Treating DVT with Anticoagulation


Anticoagulation has been the mainstay of therapy for
DVT and PE since the initial introduction of heparin into
clinical use in the 1930s. Rapid anticoagulation is
essential because thrombus progression and recurrent
embolization are 15 times higher in patients who do not
receive adequate anticoagulation within the first 48
hours.

After initial anticoagulation with heparin, long-term
anticoagulation is usually maintained with warfarin.
Warfarin should never be started without prior
heparinization because warfarin reduces the levels of
anticoagulants (eg, protein C and protein S) before it
reduces the levels of procoagulant proteins. This
produces a hypercoagulable state during the first 5-7
days. If heparin is not given during this period of
warfarin induction, many patients have worsening
thrombosis.

Before 1992, the common practice in Europe was to
start patients with DVT directly on warfarin without prior
heparinization. This practice was abandoned when
Brandjes et al demonstrated in a large randomized
prospective trial that the rate of progression of
thrombosis and of embolization was 40% when patients
were started directly on warfarin, compared with only
8% when full heparin anticoagulation was established
before warfarin was started.

Intravenous unfractionated heparin is gradually being
replaced in modern practice by subcutaneous
fractionated low molecular weight heparins. These
newer agents offer much easier dosing, a wider
therapeutic window, fewer bleeding complications, and
faster and more reliable results. Several different
preparations are available, but the various heparins are
not equivalent and each requires a different dosing
regimen.

Anticoagulation Remains the Best Therapy for VTE

Anticoagulation remains the mainstay of therapy for
Venous thromboembolism (VTE) disease, but
anticoagulation alone is far from adequate
therapy for most patients. Anticoagulation can slow or
stop the progression of a new thrombus, but it does
nothing to remove a thrombus that has already been
formed. In many cases, a deep vein thrombus treated
by anticoagulation alone fails to recanalize, leaving a
chronic obstruction to outflow that is poorly tolerated by
the patient. In other cases, the thrombus recanalizes
incompletely, leaving a narrowed channel that still
produces resistance to outflow. Even when spontaneous
recanalization is complete, it usually leaves behind a
dysfunctional leg because the thrombus destroys venous
valves and produces a valveless channel that leads to
profound venous reflux and venous hypertension.

For all these reasons, approximately 65% of patients
with DVT treated with anticoagulation alone go on to
develop a debilitating clinical syndrome of CVI, often
referred to as postphlebitic syndrome. This syndrome
can include the development of large or small varicose
bypass vessels, chronic dermatitis,
lipodermatosclerosis, chronic nonhealing ulcers, chronic
pain and swelling, an increased incidence of recurrent
DVT, and other signs and symptoms of obstructed
venous outflow or increased venous reflux.


Anticoagulation Alone is Not Enough

Nearly 90% of patients treated with anticoagulation
alone for DVT develop abnormal flow patterns in one or
more venous segments, 65% have some degree of
whole-leg reflux, and 50% develop clinical signs and
symptoms of CVI. Leg ulcers may be seen in up to 80%
of patients treated with anticoagulation alone for DVT.
Even when the thrombus is isolated to the popliteal
segment of the femoral vein, 60% of patients develop
clinical CVI if treated with anticoagulation alone.

The problem is not confined to patients with lower
extremity DVT. Subclavian vein thrombosis treated with
anticoagulation alone results in permanent obstruction
or CVI in up to 90% of cases. PE occurs in 30% of these
cases, and the thrombus extends to occlude the superior
vena cava in 10% of cases.