Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3938_Библиотеки_им_академика_М_И_Перельмана
.pdf
48 Lower Extremity Ultrasound Evaluation and Mapping for Evaluation
fi cial fascia, and the lower echogenic layer is the muscular fascia. Any vein
outside the saphenous eye is not the GSV, but an accessory saphenous, or
a tributary. In the upper thigh, there is an accessory saphenous vein that
creates a second “eye” and can easily be distinguished from the GSV
because it lies anteriolateral and parallels the course of the femoral artery
and vein. In the knee area, it is diffi cult to recognize the “saphenous eye,”
C
D
FIGURE 4-2 Continued
C. A lower calf medial perforator vein joins a tributary of the posterior arch vein and
the posterior tibial vein. It is very dilated and has refl ux. Its largest diameter was 6.7 mm.
D. The femoral vein in the midthigh is partially recanalized and has refl ux.
https://t.me/med1917
Lower Extremity Ultrasound Evaluation and Mapping for Evaluation 49
and the GSV is usually identifi ed in a triangle formed by the tibia, medial
gastrocnemius muscle, and fascial sheet. Occasionally, a large tributary
arises above the knee and may be mistakenly identifi ed as the GSV. In
general, the GSV in the thigh and the leg is often followed by parallel veins
that may be confused with the GSV. These veins lie subcutaneously and
then travel through the superfi cial fascia to enter the saphenous compart-
ment. Most of the patients have refl ux in GSV and its tributaries. The
anterior and medial accessory veins in the thigh and the posterior and
anterior arch vein in the calf are the tributaries most commonly
incompetent.
12
The SSV is found at the popliteal fossa within the triangular fascia
over the medial and lateral heads of the gastrocnemius muscle.
13
The vein
lies in the leg in a fascial compartment that is identifi ed with the ultrasound
as an “eye” similar to the GSV eye. The SSV may terminate at different
levels of the popliteal vein, may extend to the thigh, or may join the GSV
via the Giacomini vein. Termination of SSV above the popliteal vein is
now collectively termed as “thigh extension of SSV.”
14
Knowledge of the
variable anatomy of the SSV is very important, as the intervention may
be modifi ed according to the patterns of refl ux.
15,16
There is a tributary
called “popliteal fossa perforating vein” that may be misidentifi ed as
the SSV because it runs parallel to the SSV and joins separately with the
popliteal vein.
17
Refl ux in nonsaphenous veins is found in 10% of patients with CVD.
18
Most of these patients are usually multiparous women. The location
and origin of these veins are variable. Often they are found as an extension
of the pelvic veins in the thigh (vulvar and gluteal), lateral and posterior
thigh (lateral thigh system, posterolateral perforator veins, and sciatic
nerve veins), popliteal fossa (vein of the popliteal fossa, tibial nerve veins,
atypical perforators, and tributaries), and lateral knee and calf (atypical
tributaries and perforators). About 90% of these patients present with
CVD classes 1 to 3, and skin damage is present in 10%. Inaccurate clinical
evaluation has been found in one-third of cases with this type of refl ux.
Therefore, DU is ver y importa nt in identify ing refl ux in these veins because
there are many different ones and there is great variability in the patterns
of refl ux.
PERFORATING VEINS
The role of the perforator veins is controversial in the development of
venous ulcers in patient with CVD. They are seen in different planes with
the ultrasound because the direction of fl ow is different in those veins.
Transverse and oblique scanning along the course of the superfi cial veins
is more appropriate. The fascia has to be identifi ed by the examiner. The
https://t.me/med1917
50 Lower Extremity Ultrasound Evaluation and Mapping for Evaluation
fascia appears white due to high collagen content, and the perforators are
identifi ed as they travel through the fascia. About 150 perforating veins
have been identifi ed, and they are grouped based on their location.
19
However, only about 20 of them have been shown to become incompetent
and are frequently found in patients with ulceration. Most of these veins
are found in the medial and posterior calf, and they are connecting tribu-
taries of the GSV and SSV with muscular and deep axial veins.
