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136
K. Sharma and S. Vedantham
developing PTS [ 3 ] . During the past decade,
there has been a better understanding of these
late complications of DVT, and this has stimu-
lated interest in more aggressive strategies to
counter these risks (Table 14.1 ).
Basic Approach to DVT Treatment
The goals of DVT treatment are to prevent
thrombus propagation and PE, provide relief of
acute symptoms, prevent recurrence, and prevent
PTS. Anticoagulant therapy is the mainstay of
treatment of acute DVT because it markedly
reduces the incidences of fatal PE and symptom-
atic recurrent VTE [ 4 ] . The initial anticoagulant
regimen may be subcutaneous injections of low
molecular weight heparin (LMWH), monitored
intravenous unfractionated heparin (UFH), sub-
cutaneous injections of UFH, or subcutaneous
injections of fondaparinux. Although many DVT
patients can be treated as outpatients with
LMWH, patients with iliofemoral/IVC thrombo-
sis, serious comorbidities, or a higher risk of
bleeding complications are best managed ini-
tially as inpatients [
5 ] . After initial anticoagulant
treatment for 5 days, long-term anticoagulant
therapy is generally given using Vitamin K
antagonists – typically medium-intensity warfa-
rin (international normalized ratio (INR) target
2.5, range 2–3) [
4 ] . One major exception is can-
cer patients, in whom a 3–6 month course of
LMWH as initial therapy is more effective than
early transition to warfarin in preventing recur-
rent VTE [ 6, 7 ] . Because cancer patients are at
high risk for recurrent VTE, anticoagulation is
typically continued inde fi nitely or until resolu-
tion of active cancer is achieved.
The duration of anticoagulant therapy in non-
cancer patients depends upon an assessment of
the patient’s risk for recurrence. Patients with
DVT related to a reversible, time-limited major
factor (for example, major surgery or trauma) are
at relatively low risk for recurrence and 3 months
of therapy may suf fi ce. Patients with unprovoked
DVT for which a predisposing cause is not found
are at higher risk for recurrence and are treated
for longer durations ( ³ 1 year to inde fi nite).
Periodic re-assessment of the risks of recurrence
versus bleeding is performed to decide when
therapy should be discontinued.
When there is an absolute or strong relative
contraindication(s) to anticoagulant therapy,
placement of an IVC fi lter may be performed
to prevent PE. IVC fi lters are also indicated for
patients with acute VTE who have a complica-
tion or failure of anticoagulant therapy (failure
is de fi ned as recurrent PE or progression of DVT
despite therapeutic-level anticoagulation when
reasonable alternative anticoagulation regimens
have been exhausted) [
8 ] . IVC fi lters are also
often employed in selected VTE patients with
severe cardiopulmonary compromise (e.g. PE
with hypotension) and in patients who are non-
compliant with anticoagulant therapy [
9 ] . In addi-
tion, speci fi c subsets of patients who do not have
VTE but who are at particularly high risk for PE
(e.g. multiple trauma, pelvic fracture, bariatric
surgery) may bene fi t from placement of retriev-
able fi lters, but such strategies have not yet been
validated in prospective studies.
Although anticoagulant therapy is effective in
preventing fatal PE and reducing recurrent VTE,
25–50% of patients with acute proximal DVT
eventually develop PTS [ 10, 11 ] . Anticoagulant
therapy usually produces symptom improvement
Table 14.1 Commonly-used drugs for catheter-directed thrombolysis
DRUG (abbreviation)
a
FDA approval Dose range for CDT of DVT
Urokinase (UK) Pulmonary embolism 120,000–180,000 units/h
Tissue Plasminogen Activator (tPA) Myocardial infarction 0.5–1.0 mg/h
Cerebral infarction
Pulmonary embolism
Reteplase (RPA) Myocardial infarction 0.25–0.75 units/h
Tenecteplase (TNK) Myocardial infarction 0.25–0.50 mg/h
a
Note – streptokinase did receive FDA approval for systemic thrombolysis of DVT but is not used in the U.S. since an
NIH Consensus Panel later recommended against its use
https://t.me/med1917
13714 Deep Vein Thrombosis: What to Do
in DVT patients, but its time course varies con-
siderably, and some patients do not respond.
Unlike anticoagulants, thrombolytic drugs can
rapidly eliminate thrombus and thereby provide
immediate restoration of venous patency [
12 ] .
