Article 3 5/21/01 11:14 PM Page 25

Deep Venous Thrombosis

Venous thrombosis involving the deep veins is a major US health problem that affects over
2.5 million people annually. The most serious complication of a deep venous thrombosis (DVT)
is pulmonary embolism (PE), which is associated with 50,000 to 200,000 deaths each year. DVT
and PE are often silent and difficult to detect by clinical examination; however, DVT rarely occurs
in the absence of risk factors. This article reviews normal venous anatomy and discusses the
etiology of DVT, its clinical manifestations, and diagnosis. Then it reviews treatment of DVT,
highlighting the nurses role. A discussion of DVT prophylaxis based on patient risk follows. Key
words: anticoagulation, deep venous thrombosis, DVT prophylaxis, low-dose heparin, low-
molecular-weight heparin, nursing measures, unfractionated heparin, Virchows triad, warfarin

gic, and neurosurgical. Of these groups,

Anne M. Aquila, APRN orthopaedic patients appear to be espe-
Vascular Program Coordinator cially prone to thrombosis, particularly pa-
Hospital of Saint Raphael tients with hip fracture/hip replacement
New Haven, Connecticut and knee reconstruction. Patients with
various medical diseases, usually chronic,
also are at risk for thrombotic events. With
many high-risk groups identified, it is rea-
enous thrombosis involving the deep sonable then to consider ways to prevent
V veins is a major health problem in the
United States today, affecting more than
embolic phenomena. Preventive measures
are not only cost-effective, but also less
2.5 million people each year. The most risky and better tolerated by the patient
serious complication of a deep venous than specific treatment modalities.
thrombosis (DVT) is pulmonary embolism This article begins by reviewing normal
(PE), which is associated with 50,000 to venous anatomy. A discussion of the etiol-
200,000 deaths annually.1 It is impossible ogy of DVT, its clinical manifestations, and
to determine the true mortality rate be- diagnosis follows. The treatment of DVT is
cause of difficulty in diagnosing PE with then reviewed, highlighting the nurses role.
certainty in the absence of an autopsy; A discussion of DVT prophylaxis based on
moreover, many patients who die of a PE patient risk concludes the presentation.
have concomitant medical conditions that
may have contributed to their death. VENOUS ANATOMY
Both DVT and PE are often silent and
difficult to detect by clinical examination. The primary function of the systemic
It is important to keep in mind that clini- veins is to provide for the return of blood
cal examination includes attention to pa- to the right side of the heart. The veins,
tient history, not just physical examina- however, do not function simply as passive
tion because DVT rarely occurs in the conduits for the flow of blood. Instead, ve-
absence of risk factors. Several groups of nous hemodynamics are complicated by
patients at high risk for developing ve- the presence of low pressure within the
nous thromboembolic disease have been system (as compared with the arteries),
identified.2 These include patients under-
going various types of surgerygeneral, J Cardiovasc Nurs 2001;15(4):2544
orthopaedic, gynecologic-obstetric, urolo- 2001 Aspen Publishers, Inc.

25
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26 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

vein collapsibility, flow variation with res- in the smaller, more distal veins. Few
piration, the effect of gravity, and even valves are located in the femoral veins;
retrograde pulse transmission from right the vena cava and common iliac veins are
heart contraction.3 valveless.5,6

Microscopic anatomy Gross anatomy

In comparison to arteries, veins are Lower extremity veins can be concep-
thinner walled and less muscular. The tually separated into three separate but
layers of the veins, namely the intima, interconnected systems that work to-
media, and adventitia, are identifiable gether to provide total outflow for the
microscopically. The innermost layer extremity: the deep venous system, the
the intimaconsists of a confluent layer superficial venous system, and the perfo-
of endothelial cells that is in contact with rating or communicating system. The
the blood flowing within the lumen of deep veins of the legs lie beneath the deep
the vein. These cells are metabolically fascia within the leg musculature and are
active and produce prostacyclin, plasmin, well supported by surrounding tissue.
and endothelium-derived relaxing factor, They provide 90% to 95% of venous out-
which are important inhibitors of intra- flow from the leg. Deep veins above the
vascular coagulation.4 Alterations in this knee are the iliac and femoral. Deep veins
endothelial lining may play a role in the de- below the knee are the popliteal, per-
velopment of thrombus. In the larger veins, oneal, anterior tibial, and posterior tibial.
a subendothelial layer of supportive tissue Superficial veins run in the subcutaneous
can be identified within the intimal layer. tissue and are relatively poorly supported.
A primary difference between arteries The principal superficial veins of the lower
and veins is found in the composition of extremity are the greater and lesser saphe-
the media, which is generally thicker in ar- nous. The proximal ends of these veins
teries and accounts for the arterys firm empty directly into the deep venous system
and minimally distensible properties. The at the popliteal and femoral levels.
adventitia is a thin layer of loose connec- There are between four and six major
tive tissue surrounding the vein. communicating veins that traverse the
deep fascia of the legs and form a commu-
Macroscopic anatomy nication between the superficial and deep
venous circulation. They are located at the
Unlike the arteries, veins possess valves
area just superior to the medial malleolus,
along their entire length. Each valve con-
the medial calf, and the medial lower
sists of two very thin-walled cusps that
thigh.5,6 Each of these communicating
originate at opposite sides of the vein wall
veins has venous valves that normally di-
and oppose in the midline. Ordinarily,
rect flow from the superficial veins to the
valves allow for the unidirectional flow of
deep veins and prevent reflux in the oppo-
blood back to the heart. Blood is able to flow
site direction.
in a proximal direction through the valve
between the valve cusps. Reverse flow is
Venous physiology
prevented by the apposition of the two
cusps when pressure above the valve is Venous physiology is in many respects
greater than below. more complex then arterial physiology.
The location of the venous valves is Venous compliance and normal venous
variable. Generally speaking, valves are hemodynamics influence physiology in
more numerous and more closely located the venous system.
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Deep Venous Thrombosis 27