The examination starts from the medial malleolus going upward to the
knee. The posterior arch and GSV are scanned on a transverse plane for
incompetent perforator veins. Localized varicose veins are highly suspi-
cious for an underlying incompetent perforator, and that region requires
detailed evaluation. Then, the SSV is tested starting from the lateral malle-
olus and ending at its termination in the fossa or higher up. In order to
determine normal valvular function, distal compression is applied for aug-
mentation of fl ow, and the perforators are tested in combination with the
deep and superfi cial veins. The fl ow in the calf perforator veins may be
bidirectional. The net outward fl ow from deep to superfi cial veins is meas-
ured to determine refl ux.
20
In patients with signifi cant edema, dorsi/plantar
fl exion is performed to determine refl ux in these veins. This is important
because manual compression alone may not show refl ux in dilated perfora-
tor veins.
DEEP VEINS
The common femoral vein is tested from the inguinal ligament to its
union with the femoral and the deep femoral veins. Any evidence of con-
tinuous fl ow, poor augmentation, and asymmetrical waveforms to the con-
tralateral CFV should alert the examiner to extend the imaging in the iliac
veins and the inferior vena cava. The CFV should also be examined above
and below the SFJ in order to determine the presence or absence of refl ux
at the SFJ level and test the effect of the GSV on the CFV.
21
The femoro-
popliteal veins are examined along their length from the groin to the tibi-
operoneal trunk. Duplications and any pathology in them are noted. In the
popliteal fossa also, the gastrocnemial veins are being evaluated, particu-
larly those in the medial head because they are more often implicated in
CVD. Unusual veins if present—such as the popliteoprofunda vein, per-
sistent sciatic vein, and veins from the sciatic nerve and other muscular
veins—are being evaluated as well. The popliteal vein is examined care-
fully above and below its union with the SSV and gastrocnemius veins for
the reasons mentioned previously for the CFV.
In the calf, the posterior tibial, peroneal, and soleal veins are imaged
because the frequency of deep vein thrombosis in these veins is high, and
this in turn can lead to post-thrombotic refl ux. The anterior tibial veins are
https://t.me/med1917
Lower Extremity Ultrasound Evaluation and Mapping for Evaluation 51
imaged only in the presence of CVD signs and symptoms in the anterior
aspect of the calf.
ULCER BED
The ulcer bed should always be evaluated for incompetent veins includ-
ing the area surrounding the ulcer as far as 2 cm from the periphery of
the ulcer. In ulcers over the medial malleolus, the veins that need to
be tested are the GSV, the posterior arch, posterior tibial, and the pe -
roneal veins. In ulcers at the lateral malleolus, the veins are the SSV and
the peroneal veins. In ulcers on the anterior aspect of the leg, the anterior
arch of the GSV and the anterior tibial veins need to be assessed. Sterile
technique can be used for the evaluation of the ulcer bed. The surface of
the ulcer may be covered with a transparent sterile dressing, or the probe
can be covered with a sterile glove that is fi lled with ultrasonic gel.
22,23
The prevalence of deep venous refl ux has been found to be higher in
patients with venous ulcers when compared to patients with less severe
forms of CVD. In addition, it was found that the ration of outward fl ow
in these veins is longer in patients with ulcers compared to patients with-
out ulcers.
ULTRASOUND FINDINGS AND IMPLICATIONS
FOR TREATMENT
The use of DU has contributed to a better understanding of the mecha-
nisms of CVD and has changed dramatically the management of patients.
The overall involvement of the superfi cial veins was 88% in patients with
venous ulceration.
24
Refl ux confi ned to the superfi cial and perforator veins
alone was found in 40% to 50%,
24
and treatment of these veins was found
to be successful in healing the ulcers in almost 90% of patients.
25–27
When
the deep veins are involved, particularly in patients with previous throm-
bosis, the ulcer healing rate is lower, and the recurrence rate is higher.
2,3
The presence of deep vein refl ux is higher in patients with venous ulcers
compared with patients with less severe symptoms of CVD.
