapse of the vein as seen on the transverse image (right).
b A month later, the cyst (Z) has increased in size, now compressing the vein and displacing the artery. The Doppler waveform shows no spontaneous ow and only moderate augmented ow upon strong compression of the calf muscles. The sample volume is placed in the vein (longitudinal image)
3
. Fig. 3.96 (Atlas) Adventitial cystic disease of the popliteal vein.
A cyst (Z) in the wall of the popliteal (V) narrows the lumen distally.
Variable lling of the cyst causes intermittent calf swelling with symptom-free intervals. Adventitial cystic disease of the popliteal vein was
conrmed intraoperatively
256
Chapter 3 · Extremity Veins
3
. Fig. 3.97a, b (Atlas) Venous wall tumor.
The contrast medium lling defect in the venogram (a) is caused by a tumorous lesion of the venous wall depicted by ultrasound (b). Ultrasound
in longitudinal orientation shows that the wall is not disrupted. Scanning from an anteromedial approach depicts the artery near the transducer
and adjacent to the vein, which is compressible (KOMP, right section in b). Histologic workup of the surgical specimen yielded the diagnosis of a
venous wall broma
. Fig. 3.98a–c (Atlas) Entrapment syndrome.
a An entrapment syndrome of the popliteal artery very rarely involves the popliteal vein as well (see 7 Sect. 2.1.6.4.2). In the 45-year-old patient
presented here, malformation of the medial head of the gastrocnemius with a lateral extension (XX) to the lateral condyle of the femur (Insua type
II) causes stenosis of the popliteal artery with poststenotic, thrombotic dilatation (A.POP AN). The atypical lateral gastrocnemius extension in this
case also impairs blood ow in the popliteal vein (V.POP), which is compressed between the dilated artery and the lateral muscle extension (XX).
b In another case– a 35-year-old athletic patient with well-developed calf muscles presenting with calf swelling and exercise-induced pain–
ultrasound demonstrates compression of the popliteal vein by a hypertrophied gastrocnemius muscle with two strong heads but normal courses
in the popliteal fossa. The Doppler waveform obtained from the compressed popliteal vein with the patient lying in a relaxed position shows a
stenosis signal interrupted by arterial pulsation. The vein has a lumen of 2mm. The angle-corrected ow velocity is over 100cm/s and respiratory
phasicity is lost (same patient as in . Fig. 2.95 (Atlas)). In this patient with the rare combination of arterial and venous compression, calf swelling
was caused by compression of the popliteal vein at rest and exercise- induced pain by compression of the artery during plantar exion.
c Venogram: The vein appears compressed. A large popliteal artery aneurysm or a large Baker’s cyst may have a similar venographic appearance
3.3 · Atlas: Ex tremity Veins
257
3
. Fig. 3.99 (Atlas) Axillary vein– normal ndings.
Junction of axillary and subclavian veins with respiratory phasicity and
typical cardiac pulsatility of blood ow. The B-mode image on the left
depicts a venous valve
. Fig. 3.101a, b (Atlas) Jugular vein aneurysm.
Jugular vein aneurysm (V.J.) measuring 27mm in size. Aneurysms of the jugular vein can become quite large but thrombosis is very rare, and
specic treatment is rarely necessary
. Fig. 3.100 (Atlas) Thoracic outlet obstruction.
Obstruction of venous inow in the thoracic outlet by a mediastinal
tumor is indicated by dilatation of the veins in the B-mode (shown
here for the jugular vein). Blood ow is slower and cardiac pulsatility is
eliminated
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Chapter 3 · Extremity Veins
3
. Fig. 3.102a–e (Atlas) Jugular vein thrombosis– central venous catheter.
a Foreign bodies in a vein (pacemaker, central venous catheter) have thrombogenic eects. In the example, the double contour indicates the central venous catheter (KAT) in the thrombosed jugular vein (arrowheads) with residual ow near the wall depicted in blue in transverse orientation
(left). The common carotid artery is seen medial to the thrombosed jugular vein (transverse view on the left, longitudinal view on the right). Flow
in the artery is in the opposite direction. The color change from red, to black, to blue in the artery is due to a change in ow direction relative to
the ultrasound beam.
b Beginning recanalization of the jugular vein (V.J) along its course lateral to the carotid arteries (ICA and CCA) (left image) and proximally, at the
site of its junction with the subclavian vein (V.S; right image).
c In older jugular vein thrombosis, there may be partial recanalization or persistent obstruction with depiction of the vein as a connective tissue
strand with a rather thin lumen adjacent to the carotid artery. Patients in whom such a condition is identied by ultrasound before implantation
of a central venous catheter can be spared an unnecessary puncture.