Compliance sipated by the passage of blood through

the high-resistance arteriolar capillary bed
Veins are collapsible tubes, so trans-
at the level of the right atrium. With stand-
mural pressure (ie, the difference between
ing, hydrostatic pressure (ie, the pressure
the intraluminal forces acting to expand
created by the weight of the column of
the vein and the external pressures acting
blood) greatly exceeds the dynamic pres-
to compress the vein) determines their
sure and acts to impede venous return.
shape and thus their volume. Because
The driving force to overcome gravity
veins can stretch and distend, they can in-
when one is in the standing position is
crease their intraluminal volume with only
provided by the musculovenous pump or
minimal elevation in the venous pressure.
calf muscle pump (Fig 1).
This ability to accommodate large shifts in
When leg muscles contract, they raise
volume with only minimal changes in ve-
pressure in and around all the structures
nous pressure is known as compliance.5
within the deep fascia. As this pressure
within the deep veins rises above that in
Normal venous hemodynamics
the superficial veins, blood moves into the
Venous hemodynamics differs greatly larger veins in the deep system and toward
from the hemodynamics of the arterial cir- the heart; the valves in the perforating
culation. In the arterial circulation dy- system close, preventing blood reflux into
namic pressure exerted by the contraction the superficial system. With muscle relax-
of the left ventricle is the dominant force ation, pressure within the deep venous
providing a mean arterial pressure be- system falls below that in the superficial
tween 90 and 100 mm Hg. On the venous system and blood passes from the super-
side, dynamic forces have been greatly dis- ficial to the deep system via the perfora-

A Relaxation B Contraction

Fig 1. (A) Veins within the calf muscle pump during relaxation. Note the filling of the deep veins
from the perforating veins and lower leg with proper deep venous valve closure in the standing po-
sition. (B) Veins within the calf muscle pump during muscle contraction with ejection of blood to-
ward the heart. Note the proper closure of the valves of the communicating veins in a nondiseased
venous system. Source: Reprinted with permission from Hahn TL, Dalsing MC, Chronic venous dis-
ease, in Vascular Nursing, 3rd ed. V Fahey, ed., p. 366, 1999, WB Saunders Company.
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28 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

tors. Pressures in excess of 200 mm Hg can

be generated when the calf muscles con- Risk Factors Associated with Deep
tract, which is more than enough to pro- Venous Thrombosis
vide energy for venous return. With the
recumbent position, the pressure exerted I. Venous stasis
Heart disease
by gravity is eliminated and venous flow
Congestive heart failure
becomes relatively phasic in nature; it is to Myocardial infarction
a great extent driven by changes in ab- Cardiomyopathy
dominal and thoracic pressure induced by Constrictive pericarditis
Dehydration
respiration.5,6
Immobility(bed rest 72 hours,
long travel)
Paralysis
ETIOLOGY OF DVT Incompetent venous valves

Obesity (20% ideal body weight)

Pregnancy
Understanding of the pathophysiology
Surgerylasting more than
of DVT and PE dates back to 1856 when
45 minutes
Rudolph Virchow, a German pathologist, Age 40 years
first recognized the association between
the two entities. Virchows triad of (1) ve- II. Vessel wall injury
Trauma
nous stasis, (2) vessel wall injury, and
Fracture
(3) hypercoagulabilitymore appropri- Extensive burns
ately called the prothrombotic stateis Infection

generally accepted as including the main Venipuncture

precipitating factors in the generation of Intravenous infusion of irritant

solutions
venous thrombi7 (see the box titled, Risk
Previous history of deep venous
Factors Associated with Deep Venous thrombosis
Thrombosis). History of previous major surgery

III. Hypercoagulability
Venous stasis Alterations in hemostatic
mechanisms
Blood flow is normally reduced around Protein C resistance or deficiency
venous valves.1,6 Immobility, which results Antithrombin III deficiency or
when one is subjected to a period of bed resistance
Protein S deficiency
rest, serves to further alter blood flow by
Factor V R506Q (Leiden) mutation
influencing the functioning of the mus- Polycythemia vera
culovenous pump. With prolonged bed Anemias
rest, there is loss of the regular repetitive Trauma/surgery

Malignancy
muscular contraction in the legs, which im-
Oral contraceptive use
pairs the peristaltic propulsion of venous
Systemic infection
blood flow. This alteration promotes venous
stasis. While some controversy about the
role of stasis in the development of DVT ex-
ists, in the surgical patient venous stasis is
perhaps the most treatable of the causative tions that promote venous stasis include
factors.1 Stasis may develop when surgical heart disease (congestive heart failure, myo-
procedures exceed 30 minutes in duration cardial infarction, cardiomyopathy), obe-
or when general anesthesia causes veno- sity, dehydration, pregnancy, malignancy
dilation and venous stasis. Other condi- and a debilitated state, and stroke.8
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Deep Venous Thrombosis 29

Vessel wall injury monstration that some tumors release tis-

sue factor into the circulation. Tissue fac-
It has been suggested that venodilation
tor appears to be derived from not only
that occurs under general anesthesia can
neoplastic cells but also regional infil-
disrupt the endothelial or innermost lining
tration of activated macrophages around
of the vein, exposing the thrombogenic
the tumors.1,9 This thrombogenic effect of
subendothelial surface.1 Thus, a vessel that
malignant cells is of more concern in pa-
should normally not allow clot to form may
tients receiving chemotherapy, another
become obstructed by platelets and fibrin
factor associated with an increased inci-
that accumulate at the site of injury. The
dence of thromboembolic disease.
box titled, Risk Factors Associated with
Deep Venous Thrombosis lists other fac-
PATHOPHYSIOLOGY OF DVT
tors that may promote vessel wall injury.
Most venous thrombi originate behind
Hypercoagulability (prothrombotic state)
valve pockets10 (Fig 2) as the vein wall is
Hypercoagulability exists when coagu- slightly dilated behind each of the venous
lation overrides fibrinolysis. The coagula- valve leaflets. While this dilated area
tion cascade mediates intravenous throm- allows for prompt valve closure, flow is
bus formation by two basic pathways: the slower or stagnant in these small areas. It
intrinsic system and the extrinsic system. is not known whether previous damage to
Both systems lead to thrombin formation the endothelium of the vein is necessary
and the development of a fibrin clot. The
fibrinolytic system is associated with the
coagulation cascade and acts to prevent
clot propagation and allows for clot dis-
solution as healing takes place.
Although preoperative coagulation tests
cannot identify patients who will develop
DVT, there are several inherited disorders
that clearly predispose patients to its de-
velopment. The most important inhibitor
of activated factor X is antithrombin III. A
deficiency in it as well as other factors (see
the box titled Risk Factors Associated
with Deep Venous Thrombosis) may ren-
der an individual more likely to clot. Other
unexplained prothrombotic states are as-
sociated with trauma, major surgical pro-
cedures in proportion to the length of op-
eration, obesity, advanced age, and sepsis.1
In addition to an increase in coagulability
of the blood after trauma or operation, sys-
temic plasma fibrinolytic activity is re-
duced for as long as 10 days. This is Fig 2. Development of deep vein thrombosis
known to be a significant factor in the de- and pulmonary embolism. Source: Reprinted
velopment of DVT.1 from VA Fahey, Life-threatening pulmonary em-
The association of DVT and malignancy bolism, Critical Care Nursing Quarterly, Vol. 8,
has been clarified recently with the de- No. 2, p. 82, 1985, Aspen Publishers, Inc.
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30 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

