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DEEP VENOUS
THROMBOSIS
DR.SHERAZ AHMED
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Definition
Deep vein thrombosis is theformation of a blood clot in one ofthe deep veins of the body, usually
in the leg
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ETIOLOGY
DVT ususally originates in the lower extremityvenous level ,starting at the calf vein level andprogressing proximally to involve popliteal
,femoral ,or iliac system.
80 -90 % pulmonary emboli originates fromhere .
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Virchow tried
More than 100 years ago, Virchow described atriad of factors of
venous stasis,
endothelial damage, and
hypercoagulable state
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Venous stasis
prolonged bed rest (4 days or more)
A cast on the leg
Limb paralysis from stroke or spinal cord injury extended travel in a vehicle
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Hypercoagulability
Surgery and trauma responsible for up to 40% of allthromboembolic disease
Malignancy
Increased estrogen (due to a fall in protein S)Increased estrogen occurs during :
- All stages of pregnancy
- the first three months postpartum- After elective abortion.
- During treatment with oral contraceptive pills
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Inherited disorders of coagulation
deficiencies of protein S,
protein C, and
antithrombin III.
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Acquired disorders of coagulation
nephrotic syndrome results in urinary loss ofantithrombin III, this diagnosis should beconsidered in children presenting with
thromboembolic disease
Antiphospholipid antibodies acceleratecoagulation and include the lupus anticoagulant
and anticardiolipin antibodies.
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Inflammatory processes, such as systemic lupus erythematosus (SLE),
sickle cell disease, and
inflammatory bowel disease (IBD),also predispose to thrombosis, presumably due to
hypercoagulability
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Endothelial Injury
Trauma,
surgery, and
invasive procedure may disrupt venous integrity
Iatrogenic causes of venous thrombosis areincreasing due to the widespread use of centralvenous catheters, particularly subclavian and
internal jugular lines. These lines are animportant cause of upper extremity DVT,particularly in children.
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Clinical Pathophysiology
The nidus for a clot is often an intimal defect
When a clot forms on an intimal defect, thecoagulation cascade promotes clot growthproximally. Thrombus can extend from thesuperficial veins into the deep system fromwhich it can embolize to the lungs.
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Opposing the coagulation cascade is theendogenous fibrinolytic system. After the clotorganizes or dissolves, most veins will recanalize
in several weeks. Residual clots retract asfibroblasts and capillary development lead tointimal thickening.
Venous hypertension and residual clot maydestroy valves, leading to the postphlebiticsyndrome, which develops within 5-10 years
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Edema, sclerosis, and ulceration characterize thissyndrome, which develops in 40-80% of patients withDVT.
patients also can suffer exacerbations of swelling andpain, probably as a result of venous dilatation andhypertension
Pulmonary embolism (PE) is a serious complication
of DVT. Many episodes of pulmonary embolism gounrecognized, and at least 40% of patients with DVThave clinically silent PE on VQ scanning
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Presentation and Physical
Examination
Calf pain or tenderness, or both
Swelling with pitting oedema
Swelling below knee in distal deep veinthrombosis and up to groin in proximal deepvein thrombosis
Increased skin temperature
Superficial venous dilatation Cyanosis can occur with severe obstruction
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Palpate distal pulses and evaluate capillary refillto assess limb perfusion.
Move and palpate all joints to detect acute
arthritis or other joint pathology. Neurologic evaluation may detect nerve root
irritation; sensory, motor, and reflex deficits
should be noted Homans' sign: pain in the posterior calf or knee
with forced dorsiflexion of the foot
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Search for stigmata of PE such as tachycardia(common), tachypnea or chest findings (rare),and
exam for signs suggestive of underlyingpredisposing factors.
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Wells Clinical Prediction Guide
The Wells clinical prediction guide incorporates riskfactors, clinical signs, and the presence or absence ofalternative diagnoses
.Wells Clinical Prediction Guide for DVTClinicalParameterScore
Active cancer (treatment ongoing, or within 6 monthsor palliative)1
Paralysis or recent plaster immobilization 1 Recently bedridden for >3 days or major surgery
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Localized tenderness along the distribution of the deepvenous system1
Entire leg swelling1
Calf swelling >3 cm compared to the asymptomatic leg1
Pitting edema (greater in the symptomatic leg)1 Collateral superficial veins (nonvaricose)1
Alternative diagnosis (as likely or > that of DVT)
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Total of Above Score
High probability: Score 3
Moderate probability: Score = 1 or 2Low probability: Score 0
Adapted from Anand SS, et al.JAMA. 1998;
279 [14];1094
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Diagnostic Studies
Clinical examination alone is able to confirm only 20-30% of cases of DVT
Blood Tests
the D-dimer
INR.
Current D-dimer assays have predictive value for DVT,
and the INR is useful for guiding the management of patients
with known DVT who are on warfarin (Coumadin)
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D-dimer
D-dimer is a specific degradation product ofcross-linked fibrin. Because concurrentproduction and breakdown of clot characterize
thrombosis, patients with thromboembolicdisease have elevated levels of D-dimer
three major approaches for measuring D-dimer
- ELISA- latex agglutination
- blood agglutination test (SimpliRED
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False-positive D-dimers occur in patients with
- recent (within 10 days) surgery or trauma
- recent myocardial infarction or stroke
- acute infection
- disseminated intravascular coagulation
- pregnancy or recent delivery
- active collagen vascular disease, or metastaticcancer
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Imaging Studies
Invasive
venography,
radiolabeled fibrinogen. noninvasive
ultrasound
plethysmography MRI techniques
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venography
gold standard modality for the diagnosis ofDVT
Advantages
Venography is also useful if the patient has ahigh clinical probability of thrombosis and anegative ultrasound,
it is also valuable in symptomatic patients with ahistory of prior thrombosis in whom theultrasound is non-diagnostic.
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side effects
phlebitis
anaphylaxis
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Nuclear Medicine Studies
Because the radioactive isotope incorporatesinto a growing thrombus, this test candistinguish new clot froman old clot
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Plethysmography
Plethysmography measures change in lowerextremity volume in response to certain stimuli.
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Ultrasonography
color-flow Duplex scanning is the imaging testof choice for patients with suspected DVT
- Inexpensive
- noninvasive
- widely available
Ultrasound can also distinguish other causes ofleg swelling, such as tumor, popliteal cyst,abscess, aneurysm, or hematoma.
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clinical limitations
expensive
reader dependent
Duplex scans are less likely to detect non-occluding thrombi.
During the second half of pregnancy, ultrasoundbecomes less specific, because the gravid uteruscompresses the inferior vena cava, therebychanging Doppler flow in the lower extremities
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Magnetic Resonance Imaging
It detects leg, pelvis, and pulmonary thrombiand is 97% sensitive and 95% specific for DVT.
It distinguishes a mature from an immature clot.
MRI is safe in all stages of pregnancy.
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DIFFERENTIAL DIAGNOSIS
o CellulitisThrombophlebitis
o ArthritisAsymmetric peripheral edema secondary to CHF, liverdisease, renal failure, or nephrotic syndromelymphangitis
Extrinsic compression of iliac vein secondary to tumor,hematoma, or abscessHematomaLymphedema
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Muscle or soft tissue injuryNeurogenic painPostphlebitic syndrome
Prolonged immobilization or limb paralysisRuptured Baker cystStress fractures or other bony lesions
Superficial thrombophlebitisVaricose veins
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Management
Using the pretest probability score calculatedfrom the Wells Clinical Prediction rule, patientsare stratified into 3 risk groupshigh, moderate,
or low.The results from duplex ultrasound are
incorporated as follows:
If the patient is high or moderate risk and theduplex ultrasound study is positive, treat forDVT.
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If the duplex study is negative and the patient islow risk, DVT has been ruled out.
When discordance exists between the pretestprobability and the duplex study result, furtherevaluation is required.
