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Introduction
Venous thromboembolism
(VTE) is most commonly manifested as pulmonary embolism (PE) and deep venous
thrombosis (DVT) and is associated with significant morbidity and mortality.
One-third of patients present with symptoms of pulmonary embolism and ⅔ with deep
vein thrombosis. It also manifests as superficial vein thrombosis (SVT), a less
severe form of deep vein thrombosis.
All patients admitted
for major trauma, surgery or acute medical illness should be assessed for risk
of VTE and bleeding before starting prophylaxis of VTE. Studies show that appropriate VTE prophylaxis
should be given to surgical patients in Asia who are at risk.
Deep Vein
Thrombosis (DVT)
Deep vein thrombosis is
a frequent manifestation of venous thromboembolism in which there is a blood
clot blocking a deep vein. Patients are generally asymptomatic with a calf deep
vein thrombosis but become symptomatic with proximal extension of the deep vein
thrombosis and venous outflow obstruction.
Pulmonary
Embolism (PE)
Pulmonary embolism is
the blockage of the blood vessels in the lungs that is usually due to blood
clots from the veins, especially the veins in the legs and pelvis. Subsegmental
pulmonary embolism is a type of pulmonary embolism that does not involve the
proximal pulmonary arteries.
Epidemiology
The annual incidence of the
first symptomatic deep vein thrombosis episode in adults ranges from 50 to 100
per 100,000 population, 70% of which are hospital-acquired. At ages 20 to 45 years old, the incidence is higher in
women and at ages 45 to 60 years old, the incidence is higher in men. About 60%
of venous thromboembolism events occur in >65 to year-old patients. The incidence
of deep vein thrombosis is higher in African Americans and lower in Asians and
the incidence of venous thromboembolism is higher in winter with a peak in
February.
The rate of recurrent venous thromboembolism is
approximately 10% during the first year and 30% after 5 to 8 years in patients
with unprovoked deep vein thrombosis with unidentified triggering factors. The
prevalence of clinically silent pulmonary embolism increases with age in
patients with deep vein thrombosis and is higher in patients with proximal deep
vein thrombosis.
Venous thromboembolism is the third most common
cause of acute cardiovascular disease (CVD) worldwide. It is one of the most
common life-threatening cardiovascular diseases in the United States.
In Asia, VTE has long been observed to be rare, and the lowest among
the different regions. However, cases of VTE in
Asia are increasing due to the aging population, higher rates of complex
surgery, higher rates of caesarean deliveries, rising cases of obesity,
increasing cancer cases, and lower rates of thromboprophylaxis. Currently, obstetric VTE is the leading cause of
maternal death in Malaysia.
Pathophysiology
Virchow’s triad
theorizes 3 factors contributing to the development of venous thromboembolism
which are hypercoagulability, endothelial damage, and stasis.
Hypercoagulability has been associated with factor V
Leiden mutation and prothrombin gene mutation. Cancer also produces a
hypercoagulable state due to the procoagulant activity produced by malignant
cells and secondary to the effects of chemotherapeutic agents.
The major contributing risk factors include a history of trauma,
surgical procedures, spinal cord injury, long bone fractures, and previous venous
thromboembolism.
Risk Factors
The transient or reversible provoking factors for
the development of venous thromboembolism include surgery within the past 4
weeks (eg hip or knee replacement), major trauma, immobilization for at least 3
days, bedridden for ≥3 days, estrogen therapy, pregnancy or postpartum, cesarean
section, and lengthy travel (eg airline flight >8 hours).
The chronic or persistent provoking factors for the
development of venous thromboembolism include active cancer, active autoimmune
disease (eg antiphospholipid antibody syndrome, rheumatoid arthritis), chronic
infections or immobility (eg spinal cord injury), and chronic inflammatory
states (eg inflammatory bowel disease).
Other risk factors for the development of venous
thromboembolism include myocardial infarction (MI) or hospitalization for
atrial flutter or fibrillation or heart failure (HF) within the past 3 months, increasing
age, male sex, past medical history or family history of venous
thromboembolism, lower limb fracture, congestive heart failure or respiratory
failure, obesity, varicose veins, blood transfusion and
erythropoiesis-stimulating agents, prolonged computer-related "seated
immobility syndrome", and hereditary
risk factors including non-O blood type and heterozygous factor V Leiden gene
polymorphism, and deficiency of antithrombin, protein C or protein S.
Classification
Classification
of Deep Vein Thrombosis
According to the Anatomical
Level
Accurate anatomical classification is important for
diagnostic, therapeutic, and prognostic purposes as the risk of pulmonary
embolism, post-thrombotic syndrome development, and overall prognosis are
different depending on the affected veins. Deep vein thrombosis may be classified
into proximal and distal deep vein thrombosis.
Proximal deep vein thrombosis is thrombosis of the iliac,
femoral, and/or popliteal veins with or without calf deep vein thrombosis. This
includes femoropopliteal deep vein thrombosis and iliofemoral deep vein
thrombosis (which commonly occurs on the left).
Distal deep vein thrombosis is thrombosis confined
to the calf-deep veins (eg peroneal, posterior tibial, gastrocnemius, or soleal
veins). It is often associated with transient risk factors (eg recent surgery,
plaster placement for limb fracture, travel).
According to Etiology
Deep vein thrombosis may also be classified as
provoked or unprovoked based on the presence of risk factors. Unprovoked or
idiopathic deep vein thrombosis is venous thrombosis without identifiable
environmental or acquired risk factors. Provoked deep vein thrombosis occurs in
the presence of risk factors which may be transient minor or major risk factors
or persistent risk factors.
The risk of recurrence and anticoagulation therapy will differ based on the
etiology and chronicity of the risk factors. The risk of recurrence is higher
when deep vein thrombosis is provoked by a persistent and progressive risk
factor (eg cancer). The risk of recurrence after stopping anticoagulation is
very low when deep vein thrombosis is provoked by a major transient risk factor
(eg trauma, surgery, estrogen therapy, pregnancy, puerperium) provided the risk
factor is no longer present. Patients with unprovoked deep vein thrombosis have
an intermediate risk of recurrence.