for thrombus formation, however, stagnant

hypoxemia is capable of causing endothe-
lial injury and stasis retains all the proco-
agulant factors locally, leading to succes-
sive regional activation of the coagulation
cascade and further platelet and fibrin
deposition.1,11
Once a thrombus forms, it enlarges and
may extend proximally and distally, there-
by occluding the vessel lumen. Various sce-
narios may occur. If the thrombus fails to Fig 3. Classic symptom of deep vein thrombo-
obstruct the entire lumen, it is enveloped sis. Note the unilateral right leg swelling, espe-
by endothelium (recanalization) and the co- cially at thigh and calf. Source: Reprinted with
agulation or thrombogenic process ceases.12 permission from Walsh ME, Rice KL, Venous
thrombosis and pulmonary embolism, in Vas-
Even though clot formation was interrupted
cular Nursing, 3rd ed., V Fahey, ed., p. 347,
and the vessel reopened, the venous valves
1999, WB Saunders Company.
may still be destroyed by the inflammatory
reaction that accompanies the original
thrombotic process. This individual may go
on to develop a chronic venous disorder The physical findings in DVT are deter-
such as post-phlebitic syndrome. In fact, mined by location of the venous obstruc-
29% to 79% of patients with DVT will de- tion, the size of the thrombus, whether the
velop this problem.13 The thrombus also vein lumen is partially or totally obstruc-
may develop a floating tail that is highly ted, and the adequacy of the collateral cir-
susceptible to becoming dislodged and culation. Thus, physical findings may be
traveling proximally into the pulmonary ar- absent if the vein lumen is partially ob-
terial circulation, resulting in a PE. It is now structed or if collateral channels allow for
generally accepted that 90% of all clinically flow around an obstruction.
significant PEs can be traced to a lower ex- The patient may exhibit unilateral ede-
tremity DVT.8,14 ma, which results from congestion of ve-
nous, lymphatic, and capillary beds distal
CLINICAL MANIFESTATIONS to the thrombotic occlusion. An increase in
the diameter of one calf, ankle, or thigh in
DVT generally occurs in the lower ex- relation to the other or pitting edema
tremity (Fig 3), but also may occur in the in only one leg also may be observed.
upper extremities, although with a lower Homans sign, which is defined as pain in
frequency. Upper-extremity DVT is usually the calf on forced dorsiflexion of the foot, is
associated with an identifiable predispos- not a sensitive or specific test for DVT.17 A
ing condition such as a cervical rib or mus- more accurate finding is pain that occurs
cular band that causes venous compression when palpating the calf or along a vein.18
or following deep venous instrumenta- Less common manifestations include
tion.15 The more frequent use of central prominent superficial veins and a palpable
venous catheters for prolonged venous ac- cord. When a palpable cord is found it
cess, hyperalimentation, and dialysis ac- helps to differentiate a superficial phlebitis
cess and hemodynamic monitoring has led from a DVT by virtue of its subcutaneous
to an increase in catheter-related central location. The inflammatory response of the
venous thrombosis.15,16 superficial venous system also may cause
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Deep Venous Thrombosis 31

the affected extremity to be erythematous test include patient discomfort from the in-
and warm to the touch. jection, expense, and potential reaction to
Obstruction of the large veins (eg, the the contrast medium.1
iliofemoral veins) may take on the form
of phlegmasia alba dolens (white leg) or
Duplex study
phlegmasia cerulea dolens (blue leg).
Phlegmasia alba dolens is the term used to The term duplex study refers to the deter-
describe the white or milky leg caused by mination of venous flow by a combination
iliofemoral vein thrombosis with associ- of Doppler analysis and B-mode (bright-
ated arterial spasm. It is usually observed ness mode) ultrasound. Color-enhanced
in postpartum women. In this patient Doppler imaging has added to the speed
pulses may be weak or absent, and the leg and accuracy of the measurements. Ad-
is cold. Swelling occurs in later stages. vantages of the test include its ability to be
Phlegmasia cerulea dolens is commonly performed at the bedside, its noninvasive
seen in advanced stages of some cancers. and nonthrombogenic nature, and its sen-
Here there is almost total occlusion of ve- sitivity and specificity, which are compa-
nous outflow, with increased pressure rable to those of venography. It is the most
contributing to arterial inflow obstruction. appropriate initial screening test for clini-
It can lead to gangrene if left untreated. Pa- cally suspected DVT; if negative, it will
tients typically experience a sudden onset safely exclude the diagnosis of DVT in the
of pain, massive edema, and cyanosis of area studied.1,20
the extremity. The patient may be hypo- The Doppler probe can be used alone at
tensive due to interstitial fluid extravasa- the bedside to detect DVT with a high de-
tion and hemoconcentration may occur, gree of accuracy if the examiner is skilled
which further influences thrombosis.19 and experienced. Doppler tracks sound
Approximately 50% of patients with a waves created by blood moving through
DVT will be asymptomatic. Thus a sus- the vessel. It can detect the lack of flow,
pected diagnosis needs to be confirmed by the effect of compression on venous flow,
objective means. and changes in flow velocity. A negative
Doppler study is reassuring, but a positive
or equivocal test should be confirmed by
DIAGNOSTIC EVALUATION
adding B-mode ultrasound or by contrast
venography. The test is less sensitive to
Venography
calf vein thrombi but can be used in
While clinical evaluation of the patient patients who are wearing a plaster cast.
with DVT is important, it is unreliable. His- B-mode ultrasonography allows visualiza-
torically, venography was considered the tion of venous valvular movement, accel-
gold standard for providing an accurate erated blood flow in the presence of throm-
diagnosis of DVT. The test consists of the bus, and even imaging of the thrombus
injection of contrast medium into a vein in itself, depending on its age. Fresh thrombi
the foot. A tourniquet on the lower leg pro- are not echogenic but can be identified
motes filling of the deep venous system. when pressure of the probe fails to com-
Typically a positive study results when the press the walls of the vein, as would nor-
contrast media fail to fill the deep system, mally be expected. The size of the vein
with passage of contrast medium into the also can be demonstrated, and an affected
superficial system or demonstration of dis- vessel can be compared with a normal ves-
crete filling defects. Disadvantages of the sel in the same individual.
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32 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

TREATMENT OF DVT Anticoagulation remains the first-line

treatment for patients with distal and
In a patient with DVT, the goals of ther- proximal DVT. Therapy should start with
apy are to (1) minimize the risk of pul- an agent that has immediate anticoagulant
monary embolism, (2) limit further throm- effect, and it should be given at an ade-
bosis, and (3) facilitate the resolution of quate dosage. Failure to reach the pre-
existing thrombi and avoid the post- scribed intensity of anticoagulation in the
phlebitic syndrome. Traditionally, bed rest first 24 hours of treatment increases the
was recommended for about 5 days follow- risk of recurrent venous thromboembolism
ing the acute event. This time period al- 15 times.22
lowed the thrombus to stabilize and adhere
to the vein wall, thus decreasing the risk of
Anticoagulation therapy: A historical
embolization. Progressive ambulation then
perspective
was started. Today there is variability
among practitioners as to the amount of Heparin has been the standard initial
prescribed bed rest. This variability is due therapy for DVT since the 1940s. For many
in part to the shift in treatment of DVT to years, evidence of the efficacy of heparin in
the outpatient setting using low-molecular- patients with DVT was based on experi-
weight heparin (LMWH). mental studies in animals and uncontrolled
Leg elevation is recommended when clinical experience. Not until 1992 did a
the patient is lying down. The affected randomized, double-blind trial23 demon-
extremity should be elevated at least 10 strate that patients with DVT do require ini-
to 20 above the level of the heart to pro- tial treatment with full-dose heparin.
mote venous return and decrease venous Historically, admission to the hospital
congestion.21 After the acute event re- was deemed necessary for patients with
solves, graduated compression stockings DVT, so treatment with dose-adjusted
should be used to promote venous return standard (unfractionated) heparin (UH)
and decrease residual swelling, thereby could commence. In the 1980s these pa-
reducing the risk of post-phlebitic syn- tients were typically hospitalized for 7 to
drome. For proper fit, the nurse should 14 days before being discharged on oral
measure the largest calf and ankle cir- anticoagulant therapy.24 In the 1990s, it
cumference and the length from the bot- was determined that the duration of he-
tom of the heel to the bend of the knee. parin therapy could be safely shortened to
Stockings are designed so that the great- 5 days if oral anticoagulant therapy com-
est pressure is exerted at the ankle, with menced at the same time as heparin ther-
pressure decreasing proximally. Com- apy.25,26 The advent of LMWH preparations
pression stockings are discussed further made it possible to commence heparin
under nonpharmacologic (mechanical) therapy in an outpatient setting. The use of
prophylaxis for DVT. LMWHs can serve to eliminate or drasti-
Mild analgesics such as acetaminophen cally reduce hospital length of stay for in-
may be ordered to decrease pain associ- dividuals with DVT.27,28
ated with venous distention. Local moist
heat also may be applied to the affected
Comparing UH and LMWH
extremity at prescribed intervals to de-
crease pain and inflammation. Leg eleva- Heparin is a glycosaminoglycan extrac-
tion also may serve to relieve pain and ted from a variety of animal tissues such as
discomfort. porcine intestine mucosa and bovine lung
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Deep Venous Thrombosis 33

tissue. Heparin acts as an anticoagulant by be obtained. Not all patients are candi-
binding to plasma antithrombin III, the dates for outpatient therapy due to preex-
bodys naturally occurring anticoagulant. isting conditions, age, or anticipated poor
This interaction brings about a conforma- compliance; thus careful screening of pa-
tional change in antithrombin III that tients is necessary. LMWH is dosed based
greatly increases its ability to inactivate on patient weight; it may be given subcu-
coagulation enzymes, including thrombin taneously every day or twice a day, de-
and factor Xa.29 Preparations of UH consist pending on the LMWH preparation being
of a heterogeneous mixture of polysaccha- used. Oral anticoagulation with warfarin
ride chains ranging in molecular weight (Coumadin) is begun concomitantly. The
from about 3,000 to 30,000. Preparations of PT/INR is typically drawn on day 3 of war-
LMWH are derived from UH by either en- farin therapy and adjusted if needed to
zymatic or chemical depolymerization to maintain an INR of 2.0 to 3.0. The INR is
yield fragments that are one third the size monitored daily until stable and therapeu-
of UH, with a mean molecular weight of tic (INR of 2.0 to 3.0 for two consecutive
about 4,000 to 6,000.29 The anticoagulant days). Typically therapy with LMWH is
activity of both UH and LMWH resides in continued for 5 days and the INR is be-
a unique pentasaccharide sequence that is tween 2.0 and 3.0. Oral anticoagulation
randomly distributed along the heparin therapy is continued for 3 to 6 months un-
chains and binds with high affinity to anti- less patient status requires a longer dura-
thrombin III. tion of therapy.27,28 Care outside the hos-
The principal difference between UH pital increases pressure on community
and LMWH is in the inhibitory effect on facilities to provide proper anticoagulant
factor Xa and thrombin. Because of differ- therapy. Patients may be taught self-injec-
ences in their chemical composition, UH tion of LMWH at home or require assis-
has equivalent inhibitory activity against tance to administer the medication. Addi-
both thrombin and factor Xa, whereas tional teaching may be needed including
LMWH preferentially inactivates factor Xa. patient understanding of what DVT is, an
LMWH preparations have several advan- understanding of self-care activities such
tages over UH. Unlike UH, LMWH can in- as limb monitoring and medications, and
activate platelet-bound factor Xa and can follow-up care including blood drawing
resist inhibition by platelet factor 4, which and signs and symptoms to report to the
is released during clotting.29 LMWHs have health care provider.
a longer plasma half-life and a more pre-
dictable anticoagulant response to weight-
Inpatient therapy with intravenous UH
adjusted doses than UH. These properties
allow LMWHs to be given once or twice a While treatment of DVT with LMWH has
day and without laboratory monitoring.29 proved safe and effective,27,28 it will take
time for institutions and practitioners to
transition from one treatment method to
Outpatient therapy with LMWH
another. Thus, intravenous (IV) UH may be
Prior to the initiation of therapy, base- used. If inpatient therapy with IVUH is
line laboratory parameters of activated chosen, baseline laboratory parameters of
partial thromboplastin time (APTT), pro- APTT, PT/INR, and platelet count or com-
thrombin time (PT) as an international plete blood cell count are obtained. The
normalized ratio (PT/INR), and platelet goal of therapy is to maintain the APTT
count or complete blood cell count must ratio between 1.5 and 2.5 times the control.
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34 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

