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Apr 14, 2018

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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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    http://bmj.com/content/vol320/issue7247/images/large/vasabc12.f3.jpeg
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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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    http://bmj.com/content/vol320/issue7247/images/large/vasabc12.f2.jpeg
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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

    http://www.emedicine.com/EMERG/topic88.htmhttp://www.emedicine.com/EMERG/topic88.htm
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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

    http://bmj.com/content/vol320/issue7247/images/large/vasabc12.f6y.jpeg
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    C i t ki ( ti l

    http://bmj.com/content/vol320/issue7247/images/large/vasabc12.f6y.jpeg
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    Compression stockings (routinely

    recommended

    http://bmj.com/content/vol320/issue7247/images/large/vasabc12.f4.jpeg
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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.