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304 Chapter 30 Mesenteric vein thrombosis
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30.3 Venogram example of the transjugular intrahepatic por-
tosystemic shunt (TIPS) procedure showing partially occlusive
mesenteric venous thrombus (large white arrow). The stented
communication (thin black arrows) with the inferior vena cava is
readily apparent.
30.2 Magnetic resonance imaging (MRI) example of mesen-
teric vein thrombus. Contrast-enhanced MRI of the abdomen
demonstrates an acute occlusive venous thrombus (arrows)
involving the superior mesenteric vein (SMV) in both cross-sectional
(a) and coronal (b) views. The SMV is distended with an
acute-appearing thrombus.
30.4.4 Venography
Although more invasive than the cross-sectional imaging
modalities described, venography can include an assessment
of mesenteric venous patency and ow direction, venous
collaterals, and a comprehensive assessment of thrombus
burden (Figure30.3). Pressure gradients can be measured
directly, and endovascular therapies can be readily accomplished.
impaired lling of the accompanying veins, arterial spasm,
and prolonged opacication of the arterial arcades, all of
which provide indirect evidence supporting the diagnosis.
The limitations of venography include the requirement
of experienced personnel with appropriate imaging hardware. Additionally, the 2D image produced may overestimate or underestimate thrombus burden within the vessel,
depending on angulation and view. The evaluation includes
transfer of a potentially unstable patient to a uoroscopy
suite for image acquisition, which is invasive and exposes
the patient to both nephrotoxic contrast and ionizing
radiation.
Selective mesenteric angiography demonstrates
In summary, there are several imaging studies to choose
from in the evaluation of patients with suspected MVT.
The choice involves a careful clinical assessment of the
patient to determine the likelihood of MVT versus other
diagnoses. For the stable patient with reasonable creatinine clearance, contrast-enhanced CT imaging will provide
considerable clinical information. For patients who are less
stable, bedside duplex ultrasound will provide an assessment of mesenteric vascular patency; however, it requires
an experienced tech comfortable with the imaging study.
The ultimate choice of imaging will depend on the radiology expertise and machinery available at the institution
that is caring for the patient. Discussion of the patient-specic variables with the attending radiologist prior to decision making is a very valuable and fruitful place to start.
30.4.5 Blood tests
Blood tests may be very helpful but are not very specic in
the evaluation of patients with suspected MVT. The complete blood count with differentials is important for assessing both the hemoglobin and hematocrit to ensure that
occult bleeding is not overlooked. Polycythemia rubra vera,
essential thrombocythemia, leukemia, and other hematologic disorders that may predispose to venous thrombosis
can also be screened for with this test. The white blood
count will alert the physician to infections related to bowel

30.5 Treatment 305
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infarction or perforation. Elevated serum lactate levels and
metabolic acidosis will help to identify those patients with
a severely ischemic or infarcted bowel. Transaminase elevation implies additional involvement of the portal or hepatic
venous system. This is particularly relevant to the initiation
of treatment with vitamin K antagonists. Fibrin D-dimer
elevation may also be helpful in determining the timing of
thrombosis. An acute thrombus is anticipated to be accompanied by signicant D-dimer elevations. In the subacute
or chronic setting, thrombosis evolution may no longer be
associated with D-dimer abnormalities.
Thrombophilia laboratory assessment of MVT should
be considered on all MVT patients. This assessment assists
with choice of anticoagulant and guides duration of anticoagulation. The timing of the laboratory prole may be a
difcult decision to make. Ideally, one would obtain these
types of tests once the thrombus has been appropriately
treated and the patient is no longer taking warfarin or
heparin. Typically, this type of testing would be performed
more than 2 weeks after warfarin has been discontinued in
order to maximize the test sensitivity and specicity. Even
in the presence of a provoked factor such as abdominal
surgery or pancreatitis, a panel should be considered, as
thrombophilia is a known risk factor for MVT in these
situations.
