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_3953_Библиотеки_им_академика_М_И_Перельмана
.pdf
Figure 4 Intravascular ultrasound (IVUS) showing a septum not easily visualized by venogram
(left) and partially thrombosed vein (right). The adjacent artery is marked with an A. The black circle
within the vein is the IVUS catheter.
Figure 5 AP-view of transfemoral antegrade venogram, which appears normal with no obvious
stenosis (left). IVUS of the same vein at different levels showing severe proximal common iliac vein
(CIV) stenosis due to compression by transversing iliac artery, partial obstruction mid-CIV, and
normal distal CIV (right). The adjacent artery is marked with an A. The black circle within the vein is
the IVUS catheter.
Negle
´
n and Raju108
https://t.me/med1917
significantly underestimated the degree of stenosis by 30%. The venogram was actually
considered “normal” in one-fourth of limbs despite the fact that IVUS showed O50%
obstruction (39). In a similar population of limbs, the stenosis was less than 50% in 42% of
venograms but only in 10% of IVUS investigations (33). On the other hand, the venous
stenosis was found to be greater than 70% in 32% of venograms, but twice as often with the
IVUS. Using the IVUS result as the standard, the venogram had a poor sensitivity of 45%
and negative predictive value of 49% in detecting an obstruction of greater than 70%.
Intravascular ultrasound is clearly superior to venography in providing adequate
morphological information and is presently the best available method for diagnosing
clinically significant chronic iliac vein obstruction. It is also an invaluable tool for accurate
placement of iliofemoral stents ensuring stent cover of the entire diseased segment. Owing
to the lack of hemodynamic tests and inability of duplex Doppler scanning to visualize
accurately the iliac vein, it is insufficient to limit the workup of all patients with chronic
venous disease to duplex ultrasound alone. In patients with significant signs and symptoms
of CVD, transfemoral venography (preferably multi-plane) or IVUS should be utilized
more often to identify patients with potentially important venous outflow obstruction.
Good clinical results have been obtained when stenosis of greater than 50%, as
identified by IVUS, or occlusions have been stented. In selecting symptomatic patients for
IVUS investigation, one or several of these parameters have been used: (1) single-plane
venographic stenosis O30%; (2) presence of pelvic collaterals; and (3) positive invasive
pressure test (35,39). Utilizing this policy, however, 10–15% of iliofemoral veins are
found to be normal. An appropriate hemodynamic test needs to be developed.
CONCLUSION
There is rightly a general trend for avoidance of invasive studies owing to potential
complications and discomfort for the patient. This concern should, however, not lead to
complete abandonment of invasive studies, especially in the situation where they cannot
be adequately replaced by a non invasive test. Although AVP is not necessary for daily
clinical practice, obstruction testing may give valuable information in select patients.
The importance and frequency of iliofemoral venous outflow obstruction and the lack
of accurate non invasive hemodynamic tests for obstruction necessitate increasing use of
invasive morphologic studies of the iliofemoral venous outflow tract. Ascending dorsal
foot vein, transfemoral antegrade and descending venograms are still important for
mapping of the pathologic morphology in preparation for open or endovascular surgery of
the deep venous system.
KEY POINTS
† Invasive tests are often necessary to identify anatomic sites of disease for
interventional treatment.
† Ascending venography is used to detect the anatomic extent of obstruction while
descending venography is used to detect reflux. Both techniques are used for
intervention in the deep veins.
† Ambulatory venous pressure assesses the global hemodynamics of the limbs but
a normal pressure cannot exclude venous disease.
Invasive Tests—Radiological and Pressure Measurements 109
https://t.me/med1917
† Pressure measurements are used to detect obstruction and evaluate the
significance of vein stenosis. They are also useful to assess the outcome of an
intervention.
† Intravascular ultrasound is superior to venography in providing morphological
information and a valuable tool for accurate placement of iliofemoral stents.
REFERENCES
1. Welkie JF, Comerota AJ, Katz ML, Aldridge SC, Kerr RP, White JV. Hemodynamic
deterioration in chronic venous disease. J Vasc Surg 1992; 16:733–740.
2. Payne SP, Thrush AJ, London NJ, Bell PR, Barrie WW. Venous assessment using air
plethysmography: a comparison with clinical examination, ambulatory venous pressure
measurement and duplex scanning. Br J Surg 1993; 80:967–970.
3. Negle
´
n P, Raju S. A rational approach to detection of significant reflux with duplex Doppler
scanning and air plethysmography. J Vasc Surg 1993; 17:590–595.
4. Gillespie DL. Letter to the editor. J Vasc Surg 1993; 18:140.
5. Pollack AA, Wood EH. Venous pressure in teh saphenous vein in ankle in man during exercise
and changes in posture. J Appl Physiol 1949; 1:649–653.
6. Raju S, Fredericks R. Hemodynamic basis of stasis ulceration—a hypothesis. J Vasc Surg
1991; 13:491–495.
7. Nicolaides AN. Outflow obstruction. Investigations of Patients with Deep Vein Thrombosis
and Chronic Venous Insufficiency. Los Angeles, C.A.: Med-Orion Publishing Co, 1991 pp.
56–62.
8. Negle
´
n P, Raju S. Differences in pressures of the popliteal, long saphenous, and dorsal foot
veins. J Vasc Surg 2000; 32:894–901.
9. Negle
´
n P, Raju S. Ambulatory venous pressure revisited. J Vasc Surg 2000; 31:1206–1213.
10. Raju S, Fredericks R. Venous obstruction: an analysis of one hundred thirty-seven cases with
hemodynamic, venographic, and clinical correlations. J Vasc Surg 1991; 14:305–313.
11. Negle
´
n P, Thrasher TL, Raju S. Venous outflow obstruction: An underestimated contributor to
chronic venous disease. J Vasc Surg 2003; 38:879–885.
12. Back TL, Padberg FT, Jr., Araki CT, Thompson PN, Hobson RW, II. Limited range of motion
is a significant factor in venous ulceration. J Vasc Surg 1995; 22:519–523.
13. Strandness DE, Jr., Sumner DS. The effect of geometry on arterial blood flow. Hemodynamics
for Surgeons. New York: Grune&Stratton, 1975: 96–119.
14. Hurst DR, Forauer AR, Bloom JR, Greenfield LJ, Wakefield TW, Williams DM. Diagnosis and
endovascular treatment of iliocaval compression syndrome. J Vasc Surg 2001; 34:106–113.
15. Labropoulos N, Volteas N, Leon M, et al. The role of venous outflow obstruction in patients
with chronic venous dysfunction. Arch Surg 1997; 132:46–51.
16. Negle
´
n P, Raju S. Detection of outflow obstruction in chronic venous insufficiency. J Vasc Surg
1993; 17:583–589.
17. Raju S. A pressure-based technique for the detection of acute and chronic venous obstruction.
Phlebology 1988; 3:207–216.
18. Raju S. New approaches to the diagnosis and treatment of venous obstruction. J Vasc Surg
1986; 4:42–54.
19. Albrechtsson U, Einarsson E, Eklof B. Femoral vein pressure measurements for evaluation of
venous function in patients with postthrombotic iliac veins. Cardiovasc Intervent Radiol 1981;
4:43–50.
20. Negus D, Cockett FB. Femoral vein pressures in post-phlebitic iliac vein obstruction. Br J Surg
1967; 54:522–525.
21. Illig KA, Ouriel K, DeWeese JA, Riggs P, Green RM. Increasing the sensitivity of the
diagnosis of chronic venous obstruction. J Vasc Surg 1996; 24:176–178.
Negle
´
n and Raju110
https://t.me/med1917
22. Rigas A, Vomvoyannis A, Giannoulis K, Antipas S, Tsardakas E. Measurement of the femoral
vein pressure in edema of the lower extremities. Report of 50 cases. J Cardiovasc Surg (Torino)
1971; 12:411–416.
23. Raju S, Owen S, Jr., Negle
´
n P. The clinical impact of iliac venous stents in the management of
chronic venous insufficiency. J Vasc Surg 2002; 35:8–15.
24. Raju S, Negle
´
n P. Popliteal vein entrapment: a benign venographic feature or a pathologic
entity? J Vasc Surg 2000; 31:631–641.
25. Raju S, Fountain T, Negle
´
n P, Devidas M. Axial transformation of the profunda femoris vein.
J Vasc Surg 1998; 27:651–659.
26. Kistner RL, Ferris EB, Randhawa G, Kamida CA. Method of performing descending
venography. J Vasc Surg 1986; 4:464–468.
27. Morano JU, Raju S. Chronic venous insufficiency: assessment with descending venography.
Radiology 1990; 174:441–444.
28. Herman RJ, Neiman HL, Yao JS, Egan TJ, Bergan JJ, Malave SR. Descending venography:
a method of evaluating lower extremity venous valvular function. Radiology 1980;
137:63–69.
29. Kistner RL. Transvenous repair of the incompetent femoral vein valve. In: Bergan JJ, Yao JS,
eds. Venous Problems. London: Year Book Medical Publishers, 1978:493–509.
30. Negle
´
n P, Raju S. A comparison between descending phlebography and duplex Doppler
investigation in the evaluation of reflux in chronic venous insufficiency: a challenge to
phlebography as the “gold standard.” J Vasc Surg 1992; 16:687–693.
31. Juhan C, Hartung O, Alimi Y, Barthelemy P, Valerio N, Portier F. Treatment of nonmalignant
obstructive iliocaval lesions by stent placement: mid-term results. Ann Vasc Surg 2001;
15:227–232.
32. Thomas ML, Fletcher EW, Cockett FB, Negus D. Venous collaterals in external and common
iliac vein obstruction. Clin Radiol 1967; 18:403–411.
33. Negle
´
n P, Raju S. Intravascular ultrasound scan evaluation of the obstructed vein. J Vasc Surg
2002; 35:694–700.
34. Forauer AR, Gemmete JJ, Dasika NL, Cho KJ, Williams DM. Intravascular ultrasound in the
diagnosis and treatment of iliac vein compression (May-Thurner) syndrome. J Vasc Interv
Radiol 2002; 13:523–527.
35. Negle
´
n P, Raju S. Balloon dilation and stenting of chronic iliac vein obstruction: technical
aspects and early clinical outcome. J Endovasc Ther 2000; 7:79–91.
36. Ahmed HK, Hagspiel KD. Intravascular ultrasonographic findings in May-Thurner syndrome
(iliac vein compression syndrome). J Ultrasound Med 2001; 20:251–256.
37. Satokawa H, Hoshino S, Iwaya F, Igari T, Midorikawa H, Ogawa T. Intravascular Imaging
Methods for Venous Disorders. Int J Angiol 2000; 9:117–121.
38. Brice JG, Dowsett DJ, Lowe RD. The effect of constriction on carotid blood-flow and pressure
gradient. Lancet 1964; 18:84–85.
39. Negle
´
n P, Berry MA, Raju S. Endovascular surgery in the treatment of chronic primary and
post-thrombotic iliac vein obstruction. Eur J Vasc Endovasc Surg 2000; 20:560–571.
Invasive Tests—Radiological and Pressure Measurements 111
https://t.me/med1917
https://t.me/med1917
10
Diagnosis of Deep Vein Thrombosis
Luis Leon
Division of Vascular Surgery, Loyola University Medical Center, Maywood, IIlinois,
U.S.A.
Nicos Labropoulos
Vascular Laboratory, Division of Vascular Surgery, New Jersey Medical School, Newark,
New Jersey, U.S.A.
INTRODUCTION AND MAGNITUDE OF THE PROBLEM
Deep vein thrombosis (DVT) is a serious condition that frequently occurs in the inpatient
setting but may also affect otherwise healthy subjects. It is rare in the young and it is more
often found in the elderly (1). Inpatients O64 years old in sub-acute care facilities have
a high prevalence of DVT despite the use of prophylaxis (2).
DVT has a silent nature. About a third of patients who present with its signs and
symptoms will have the disease. This, combined with the low autopsy rate in most
countries, makes its real occurrence unknown. Estimated yearly figures from
a community-based study in the United States revealed 170,000 new cases and 99,000
admissions for recurrent cases of symptomatic DVT and pulmonary embolism (PE), its
most feared complication, in patients treated in short-stay hospitals (3).
PATHOPHYSIOLOGY
Endothelial damage, hypercoagulability, and stasis have been recognized for over 150
years to be the three elements associated with venous thromboembolism (VTE), with often
two of those three factors needed for its initiation. Therefore, its etiology is multifactorial
with each component having different impacts on different patients.
The vein wall has been extensively analyzed and it is no longer viewed as a mere
passive conduit of blood. The endothelium and the subendothelium are key structures in
the development of VTE. The endothelium is a negatively charged physical barrier that
protects the blood from the thrombogenic subendothelium, produces pro- and anti-
coagulant substances, inhibits thrombosis and platelet aggregation and promotes
fibrinolysis. After trauma, leukocyte adhesion and transmigration disrupt the endothelium
and expose the subendothelium, providing a surface for the beginning of coagulation (4,5).
Circulating platelets are activated and platelet aggregation starts as the first step in the
formation of a hemostatic plug.
Antithrombin III, protein C and protein S deficiencies and mutations of factor V
and prothrombin genes have been recently associated with the development of venous
113
https://t.me/med1917
thrombosis (6). The activated protein C resistance phenotype associated with an abnormal
factor V Leiden and the G20210A prothrombin gene mutations are the most common
findings in patients with VTE (7). The use of oral contraceptives, pregnancy and
malignancies also increase the risk for VTE (6). A pooled analysis of eight case-control
studies revealed an odds ratio for VTE of 4.9 (95% CIZ4.1–5.9) for factor V Leiden and
3.8 (3.0–4.9) for the factor II G20210A mutation. In double heterozygotes it increased to 20
(11.1–36.1). The overall odds ratio for VTE associated with the use of oral contraceptives
was 2.29 (1.72–3.04). If oral contraceptives users were associated with a factor V Leiden
carrier, the odds ratio was 10.25 (5.69–18.45) and 7.14 (3.39–15.04) for a factor II mutation
carrier (8).
Thrombosis often begins in areas of blood flow stasis, usually in a vein valve or in
intramuscular veins, from local factors, such as venous mechanical compression and
prolonged immobility and from systemic factors such as blood sluggishness (9). Stasis
determines the site of thrombosis and probably represents the most important factor in
postoperative and posttrauma patients with limited activity. Together with endothelial
damage, they act as cofactors in the development of VTE inducing platelet activation and
blood clotting. Studies have shown that P-selectins have a role in vein wall cytokine
elevation, edema and thrombosis days after stasis. Selectins are the mediators of leukocyte
interaction with the endothelium and platelets. A CD 15-selectin is involved in the transfer
of tissue factor from leukocytes to platelets for them to be able to initiate and propagate
thrombosis. Its immunoneutralization may potentially have a clinical role in VTE (10).
Large varicose veins with sluggish flow are often a place for spontaneous thrombosis.
In immobilized patients, there is prolonged stasis at the calf level. Not surprisingly,
it has been suggested that DVT often begins in these veins and then propagates
proximally (11,12).
NATURAL HISTORY OF VENOUS THROMBOSIS
Superficial
Most thrombotic episodes of the great saphenous vein (GSV) start in the calf and are often
self-limiting. When limited to the calf they are a rare cause of symptoms or of
symptomatic PE. They represent a more serious condition if they extend above the knee,
with a 33% prevalence of documented PE (95% confidence interval [CI]Z14.6–57) (13).
Most of the studies that deal with concomitant superficial thrombophlebitis (STP)
and DVT and/or PE in the literature are of a retrospective nature and include a small
number of subjects. DVT in association with saphenous thrombosis ranges from 6% to
53%. Thrombus can propagate in a contiguous and in a non contiguous manner. From 53
patients with clinical manifestations of STP and diagnosed with DVT, evidence of direct
contiguous propagation was found in 75.5%, and the rest was non contiguous calf
involvement at the posterior tibial and soleal levels (14). Contiguous extension has been
proposed through three different routes (15). Most occur from the GSV into the femoral
vein, and this route appears to be the most significant (14,15). Less common, the thrombus
extends from the small saphenous vein (SSV) into the popliteal vein through the
saphenopopliteal junction. Extension through perforators can also occur, either directly
to involve the tibial veins or indirectly through the soleal veins (14). Thrombosis can, in
theory, also extend from the deep veins to the superficial ones, but this has not been
evaluated (Fig. 1). Patients with STP should have their deep veins evaluated even if we
accept the lowest DVT prevalence of 5.6% reported (16).
Leon and Labropoulos114
https://t.me/med1917
Fifty-six patients with clinical evidence of STP underwent ascending venography
(AV), and evidence of DVT was found in nine. The prevalence of DVT in patients with
varicose veins was 44% in contrast with 2.6% in patients without them (p!0.01). The site
of STP did not influence the presence or absence of DVT. Another important finding was
that no patients with varicose veins developed a malignancy on follow-up whereas two
patients without varicosities did. Both patients had venographic evidence of DVT on
initial studies (11).
Deep
Recurrent events after a first episode of DVT are not uncommon and its risk persists
for many years. Three hundred fifty-five patients were followed after a first DVT and
a cumulative incidence of recurrent VTE of 17.5% after two years, 24.6% after five and
30.3% after eight years was found (17). This risk was significantly higher in patients with
cancer or hypercoagulable states compared to that associated with surgery or trauma (18).
After DVT, up to 79% of limbs may develop edema, pain, lipodermatosclerosis or
skin ulcers, condition known as the post-thrombotic syndrome (PTS), mostly due to vein
reflux. Persistent venous obstruction may also play a role but is seen less often. PTS was
found in 22%, 28% and 29% after two, five and eight years, respectively (17,19).
Ipsilateral recurrent DVT was strongly associated with its development (hazard ratioZ
6.4). Furthermore, the eight-year survival of this cohort was 70.2% indicating a substantial
mortality associated with this disease (17,19).
Untreated above-the-knee DVT has a 50% risk for PE and a 10% risk for fatal PE
(20,21). However, the optimum length of anticoagulation remains unknown. Traditionally,
patients are anticoagulated for three to six months. With time, re-canalization or collateral
development occurs and these translate into clinical improvement. Recanalization begins
within the first week from the acute episode and the thrombus load is significantly reduced
Figure 1 Normal popliteal and gastrocnemial veins. The popliteal vein is duplicated. All veins are
fully compressed and free of thrombus as seen on the right screen. The popliteal artery is non-
compressible under light compression and is the only vessel seen. The patient was a 60-year-old
female with right knee pain for the past 15 years, complaining of difficulty getting up and down the
stairs, as well as standing. She underwent an uneventful right total knee arthroplasty. Postoperatively,
the patient complained of right calf pain.
Diagnosis of Deep Vein Thrombosis 115
https://t.me/med1917
mostly in the first three months. About 56% of patients have complete thrombus resolution
as shown by Duplex ultrasound (DUS) (22). Thrombosis evolution after an acute event
appears to be a dynamic process with spontaneous lysis of the original thrombus and
further thrombosis occurring as competing processes (18). Thrombus remodeling in the
acute phase occurs in 44%. This includes, ascending, descending or bidirectional
propagation and lysis (23). DUS analysis of the affected veins can aid to individualize
management. Residual venous thrombosis is associated with a 2.4 hazard ratio (95%
CIZ1.3–4.4; pZ0.004) to develop recurrent DVT and these patients may need longer
anticoagulation (24).
Children
Acute DVT in children was found to be rare after studying 1997 patients !18 years old
hospitalized for O72 hours who had Rtwo risk factors for the development of DVT
(history of DVT or PE, recent surgery, immobilization, trauma, acute neurologic deficits,
cancer, sepsis, O150% ideal body weight, hypercoagulable states and the presence of
a femoral venous catheter) and had at least one screening duplex scan. Nineteen females
and forty males were enrolled. Over a nine-month follow up one patient developed DVT.
DVT prophylaxis and screening was deemed unnecessary in children with %two risk
factors for its development (25).
DIAGNOSIS
Ascending Venography
Ascending Venography is the accepted gold standard for the diagnosis of DVT. It is
routinely performed with venous contrast injection in the dorsum of the foot using a 21- or
22-gauge butterfly needle. Pedal, calf, thigh and pelvic veins are outlined. To enhance
detailed vision of the venous anatomy a direct popliteal or common femoral vein (CFV)
puncture can be done with subsequent passage of a catheter for selective injection of
contrast (Fig. 2).
An intraluminal filling defect is a definitive finding for acute DVT (26). Well-
developed collaterals, linear webs and synechiae within the veins also imply vein
occlusion but of an older age. Acute DVT can be overimposed showing as a more rounded
and larger filling defect. Non filling veins or abrupt termination of the contrast column are
considered by some to be an indirect sign of DVT. Others have debated that finding.
Bjorgell et al. (27) prospectively studied the occurrence of DVT in 100 consecutive
patients with isolated, non filling deep veins as seen on AV. Using DUS, they found that
about one-third of patients had DVT, a third of them had concomitant incidental findings
that explained the non filling and a third had no identifiable pathology. They can be due
to extrinsic or intrinsic pressure changes with abnormal flow patterns that may lead to
interpretation errors (26).
Reaction to iodinated contrast, postprocedural DVT (reported in 1.3–7% of cases)
(28,29) and skin necrosis from extravasation are among its most important compli-
cations (26). It also has limitations with regard to costs, patient’s discomfort and inability
to show other conditions that may explain the patient symptomatology. Its use is currently
restricted for equivocal cases after noninvasive testing, for catheter-directed thrombolysis
is considered, when thrombectomy is planned, or if the information is essential to consider
an intervention (26).
Leon and Labropoulos116
https://t.me/med1917
Duplex Ultrasound Examination
DUS has clear advantages over AV with respect to its noninvasive nature, portability,
lower cost, patient comfort, ability to image all the individual veins and tributaries, to
differentiate acute from chronic thrombi and it can be repeated as many times as needed.
Furthermore, it can detect other pathologies that may explain the patients’ symptoms and
potentially alter their management. Baker’s cysts, enlarged hematomas, lymph nodes,
musculoskeletal injuries, vascular anomalies, aneurysms and tumors are often
encountered. It became the method of choice for the diagnosis of DVT (30).
The excellent sensitivity and specificity of DUS for symptomatic proximal DVT is
well recognized. The results of several prospective studies including at least 40 patients in
their analysis are summarized in Table 1 (31–36). However, screening for asymptomatic
DVT in high-risk patients and in patients with isolated calf vein DVT is considered
unwarranted by some authors (37,38) due to a sensitivity of 62% (95% CIZ54%–70%),
a specificity of 97% (CIZ96%–98%), and a positive predictive value (PPV) of 66%
(CIZ58%–74%) fordetecting proximal thrombi. This does not reflect our experience. Such
results are due to inadequate experience and training in identifying non-occlusive thrombi
and those located in the calf veins. Furthermore, improved results have been possible,
mainly due to intensive training and to modern and better equipment. These results were
independent of thrombus size and were superior to AV in its identification (23,39,40).
DUS combines a Doppler mode that yields functional information about
spontaneous and phasic vein flow and about the function of the vein valves, and
a B-mode, that offers real-time anatomic information of the vein wall and lumen and can
visualize intraluminal thrombus.
Figure 2 Acute thrombosis of the common femoral vein and the saphenofemoral junction. Both
veins are distended, partially compressible and containing thrombus. The thrombus is echolucent
(dark), which indicates that it is fresh. The patient is a 79-year-old male with history of congestive
heart failure and mitral valve disease. He underwent cardiac catheterization five days prior to
admission through a right common femoral artery approach. He stated that the right groin was
slightly swollen after catheterization that worsened progressively. Doppler ultrasound of the right
lower extremity demonstrated a pseudoaneurysm of the right common femoral artery and DVT of
the right common femoral and iliac veins. Abbreviation: DVT, deep vein thrombosis.
Diagnosis of Deep Vein Thrombosis 117
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана