Добавил:
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_3656_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
30.08.2026
Размер:
49 Мб
Скачать
340 Indications, techniques, and results of inferior vena cava filters
https://t.me/med1917
10. Hirsh J. Oral anticoagulant drugs. N Engl J Med 1991;324(26):1865–75.
11. Harrington R and Ansell J. Risk–benefit assessment of anticoagulant therapy. Drug Saf 1991;6(1):54– 69.
12. Schmitt BP and Adelman B. Heparin-associated
thrombocytopenia: A critical review and pooled analysis. Am J Med Sci 1993;305(4):208–15.
13. Landefeld CS and Beyth RJ. Anticoagulant-related bleeding: Clinical epidemiology, prediction, and prevention. Am J Med 1993;95(3):315–28.
14. Eby CS. Warfarin-induced skin necrosis. Hematol Oncol Clin North Am 1993;7(6):1291–300.
15. Hull RD, Raskob GE, Rosenbloom D etal. Optimal therapeutic level of heparin therapy in patients with venous thrombosis. Arch Intern Med 1992;152(8):1589–95.
16. Hull RD, Raskob GE, Brant RF, Pineo GF, and Valentine KA. The importance of initial heparin treatment on long-term clinical outcomes of anti­thrombotic therapy. The emerging theme of delayed recurrence. Arch Intern Med 1992;152(8):2317–21.
17. Falanga A and Donati MB. Pathogenesis of throm­bosis in patients with malignancy. Int J Hematol 2001;73(2):137–44.
 ◆
18. Pasquale M and Fabian TC. Practice management guidelines for trauma from the Eastern Association for the Surgery of Trauma. J Tra uma 1998;44(6):941– 56; discussion 956–7.
19. Pacilli A, Faggioli G, Stella A, and Pasquinelli G. Anupdate on therapeutic angiogenesis for peripheral vascular disease. Ann Vasc Surg 2010;24(2):258 –68.
20. Rosen MP, Porter DH, and Kim D. Reassessment of vena caval filter use in patients with cancer. J Vasc Interv Radiol 1994;5(3):501–6.
21. Shackford SR, Davis JW, Hollingsworth-Fridlund P, Brewer NS, Hoyt DB, and Mackersie RC. Venous thromboembolism in patients with major trauma. AmJ Surg 1990;159(4):365–9.
22. Khansarinia S, Dennis JW, Veldenz HC, Butcher JL, and Hartland L. Prophylactic Greenfield filter place­ment in selected high-risk trauma patients. J Vasc Surg 1995;22(3):231–5; discussion 235–6.
 ●
23. Rogers FB, Strindberg G, Shackford SR etal. Five-year follow-up of prophylactic vena cava filters in high-risk trauma patients. Arch Surg 1998;133(4):406–11; discussion 412.
24. McMurtry AL, Owings JT, Anderson JT, Battistella FD, and Gosselin R. Increased use of prophylac­tic vena cava filters in trauma patients failed to decrease overall incidence of pulmonary embolism. J Am Coll Surg 1999;189(3):314–20.
25. Rowland SP, Dharmarajah B, Moore HM etal. Inferior vena cava filters for prevention of venous thromboembolism in obese patients undergoing bariatric surgery a systematic review. Ann Surg 2015;261(1):35 –45.
26. McClendon J, O’Shaughnessy BA, Smith TR etal. Comprehensive assessment of prophylactic pre­operative inferior vena cava filters for major spi­nal reconstruction in adults. Spine (Phila Pa 1976) 2012;37(13):1122–9.
27. Ozturk C, Ganiyusufoglu K, Alanay A, Aydogan M, Onat L, and Hamzaoglu A. Efficacy of prophylactic placement of inferior vena cava filter in patients undergoing spinal surgery. Spine (Phila Pa 1976) 2010;35(20):1893–6.
28. Lin J, Proctor MC, Varma M, Greenfield LJ, Upchurch GR Jr., and Henke PK. Factors associ­ated with recurrent venous thromboembolism in patients with malignant disease. J Vasc Surg 2003;37(5):976–83.
29. Gitter MJ, Jaeger TM, Petterson TM, Gersh BJ, and Silverstein MD. Bleeding and thromboembolism during anticoagulant therapy: A population-based study in Rochester, Minnesota. Mayo Clin Proc 1995;70(8):725–33.
30. Prandoni P, Lensing AWA, Piccioli A etal. Recurrent venous thromboembolism and bleeding complica­tions during anticoagulant treatment in patients with cancer and venous thrombosis. Blood 2002;100(10):3484–8.
31. Ihnat DM, Mills JL, Hughes JD, Gentile AT, Berman SS, and Westerband A. Treatment of patients with venous thromboembolism and malignant disease: Should vena cava filter placement be routine? J Vasc Surg 1998;28(5):800–7.
32. Krauth D, Holden A, Knapic N, Liepman M, and Ansell J. Safety and efficacy of long-term oral anticoagulation in cancer patients. Cancer 1987;59(5):983–5.
33. Laporte S, Mismetti P, Décousus H etal. Clinical predictors for fatal pulmonary embolism in 15,520 patients with venous thromboembolism: Findings from the Registro Informatizado de la Enfermedad TromboEmbolica venosa (RIETE) Registry. Circulation 2008;117(13):1711– 6.
34. Somarouthu B, Yeddula K, Wicky S, Hirsch JA, and Kalva SP. Long-term safety and effectiveness of inferior vena cava filters in patients with stroke. JNeurointerv Surg 2011;3(2):141–6.
