Management of Deep venous thrombosis.
nUsing
the pretest probability score calculated from the Wells Clinical
Prediction rule, patients are stratified into 3 risk groups—high,
moderate, or low.
nThe
results from duplex ultrasound are incorporated as follows:
nIf
the patient is high or moderate risk and the duplex ultrasound study is
positive, treat for DVT.
nIf
the duplex study is negative and the patient is low risk, DVT has been
ruled out.
•When
discordance exists between the pretest probability and the duplex study
result, further evaluation is required.
nIf
the patient is high risk but the ultrasound study was negative, the
patient still has a significant probability of DVT
na
venogram to rule out a calf vein DVT
nsurveillance
with repeat clinical evaluation and ultrasound in 1 week.
nresults
of a D-dimer assay to guide management
n
If the patient is low risk but the ultrasound study is positive, some
authors recommend a second confirmatory study such as a venogram before
treating for DVT
EMERGENCY DEPARTMANT CARE
nThe
primary objectives of the treatment of DVT are to
nprevent
pulmonary embolism,
nreduce
morbidity, and
n
prevent or minimize the risk of developing the postphlebitic syndrome.
nAnticoagulation
nThrombolytic
therapy for DVT
nSurgery
for DVT
nFilters
for DVT
nCompression
stockings
Anticoagulation
nHeparin
prevents extension of the thrombus
nHeparin's
anticoagulant effect is related directly to its activation of antithrombin
III. Antithrombin III, the body's primary anticoagulant, inactivates
thrombin and inhibits the activity of activated factor X in the
coagulation process.
nHeparin
is a heterogeneous mixture of polysaccharide fragments with varying
molecular weights but with similar biological activity. The larger
fragments primarily interact with antithrombin III to inhibit thrombin.
n
The low molecular weight fragments exert their anticoagulant effect by
inhibiting the activity of activated factor X. The hemorrhagic
complications attributed to heparin are thought to arise from the larger
higher molecular weight fragments.
nThe
optimal regimen for the treatment of DVT is anticoagulation with heparin
or an LMWH followed by full anticoagulation with oral warfarin for 3-6
months
nWarfarin
therapy is overlapped with heparin for 4-5 days until the INR is
therapeutically elevated to between 2-3.
nAfter
an initial bolus of 80 U/kg, a constant maintenance infusion of 18 U/kg is
initiated. The aPTT is checked 6 hours after the bolus and adjusted
accordingly. .
nThe
aPTT is repeated every 6 hours until 2 successive aPTTs are therapeutic.
Thereafter, the aPTT is monitored every 24 hours as well as the hematocrit
and platelet count.
Advantages of Low-Molecular-Weight Heparin Over
Standard Unfractionated Heparin
nSuperior
bioavailability
nSuperior
or equivalent safety and efficacy
nSubcutaneous
once- or twice-daily dosing
nNo
laboratory monitoring*
nLess
phlebotomy (no monitoring/no intravenous line)
nLess
thrombocytopenia
nEarlier/facilitated
At
the present time, 3 LMWH preparations,
nEnoxaparin,
nDalteparin,
and
nArdeparin
warfarin
n
Interferes with hepatic synthesis of vitamin K-dependent coagulation
factors
nDose
must be individualized and adjusted to maintain INR between 2-3
n2-10
mg/d PO
ncaution
in active tuberculosis or diabetes; patients with protein C or S
deficiency are at risk of developing skin necrosis
Thrombolytic therapy for DVT
nAdvantages
include
nprompt
resolution of symptoms,
nprevention
of pulmonary embolism,
nrestoration
of normal venous circulation,
npreservation
of venous valvular function,
nand
prevention of postphlebitic syndrome.
Thrombolytic therapy does not prevent
nclot
propagation,
n
rethrombosis, or
n
subsequent embolization.
n
Heparin therapy and oral anticoagulant therapy always must follow a course
of thrombolysis.
nThrombolytic
therapy is also not effective once the thrombus is adherent and begins to
organize
nThe
hemorrhagic complications of thrombolytic therapy are formidable (about 3
times higher), including the small but potentially fatal risk of
intracerebral hemorrhage.
The
uncertainty regarding thrombolytic therapy likely will continue
Surgery for DVT
n
indications
n
when anticoagulant therapy is ineffective
n
unsafe,
n
contraindicated.
nThe
major surgical procedures for DVT are clot removal and partial
interruption of the inferior vena cava to prevent pulmonary embolism.
