dvt presentation in orthopaedics pov.pptx

Deep vein thrombosis

1. DEEP VEIN THROMBOSIS Presented by Dr. Lakshay Sharma PG resident Orthopaedics (1 st year)

2. DEEP VEIN THROMBOSIS A thrombus is a mass formed from blood constituents within a vessel or the heart during life. A venous thrombus is the formation of a semi-solid coagulum within flowing blood in the venous system.

3. The incidence of DVT ranges between 5 and 9 per 10,000 person-years in the general population . T he incidence of VTE (DVT and PE combined) is approximately 14 per 10,000 person-years. Major surger ies have a significant incidence of perioperative DVT (15 to 40%). Major trauma : 40- 80% . Hip or knee surgery : 40- 60% . Spina l injury : 60-80% .

4. EPIDEMIOLOGY OF DVT It occurs in about 1 to 2 persons per 1,000 population. 20 – 30% of general surgical patients . Male :Female = 1:1 This incidence increases with increasing age, doubling with each decade of life after 40 More than two thirds of these patients have DVT alone, and the 30% will have symptomatic pulmonary embolism with mortality of 17% .

5. Major general , urological , OBG, C a rdiothorac i c,vascul a r or neruological surgery . Age > 40 yrs . Mahor medical illness . Major trauma or burns . Minor surgery or trauma in pat with previous DVT, PE . Orthopedic surgery or amputation of LL . Lower limb paral y sis . Major pelvic or abdominal surgery for cancer . Major surgery, trauma or illness with previous DVT, PE, Thrombophillia . Full limb paralysis . Maojor limb amputation . Moderate risk High risk

6. 50 to 60% of DVT cases are asymptomatic . The recurrence rate with anticoagulation therapy has been noted to be 6% to 7% in 6 months . DVT in upper extremity is less common- 5% of all documented DVT but one third result ing in PE .

7. . Activation of Coagulation Virchow's Triad PATHOPHYSIOLOGY

8. PATHOPHYSIOLOGY Starts as a platelet nidus, usually in the venous valves of the calf. Platelet adhere to the endothelium and to each other forming a projecting mass . The liberation of thromboplastin initiates a chemical cascade leading to activation of coagulation pathway. If the rate of flow is slow , rbc are entangled so that the lumen is occluded . In front and behind platelet mass, the blood stagnates further formation of fibrin takes place, resulting in a large solid coagulum .

9. SEQUELAE OF THROMBOSIS Fibrinolysis Organisation Calcification Incorporation Embolism

10. A thrombus often develops in the soleal veins of the calf . Propagate and extend up to next venous branch and break down to embolize . Thrombus localise to calf have less tendency to embolise than thromboi that extend to the thigh ve ins. Aproximately 20% of cases of calf DVT propagate to the thigh, and 50% of cases of thigh or proximal DVT embolize .

11. Malignancy Tumor cell activation of clotting cascade . Indirect clotting activation . Reactive thrombocytosis . Endothelial injury Adhesion of tumor cells . Chemotherapeutic drugs . Venous stasis Immobility, venous obstruction, inc pressure, inc blood viscosity . Reduced clerance of activated clotting factors . Endothelial hypoxia- inc expression of TF . RISK FACTORS

12. HYPER COAGUABLE STATES Primary De activation of protein C Impaired heparin binding of antithrombin III Downregulation of membrane associated plas min production Inc serum prothrombin levels Decrease thrombogenic inhibitors (antithrombin lll , protein C, Protein S ) Secondary Antiphospholipid syndrome Venous trauma Surgery Cancer Chemotherapy Myeloproliferative syndromes Heparin induced thrombopathy

13. R ISK FACTORS FOR DVT

14. CLINICAL PRESENTATION Pain and swelling in calf region. Bilateral presentation is quite uncommon ( 30% ) Asymptomatic cases may present as features of pulmonary embolism Pleuritic chest pain, haemoptysis and SOB Phlegmasia alba dolens (white leg) and phlegmasia cerulea dole ns