d In this patient with Hodgkin lymphoma, the mesh-like pattern is a stent placed to maintain patency of the jugular vein obstructed by lymphoma
in the thoracic outlet.
e After stenting of the compressed jugular vein (left image), the patient developed thrombosis of the subclavian (V.SUBCL) and axillary veins
(V.AX, right image)
3.3 · Atlas: Ex tremity Veins
259
3
. Fig. 3.103a–c (Atlas) Axillary vein thrombosis– thrombolytic therapy.
a Hypoechoic and homogeneous thrombi in the axillary and subclavian veins with clear demarcation from the wall indicate acute thrombosis. The
vein is markedly dilated compared to the artery posterior to it. Collateral veins are depicted anteriorly.
b Following two cycles of thrombolytic therapy with ultrahigh-dose streptokinase administration, color duplex imaging demonstrates beginning
recanalization. There is complete recanalization of the distal axillary vein (ow depicted in red, toward transducer). In the proximal axillary vein
(left section), there is ow along one side of the thrombus (blue, due to change in ow direction relative to transducer). A chest wall collateral is
seen anteriorly. The transverse view (middle section) depicts a larger hypoechoic mural thrombus in an otherwise patent axillary vein with ow
in blue. The compression test conrms a thrombus and excludes a ow phenomenon due to inadequate instrument settings (right section). The
patent lumen is collapsed and only the thrombosed, noncompressible portion is still identiable as a hypoechoic structure. The transverse scans
depict the axillary artery (A) posterocranially (CL=clavicle).
c There is full recanalization of the vein after another cycle of thrombolytic therapy. The Doppler waveform demonstrates respiratory phasicity and
cardiac pulsatility of venous blood ow (M-shaped prole). The restoration of cardiac pulsatility indicates that thrombolytic therapy was initiated
at an early stage; an older thrombus would have caused inammatory changes and rigidity of the venous wall
. Fig. 3.104a, b (Atlas) Recanalization.
a Thrombosis of the axillary vein as in the case presented in . Fig.3.103 (Atlas); however, ve cycles of thrombolytic therapy are necessary before
signs of recanalization appear (transverse image on the left, longitudinal image on the right).
b Recanalization of the axillary vein is complete after another three cycles, but the wall is still markedly thickened as indicated by the hypoechoic
structure surrounding the patent lumen (blue). The Doppler waveform shows no cardiac modulation of blood ow due to rigidity of the wall
resulting from postthrombotic inammatory changes and possible deposition of thrombotic material. Thrombogenic wall lesions have a high risk
of early recurrence. In this patient, recurrent thrombosis of the axillary vein with occlusion was seen 2days later despite adequate heparinization
260
Chapter 3 · Extremity Veins
3
. Fig. 3.105a–e (Atlas) Costoclavicular compression syndrome with thrombosis.
a A 17-year-old patient presented with a 5-day history of swelling of the right arm and lividity of the hand and lower arm. She reported recurrent
transient but very mild swelling of the arm. Ultrasound identied a short thrombus at the junction of the subclavian vein with the axillary vein
immediately distal to the costoclavicular space.
b Upstream of the thrombus, the axillary vein is patent and the Doppler waveform indicates disturbed drainage with loss of respiratory phasicity
and cardiac pulsatility.
c Proximal to the clavicle, the subclavian vein is patent and shows normal ow with respiratory and cardiac variation.
d After 3cycles of ultrahigh- dose streptokinase, recanalization of the vein was observed, and duplex ultrasound conrmed the suspected costo-
clavicular compression syndrome as the underlying cause of thrombosis. The Doppler waveform from the supine position with the arm relaxed
shows a normal ow prole.
e Upon strong pulling of the arm in the posteroinferior direction, the vein becomes dilated distal to the costoclavicular space due to congestion.
With the transducer in the infraclavicular fossa, the dilated subclavian and axillary veins as well as collateral veins (KOL) are seen. No ow signal is
detected immediately distal to the costoclavicular space, indicating compression- induced occlusion of the subclavian vein. Valves (KL) are seen in
the dilated lumen. (CL=clavicle). A Doppler waveform should be obtained to document the costoclavicular compression syndrome because the
color duplex ndings are dicult to quantify and are more susceptible to artifacts as a result of the maneuvers performed to induce compression
3.3 · Atlas: Ex tremity Veins
261
. Fig. 3.106 (Atlas) Costoclavicular compression syndrome.
The passage of the vein through the costoclavicular space between the clavicle and the rst rib is dicult to depict due to acoustic shadowing.