If the patient is high risk but the ultrasoundstudy was negative, the patient still has asignificant probability of DVT
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a venogram to rule out a calf vein DVT
surveillance with repeat clinical evaluation andultrasound in 1 week.
results of a D-dimer assay to guide management
If the patient is low risk but the ultrasoundstudy is positive, some authors recommend asecond confirmatory study such as a venogrambefore treating for DVT
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EMERGENCY DEPARTMANT
CARE
The primary objectives of the treatment of DVTare to :
- prevent pulmonary embolism
- reduce morbidity
- prevent or minimize the risk of developing thepostphlebitic syndrome.
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Anticoagulation
Thrombolytic therapy for DVT
Surgery for DVT Filters for DVT
Compression stockings
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Anticoagulation
Heparin prevents extension of the thrombus
Heparin's anticoagulant effect is related directlyto its activation of antithrombin III.Antithrombin III, the body's primaryanticoagulant, inactivates thrombin and inhibitsthe activity of activated factor X in the
coagulation process.
Heparin is a heterogeneous mixture of
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Heparin is a heterogeneous mixture of
polysaccharide fragments with varying molecular
weights but with similar biological activity. Thelarger fragments primarily interact with
antithrombin III to inhibit thrombin.
The low molecular weight fragments exert theiranticoagulant effect by inhibiting the activity ofactivated factor X. The hemorrhagic
complications attributed to heparin are thoughtto arise from the larger higher molecular weightfragments.
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The optimal regimen for the treatment of DVTis anticoagulation with heparin or an LMWHfollowed by full anticoagulation with oral
warfarin for 3-6 months
Warfarin therapy is overlapped with heparin for4-5 days until the INR is therapeutically elevated
to between 2-3.
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After an initial bolus of 80 U/kg, a constantmaintenance infusion of 18 U/kg is initiated.The aPTT is checked 6 hours after the bolus and
adjusted accordingly. .
The aPTT is repeated every 6 hours until 2successive aPTTs are therapeutic. Thereafter,
the aPTT is monitored every 24 hours as well asthe hematocrit and platelet count.
Advantages of Low-Molecular-
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Advantages of Low Molecular
Weight Heparin Over
Standard Unfractionated Heparin
Superior bioavailability
Superior or equivalent safety and efficacy Subcutaneous once- or twice-daily dosing
No laboratory monitoring*
Less phlebotomy (no monitoring/no intravenous line) Less thrombocytopenia
Earlier/facilitated
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At the present time, 3 LMWH preparations:
Enoxaparin
Dalteparin
Ardeparin
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warfarin
Interferes with hepatic synthesis of vitamin K-dependent coagulation factors
Dose must be individualized and adjusted to
maintain INR between 2-3
2-10 mg/d PO
caution in active tuberculosis or diabetes;patients with protein C or S deficiency are at riskof developing skin necrosis
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Thrombolytic therapy for DVT
Advantages include :
- prompt resolution of symptoms
- prevention of pulmonary embolism
- restoration of normal venous circulation
- preservation of venous valvular function
- prevention of postphlebitic syndrome
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Thrombolytic therapy does not prevent :
Clot propagation
Re-thrombosis
Subsequent embolization
Heparin therapy and oral anticoagulant therapy
always must follow a course of thrombolysis.
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Thrombolytic therapy is also not effective once thethrombus is adherent and begins to organize
The hemorrhagic complications of thrombolytictherapy are formidable (about 3 times higher),including the small but potentially fatal risk ofintracerebral hemorrhage.
The uncertainty regarding thrombolytic therapy likelywill continue
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Surgery for DVT
indications
when anticoagulant therapy is ineffective
unsafe
contraindicated.
The major surgical procedures for DVT are clot
removal and partial interruption of the inferiorvena cava to prevent pulmonary embolism.
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These pulmonary emboli removed at autopsy look likecasts of the deep veins of the leg where they originated.
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This patient underwent a thrombectomy. The thrombus has been
laid over the approximate location in the leg veins where it
developed.