Systemic administration of thrombolytic drugs
was tested in randomized trials – although meta-
analyses suggest that it did reduce PTS rates, it
was associated with unacceptably high major
bleeding rates [ 12– 14 ] . Surgical thrombectomy,
used in patients with acute iliofemoral DVT, also
appears to reduce PTS but is excessively invasive
for routine use in acute DVT patients [ 15, 16 ] .
Catheter-directed intrathrombus thrombolysis
(CDT) is a targeted, image-guided therapy in
which a thrombolytic drug is infused or injected
directly into the venous thrombus through a cath-
eter which is embedded in the thrombosed vein
using imaging guidance [ 17 ] . In observational
series and a prospective registry, CDT has been
reported to rapidly restore venous patency and
relieve acute DVT symptoms [ 18, 19 ] . In all three
studies which compared CDT + anticoagulation
versus anticoagulation alone in acute iliofemoral
DVT patients, the patients receiving CDT had
better outcomes in terms of physiological venous
function, PTS, and/or quality of life; however, all
three studies had signi fi cant methodologic limita-
tions [ 20– 22 ] . Hence, the routine use of CDT for
acute DVT remains controversial due to the
absence of evidence from randomized trials that
it can prevent PTS and concern that it may
increase the risks and costs of therapy [
6, 23 ] .
For these reasons, careful patient screening
should be used to determine which patients are
best suited for CDT. Patients with limb-threaten-
ing phlegmasia, IVC thrombosis with involvement
of the suprarenal IVC, or continued marked func-
tional impairment despite an initial course of ther-
apeutic anticoagulation are solid candidates.
Appropriate candidates for CDT must have symp-
tomatic venous thrombosis documented by imag-
ing and have no contraindications to anticoagulation
or thrombolysis. In the lower extremity, patients
with acute iliofemoral DVT represent an ideal
patient cohort and should be offered a balanced
discussion of the risks and possible bene fi ts of
CDT for prevention of PTS. In acute iliofemoral
DVT patients in whom CDT has failed or is con-
traindicated, surgical venous thrombectomy is a
reasonable alternative. Selected patients with acute
axillosubclavian venous thrombosis are also rea-
sonable CDT candidates, either alone or with
adjunctive surgical thoracic outlet decompression.
Endovascular Treatment Technique
Step 1: Venous access: In most cases of lower
extremity DVT, the ipsilateral popliteal vein or
lesser saphenous vein is used for access into the
deep venous system. Tibial vein access can be
used when thrombus extends into or below the
popliteal vein.
Step 2: Diagnostic Venogram: Catheter venog-
raphy is essential to provide the anatomical road-
map necessary for treatment. In addition to
de fi ning the extent of thrombosis and/or associ-
ated stenosis, venographic criteria can occasion-
ally be employed to render an educated guess as
to whether acute and/or chronic thrombus is pres-
ent. In general, successful clot dissolution is more
likely for acute thrombus.
Step 3: Selection of Thrombus Removal
Approach: In current practice, a number of options
are available for removal of acute thrombus: (a)
catheter-directed intrathrombus infusion – although
no drug is FDA approved for DVT therapy per se, a
number of drugs have been safely used in off-label
fashion, including urokinase (120,000–180,000
units/h), tissue plasminogen activator (0.5–1.0 mg/h),
reteplase (0.25–0.75 units/h), and tenecteplase
(0.25–0.5 units/h). This “drug-only” approach is a
time-tested method of obtaining thrombus removal
but has the disadvantage of long infusion times (24–27 h
typically) [ 18 ] ; (b) “ fi rst-generation” pharmacome-
chanical thrombolytic techniques, in which cathe-
ter-directed drug infusion is combined with use of a
thrombectomy device which macerates and/or aspi-
rates thrombus. These approaches have been associ-
ated with reduced infusion time, drug dose, and
hospital resource use during therapy [ 24, 25 ] ; (c)
ultrasound-assisted thrombolysis, in which a spe-
cially designed catheter is used to simultaneously
deliver a thrombolytic drug infusion and low-power
ultrasound energy which may loosen fi brin strands,
augment drug dispersion, and thereby speed ther-
apy; and (d) single-session pharmacomechanical
CDT (see Fig. 14.1 ), in which up-front bolus or
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138
K. Sharma and S. Vedantham
https://t.me/med1917
13914 Deep Vein Thrombosis: What to Do
Fig. 14.1 Pharmacomechanical CDT in a patient with
iliofemoral DVT The top two images from the initial veno-
gram obtained from a popliteal approach demonstrate throm-
bus within the femoral and iliac veins. The middle two images
demonstrate position of the proximal and distal occlusion
balloons on the Trellis device prior to treatment. The bottom
two images from the fi nal post treatment venogram demon-
strate a good result following single session combined phar-
macomechanical CDT. In this case, adjunctive venous stenting
was performed because of an underlying iliac vein stenosis
pulse-spray intrathrombus drug administration is
combined with thrombectomy device use with the
intent of providing on-table complete thrombus
removal [ 26, 27 ] . To date, there have been no pro-
spective comparisons of these therapies to deter-
mine which is most effective.
