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_3771_Библиотеки_им_академика_М_И_Перельмана.pdf
180 Indrani Sen and Manju Kalra
A.
13
Patency rate (%)
Grafts at Risk
Primar y
Assisted Primary
Secondary
B.
100
80
60
40
20
100
80
85%
81%
75% 75%
68%
68%
58%
45%
45%
Primary
Assisted Primary
Secondary
0
0
1
2
3
4
5
Ye ars
42
42
42
27
25
27
96% 96%
19
18
21
16
12
15
96% 96%
70%
13
12
12
13
12
12
60
44%
40
Primary
20
Patency rate (%)
Assisted Primary
Secondary
0
4
4
3
3
5
2
1
1
Number at Risk
Primary
Assisted Primary
Secondary
0
28
28
28 18
1
2
3
Ye ars
21
16
13
8
9
7
9
Figure 17.5 (A) Cumulative primary, assisted primary and secondary patency rates at 1, 3 and 5years of open
surgical reconstruction (n= 42). Solid bars represent SEM <10%. (B) Cumulative primary, assisted primary
and secondary patency rates at 1 and 3years of endovascular repair (n=28). Solid bars represent SEM <10%.
(From Rizvi,AZ, etal. Benign superior vena cava syndrome: stenting is now the first line of treatment. J Vasc
Surg 47(2): 372–380, 2008.)
Management of Benign Disease of the Deep Venous System 181
A. B.
2
Interventions
4 4
#
50
40
30
20
Patients
10
%
0
Secondary Interventions
%
of Patients
10 10
9
8
7
6
5
3
2
1
12 - 36
1 - 12
days
mo mo mo days mo mo mo
0
Interventions
%
0
2
0
50
40
30
20
Patients
10
0
Secondary Interventions
#
of Patients
%
30 3636< >
< >1 - 12 12 - 36
9
8
7
6
5
4
3
2
0
1
Figure 17.6 Treatment of benign superior vena cava syndrome. Secondary interventions are required to
maintain patency in (A) the open surgical group (n = 42) and (B) the endovascular group (n= 28). The
bars represent the percentage of patients in each group, and the line graphs represent the total number of
interventions. (From Rizvi, AZ, etal. Benign superior vena cava syndrome: stenting is now the first line of
treatment. J Vasc Surg 47(2): 372–380, 2008.)
REFERENCES
1. Wilson LD, Detterbeck FC, Yahalom J. Superior vena cava syndrome with malignant causes.
New England Journal of Medicine. 2007;356(18):1862–9.
2. Rice TW, Rodriguez RM, Light RW. The superior vena cava syndrome: Clinical characteristics
and evolving etiology. Medicine (Baltimore). 2006;85(1):37–42.
3. Stanford W, Doty DB. The role of venography and surgery in the management of patients with
superior vena cava obstruction. Annals of Thoracic Surgery. 1986;41(2):158–63.
4. Gwon DI, Ko GY, Kim JH, Shin JH, Yoon HK, Sung KB. Malignant superior vena cava syndrome: Acomparative cohort study of treatment with covered stents versus uncovered stents.
Radiology. 2013;266(3):979–87.
5. Crowner J, Marston W, Almeida J, McLafferty R, Passman M. Classification of anatomic involvement of the iliocaval venous outflow tract and its relationship to outcomes after iliocaval venous
stenting. Journal of Vascular Surgery: Venous and Lymphatic Disorders. 2014;2(3):241–5.
6. Haddad MM, Thompson SM, McPhail IR, Bendel EC, Kalra M, Stockland AH, etal. Is longterm anticoagulation required after stent placement for benign superior vena cava syndrome?
Journal of Vascular and Interventional Radiology. 2018;29(12):1741–7.
7. Azizi AH, Shafi I, Zhao M, Chatterjee S, Roth SC, Singh M, etal. Endovascular therapy for
superior vena cava syndrome: A systematic review and meta-analysis. EClinicalMedicine.
2021;37:100970.
8. Maleux G, Gillardin P, Fieuws S, Heye S, Vaninbroukx J, Nackaerts K. Large-bore nitinol stents
for malignant superior vena cava syndrome: Factors influencing outcome. American Journal of
Roentgenology. 2013;201(3):667–74.
9. Haddad MM, Simmons B, McPhail IR, Kalra M, Neisen MJ, Johnson MP, etal. comparison of
covered versus uncovered stents for benign superior vena cava (svc) obstruction. Cardiovascular
and Interventional Radiology. 2018;41(5):712–7.
10. Fagedet D, Thony F, Timsit J-F, Rodiere M, Monnin-Bares V, Ferretti G, etal. Endovascular
treatment of malignant superior vena cava syndrome: Results and predictive factors of clinical
efficacy. Cardiovascular and Interventional Radiology. 2013;36(1):140–9.
182 Indrani Sen and Manju Kalra
11. Fagedet D, Thony F, Timsit JF, Rodiere M, Monnin-Bares V, Ferretti GR, etal. Endovascular
treatment of malignant superior vena cava syndrome: Results and predictive factors of clinical
efficacy. Cardiovascular and Interventional Radiology. 2013;36(1):140–9.
12. Dinkel HP, Mettke B, Schmid F, Baumgartner I, Triller J, Do DD. Endovascular treatment of
malignant superior vena cava syndrome: Is bilateral wallstent placement superior to unilateral
placement? Journal of Endovascular Therapy. 2003;10(4):788–97.
13. Dartevelle PG, Chapelier AR, Pastorino U, Corbi P, Lenot B, Cerrina J, et al. Long-term
follow-up after prosthetic replacement of the superior vena cava combined with resection of
mediastinal-pulmonary malignant tumors. Journal of Thoracic and Cardiovascular Surgery.
1991;102(2):259–65.
14. Da Ines D, Chabrot P, Cassagnes L, Merle P, Filaire M, Ravel A, et al. [Endovascular treatment of SVC syndrome from neoplastic origin: Areview of 34 cases]. Journal de Radiologie.
2008;89(7–8 Pt 1):881–90.
15. Borsato GW, Rajan DK, Simons ME, Sniderman KW, Tan KT. Central venous stenosis associated
with pacemaker leads: Short-term results of endovascular interventions. Journal of Vascular and
Interventional Radiology. 2012;23(3):363–7.
16. Barshes NR, Annambhotla S, El Sayed HF, Huynh TT, Kougias P, Dardik A, etal. Percutaneous
stenting of superior vena cava syndrome: Treatment outcome in patients with benign and malignant etiology. Vascular. 2007;15(5):314–21.
17. Anton S, Oechtering T, Stahlberg E, Jacob F, Kleemann M, Barkhausen J, et al. Endovascular stent-based revascularization of malignant superior vena cava syndrome with concomitant implantation of a port device using a dual venous approach. Supportive Care in
Cancer: Official Journal of the Multinational Association of Supportive Care in Cancer.
2018;26(6):1881–8.
18. Sen I, Kalra M, Gloviczki P. Interventions for superior vena cava syndrome. Journal of Cardiovascular Surgery (Torino). 2022;63(6):674–81.
19. Léon D, Rao S, Huang S, Sheth R, Yevich S, Ahrar K, etal. Literature review of percutaneous
stenting for palliative treatment of malignant superior vena cava syndrome (SVCS). Academic
Radiology. 2022;29 (Suppl 4):S110–S20.
20. Anaya-Ayala JE, Smolock CJ, Colvard BD, Naoum JJ, Bismuth J, Lumsden AB, etal. Efficacy of
covered stent placement for central venous occlusive disease in hemodialysis patients. Journal of
Vascular Surgery. 2011;54(3):754–9.
21. Smayra T, Otal P, Chabbert V, Chemla P, Romero M, Joffre F, etal. Long-term results of endovascular stent placement in the superior caval venous system. Cardio Vascular and Interventional Radiology. 2001;24(6):388–94.
22. García Mónaco R, Bertoni H, Pallota G, Lastiri R, Varela M, Beveraggi EM, etal. Use of selfexpanding vascular endoprostheses in superior vena cava syndrome. European Journal of
Cardio-Thoracic Surgery: Official Journal of the European Association for Cardio-Thoracic
Surgery. 2003;24(2):208–11.
23. Breault S, Doenz F, Jouannic AM, Qanadli SD. Percutaneous endovascular management of
chronic superior vena cava syndrome of benign causes: Long-term follow-up. European Radiology. 2017;27(1):97–104.
24. Karakhanian WK, Karakhanian WZ, Belczak SQ. Superior vena cava syndrome: Endovascular
management. Journal Vascular Brasileiro. 2019;18:e20180062.
25. McDevitt JL, Goldman DT, Bundy JJ, Hage AN, Jairath NK, Gemmete JJ, etal. Gianturco
Z-stent placement for the treatment of chronic central venous occlusive disease: Implantation
of 208 stents in 137 symptomatic patients. Diagnostic and Interventional Radiology (Ankara,
Turkey). 2021;27(1):72–8.
26. Aung EY, Khan M, Williams N, Raja U, Hamady M. Endovascular stenting in superior vena
cava syndrome: Asystematic review and meta-analysis. Cardiovascular and Interventional Radiology. 2022;45(9):1236–54.
27. Kordzadeh A, Askari A, Hanif MA, Gadhvi V. Superior vena cava syndrome and wallstent:
Asystematic review. Annals of Vascular Diseases. 2022;15(2):87–93.
Management of Benign Disease of the Deep Venous System 183
28. Kitrou PM, Steinke T, El Hage R, Ponce P, Lucatelli P, Katsanos K, etal. Paclitaxel-coated balloons for the treatment of symptomatic central venous stenosis in vascular access: Results From
a European, multicenter, single-arm retrospective analysis. Journal of Endovascular Therapy.
2021;28(3):442–51.
29. Kee ST, Kinoshita L, Razavi MK, Nyman UR, Semba CP, Dake MD. Superior vena cava syndrome: Treatment with catheter-directed thrombolysis and endovascular stent placement. Radiology. 1998;206(1):187–93.
30. Danışman N, Çeneli D, Kültürsay B, Yılmaz C, Alizade E. Endovascular treatment of vena cava
superior syndrome using angiojet thrombectomy due to COVID-19 infection. Kardiologia Polska. 2022.
31. Ramjit A, Chen J, Konner M, Landau E, Ahmad N. Treatment of superior vena cava syndrome
using angiojet™ thrombectomy system. Cardiovascular and Interventional Radiology Endovascular. 2019;2(1):28.
32. Sessions KL, Anderson JH, Johnson JN, Taggart NW. AngioJet(™) thrombolysis of SVC
thrombosis after orthotopic heart transplantation: A case report. Pediatric Transplantation.
2016;20(5):723–6.
33. Ahmed O, Kuo WT. Laser-assisted venous thrombectomy for treatment of recurrent in-stent
restenosis and superior vena cava syndrome. Journal of Vascular and Interventional Radiology.
2016;27(4):603–6.
34. Sousou JM, Sherard DM, Edwards JR, Negron-Rubio E. Successful removal of a thrombus in
the setting of SVC syndrome using the INARI FlowTriever device. Radiology Case Reports.
2022;17(3):744–7.
35. Hanser A, Sieverding L, Hauser TK, Wiegand G, Hofbeck M. Stent-retriever thrombectomy in
the treatment of infants with acute thrombosis of the superior vena cava and innominate vein.
Catheterization and Cardiovascular Interventions: Official Journal of the Society for Cardiac
Angiography & Interventions. 2019;93(6):E357–E61.
36. Rizvi AZ, Kalra M, Bjarnason H, Bower TC, Schleck C, Gloviczki P. Benign superior vena
cava syndrome: Stenting is now the first line of treatment. Journal of Vascular Surgery.
2008;47(2):372–80.
37. Erben Y, Bjarnason H, Oladottir GL, McBane RD, Gloviczki P. Endovascular recanalization for
nonmalignant obstruction of the inferior vena cava. Journal of Vascular Surgery: Venous and
Lymphatic Disorders. 2018;6(2):173–82.
38. Murphy EH, Johns B, Varney E, Raju S. Endovascular management of chronic total occlusions
of the inferior vena cava and iliac veins. Journal of Vascular Surgery: Venous and Lymphatic
Disorders. 2017;5(1):47–59.
39. Morris RI, Jackson N, Smith A, Black SA. A systematic review of the safety and efficacy
of inferior vena cava stenting. European Journal of Vascular and Endovascular Surgery.
2023;65(2):298–308.
40. Kalra M, Gloviczki P, Andrews JC, Cherry KJ, Bower TC, Panneton JM, etal. Open surgical
and endovascular treatment of superior vena cava syndrome caused by nonmalignant disease.
Journal of Vascular Surgery. 2003;38(2):215–23.
41. Chiu CJ, Terzis J, MacRae ML. Replacement of superior vena cava with the spiral composite
vein graft. Aversatile technique. The Annals of Thoracic Surgery. 1974;17(6):555–60.
42. Manju Kalra IS, Bjarnason H, Gloviczki P. Superior vena cava occlusion and management.
Rutherford’s Vascular Surgery and Endovascular Therapy. 2023, Chapter162, 2148–2162.e2.
43. Mistirian AA, Balmforth DC, Oo A, Lawrence D. Open repair of superior vena cava syndrome with
high intracranial pressures using a ‘Y’ graft. Annals of Thoracic Surgery. 2022;113(4):e283–e6.
44. Uceda PV, Feldtman RW, Ahn SS. Long term results of bypass graft to the right atrium in the
management of superior vena cava syndrome in dialysis patients. Annals of Vascular Surgery.
2021;74:321–9.
45. Colombier S, Girod G, Niclauss L, Danzer D, Eeckhout E, Qanadli SD, etal. Total endovascular
repair of post-trauma ascending aortic pseudoaneurysm and secondary superior vena cava syndrome. Annals of Vascular Surgery. 2019;61:468.e13–e17.
184 Indrani Sen and Manju Kalra
46. Fichelle JM, Baissas V, Salvi S, Fabiani JN. [Superior vena cava thrombosis or stricture secondary to implanted central venous access: Six cases of endovascular and direct surgical treatment
in cancer patients]. Journal de medecine vasculaire. 2018;43(1):20–8.
47. Li H, Jiang X, Sun T. Open surgery repair for superior vena cava syndrome after failed endovascular stenting. Annals of Thoracic Surgery. 2014;97(4):1445–7.
48. Firstenberg MS, Blais D, Abel E, Go MR. Superior vena cava bypass with cryopreserved ascending aorta allograft. Annals of Thoracic Surgery. 2011;91(3):905–7.
49. Kennedy DP, Palit TK. Reconstruction of superior vena cava syndrome due to benign disease
using superficial femoral vein. Annals of Vascular Surgery. 2010;24(4):555.e7–e12.
50. Dedeilias P, Nenekidis I, Hountis P, Prokakis C, Dolou P, Apostolakis E, etal. Superior vena cava
syndrome in a patient with previous cardiac surgery: What else should we suspect? Diagnostic
Pathology. 2010;5:43.
51. Doty JR, Flores JH, Doty DB. Superior vena cava obstruction: Bypass using spiral vein graft.
Annals of Thoracic Surgery. 1999;67(4):1111–6.
52. Alimi YS, Gloviczki P, Vrtiska TJ, Pairolero PC, Canton LG, Bower TC, etal. Reconstruction
of the superior vena cava: Benefits of postoperative surveillance and secondary endovascular
interventions. Journal of Vascular Surgery. 1998;27(2):287–301.
53. AbuRahma AF, Robinson PA, Boland JP. Clinical, hemodynamic, and anatomic predictors
of long-term outcome of lower extremity venovenous bypasses. Journal of Vascular Surgery.
1991;14(5):635–44.
54. Garg N, Gloviczki P, Karimi KM, Duncan AA, Bjarnason H, Kalra M, etal. Factors affecting
outcome of open and hybrid reconstructions for nonmalignant obstruction of iliofemoral veins
and inferior vena cava. Journal of Vascular Surgery. 2011;53(2):383–93.
Chapter 18
Evidence-Based Management of Venous Aneurysms
Reid C. Mahoney, Leo Daab, and Gregory Moneta
INTRODUCTION
(1)
Venous aneurysms are rare and were first described by Osler in 1913.
presentations, from asymptomatic, incidentally discovered on imaging or at surgery, to presenting with pain, thrombosis, palpable mass, deep venous thrombosis, pulmonary embolus,
or death. There are no management strategies based on level one evidence; management is
generally individualized and/or based on case studies and case series.
Venous aneurysms have been reported to involve most major veins.
include aneurysm, varix, and phlebectasia.
(3)
For the purposes of this chapter, any venous
dilatation will be termed “aneurysm.” Venous aneurysm can be defined as a solitary area of
localized venous dilation that communicates with a main venous structure by a single channel
and does not have an association with a surgical arteriovenous communication, pseudoaneurysm, or involve vein proximal to venous stenosis or obstruction.
(4)
Herein we present the current understanding of the etiology and pathophysiology of venous
aneurysms, including their relation to congenital conditions. This is followed by a discussion
of venous aneurysm presentation and management based on anatomic location, size, imaging,
and clinical presentation.
They have varying
(2)
Synonymous terms
ETIOLOGY AND PATHOPHYSIOLOGY
Little is known about the etiology and the pathogenesis of venous aneurysms. Thinning of
the venous walls occurs with aging. Acombination of congenital and mechanical factors,
including potential prior trauma, may also stimulate the formation of venous aneurysms.
(5)
Venous reflux and venous hypertension are suggested as likely contributors to the etiology
of aneurysmal degeneration.
fibers in the vein walls are seen histologically; hyalinization of the intima can also occur.
(6)
Reduced amount and size of smooth muscle cells and elastin
(7)
An
early investigation of the popliteal vein by Lev and Saphir proposed that areas associated with
stress were prone to hypertrophy of the vein, while thinning of the venous wall was seen in
areas that were in direct apposition with the artery, perhaps indicating external force may be
a cause of venous aneurysmal changes.
(3)
Schatz and Fine, in one of the first series of venous
aneurysms, noted two commonly found histologic changes: an increase in fibrous connective
tissue with decrease in smooth muscle cells and an increase or decrease in fibrous connective
tissue and elastic tissue.
lar venous aneurysms, including increased levels of matrix metalloproteinases.
(2)
Degenerative histologic changes are described for internal jugu-
(8)
Histology,
however, appears to be more variable for popliteal venous aneurysms, perhaps in response to
gravitational forces, tending to have thickened and fibrosed intima and regions of increased
smooth muscle cells.
DOI: 10.1201/9781003316626-21 185
(7)
186 Reid C. Mahoney, et al.
Venous aneurysms appear to have equal distribution between sexes and a wide range of
age at discovery is noted.
(6)
Most patients with venous aneurysms will not have an associated genetic mediated pathway or syndrome. However, there are known genetic syndromes
that increase a patient’s chance of having venous pathology, including malformations and
aneurysms. Blue rubber bleb nevus syndrome is a rare syndrome of venous malformations
primarily affecting the gastrointestinal tract. It is generally sporadic but can be transmitted
in an autosomal dominant manner and has been associated with inferior vena cava (IVC)
aneurysm.
(9)
Klippel-Trenaunay syndrome is a well-known disorder that results in a wide
range of lymphatic and venous anomalies including agenesis, hypoplasia, atresia, valvular
incompetence, external compression by fibrous bands, and aneurysmal degeneration.
(6)
These
anomalies most frequently involve the lower extremity.
MANAGEMENT
Lower Extremity Venous Aneurysms
Popliteal Venous Aneurysms
The popliteal vein appear to be the most common site of venous aneurysms.
is variable, from asymptomatic to pain, deep venous thrombosis, pulmonary embolism, or
death from pulmonary embolism.
(7)
Popliteal venous aneurysms are the most common venous
aneurysm to present with pulmonary embolism (PE), with rates as high as 70% of patients
afflicted with popliteal venous aneurysms.
(7)
Interestingly, size does not appear to impact the
risk of pulmonary embolism. Rupture rates are not known but appear to be exceedingly low
as there are no reports describing rupture of a primary popliteal venous aneurysm.
Large popliteal venous aneurysms may be palpable to the patient or healthcare provider,
but most popliteal venous aneurysms are diagnosed utilizing ultrasound. CT and MRI can
also be used for diagnosis and, if elected, operative planning. Size criteria to define a popliteal
venous aneurysm has been debated, but most often two to three times the size of a normal
popliteal vein is considered aneurysmal. This equates to approximately 1.5 to 2cm in diameter representing an aneurysmal popliteal vein.
(7)
Once a patient has been diagnosed with
a popliteal venous aneurysm, further investigation is warranted to ensure no other venous
aneurysms are present, including the contralateral popliteal vein.
Symptoms, aneurysm size, mass effect, and the presence or absence of associated intraluminal thrombus (Figure18.1) influence management. Medical management with anticoagulation
has been the mainstay of treatment for popliteal venous aneurysms. However, anticoagulation alone does not appear to prevent thromboembolic events. Nasr et al demonstrated 43%
of patients with popliteal venous aneurysms treated with anticoagulation alone went on to
develop thromboembolic complications, including one death from pulmonary embolism.
Given their propensity to lead to catastrophic results, including pulmonary embolism and
death, intervention for symptomatic aneurysms is widely accepted. Management of asymptomatic popliteal aneurysm is less clear but is likely still best managed surgically in reasonably
fit patients to avoid the potential of future complications.
Surgical management of popliteal venous aneurysms is variable between aneurysmectomy
and venorrhaphy or resection with venous interposition graft.
(1)
Posterior approach appears
to be the most common. Additional options include the use of PTFE graft and the use of patch
venoplasty.
(1)
Outcomes appear to be similar regardless of surgical approach. This indicates
(3)
Presentation
(10)
Evidence-Based Management of Venous Aneurysms 187
Figure 18.1 Popliteal venous aneurysm with intraluminal thrombus.
individual case planning based on patient presentation, anatomy of the aneurysm, and surgeon preference appears to be a reasonable tactic for treatment. It should be noted that one
review does demonstrate higher rates of postoperative thrombosis in venous interposition
grafts; this finding has not been replicated in other reviews.
(1)
The role of anticoagulation pre
and postoperatively appears institution dependent, but most surgeons will treat with anticoagulation until the postoperative period, with some surgeons recommending continuing
anticoagulation for up to 3 months after surgery.
(10)
Iliac and Common Femoral Venous Aneurysms
Iliac venous aneurysms are quite rare, although aneurysms of the common, external, and
internal iliac vein have been reported. Arecent review reported 50 cases of iliac venous aneurysms, noting a 2:1 male to female ratio.
(11)
Most cases included in this review were related to
trauma or arteriovenous fistula and thus not primary aneurysms. Of those that were primary
aneurysms, approximately 70% were found in women, and the majority were found in the
left external iliac vein. This is likely due to extrinsic trauma/forces from the right common
iliac artery as a variant of May-Thurner syndrome.
(12)
Abdominal pain, back pain, leg swelling, and pulmonary embolism have been reported in primary iliac venous aneurysm. Most
patients are asymptomatic, and rupture has never been reported.
(13)
Although the data is less
compelling than for popliteal venous aneurysms, given the risk of thrombosis and pulmonary
embolism, surgical treatment of primary iliac venous aneurysms is reasonable in suitable risk
188 Reid C. Mahoney, et al.
patients. Venorrhaphy, venoplasty, bypass, and ligation are all possible options, although ligation should only be performed if there is adequate collateral drainage.
One report details coil embolization of a common femoral vein aneurysm,
(14)
but coiling
does not seem to eliminate the potential for thromboembolic events, and management akin
to popliteal or iliac veins seems more prudent.
Lower Extremity Superficial Venous Aneurysms
Superficial venous aneurysms of the lower extremity are less common than deep aneurysms
and likely represent an overall benign process. They may be discovered in an evaluation for
symptoms consistent with chronic venous disease (Figure18.2). The most common presenting symptoms include pain, swelling, and a palpable mass. Cosmesis is the most common
reason to intervene. There have been reports of deep venous thrombosis and pulmonary
embolism from superficial venous aneurysms of the lower extremity; however, it appears that
the risk of thromboembolic events remains quite low.
can compress the sural nerve, causing significant pain within the distribution of the nerve.
(2)
Small saphenous venous aneurysms
(4)
The most common surgical approaches are aneurysmectomy and venorrhaphy or excision
and interposition grafting. Ligation is a viable option if the deep venous system remains patent. Endovascular treatment is likely to leave a large palpable mass if used for superficial
venous aneurysms.
Figure 18.2 Ultrasound of an accessory saphenous vein aneurysm discovered in an evaluation for chronic
venous disease.
Evidence-Based Management of Venous Aneurysms 189
Upper Extremity, Internal Jugular, and Thoracic Venous
Aneurysms
Primary axillary venous aneurysms are distinctly uncommon. Although possible, thromboembolic events are quite rare in upper extremity aneurysms, including in the axillary vein.
There is a case report of axillary venous aneurysm and associated pulmonary embolus.
However, in a study of 30 patients with venous aneurysms, four axillary venous aneurysms
were encountered, and none of these patients had thromboembolic events.
(2)
Reasons to intervene surgically include symptoms of compression or pain and cosmetic reasons. If there is
concern for the possibility of VTE, such as thrombus within the aneurysm, it is reasonable
to consider surgical treatment or anticoagulation. Surgical treatment options are similar to
those for lower extremity aneurysms, including aneurysmectomy and venorrhaphy, excision
with grafting, or ligation.
Cephalic, brachial, and basilic venous aneurysms unrelated to arteriovenous fistula formation are rare, although one case series did include an asymptomatic cephalic vein aneurysm.
It is unlikely that they would require intervention unless they are causing significant cosmetic
issues or symptoms.
(15)
(4)
Figure 18.3 Internal jugular venous aneurysm.