Deep Vein Thrombosis

Wikis > Peripheral Vascular Disease > 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)

Pathology:
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

Hypercoagulability:
• 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

Treatment:
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

http://reference.medscape.com/calculator/dvt-probability-wells-score

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