Transcript Upper Ext DVTs

Upper Extremity
Deep Vein Thrombosis
4/6/10
Definition
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Originally described in late 19th century by
Paget and von Schroetter.
Thrombosis in any of the following veins:
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Ulnar/Radial/Interosseous
Brachial
Axillary
Subclavian
Jugular/Brachiocephalic/SVC
Basilic and cephalic are considered superficial
Dark Blue: Deep vein
Blue: Superficial vein
Incidence
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Prior to 1970, accounted for < 2% DVTs
May now account for 4-8%, higher in
critical care areas (up to 33% in some
studies).
Male≈Female
Idiopathic UE DVT tend to be in younger
patients.
Etiology
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Virchow’s Triad:
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Venous trauma (Endothelial wall)
Venous stasis (external compression)
Hypercoagulability
Dark Blue: Deep vein
Blue: Superficial vein
Red: “Choke” points
Risk Factors
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Trauma/Surgery
Malignancy/XRT
Inherited Hypercoagulable states
Anatomical deformities/Malformations (e.g.
Cervical ribs)
Hyperviscosity (Sickle cell/Polycythemia)
Athletes (with repetitive motions of arms)/”Effort
thrombosis”/Paget-von-Schroetter syndrome
Thoracic Outlet Syndrome
Previous DVT/VTE
Risk Factors
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Venous catherization
Oral contraceptives/Hormone Replacement Therapy
Tobacco
Obesity
CHF
Nephrotic syndrome/PNH
Lymphedema
Hyperhomocysteinemia
Thrombophlebitis
Symptoms
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Arm/Neck/Facial swelling
Arm/Neck/Facial pain
Erythema
Bluish discoloration
Collateral Venous distention (including
chest veins)
Fever
Diagnosis
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D-Dimer: High sensitivity/Low specificity.
Measures degradation product of cross-linked
fibrin
Doppler Ultrasound: High sensitivity and
specificity, though operator dependent.
Venography: Gold standard. Requires contrast
MRI: Relatively low sensitivity/High specificity.
Limited due to time constraints/cost
Complications
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Pulmonary Embolism
Historically, 1% PE were attributed to UE
DVTs.
More likely 5-10%.
More centrally located the thrombosis, the
higher the risk of PE (Subclavian >
Brachial)
Complications - PE
QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.
Complications
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Recurrent DVT/PE:
Risk increases on a yearly basis
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2% in 1st year
4% in 3rd year
7% in 5th year
Risk is further increased in malignancy
Complications
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Post-thrombotic syndrome: 15-25% of
patients with UE DVT may develop PTS.
Characterized by persistent/severe pain
and persistent edema.
Can often be debilitating adversely
affecting quality of life.
Treatment
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American College of Chest Physicians:
Recommends the UE DVT be treated the
same as LE DVT.
Treatment was shown to decrease the
recurrence of DVT/PE in two prospective
cohort studies.
Q u ic k T im e ™ a n d a
T I F F ( Un c o m p r e s s e d ) d e c o m p r e s s o r
a r e n e e d e d t o s e e t h is p ic t u r e .
Treatment
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Heparin (Unfractionated): Activates
antithrombin III, which inactivates
thrombin. Also inhibits factor Xa and factor
IXa.
Requires monitoring of the aPTT (1.5X
baseline PTT) due to heparin-binding
proteins (which tend to increase during
illness).
Half-life: 60 min when given IV.
Can be reversed with protamine sulfate.
Treatment
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Low-molecular weight heparin (LMWH)
Less affected by heparin-binding proteins
More active against antithrombin III
Lower rate of HIT.
Reversal with protamine sulfate is limited
Treatment
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Fondaparinux (Arixtra): Binds to
antithrombin, which inhibits factor Xa.
No action against thrombin
Not metabolized, renally excreted.
Half-life 15 hrs
Treatment
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Direct thrombin inhibitors:
Lepirudin, renally excreted.
Argatroban
Can inhibit clot-bound thrombin
Not affected by circulating inhibitors of
heparin (released by platelets)
Does not cause HIT.
Treatment
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Vitamin K antagonists:
Warfarin (Coumadin): Inhibits Vitamin K epoxide
reductase, which recycles oxidized Vit K. Initially
developed as a rodenticide (rat poison).
Acenocoumarol: Outside US, shorter half life
than warfarin.
Phenprocoumon: Outside US, longer half life
than warfarin.
INR goal 2-3
Future
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Ximelagatran: PO Direct thrombin inhibitor.