Step 4: Repeat Venography and Adjunctive
Interventions: After thrombus removal, the
treated vein is examined venographically for
underlying obstructive lesions (e.g. iliac vein
stenosis due to May-Thurner Syndrome). If
present, iliac vein lesions are treated with stent
placement and femoropopliteal vein lesions
are treated with balloon angioplasty in order to
prevent early re-thrombosis due to fl ow stasis
[ 17, 19, 28 ] .
Step 5: Evidence-Based PTS Prevention
Measures: It is important to recognize that CDT
has not been conclusively shown to prevent PTS.
However, recurrent ipsilateral DVT is associated
with PTS and therefore the post-CDT transition to
anticoagulant therapy should be closely monitored
as an important aspect of PTS prevention. The eti-
ology of DVT should be categorized (i.e. transient
reversible risk factor, cancer-related, thrombo-
philia-related, or unprovoked) and an appropriate
anticoagulant regimen chosen. In addition, the use
of 30–40 mmHg, knee-high elastic compression
stockings has been shown in two single-center ran-
domized controlled trials to prevent PTS – these
should be prescribed to patients as soon as the acute
DVT symptoms permit (Table 14.2 ) [ 10, 11 ] .
Fig. 14.1 (continued)
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140
K. Sharma and S. Vedantham
Conclusion
Acute DVT is an extremely common problem
and often leads to death or major disability.
Major advances made during the last decade
now allow better diagnosis and treatment of
acute DVT. These include use of LMWHs
which allow outpatient therapy, the advent of
retrievable IVC fi lters, and improved throm-
bus removal methods. These advances, and an
improved understanding of PTS-associated
morbidity, portend an increasing use of aggres-
sive strategies to optimize treatment outcomes
in DVT patients.
Pearls and Pitfalls
1. Inability to adequately maintain patients in the
therapeutic window: When using UFH, a PTT
value of 1.5–2.5 times control represents the
usual target range. The use of weight-based
UFH nomograms improves the ability to rap-
idly reach and maintain therapeutic anticoagu-
lant levels [ 31 ] . Initial therapy with UFH or
LMWH should be transitioned to oral warfa-
rin with at least 5 days of overlap.
2. Inability to determine appropriate duration of
treatment: The proper duration of therapy is
dependent upon an individualized risk factor
analysis which incorporates results of any hyper-
coagulability testing. In general, 3 months of
anticoagulant therapy is acceptable for patients
with time-limited, reversible risk factors. Patients
with major continuing risk factors or idiopathic
DVT bene fi t from durations ³ 12 months since
the underlying risk of recurrent VTE is higher.
3. Heparin-induced thrombocytopenia (HIT):
Complications of HIT can be avoided by moni-
toring platelet counts in patients receiving UFH.
Alternative anticoagulants such as bivalirudin,
lepirudin and argatroban may be used [
6 ] .
4. Avoiding CDT-related bleeding: Hematocrit,
platelet count, INR, PTT, and fi brinogen
should be monitored during fi brinolytic drug
infusions. Therapy should be immediately
stopped if sentinel bleeding is noted, if the
hematocrit drops precipitously, or if the
fi brinogen level dips below 100 mg/dl.
Table 14.2 Evidence-based prevention of the post-thrombotic syndrome
DVT treatment method Effectively prevents PTS Methodology of supporting studies References
Anticoagulant therapy Probably somewhat effective
Direct: prospective registry in which PTS
more common in patients with subthera-
peutic INR > 50% of the time.
[
29 ]
Indirect: prospective registries and RCTs
in which PTS more common in patients
with recurrent ipsilateral DVT.