In this area, the vein can only be evaluated if tangential beam orientation is achieved in slender patients. Under these conditions, a continuous
high-frequency stenosis signal will be obtained from this vein segment with increasing abduction of the arm. This maneuver may even lead to
complete occlusion of the subclavian vein. The ndings presented were obtained in a 29-year-old patient with costoclavicular compression syndrome (same patient as in . Fig.3.105 (Atlas), before thrombosis). As in most cases of this syndrome, the subclavian artery was not compressed
and showed triphasic ow in the duplex examination. In this patient, the same duplex ndings could be elicited when the outwardly rotated arm
was pulled in the posteroinferior direction. Extreme hyperabduction can induce compression of the subclavian vein in the costoclavicular space
with demonstration of disturbed venous return in the Doppler waveform also in subjects without clinical symptoms of compression syndrome.
For this reason, the hyperabduction test must be interpreted with caution. An abnormal Doppler waveform sampled while the outwardly rotated
arm is being pulled posteroinferiorly is a more specic sign of the costoclavicular compression syndrome
3
262
Chapter 3 · Extremity Veins
3
. Fig. 3.107a–e (Atlas) Follow-up of subclavian vein thrombosis after pacemaker implantation.
a One week after pacemaker implantation, ultrasound demonstrates thrombosis of the subclavian vein (left) and of the axillary vein (right). Only
isolated segments of the partially thrombosed axillary vein show ow signals when scanned with a low PRF.The subclavian vein (V.S) is completely thrombosed to the level of entry of the jugular vein (V.J). The pacemaker probe (PM) is identied by the hyperechoic double reection in
the lumen.
b The Doppler waveform from the brachial vein shows the band-like ow prole with absence of respiratory phasicity typical of upstream ow
obstruction (thrombosis).
c After only 2days of low-molecular heparin (weight-adjusted therapeutic dose), the patient shows surprisingly early spontaneous recanalization.
Residual thrombi are seen only around the pacemaker probe (PM). Moreover, there is narrowing of the subclavian vein as it enters the conuence
(aliasing, but without demonstration of ow obstruction in the Doppler waveform).
d The axillary vein is completely recanalized with restoration of respiratory phasicity and cardiac pulsatility (conrming absence of a central ow
obstruction).
e The brachial vein now exhibits respiratory phasicity of ow with slight cardiac pulsatility, consistent with elimination of the ow obstruction
(same sampling site as in b)
. Fig. 3.108 (Atlas) Thrombophlebitis of arm veins.
Using the artery as a landmark, the examiner can distinguish deep veins from supercial veins and thus differentiate between thrombosis and thrombophlebitis.
In the example, the ndings rule out venous thrombosis
(brachial vein with ow displayed in blue, compressible
as shown on the right) and conrm thrombophlebitis
(basilic vein not compressible, supercial course, no
accompanying artery)
263
Arteriovenous Fistulas
4.1 Clinical Role ofArteriovenous Fistula Evaluation – 264
4.1.1 Background – 264
4.1.2 Diagnostic Evaluation ofPatients withAbnormal
andSurgically Created Fistulas – 264
4.1.2.1 Types ofAV Fistulas – 264
4.1.2.2 Creation ofaHemodialysis Access – 264
4.1.2.3 Indications forColor Duplex Ultrasound – 265
4.2 Examination Protocol, Technique, andDiagnostic Role – 266
4.2.1 Congenital andAcquired Fistulas – 266
4.2.2 Hemodialysis AV Fistula – 267
4.2.2.1 Time-Ecient Ultrasound Workup ofHemodialysis
Access Problems – 268
4
4.3 Doppler Waveform Changes Characteristic
ofAV Fistulas – 269
4.4 Fistula Maturation andFlow Volume Measurement – 269
4.5 Documentation – 270
4.6 Vascular Mapping Prior toAV Fistula Creation – 270
4.7 Hemodialysis Access Complications – 271
4.7.1 Hemodialysis Access Stenosis – 271
4.7.1.1 Causes ofHemodialysis Access Stenosis – 271
4.7.1.2 Stenosis Detection andGrading – 271
4.7.1.3 Proximal Feeding Artery Stenosis – 273
4.7.2 Diagnostic Evaluation forSpecic Hemodialysis
Access Problems – 273
4.7.2.1 Peripheral Ischemia – 273
4.7.2.2 Hemodialysis Access Aneurysm – 275
4.7.2.3 Inadequate or Excessive Fistula Flow – 275
4.7.2.4 Arm Swelling – 277
4.8 Diagnostic Role ofDuplex Ultrasound Compared
withOther Modalities – 277
4.8.1 Therapeutic Decision-Making – 277
4.8.2 Surveillance Programs? – 278
4.9 Atlas: Arteriovenous Fistulas – 279
© Springer International Publishing AG, part of Springer Nature 2018
W. Schäberle, Ultrasonography in Vascular Diagnosis, https://doi.org/10.1007/978-3-319-64997-9_4