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310 Anticoagulation Therapy
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*11. Wein L, Wein S, Haas SJ, et al. Pharmacological venous thromboembolism prophylaxis
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Chapter
VENOUS THROMBOEMBOLISM
TREATMENT
Snehal H. Bhatt and Michael P. Gulseth
INTRODUCTION
Venous thromboembolism (VTE) is comprised of deep vein thrombosis (DVT) and
pulmonary embolism (PE) and affects between 350,000–600,000 patients each
year. In addition, it has been estimated that up to 100,000 patients directly or
indirectly die of this disease process annually.1 Optimal treatment of VTE is critical
to prevent death and future recurrence as well as minimize the risk of complications
such as post-thrombotic syndrome (PTS) and chronic thromboembolic pulmonary
hypertension (CTEPH).
VENOUS THROMBOEMBOLISM OVERVIEW
DVT, in the lower extremity, typically begins in a calf vein and can propagate
proximally to the popliteal vein and higher. Lower extremity DVT is 10 times more
common than upper extremity DVT. In the upper extremity, DVT typically has an
iatrogenic cause such as internal cardiac defibrillators, pacemakers, or in-dwelling
central venous catheters (e.g., peripherally inserted central catheter [PICC] line).
For DVT of the upper extremity, the risk increases with the diameter of inserted
catheters and number of lumens used.
PE occurs when a DVT embolizes to the lungs (see Figure 13-1). Patients
with signs and symptoms of shock, elevated cardiac biomarkers, and signs of
right ventricular (RV) dysfunction are classified as having massive PE. Massive
PE accounts for 5–10% of all PE cases and indicates extensive thrombus affecting over half of the pulmonary vascular tree. Classic symptoms include syncope,
hypotension, dyspnea, and cyanosis. Patients with massive PE often present in
shock and can die. Patients who have cardiac manifestations (e.g., RV dysfunction,
release of cardiac enzymes) but who are hemodynamically stable are classified as
having submassive PE, which represents 20–25% of all PE cases. The remaining
70–75% of patients with PE are classified as having nonmassive PE and have a
good prognosis for recovery.
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FIGURE 13-1. Pathophysiology of DVT and PE
Pulmonary emboli usually originate in the deep veins of the leg. The thrombus typically
originates around the venous valves and other areas of stasis. Thrombi that extend
above the knee or originate above the knee are at a higher risk of embolization.
Pulmonary emboli travel through the venous system, into the right side of the heart, to
the lungs.
Source: Image printed with permission from The Mayo Foundation for Medical
Education and Research. All rights reserved. http://healthletter.mayoclinic.com/
common/images/609/Deep_vein_thrombosis_lg.jpg
Common Areas for Venous Thrombosis
•
Lower extremity DVT.
•
Lower extremity superficial vein thrombosis.
•
Upper extremity DVT (UEDVT) represents approximately 10% of all DVT cases.
See Tables 13-1 and 13-2 for veins found in the upper and lower extremities.
See Figure 13-2 of lower extremity venous anatomy.
2
VENOUS THROMBOEMBOLISM TREATMENT 315
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• DVT can embolize; superficial vein thrombi do
not (unless they extend into a deep vein).
Isolated calf DVTs are less likely to embolize than
•
proximal DVTs.
•
Proximal DVTs are any DVTs that occur above
the level of the knee (popliteal vein) and higher.
Patients with DVT can often present with
•
nonspecific symptoms such as leg pain or
tenderness, warmth, discoloration, swelling, and
surface vein distention.
TABLE 13-1: Lower Extremity Venous Anatomy
Deep Veins of the Lower Leg Superficial Lower Limb Veins
Proximal veins
Deep femoral vein
External iliac vein
Femoral vein
Gluteal vein
Iliac vein
Medial and lateral circumflex femoral veins
Mid-thigh perforator (Hunterian) vein
Popliteal vein
Calf veins
Anterior and posterior tibial veins
Dorsal and plantar metatarsal veins
Fibular veins
Gastrocnemius vein
Genicular veins
Peroneal vein
Plantar digital veins
Soleal vein
Sural veins
Proximal veins
Anterior lateral thigh vein
External pudendal veins
Great saphenous vein
Intra saphenous vein
Small saphenous vein
Superficial circumflex iliac vein
Superficial epigastric vein
Vein of Giacomini
Calf veins
Accessory saphenous vein
Dorsal venous arch
Dorsal venous network
Femoropopliteal vein
Great saphenous vein
Plantar venous network
Plantar venous arch
Posterior arch vein
TABLE 13-2: Upper Extremity Venous Anatomy
Deep Veins of the Upper Extremity Superficial Upper Extremity Veins
Anterior interosseous veins
Axillary vein
Brachial veins
Deep palmar venous arch
Posterior interosseous veins
Radial veins
Subclavian vein
Ulnar veins
Palmar metacarpal veins
Accessory cephalic vein
Basilic vein
Cephalic vein
Median antebrachial vein
Median basilica vein
Median cephalic vein
Median cubital vein
Dorsal venous network of the hand
Superficial palmar venous arch
316 Anticoagulation Therapy
Adductor
hiatus
Adductor
canal
Fe
Deep
fe
Lateral
circumfl
fe
Ante
tibial
Shor
saphenou
ve
saphenous
saphenous
Dorsal
netwo
the
Inguina
ligament
P
Anterior vi
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l
ex
moral veins
moral vein
moral vein
opliteal vein
rior
veins
t
ins
venous
rk of
foot
External
iliac vein
Medial
circumflex
veins
saphenous
vein
Accessory
saphenous
vein
Posterior
tibial veins
Genicular
veins
Long
saphenous
vein
s
Posterior view
Popliteal
vein
Short
vein
Anterior
tibial
vein
Fibular
veins
Short
vein
Lateral
malleolus
ew
FIGURE 13-2. Lower Extremity Venous Anatomy
VENOUS THROMBOEMBOLISM TREATMENT 317
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See Figure 13-3 of upper extremity venous anatomy.
• Most UEDVTs are associated with central venous
catheters.
3
• UEDVT is treated with anticoagulation therapy
similar to that of lower extremity DVT with
regard to initial therapy and duration of therapy,
although randomized controlled trials have not
been performed in patients with UEDVT.
Routine removal of the central venous catheter
•
is not recommended, but can be considered
when there is concern for infection or if there are
contraindications to anticoagulation therapy.
Subclavian vein
Axillary vein
Thoracoepigastric vein
Thoracodorsal vein
Brachial veins
FIGURE 13-3. Upper Extremity Venous Anatomy
Anterior interosseous
veins
Radial veins
Deep arm veins
Ulnar veins
Deep palma
venous arch
Palmar
metacarpal
veins
Palmar
digital veins
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PARADOXICAL EMBOLISM
In some patients with atrial septal defects (i.e., a patent foramen ovale [PFO]),
DVTs that embolize can cross over from the right atrium to the arterial system
via the left atrium and left ventricle (see Figure 13-4).
Embolus (blood clot) from a vein in leg or pelvis enters right atrium.
1.
2. Embolus passes through defect in septum between right and left atria, and enters
left artrium.
3.
Embolus enters left ventricle, and is then pumped into the aorta and hence into the
brain, causing a stroke.
* Narrowing of the pulmonary artery causes increased pressure differential between
right and left side of heart, expediting passage of embolus from right to left atrium.
FIGURE 13-4. Paroxysmal Embolism
Source: Image reprinted with permission from Medscape Drugs & Diseases (http://
emedicine.medscape.com/), 2016; available at: http://emedicine.medscape.com/
article/460607-overview.
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PROVOKING RISK FACTORS FOR VTE
See Table 13-3.
TABLE 13-3: Common Provoking (Reversible) Risk Factors for
4
VTE
Common Provoking Risk Factors
Major risk
Hospitalization
•
•
Plaster cast immobilization
Surgery
•
Minor risk
• Estrogen therapy
• Flight >8 hours
•
Leg injury
Pregnancy
•
DIAGNOSIS OF DEEP VEIN THROMBOSIS
The diagnosis of DVT involves a thorough review of patient history and signs
and symptoms, recognizing that in some patients, these may be unremarkable. Imaging of the leg veins by duplex ultrasonography with compression
is often performed to aid in the diagnosis of DVT. Venography is rarely used
due to invasive nature and dye exposure.
DVT Signs/Symptoms*
•
Calf tenderness
•
Erythema
•
Increased leg warmth
•
Leg swelling
•
Pain in the back of the knee when the foot is dorsiflexed (Homans’ sign)
•
Pain in the leg
•
Palpable superficial veins
*Key point: These are very nonspecific signs/symptoms; objective testing is
needed to confirm the diagnosis.
DVT Diagnostic Testing
Role of D-Dimer Testing in Establishing the Diagnosis of DVT
•
D-dimer is a degradation product that is produced from the breakdown of a
fibrin blood clot.
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