DEEP VEIN THROMBOSIS.

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Presentation transcript:

DEEP VEIN THROMBOSIS

DEFINITION : VENOUS THROMBOEMBOLISM Composite term for DVT &PE The presence of thrombus with in deep veins is termed as deep vein thrombosis It is a life threatening condition that may lead to sudden death in the short term or long term. morbidity due to the development of post thrombotic limb and venous ulceration

CLASSIFICATION : PROXIMAL DVT :thrombus formed in veins above the knee joint (femoral, iliac, popliteal) DISTAL DVT : those formed below the knee joint (calf veins)

FACT Venous thrombosis are difficult to recognize clinically. The documented cases probably represent only tip of the Ice Berg. SILENT KILLER

EPIDEMIOLOGY M:F 1.2:1 Age more than 40 years. VT occur in more than 50% of patient’s having orthopaedic surgical procedures. 10 to 20% of patient with idiopathic DVT have or develop cancer. 1/3rd to 1/4th patient having proximal DVT may develop PE. About 10% of hospital deaths attributable to PE (from DVT)

Calf vein - most common Ilio femoral - most symtomatic IVC - most lethal

AIR TRAVEL AND DVT Up to 1 out of 10 air line passengers develop small asymptomatic blood clots. Due to hypoxia and reduced cabin pressure. VT occurs in patients regularly without any damaged to the blood vessels.

VTE Risk Patient Factors Age Previous VTE Malignancy Advancing age Obesity Prolonged immobility Trauma Surgery Pregnancy/ postpartum Indwelling central venous catheter Deficiency of anti-thrombin III Protein C or S Contd...

Paralysis of lower limbs Polycythaemia Medical illness stroke MI CHF pneumonia COPD infections nephrotic syndrome inflammatory bowel disease Oral contraceptives Varicose veins

Pregnancy and postpartum period. Immobilization longer than 3 days Major surgery in previous 4weeks Long air or car trips >4hrs in previous 4 weeks

PATHO-PHYSIOLOGY VIRCHOW`S TRIAD Predisposing Factors : Stasis Vascular damage Hyper coagulability Imbalance between thrombogenesis & thrombolytic agents

FATE OF THROMBUS: Propagation Embolization Dissolution Organization & recanalization ORGIN DVT usually originates from veins of calf around the valve cusps or with in soleal plexus A minority of cases occurs directly in ilio femoral veins

In practical terms the development of VT is best understood as activation of coagulation in areas of reduced blood flow. Majority of calf vein thrombus dissolve completely. Only 20% progress proximally. Propagation occurs before embolization.

The process of adherence and organization of venous thrombus does not begin until 5 to 10 days after thrombus formation. This non adherent thrombus may propagate or embolise. Propagation or organization of venous thrombus  destruction of valves & varying degree of venous outflow obstruction  chronic venous insufficiency.

VTE RESULTS IN Fatal PE Non-fatal PE Post-thrombotic syndrome

POST-PHLEBETIC SYNDROME Consequence of recanalization of major venous thrombus Due to incompetence of valves Long term morbidity Causes chronic edema &venous ulcers

CLINICAL FEATURES Swelling/edema most specific sign unilateral Leg pain (50%) non specific Redness/erythema over the thrombus Tenderness(75%) calf or along the involved veins does not correlate size, site, extent Low grade pyrexia Signs and symptoms of PE

HOMAN`S SIGN Pain or discomfort in leg on forceful dorsiflexion of foot with knee straight Present only in 10% of confirmed DVT Highly non-specific Present in 50% of cases with out DVT Misleading sign No longer used

DIFFERENTIAL DIAGNOSIS In approximately 70% of patients with clinically suspected DVT, alternate diagnoses are ultimately found as follows: Arthritis Cellulitis, lymphangitis Hematoma Lymphedema Muscle or soft tissue injury Neurogenic pain Postphlebitic syndrome Prolonged immobilization or limb paralysis Ruptured Baker cyst Stress fractures or other bony lesions Superficial thrombophlebitis Varicose veins

INVESTIGATION D- dimer level : This cross-linked fibrin degradation product is an indication that thrombosis is occurring , and that the blood clot is being dissolved by plasmin. D-dimer is measured by latex agglutination or by an enzyme-linked immunosorbent assay (ELISA) test that is considered positive if the level is greater than 500 ng/mL Other blood tests Complete blood count (CBC) Primary coagulation studies (PT ,PTT ,Fibrinogen ) Liver Enzymes Renal function and electrolytes .

Protein S, protein C, anticromin III,, antiphospholipid antibodies and homocysteine levels can be measured.  investigations for these abnormalities are primarily indicated when DVT is diagnosed in patients younger that 35 years or when venous thrombosis is detected in unusual sites.

INVESTIGATION CONTRAST VENOGRAPHY DUPLEX ULTRASONOGRAPHY IMPEDANCE PLETHYSMOGRAPHY MRI CONTRAST C.T.

TREATMENT MEDICAL TREATMENT Bed rest Affected limb is elevated above the level of heart. Anticoagulant prevent thrombus propagation and allow the endogenous lytic system to operate Pain relief.

UNFRACTIONED HEPARIN Initial bolus 7500 to 10000 IU followed by continuous in infusion to 1000 to 1500 IU/hr. Infusion rate adjusted so that aPTT is approx twice the control value Every 6 hrs aPTT monitered till therapeutic range is reached Duration :5 days Discontinue when platelet count <75,000

LOW MOLECULAR WT HEPARIN Effective and better than conventional heparin. Different preparations available. Administered SC in fixed doses once or twice daily. Duration -7 to 14 days Anticoagulant effect by inhibiting the activated factor X. Hemorrhagic complications doesn’t occur

WARFARIN To be taken along with heparin for initial 4 to5 days. Dose adj to maintain prothrombin time at INR 2.0 to3.0 Continued for 3 to6 months for pts with acute idiopathic DVT For recurrent DVT/PE low intensity warfarin continued indefinitely maintaining INR 1.5 to2.0

THROMBOLYTICS Early administration Prompt resolution of symptoms Accelerate clot lysis Preserve venous valves Decrease the potential for developing post- phlebitic syndrome

Does not prevent clot propagation or rethrombosis. Heparin and oral anti coagulant therapy must follow a course of thrombolysis. Haemorraghic complications reduced by regionally administering with flouroscopic control. Streptokinase,urokinase.

SURGICAL TREATMENT Indicated when anticoagulant therapy is ineffective, unsafe or contraindicated. Major surgical procedures : clot removal and partial interruption of IVC to prevent PE.

THROMBECTOMY FILTERS FOR DVT To restore venous patency and valvular function. Alone it is not indicated because rethrombosis is frequent. Heparin therapy is a necessary adjunct. Best reserved for patients with massive vein thrombosis when limb viability is at risk. FILTERS FOR DVT First suggested by Trousseau in 1868. introducing intracaval devices percutaneosly and floating them into position with fluoroscopy is the procedure of choice for filter placement.

ACCEPTED INDICATION FOR FILTER PLACEMENT Severe hemorrhage complications of anticoagulant therapy. Absolute contra indications to anticoagulation. Failure of anticoagulation such us new or recurrent VTE or PE.

prophylaxis - yes or no? YES - Overall reduction in DVT and PE is by 40% to 60%

PROPHYLAXIS Designed to address stasis & coagulation Usually combination of therapies EARLY MOVT & REHABLITATION MECHANICAL METHODS lower extremity exercises graded compression stockings intermittent pneumatic compression devices

PREVENTION OF TRAVELER`S THROMBOSIS Graduated compression stockings Exercise Avoid alcohol &sleeping tablets HIGH RISK PATIENTS LMWH ,single dose SC before the flight

DVT IN UPPER LIMB PAGET VON SCHROTTER DISEASE Axillary and sub clavian vein thrombosis Reduced incidence Thoracic outlet synd &cervical ribs Thrombolytic therapy is treatment of choice Since restoring venous patency more important in upper limb

Complications Early- Progression Pulmonary embolism Paradoxical embolism Acute compartment syndrome venous gangrene Late - Rec DVT, Post phlebitic syndrome