7,2 8, 29
Overall,
the involvement of deep venous insuffi ciency in venous ulcer disease has
been shown to be up to 56%.
24
Also, a documented episode of thrombosis
is found in one-third of patients with ulcers, which is signifi cantly higher
compared to those without an ulcer (Figure 4-3).
24,30
Refl ux confi ned to
the deep veins alone is found in 12%, while obstruction alone is detected
in about 2%.
24,30
In a recent prospective multicenter study, of the 2.6%
(21/799) of limbs that appeared to be venous in origin, no venous
https://t.me/med1917
52 Lower Extremity Ultrasound Evaluation and Mapping for Evaluation
abnormality was found.
31
These patients had many different pathologies
such as carcinomas, infections, vasculitis, hematologic abnormalities, etc.
DU MAPPING FOR GUIDING TREATMENT
Recently, with the evolution of endovenous ablation techniques such as
the radiofrequency, laser, and foam sclerotherapy, DU is of major impor-
tance, since these methods are being performed with DU guidance.
32–34
DU is used to select the patients during the procedures and follow-up. In
this way, only the involved veins are being treated under direct vision. The
outcome of the treatment in these veins and its effect in the untreated veins
are evaluated. Residual from recurrent disease is identifi ed, and also
thrombosis and neovascularization are detected as well.
35,36
REFERENCES
1. Bergan JJ, Schmid-Schonbein GW, Smith PD, Nicolaides AN, Boisseau MR, Eklof B.
Chronic venous disease. N Engl J Med. 2006;355:488–498.
2. Gloviczki P, Bergan JJ, Rhodes JM, et al. Mid term results of endoscopic perforator vein
interruption for chronic venous insuffi ciency: Lessons learned from the North American
FIGURE 4-3 Femoral and popliteal vein old thrombosis (two previous episodes in the
same site) with partial recanalization and severe refl ux (>5 seconds). The patient had an
ulcer in the lateral malleolus and also refl ux in the SSV from the popliteal fossa to the ulcer.
Ligation and stripping of the SSV healed the ulcer in 2 months. The duration of refl ux in
the femoral and popliteal veins was reduced to 2 seconds. However, the ulcer recurred after
5 months.
https://t.me/med1917
Lower Extremity Ultrasound Evaluation and Mapping for Evaluation 53
subfascial endoscopic perforator surgery registry. The North American Study Group.
J Vasc Surg. 1999;29:489–502.
3. Scriven JM, Bianchi V, Hartshorne T, et al. A clinical and hemodynamic investigation
into the role of calf perforating vein surgery in patients with venous ulceration and deep
venous incompetence. Eur J Endovasc Surg. 1998;16:148–152.
4. Labropoulos N, Tiongson J, Pryor L, et al. Defi nition of venous refl ux in lower extremity
veins. J Vasc Surg. 2003;38:793–798.
5 Vasdekis SN, Clarke GH, Nicolaides AN. Quantifi cation of venous refl ux by means of
DU. J Vasc Surg. 1989;10:670–677.
6. Van Bemmelen PS, Bedford G, Beach K, Strandness DE. Quantitative segmental evalu-
ation of venous valvular refl ux with duplex ultrasound scanning. J Vasc Surg. 1989;10:
425–431.
7. Labropoulos N, Delis K, Nicolaides AN, Leon M, Ramaswami G. The role of the dis-
tribution and anatomic extent of refl ux in the development of signs and symptoms in
chronic venous insuffi ciency. J Vasc Surg. 1996;23:504–510.
8. Eklof B, Rutherford RB, Bergan JJ, et al. American Venous Forum International Ad
Hoc Committee for Revision of the CEAP Classifi cation. Revision of the CEAP clas-
sifi cation for chronic venous disorders: Consensus statement. J Vasc Surg. 2004;40:
1248–1252.
9. Labropoulos N, Leon L, Engelhorn CA, et al. Sapheno-femoral junction refl ux in
patients with a normal saphenous trunk. Eur J Vasc Endovasc Surg. 2004;28:595–599.