35. Burbridge BE, Walker DR, and Millward SF. Incorporation of the Gunther temporary inferior vena cava filter into the caval wall. J Vasc Interv Radiol 1996;7(2):289–90.
36. De Gregorio MA, Gamboa P, Bonilla DL etal. Retrieval of Gunther Tulip optional vena cava filters 30 days after implantation: A prospec­tive clinical study. J Vasc Interv Radiol 2006;17(11 Pt1):1781–9.
37. Terhaar OA, Lyon SM, Given MF, Foster AE, McGrath F, and Lee MJ. Extended interval for retrieval of Günther Tulip filters. J Vasc Interv Radiol 20 04;15(11):1257– 62.
References 341
https://t.me/med1917
38. Nicholson W, Nicholson WJ, Tolerico P etal. Prevalence of fracture and fragment embolization of Bard retrievable vena cava filters and clinical implica­tions including cardiac perforation and tamponade. Arch Intern Med 2010;170(20):1827–31.
39. Lorch H, Welger D, Wagner V etal. Current practice of temporary vena cava filter insertion: A multicenter registry. J Vasc Interv Radiol 2000;11(1):83–8.
40. Yamagami T, Kato T, Iida S, Tanaka O, and Nishimura T. Retrievable vena cava filter placement during treatment for deep venous thrombosis. Br J Radiol 2003;76(910):712–8.
 ●
41. 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. N Engl J Med 1998;338(7):409–16.
 ●
42. Decousus H. Eight-year follow-up of patients with permanent vena cava filters in the prevention of pulmonary embolism: The PREPIC (Prévention du Risque d’Embolie Pulmonaire par Interruption Cave) randomized study. Circulation 20 0 5;112 (3): 416 – 2 2.
43. Chuu WM, Wang NY, and Perry D. Vena caval filters for the prevention of pulmonary embolism. N Engl J Med 1998;339(1):46; author reply 47–8.
44. Murphy TP, Trerotola SO, and Vogelzang RL. Vena caval filters for the prevention of pulmonary embo­lism. N Engl J Med 1998;339(1):46–7; author reply 47–8.
45. Greenfield LJ and Proctor MC. Vena caval filters for the prevention of pulmonary embolism. N Engl J Med 1998;339(1):47; author reply 47–8.
46. Mismetti P, Laporte S, Pellerin O etal. Effect of a retrievable inferior vena cava filter plus anticoagula­tion vs anticoagulation alone on risk of recurrent pulmonary embolism. JAMA 2015;313(16):1627–35.
47. Kim HS, Young MJ, Narayan AK, Hong K, Liddell RP, and Streiff MB. A comparison of clinical outcomes with retrievable and permanent inferior vena cava filters. J Vasc Interv Radiol 2008;19(3):393–9.
48. Andreoli JM, Lewandowski RJ, Vogelzang RL, and Ryu RK. Comparison of complication rates associ­ated with permanent and retrievable inferior vena cava filters: A review of the MAUDE database. J Vasc Interv Radiol 2014;25(8):1181–5.
49. Kim D, Schlam BW, Porter DH, and Simon M. Insertion of the Simon Nitinol caval filter: Value of the antecubital vein approach. AJR Am J Roentgenol 1991;157(3):521–2.
50. Passman MA, Dattilo JB, Guzman RJ, and Naslund TC. Bedside placement of inferior vena cava filters by using transabdominal duplex ultrasonography and intravascular ultrasound imaging. J Vasc Surg 2005;42(5):1027–32.
51. Corriere MA, Passman MA, Guzman RJ, Dattilo JB, and Naslund TC. Comparison of bedside transabdominal duplex ultrasound versus contrast
venography for inferior vena cava filter placement: What is the best imaging modality? Ann Vasc Surg 2005;19(2):229–34.
52. Lucas DJ, Dunne JR, Rodriguez CJ etal. Dedicated tracking of patients with retrievable inferior vena cava filters improves retrieval rates. Am Surg 2012;78(8):870–4.
 ●
53. Lynch FC. A method for following patients with retrievable inferior vena cava filters: Results and lessons learned from the first 1,100 patients. J Vasc Interv Radiol 2011; 2 2(11):1507–12.
54. Ballew KA, Philbrick JT, and Becker DM. Vena cava filter devices. Clin Chest Med 1995;16(2):295–305.
55. Rousseau H, Perreault P, Otal P etal. The 6-F Nitinol TrapEase inferior vena cava filter: Results of a prospective multicenter trial. J Vasc Interv Radiol 20 01;12(3):299–304.
56. Streiff MB. Vena caval filters: A comprehensive review. Blood 2000;95(12):3669–77.
 ●
57. Greenfield LJ and Proctor MC. The percutaneous Greenfield filter: Outcomes and practice patterns. JVasc Surg 2000;32(5):888–93.
58. Vena Caval Filter Consensus Conference. Recommended reporting standards for vena caval filter placement and patient follow-up. J Vasc Surg 1999;30(3):573–9.
 ◆
59. Grassi CJ, Swan TL, Cardella JF etal. Quality improvement guidelines for percutaneous permanent inferior vena cava filter placement for the prevention of pulmonary embolism. SCVIR Standards of Practice Committee. J Vasc Interv Radiol 20 01;12(2):137– 41.
60. Becker DM, Philbrick JT, and Selby JB. Inferior vena cava filters. Indications, safety, effectiveness. Arch Intern Med 1992;152(10):1985–94.
61. Greenfield LJ and Proctor MC. Current treatment and prevention of pulmonary embolus with the Greenfield filter. Surg Technol Int 1993;2:289–91.
 ●
62. Greenfield LJ and Michna BA. Twelve-year clinical experience with the Greenfield vena caval filter. Surgery 1988;104(4):706–12.
63. Greenfield LJ. Current indications for and results of Greenfield filter placement. J Vasc Surg 1984;1(3):5 02–4.
64. Greenfield LJ, Peyton R, Crute S, and Barnes R. Greenfield vena caval filter experience: Late results in 156 patients. Arch Surg 1981;116(11):1451– 6.
65. Greenfield LJ, Zocco J, Wilk J, Schroeder TM, and Elkins RC. Clinical experience with the Kim-Ray Greenfield vena caval filter. Ann Surg 1977;185(6):692–8.
66. Jarrell BE, Szentpetery S, Mendez-Picon G, Lee HM, and Greenfield LJ. Greenfield filter in renal trans­plant patients. Arch Surg 1981;116(7):9 3 0 –2.
67. Hux CH, Wapner RJ, Chayen B, Rattan P, Jarrell B, and Greenfield L. Use of the Greenfield filter for thromboembolic disease in pregnancy. Am J Obstet Gynecol 1986;155(4):734–7.
342 Indications, techniques, and results of inferior vena cava filters
https://t.me/med1917
68. Athanasoulis CA, Kaufman JA, Halpern EF, Waltman AC, Geller SC, and Fan CM. Inferior vena caval filters: Review of a 26-year single-center clinical experience. Radiology 2000;216(1):54–66.
69. David W, Gross WS, Colaiuta E, Gonda R, Osher D, and Lanuti S. Pulmonary embolus after vena cava filter placement. Am Surg 1999;65(4):341–6.
70. Matchett WJ, Jones MP, McFarland DR, and Ferris EJ. Suprarenal vena caval filter placement: Follow-up of four filter types in 22 patients. J Vasc Interv Radiol 1991;9(4):588–93.
71. Hoffman MJ and Greenfield LJ. Central venous septic thrombosis managed by superior vena cava Greenfield filter and venous thrombectomy: A case report. J Vasc Surg 1986;4 (6): 6 0 6 –11.
72. Pais SO, De Orchis DF, and Mirvis SE. Superior vena caval placement of a Kimray–Greenfield filter. Radiology 1987;165(2):385– 6.
73. Owen EW, Schoettle GP, and Harrington OB. Placement of a Greenfield filter in the superior vena cava. Ann Thorac Surg 1992;53(5):896–7.
74. Ascher E, Hingorani A, Tsemekhin B, Yorkovich W, and Gunduz Y. Lessons learned from a 6-year clinical experience with superior vena cava Greenfield filters. J Vasc Surg 2000;32(5):881–7.
75. Owens CA, Bui JT, Knuttinen MG, Gaba RC, and Carrillo TC. Pulmonary embolism from upper extremity deep vein thrombosis and the role of superior vena cava filters: A review of the literature. J Vasc Interv Radiol 2010;21(6):779–87.
76. Angel LF, Tapson V, Galgon RE, Restrepo MI, and Kaufman J. Systematic review of the use of retriev­able inferior vena cava filters. J Vasc Interv Radiol 2011;2 2(11):1522–30.e 3 .
77. Hann CL and Streiff MB. The role of vena caval filters in the management of venous thromboembolism. Blood Rev 2005;19(4):179–202.
 ◆
78. Caplin DM, Nikolic B, Kalva SP, Ganguli S, Saad WEA, and Zuckerman DA. Quality improvement guidelines for the performance of inferior vena cava filter placement for the prevention of pulmonary embolism. J Vasc Interv Radiol 2011;22(11):1499 – 5 0 6 .
Superficial thrombophlebitis
https://t.me/med1917
BENJAMIN JACOBS AND DAWN M. COLEMAN
27
27.1 Introduction 343
27.2 Epidemiology 343
27.3 Clinical presentation 343
27.4 Etiology 343
27.1 INTRODUCTION
Supercial venous thrombophlebitis (SVT) is common, although its incidence is likely underestimated, as many cases are subclinical and go unreported. ere are a num­ber of misconceptions about this diagnosis amongst phy­sicians, the most pernicious of which is that it is entirely benign, oering no life- or limb-threatening complica­tions. While this is true of some cases, SVT carries a risk of association and progression to deep vein thrombosis (DVT) and pulmonary embolism (PE). Consequently, a thorough understanding of the pathophysiology, diagno­sis, and management of SVT is of great importance to the venous health physician.
27.2 EPIDEMIOLOGY
e incidence of SVT approximates 1:1000, although this is generally believed to reect an underestimate. SVT aects almost 125,000 patients in the United States annually.1 e average age at diagnosis ranges from 54 to 65 years; SVT aects females more than males. encountered risk factor is the presence of lower extremity varicose veins, occurring in 62% of SVT patients. Other associated risk factors include increasing age, obesity, tobacco use, previous history of DVT or SVT, pregnancy and the puerperium, oral contraceptives, hormone­replacement therapy, immobilization, recent surgery, and trauma.
4
2,3
e most commonly
27.3 CLINICAL PRESENTATION
Patients will present in most cases with pain and ery­thema overlying the aected supercial vein, along with a
27.5 Diagnosis 345
27.6 Treatment 345
27.7 Conclusion 346
References 347
palpable “cord” and edema of the surrounding so tissue. Low-grade fever or malaise may be present. e supercial veins of the upper or lower extremities, the breast in the case of Mondor’s disease, or the dorsal veins of the penis may all be aected by SVT. e most common locations aected by SVT include the great saphenous vein (GSV) and its tributaries, followed by the cephalic and basilic veins of the upper extremity.4 e diagnosis of progres­sion to DVT is oen accompanied by a worsening of symptoms.
5
27.4 ETIOLOGY
Traditionally, the pathophysiology of venous thrombo­embolic disease has been attributed to Virchow’s triad of endothelial injury, stasis, and hypercoagulability. As our understanding of this triad has deepened, the importance of inammatory mediators and broadened hypercoaguable states, like malignancy and obesity, has emerged. e etiol­ogy of SVT is complex and oen multifactorial; it remains an area of active discovery.
27.4.1 Superficial thrombophlebitis and
lower extremity varicosities
Lower extremity varicosities and lower extremity venous insuciency are the most common risk factors for SVT. Varicose veins are comorbid with SVT in up to two-thirds of patients with SVT, and up to 70% of patients may have associated supercial venous insuciency. reported that only 3%–20% of SVT patients with varicose veins will develop DVT, compared to 44%–60% of those without varicosities. patients with varicose veins has a dierent pathophysiology
7–9
erefore, it may be that SVT in
6
It has been
343
344 Superficial thrombophlebitis
https://t.me/med1917
from those without varicose veins. However, in a more recent study, no increased incidence of DVT or PE was noted when comparing patients with and without varicose veins in the 186 SVT patients identied.2 Consequently, the question of whether SVT patients with or without associated varicose veins should be thought of as separate classications remains ambiguous.10 Conversely, address­ing those patients with SVT involving varicose veins only is essential. is type of SVT may remain localized to the cluster of tributary varicosities or may, from time to time, extend into the GSV.2 Supercial venous thrombosis is fre­quently found in varicose veins surrounding venous stasis ulcers.
27.4.2 Disease progression to DVT and PE
In as much as the primary threat to the patient with SVT is due to the potential for venous thromboembolism (VTE), it is important to clarify the connection between these enti­ties. It has been shown that SVT can progress to DVT via proximal extension of thrombus into the deep system, but it also, perhaps counterintuitively, has been shown to arise in association with SVT in non-contiguous vessels.
2,3
Concomitant DVT can be present but asymptom­atic at presentation for SVT, and identied only on deep vein ultrasound studies. Decousus et al. noted that 25% of patients presenting with SVT demonstrated concomi­tant DVT at presentation, and importantly, almost half of these DVT cases were not contiguous with the SVT.3 Of the 586 patients studied with isolated SVT, 10% went on to develop VTE during the study period. Across series, the incidence of proximal progression into the deep system ranges between 7% and 44%.
4,11
e most common route of extension is from the GSV via the saphenofemoral junc­tion (SFJ) into the femoral vein.
9,12
Progression to VTE may also result from short saphenous vein SVT progression into the popliteal vein, and into the deep system via perforating
4
veins.
Chengelis et al. identied a group of 263 patients with isolated SVT without evidence of deep venous involvement by duplex ultrasound examination. Surveillance duplex ultrasonography performed approximately 1 week follow­ing SVT diagnosis revealed progression to deep venous involvement in 30 patients (11%) and specically 16% of those with GSV SVT had extension into the femoral vein— most commonly via the SFJ (85%).
9
Proximity of supercial thrombus to the SFJ inuences the likelihood of progres­sion; SVT location within 1 cm of the SFJ confers a high risk of DVT progression.
5
27.4.3 Associated hypercoagulability
Which patients, if any, presenting with SVT merit workup for hypercoaguable states remains an area of contro­versy and active research. ere are no current guidelines that support concise recommendations. Martinelli et al.’s
case–control study tested 63 ‘low-risk’ patients (dened by the absence of malignancy, autoimmune disease, and lower extremity varicosities) for factor V Leiden muta­tion, prothrombin G20210A mutation, and deciencies in antithrombin III (AT III), protein C, and protein S.11 An increased risk of SVT was identied in patients with inher­ited coagulopathies. Risk of SVT was increased approxi­mately six-fold for factor V Leiden mutation, four-fold for the prothrombin G20210A mutation, and 13-fold for the combined factor deciencies. Similarly, de Moerloose et al. demonstrated that the presence of factor V Leiden mutation increased risk of SVT, although this was no lon­ger statistically signicant aer controlling for obesity.13 Additionally, patients with SVT not associated with lower extremity varicosities were more likely to have an inherited hypercoaguable state.
Another study of 29 patients with SVT investigated this relationship.14 All patients underwent duplex ultrasonog­raphy of the supercial and deep venous systems. Patients with isolated SVT were treated with non-steroidal anti­inammatory drugs (NSAIDs) and those with DVT were treated with heparin and warfarin. ese patients had a similar coagulation prole performed that included pro­tein C antigen and activity, activated protein C resistance, protein S antigen and activity, AT III, and the lupus antico­agulant. Twelve patients (41%) were found to have abnormal results consistent with a hypercoaguable state. Five of the patients (38%) with combined SVT and DVT and seven of the patients (44%) with SVT alone were found to be hyper­coaguable. Four patients had decreased levels of AT III only and four patients were identied with activated protein C (APC) resistance. One patient had decreased protein C and protein S, and three patients had deciencies of AT III, protein C, and protein S. e most prevalent anticoagulant deciency was AT III. Furthermore, in a subsequent sepa­rate set of data examining patients with recurrent SVT, anti­cardiolipin antibodies were detected in 33% of patients.
15
ese ndings and others suggest that patients with SVT may have an increased risk of an underlying hypercoaguable state, although not all studies have revealed such a strong association.
4,16,17
Consequently, whether routine testing of these patients is necessary remains unclear. It is reasonable to conclude that those patients presenting with SVT in the absence of any clear risk factor, especially if recurrent, merit such investigation.
27.4.4 Upper extremity SVT
e most common etiologic factor in upper extremity SVT is trauma associated with an intravenous cannula and intra­venous infusions resulting in caustic endothelial damage. Treatment consists of cannula removal and warm com­presses. e resultant lump may persist for months notwith­standing this treatment. Extension of upper extremity SVT into upper extremity DVT or PE is a very rare occurrence when compared with lower extremity SVT.
18
27.6 Treatment 345
https://t.me/med1917
27.4.5 Suppurative SVT
Suppurative SVT (SSVT) is also associated with the use of an intravenous cannula; however, SSVT may be lethal, given its association with septicemia. e associated signs and symptoms of SSVT include purulence at an intrave­nous site, fever, leukocytosis, and local intense pain.19 Treatment consists of catheter removal, warm compresses, NSAIDs and broad-spectrum intravenous antibiotics (tai­lored to qualitative blood culture results). Surgery should be reserved for patients with SSVT who fail conservative management and require source control for persistent sepsis, including exploration, abscess drainage, and full venous resection to the extent that brisk back-bleeding is encountered.
27.4.6 Migratory SVT
Migratory thrombophlebitis was rst described by Jadioux in 1845 as an entity characterized by repeated thrombo­sis developing in the supercial veins at varying sites, but most commonly in the lower extremity.20 is entity may be associated with carcinoma and may precede diagnosis of the carcinoma by several years. Consequently, a workup for occult malignancy may, in fact, be warranted when the diagnosis of migratory thrombophlebitis is made.
27.4.7 Mondor’s disease
Mondor’s disease is dened as thrombophlebitis of the tho­racoepigastric vein of the breast and chest wall. It can be associated with breast carcinoma or hypercoaguable state, although cases have been reported with no identiable cause.21 Recently, the term has also been applied to SVT of the dorsal vein of the penis.
22
27.5 DIAGNOSIS
Duplex ultrasound scanning is the diagnostic modality of choice for the evaluation of DVT and SVT. e availability of reliable duplex ultrasonography of the deep and super­cial venous systems has made routine determination of the location and extent of venous thrombosis accurate and prac­tical. Furthermore, the extent of involvement of the deep and supercial systems can be more accurately assessed uti­lizing this modality; routine clinical examination may not precisely evaluate the proximal extent of the involvement of the deep or supercial systems. Duplex imaging of patients with SVT has revealed concomitant DVT in 5%–40% of patients. of these patients’ DVTs may not be contiguous with the SVT, or may even be in the contralateral lower extremity. Consequently, bilateral imaging is necessary. Duplex ultra­sound is also noninvasive, inexpensive, and may be easily repeated for surveillance examinations. Venography, alter­natively, has fallen out of favor, with little indication.
2,23–26
It is important to note again that up to 25%
2
27.6 TREATMENT
e extent of thrombus burden, thrombus location, the presence of concomitant DVT, and associated local infec­tion should direct SVT treatment. Ambulation, warm com­presses, elastic compression, intermittent elevation, and NSAIDs remain appropriate for cases of mild SVT in order to alleviate the inammatory reaction.27 While NSAIDs have been shown to signicantly reduce the risk of SVT extension and/or recurrence by 67% compared to placebo, this therapy oers no protection against VTE, nor resolu­tion of local signs and/or symptoms.
erapeutic anticoagulation and venous ligation or abla­tion have become increasingly popular for decreasing the risk of DVT in patients with SVT that demonstrate throm­bus extension toward the level of the SFJ or carry additional risk factors for DVT extension. Historically, thrombus within 3 cm of the SFJ was felt to warrant surgical ligation of the SFJ with or without simultaneous GSV stripping/ ligation, while more recent data support anticoagulation and compression over surgical measures.
A 1999 prospective trial comparing various anticoagu­lant treatment groups (prophylactic unfractionated heparin, prophylactic low-molecular-weight heparin [LMWH], and therapeutic warfarin) to elastic compression alone or saphe­nous ligation identied lower rates of SVT extension in the anticoagulant treatment groups by surveillance imaging, without major bleeding complication.31 Several contempo­rary trials have followed, further supporting the benets of anticoagulation for SVT. e 2003 SVT Enoxaparin Study Group published their double-blind randomized trial com­paring 8 days of treatment for SVT with prophylactic enoxa­parin (40 mg) daily, therapeutic enoxaparin (1.5 mg/kg) daily, oral tenoxicam, and placebo for 8–12 days.32 e inci­dence of deep and supercial venous thromboembolism was signicantly decreased in all treatment groups (from 30.6% in the placebo group to 8.3% in the prophylactic enoxaparin group, 6.9% in the therapeutic enoxaparin group, and 14.9% in the tenoxicam group) without any hemorrhagic morbid­ity or heparin-induced thrombocytopenia. e randomized controlled Vesalio trial compared 1 month of prophylactic versus therapeutic doses of nadroparin for SVT.33 ese authors failed to demonstrate a dierence in thrombus pro­gression or VTE in either group, and moreover, they failed to meet recruitment goals, resulting in premature study termination.
A contemporary multicenter, randomized, double-blind, placebo-controlled trial reported on the safety and ecacy of fondaparinux for SVT.34 Approximately 3000 patients with acute, symptomatic lower limb SVT involving a seg­ment of at least 5 cm in length located at least 3 cm dis­tal to the SFJ were assigned to 45 days of treatment with fondaparinux (2.5 mg subcutaneously daily) or placebo. e fondaparinux group demonstrated an 85% lower rate of PE or DVT than the placebo group aer 77 days, along with a signicantly reduced rate of symptomatic SVT recurrence
27, 28
29,30
346 Superficial thrombophlebitis
Algorithm
https://t.me/med1917
or extension to the SFJ without major hemorrhage or alter­native morbidity.
Most recently, a 14-day treatment course of daltepa­rin (200 U/kg at presentation followed by 10,000 U daily) for SVT was identied as superior to ibuprofen (800 mg three times daily) for both major upper and lower SVT.35 Interestingly, this benet was lost by the 3-month follow­up, and thrombus extension, including VTE, occurred in the time period following cessation of dalteparin and ibuprofen dosing, suggesting the treatment duration (2 weeks) may have been too brief. Finally, both therapies signicantly reduced symptoms of pain during the treat­ment periodand appeared safewithout episodes of major or minor hemorrhage.
A 2013 Cochrane review including 30 randomized controlled trials and 6507 patients with SVT summa­rized that: both LMWH and NSAIDs reduce SVT exten­sion and recurrence without any eect on symptomatic VTE; topical treatments relieve local symptoms; surgical treatment and elastic stockings oer a lower rate of VTE and SVT progression over elastic stockings alone; and fondaparinux appears to be an adequate treatment option as it oers a signicant reduction in symptomatic VTE and SVT extension/recurrence.36 e 2012 American College of Chest Physicians CHEST guidelines advocate medical treatment with a prophylactic dose of fondaparinux or LMWH for 45 days over no anticoagulation (grade 2B) for patients with SVT of the lower limb that measures at least 5 cm in length, with grade 2C evidence favoring a daily dose of fondaparinux (2.5 mg) over a prophylactic dose of LMWH for patients with SVT being treated with anticoagulation.
37
Finally, GSV disconnection and ligation at the SFJ remains appropriate for patients with SVTwhocannot tol­erate anticoagulation and demonstrate moderatethrom­bus burden (i.e., 5 cm in length or within 3 cm of the SFJ). Surgical treatment with GSV ablation and phle­bectomies of the involved branch varicosities should be considered as the optimal treatments for patients with symptomatic SVT and evidence of venous insuciency by duplex ultrasound in order to prevent recurrent phlebitis aer the phlebitis has resolved, which is typically staged by 3–6 months.
27.7 CONCLUSION
In conclusion, SVT is common and carries a risk of asso­ciation and progression to DVT and PE. e vein health physician must consider an individualized treatment plan. While patients with milder forms of SVT may be success­fully managed with NSAIDs, compression, and warm compresses, those with moderate disease, dened as SVT located 3 cm distal to the SFJ and 5 cm in length, should be managed more aggressively, with either prophylactic LMWH or fondaparinux. erapeutic anticoagulation should be considered for any patient that develops DVT or PE. For patients who cannot tolerate anticoagulation, GSV disconnection and ligation at the SFJ are appropriate when thrombus burden is moderate. Surgical treatment with GSV ablation and phlebectomies of the involved branch varicosities should be considered as the optimal treat­ments for patients with symptomatic SVT and evidence of venous insuciency conrmed by duplex ultrasound, which is usually performed aer the phlebitis has resolved.
SVT
- <5 cm of thrombus length
Mild
Moderate
- At least 3 cm distal to SFJ
At least 5 cm of thrombus length
Associated venous insufficiency
Associated VTE
- or -
Thrombus <3 cm from (or involving) the
SFJ
NSAIDs
Compression
Warm compresses
Fondaparinux 2.5 mg daily
- or -
LMWH 40 mg daily
Medical management (as above) and
interval GSV ablation and phlebectomy
Therapeutic anticoagulation
Guidelines 3.11.0 of the American Venous Forum on superficial thrombophlebitis
https://t.me/med1917
References 347
No. Guideline
3.11.1 For saphenous vein thrombophlebitis within 3 cm of the saphenofemoral or saphenopopliteal junction, we recommend therapeutic anticoagulation.
3.11.2 For moderate thrombophlebitis with at least 5 cm thrombus length and at least 3 cm distal to the saphenofemoral junction, we recommend fondaparinux 2.5 mg daily or low-molecular-weight heparin 40 mg daily for 45 days.
3.11.3 For thrombophlebitis localized in the distal segment or in tributaries of the great saphenous vein with thrombus length <5 cm, we suggest ambulation, warm soaks, and non-steroidal anti-inflammatory agents.
3.11.4 For moderate thrombophlebitis as described above, or thrombophlebitis within 3 cm of the saphenofemoral junction, if anticoagulation is contraindicated, high ligation and division of the great saphenous vein is suggested.
3.11.5 In patients with saphenous thrombophlebitis, we suggest ablation once the inflammation resolved if there is evidence of venous insufficiency confirmed by duplex ultrasound scanning.
Grade of
recommendation
(1: strong; 2:
weak)
1 B
1 B
2 B
2 B
2 B
Grade of evidence
(A:high quality;
B:moderate quality;
C:low or very low quality)
REFERENCES
1. DeWeese MS. Nonoperative treatment of acute superficial thrombophlebitis and deep femoral venous thrombosis. In: Ernst C, Stanley JC, eds. Current Therapy in Vascular Surgery, 2nd Ed. Philadelphia, PA: BC Decker, 1991, 952–60.
2. Lutter KS, Kerr TM, Roedersheimer LR etal. Superficial thrombophlebitis diagnosed by duplex scanning. Surgery 1991;110 : 42–6.
3. Decousus H, Quere I, Presles E etal. Superficial venous thrombosis and venous thromboembolism a large prospective epidemiologic study. Ann Intern Med 2010;152:218–24.
4. Leon L, Giannoukas AD, Dodd D etal. Clinical sig­nificance of superficial vein thrombosis. Eur J Vasc Endovasc Surg 2005;2 9 :10 –7.
5. Dalsing MC. The case against anticoagula­tion for superficial venous thrombosis. Dis Mon 2010;56:582–9.
6. Meissner MH, Wakefield TW, Ascher E etal. Acute venous disease: Venous thrombosis and venous trauma. J Vasc Surg 2007;46:S25–53.
7. Bergqvist D and Jaroszewski H. Deep vein thrombo­sis in patients with superficial thrombophlebitis of the leg. BMJ 1986;292:658–9.
8. Prountjos P, Bastounis E, Hadjinikolaou L etal. Superficial venous thrombosis of the lower extremi­ties co-existing with deep venous thrombosis.
A phlebographic study on 57 cases. Int Angiol 1991;10:263 –5.
9. Chengelis DL, Bendick PJ, Glover JL etal. Progression of superficial venous thrombosis to deep vein thrombosis. J Vasc Surg 1996;24:745–9.
10. Marchiori A, Mosena L, and Prandoni P. Superficial vein thrombosis: Risk factors, diagnosis, and treat­ment. Semin Thromb Hemost 2006;23:737–43.
11. Martinelli I, Cattaneo M, Taioli E etal. Genetic risk factors for superficial vein thrombosis. Thromb Haemost 1999;82:1215–7.
12. Blumenberg RM, Barton E, Gelfand ML, Skudder P, and Brennan J. Occult deep venous thrombosis com­plicating superficial thrombophlebitis. J Vasc Surg 1998;27:338 –43.
13. de Moerloose P, Wutschert R, Heinzmann M etal. Superficial vein thrombosis of lower limbs: Influence of factor V Leiden, factor II G20210A, and over­weight. Thromb Haemost 1998;80:239–41.
14. Hanson JN, Ascher E, DePippo P etal. Saphenous vein thrombophlebitis (SVT): A deceptively benign disease. J Vasc Surg 1998;27:677–80.
15. de Godoy JM, Batigalia F, and Braile DM. Superficial thrombophlebitis and anticardiolipin antibodies— Report of association. Angiology 2001;52:127–9.
16. Leon LR Jr. and Labropoulos N. Superficial vein thrombosis and hypercoagulable states: The evidence. Perspect Vasc Surg Endovasc Ther 20 05;17:43 –6.
348 Superficial thrombophlebitis
https://t.me/med1917
17. Karthanos C, Sfyroeras G, Drakou A etal. Superficial vein thrombosis in patients with varicose veins: Role of thrombophilia factors, age and body mass. Eur J Vasc Endovasc Surg 2012;43:355–8.
18. Sassu GP, Chisholm CD, Howell JM, and Huang E. A rare etiology for pulmonary embolism: Basilic vein thrombosis. J Emerg Med 19 90;8:45 –9.
19. Hammond JS, Varas R, and Ward CG. Suppurative thrombophlebitis: A new look at a continuing prob­lem. South Med J 1988;81:969–71.
20. Glasser ST. Principles of Peripheral Vascular Surgery. Philadelphia, PA: FA Davis, 1959.
21. Mayor M, Buron I, de Mora JC etal. Mondor’s dis­ease. Int J Dermatol 2000;39:922–5.
22. Sasso F, Gulino G, Basar M etal. Penile Mondor’s disease: An underestimated pathology. Br J Urol 1996;77:729–32.
23. Talbot SR. Use of real-time imaging in identifying deep venous obstruction: A preliminary report. Bruit 1982;6:41–2.
24. Skillman JJ, Kent KC, Porter DH, and Kim D. Simultaneous occurrence of superficial and deep thrombophlebitis in the lower extremity. J Vasc Surg 1990;11: 818 –23.
25. Jorgensen JO, Hanel KC, Morgan AM, and Hunt JM. The incidence of deep venous thrombosis in patients with superficial thrombophlebitis of the lower limbs. J Vasc Surg 1993;18:70–3.
26. Schonauer V, Kyrle PA, Weltermann A etal. Superficial thrombophlebitis and risk for recur­rent venous thromboembolism. J Vasc Surg 2003;37:834–8.
27. Lee JT and Kalani MA. Treating superficial venous thrombophlebitis. J Natl Compr Canc Netw 2008;6:760–5.
28. Quenet S, Laporte S, Decousus H etal.; STENOX Group. Factors predictive of venous thrombotic complications in patients with isolated superficial vein thrombosis. J Vasc Surg 2003;38:944–9.
29. Lohr JM, McDevitt DT, Lutter KS etal. Operative management of greater saphenous thrombophlebi­tis involving the saphenofemoral junction. Am J Surg 1992;164:269–75.
30. Lozano FS and Almazan A. Low-molecular-weight heparin versus saphenofemoral disconnection for the treatment of above-knee greater saphe­nous thrombophlebitis: A prospective study. Vasc Endovascular Surg 2003;37:415–20.
31. Belcaro G, Nicolaides AN, Errichi BM etal. Superficial thrombophlebitis of the legs: A randomized, con­trolled, follow-up study. Angiology 1999;50:523–30.
32. Superficial Thrombophlebitis Treated by Enoxaparin Study Group. A pilot randomized double-blind comparison of a low-molecular-weight heparin, a nonsteroidal anti-inflammatory agent, and placebo in the treatment of superficial vein thrombosis. Arch Intern Med 20 0 3;163:1657– 6 3.
33. The Vesalio Investigators Group. High vs. low doses of low-molecular-weight heparin for the treat­ment of superficial vein thrombosis of the legs: A double-blind, randomized trial. J Thromb Haemost 20 0 5 ; 3 :115 2 – 7.
34. Decousus H, Prandoni P, Mismetti P et al. Fondaparinux for the treatment of superficial­vein thrombosis in the legs. N Engl J Med 2010;363:1222–32.
35. Rathbun SW and Aston CE. A randomized trial of dalteparin compared with ibuprofen for the treat­ment of superficial thrombophlebitis. J Thromb Haemost 2012;10:883–39.
36. Di Nisio M, Wichers IM, and Middeldorp S. Treatment for superficial thrombophlebitis of the leg. Cochrane Database Syst Rev 2013;4:CD004982.
37. 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;141:419S–94S.
Mesenteric vein thrombosis
https://t.me/med1917
WALDEMAR E. WYSOKINSKI AND ROBERT D. McBANE
28
28.1 Introduction 349
28.2 Etiology 350
28.3 Clinical presentation 351
28.4 Treatment 354
28.1 INTRODUCTION
Mesenteric vein thrombosis (MVT) was rst described by Elliot in 1895.1 Four decades later, Warren and Eberhard2 recognized this as a distinct clinical entity and an impor­tant cause of bowel infarction. Now, 120 years aer the rst description, MVT remains a serious thrombotic disorder that is dicult to both diagnose and treat.3 It is important to recognize very unique features of the mesenteric venous circulation that impact on the thrombotic process:
ere is a noticeable variation in mesenteric blood ow and viscosity associated with the time of day, nutrition intake, physical activity, emotional stress, diarrheal and/or vomiting related uid loss, and dehydration from poor uid intake.
Mesenteric venous blood is rich in nutrients and intesti­nal elements such as microbial ora and both senescent and damaged cells.
is circulation is subject to a number of blood-borne gastrointestinal peptides such as glucagon, vasoactive intestinal polypeptide (VIP), and cholecystokinin, which may further impact hemostasis and blood ow, particularly as mesenteric circulation is richly inner­vated by the sympathetic nervous system.
e mesenteric veins do not contain venous valves, at least not in the larger channels.4 is is important, as venous thrombi, occurring in the deep veins of the leg are thought to originate in the valve pockets; therefore, spatial and structural dierences between leg vein and mesenteric vein thrombi might exist.
Finally, the interrelationship of the mesenteric venous circulation with splenic and portal vein ow is such that a local pro-thrombotic milieu related to splenic or liver pathology (malignancy, inammation, or infection)
28.5 Outcomes 354
28.6 Conclusions 355
References 355
increases the propensity for thrombus propagation into the mesenteric venous segment. rombosis of one venous segment alters blood ow within the entire system; in particular, occlusion of the portal system will have a huge impact on venous blood stagnation within the mesenteric vein.
For these combined reasons, the mesenteric venous circulation is entirely unique and thrombosis occurring within this system should be considered as a distinct entity requiring special consideration and evaluation.
e incidence of MVT in the general population is poorly dened, but seems to be rather uncommon. Kazmers noted that MVT may be found in as few as one in 1000 laparoto-
5
e incidence of MVT has increased in Sweden from
mies.
2.0 per 100,000 patient-years between 1970 and 1982 to 2.7 per 100,000 patient-years between 2000 and 2006.6 e age at presentation varies from 45 to 80 years and both gen­ders are equally represented. be limited to the mesenteric veins or may propagate to or from other regional vessels. of patients with intestinal ischemia. and symptomatology is determined by both the aggression of the thrombotic process and the extent of venous segments involved, determining the possibility of collateral circulation development. e superior mesenteric vein is much more frequently involved relative to the inferior mesenteric vein.
Patients with acute MVT may note a sudden onset of abdominal pain, which may quickly progress within hours to include signs of peritonitis with bowel infarction. Patients with subacute onset present primarily with abdominal pain that has developed over days to weeks. neither bowel infarction nor chronic complications ( variceal hemorrhage) are likely. Occasionally, however, patients with prominent and persistent abdominal pain
3,5–14
Venous thrombosis may
6– 8,14
MVT accounts for 5%–15%
9–12
e clinical course
8–11
In these patients,
10
349