15. Phlegmasia alba dolens : Deep venous channels of the extremity are affected while sparing collateral veins and therefore maintaining some degree of venous return. Present with blanching of the extremity, edema and discomfort Phlegmasia cerulea dolens: Occurs with extension of thrombus into the collateral venous system, resulting in limb pain and swelling with cyanosis a sign of arterial ischemia

16. Physical signs Pitting edema . Dilated superficial veins . stiff calf and tenderness over the course of the deep veins Erythema . Bluish discoloration . Absent or decreased pulse . Homans’ sign – resistance (not pain) of the calf muscles to forcible dorsiflexion . Pratt's sign : Squeezing of posterior calf elicits pain Low grade fever . PE- cyanosis, dyspnoea, raised neck veins, a fixed split second heart sound and a pleural rub .

17. DIFFERENTIAL DIAGNOSIS Cellulitis, lymphangitis Lymphedema Varicose veins Superfical thrombophlibitis

18. Clinical Parameter Score (wells score) Score Active cancer (treatment ongoing, or within 6 mo or palliative) +1 Paralysis or recent plaster immobilization of the lower extremities +1 Recently bedridden for >3 d or major surgery <4 wk +1 Localized tenderness along the distribution of the deep venous system +1 Calf swelling >3 cm compared with the asymptomatic leg +1 Pitting edema (greater in the symptomatic leg) +1 Previous DVT documented +1 Collateral superficial veins (non varicose) +1 Alternative diagnosis (as likely or greater than that of DVT) -2 W ELLS SCORE FOR DVT

19. Total of Above Score High probability > 3 Moderate probability 1 or 2 Low probability < WELLS SCORE

20. LAB CBC PT ,PTT , INR ESR D-dimer Protein C , S Antithrombin III LFT RFT

21. I M AGING DUPLEX ULTRASOUND combines real-time B-mode ultrasound with pulsed Doppler capability. HELICAL CT VENOGRAPHY CONTRAST VENOGRAPHY MRI OTHERS CHEST X-RAY ECHO PULMO N A R Y A R TERIOGRAPHY

22. D UPLEX ULTRASONOGRAPHY Sensitivity in calf vein 73% Sensitivity in proximal vein 95-97% Specificity 95-98% lack of spontaneous flow inability to compress the vein absence of color filling of the lumen by color flow DUS, loss of respiratory flow variation, Venous distension

23. Ad v ant a ge helpful to differentiate venous thrombosis from hematoma, Baker cyst, abscess, and other causes of leg pain and edema. Non-invasive inexpensive Disad v ant a ge Venous thrombi in iliac and tibial vein are difficult to visualize not be able to differentiate between old and new clots

24. CT VENOGRAPHY ( GOLD STAND A RD ) The gold standard investigation is intravenous CT venography .

25. D-dimer testing D-dimer antibodies account for their high sensitivity for venous thrombo - embolism. D-dimer level may be elevated in any medical condition where clots are form ed . The D-dimer assays have low specificity for DVT .

26. D-dimer results should be used as follows : A negative D-dimer assay result rules out DVT in patients with low-to-moderate risk and a Wells DVT score less than 2. All patients with a positive D-dimer assay result and all patients with a moderate-to-high risk of DVT (Wells DVT score > 2) require a diagnostic study (duplex ultrasonography).

27. PROPHYLAXSIS All patient admitted should be assessed for risk for DVT Overall, low-dose UFH and LMWH reduce the risk for symptomatic and non symptomatic VTE by 60 to 70%. Low risk compression stockings, Early mobilisation and leg elevation Moderate risk Leg elevation, early mobilization, and either graduated compression stockings or s/c UFH or LMWH High risk Leg elevation, early mobilisation, TED s tockings , UFH or LMWH

28. Heparin 5,000 unit ,S/C 2 hours before surgery and every 8 or 12 hourly Graduated elastic compression (GEC) stockings reduce the incidence of asymptomatic DVT by approximately 50-60% Intermittent pneumatic compression (IPC) reduces the incidence of asymptomatic DVT by approximately 69% Aspirin reduces DVT by 30% and PE by 50% Prophylactic insertion of IVC filters Fondaparinux has similar results like LMWH

29. In the Women's Health Study, supplementation with vitamin E (alpha-tocopherol, 600 IU every other day) reduced the risk of venous thrombo embolism in women, especially those with a prior history or genetic predisposition. High-risk patients should also be prescribed a single prophylactic subcutaneous 40 mg dose of enoxaparin prior to a long plane trip (>6 h).