10. Caggiati A, Ricci S. The long saphenous vein compartment. Phlebology. 1997;12:
107–111.
11. Caggiati A. Fascial relationships of the long saphenous vein. Circulation. 1999;100:
2547–2549.
12. Labropoulos N, Kang SS, Mansour MA, Giannoukas AD, Buckman J, Baker WH.
Primary superfi cial vein refl ux with competent saphenous trunk. Eur J Vasc Endvasc
Surg. 1999;18:201–206.
13. Caggiati A. Fascial relationships of the short saphenous vein. J Vasc Surg. 2001;
34:241–246.
14. Caggiati A, Bergan JJ, Gloviczki P, Eklof B, Allegra C, Partsch H. International Inter-
disciplinary Consensus Committee on Venous Anatomical Terminology. Nomenclature
of the veins of the lower limb: Extensions, refi nements, and clinical application. J Vasc
Surg. 2005;41:719–724.
15. Labropoulos N, Giannoukas AD, Delis K, et al. The impact of isolated lesser saphenous
vein system incompetence on clinical signs and symptoms of chronic venous disease.
J Va sc Surg. 2000;32:954–960.
16. Delis KT, Knaggs AL, Khodabakhsh P. Prevalence, anatomic patterns, valvular com-
petence, and clinical signifi cance of the Giacomini vein. J Vasc Surg. 2004;40:
1174–1183.
17. Delis KT, Knaggs AL, Hobbs JT, Vandendriessche MA. The nonsaphenous vein of the
popliteal fossa: Prevalence, patterns of refl ux, hemodynamic quantifi cation, and clinical
signifi cance. J Vasc Surg. 2006;44:611– 619.
18. Labropoulos N, Tiongson J, Pryor L, et al. Nonsaphenous superfi cial vein refl ux. J Vasc
Surg. 2001;34:872–877.
19. Limborgh J van. L’anatomie du système veineux de l’extremité inférieure en relation
avec la pathologie variqueuse. Folia Angiol. 1961;8:240–257.
20. Labropoulos N, Mansour MA, Kang SS, Gloviczki P, Baker WH. New insights into
perforator vein incompetence. Eur J Vasc Endovasc Surg. 1999;18:228–234.
21. Labropoulos N, Tassiopoulos AK, Kang SS, Mansour MA, Littooy FN, Baker WH.
Prevalence of de ep venous refl u x in p atients wit h prima ry superfi cial vein incompetence.
J Vasc Surg. 2000;32:663–668.
https://t.me/med1917
54 Lower Extremity Ultrasound Evaluation and Mapping for Evaluation
22. Hanrahan LM, Araki CT, Rodriguez AA, Kechejian GJ, LaMorte WW, Menzoian JO.
Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc
Surg. 1991;3:805–812.
23. Labropoulos N, Giannoukas AD, Nicolaides AN, Leon M, Ramaswami G, Volteas N.
New insights into the pathophysiologic condition of venous ulceration with color fl ow
duplex imaging: Implications for treatment? J Vasc Surg. 1995;22:45–50.
24. Tassiopoulos AK, Golts E, Oh DS, Labropoulos N. Current concepts in chronic venous
ulceration. Eur J Vasc Endovasc Surg. 2000;20:227–232.
25. Bello M, Scriven M, Hartshorne T, et al. Role of superfi cial venous surgery in the treat-
ment of venous ulceration. Br J Surg. 1999; 86 :755–759.
26. Darke SG, Penfold CAD. Venous ulceration and saphenous ligation. Eur J Vasc Surg.
1992;6:4–9.
27. Burnand KG, Thomas ML, O’Donnell TF Jr, Browse NL. Relation between postphle-
bitic changes in the deep veins and results of surgical treatment of venous ulcers. Lancet.
1976;1:936–938.
28. Labropoulos N. CEAP in clinical practice. Vasc Surg. 1997;31:224–225.
29. Labropoulos N. Clinical correlation to various patterns of refl ux. Vasc Surg. 1997;31:
242–248.
