DEEP VENOUS THROMBOSIS

Deep vein thrombosis is the formation of a blood clot in one of the deep veins of the body, usually in the leg

THIN WALLED, DISTENSIBLE, COLLAPSIBLE BICUSPID VALVES TRANSPORT AND RESERVOIR OF BLOOD ENDOTHELIUM RELEASES EDRF AND PROSTACYCLIN WHICH PROVIDE NON-THROMBOGENIC SURFACE AND PREVENT PLATELET AGGREGATION

PROXIMAL DVT :Thrombus formed in veins above the knee jt (femoral, iliac, popliteal) DISTAL DVT :Those formed below the knee jt (calf veins)
Calf vein - most common Ilio femoral - most symtomatic IVC - most lethal

DVT is a common condition that affects about 1 person per 1,000 population per year. Associated with many medical conditions but is a relatively common complication of trauma. About 20% of multiply injured patients die as a result of a DVT. one of the most significant complications after THA & TKA, possibly resulting in life-threatening PE. In early reports of total hip arthroplasty without routine prophylaxis, venous thrombosis occurred after total hip replacement in 50% of patients, and fatal pulmonary emboli occurred in 2%. The of mechanical or pharmaceutical prophylaxis has been reported to range from 40% to 84%.

Proximal thrombi, in the popliteal vein and above, occur in 9% to 20% of patients and have been thought to pose a greater risk of PE than thrombi in calf veins, which have been reported in 40% to 60% of patients. Thrombi in the calf veins have a propensity to propagate proximally, as documented in 6% to 23% of patients. The risk of DVT is increased by five times in patients with femoral or tibial diaphyseal fractures. In elective hip surgery the use of regional anesthesia reduced the incidence of proximal vein DVT from 73% to 23% compared with general anesthesia. 80-90% occur in operated limb

Clinical Risk Factors

Advanced age Fracture of pelvis, hip, femur, or tibia Paralysis or prolonged immobility Prior venous thromboembolic disease Operation involving abdomen, pelvis, or lower extremities Obesity Congestive heart failure Myocardial infarction Stroke Pregnancy / postpartum Indwelling central venous catheter malignancy

Hemostatic Abnormalities (Hypercoagulable States)

Antithrombin III deficiency Protein C deficiency Protein S deficiency Dysfibrinogenemia Lupus anticoagulant and antiphospholipid antibodies Myeloproliferative disorder Heparin-induced thrombocytopenia Disorders of plasminogen and plasminogen activation

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Stasis of blood flow Endothelial damage Hypercoagulability

Venous thrombi are mainly composed of fibrin and erythrocytes together with platelets and leucocytes. They usually form in venous sinuses in the deep veins of the calf and in veins damaged by trauma. Damage to the endothelium of the veins leads to platelet adhesion, leucocyte accumulation, and the activation of the intrinsic and extrinsic pathways. Venous stasis during surgery or as a result of trauma may contribute by slowing the clearance of coagulative factors. This is particularly important in lower limb surgery because the normal pumping action of the calf muscles may be slowed or abolished. There is a clear association between DVT and PE. About 50% of patients with a proven DVT develop PE, and about 70% of patients with confirmed PE have asymptomatic DVTs. Pulmonary emboli can take the form of multiple small emboli or a single large, often fatal embolus. Most significant PEs arise from the proximal veins

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Propagation Embolization Dissolution Organization & recanalisation

Most of the thrombi originate in the deep venous system of the lower extremities. Large thrombi lodge at the bifurcation of the main pulmonary artery or the lobar branches, accumulate and may cause haemodynamic compromise. Smaller thrombi continue distally, occluding smaller vessels in the lung periphery. These are more likely to produce pleuritic chest pain by initiating an inflammatory response adjacent to the parietal pleura. Most pulmonary emboli are multiple, and the lower lobes are involved more commonly than the upper lobes

Calf pain or tenderness, or both Swelling with pitting oedema Swelling below knee in distal deep vein thrombosis and up to groin in proximal deep vein thrombosis Increased skin temperature Superficial venous dilatation Cyanosis can occur with severe obstruction

Early in course may/may not have symptoms Even in advanced DVT ---may not have symptoms Pain and swelling are highly nonspecific. Large studies with venogram/duplex scan have shown DVT to be present only in 50% of clinically suspected patients.

 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

Unexplained shortness of breath Chest pain and/or palpitations Anxiety and/or sweating Coughing/coughing up blood Fatigue and/or fainting

Massive DVT obliterates major deep vein sparing collateral veins Pain,pitting edema,blanching,NO CYANOSIS

Affects collateral veins --> massive fluid sequestration edema Very painful(compartment syndrome/arterial insufficiency),CYANOSIS(blue limb)

Active cancer (treatment ongoing, or within 6 months or palliative) 1 Paralysis or recent plaster immobilization 1 Recently bedridden for >3 days or major surgery within12 wks 1 Localized tenderness along the distribution of the deep venous system 1 Entire leg swelling 1 Calf swelling >3 cm compared to the asymptomatic leg 1 Pitting edema 1 Collateral superficial veins (nonvaricose)1 Alternative diagnosis at least as likely that of DVT) -2

High probability: Score of 3 or more Moderate probability: Score = 1 or 2 Low probability: Score 0

 Invasive venography, radiolabeled fibrinogen

Noninvasive ultrasound, plethysmography, MRI techniques

Lab D-dimer

Combination of realtime B modeUSG with Doppler flow studies. Most commonly performed test 95% specificity/sensitivity Findings: lack of spont.flow inability to compress the vein absense of colour filling of lumen loss of respiratory flow variation

Disadvantages reader dependent Duplex scans are less likely to detect non-occluding thrombi. During the second half of pregnancy, ultrasound becomes less specific, because the gravid uterus compresses the inferior vena cava, thereby changing Doppler flow in the lower extremities Not able to differentiate to old and new clots in patients with acute recurrent DVT
useful for visualization of proximal vein DVT and is less effective for calf vein DVT.

Was used often prior to DUS Infrequent today Principle: resistance of flow of electricity between two electrodes occurs as volume of extremity changes in response to blood flow Sensitive and specific for proximal vein thrombosis

Seldom used now IV administration of radioactive fibrinogen and monitor for increased uptake in fibrin clot

Most definitive test for Dx Its gold standard when compared to others Small catheter is inserted in dorsum of foot and radio opaque contrast is injected and radiographs are taken Used when other test are inconclusive. Drawbacks : Allergic reactions, contrast induced DVT, technical problems, inter observer variability and lack of availability.

D-dimer is a specific degradation product of crosslinked fibrin. patients with thromboembolic disease have elevated levels of D-dimer Elevated in any medical condition where clots form. Rised in trauma, recent surgery, haemorrhage, cancer and sepsis. It has high sensitivity and low specificity for VTE. Levels elevated in DVT for seven days. After clot organisation and adherence the levels decrease Approaches for measuring D-dimer ELISA latex agglutination blood agglutination test

 Current evidence strongly

supports the use of a D-dimer assay in the clinical algorithm of suspected DVT. A negative D-dimer assay R/O DVT in patients with low-to-moderate risk (Wells DVT score <2). All patients with positive D-dimer assay and all patient with a moderate-to-high risk of DVT ( Wells DVT score >=2) require a diagnostic study.

 Increasingly used. Accuracy approaches to that of contrast

venograghy,DUS Diagnostic test of choice for suspected iliac vein & IVC thrombosis,2nd &3rd trimester of pregnancy (gravid uterus alters doppler flow characteristics). In suspected calf vein thrombosis it is more sensitive than other non invasive study. Expense, lack of general availability and technical issues limit its use.

Cellulitis Thrombophlebitis Arthritis Asymmetric peripheral edema secondary to CHF, liver disease, renal failure, or nephrotic syndrome lymphangitis Extrinsic compression of iliac vein secondary to tumor, hematoma, or abscess 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

Goal: to decrease morbidity and mortality of VTE/PE Current recommendation: use of one or more pharmacologic or mechanical methods Methods: UFN,LMWH, Elastic stockings, intermittent pneumatic compression(IPC) Overall reduction in DVT and PE is by 40% to 60%

Ideidentify any patiant who is at risk. Prevent dehydration. During operation avoid prolonged calf compression. Passive leg exercises should be encourged whilst patient on bed. Foot of bed should be elevated to increase venous return. Early mobilization should be rule for all surgical patient

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Low risk general surg(minor surg,<40y, no risk factor Early ambulation Mod risk general surg(minor +risk factor, major surg, >40y) UFH,LMWH,ES, IPC THR LMWH(started 12 hr before surg) or warfarin started preop or immediate post op TKR LMWH/warfarin

Binds to antithrombin and potentiates its action of inhibition of thrombin &factor Xa

T1/2 90 min Level monitored every 6hr by aPTT IV bolus----> continuous drip Bolus 80 IU/kg Drip 18 IU/kg/hr Start warfarin after 1 day of infusion Mixture continue for 4-5 days, INR@ 2-3 Stop heparin 2 days after reaching desired INR

Side effects of heparin bleeding heparin induced thrombocytopenia osteopenia

Derived from UFH using depolymerisation Advantages of LMWH Over UFH 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, Less osteopenia Earlier/facilitated

Currently four LMWH are available. Enoxaparin Tinazaparin Dalteparin Nadroparin Only enoxaparin and tinazaparin approved by FDA for DVT prophylaxis.

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Acts in liver by inhibition of vit.k dependant factors II,VII,XI,X Takes several days to achieve full effect Hence heparin has to be continued for some time T1/2 40 hrs, INR@ 2-3 ,dose 2-10 mg/d Should be withheld 2-3 days prior to any surgery S/E: Bleeding(t/t fresh frozen plasma) Skin necrosis, drug interactions

First chemically synthesized(no animal product) Specifically inactivates factor Xa Recommended as prophylactic for hip/kne surgery

Hirudin Argatroban Oral heparin(ximelagatran)

patients undergoing THR/TKR, the American College of Chest Physicians has recommended one of the following three anticoagulant agents: LMWH, fondaparinux, or adjusted-dose vitamin K antagonist (INR target 2.5; range 2.0 to 3.0) It is recommended that patients undergoing hip or knee arthroplasty or hip fracture surgery receive thromboprophylaxis for at least 10 days The continuation of prophylaxis after the patient has been discharged presents a dilemma. If anticoagulants are to be continued after hospital discharge, preparation must be made for monitoring their effects. Most of the centres use LMWH or warfarin for 10 to 14 days postoperatively, along with mechanical compression devices during the initial hospital stay. Enteric-coated aspirin is used in low-risk patients for another 4 weeks after the LMWH or warfarin is discontinued. High-risk patients, particularly patients with previous history of thromboembolism, are maintained on LMWH or warfarin for at least 6 weeks postoperatively

Despite early mobilization, mechanical and pharmacological prophylaxis, and careful clinical monitoring, some patients develop deep vein thrombosis and pulmonary embolism and require full therapeutic anticoagulation

Advantages prompt resolution of symptoms, prevention of pulmonary embolism, restoration of normal venous circulation, preservation of venous valvular function, and prevention of postphlebitic syndrome but few <10% are candidates 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

Thrombolytic agents(activate plasminogen---> fibrin degradation)

1. streptokinase : antigenic, inhibited by Ab 250000 IU/IV loading 100000 IU/hr 2.Urokinase: 4400IU/kg---> 2200IU/kg/hr x 12hrs
3. tPA : 100mg infusion over 2hrs

To decrease bleeding complications and increase efficacy ---->catheter directed thombolytic agent is administered into thrombus

Filters emboli in patients of DVT/PE,and allow continuous flow through IVC

Indications Pulmonary embolism with contraindication to anticoagulation Recurrent pulmonary embolism despite adequate anticoagulation clot despite anticoagulation

Inferior vena cava filters reduce the rate of pulmonary embolism but have no effect on the other complications of deep vein thrombosis Complications insertion site thrombois filter migration erosion of vessel wall obstruction

Reserved with who worsen with anticoagulant therapy and Phlegmasia cerulea dolens
major surgical procedures for DVT are clot removal and partial interruption of the inferior vena cava to prevent pulmonary embolis

This patient underwent a thrombectomy. The thrombus has been laid over the approximate location in the leg veins where it developed.

These pulmonary emboli removed at autopsy look like casts of the deep veins of the leg where they originated

Special group of pts very high risk for DVT & may reach up to 60 to 80% with out prophylaxis (THR) Assymptomatic DVT common in >50% of all patients PE develop in 10 to 20 % of pts Even with prophylaxis DVT & PE remains the most common cause for emergency readmission and death in joint replacement pts

Pre-op Immobilization (stasis)

Trigger of tissue factor reamed products (THR)

tissue debris ,fat activation of coagulation

Distortion of Femoral and Poplietal viens

retraction,twisting,manipulation damage to vessel wall

Prolonged post-op Immobilization.