24,25
30.5 TREATMENT
30.5.1 Medical management
The appropriate treatment of patients with MVT involves
multidisciplinary input from both medical and surgical services. Clinical observations suggest that immediate anticoagulation with heparin early in the course of the disease
improves survival, reduces thrombus propagation, and
reduces the risk of recurrence.
ing is not necessarily a contraindication to anticoagulant
therapy, but the risk of bleeding must be weighed against
the risk of bowel infarction. This decision requires careful and thorough patient evaluation, including measures
of bowel ischemia, thrombus burden and acuity, collateral
circulation, and an assessment of bleeding risk. Although
improved survival rates have been shown among patients
receiving anticoagulant therapy, the need for chronic anticoagulant therapy in these patients is less clear. Observational studies suggest that chronic anticoagulant use
reduces the incidence of recurrent venous thrombosis and
promotes recanalization of the thrombosis and prevents
its propagation.
anticoagulant therapy, however, have not been dened by
randomized trials. In general, anticoagulation should be
continued until provoking factors have been eliminated, if
possible. In those patients whose MVT can be attributed
to temporary risk factors, 3–6 months of anticoagulants
is likely reasonable. If genetic thrombophilia is uncovered
28
The efcacy and optimal duration of
18,26,27
Gastrointestinal bleed-
during the patient’s workup, indenite anticoagulation
may be warranted.
Empiric antibiotics are often used during early treatment to prevent bacterial translocation. However, observational data suggest there is no signicant benet in
mortality with the use of empiric antibiotics.
not been shown to reduce bacterial translocation, but there
has been a reported increased rate of Clostridium difcile
infection. Therefore, unless patients are suspected to have
an intra-abdominal infection or sepsis, antibiotics should
be used sparingly.
30
They have
30.5.2 Endovascular interventions
With the rise in endovascular techniques, various endovascular approaches to treating MVT have been reported.
Endovascular therapies are generally pursued for very
select patients with MVT that is early in the diagnosis,
without any signs of bowel ischemia or sepsis. As such,
potential candidates for these approaches are patients
who do not have a surgical intervention planned and those
at low risk for bleeding complications. This is generally
suggested in noncirrhotic patients and patients without
a malignancy, owing to the bleeding risk associated with
30
both.
Endovascular approaches have been described to
be safe and effective in the available series. However, due
to the relative rarity of MVT, the majority of these reports
are single-center case series and are thus difcult to gen-
30,31
eralize.
tion following in 75%–100% of patients and resolution
of symptoms in 85%–100% of patients. However, bleeding complication rates vary and are poorly described.
DiMunno et al. report that percutaneous treatment of
MVT reduces the development of portal hypertension by
40%.
randomized control trials into the benets of endovascular
therapies for MVT is warranted.
treatment of MVT, there are multiple reported approaches.
Access can be gained by cannulation of the portal venous
system via a percutaneous transhepatic or transjugular
approach. These approaches allow for mechanical thrombectomy. Catheter-directed thrombolysis can also be
performed through these routes, as well as others. Catheter-directed thrombolysis initiated through indirect cannulation of the superior mesenteric artery has also been
described. Additionally, if the patient is planned for surgical intervention and laparotomy, direct intraoperative
catheterization can be achieved for thrombectomy. Prospective trials are needed to further investigate the safety
proles of these approaches.
The available reports quote thrombus resolu-
32–34
34
Further investigation with comparative studies and
With regard to procedural technique to percutaneous
30.5.3 Surgical treatment
While the majority of patients with MVT can be treated
safely with anticoagulation alone, there is a portion of
30

306 Chapter 30 Mesenteric vein thrombosis
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30.4 Computed tomography angiography shows (A) thrombus within the lumen of the superior mesenteric vein (SMV; circle) in a
patient without evidence of bowel ischemia and
gestive of bowel ischemia (arrows).
(B) intraluminal thrombus in the SMV (circle) of a patient with dilated bowel, sug-
patients who require surgical exploration and bowel resection. At our institution, we found that approximately 16%
of patients presenting with MVT will require surgical
intervention.
8
MVT accompanied by evidence of peritonitis or bowel infarction warrants surgical intervention
and resection of the involved bowel (Figure30.4). Other
clinical ndings that may suggest bowel ischemia include
leukocytosis, lactic acidosis, or signs of sepsis. The key to
successful surgery is to resect sufcient bowel to ensure
proper anastomotic healing while preserving as much
viable intestine as possible. The decision-making process
may be complex and may require the technical skill and
expertise of a surgeon who has familiarity with operations
of this type. Management is dictated by the intraoperative
ndings, which range from segmental bowel ischemia to
widespread mesenteric necrosis. Bowel perforation may or
may not be present. Often, the surgical procedure is staged
with a repeat (“second-look”) laparotomy performed 1
day later. Postoperatively, anticoagulants should be initiated as soon as hemostasis is adequately achieved. Thrombectomy remains a potential treatment option for selected
patients but does add to the operative time, so a multidisciplinary approach may be helpful with this complex clinical
decision making.
