compression devices postoperatively, and the use of LMWH or IV heparin in the postoperative period.
Some use closed suction drainage of wounds to avoid hematoma and seroma formation. Warfarin should
have an initial target INR range of 2.0 to 2.5 for the first 6 weeks and some would advocate a
subsequent decrease to 1.7 to 2.0 until 4 months when it is discontinued. Adjustments are made to
accommodate those with an increased risk of thrombosis. One suggested that long-term regimen is
“minidose” warfarin, which utilizes daily doses of 1 to 2.5 mg to prevent thrombosis.180,389 Although
many surgeons encourage the use of compressive support, patients often do not comply but still have
acceptable clinical results.182,183
Valve repair procedures are well tolerated by most patients and have a low morbidity, as well as
essentially zero mortality in most series.154 Hematoma and seroma formation are noted in less than 15%
of cases, depending on the level of anticoagulation used.182,378,390–392 DVT occurs in less than 10% of
cases in most series and even if higher is not associated with clinical sequelae, while the pulmonary
emboli risk is well less than 1%.180–182,378,390–392 Wound infections have been seen in 2% to 7% of
cases.180,182,378,392
Kistner et al. reported long-term follow-up of internal valvuloplasty spans over decades and is
reported in life-table format (Fig. 98-4). Valve competency is 60% to 70% at 5 years in most
series.181–183,229,375,377,393–398 In general, a patent and competent valve translates into clinical
improvement and a healed ulcer, while the reverse is true with recurrent reflux. This is true for all types
of single station venous valvular reconstructions.
External valvuloplasty without direct cusp repair (isolated wall diameter reduction) appears to
perform less well in all aspects than open valvuloplasty.229,392 However, the “transcommissural”
technique that does directly repair the slack valve cusps performs much like open valvuloplasty with a
competency rate of more than 60% at 3 years and >70% ulcer free rate up to 5 years.382 External
banding performs adequately in select cases or as adjunctive procedures during other venous valve
surgery.229,383,384
Valve transposition demonstrates clinical improvement in 50% to 60% of patients after 3 to 5 years of
follow-up.154,181,182,388–391,393–397 The valve competency rate varies from 30% to 80% and is reflected in
the clinical improvement noted.154,181,182,388–391,393–397
Figure 98-4. Life-table demonstrates the cumulative clinical success rate based on type of valve reconstruction procedure. The
valve repair operation is valvuloplasty as performed by Kistner and associates via the Kistner technique. “Other operations” refer to
valve transpositions (n = 14), superficial femoral vein valve transplantations (n = 2), and combined valve repair and transposition
procedures (n = 3). Numbers in parentheses indicate the number of valve repairs remaining in the study at that time point.
Significant difference exists between valve repair and other operations. (After Masuda EM, Kistner RL. Long-term results of venous
valve reconstruction: a four to twenty-one year follow-up. J Vasc Surg 1994;19:391.)
Valve transplantation is undertaken in the most complex and difficult conditions. Clinical
improvement is seen in about 50% of patients even at 8 years of follow-up, and it remains a good
option in cases where other techniques are not possible.153,154,379 There does not appear to be a
difference between reported competency rates or clinical results when considering the location of valve
repair (femoral vs. popliteal), but overall the competency rates reported are inferior to internal
valvuloplasty.376,385,397,399–404 There are data to support that contention that repairing multiple valves in
the same axial system translates into longer clinical benefit, but this approach does, of course, add risks
at the initial operative intervention.382,383,392,405
In general, patients with postthrombotic reflux tend to have more problems maintaining healed ulcers
than those with a primary etiology of reflux, as noted from the results of internal valvuloplasty
(generally a primary etiology) versus those requiring transplantation or a transposition operative
2820
approach.182 Review of pertinent data has resulted in guidelines to reference when treating patients
with C4b
, C5, and C6 disease.276 It is suggested that in such patients with structurally preserved deep
venous valves, individual valve repair can be offered (grade 2C). If no structurally intact exists, then
valve transposition or transplantation is suggested treatment (grade 2C).
Valve Substitutes
Autogenous tissues appear to be the only material that currently can act as a substitute valve with some
hope of success in the clinical arena. Using donor vein, after trimming adventitia and part of the media,
to fashion semilunar cusps within the deficient recipient vein, Raju and Hardy180 have reported
acceptable clinical results. Another approach invaginates a stump of the long saphenous vein into the
femoral vein to fashion a bicuspid valve, 19 of 20 reconstructions were patent and competent at a mean
of 10 months with one valve demonstrating reflux.406 No other series have reproduced these findings to
date. The newest innovation has been to use an ophthalmic knife or other fine tool to dissect the
intima/media wall of the thickened postthrombotic vein wall into one or two sheets and thereby fashion
the valve cusp(s).407 This technique has been reproduced by another investigator.408 A recent
improvement has been to place two sutures on the cusp(s) to hold the valve in the semiopen position
and thereby to prevent valve collapse and improve neovalve competence. The results with this
modification include 21 operations (mean follow-up 11 months) with all valves competent, a 95% ulcer
healing rate and two recurrences (9.5%).409 In this highly select group of patients, the SVS/AVF
Guidelines Committee suggests consideration of autogenous valve substitutes in addition to standard
compression therapy to aid in venous ulcer healing and recurrence prevention (grade 2C).276
Venous Ulcer Wound Care
The quest to heal venous ulcers has generated a myriad of potential topical agents to aid in ulcer
healing. Topical antibiotics and dressings containing antimicrobials may retard wound healing and cause
allergic reactions and are not recommended for the treatment of venous ulcers.276,410 Growth factors
and cytokines in addition to compression when provided as isolated topically applied agents have not
demonstrated efficacy when compared to placebo. Review of the literature demonstrates inconsistent
results or studies with insufficient data to determine with any certainty the efficacy of such
adjuvants.411,412 A number of topical dressings applied on the ulcer bed and beneath the compression
dressing have been investigated to determine if ulcer healing could be improved. Hydrocolloids (e.g.,
DuoDerm), foams (e.g., Allevyn), alginates (e.g., Sorbsan), hydrogels (e.g., Intrasite Gel, or Debrican),
and others (e.g., Opsite) have been studied. Insufficient data is available to make firm conclusions, but
it is clear that the nature and amount of the exudates present may provide a rationale for the benefit of
one or the other of these dressings in a given patient.413–415 The SVS/AVF 33.Guidelines Committee
suggests that the wound dressing be selected, which absorbs wound exudates and protects the periulcer
skin from damage (grade 2B).276
Surgical debridement to healthy tissue, when required, benefits the rate of ulcer healing and does not
lead to a higher risk of systemic infection.410,416–418 It is especially beneficial when evaluated as
adjuvant care to the standard methods of venous ulcer wound care.414,419 The use of local anesthetic
during debridement of venous leg ulcers has been found statistically beneficial in lowering pain scores
in a Cochrane analysis of six trials.420 This and other pertinent data are the basis of recent guidelines for
optimal patient care.276 Surgical debridement is recommended to remove slough, nonviable tissue and
eschar (grade 1B) using local anesthesia to minimize discomfort (grade 1B).
Hydrosurgical, enzymatic, and larval therapy are effective methods of venous ulcer debridement, but
none have been found more effective than surgical debridement and can be more expensive. Current
guidelines suggest each as a potential alternative to surgical debridement when a trained practitioner is
not available to provide surgical debridement (grade 2B/C).276
For resistant venous ulcers, defined as those that fail to demonstrate improvement in a minimum of 4
to 6 weeks of standard wound therapy, adjuvant wound therapy options should be considered.276,421
These ulcers can be extensive, and skin grafting allows for coverage of raw surfaces to speed the healing
process. Once the ulcer has a clean base of granulation tissue, a split-thickness skin graft can be applied.
There are reports on improved healing with skin grafting for chronic venous ulceration.422 Skin grafting
is generally considered only when ulcer healing has not occurred following diligent conservative
management.423 An alternative or precursor to an autologous skin graft may be one of a variety of skin
substitutes. A number of skin substitutes have been used to aid in venous ulcer healing (e.g., fresh
allografts, porcine dermis) but for most there are insufficient data available to determine whether
2821
venous ulcer healing is improved.424 However, the biologically active bilayered human skin equivalent
with an allogenic epidermal and dermal layer has demonstrated more promise and statistically
improved the time to complete healing.414,424,425 Porcine small intestine submucosa (SIS) is primarily a
collagen-based extracellular matrix with retained biologically active components. In a study of SIS and
when adjusted for ulcer size, SIS was three times as likely to heal as the control group (P = 0.007) and
at 6 months there was no recurrence in the SIS group.419 This manuscript was included in a review of
the literature as an RCT demonstrating significance when used to heal venous ulcers.414 The use of these
skin substitutes is suggested as guideline adjuvant therapy in recalcitrant venous ulcer care (grade 2
A/B).276
The Pelvic Congestion Syndrome
This distressing clinical condition can result from gonadal vein and/or hypogastric vein reflux. Pelvic
pain is a constant complaint and can be disabiling. Gonadal vein reflux may be best managed with
gonadal vein excision due to its many areas of potential reflux, but an endovascular approach using
coils, sclerosants, or a combination can also be successful and is the most common approach
currently.426 Hypogastric vein reflux may be best managed by percutaneous embolization.427 When the
elimination of proximal reflux does not resolve superficial varicosities, the management involves
techniques used for saphenous vein branch varicosities.
2822
References
1. Heit JA. The epidemiology of venous thromboembolism in the community. Arterioscler Thromb Vasc
Biol 2008;28:370–372.
2. Bauer KA, Rosendaal FR, Heit JA. Hypercoagulability: too many tests, too much conflicting data.
Hematology (Am Soc Hematol Educ Program) 2002:353–368.
3. Henke PK, Schmaier A, Wakefield TW. Thrombosis Due to Hypercoagulable States Chapter 34. Elsevier
Saunders; 2005.
4. Goldhaber SZ, Tapson VF. A prospective registry of 5,451 patients with ultrasound-confirmed deep
vein thrombosis. Am J Cardiol 2004;93:259–262.
5. Thomas S, Goodacre S, Sampson F, Van Beek E. Diagnostic value of CT for deep vein thrombosis:
results of a systematic review and meta-analysis. Clin Radiol 2008;63:299–304.
6. Theodorou SJ, Theodorou DJ, Kakitsubata Y. Sonography and venography of the lower extremities
for diagnosing deep vein thrombosis in symptomatic patients. Clin Imag 2003;27:180–183.
7. Goodman LR, Stein PD, Matta F, et al. CT venography and compression sonography are
diagnostically equivalent: data from pioped II. Am J Roentgenol 2007;189:1071–1076.
8. Kearon C, Ginsberg JS, Kovacs MJ, et al. Comparison of low-intensity warfarin therapy with
conventional-intensity warfarin therapy for long-term prevention of recurrent venous
thromboembolism. N Engl J Med 2003; 349:631–639.
9. Cornuz J, Ghali WA, Hayoz D, et al. Clinical prediction of deep venous thrombosis using two risk
assessment methods in combination with rapid quantitative D-dimer testing. Am J Med
2002;112:198–203.
10. Vandy FC, Stabler C, Eliassen AM, et al. Soluble P-selectin for the diagnosis of lower extremity
deep venous thrombosis. J Vasc Surg Venous Lymphat Disord 2013;1:117–125.
11. Johnson SA, Stevens SM, Woller SC, et al. Risk of deep vein thrombosis following a single negative
whole-leg compression ultrasound. JAMA 2010;303:438–445.
12. Schellong SM, Schwarz T, Halbritter K, et al. Complete compression ultrasonography of the leg
veins as a single test for the diagnosis of deep vein thrombosis a prospective clinical outcome study.
Thromb Haemost 2003;89:228–234.
13. Decousus H, Quéré I, Presles E, et al. Superficial venous thrombosis and venous thromboembolism:
a large, prospective epidemiologic study. Ann Int Med 2010;152:218–224.
14. Decousus H, Prandoni P, Mismetti P, et al. Fondaparinux for the treatment of superficial-vein
thrombosis in the legs. N Engl J Med 2010;363:1222–1232.
15. Wells PS, Ginsberg JS, Anderson DR, et al. Use of a clinical model for safe management of patients
with suspected pulmonary embolism. Ann Intern Med 1998;129:997–1005.
16. Wells P, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients
probability of pulmonary embolism: increasing the models utility with the simpliRED D-dimer.
Thrombo Heamost 2000;83:416–420.
17. Wicki J, Perrier A, Perneger TV, et al. Predicting adverse outcome in patients with acute
pulmonary embolism: A risk score. Thromb Haemost 2000;84:548–552.
18. van Belle A, Buller HR, Huisman MV, et al. Effectiveness of managing suspected pulmonary
embolism using an algorithm combining clinical probability, D-dimer testing, and computed
tomography. JAMA 2006; 295:172–179.
19. Hunt JM, Bull TM. Clinical review of pulmonary embolism: diagnosis, prognosis, and treatment.
Med Clin North Am 2011;95:1203–1222.
20. Stein PD, Terrin ML, Gottschalk A, et al. Value of the ventilation/perfusion scan in acute pulmonary
embolism. Results of the prospective investigation of pulmonary embolism diagnosis (pioped). The
pioped investigators. JAMA 1990;263:2753–2759.
21. Worsley DF, Alavi A. Comprehensive analysis of the results of the pioped study. Prospective
investigation of pulmonary embolism diagnosis study. J Nucl Med 1995;36:2380–2387.
22. Henzler T, Schoenberg SO, Schoepf UJ, et al. Diagnosing acute pulmonary embolism: systematic
review of evidence base and cost-effectiveness of imaging tests. J Thorac Imag 2012;27:304–314.
2823
23. Stein PD, Chenevert TL, Fowler SE, et al. Gadolinium-enhanced magnetic resonance angiography
for pulmonary embolisma multicenter prospective study (pioped iii). Ann Int Med 2010;152:434–
443.
24. Wilbur J, Shian B. Diagnosis of deep venous thrombosis and pulmonary embolism. Am Fam
Physician 2012;86:913–919.
25. Prandoni P, Bernardi E. Upper extremity deep vein thrombosis. Curr Opin Pulm Med 1999;5:222–
226.
26. Hull RD, Raskob GE, Brant RF, et al. Relation between the time to achieve the lower limit of the
APTT therapeutic range and recurrent venous thromboembolism during heparin treatment for deep
vein thrombosis. Arch Intern Med 1997;157:2562–2568.
27. Prandoni P, Lensing AW, Cogo A, et al. The long-term clinical course of acute deep venous
thrombosis. Ann Intern Med 1996;125:1–7.
28. Bates SM, Ginsberg JS. Treatment of deep-vein thrombosis. N Engl J Med 2004;351:268–277.
29. Ageno W, Turpie A. Low-molecular-weight heparin in the treatment of pulmonary embolism. Semin
Vasc Surg 2000;13:189–193.
30. van Dongen CJ, van den Belt AG, Prins MH, Lensing AW. Fixed dose subcutaneous low molecular
weight heparins versus adjusted dose unfractionated heparin for venous thromboembolism. The
Cochrane Library. 2004;(4):CD001100.
31. Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: antithrombotic
therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based
clinical practice guidelines. Chest 2012;142(6):1698–1704.
32. Palareti G, Cosmi B, Legnani C, et al. D-Dimer testing to determine the duration of anticoagulation
therapy. N Engl J Med 2006;355:1780–1789.
33. Ridker PM, Goldhaber SZ, Danielson E, et al. Long-term, low-intensity warfarin therapy for the
prevention of recurrent venous thromboembolism. N Engl J Med 2003;348:1425–1434.
34. Cosmi B, Legnani C, Cini M, et al. D-Dimer levels in combination with residual venous obstruction
and the risk of recurrence after anticoagulation withdrawal for a first idiopathic deep vein
thrombosis. Thromb Haemost 2005;94:969–974.
35. Hull RD, Marder VJ, Mah AF, et al. Quantitative assessment of thrombus burden predicts the
outcome of treatment for venous thrombosis: a systematic review. Am J Med 2005;118:456–464.
36. Kearon C. Natural history of venous thromboembolism. Circulation 2003;107:I22–130.
37. Prandoni P, Lensing AW, Prins MH, et al. Residual venous thrombosis as a predictive factor of
recurrent venous thromboembolism. Ann Intern Med 2002;137:955–960.
38. Kearon C, Akl EA. Duration of anticoagulant therapy for deep vein thrombosis and pulmonary
embolism. Blood. 2014;123(12):1794–1801.
39. Linkins L-A, Choi PT, Douketis JD. Clinical impact of bleeding in patients taking oral anticoagulant
therapy for venous thromboembolism a meta-analysis. Ann Intern Med 2003;139:893–900.
40. Almeida JI, Coats R, Liem TK, et al. Reduced morbidity and mortality rates of the heparin-induced
thrombocytopenia syndrome. J Vasc Surg 1998;27:309–314; discussion 315–306.
41. Greinacher A, Michels I, Mueller-Eckhardt C. Heparin-associated thrombocytopenia: the antibody is
not heparin specific. Thromb Haemost 1992; 67:545–549.
42. Alving BM. How I treat heparin-induced thrombocytopenia and thrombosis. Blood 2003;101:31–37.
43. Baldwin ZK, Spitzer AL, Ng VL, et al. Contemporary standards for the diagnosis and treatment of
heparin-induced thrombocytopenia (HIT). Surgery 2008;143:305–312.
44. Guyatt G, Akl E, Crowther M, et al; American College of Chest Physicians Antithrombotic Therapy
and Prevention of Thrombosis Panel. Executive summary: antithrombotic therapy and prevention of
thrombosis: American College of Chest Physicians evidence-based clinical practice guidelines. Chest
2012;141:7S–47S.
45. van dongen CJ, Mac Gillavry MR. Once versus twice daily LMWH for the initial treatment of
venous thromboembolism. Cochrane Database Syst Rev 2005. doi:
10.1002/14651858.CD003074.pub2
46. Merli G, Spiro TE, Olsson C-G, et al. Subcutaneous enoxaparin once or twice daily compared with
intravenous unfractionated heparin for treatment of venous thromboembolic disease. Ann Intern
2824
Med 2001;134: 191–202.
47. Lee AY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus a Coumadin for the
prevention of recurrent venous thromboembolism in patients with cancer. N Engl J Med
2003;349:146–153.
48. Bergqvist D, Agnelli G, Cohen AT, et al. Duration of prophylaxis against venous thromboembolism
with enoxaparin after surgery for cancer. N Engl J Med 2002;346:975–980.
49. Turpie AG, Bauer KA, Eriksson BI, et al. Fondaparinux vs enoxaparin for the prevention of venous
thromboembolism in major orthopedic surgery: a meta-analysis of 4 randomized double-blind
studies. Arch Intern Med 2002;162:1833–1840.
50. Wolozinsky M, Yavin YY, Cohen AT. Pharmacological prevention of venous thromboembolism in
medical patients at risk. Am J Cardiovasc Drugs 2005;5:409–415.
51. Agnelli G, Bergqvist D, Cohen AT, et al. Randomized clinical trial of postoperative fondaparinux
versus perioperative dalteparin for prevention of venous thromboembolism in high-risk abdominal
surgery. Br J Surg 2005;92:1212–1220.
52. Eriksson BI, Lassen MR. Duration of prophylaxis against venous thromboembolism with
fondaparinux after hip fracture surgery: a multicenter, randomized, placebo-controlled, doubleblind study. Arch Intern Med 2003;163:1337–1342.
53. Buller HR, Davidson BL, Decousus H, et al. Fondaparinux or enoxaparin for the initial treatment of
symptomatic deep venous thrombosis: a randomized trial. Ann Intern Med 2004;140:867–873.
54. Buller HR, Davidson BL, Decousus H, et al. Subcutaneous fondaparinux versus intravenous
unfractionated heparin in the initial treatment of pulmonary embolism. N Engl J Med
2003;349:1695–1702.
55. Schulman S, Kearon C, Kakkar AK, et al. Dabigatran versus warfarin in the treatment of acute
venous thromboembolism. N Engl J Med 2009;361:2342–2352.
56. Schulman S, Kearon C, Kakkar AK, et al. Extended use of dabigatran, warfarin, or placebo in venous
thromboembolism. N Engl J Med 2013;368:709–718.
57. Bauersachs R, Berkowitz SD, Brenner B, et al; EINSTEIN Investigators. Oral rivaroxaban for
symptomatic venous thromboembolism. N Engl J Med 2010;363:2499–2510.
58. Bailey AL. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism. N Engl J Med
2012;366:1287–1297.
59. Agnelli G, Buller HR, Cohen A, et al. Oral apixaban for the treatment of acute venous
thromboembolism. N Engl J Med 2013;369:799–808.
60. Agnelli G, Buller HR, Cohen A, et al. Apixaban for extended treatment of venous thromboembolism.
N Engl J Med 2013;368:699–708.
61. Büller HR, Décousus H, Grosso MA, et al. Edoxaban versus warfarin for the treatment of
symptomatic venous thromboembolism. N Engl J Med 2013;369:1406–1415.
62. Knepper J, Horne D, Obi A, et al. A systematic update on the state of novel anticoagulants and a
primer on reversal and bridging. J Vasc Surg Venous Lymphat Disord 2013;1:418–426.
63. Kolbach D, Sandbrink MW, Hamulyak K, et al. Non-pharmaceutical measures for prevention of
post-thrombotic syndrome. Cochrane Database Syst Rev. 2004;(1):CD004174.
64. Kahn SR, Shapiro S, Wells PS, et al. Compression stockings to prevent post-thrombotic syndrome: a
randomised placebo-controlled trial. Lancet 2014;383(9920):880–888.
65. Aschwanden M, Labs KH, Engel H, et al. Acute deep vein thrombosis: early mobilization does not
increase the frequency of pulmonary embolism. Thromb Haemost 2001;85:42–46.
66. Partsch H. Ambulation and compression after deep vein thrombosis: dispelling myths. Semin Vasc
Surg 2005;18:148–152.
67. Greenfield LJ, Proctor MC. Twenty-year clinical experience with the greenfield filter. Cardiovasc
Surg 1995;3:199–205.
68. Usoh F, Hingorani A, Ascher E, et al. Prospective randomized study comparing the clinical
outcomes between inferior vena cava greenfield and trapease filters. J Vasc Surg 2010;52:394–399.
69. Berry RE, George JE, Shaver WA. Free-floating deep venous thrombosis. A retrospective analysis.
Ann Surg 1990;211:719–712; discussion 712–713.
70. Langan EM III Miller RS, Casey WJ III, et al. Prophylactic inferior vena cava filters in trauma
2825
patients at high risk: follow-up examination and risk/benefit assessment. J Vasc Surg 1999;30:484–
488.
71. Sugerman HJ, Sugerman EL, Wolfe L, et al. Risks and benefits of gastric bypass in morbidly obese
patients with severe venous stasis disease. Ann Surg 2001;234:41–46.
72. Chiou AC. Beside placement of IVC filters. Endovasc Today 2005;4: 60–63.
73. Kearon C, Kahn SR, Agnelli G, et al. Antithrombotic therapy for venous thromboembolic disease:
American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest
2008;133: 454S–545S.
74. Decousus H, Leizorovicz A, Parent F, et al. A clinical trial of vena caval filters in the prevention of
pulmonary embolism in patients with proximal deep-vein thrombosis [Prevention du risque
d’embolie pulmonaire par interruption cave study group]. N Engl J Med 1998;338:409–415.
75. Meissner MH, Manzo RA, Bergelin RO, et al. Deep venous insufficiency: the relationship between
lysis and subsequent reflux. J Vasc Surg 1993;18:596–605; discussion 606–608.
76. Semba CP, Dake MD. Iliofemoral deep venous thrombosis: aggressive therapy with catheterdirected thrombolysis. Radiology 1994;191: 487–494.
77. Mewissen MW, Seabrook GR, Meissner MH, et al. Catheter-directed thrombolysis for lower
extremity deep venous thrombosis: report of a national multicenter registry. Radiology
1999;211:39–49.
78. Elsharawy M, Elzayat E. Early results of thrombolysis vs anticoagulation in iliofemoral venous
thrombosis. A randomised clinical trial. Eur J Vasc Endovasc Surg 2002;24:209–214.
79. Enden T, Haig Y, Kl⊘w NE, et al; CaVenT Study Group. Long-term outcome after additional
catheter-directed thrombolysis versus standard treatment for acute iliofemoral deep vein
thrombosis (the caVenT study): a randomised controlled trial. Lancet 2012;379:31–38.
80. Baekgaard N, Broholm R, Just S, et al. Long-term results using catheter-directed thrombolysis in
103 lower limbs with acute iliofemoral venous thrombosis. Eur J Vasc Endovasc Surg 2010;39:112–
117.
81. Comerota AJ, Grewal N, Martinez JT, et al. Postthrombotic morbidity correlates with residual
thrombus following catheter-directed thrombolysis for iliofemoral deep vein thrombosis. J Vasc
Surg 2012;55:768–773.
82. Raju S. Critical issues in ulcer prevention in postthrombotic disease. J Vasc Surg 2010;52:67S–69S.
83. Turpie AG. Thrombolytic agents in venous thrombosis. J Vasc Surg 1990; 12:196–197.
84. Goldhaber SZ. Pulmonary embolism. Lancet 2004;363:1295–1305.
85. Sharma GV, Folland ED, McIntyre KM, et al. Long-term benefit of thrombolytic therapy in patients
with pulmonary embolism. Vasc Med 2000;5: 91–95.
86. Goldhaber SZ, Haire WD, Feldstein ML, et al. Alteplase versus heparin in acute pulmonary
embolism: randomised trial assessing right-ventricular function and pulmonary perfusion. Lancet
1993;341:507–511.
87. Jerjes-Sanchez C, Ramirez-Rivera A, Arriaga-Nava R, et al. High dose and short-term streptokinase
infusion in patients with pulmonary embolism: prospective with seven-year follow-up trial. J
Thromb Thrombolysis. 2001;12:237–247.
88. Konstantinides S, Geibel A, Olschewski M, et al. Association between thrombolytic treatment and
the prognosis of hemodynamically stable patients with major pulmonary embolism: results of a
multicenter registry. Circulation 1997;96:882–888.
89. Eid-Lidt G, Gaspar J, Sandoval J, et al. Combined clot fragmentation and aspiration in patients with
acute pulmonary embolism. Chest 2008;134: 54–60.
90. Eklof B, Kistner RL. Is there a role for thrombectomy in iliofemoral venous thrombosis? Semin Vasc
Surg 1996;9:34–45.
91. Juhan CM, Alimi YS, Barthelemy PJ, et al. Late results of iliofemoral venous thrombectomy. J Vasc
Surg 1997;25:417–422.
92. Meneveau N, Seronde MF, Blonde MC, et al. Management of unsuccessful thrombolysis in acute
massive pulmonary embolism. Chest 2006;129: 1043–1050.
93. Lutter KS, Kerr TM, Roedersheimer LR, et al. Superficial thrombophlebitis diagnosed by duplex
scanning. Surgery 1991;110:42–46.
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