Filters for DVT
nIndications
for insertion of an inferior vena cava filter
nPulmonary
embolism with contraindication to anticoagulation
nRecurrent
pulmonary embolism despite adequate anticoagulation
nControversial
indications:
nDeep
vein thrombosis with contraindication to anticoagulation
nDeep
vein thrombosis in patients with pre-existing pulmonary hypertension
nFree
floating thrombus in proximal vein
nFailure
of existing filter device
nPost
pulmonary embolectomy
nInferior
vena cava filters reduce the rate of pulmonary embolism but have no effect
on the other complications of deep vein thrombosis. Thrombolysis should be
considered in patients with major proximal vein thrombosis and threatened
venous infarction
Compression stockings (routinely recommended
Further Inpatient Care
nMost
patients with confirmed proximal vein DVT may be treated safely on an
outpatient basis. Exclusion criteria for outpatient management are as
follows:
nSuspected
or proven concomitant pulmonary embolism
nSignificant
cardiovascular or pulmonary comorbidity
nMorbid
obesity
nRenal
failure
nUnavailable
or unable to arrange close follow-up care
nPatients
are treated with a low molecular weight heparin and instructed to initiate
therapy with warfarin 5 mg PO the next day. Low molecular weight heparin
and warfarin are overlapped for about 5 days until the international
normalized ratio (INR) is therapeutic.
nIf
inpatient treatment is necessary, low molecular weight heparin is
effective and obviates the need for IV infusions or serial monitoring of
the PTT.
nWith
the introduction of low molecular weight heparin, selected patients
qualify for outpatient treatment only if adequate home care and close
medical follow-up care can be arranged.
nPlatelets
also should be monitored and heparin discontinued if platelets fall below
75,000.
nWhile
on warfarin, the prothrombin time (PT) must be monitored daily until
target achieved, then weekly for several weeks. When the patient is
stable, monitor monthly.
nSignificant
bleeding (ie, hematemesis, hematuria, gastrointestinal hemorrhage) should
be investigated thoroughly since anticoagulant therapy may unmask a
preexisting disease (eg, cancer, peptic ulcer disease, arteriovenous
malformation).
Duration of anticoagulation in patients with deep
vein thrombosis
nTransient
cause and no other risk factors: 3 months
nIdiopathic:
3-6 months
nOngoing
risk for example, malignancy: 6 -12 months
nRecurrent
pulmonary embolism or deep vein thrombosis: 6-12 months
nPatients
with high risk of recurrent thrombosis exceeding risk of anticoagulation:
indefinite duration (subject to review)
Further Outpatient Care:
nPatients
with suspected or diagnosed isolated calf vein DVT may be discharged
safely on a nonsteroidal anti-inflammatory drug (NSAID) or aspirin with
close follow-up care and repeat diagnostic studies in 3-7 days to detect
proximal extension.
nAt
certain centers, patients with isolated calf vein DVT are admitted for
full anticoagulant therapy.
nPatients
with suspected DVT but negative noninvasive studies need to be reassessed
by their primary care provider within 3-7 days.
nPatients
with ongoing risk factors may need to be restudied at that time to detect
proximal extension because of the limited accuracy of noninvasive tests
for calf vein DVT.
Complications
nAcute
pulmonary embolism
n
Hemorrhagic complications
nChronic
venous insufficiency
Prognosis:
nAll
patients with proximal vein DVT are at long-term risk of developing
chronic venous insufficiency.
nAbout
20% of untreated proximal (above the calf) DVTs progress to pulmonary
emboli, and 10-20% of these are fatal. With aggressive anticoagulant
therapy, the mortality is decreased 5- to 10-fold.
nDVT
confined to the calf virtually never causes clinically significant emboli
and thus does not require anticoagulation
Patient Education:
nAdvise
women taking estrogen of the risks and common symptoms of thromboembolic
disease.
nDiscourage
prolonged immobility, particularly on plane rides and long car trips
Deep vein thrombosis in pregnancy
nNormal
pregnancy is a hypercoagulable state
n
Deep vein thrombosis occurs antepartum in 0.6/1000 women aged < 35 years
and 1.2/1000 women >35 and postpartum in 0.3/1000 and 0.7/1000
respectively
n
Age, operative delivery, personal or family history, and
thrombophilia are particular risks
n
Heparin does not cross the placenta and is not secreted in breast
milk
n
nProlonged
heparin therapy raises concerns about osteoporosis, heparin-induced
thrombocytopenia, and allergy
n
The combined contraceptive pill increases the relative risk of deep
vein thrombosis by 3-4 times
n
Hormone replacement therapy also increases the relative risk of
deep vein thrombosis by 3-4 times but is associated with a 10 fold
higher absolute risk because of the older age group
nAnticoagulation
should be restarted in the puerperium and continued for six weeks to three
months.
nWarfarin
is usually contraindicated during pregnancy because it is teratogenic and
increases risk of maternal and fetal haemorrhage perinatally. It can be
restarted 48 hours after delivery.
Prophylaxis
|