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Filters for DVT
Indications for insertion of an inferior vena
cava filter
- Pulmonary embolism with contraindication to
anticoagulation
- Recurrent pulmonary embolism despite adequateanticoagulation
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Controversial indications:
Deep vein thrombosis with contraindication toanticoagulation
Deep vein thrombosis in patients with pre-existing pulmonary hypertension
Free floating thrombus in proximal vein
Failure of existing filter device Post pulmonary embolectomy
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Inferior vena cava filters reduce the rate ofpulmonary embolism but have no effect on theother complications of deep vein thrombosis.
Thrombolysis should be considered in patientswith major proximal vein thrombosis andthreatened venous infarction
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C i t ki ( ti l
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Compression stockings (routinely
recommended
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Further Inpatient Care
Most patients with confirmed proximal vein DVT maybe treated safely on an outpatient basis. Exclusioncriteria for outpatient management are as follows:
- Suspected or proven concomitant pulmonary embolism- Significant cardiovascular or pulmonary comorbidity
- Morbid obesity
- Renal failure- Unavailable or unable to arrange close follow-up care
Patients are treated with a low molecular weight
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gheparin and instructed to initiate therapy with warfarin5 mg PO the next day. Low molecular weight heparin
and warfarin are overlapped for about 5 days until theinternational normalized ratio (INR) is therapeutic.
If inpatient treatment is necessary, low molecular
weight heparin is effective and obviates the need forIV infusions or serial monitoring of the PTT.
With the introduction of low molecular weight
heparin, selected patients qualify for outpatienttreatment only if adequate home care and closemedical follow-up care can be arranged.
Platelets also should be monitored and heparin
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pdiscontinued if platelets fall below 75,000.
While on warfarin, the prothrombin time (PT) must
be monitored daily until target achieved, then weeklyfor several weeks. When the patient is stable, monitormonthly.
Significant bleeding (ie, hematemesis, hematuria,gastrointestinal hemorrhage) should be investigatedthoroughly since anticoagulant therapy may unmask a
preexisting disease (eg, cancer, peptic ulcer disease,arteriovenous malformation).
Duration of anticoagulation in patients
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g pwith deep vein thrombosis
Transient cause and no other risk factors: 3 months
Idiopathic: 3-6 months
Ongoing risk for example, malignancy: 6 -12 months
Recurrent pulmonary embolism or deep veinthrombosis: 6-12 months
Patients with high risk of recurrent thrombosis
exceeding risk of anticoagulation: indefinite duration(subject to review)
Further Outpatient Care:
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Further Outpatient Care:
Patients with suspected or diagnosed isolatedcalf vein DVT may be discharged safely on anonsteroidal anti-inflammatory drug (NSAID)
or aspirin with close follow-up care and repeatdiagnostic studies in 3-7 days to detect proximalextension.
At certain centers, patients with isolated calf
vein DVT are admitted for full anticoagulanttherapy.
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Patients with suspected DVT but negativenoninvasive studies need to be reassessed bytheir primary care provider within 3-7 days.
Patients with ongoing risk factors may need tobe restudied at that time to detect proximalextension because of the limited accuracy of
noninvasive tests for calf vein DVT.
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Complications
Acute pulmonary embolism
Hemorrhagic complications
Chronic venous insufficiency
Prognosis:
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Prognosis:
All patients with proximal vein DVT are atlong-term risk of developing chronic venousinsufficiency.
About 20% of untreated proximal (above thecalf) DVTs progress to pulmonary emboli, and10-20% of these are fatal. With aggressiveanticoagulant therapy, the mortality is decreased5- to 10-fold.
DVT confined to the calf virtually never causesclinically significant emboli and thus does not
require anticoagulation
Patient Education:
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Patient Education:
Advise women taking estrogen of the risks andcommon symptoms of thromboembolic disease.
Discourage prolonged immobility, particularlyon plane rides and long car trips
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PROPHYLAXIS
Ideidentify any patiant who is at risk. Prevent dehydration.
During operation avoid prolonged calf compression.
Passive leg exercises should be encourged whilst patienton bed.
Foot of bed should be elevated to increase venousreturn.
Early mobilization should be rule for all surgical patients.