Traditionally, the patient was given a bolus greater than 70 years. Thus, when admin-
dose of 5,000 units of heparin followed by istering heparin therapy, the nurse must be
a continuous heparin infusion of 1,000 to attuned to major bleeding such as intracra-
1, 500 units/hour. Of primary importance nial or retroperitoneal as well as minor
is using adequate doses of heparin (at least bleeding that might take the form of easy
a 5,000-unit bolus) followed by an intra- bruising, blood in the urine or stool, epis-
venous infusion of 30,000 units/day. Ad- taxis, or hematemesis. Patients need to
justing heparin doses in response to APTT be aware of the bleeding risk and know
values also is important, especially in pa- the importance of reporting any bleeding
tients receiving subtherapeutic doses of he- noted. Serious bleeding associated with
parin. Some patients may have persistently IVUH therapy may require administration
subtherapeutic APTT values despite re- of protamine sulfate, a strongly basic pro-
ceiving high therapeutic doses of heparin. tein that binds and neutralizes heparin.
Heparin levels may assist in the treatment Each milligram of protamine neutralizes
of these patients.29 approximately 100 units of heparin. Prota-
Since appropriate dosage adjustments of mine may cause hypotension and should
intravenous heparin therapy can be prob- be given slowly over 10 minutes.29 LMWH
lematic, studies30,31 have reviewed the use is not associated with increased major
of dose-adjusted nomograms. They have bleeding compared with standard heparin
demonstrated that by dosing heparin based in acute venous thromboembolism.32
on weight, a therapeutic APTT is more Heparin-induced thrombocytopenia
likely to be achieved in the first 24 hours. (HIT) is a well-recognized complication of
When APTT is therapeutic, it is initially heparin therapy. It is caused by antibodies,
obtained daily. Continuous heparin infu- predominantly immunoglobulin G (IgG),
sion continues for 3 to 4 days. Oral antico- that activate platelets, leading to thrombo-
agulation with warfarin is started within cytopenia. HIT may occur in an early be-
the first 24 hours of heparin dosing and nign, reversible nonimmune form where
when the APTT is within the prescribed the platelet count recovers despite heparin
therapeutic range. therapy.29
Late thrombocytopenia is IgG mediated.
It is associated with a substantial risk of
Heparin side effects or complications
thrombotic complications and will usually
and nursing considerations
persist unless heparin therapy is discon-
Bleeding is the major complication of tinued. The frequency of this form of HIT is
anticoagulant therapy, and there is a strong uncertain due to its patient population def-
relationship between the intensity of anti- inition, definition of thrombocytopenia,
coagulant therapy and the risk of bleeding. dose and duration of heparin therapy, and
Any heparin preparation has the potential the heparin preparation used. In the previ-
to induce bleeding by inhibiting blood co- ously unexposed patient, platelet count be-
agulation, impairing platelet function, and gins to fall 5 to 10 days after starting ther-
increasing capillary permeability. Based apy, although overt thrombocytopenia may
on data reviewed at the fifth American Col- not be reached for a few more days.29 Mon-
lege of Chest Physicians (ACCP) confer- itoring of platelets is recommended at in-
ence,32 the risk of bleeding associated with tervals, often beginning day 3 of therapy
IVUH in patients with acute venous throm- and then every other day while the patient
boembolism is less than 3%. There is some is receiving heparin. In the previously ex-
evidence to suggest that this bleeding risk posed patient, platelet count may begin
increases with heparin dosage and age to fall within 24 hours. Thrombosis attri-
Article 3 5/21/01 11:14 PM Page 35

Deep Venous Thrombosis 35

butable to HIT occurs in about 1% of IVUH or subcutaneous LMWH. Dosing is

patients who receive intravenous thera- very individualized and is based on the
peutic heparin for more than 5 days. Ve- PT/INR. Studies have compared 5-mg and
nous thrombosis is more common than 10-mg loading doses in the initiation of
arterial thrombosis. Once heparin is dis- warfarin therapy. A 5-mg loading dose has
continued, platelet counts will be within been shown to produce less excessive an-
the normal range for 90% of individuals ticoagulation than a 10-mg loading dose.34
within 1 week. The optimal management As warfarin is not fully effective in in-
of HIT is uncertain. A consensus is emerg- hibiting the clotting process for 3 to 4 days,
ing that agents that rapidly control throm- overlapping with IVUH or LMWH is rec-
bin generation (danaparoid, hirudin, and ommended with heparin stopped once the
argatroban) are likely to be effective for the INR has reached 2.0 to 3.0.
treatment of HIT.29 The incidence of throm- Oral anticoagulation is generally contin-
bocytopenia is reduced with LMWH, per- ued for 3 to 6 months to prevent recurrent
haps due to reduced binding to platelets.29 thrombosis in patients with proximal vein
Osteoporosis is usually seen only with thrombosis and symptomatic calf vein
long-term UH therapy as it is thought thrombosis. For patients with recurrent
to cause direct resorption of bone. The venous thrombosis, antithrombin III defi-
reduction in osteoporosis demonstrated ciency, protein C deficiency, protein S de-
with LMWH is possibly due to reduced ficiency, and malignant neoplasms, antico-
binding to osteoblasts that results in less agulation may be maintained indefinitely.
activation of osteoclasts and an associated Special consideration must be given to
reduction in bone loss.29 the effects of dietary vitamin K on warfarin
levels. Patients are instructed to maintain a
consistent diet and avoid eating large quan-
Anticoagulation with warfarin
tities of foods high in vitamin K such as dark
Warfarin prevents thrombosis by inhibit- green leafy vegetables. Many drugs also in-
ing the synthesis of functionally active teract with warfarin and may potentiate or
vitamin Kdependent clotting factors II, inhibit its effect. A detailed list of the pa-
VII, IX, and X.33 These vitamin Kdepend- tients medications should be reviewed
ent clotting factors vary considerably in prior to dosing warfarin.
their half-lives (II, 60 to 120 hours; VII, 5
to 6 hours; IX, 17 to 40 hours; X, 20 to
Warfarin side effects and nursing
48 hours). Due to this variability in clearing
considerations
the vitamin Kdependent clotting factors
from the body, warfarin is not fully effec- As previously noted, bleeding is a risk of
tive in inhibiting the clotting process for 3 anticoagulant therapy. The major determi-
to 4 days. nants of oral anticoagulant-induced bleed-
Progress has been made in the control of ing are the intensity of the anticoagulant
oral anticoagulant therapy because the im- effect, patient-specific characteristics, and
portance of reporting PT results as an INR the duration of therapy. There is good evi-
is now recognized. A recommendation of dence to suggest that lower-intensity oral
an INR of 2.0 to 3.0 is made for treatment anticoagulant therapy aiming for an INR of
of venous thrombosis and PE as well as for 2.5 (range 2.0 to 3.0) is associated with a
prophylaxis of venous thrombosis in high- lower risk of bleeding than therapy tar-
risk surgery.33 geted at a higher intensity.33
Dosing with warfarin is usually begun A nonhemorrhagic side effect of war-
simultaneously with the initiation of farin is skin necrosis. This uncommon
Article 3 5/21/01 11:14 PM Page 36