Denied approval by FDA in 2004
Pulled from market in 2006
Found to have caused severe liver
damage and heart attacks.
Future
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Rivaroxaban: PO Factor Xa inhibitor
Compared to LMWH in orthopedic surgery
patients in several trials.
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Reduced LE DVT/nonfatal PE/death with no
significant difference in major bleeding.
Approved in Europe and Canada for DVT
prophylaxis in orthopedic surgery patients.
May potentially be used in HIT?
Future
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Dabigatran: PO direct thrombin inhibitor.
RECOVER trial: End point recurrent VTE/fatal
PE:
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2.4% dabigatran vs 2.1% warfarin
Hazard ratio 1.1, dabigatran not inferior
1.6% major bleeding dabigatran vs 1.9% warfarin, not
significant
Significant reduction in all bleeding with dabigatran of
29%
Approved for DVT prophylaxis in orthopedic
surgery patients in Europe and Canada.
Treatment Duration
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First DVT: Provoked: 3-6 months
Unprovoked: 6-12 months
DVT with cancer/antiphospholipid
syndrome: Life-long therapy
Second DVT: Life-long therapy
Treatment
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Catheter-directed thrombolysis: Infuses a thrombolytic
agent (usually tPA) between two inflated balloons via a
catheter.
Early restoration of venous patency/improved venous
return/Decreases pain/discomfort.
No change in rates of recurrent DVT/PE/bleeding/PTS.
Contraindications include hemorrhage/recent
neurosurgery
ACCP recommends against routine use (Grade 1C).
With severe symptoms of recent onset with low risk of
bleeding, may be used (Grade 2C)
Treatment
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SVC Filter
Rates of PE 2.4% and PTS 0% in one study
(n=41).
Another study showed no episodes of PE
(n=72).
ACCP recommends against routine use (Grade
1C). If anticoagulation contraindicated and DVT
progression occurs, then SVC may be placed
(Grade 2C).
Treatment
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Graded Compression sleeves/Elastic
bandages
Useful in relieving symptoms of persistent
pain/swelling such as in PTS.
ACCP: Routine use not recommended
(Grade 2C), except in patients with
persistent pain (Grade 2C)
Treatment
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Graded Compression sleeves/Elastic
bandages
Useful in relieving symptoms of persistent
pain/swelling such as in PTS.
ACCP: Routine use not recommended
(Grade 2C), except in patients with
persistent pain (Grade 2C)
Treatment
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In a retrospective study of 189 Surgical
ICU patients, 33% had UE DVTs,
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Central catheters (45%) was the highest risk
factor identified
6% had PE, all nonfatal, all with IJ clots
60% were anticoagulated
No difference in LOS/survival to 30 days, and
1 year mortality
Treatment
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RIETE Registry:
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512 of 11564 DVTs were UE DVT (4.4%)
9% had PE (vs 29% for LE DVT)
3 month outcomes of major bleeding/fatal
bleeding/recurrent DVT/recurrent PE were
similar between UE and LE DVTs
Slightly higher mortality rate for UE DVTs
Cancer patients had increased rates in
recurrent DVT/PE/major bleeding.
56% of patients had received anticoagulation.
Conclusions
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Most studies are retrospective or cohort
studies with small numbers of patients.
ACCP recommends to treat UE DVTs
same as LE DVTs
Use heparin/LMWH, until INR therapeutic
with coumadin (INR goal 2-3)
Thrombolysis/Thrombectomy/SVC Filter
not routinely indicated.
Future PO meds may replace warfarin
References
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Chest 2008; 133; 454S-545S.
Chest January 2008 vol. 133 no. 1 143-148
Dabigatran versus Warfarin in the Treatment of Acute Venous
Thromboembolism. NEJM 361: 2342-2352. Dec 10, 2009.
Hingorani A, Ascher E, Lorenson E, et al. Upper extremity deep venous
thrombosis and its impact on morbidity and mortality rates in a hospitalbased population J Vasc Surg 1997;26:853–60.
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Hingorani A, Ascher E, Markevich N, et al. Risk factors for mortality
in patients with upper extremity and internal jugular deep venous
thrombosis J Vasc Surg 2005;41:476–8.
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Paget J., London: Longmans, Green & Co; 1875. Clinical lectures and
essays.
Prandoni P, Polistena P, Bernardi E, et al. Upper-extremity deep vein
thrombosis: risk factors, diagnosis and complications Arch Intern Med
1997;157:57–62.
Vascular. 2008;16(2):73-79.
von Schroetter L. Nothnagel Handbuch der Pathologie und Therapie Holder
1884
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