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(VTE)
EricWongandSultanChaudhry
Facultyreviewer:Dr.PeterL.Gross,AssociateProfessor,DivisionofHematology
andThromboembolism,DepartmentofMedicine(McMasterUniversity)
Definition
Deep vein thrombosis (DVT) and pulmonary embolism (PE) are
manifestations of the same pathological entity, called venous
thromboembolism (VTE).
An embolus is any intravascular material that migrates from its original location to
occlude a distal vessel. Although the embolus can be a blood clot (thrombus), fat, air,
amniotic fluid, or tumour, a PE is usually caused by a thrombus originating from the deep
veins in the legs (deep venous thrombosis, DVT).
Arterialvs.venousthrombosis
Mechanis
atherosclerotic plaques.
Location
Diseases
Ischemic stroke
Limb
Pulmonary embolism
claudication/ischemia
Compositi
on
Mainly platelets
Mainly fibrin
Treatment
Etiology
Hypercoagulability
Stasis
Endothelial damage
VTE often arise from the synergistic effects of multiple risk factors, for
example, when a patient with inherited factor V Leiden mutation uses oral
contraceptives (acquired risk on genetic risk background).
Triad component
Hypercoagulabilit
Changes in blood
coagulation
pathway, shifting
balance toward
coagulation
60.
Stasis
The slowing or
stopping of blood
flow
Endothelial
damage
Normal endothelium
is antithrombotic.
Hypertension
Cigarette smoking
Endothelial damage: Exposure of subendothelial
tissue factor and collagen, which offer a substrate for
platelet binding, activation and aggregation; leading to
clot formation.
Major surgery
Trauma
PathophysiologyofDVT
Venous valves are avascular, which, in conjunction with reduced flow of oxygenated
blood in veins, predisposes the endothelium to be hypoxemic. The endothelium around
valves responds by expressing adhesion molecules that attract leukocytes. These cells
transfer tissue factor to the endothelium, which can complex with activated factor
VII to begin the coagulation cascade via the extrinsic pathway. The main component of
these venous thrombi is fibrin (as product of coagulation cascade) and red blood cells,
which get trapped in the clot. Platelets also contribute, but to a lesser extent.
The skeletal muscle pump helps prevent DVT by moving blood past the valves (i.e.
reducing venous stasis), which washes away activated clotting factors that can otherwise
propagate the initial thrombus.
If a clot forms and does not resolve (see below), it will extend proximally into
the popliteal and femoral veins (proximal veins). 25% of calf DVTs will extend
proximally within 7 days. While calf DVTs are usually asymptomatic and do not give rise
to significant PEs, proximal DVTs are more likely symptomatic and can embolize to form
dangerous PEs.
By the numbers
PathophysiologyofPE
Hellenic J Cardiol. 2007 Mar-Apr;48(2):94-107.
Circulation. 2003 Dec 2;108(22):2726-9.
Effectsofmechanicalocclusion
Effectsofchemicalmediators
Hemodynamicconsequences
RV ischemia
o
Right-sided (backward) heart failure: increased jugular venous pressure
(JVP)
Decreased left ventricular filling: because of bowing of interventricular septum to
left side from RV hypertrophy
o
Left-sided (forward) heart failure: hypotension, syncope, cardiogenic shock
Resolution
ClinicalfeaturesofDVT
Signs
Mechanism
Asymmetric
Pitting
leg/calf
swelling
edema on
affect side
Pain,
Localized
erythema
tenderness
along deep
venous
system
Homans sign
Dilated
Palpable cord
superficial
veins (non-
varicose)
ClinicalfeaturesofPE
Corresponding
Mechanism
ms
sign(s)
Dyspnea
Tachypnea*,
wheezing
platelets.Dyspnea is a symptom
of central, which causes more severe
Parasternal heave,
Palpitatio
ns
Hemodynamic
signs: Tachycardia
Pleuritic
chest
pain
effusion (stony
dullness on
percussion,
decreased fremitus)
Hemoptys
is and
cough
Syncope
Hypotension,
cyanosis
DiagnosisofDVT
Diagnosis starts with history (risk factors) and physical, which can be
used to generate a pretest probability using a validated clinical
prediction rule, such as the Wells DVT score (see JAMA reference
above). Patients with high likelihood of DVT can be further tested
with compression ultrasonography, where the length of the proximal
veins (popliteal and femoral) is sequentially compressed with the
ultrasound probe. Normal veins are easily occluded with moderate
external compression, but a DVT will prevent occlusion of the vein lumen.
Ultrasonography is both sensitive and specific for DVTs.
A D-dimer level can be done to rule-out DVT in individuals with low pretest
probability (see discussion in Diagnosis of PE).
Contrast venography is considered the gold standard for diagnosis of DVT, although
this is rarely done because it is invasive, expensive, and not readily available. Contrast is
injected into the dorsal foot vein, and the leg is imaged with CT scan or MRI.
DiagnosisofPE
JAMA. 2003 Dec 3;290(21):2849-58.
Poin
ts
than PE
3 Tachycardia: heart rate > 100
1.5
1.5
OR
Surgery in the previous 4
weeks
5 Previous DVT or PE
1.5
6 Hemoptysis
7 Malignancy
probability
Moderate (2-6): 20%
High (>6): 63%
Thromb Haemost. 2000
Mar;83(3):416-20.
Treatment
Chest. 2012 Feb;141(2 Suppl):e419S-94S.
The goals of treatment for VTE are (i) anticoagulation to prevent further
clot generation and (ii) thrombolysis if the thrombus is large enough to
cause hemodynamic compromise.
Anticoagulation: Reduces further clot formation
Any of the agents for acute anticoagulation can be used for chronic
anticoagulation, but they are less convenient for outpatients due to the
need for daily injections. Oral anticoagulation drugs are the mainstay
for outpatient anticoagulation. Vitamin K antagonists (e.g.
Contraindications to anticoagulation
Inferior vena cava (IVC) filter: Temporary IVC filters can be placed to stop the
movement of clots from the deep veins of the lower extremity from travelling to the
pulmonary vasculature.