36 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

complication is usually observed on the Operative thrombectomy

third to eighth day of therapy. It results
Direct surgical removal of a thrombus
when thrombi form in the small vessels
from the deep veins of the leg by way of the
and adipose tissue. This tissue becomes
common femoral vein has been facilitated
necrotic and sloughs, promoting infection.
by the use of embolectomy catheters for
Sites affected by this process include the
the extraction of clot. Surgery is usually re-
breasts, thighs, buttocks, and legs.35 Stud-
served for those patients with phlegmasia
ies point to a correlation between protein
cerulea dolens who are at risk of limb loss
C deficiency36 and, to a lesser extent, pro-
or who demonstrate extensive ileofemoral
tein S deficiency and skin necrosis. Treat-
vein thrombosis and impending venous
ment includes cessation of the drug, re-
gangrene.1
sumption of heparin therapy or increased
dosage, and comfort measures. Surgical
Inferior vena caval interruption
debridement, topical antibacterial oint-
ments, and skin grafting may be necessary Adequate anticoagulation is usually ef-
with more extensive tissue damage.37 For fective in managing DVT. However, in se-
patients who may require long-life antico- lect circumstances (see the box titled In-
agulant therapy, warfarin may be restarted dications for Vena Caval Filter Placement),
at a low dose, with heparin given con- vena caval interruption is performed. The
comitantly and gradually increased over most popular method of inferior vena caval
several weeks. This approach should interruption is placement of a filter.1 This
avoid an abrupt fall in protein C levels be- six-legged device can be inserted through
fore there is a reduction in the levels of fac- the internal jugular vein or femoral vein
tors II, IX, and X.35,36 and advanced into place in the inferior
vena cava using fluoroscopic guidance. The
long-term patency rate of the filter is 98%.
Thrombolytic therapy
Complications of filter placement include
Thrombolytic agents affect the coagula- recurrent emboli, venous insufficiency, air
tion cascade by acting directly or indirect- embolism, and improper placement or mi-
ly on plasminogen, effecting its conversion gration of the device.1,38
to plasmin and promoting fibrinolysis.
Streptokinase (SK) and tissue plasminogen PREVENTION OF DVT
activator (tPA) are the agents currently ap-
proved for clinical use in venous throm- The goal of prophylaxis in patients with
boembolic disease. The application and risk factors for DVT is to prevent both its
duration of thrombolytic therapy in the occurrence and its consequences, mainly
treatment of DVT and PE remain variable. pulmonary emboli and post-phlebitic syn-
In the treatment of DVT, it appears that drome. Patients with DVT often have no
early use of a thrombolytic such as SK can symptoms, and therefore its detection is
decrease subsequent pain, swelling, and likely to be delayed. Of the patients who
loss of venous valves and may reduce the will eventually die of PE, two thirds sur-
incidence of post-phlebitic syndrome.38 vive less than 30 minutes after the event
Work is still needed as to the optimum not long enough for most forms of treat-
dose and duration of thrombolytic therapy ment to be effective.2 Preventing DVT in
for DVT and PE. In DVT, SK is approved patients at risk is clearly preferable to
for 48 to 72 hours of intravenous therapy. treating the condition after it appears, a
All thrombolytic agents act systemically, view that is supported by cost-effective-
thus bleeding is a risk. ness analysis.2
Article 3 5/21/01 11:14 PM Page 37

Deep Venous Thrombosis 37

Indications for Vena Caval Filter Placement

Recurrent thromboembolism despite adequate anticoagulation

Confirmed deep venous thrombosis or thromboembolism with a contraindication to anti-
coagulation therapy
Complication of anticoagulation requiring discontinuation of therapy
Recurrent pulmonary embolism with associated pulmonary hypertension and cor
pulmonale
Propagating or free-floating thrombus
Immediately following pulmonary embolectomy
Prophylaxis in high-risk patients
Propagating or free-floating thrombus
Occlusion of more than 50% of the pulmonary vascular bed and patient unable to
tolerate additional embolism
Patient with extension/propagation of iliofemoral thrombus despite anticoagulation