30.6 OUTCOMES
Mortality rates have been reported to be as high as 32%
in MVT.
to be less than 12%, with no signicant difference when
bowel resection is required.
mortality rates of MVT as high as 25%; however, these
are usually in systemically ill patients who do not present in the acute setting.
28,35
One-year mortality rates have been reported
8
Some studies have reported
36–38
When patients present acutely
and there is prompt treatment, mortality rates have been
reported to be as low as 1.25%.
yielded improved outcomes over time results with declining mortality rates.
39
Delay of diagnosis and intervention,
2
Recent reports have
postsurgical complications, and underlying malignancy
carry worse prognoses. The recurrence rate of venous
thrombosis in these patients is not completely clear.
Although the rates are said to be increased, Kumar and
Kamath reported only two recurrences among 30 patients
with MVT limited to the superior mesenteric vein over
a median follow-up of 18 months.
40
Recurrent thrombosis was noted in 5 out of 39 patients with combined
porto-mesenteric-splenic thrombosis during a median
follow-up period of 27 months. These data suggest recurrence rates of 5%–6% per year. Morasch etal. reported
that all 22 long-term survivors of MVT (19 treated with
warfarin) were thrombosis free at the last follow-up visit
(mean 57.7-month period).
37
Anticoagulant treatment has been associated with an
essentially unchanged rate of major bleeding, at 3.9 per
100 patient-years, but a lower rate of thrombotic events,
at 5.6 per 100 patient-years. When anticoagulation was
discontinued, rates were 1.0 per 100 patient-years for
bleeding and 10.5 per 100 patient-years for thrombosis recurrence.
37
The highest rates of major bleeding and
thrombotic events are reported to be cirrhotics, while
the lowest rates of bleeding are observed in patients with
thrombosis secondary to transient risk factors.
8,41
30.7 CONCLUSION
MVT, although less common than arterial thrombosis,
remains an important cause of mesenteric ischemia. The
incidence of MVT is increased in patients with underlying

References 307
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thrombophilia, malignancy, and abdominal infection or
surgery. There can be considerable delay in the diagnosis of
MVT because of a low degree of clinical suspicion and the
nonspecic clinical presentation. CT angiography and magnetic resonance angiography are the preferred methods for
MVT diagnosis, although other imaging techniques such as
duplex ultrasonography can be utilized as well. Immediate
use of anticoagulation is recommended as rst-line therapy
and can improve outcomes. Surgery should be limited to
patients with peritonitis or perforation, with the objective
of conserving as much bowel as possible yet ensuring viable
margins. The safety and efcacy of endovascular techniques
for the treatment of MVT remain unknown. MVT has lower
morbidity and mortality than arterial mesenteric ischemia.
Guidelines 30.0 of the American Venous Forum on mesenteric vein thrombosis
No. Guideline Grade of
30.1 For evaluation of patients with suspected mesenteric vein thrombosis (MVT), we recommend
computed tomography angiography and magnetic resonance angiography.
30.2 For patients with MVT, we recommend immediate anticoagulation to improve outcomes. 1
30.3 For patients with MVT and evidence of peritonitis or perforation, we recommend surgery. 1
30.4 For patients with MVT and high-risk inherited thrombotic disorders or other permanent risk for
thrombosis, we recommend long-term anticoagulation.
recommendation
1
(strong)
(strong)
(strong)
1
(strong)
30
Quality of
evidence
B
(moderate)
B
(moderate)
B
(moderate)
B
(moderate)
REFERENCES
★ Systematic review
♦ Guidelines
1. Elliot JW. II. The operative relief of
gangrene of intestine due to occlusion of
the mesenteric vessels. Ann Surg. 1895
Jan;21(1):9–23.
2. Blumberg SN, Maldonado TS.
Mesenteric venous thrombosis. J Vasc
surgery Venous Lymphat Disord. 2016
Oct;4(4):501–7.
3. Acosta S, Ogren M, Sternby N-H,
Bergqvist D, Björck M. Mesenteric
venous thrombosis with transmural
intestinal infarction: Apopulation-based
study. J Vasc Surg. 2005 Jan;41(1):
59–63.
4. Acosta S, Alhadad A, Svensson P, Ekberg
O. Epidemiology, risk and prognostic
factors in mesenteric venous thrombosis.
Br J Surg. 2008 Oct;95(10):1245–51.
5. Harnik IG, Brandt LJ. Mesenteric
venous thrombosis. Vasc Med. 2010
Oct;15(5):407–18.
6. Rajasekhar A, Zumberg M. Venous
thromboses at unusual sites. Consult
Hemost Thromb. 2019:300–37.
7. Rhee RY, Gloviczki P. Mesenteric venous
thrombosis. Surg Clin North Am. 1997
Apr;77(2):327–38.
8. Andraska E, Haga L, Reitz K,
Li X, Ramos R, Avgerinos E, etal.
Acute superior mesenteric venous
thrombosis results in high rates of
readmission and morbidity. J Vasc
surgery Venous Lymphat Disord. 2020
Sep;8(5):748–55.
9. Condat B, Pessione F, Helene Denninger
M, Hillaire S, Valla D. Recent portal or
mesenteric venous thrombosis: Increased
recognition and frequent recanalization
on anticoagulant therapy. Hepatology.
2000 Sep;32(3):466–70.
10. Zhang J, Duan ZQ, Song QB, Luo YW,
Xin SJ, Zhang Q. Acute mesenteric
venous thrombosis: Abetter outcome
achieved through improved imaging
techniques and a changed policy of clinical management. Eur J Vasc Endovasc
Surg Off J Eur Soc Vasc Surg. 2004
Sep;28(3):330–34.
11. Finazzi G, De Stefano V, Barbui T.
Splanchnic vein thrombosis in myeloproliferative neoplasms: Treatment
algorithm 2018. Blood Cancer J. 2018
Jun;8(7):64.
12. Rhee RY, Gloviczki P, Finazzi G, De
Stefano V, Barbui T. Splanchnic vein
thrombosis in myeloproliferative
neoplasms: Treatment algorithm
2018. Surg Clin North Am. 2018
Apr;8(2):64.
13. Austin SK, Lambert JR. The JAK2
V617F mutation and thrombosis. Br J
Haematol. 2008 Nov;143(3):307–20.
14. Colaizzo D, Amitrano L, Tiscia GL,
Scenna G, Grandone E, Guardascione
MA, etal. The JAK2 V617F mutation
frequently occurs in patients with portal
and mesenteric venous thrombosis. J
Thromb Haemost. 2007 Jan;5(1):55–61.
15. Sutkowska E, McBane RD, Tafur AJ,
Sutkowski K, Grill DE, Slusser JP,
etal. Thrombophilia differences in
splanchnic vein thrombosis and lower
extremity deep venous thrombosis in
North America. J Gastroenterol. 2013
Oct;48(10):1111–8.
16. Singal AK, Kamath PS, Tefferi A. Mesenteric venous thrombosis. Mayo Clin
Proc. 2013 Mar;88(3):285–94.
17. Klar E, Rahmanian PB, Bücker A,
Hauenstein K, Jauch K-W, Luther B.
Acute mesenteric ischemia: Avascular
emergency. Dtsch Arztebl Int. 2012
Apr;109(14):249–56.
18. Maldonado TS, Blumberg SN, Sheth
SU, Perreault G, Sadek M, Berland T,
etal. Mesenteric vein thrombosis can be
safely treated with anticoagulation but
is associated with signicant sequelae
of portal hypertension. J Vasc surgery
Venous Lymphat Disord. 2016 Oct;4(4):
400–6.
★
19. Acosta S, Salim S. Management of
acute mesenteric venous thrombosis:
Asystematic review of contemporary
studies. Scand J Surg SJS Off organ
Finnish Surg Soc Scand Surg Soc. 2021
Jun;110(2):123–9.
★
20. Hall TC, Garcea G, Metcalfe M, Bilku
D, Dennison AR. Management of acute
non-cirrhotic and non-malignant portal
vein thrombosis: Asystematic review.
World J Surg. 2011 Nov;35(11):
2510–20.

308 Chapter 30 Mesenteric vein thrombosis
https://t.me/med1917
21. Feldman ZM, Wang LJ, Chou EL, Latz
CA, Sumpio BJ, Eagleton MJ, etal.
Venous mesenteric ischemia carries high
procedural burden and elevated mortality in patients with severe presentation.
J Vasc surgery Venous Lymphat Disord.
2021 Nov;9(6):1479–87.
22. Aschoff AJ, Stuber G, Becker BW,
Hoffmann MHK, Schmitz BL, Schelzig
H, etal. Evaluation of acute mesenteric
ischemia: Accuracy of biphasic mesenteric multi-detector CT angiography.
Abdom Imag. 2009;34(3):345–57.
23. Bradbury MS, Kavanagh P V, Bechtold
RE, Chen MY, Ott DJ, Regan JD, etal.
Mesenteric venous thrombosis: Diagnosis and noninvasive imaging. Radiogr
Rev Publ Radiol Soc North Am Inc.
2002;22(3):527–41.
24. Parikh M, Adelsheimer A, Somoza E,
Saunders JK, Ude Welcome A, Chui P,
etal. Factor VIII elevation may
contribute to portomesenteric vein
thrombosis after laparoscopic sleeve
gastrectomy: Amulticenter review
of 40 patients. Surg Obes Relat Dis
Off J Am Soc Bariatr Surg. 2017
Nov;13(11):1835–9.
25. Boiko JR, Srinath AI, Cooper JD.
Portomesenteric venous thrombosis in
previously healthy adolescents presenting
with subacute abdominal pain.
Clin Pediatr (Phila). 2016
Sep;55(10):975–8.
♦26. Björck M, Koelemay M, Acosta S, Bastos
Goncalves F, Kölbel T, Kolkman JJ, etal.
Editor’s choice—Management of the
diseases of mesenteric arteries and veins:
Clinical practice guidelines of the European Society of Vascular Surgery (ESVS).
Eur J Vasc Endovasc Surg Off J Eur Soc
Vasc Surg. 2017 Apr;53(4):460–510.
27. Hmoud B, Singal AK, Kamath PS.
Mesenteric venous thrombosis. J Clin
Exp Hepatol. 2014 Sep;4(3):257–63.
28. Russell CE, Wadhera RK, Piazza
G. Mesenteric venous thrombosis. Circulation [Internet]. 2015
May5;131(18):1599–603. https://
doi.org/10.1161/CIRCULATIONAHA.114.012871
30. Lewcun JA, Khatun R, Allen S, Hazelton
JP, Cooper A. Patient outcomes in
mesenteric venous thrombosis treated
with empiric antibiotics. Am Surg. 2021
Apr;87(4):658–63.
30. Oguslu U, Uyanik SA, Cenkeri HÇ, Atli
E, Yilmaz B, Gümüş B. Transhepatic
pharmacomechanical thrombectomy
of symptomatic acute noncirrhotic,
nonmalignant portomesenteric venous
thrombosis: Midterm results. AJR Am J
Roentgenol. 2021 Aug;217(2):418–25.
31. Rabuf P, Vagnarelli S, Bruni A, Antonuccio G, Ambrogi C. Percutaneous
pharmaco-mechanical thrombectomy of
acute symptomatic superior mesenteric
vein thrombosis. Cardiovasc Intervent
Radiol. 2020 Jan;43(1):46–54.
32. Hollingshead M, Burke CT, Mauro
MA, Weeks SM, Dixon RG, Jaques PF.
Transcatheter thrombolytic therapy
for acute mesenteric and portal vein
thrombosis. J Vasc Interv Radiol. 2005
May;16(5):651–61.
33. Cai W, Li X, Shu C, Qiu J, Fang K, Li M,
etal. Comparison of clinical outcomes
of endovascular versus open revascularization for chronic mesenteric ischemia:
Ameta-analysis. Ann Vasc Surg. 2015
Jul;30(5):934–40.
34. Di Minno MND, Milone F, Milone M,
Iaccarino V, Venetucci P, Lupoli R, etal.
Endovascular thrombolysis in acute
mesenteric vein thrombosis: A3-year
follow-up with the rate of short and
long-term sequaelae in 32 patients.
Thromb Res. 2010 Oct;126(4):305–8.
★35. Schoots IG, Koffeman GI, Legemate
DA, Levi M, van GulikTM. Systematic
review of survival after acute mesenteric
ischaemia according to disease aetiology.
Br J Surg. 2004 Jan;91(1):17–27.
36. Dentali F, Ageno W, Witt D, Malato
A, Clark N, Garcia D, etal. Natural
history of mesenteric venous thrombosis in patients treated with vitamin K
antagonists: Amulti-centre, retrospective
cohort study. Thromb Haemost. 2009
Sep;102(3):501–4.
37. Morasch MD, Ebaugh JL, Chiou AC,
Matsumura JS, Pearce WH, Yao JS.
Mesenteric venous thrombosis: Achanging clinical entity. J Vasc Surg. 2001
Oct;34(4):680–4.
38. Hedayati N, Riha GM, Kougias P,
Huynh TT, Cheng C, Bechara C,
etal. Prognostic factors and treatment outcome in mesenteric vein
thrombosis. Vasc Endovascular Surg.
2008;42(3):217–24.
39. Salim S, Zarrouk M, Elf J, Gottsäter A,
Ekberg O, Acosta S. Improved prognosis
and low failure rate with anticoagulation as rst-line therapy in mesenteric
venous thrombosis. World J Surg. 2018
Nov;42(11):3803–11.
40. Kumar S, Sarr MG, Kamath PS. Mesenteric venous thrombosis. N Engl J Med.
2001 Dec;345(23):1683–8.
41. Wang L, Guo X, Bai Z, Yin Y, Xu S,
Pan J, etal. Impact of asymptomatic
superior mesenteric vein thrombosis
on the outcomes of patients with liver
cirrhosis. Thromb Haemost. 2022
Dec;122(12):2019–30.

PART
Management of chronic venous disorders
https://t.me/med1917
SUB-PART A: General considerations
Edited by Michael C. Dalsing
31 Clinical presentation and assessment of patients with venous disease
Sarah Onida, Tristan R. A. Lane, and Alun H. Davies
32 Diagnostic algorithm for chronic venous disorders
Amani D. Politano and Robert B. McLafferty
33 Compression therapy for chronic venous disease and venous ulceration
Sergio Gianesini, Leo J. Daab, Erica Menegatti, Yung-Wei Chi, Hugo Partsch, and Gregory L. Moneta
34 Drug treatment for chronic venous disease
Monika L. Gloviczki and Joseph D. Raffetto
4

https://t.me/med1917

CHAPTER
31
https://t.me/med1917
Clinical presentation and assessment
of patients with venous disease
Sarah Onida, Tristan R. A. Lane, and Alun H. Davies
31.1 INTRODUCTION
Venous presentations are among the most common complaints in patients seeking assessment in primary and secondary care vascular clinics.
signs may be nonspecic and difcult to assess. It is therefore important to have a comprehensive understanding of
the presentations of venous disease to ensure patients are
diagnosed and managed appropriately.
1
Patient symptoms and clinical
31.2 THE UPPER LIMB
Vascular disorders of the upper extremity are less common
than in the lower limb, affecting approximately 10% of
the population.
importance in day-to-day activities. Furthermore, the vascular tree of the upper limb plays an important role in
individuals with chronic disease, for example, with respect
to the formation of arteriovenous stulae for dialysis or
for the administration of long-term intravenous therapy.
Venous pathology affecting the dominant arm can be life
changing for an individual and can potentially cause considerable disability.
31.2.1 Trauma
Acute trauma and repetitive micro-trauma can both result
in vascular disorders of the upper limb. This is particularly
prevalent in middle-aged males employed in manual labor
or young males involved in acute traumatic injury. Individuals working with handheld vibrating tools may be subject
to chronic micro-trauma.
31.2.2 Intermittent subclavian/upper
Although uncommon, compression of the subclavian
vein can result in intermittent symptomatology, including
intermittent swelling, discomfort, and tightness (relieved
by rest) and abnormally prominent supercial veins. These
symptoms are aggravated in the erect position or when
the arm is raised (e.g., when typing, driving, or painting
a ceiling).
2
The upper limb is clearly of paramount
extremity vein obstruction
Thoracic outlet syndrome (TOS) may present in this
3
manner,
rib, a congenital brous band compressing neurovascular
structures, or compression at the costoclavicular junction.
TOS may be neurological or vascular in nature according to the structure compressed: the brachial plexus and
subclavian artery in the interscalene triangle or the subclavian vein in the costoclavicular space. Patients with
these symptoms should be evaluated with their shoulders
in the neutral position and in specic stress tests to elicit
signs and symptoms. These include braced in the military
position (Figure 31.1) or with arms hyperabducted and
externally rotated at the shoulder (Figure 31.2), as this
will result in the subclavian vein being compressed by the
scissor-like closure of the costoclavicular space. Arm discomfort, swelling, and venous distension in this position
suggest intermittent venous outow obstruction. However,
as with arterial thoracic outlet obstruction, these ndings
can be reproduced in approximately 50% of asymptomatic
individuals at the extremes of movement.
vers are useful in assessing patients but have been reported
to have low sensitivity and specicity.
thrombosis is a likely outcome of intermittent obstruction,
active investigations with a view to surgical decompression
are indicated.
usually secondary to the presence of a cervical
4
These maneu-
5
As subclavian vein
31.2.3 Subclavian/upper vein thrombosis
31.2.3.1 Primary upper extremity deep venous
thrombosis
Deep venous thrombosis (DVT) can arise as a result of
hypercoagulable disorders or acute or recurrent trauma to
a blood vessel.
Paget–Schroetter syndrome (effort vein thrombosis)
describes a syndrome of axillosubclavian vein thrombosis
associated with repetitive upper limb activities. The syndrome is due to repeated trauma to the endothelium of the
subclavian vein, which may be secondary to the presence of
the anatomical abnormalities, leading to the development
of venous TOS. This syndrome is more common in young,
healthy men undertaking manual work, preferentially
involving the dominant arm. Patients are usually symptomatic, presenting with arm discomfort, pain, swelling, and
dilated veins across the shoulder and upper arm (Urschel
DOI: 10.1201/9781003328971-35
311311

312 Chapter 31 Clinical presentation and assessment of patients with venous disease
retraction of shoulder
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Backward and downward
31.1 Compression of the subclavian vein in the military position. When the shoulder is retracted backward and downward, the sub-
clavian vein is narrowed by the scissoring action of the clavicle and the rst rib.
Source: (Adapted from Adams JT et al. Surgery 1968;63:147–65.)
31.2 Compression of the subclavian vein with hyperabduction of the arm. With hyperabduction and external rotation of the arm, the
clavicle rotates backward and downward and causes compression of the subclavian vein secondary to narrowing of the costoclavicular space.
Source: (Adapted from Adams JT et al. Surgery 1968;63:147–65.)
sign).6 The arm may be pale, cyanotic, or red. Patients
usually present acutely or subacutely, with sudden onset
of symptoms. Often, patients can identify a precipitating
event, such as a sports injury.
Pulmonary embolism (PE) following upper extremity
DVT (UEDVT) has been reported to occur in 2%–35% of
individuals.
7
Post-thrombotic syndrome, characterized by
chronic pain, heaviness, and swelling, develops in up to 45%
of individuals with UEDVT, while recurrent thrombosis is
affects up to 9.8% at 3 years.
of UEDVT in young men and its preferential involvement of
the dominant arm, this can lead to considerable functional
disability and a profound impact on quality of life.
Compression ultrasound with duplex assessment is a
recommended initial investigation. Formal venography
is the gold-standard diagnostic modality; however, due
to its invasive nature, this is not usually performed as a
8
Considering the prevalence
9
rst investigation. Contrast computed tomography (CT)
venography provides a noninvasive option to permit the
assessment of venous anatomy. Further imaging modalities, including cervical spine radiography and magnetic
resonance imaging (MRI), can reveal bony or soft tissue
abnormalities that may have caused the DVT.
The initial management comprises anticoagulation. In
highly symptomatic patients, thrombus removal strategies
can be considered, including catheter-directed or pharmacomechanical catheter-directed thrombolysis (CDT and
PCDT) with or without venoplasty followed by surgery for
thoracic outlet decompression in selected cases.
10
31.2.3.2 Secondary UEDVT
DVT can result from direct trauma to the vessel—this can
be iatrogenic or secondary to central venous cannulation,
catheterization, or pacemaker insertion. Central venous

31.2 The upper limb 313
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catheters present a signicant risk of thrombosis, which
is reported to occur in 14%–18% of cases. Recurrent
intervention to the central veins can lead to stenosis and
thrombosis. Unlike primary UEDVT, the onset of obstruction is gradual with recurrent intervention. Patients, therefore, have time to develop a collateral circulation and be
asymptomatic. When present, the symptoms may be vague
shoulder or neck discomfort or arm edema. Alternatively,
patients can present with a nonfunctioning line; venous
duplex imaging or a “linogram” (contrast injection) can
reveal the thrombosis. Treatment involves thrombolysis if
the thrombus is extensive, or simply removal of the line
and anticoagulation. Lines should be placed, if possible, in
the internal jugular, cephalic, or external jugular vein, as
chronic venous scarring with narrowing (stenosis) is particularly common following direct subclavian vein cannulation. A history of central venous cannulation is important
in patients being considered for hemodialysis access and/or
arterial reconstruction using an upper limb venous conduit
due to the possibility of stenosis, especially in case of prior
subclavian vein usage. If present, postoperative limb swelling may result in considerable patient morbidity.
31.2.3.2.1 Superficial venous thrombophlebitis
Supercial venous thrombophlebitis (SVT) is characterized
by localized pain, redness, and swelling over a segment of
a supercial vein. Iatrogenic injury, secondary to venous
cannulation, is the most common cause, and is usually
self-limiting. In some cases, the disease can be recurrent
and persistent. Spontaneous thrombophlebitis, especially
if recurrent, may be associated with malignant disease or
thrombophilia. Upon examination, palpation will reveal
tenderness over an underlying thrombus in the vein, with
surrounding induration and erythema. If the thrombus is
localized and not infected, there may be considerable distal
swelling. Thrombus propagation to the deep veins is rare.
A history of thrombophlebitis is important, as it may have
important consequences for venous access and the utility of
an arm vein for arterial bypass.
31.2.3.2.2 Phlegmasia cerulea dolens
This affects the upper limb very rarely and tends to occur
in patients with advanced malignancy, often being treated
with chemotherapy via an indwelling central venous catheter. Phlegmasia is characterized by extensive thrombosis
affecting not only the major veins but also the venules
and the microcirculation. It is characterized by severe pain
associated with intense swelling and discoloration of the
affected limb. Development of compartment syndrome is
a potential complication and may even progress to venous
gangrene requiring amputation. Further complications
include PE and death.
31.2.3.2.3 Post-thrombotic syndrome
Post-thrombotic syndrome (PTS) is reported in 30%–70%
of patients following a primary subclavian vein thrombosis
and consist of chronic discomfort, heaviness, and swelling, particularly in positions that compress collaterals in
the costoclavicular space. However, the skin changes commonly found in the lower limb are extremely rare. PTS in
the upper limb is more commonly associated with unprovoked primary DVT than secondary DVT.
11
31.2.3.2.4 Arteriovenous malformations
These can be frequently misdiagnosed and are associated
with localized limb hypertrophy. Examples include Klippel-Trenaunay syndrome (KTS) and Parkes Weber syndrome (PWS); they usually affect the lower limb and are
discussed in further detail in the next section.
31.2.4 Examination findings
31.2.4.1 Inspection
Simply inspecting the arm and comparing it with the contralateral limb can yield useful clinical information. The
examination process can help eliminate arterial, lymphatic,
orthopedic, or rheumatologic pathology from the differential diagnoses.
Inspection should aim to identify the following: swelling, hypertrophy, discoloration, pallor, venous collaterals,
prominent veins, scars and/or puncture sites, evidence of
previous trauma, presence of indwelling catheters, and
peripheral venous catheters.
31.2.4.2 Palpation
This can help determine:
1. Differences in temperature
2. Tenderness over an inamed supercial vein or in the
supraclavicular fossa
3. Evidence of obstructing pathology in the axilla and/or
supraclavicular fossa (e.g., enlarged lymph nodes or a
palpable cervical rib)
4. Hard and “cordlike” veins suggesting previous throm-
bophlebitis
5. Presence of a full complement of pulses; presence of any
abnormal pulsations, either venous or arterial (arteriovenous stula or malformation)
6. Presence of a palpable thrill
7. Presence of pitting edema
8. Allen test to conrm the arterial inow to the hand and
completeness of the palmar arch
31.2.4.3 Percussion
The presence of incompetence can be grossly assessed by the
“tap test” of Chevrier. This is performed with the patient
standing. One hand is placed on the proximal thigh, tapping dilated veins, while the other feels for a transmitted
impulse in the veins of the lower leg. Venous return should
ow from the foot to the groin. A palpable thrill in the
lower leg veins is suggestive of continuity in the column of
blood, implying the presence of nonfunctional valves and,
therefore, venous incompetence.
31.2.4.4 Auscultation
Listen for a continuous machinery murmur, which might
indicate an arteriovenous malformation.
31.2.4.5 Additional steps
The blood pressure should be measured in each arm, and
a full neurovascular examination should be performed.
If the arm is swollen, the examination should include the
axilla for lymphadenopathy and the breast to exclude
31
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