30. Labropoulos N, Patel PJ, Tiongson JE, Pryor L, Leon LR, Tassiopoulos AK. Patterns
of venous refl ux and obstruction in patients with skin damage due to chronic venous
disease. Vasc Endovasc Surg. 2007;41:33–40.
31. Labropoulos N, Manalo D, Patel N, Tiongson JE, Pryor L, Giannoukas AD. Uncommon
leg ulcers. J Vasc Surg. 2007;45:568–573.
32. Lurie F, Creton D, Eklof B, et al. Prospective randomised study of endovenous radio-
frequency obliteration (closure) versus ligation and vein stripping (EVOLVeS): Two-
year follow-up. Eur J Vasc Endovasc Surg. 2005;29:67–73.
33. Almeida JI, Raines JK. Radiofrequency ablation and laser ablation in the treatment of
varicose veins. Ann Vasc Surg. 2006;20:547–552.
34. Guex JJ. Foam sclerotherapy: An overview of use for primary venous insuffi ciency.
Semin Vasc Surg. 2005;18:25–29.
35. Perrin MR, Labropoulos N, Leon LR Jr. Presentation of the patient with recurrent
varices after surgery (REVAS). J Vasc Surg. 2006;43:327–334.
36. van Rij AM, Jones GT, Hill GB, Jiang P. Neovascularization and recurrent varicose
veins: More histologic and ultrasound evidence. J Vasc Surg. 2004;40:296–302.
https://t.me/med1917
55
5
Hypercoagulable States
Associated with Chronic
Venous Insuffi ciency
Jose L. Trani Jr. and
Jeffrey H. Lawson
INTRODUCTION
Venous disorders affect a signifi cant percentage of the U.S. population,
as many as one in 1,000 persons annually.
1
For many patients with deep
venous thrombosis (DVT), the clinical course following an initial throm-
botic event may be complicated by further manifestations of venous disease
formerly referred to as the post-thrombotic syndrome. In patients who
progress to chronic venous insuffi ciency (CVI), the currently accepted
terminology, approximately 4% will progress to develop venous ulcer-
ation.
2
Chronic venous insuffi ciency is a direct result of sustained venous
hypertension, as described elsewhere in this volume. Over time, the per-
sistence of venous hypertension leads to the most severe form of chronic
venous insuffi ciency: chronic venous ulceration. A combination of factors
including high thrombotic recurrence rates, ineffective anticoagulant treat-
ment, and a poorly understood disease process makes venous ulceration
diffi cult to both prevent and manage.
3
Identifi ed causes in the development
of chronic venous insuffi ciency include a family history of venous insuffi -
ciency, especially of maternal origin, and a history of vigorous exercise.
Subsequent chronic venous ulceration includes persistent untreated primary
venous insuffi ciency and repetitive post-thrombotic episodes of recurrent
DVT.
3,4
The CVI syndrome is a combination of sequelae of a deep venous
thrombosis. Studies demonstrate that this syndrome may occur in more
Venous Ulcers
Copyright © 2007 by Academic Press, Inc.
All rights of reproduction in any form reserved.
https://t.me/med1917
56 Hypercoagulable State s Associated with Chronic Venous Insuffi ciency
than 50% of patients who have symptomatic deep venous thrombosis.
5
The
underlying pathophysiology of the thrombotic event leading to post-throm-
botic syndrome is the resultant scarring from thrombus resolution that
leads to valve incompetence and subsequent distal venous hypertension.
6
At least one risk factor is identifi ed in the majority of patients who have a
symptomatic deep venous thrombosis. Many patients have multiple risk
factors that contribute to their CVI.
7
The inciting procoagulant etiologies
for developing thromboses may be divided into inherited and acquired
thrombophilias (Table 5-1). The overall prevalence of thrombophilia, both
inherited and acquired, in patients who proceed to develop CVI is reported
to be as high as 41%. This is similar to the reported prevalence of throm-
bophilia in patients with an antecedent deep vein thrombosis, making
thrombophilias an important contributors to CVI.