A number of clinical risk factors for mately 50% of deep vein thrombi were de-
DVT have been identified. Based on these tected on the first postoperative day and
risk factors, patients can be classified as 30% on the second, suggesting that a large
at risk for the development of calf vein percentage develop in the operating room.
or proximal vein thrombosis as well as So while early ambulation should be en-
clinical or fatal PE (Table 1). Prophylac- couraged in all patients, it should be re-
tic measures can then be instituted that lied on as the sole method for DVT pre-
are tailored to meet each patients risk vention in only those patients under age
(Table 2). The primary prophylactic meth- 40 with no additional risk factors who un-
ods have been clinically evaluated and are derwent procedures less than 30 minutes
directed at one or more elements of Vir- in duration.2
chows triad. They include nonpharma-
cologic (mechanical) and pharmacologic
modalities. Graduated compression stockings
Simple elastic stockings or support
Mechanical modalities and nursing hose, the forerunners of the graduated
considerations compression stocking, have been shown to
be entirely without value. This fact, com-
bined with common misconceptions about
Early ambulation
the various mechanical prophylactic op-
Early ambulation is accepted as increas- tions, has caused confusion about the pro-
ing venous flow and reducing venous sta- phylactic use of all stockings. The only
sis even though it has not been subjected kind of stocking that has been shown to
to rigorous clinical trials. It is important to be effective is the graduated compression
get patients up and moving as soon as pos- stocking, which achieves highest compres-
sible, however, many patients develop sion at the ankle, with gradually decreasing
thrombi during surgery and immediately pressure continuing up the leg.3941 Com-
postoperatively before activity and pro- pression pressure applied from the stan-
gressive ambulation can be instituted. dard hospital graduated compression stock-
One study39 demonstrated that approxi- ing is: ankle, 20 to 30 mm Hg; midcalf, 14 to
Article 3 5/21/01 11:14 PM Page 38

38 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

Table 1. Classification of level of risk

% Calf % Proximal
vein vein % Clinical % Fatal
thrombosis thrombosis PE PE

Low
Uncomplicated minor 2 0.4 0.2 0.002
surgery in patients 40 years
with no clinical risk factors
Moderate
Any surgery (major or minor) 1020 24 12 0.10.4
in patients 4060 years
with no additional risk
factors; major surgery in
patients 40 years with no
additional risk factors; minor
surgery in patients with
risk factors
High
Major surgery in 2040 48 24 0.41.0
patients 60 years without
additional risk factors;
major surgery in patients
4060 years with additional risk
factors; patients with myocardial
infarction and medical patients
with risk factors
Highest
Major surgery in patients 4080 1020 410 15
40 years plus prior venous
thromboembolism or malignant
disease or hyper-coagulable
state; patients with elective
major lower extremity
orthopaedic surgery, hip fracture,
stroke, multiple trauma, or spinal
cord injury

PE, pulmonary embolus.

Source: Adapted with permission from GP Clagett, FA Anderson, W Geerts, et al, Prevention of Venous
Thromboembolism, Chest, Vol. 114, pp. 531S560S, 1998.

21 mm Hg; and midthigh, 8 to 13 mm Hg. fully ambulatory. Despite the availability

Stockings prevent DVT by augmenting the of different lengths, knee-high stockings
velocity of venous return from the legs, are more effective in the prevention of
thereby reducing venous stasis.2,4042 DVT, less expensive, and easier to apply.
Typically stockings are applied before As Table 2 illustrates, stockings can be
surgery and are worn until the patient is used alone in low-risk patients or be com-
Article 3 5/21/01 11:14 PM Page 39

Deep Venous Thrombosis 39

Table 2. Patient risk category and regimens to prevent venous thromboembolism

Method Description Patient risk

Graduated compression Applied before surgery Low/moderate

stockings* and worn until fully
ambulatory
Intermittent pneumatic Begun immediately before Low/moderate
compression* surgery and continued until
fully ambulatory
Venous foot pump* Applied before surgery and High/orthopaedic
worn until fully ambulatory surgery
Low-dose unfractionated 5,000 units given subcutaneously Moderate/high
heparin (LDUH) every 812 hours, starting
12 hours before surgery
Low-molecular-weight Various doses depending on Moderate/high/highest
heparin (LMWH) preparation and class
Mini-dose warfarin 1 mg/day begun 1014 Highest
days before surgery; goal:
INR of 1.5 after surgery
Pre- and postoperative 12.5 mg/day 514 days Highest
two-step warfarin before surgery aiming for
2- to 3-second increase in
prothrombin time during
surgery; 2.55 mg/day aiming
for prothrombin time ratio of
1.31.5 (INR 2:3) in the post-
operative period
Moderate-dose warfarin 5 mg the day of or the day after Highest
surgery; adjust dose for
prothrombin time ratio 1.31.5
(INR 2:3) by day 5

INR, international normalized ratio.

*May be combined with LDUH or LMWH in highest risk patients.
Source: Adapted with permission from GP Clagett, FA Anderson, W Geerts, et al, Prevention of Venous
Thromboembolism, Chest, Vol. 114, pp. 531S560S, 1998.

bined with other modalities in moderate- decreased strength or manual dexterity. To

or high-risk patients.2 Stockings need to fit apply a graduated compression stocking, it
properly and be applied correctly. If too is helpful to first turn it inside out as far as
tight, they may exert a tourniquet effect, the heel. Then, placing thumbs inside the
thereby promoting venous stasis, the very foot part, slip the stocking on until the heel
problem trying to be prevented. A tight is properly aligned.42 The fabric then can be
stocking also can cause redness and pro- gathered up and eased over the ankle and
mote skin breakdown. If too loose, the up the leg. Some stockings are equipped
stocking will not provide adequate com- with devices that make application easier.
pression. Stockings should be removed at least once
Due to their design, compression stock- a day to inspect the legs and feet for redness
ings may be difficult to apply for those with and skin breakdown. Stockings are avail-
Article 3 5/21/01 11:14 PM Page 40

40 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

able in several ready-made sizes, but also nursing units. Proper positioning of the
can be custom-made. sleeves should be assessed, and the sleeves
should be removed at specified intervals
daily to inspect the skin for redness or
Intermittent (external) pneumatic
breakdown.
compression
Intermittent (external) pneumatic com-
Venous foot pump
pression (IPC) is a noninvasive method of
preventing DVT. Two inflatable sleeves Venous foot pumps were developed to
applied to the patients lower leg replicate mimic the natural effects of walking and
the pumping action of the musculovenous weight-bearing on the circulation in the feet
pump. Available devices provide single- and legs and provide an alternative to the
chamber (uniform) or sequential (segmen- traditional thigh or calf compression de-
tal) compression and consist of the sleeves vice.45 The foot device consists of inflation
that are connected via air tubes to a pump pads and rigid sole feet covers that wrap
(compression unit). With single-chamber around the arch of the foot and connect via
compression, a uniform pressure in alter- hoses to a compression unit or pump.
nating equal cycles is applied to the limb. When the foot pads inflate there is com-
Sequential compression provides a wave- pression, stretching, and flattening of the
like or milking action as the graded pres- entire plantar plexus located in the dorsum
sure changes sequentially cephalad along of the foot. The compression of the venous
the leg. The pattern of intermittent com- plantar plexus enhances venous blood
pression reduces venous pooling and in- flow, thereby decreasing the risk of DVT.
creases the velocity of venous flow, Foot pumps have been used as a primary
thereby decreasing stasis. IPC also in- method of prophylaxis in orthopaedic pro-
creases blood fibrinolytic activity as its cedures and may be combined with phar-
gentle squeeze stimulates the release of tis- macologic modalities as well.4648 The foot
sue plasminogen activator from the en- pads should be checked for proper place-
dothelial layer of the vein wall.2,8,39,41,43 IPC ment and proper inflation at predetermined
is well suited for patients who cannot tol- intervals. The skin also should be checked
erate anticoagulant therapy because of for irritation. The device is contraindicated
bleeding risk. These include neurosurgical in patients with conditions where an in-
patients and those undergoing urologic crease of fluid to the heart may be detri-
and prostate surgery. IPC also may be com- mental (ie, congestive heart failure) or in
bined with pharmacologic modalities in the setting of an acute DVT.
the very-high-risk patient (Table 2) and
also may show benefit when combined Pharmacologic modalities and nursing
with LMWH or low-dose UH (LDUH) in considerations
other patient groups.2 The devices should
Low-dose unfractionated heparin
not be used in individuals with evidence
of lower extremity ischemia related to pe- LDUH is usually given in a dose of
ripheral artery disease or those with an 5,000 units subcutaneously 1 to 2 hours
acute DVT. Sleeves should be applied cor- preoperatively, and then 5,000 units every
rectly, and their application should be 8 to 12 hours until the patient is dis-
checked periodically. One study44 de- charged.2,8 Dosing does not require anti-
scribed proper application of IPC devices coagulant monitoring due to its minimal
in only 78% of patients in an intensive effect on the APTT. Heparin dosed as dis-
care unit and in 48% of patients on routine cussed is effective in preventing not only
Article 3 5/21/01 11:14 PM Page 41

Deep Venous Thrombosis 41

calf vein thrombosis, but also proximal wound hematomas increase with LDUH as
vein thrombosis and major PE.2 It can be well as LMWH; this can be an important
used alone in moderate-risk patients or in problem resulting in wound infection, de-
combination with mechanical modalities hiscence, and infection of a prosthetic de-
for those at very high risk (Table 2). The vice placed at the time of surgery.49
risk of serious bleeding with LDUH pro-
phylaxis is less than 2%.32
Low-molecular-weight heparin
Contraindications for LDUH include
any previous reaction to heparin such Like LDUH, the LMWH agents are gen-
as thrombocytopenia or urticaria, major erally given subcutaneously before surgery
trauma, intracranial lesions, spinal lesions, and then once or twice daily until the pa-
or eye surgery. It is important to note that tient is discharged. Dosing regimens for

Nursing Measures To Prevent Deep Venous Thrombosis

Identify risk factors present in the patient that predispose him or her to deep venous throm-
bosis; reevaluate patient status frequently.
Implement ordered prophylactic regimen.
Nonpharmacologic (mechanical)
a. Graduated compression stockings
b. Intermittent (external) pneumatic compression
c. Venous foot pump
Pharmacologic
a. Subcutaneous low-dose unfractionated heparin
b. Subcutaneous low-molecular-weight heparin
c. Oral anticoagulants
Document patient tolerance to ordered prophylactic regimen(s).
Assess all extremities on a regular basis.
Pain/tenderness
Unilateral edema
Erythema
Warmth
Encourage early ambulation and the performance of active leg exercises every hour while
patient is awake.
Perform passive range of motion exercises every shift if patient is immobile.
Monitor for low-grade fever to detect thrombophlebitis.
Encourage fluid intake to avoid dehydration; maintain accurate intake and output.
Use stool softeners to avoid straining, which increases venous pressure.
Avoid use of knee gatch.
Patient education
What deep venous thrombosis is and why it develops
Risk factor awareness; highlight any risk factors patient possesses such as orthopaedic
surgery, older age, a long general surgery operation, malignancy
Signs and symptoms (if deep venous thrombosis occurred, review with the patient his or
her own signs/symptoms if present)
Methods to prevent deep venous thrombosis
a. Perform regular activity such as walking, cycling, and swimming to promote venous
return.
b. Avoid prolonged sitting/standing.
c. Elevate legs with prolonged sitting.
d. Avoid constrictive garments: garters, girdles, tight-fitting stockings.
Article 3 5/21/01 11:14 PM Page 42

42 JOURNAL OF CARDIOVASCULAR NURSING/JULY 2001

prophylaxis are specific for each LMWH ing total knee or hip replacement. The box
preparation and also vary with patient risk titled Nursing Measures To Prevent Deep
category and type of surgery or injury.2 Venous Thrombosis summarizes nursing
In all patients having spinal or epidural management measures.
catheters for regional analgesia, LMWH

should be used with caution.2
PE remains the most common preventa-
ble cause of death in hospitalized patients.
Oral anticoagulants
It is most often a complication of venous
Warfarin may be started the day of or thrombosis that originates in the deep
day after surgery at a dose of 5 mg. The veins of the legs. Patients present with a
dose is adjusted thereafter, aiming for an variety of risk factors that predispose them
INR of 2.0 to 3.0 by day 5.2,49 This type of to DVT and subsequent PE. The presence
dosing is referred to as adjusted-dose peri- of one or more of these risk factors enables
operative warfarin. Dosing according to appropriate prophylactic regimens to be
this method may not prevent the formation instituted.
of small venous thrombi that form soon The nurse plays a key role in preventing
after surgery. However, it is effective for DVT by educating the patient regarding his
inhibiting the extension of these thrombi or her prophylactic regimen as well as
and may prevent clinically significant PE. monitoring patient adherence and toler-
Warfarin also may be dosed via a pre- and ance to that regimen. Being aware of pa-
postoperative two-step method or via a tients at risk and knowledgeable regarding
mini-dose method. Parameters for the INR the signs and symptoms of DVT will allow
are followed with either dosing method. for prompt identification, management,
Warfarin is most commonly reserved for and education of the patient should DVT
high-risk patients such as those undergo- occur.

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