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Does This Patient Have Deep Vein Thrombosis?

Discussion in 'General Issues and Discussion Forum' started by Admin2, Jan 10, 2006.

  1. Admin2

    Admin2 Administrator Staff Member

    Members do not see these Ads. Sign Up.
    This is what evidence based practice is all about:

    Does This Patient Have Deep Vein Thrombosis?

    JAMA. 2006;295:199-207.

  2. Craig Payne

    Craig Payne Moderator

    These are from some lecture notes I have:

    Deep Vein Thrombosis
    Complete or partial occlusion of vein by thrombosis. Common cause of in-hospital mortality.
    80% of time in calf muscles – usually around valve cusps or in soleal plexus --> 20% move proximally --> can result in fatal pulmonary embolism.

    Risk Factors:
    • Virchow’s triad (venous stasis, vessel wall injury, hypercoaguable state) --> primary mechanism for DVT
    • age (increasing age increases risk, but mechanism is not known – may be related to mobility, the decreased fibrinolytic response)
    • immobilisation > 3 days (venous stasis)
    • pregnancy and postpartum period
    • major surgery (trauma to blood vessels and period of immobilisation after)
    • oral contraceptives
    • obesity (impaired fibrinolytic activity and immobility)
    • long plane or car trips
    • medical conditions – cancer; previous DVT; CVA; CHF; nephrotic syndrome; ulcerative colitis
    • fractures and other trauma (especially if immobilised)

    Thrombus is composed or red blood cells, platelets and leukocytes bound together with fibrin.
    Pathogenesis is due to vessel wall damage, venous stasis and increased activation of clotting factors (hypercoagulability) – Virchow’s triad.

    Venous stasis/alteration in blood flow:
    • occurs during immobility (eg loss of calf muscle venous pump; during surgery)
    • also affected by arrhythmias, myocardial infarction, congestive heart failure, obesity, varicose veins
    • arterial turbulence contributes

    Injury to vessel wall:
    • endothelial injury has a strong influence on the formation of a thrombus
    • if vessel wall is damaged --> platelets adhere to exposed subendothelium collagen --> platelet aggregation --> activation of coagulation pathway
    • eg may occur during surgery, trauma, burns, IV lines

    • a number of acquired and hereditary hypercaogulable states have been identified
    • eg postpartum, postoperative, severe trauma, cancer, oral contraceptives, obesity, nephrotic syndrome, congestive heart failure

    Clinical Features:
    Related to degree of venous obstruction – most do not produce significant venous obstruction and collaterals may rapidly develop. Many are asymptomatic but if symptomatic include: nonspecific painful swollen leg with dilated superficial veins; pulses usually present; unilateral oedema; nontender oedema of collateral superficial veins; Homan’s sign – dorsiflexion of foot causes pain in calf – only present in 1/3rd; venous distension; prominence of subcutaneous veins; may have low grade fever; may develop reddish purple hue to lower limb (phlegmasia cerulea dolens); 10% --> signs of pulmonary embolism.
    Radiography – contrast venography; duplex ultrasound; MRI; nuclear medicine; 125 I-fribinogen scan
    Differential diagnosis – muscle aches; muscle/tendon strain; fibromyalgia; cellulitis; thrombophlebitis; achilles tendonitis; calf strain; intermittent claudication; arthritis; haematoma; referred pain; varicose veins; ruptured Bakers cyst; lymphedoema; varicose veins.

    Signs of pulmonary embolism – tachypnoea, cyanosis, hypoxia, pleural effusion, wheeze

    Emergency treatment – aim is to prevent pulmonary embolism --> anticoagulation (heparin); thrombolytic therapy (stretokinase); compression stockings; surgery (thromboectomy) when anticoagulant is ineffective or can’t be used.

    Prophylactic measures – increased mobility, aspirin, thrombolytic therapy, heparin, warfarin, compression stockings, foot pump systems

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