[
3, 10, 11 ]
Elastic compression
stockings (30–40 mmHg,
knee-high, used soon after
DVT diagnosis)
Yes, reduces risk of
developing PTS by 50%
Two single-center RCTs [
10, 11 ]
Early ambulation/
compression
Probably yes One single-center RCT [
30 ]
Catheter-directed
thrombolysis
Probably yes
Indirect: One prospective non-randomized
comparative cohort study in which 5-year
PTS was reduced with CDT, one
case-control study in which 20-month
QOL was superior with CDT, and one
single-center RCT in which 6-month
venous function was superior with CDT
[
20– 22 ]
Surgical thrombec-
tomy + AV fi stula creation
Probably yes for iliofemoral
DVT
One single-center RCT [
15, 16 ]
Systemic thrombolysis Probably yes Meta-analyses of RCTs [
13, 14 ]
RCT randomized controlled trial
https://t.me/med1917
14114 Deep Vein Thrombosis: What to Do
Keys to Success
1. Categorize DVT patients as those with time-
reversible risk factors, those with cancer-
related DVT, and those with thrombophilias or
idiopathic DVT. The appropriate type and
duration of anticoagulant therapy are directly
dependent upon this categorization.
2. Have a system in place for anticoagulant ther-
apy monitoring at your institution. Incorporate
evidence-based measures to prevent PTS, such
as ensuring compliance with elastic compres-
sion stockings, into the routine of the antico-
agulant clinic.
3. To select patients for CDT, use an individualized
approach based upon a rigorous pre-treatment
screening evaluation. Conditions which may
promote bleeding should be actively sought and
a low threshold should be applied to exclude
patients from receiving CDT. Patients with
malignancies known to metastasize to the central
nervous system should undergo brain imaging
prior to CDT. The patient’s medications and
drug allergies should be reviewed, and particular
note should be taken of medications that
in fl uence coagulation or platelet function. The
patient’s life expectancy, anticipated activity
level, and acute symptom severity should also be
factored into the global assessment of the
patient’s suitability for CDT.
4. When performing CDT, use ultrasound guid-
ance to obtain venous access – this helps pre-
vent inadvertent arterial punctures which can
cause local bleeding complications following
initiation of thrombolysis. Use thrombectomy
devices with CDT to speed therapy and reduce
fi brinolytic drug dose – this may help to reduce
major bleeding.
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143
N.S. Sadick et al. (eds.), Practical Approach to the Management and Treatment of Venous Disorders,
DOI 10.1007/978-1-4471-2891-5_15, © Springer-Verlag London 2013
1 5
Introduction
Super fi cial vein thrombosis (SVT), also known
as super fi cial thrombophlebitis, is a thrombosis
occurring in a super fi cial vein, most often in the
lower limbs. It has been estimated that approxi-
mately 125,000 clinically diagnosed cases of
SVT are reported annually in the United States
[ 1, 2 ] . Mortality with SVT is low (0–1% 3-month
mortality) [ 3, 4 ] ; however, SVT can progress to
venous thromboembolism (VTE), which has a
30-day mortality rate as high as 28% and a 1-year
mortality rate as high 36.4% [ 5 ] .
Epidemiology and Etiology
The mean age of SVT presentation is approxi-
mately 60 years [
3, 6– 8 ] . A higher incidence of
SVT in females has been reported [
3, 6– 8 ] , possi-
bly related to increased incidence of varicose veins
with pregnancy [ 9 ] . Varicose veins are the cause of
SVT in 70% of cases [ 3, 6, 8 ] . Underlying condi-
tions, such as cancer, autoimmune disease, and
acquired or immune thrombophilia, should be
investigated in patients with SVT without varicose
veins and in the case of idiopathic migrant or recur-
rent SVT [ 6, 7, 10– 12 ] . Other risk factors for SVT
are similar to those with VTE and include obesity,
history of VTE, hormone therapy, age >65 years,
recent surgery, trauma, pregnancy, oral contracep-
tives, inherited thrombophilia [ 13 ] , acquired throm-
bophilia, long-haul fl ight, prolonged immobilization,
cancer, and sclerotherapy [ 3, 6, 7 ] . In a large, ran-
domized study, the most important factors were
obesity, age > 65 years, history of VTE, and hor-
mone therapy [ 4 ] . In this study, approximately 20%
of patients were obese, 50% were >65 years of age,
15% had a history of VTE, and 12% were taking
hormone therapy [
4 ] . Endovenous laser and radiof-
requency ablation of the saphenous vein to treat
varicose veins is also a risk factor for SVT, espe-
cially in cases of incomplete obliteration [
14 ] .