8
The remainder of the
chapter will be devoted to a discussion of the major inherited and acquired
thrombophilias, as well as their relationship to CVI in general and venous
ulceration in particular.
INHERITED THROMBOPHILIA CONDITIONS
Inherited thrombophilias are characterized by a genetic predisposition
to venous thrombotic events. They are frequently the cause of vascular
thrombosis in younger individuals (less than 45–50 years of age) and may
contribute to deep venous thrombosis at any age. Attempts have been
made to quantify the risk of developing a deep venous thrombus in patients
with inherited thrombophilias. Between 8% and 13% of patients in an
unselected patient population who present with a fi rst deep venous throm-
bus will have a genetic anticoagulant defi ciency. Early studies took into
account all major coagulation disorders with the exception of factor V
TABLE 5-1 Inherited and Acquired Thrombophilias That Increase the Risk of
Developing a Deep Vein Thrombosis
Inherited Acquired
Factor V Leiden mutation antiphospholipid syndrome
Activated protein C mutations anticardiolipin antibodies
Antithrombin mutations Lupus anticoagulant antibodies
Protein C mutations Hyperhomocysteinemia
Protein S mutations Activated protein C resistance
Elevated factor VIII Malignancy
Prothrombin gene mutation Autoimmune disorders, etc.
Dysfi brinogenemia
https://t.me/med1917
Hypercoagulable State s Associated with Chronic Venous Insuffi ciency 57
Leiden mutation.
9
For this particular disorder, two separate studies have
determined that in patients with a fi rst-time deep venous thrombosis or
pulmonary embolism, 12% to 19% of patients were positive for the factor
V Leiden mutation.
9
Factor V Leiden Mutation
Factor V Leiden mutation is the most common prothrombotic genetic
defect. It is present in approximately 5% of all Caucasians, and it accounts
for 40% to 50% of all cases of inherited thrombophilia. Biochemically, the
etiology of the factor V Leiden mutation is a point mutation resulting in
an arginine to glutamine substitution at position 506 in coagulation factor
V. This alteration results in an inability of activated protein C to cleave
factor Va, promoting coagulation via continued thrombin production.
10
The factor V Leiden mutation is among the most prevalent inherited
thrombophilia condition identifi ed in patients with a fi rst deep venous
thrombosis. MacKenzie and colleagues also identifi ed the factor V Leiden
mutation as a specifi c thrombophilia condition associated with chronic
venous ulceration in the setting of a previous deep vein thrombosis.
8
Sepa-
rate studies have determined that this mutation is present in 36% of all
patients with post-thrombotic leg ulcers.
10
Post-thrombotic venous ulcer-
ation accounts for 30% to 60% of all lower extremity venous ulcerations.
Initial screening for factor V Leiden mutations requires measurements of
the aPTT with and without the addition of a standard amount of activated
protein C in order to produce an activated protein C ratio. Second-
generation tests included diluting the patient plasma in order to produce a
more standard assay. In the current era, most authorities recommend using
a PCR-based screen to identify the factor V Leiden mutation.
As indicated previously, the factor V Leiden mutation has been detected
in up to 20% of individuals with a venous thrombotic event.
11
Also, a sepa-
rate study that evaluated patients with chronic venous ulceration deter-
mined that 13% of patients with a venous ulcer also had a factor V Leiden
mutation.
8
As this mutation is present in 5% of the population, a 4–5-fold
risk of developing a deep venous thrombosis is conferred among carriers
(Table 5-2).
Although the factor V Leiden mutation is the most common form of
activated protein C resistance, other mutations in factor V may produce
similar procoagulant effects. In addition, activated protein C resistance
m ay be a n a c qu i re d co ndit i on , mo s t c o mm o nl y associat e d w ith the a nt iph o s-
pholipid syndrome.
Antithrombin Defi ciency
Antithrombin (formerly known as antithrombin III) is a vitamin K-
independent glycoprotein that functions to inhibit thrombin as well as
activated factors of the intrinsic clotting cascade (including factors IXa and
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана