ARTICLE
Saphenous vein thrombophlebitis (SVT) is generally characterized by lack
of significant progression and quick resolution. In most cases it may
be treated effectively by means of external graduated compression and
non-steroidal anti-inflammatory therapy. If thrombophlebitis affects a
larger area and deeper veins show involvement, the guidelines of the German
Phlebological Society state that the patient must be treated with heparin
and concomitant oral anticoagulants. Conventional or low-weight heparin
is to be adminstered immediately in therapeutic doses [1]. The treatment
options have still not been compared with each other, and therefore still
have to be proven. Deep venous involvement and the risk of pulmonary embolism
have been reported much more frequently with SVT than commonly thought
[2-6].
Recently there has been an increase in reports of clinically and phlebographically
undiagnosed involvement of the saphenofemoral junction and of the deep
vein system, as technical improvements in duplex and colour-coded duplex
sonography now allow detailed examination of the extent of SVT [7]. There
remains controversy [3, 5, 8-10] regarding whether superficial and deep
vein thromboses can develop simultaneously at different sites, as well
as whether deep vein thromboses lead to involvement of the superficial
venous system [11]. In terms of the danger to the patient, the most clinically
important consequence of SVT is ascending progression into the deep venous
system through the saphenofemoral junction [12]. In 70% of these cases,
there is involvement of the femoral vein. When this occurs, free-floating
thrombi and the concomitant danger of embolisation into the lung are shown
to be common [4, 13-16]. Zollinger et al. reported an incidence
of pulmonary embolism in 10.1% of the patients they examined with femoral
thrombophlebitis [17]. Pacouret et al., however, did not observe
a higher risk for pulmonary embolism in their study of 95 patients [18].
The diagnosis of thrombophlebitis of large veins and the determination
of localization and proximal expansion of a thrombus is therefore of particular
importance in estimating the risk of embolism and subsequent choice of
treatment. Some believe that ascending phlebography is still a gold standard
or reference for diagnosing deep venous thromboses in the legs [19, 20].
Yet the proximal great saphenous vein and the saphenofemoral junction
are especially difficult to assess with this diagnostic technique with
multiple reports of false-negative findings [8, 15, 21-23]. Colour duplex
sonography features high levels of sensitivity and specificity, even in
depicting floating thrombi in the area of the saphenofemoral junction
[8, 24]. In this case report, we discuss a patient with a free-floating
thrombus in the left femoral vein to illustrate diagnostic pitfalls and
to discuss therapy of extension of thrombus from the great saphenous vein,
the so-called "collar button thrombosis".
Case report
History
A 73-year-old male presented with chronic venous insufficiency of the
left lower extremity which had been accompanied for one year by an increasing
sensation of heaviness and oedema. There was no known previous history
of thrombosis or thrombophlebitis. The patient had been wearing a thigh
high graduated compression stocking (30-40 mmHg) for three weeks with
improvement of symptoms. Just prior to the visit, the patient noted some
minor pain in the left chest without shortness of breath or coughing.
Family history was positive for deep venous thrombosis of the lower
extremities in the father. The patient did not take any medication on
a regular basis.
Physical examination
The patient measured 171 cm and 70 kg and was in a good state of general
health. An examination of the lower extremities revealed a dilated, partially
distended great saphenous vein on the left side, which was not sensitive
to pressure and had varicose lateral tributaries in the dorsal proximal
calf in the medial area of the knee. A tender, sinuous vein on the back
of the right thigh was visible all the way to the lateral side of the
right lower extremity. There was neither unilateral increase in size nor
oedema. The posterior and anterior tibial arteries were easily palpable
on both ankles. Blood pressure measured 155/90 mmHg on the right and 175/105
on the left; heart rate was 68 bpm.
Laboratory
All parameters were determined before any therapy began. Functional
protein S deficiency (35%, normal levels 60-140%) and decreased antithrombin
III levels (63.97%, normal levels: 75-125%) were detected. APC sensitivity
was low at 1.24 (normal levels: 1.8-2.13). The factor-V analysis showed
a heterozygous gene mutation on one allele. ESR measured 2/6. Other laboratory
values were in the normal range.
Diagnostic evaluation
Arterial Doppler: there was no evidence of peripheral arterial
occlusive disease.
Light reflection rheography: right borderline normal venous backflow
(23 s); evidence of abbreviated venous backflow time (T = 14 s) on the
left. No normalization could be obtained after administration of an occlusion
test (T = 19 s).
Venous occlusion plethysmography: venous capacity after a 3 min
interval on both sides was slightly increased at 5.1 ml/100 ml tissue.
Venous outflow was in normal ranges on both sides (r. 53 ml and l. 61
ml/100 ml tissue per min).
Colour duplex sonography of the veins of the lower extremities:
The right lower extremity showed a clinically normal superficial and
deep venous system.
A wide junctional valve was found on the left and shown to be incompetent
upon administration of the Valsalva pressure test. In the saphenofemoral
junction area of the great saphenous vein a mobile finger-like and largely
sonogenic structure was notable; it extended into the lumen of the femoral
vein and floated upon breathing (Figs.
1 and 2). The diameter
of the femoral vein at rest was 1.22 cm. The lumen was almost completely
displaced due to the structure (diameter 1.00 cm). In the deep femoral
and tibial veins distal compression yielded a good flow. A Valsalva test
showed no evidence of retrograde blood flow. The entire great saphenous
vein was non-compressible. The final interpretation was floating thrombus
into the left femoral vein with concomitant pre-existing ascending thrombophlebitis
of the great saphenous vein.
Electrocardiography: sinus rhythm at a rate of 68/min; indeterminate
axis. No cardiac conduction disorders or repolarisation disorders. No
evidence of dilation of right ventricle.
Treatment and course
Immediately after diagnosis, subcutaneous low-molecular-weight heparin
in therapeutic dosage (0.6 ml Nadroparin-Fraxiparin® s.c.
at 70 kg BW) was administered. The patient was transferred to hospital
on the same day to determine the further course of treatment (thrombectomy,
thrombolysis, anticoagulation). Once admitted, additional phlebography
and duplex sonography of the left lower extremity were performed. Ascending
phlebography revealed no obstruction in the entire deep venous system
(crural veins, popliteal vein, superficial femoral vein, deep femoral
vein, common femoral vein, external femoral vein, lower inferior vena
cava). However there was no evidence seen of newly developed or older
thrombotic material (Fig. 3A
and B). The conclusion was that the apparent filling defect in
the saphenofemoral junction area could be explained by an influx phenomenon
and did not correspond to a thrombus or to a floating thrombus. Duplex
sonography revealed a thickened vein wall with an older adherent thrombus
near the femoral vein with no evidence of floating thrombus.
Based on these findings, the patient was released without additional
therapy. A colour duplex sonographic follow-up exam was performed on the
next day in our surgery. This showed that the thrombus was unchanged in
its size and shape. The patient was re-admitted to hospital, where a thrombectomy
was indicated and then promptly performed. The intraoperative diagnosis
was a large floating and adherent, older thrombus extending from the great
saphenous vein into the femoral vein. Histology showed small passages
of a wall of a vein with foci of fibroses and macrophages (apparently
a developing thrombus) and segments of an older coagulation thrombus with
signs of organization. There was no evidence of malignancy. Post-operative
heparinisation with Fraxiparin (2 x 0.6 ml s.c. per day) occurred
for a three-month period as the patient rejected oral anticoagulant therapy.
Compression therapy was continued. A long-term anticoagulant therapy was
rejected by the patient in spite of extensive discussion of consent.
Discussion
Ascending thrombophlebitis of the great saphenous vein with extension
into the femoral vein greatly increases the risk of pulmonary embolism
[4, 5, 12-17, 25, 26]. Ascending contrast phlebography was introduced
by Bauer in 1940 to diagnose deep venous thromboses [27] and is still
considered by some as the reference standard for verifying or ruling out
the presence of thromboses [18, 19, 28, 29]. Limitations of phlebography
include failure to adequately visualize the deep femoral vein [30], verification
of thrombosis of the gastrocnemius and soleus veins [20, 23] and the need
for an experienced eye to distinguish between old and new thrombus [23].
Other drawbacks include risks of allergy to contrast medium, renal complications
[31], and puncture of the dorsal venous arch [28, 31].
Colour-coded high-resolution duplex sonography has numerous advantages
as a non-invasive procedure which allows simultaneous morphologic and
haemodynamic depictions of the superficial and deep vein system [8, 12,
14-16, 22, 24, 28, 31-34]. Compression sonography (B-mode compression
sonography) without colour-coded flow imaging and pulsed Doppler technique
makes it possible to differentiate between open and thrombotic vascular
lumen. Saphenofemoral junction areas, deep femoral veins and muscular
veins can be clearly shown with free-floating thrombus clearly distinguished
from adherent material. The newly developed power Doppler mode allows
visualization of very slow marginal or residual flow in thrombotic veins
with a mild compression manoeuvre [35]. The lowest detectable flow with
the power doppler technique is 0.5 mm/s (in vitro measurements)
[36]. Duplex allows non-invasive monitoring of clot progression and therapy
which can be repeated frequently if necessary.
The ability to diagnose by duplex ultrasound, however, is dependent
upon use of modern, high-resolution ultrasound equipment which makes exact,
clear images possible for optimal diagnosis. Examination results also
depend on the individual training and experience of the operator. A pulse
repetition frequency in the colour depiction that is too high brings about
an aliasing effect, or it images colours poorly or not at all in cases
of slow rates of blood flow [35]. Often it is difficult to show the course
of the tibial veins, especially in the case of overweight or oedematous
extremities.
In our case report, a floating thrombus in the region of the saphenofemoral
junction could not be confirmed in the hospital either by phlebography
or by duplex sonography. It is known that thromboses at the junction of
the great and small saphenous veins can not always be detected using phlebolography
[8, 15, 21-23, 32]. An inconsistent filling defect near the saphenofemoral
junction on the venogram was mistakenly interpreted as an influx phenomenon
of blood without contrast medium [23]. The colour duplex false-negative
findings were probably due to the fact that the non-occlusive thrombus
or floating thrombus appeared unchanged during the colour duplex exam
by breathing and modulation compression tests [35].
False-positive results are also possible when duplex sonography is used.
In a study by Kock et al., for example, even experienced angiologic
examiners with high-quality equipment could not intraoperatively confirm
11% of the cases of preoperatively diagnosed thrombi around the saphenofemoral
junctions [26]. Another study also found no intraoperative correlation
in 11% of the cases in which duplex sonography had previously "confirmed"
thromboses near the saphenofemoral junction (floating thrombus in the
femoral vein; up to the proximal saphenofemoral valve; or within the saphenofemoral
junction area). In six out of seven cases, however, free-floating thrombi
were correctly identified using colour duplex sonography [6], a fact which
reflects the high sensitivity and specificity of this method.
Verrel et al. suggested a four-stage classification of ascending
varicophlebitis so that therapeutic recommendations could be standardized
and categorized; its localization and extent would determine whether treatment
is to be performed with maintenance therapy or operation [37]. These statements,
however, are given as recommendations which still have to be proven.
A case of isolated thrombophlebitis in which the proximal end of the
thrombus is at a safe distance from the saphenofemoral junction is thus
to be treated with non-steroidal, anti-inflammatory therapy, subcutaneous
administration of heparin and compression therapy (type I). The therapy
of thrombophlebitis near the saphenofemoral junction includes the out-patient
subcutaneous administration of therapeutic dosages of low-molecular heparins
with concomitant high-resolution colour duplex sonographic monitoring.
If the proximal end of the thrombus reaches the beginning of the saphenofemoral
area, the therapy of choice is a saphenofemoral junction ligation and
saphenectomy (type II) [9, 37]. In the case of extension of the thrombus
into the deep venous system (type III) or the presence of floating thrombi,
a thrombectomy is also to be recommended [37] and/or oral anticoagulant
therapy for 2-6 months [9, 18, 37, 38]. Type IV according to Verrel et
al. describes the exceptional situation of a thrombus extended via
insufficient perforator veins and is predominantly treated with maintenance
therapy. Treatment is thus guided by the extent and location of thrombophlebitis.
This is best revealed by colour duplex sonography by trained operators.
CONCLUSION In
summary colour duplex sonography offers valuable information about the morphology
and haemodynamics of the deep and superficial venous systems, especially
the saphenofemoral junction. Phlebography may be misinterpreted in this
region. Due to the danger of pulmonary embolisms when benign thrombophlebitis
of the large veins extend into the deep venous system, (colour) duplex sonographic
monitoring on a regular basis is recommended, especially since the clinical
symptoms may be unreliable in comparison to the sonographically demonstrated
proximal extension of the thrombosis.
Article accepted on 14/4/01 REFERENCES
1. Korting HC, Callies R, Reusch M, Schlaeger M, Schöpf E,
Sterry Wl. (eds). Dermatologische Qualitätssicherung. Leitlinien
und Empfehlungen. 1st edn., München, Bern, Wien, New York: Zuckschwerdt,
2000: 156.
2. Bergquist D, Jaroszewski H. Deep vein thrombosis in patients
with superficial thrombophlebitis of the leg. Br Med J 1986; 292:
658-9.
3. Blätter W. Komplikationen der Thrombophlebitis superficialis.
Schweiz Med Wschr 1993; 123: 223-8.
4. Chengelis DL, Bendick PJ, Glover JL, Brown OW, Ranval TJ.
Progression of superficial venous thrombosis to deep vein thrombosis.
J Vasc Surg 1996; 24: 745-9.
5. Jorgensen JO, Hanel KC, Morgan JM, Hunt JM. The incidence
of deep venous thrombosis in patients with superficial thrombophlebitis
of the lower limbs. J Vasc Surg 1993; 18: 70-3.
6. Krause U, Kock HJ, Kröger K, Albrecht K, Rudofsky G.
Prevention of deep venous thrombosis associated with superficial thrombophlebitis
of the leg by early saphenous vein ligation. VASA 1998; 27: 34-8.
7. Becker F. Superficial venous thrombosis of the lower limbs.
Rev Prat 1996; 46: 1225-8.
8. Habscheid W. Stellenwert der Duplexsonographie in der Beinvenendiagnostik.
Dtsch Med Wschr 1998; 123: 1185-90.
9. Lohr JM, McDevitt DT, Lutter KS, Roedersheimer LR, Sampson
MG. Operative management of greater saphenous thrombophlebitis involving
the saphenofemoral junction. Am J Surg 1992; 164: 269-75.
10. Prountjos P, Bastounis E, Hadjinikolaou L, Felekuras E, Balas
P. Superficial venous thrombosis of the lower extremities co-existing
with deep venous thrombosis. A phlebographic study on 57 cases. Inter
Ang 1991; 10: 63-5.
11. Welger D, Müller JH. Assoziierte thrombotische Prozesse
des oberflächlichen, perforierenden und intramuskulären Venensystems
bei Patienten mit akuter Phlebothrombose der unteren Extremitäten.
Z Ges Inn Med Grenzgeb 1988; 43: 15-8.
12. Lutter KS, Kerr TM, Roedersheimer LR, Lohr JM, Sampson MG,
Cranley JJ. Superficial thrombophlebitis diagnosed by duplex scanning.
Surgery 1991; 110: 42-6.
13. Blumenberg RM, Barton E, Gelfand ML, Skudder P, Brennan J.
Occult deep venous thrombosis complicating superficial thrombophlebitis.
J Vasc Surg 1998; 27: 338-43.
14. Pulliam CW, Barr SL, Ewing AB. Venous duplex scanning in
the diagnosis and treatment of progressive superficial thrombophlebitis.
Ann Vasc Surg 1991; 5: 190-5.
15. Schonhofer B, Bechtold H, Renner R, Bundschu HD. Sonographische
Befunde bei Varikophlebitis der Vena saphena magna. Dokumentation von
Thrombuswachstum und -ablösung mit asymptomatischer Lungenembolie.
Dtsch Med Wschr 1992; 117: 51-5.
16. Yucel EK, Egglin TK, Waltman AC. Extension of saphenous thrombophlebitis
into the femoral vein: demonstration by color flow compression sonography.
J Ultrasound Med 1992; 11: 285-7.
17. Zollinger RW, Williams RD, Briggs DO. Problems in the diagnosis
and treatment of thrombophlebitis. Arch Surg 1962; 85: 18-22.
18. Pacouret G, Alison D, Pottier JM, Bertrand P, Charbonnier
B. Free-floating thrombus and embolic risk in patients with angiographically
confirmed proximal deep venous thrombosis. A prospective study. Arch
Intern Med 1997; 157: 305-8.
19. Lensing AWA, Büller HR, Prandoni P, Batchelor D, Molenaar
AHM, Cogo A, Vigo M, Huisman PM, Wouter ten Cate J. Contrast venography,
the gold standard for the diagnosis of deep vein thrombosis: improvement
in observer agreement. Thromb Haemost 1992; 76: 8-12.
20. Hach W, Hach-Wunderle V. Der Stellenwert von Phlebographie
und Duplex-Sonographie für die Diagnostik der tiefen Bein- und Beckenvenenthrombose.
Gefässchirurgie 1998; 3: 235-41.
21. Barrellier MT, Jouen E, Creveuil C. Discrepancies between
the results of phlebography and Doppler ultrasonography in the diagnosis
of asymptotic venous thrombosis after total hip prostesis. False negatives
of phlebography or false positives of Doppler ultrasonography. J Mal
Vasc 1998; 23: 183-90.
22. Krings W, Adolph J, Diederich S, Urhahne S, Vassalllo P,
Peters PE. Diagnostik der tiefen Bein und Beckenvenenthrombose mit hochauflösender
real-time und CW-Dopplersonographie. Treffsicherheit und Grenzen. Radiologie
1990; 30: 525-31.
23. Weber J, May R: In: Funktionelle Phlebologie. Stuttgart-New
York: Thieme, 1990: 398-410.
24. Labropoulus N, Leon M, Kalodiki E, al Kutoubi A, Chan P,
Nicolaides AN. Colour flow duplex scanning in suspected acute deep vein
thrombosis; experience with routine use. Eur J Vasc Endovasc Surg
1995; 9: 49-52.
25. Hafner CD, Cranley JJ, Krause RJ, Strasser ES. A method of
managing superficial thrombophlebitis. Surgery 1964; 55: 201-6.
26. Kock HJ, Krause U, Albrecht KH, van der Laan E, Rudofky G,
Eigler FW. Die Crossektomie bei aszendierender oberflächlicher Thrombophlebitis
der Beinvenen. Zentralbl Chir 1997; 122: 795-800.
27. Bauer G. A venographic study of thromboembolic problems.
Acta Chir Scand 1940; 84 (suppl. 161): 1-7.
28. Baxter GM, McKechnie S, Duffy P. Colour doppler ultrasound
in deep venous thrombosis: a comparison with venography. Clinical Radiology
1990; 42: 32-6.
29. Hach W, Hach-Wunderle V. Chirurgische und konservative Behandlung
einer transfaszial progredierenden Varikophlebitis der Stammvenen und
der Perforansvenen. Gefässchirurgie 1996; 1: 172-6.
30. Habscheid W. Die isolierte Thrombose der Vena profunda femoris
als Emboliequelle. Dtsch Med Wschr 1999; 124: 793-6.
31. Beuchel G, Stadler R. Wertigkeit farbkodierter Duplexsonographie
in der Diagnostik der epifaszialen Beinvenen. Z Hautkr 1994; 69:
227-32.
32. Appel J, Taute BM, Seifert H, Podhaisky H. Duplexsonographische
Aspekte der postoperativen Thrombosediagnostik. Vasomed 1998; 10:
348-52.
33. Becker D, Gunter E, Strauss R, Cidlinsky K, Tomandl B, Kalden-Nemeth
D, Neureiter D, Lang W, Hahn EG. Color Doppler imaging versus phlebography
in the diagnosis of deep leg and pelvic vein thrombosis. J Ultrasound
Med 1997; 16: 31-7.
34. Wells PS, Hirsh J, Anderson DR, Lensing AW, Foster G, Kearon
C, Weitz J, D´Ovidio R, Cogo A, Prandoni P. Accuracy of clinical
assessment of deep-vein thrombosis. Lancet 1995; 345: 1326-30.
35. Karasch T. Fallstricke der farbkodierten Duplexsonographie.
VASA 1998; 53 (suppl.): 27-33.
36. Sohn C, Weskott HP. The sensitivity of new color systems
in blood-flow diagnosis. The maximum entropy method and angio-color-comparative
in vitro flow measurements to determine sensitivity. Surg Endosc
1997; 11: 1040-4.
37. Verrel F, Steckmeier B, Parzhuber A, Spengel FA, Rauh G,
Reininger CB. Die aszendierende Varikophlebitis. Klassifikation und Therapie.
Gefässchirurgie 1999; 4: 13-9.
38. Ascer E, Lorensen E, Pollina RM, Gennaro M. Preliminary results
of a nonoperative approach to saphenofemoral junction thrombophlebitis.
J Vasc Surg 1995; 22: 616-21.
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