The incidence of thrombophilia is also
increased in patients with SVT [
10, 13, 15– 17 ] . It
may be useful to evaluate patients with SVT who
do not have varicose veins and have one other
risk factor for SVT for markers of thrombophilia
including protein S de fi ciency, protein C
de fi ciency, anticardiolipin antibodies, beta2 gly-
coprotein, factor V Leiden, prothrombin muta-
tion, antithrombin de fi ciency, lupus anticoagulant,
methylene tetrahydrofolate reductase de fi ciency,
and fasting serum homocysteine [
10, 13, 16,
18– 20 ] .
Super fi cial Vein Thrombosis
Joseph A. Caprini and Michael J. Verta
J. A. Caprini , M.D., M.S., FACS, RVT (*)
Louis W. Biegler Professor of Surgery ,
Division of Vascular Surgery, Department of Surgery ,
NorthShore University HealthSystem ,
Evanston , IL , USA
The University of Chicago Pritzker School of Medicine ,
Chicago , IL , USA
e-mail: jcaprini2@aol.com
M. J. Verta , M.D.
Department of Surgery , Northwestern University
Feinberg School of Medicine ,
Chicago , IL , USA
e-mail: michael_verta@cdh.org
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144
J.A. Caprini and M.J. Verta
With SVT, thrombi are most often found in the
saphenous veins and their tributaries [
3, 7 ] , more
frequently in varicose tributaries than in the
saphenous trunk [ 7, 21 ] . The greater saphenous
vein (GSV) is the most common site (60–80% of
cases) [
3, 7, 8 ] . The smaller saphenous vein
(SSV) is the site in approximately 10–20% of
cases [
3, 7, 8 ] . The upper limbs and neck are
other locations for SVT [
3 ] .
Complications
SVT recurrence or proximal extension is an
important complication with SVT [ 3, 7 ] . In addi-
tion, SVT is a risk factor for VTE [ 22 ] . It can
precipitate or be associated with deep vein throm-
bosis (DVT) and can cause pulmonary embolism
(PE). The presence of DVT in association with
SVT ranges from 6% to 53%, and concomitant
PE has been reported to range from 0% with
symptomatic PE to as high as 33% with lung
scanning (Table 15.1 ) [ 7, 23 ] . The wide range is
most likely due to differences in study design
including how ultrasonography was performed in
the different studies, the location of DVT sought
(proximal or distal, with or without muscular
involvement), patient characteristics, type of SVT
considered, and diagnostic methods used [ 3, 6 ] .
In a post-hoc analysis of the STENOX trial,
which was a randomized, controlled trial in which
risk factors for thrombotic complications were
Table 15.1 SVT and concomitant and subsequent VTE [ 7 ]
Author Patients (N) DVT (%) PE (%) Diagnosis Treatment
Gervais (1956) [
51 ] 64 6 – Surgery Surgery
Gjores (1962) [
42 ] 40 32 5 – Surgery
Zollinger (1962) [
52 ] 335 – 10.1 Clinical –
Hafner (1964) [
26 ] 133 17 – Surgery –
Lofgren (1981) [
21 ] 163 8 – Clinical Surgery
Husni (1982) [
9 ] 139 7 – – Surgery
Plate (1985) [
41 ] 28 14 – VNG, VQ Surgery
Bergqvist (1986) [
53 ] 56 16 – VNG –
Skillman (1990) [
54 ] 42 12 – VNG, IPG, DUS Medical
Lutter (1991) [
8 ] 186 28 4 DUS –
Prountjos (1991) [
55 ] 57 20 – VNG –
Pulliam (1991) [
56 ] 20 30 (15 propagated to
DVT during study)
0 DUS Surgery
Lohr (1992) [
40 ] 43 53 – DUS Surgery
Blattler (1993) 25 44 DUS, VNG Medical
Jorgensen (1993) [
57 ] 44 23 – DUS –
Ascer (1995) [
33 ] 20 40 0 DUS Medical
Chengelis (1996) [
58 ] 263 11 – – –
Somjen (1996) [
59 ] 53 56.6
³ 2.3
DUS, VQ –
Bounameaux (1997) [
60 ] 551 5.6 – VNG, DUS –
Blumenberg (1998) [
2 ] 213 (232 limbs) 8.6 (2.6 propagated
to DVT during study)
0.93 DUS Medical
Belcaro (1999) [
29 ] 562 6.8 – DUS Various
Verlato (1999) [
23 ] 21 – 33.3 DUS, VQ, CXR –
Murgia (1999) [
61 ] 85 25.3 – DUS –
Unno (2002) [
11 ] 51 11.8 7.8 DUS –
Ascher (2003) [
34 ] 32 65.6 – DUS Medical
Adapted with permission from Leon et al. [
7 ] . Copyright Elsevier 2005
DUS duplex ultrasound, VNG venography, VQ ventilation perfusion lung scan, IPG impedance plethysmography, CXR
chest X-ray
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14515 Super fi cial Vein Thrombosis
studied, multivariate analysis found that throm-
botic complications (DVT, PE, or SVT recur-
rence and/or extension) with SVT were
signi fi cantly increased ( P £ .03, with a two- or
three-fold increased risk associated with each
factor) in patients who were male, had a history
of VTE, had a short interval ( £ 7 vs >7 days)
between symptom onset and diagnosis of SVT, or
had severe chronic venous insuf fi ciency (stage 3
of the Porter classi fi cation [
24 ] ) [ 25 ] . Short inter-
val between symptom onset and diagnosis as an
independent predictor of SVT may re fl ect that, in
patients with this characteristic, SVT was pro-
gressive; in contrast, in patients with chronic
SVT, the disease was not progressive or had
already progressed to a thrombotic complication,
thereby rendering the patient ineligible for the
study [ 25 ] . Severe chronic venous insuf fi ciency
was the only factor found to be a signi fi cant inde-
pendent predictor of the more speci fi c complica-
tion of DVT or PE and was associated with a
more than fourfold increased risk for this compli-
cation ( P = .018). Other factors that have been
suggested to be associated with increased risk for
thrombotic complications with SVT include
thrombus in the GSV [ 2, 8 ] , location of the throm-
bus head <1 cm from the sapheno-femoral junc-
tion (SFJ), age > 60, bed rest, and bilateral SVT
[ 3, 8 ] .
Contiguous extension of the thrombotic pro-
cess from the super fi cial to the deep veins occurs
most commonly by extension from the GSV
into the femoral vein but can also occur by
extension from the SSV into the popliteal vein
through the sapheno-popliteal junction (SPJ) or
through perforating veins to deep venous struc-
tures [ 7, 26 ] .
These data challenge the belief that SVT is
always a benign and trivial disease that can be
treated symptomatically with nonsteroidal
antiin fl ammatory drugs (NSAIDs) and com-
pression alone. The objective of this chapter is
to review the methods for diagnosis of SVT as
well as the available data on the treatment of
SVT in order to provide practical recommenda-
tions for the optimal management of SVT that
take into account the risk of VTE in patients
with SVT.
Diagnosis
Clinical signs of SVT include pain, erythema,
and swelling around a super fi cial vein that on
palpation feels like a cord [
3, 6, 7 ] . Although
these clinical signs are usually easily recognized,
clinical examination is not suf fi cient for differen-
tial diagnosis of SVT or for determining the
extent of the condition.
Duplex ultrasound scanning (DUS) of the
super fi cial and deep venous systems of the leg
is required to con fi rm the diagnosis of SVT [ 3,
6, 12 ] , rule out concomitant DVT [ 3, 6, 12 ] ,
and visualize the thrombus head to determine
its location regarding the SFJ and SPJ [ 3, 6 ] .
DUS may also be used to determine if SVT
treatment is successful in resolving the throm-
bus and ensuring that DVT has not subse-
quently developed [ 7 ] .
Treatment
The optimal treatment of SVT is not well estab-
lished due to the lack of quality randomized, con-
trolled clinical trials in this patient population.
Agents that have been studied in the treatment of
SVT include nonsteroidal antiin fl ammatory drugs
(NSAIDs), elastic compression stockings, anti-
coagulants, and surgery. Elastic compression
should be used as an adjunctive in all patients if
tolerated regardless of the associated conditions;
however, compression alone is not suf fi cient for
treatment of SVT [ 7, 27– 29 ] .
NSAIDs are used by some physicians in
patients with SVT where the thrombus is located
away from the SFJ or SPJ or for SVT at lower
levels without evidence of DVT [
7 ] . However,
limited data suggest that NSAIDs may not relieve
symptoms as well as anticoagulation and may be
insuf fi cient for prevention of VTE (Table 15.2 )
[
4, 30 ] . In addition, NSAIDs, including aspirin,
are proven not to be effective in prevention of
VTE in patients who have undergone orthopedic
surgery, general surgery, and in medical patients [ 31 ] .
These drugs may also be associated with the
development of gastrointestinal complications
including bleeding.
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