30. T R E A TME N T Principles are: To prevent clot propagation . Reduce the risk of PE . Enhance the resolution of the clot to minimize the post – thrombotic syndrome Options are Anticoagulants/ Pharmacotherapy Catheter directed intra-thrombus thrombolysis Inferior vena caval filters Venous thrombectomy

31. AN TICOAGULATION THERAPY HEPARIN Blocks th e coagulat ion pathway at factors IXa, Xa, XIa, XII and thrombin to antithrombin-III . Discourage further clot formation and facilitate endogenous clot lysis O nset of action 10-18 mins IV 20-60 min S/C ( peak at 4-6 hrs n last up to 12 hrs) Half life – 90 mins Safe in pregnancy Monitoring done with APTT 6 hrly (1.5 to 2.5 times) Platelet count should be done every 3 days APTT >1.5 should be achieved with in 24 hrs

32. Heparinization Continous IV infusion Loading dose- 5000 to 10000 unit( 80 U/kg) Continuous infusion- 1300 units /hour (18 U/Kg) Intermittent intravenous adminstration 70-100 units /kg every 4 hours Subcutaneous adminstration 5000 unit every 8 0r 12 hourly Should be continued for 4-6 days Oral anticoagulant after 24 hours and overlapped for 4 days Heparin should be discontinued when INR is >2 for 2 consecutive days Warfarin is continued for minimum 3 months to maintain INR between 2.0 to 4.5

33. Advantages of Low Molecular Weight Heparin Greater activity against factor Xa Lower risk of bleeding Longer half life(4-6 hrs) Produce little effect on test APTT or PT so no need of monitoring Can be started simultaneously with warfarin Weight-based once- or twice-daily SC LMWH injections Incidence of HIT is<2% Can be used as outpatient therapy Less recurrence (8.6% vs 6.9%)

34. Adverse affects Haemorrhage 5% Heparin induced Thrombocytopenia( HAAbs ) Hypersensitivity H yperkalemia

35. W A R F A R IN Inhibits the enzyme vitamin K epodxide Thus indirectly inhibit the the synthesis of vitamin K dependent clotting factors . 5mg orally Onset: 36 -48hrs Duration: 2-6 days Half life: 36-40hrs Bioavailability: 100% The target INR 2 to 3 Adverse affects Haemorrhage (0.5 to 1% per month) Skin necrosis Teratogenecity Liver damage

36. N E WER AGE N TS Fondaparinux synthetic pentasaccharide Its five-polysaccharide sequence binds and activates antithrombin, causing specific inhibition of factor Xa . The drug is administered SC once daily with a weight- based dosing protocol: 5 mg, 7.5 mg, or 10 mg for patients weighing <50 kg, 50 to 100 kg, or >100 kg, respectively Half life is 17 hrs

37. Direct Thrombin inhibitors R ecombinant hirudin, argatroban, and bivalirudin B ind to thrombin, inhibiting the conversion of fibrinogen to fibrin as well as thrombin-induced platelet activation. reserved for (a) patients in whom there is a high clinical suspicion or confirmation of HIT, and (b) patients who have a history of HIT or test positive for heparin- associated antibodies administered for at least 7 days, or until the platelet count normalizes.

38. LONG TERM ANTI THROMBOTIC THERAPY FOR DVT

39. INFERIOR VENACAVAL FILTER Kimray-Greenfield filter in 1973 . Traps emboli as small as 3mm . Made of titanium or nickel titanium alloy . Placed percutaneously under LA via the common femoral, internal juglar or antecubital vein . Positioned in the infra-renal cava vein. 20 years follow up – 96 % patency . Complications associated with IVC filter placement include insertion site thrombosis, filter migration, erosion of the filter into the IVC wall, and IVC thrombosis. The rate of fatal complications is <0.12%

40. Absolute indication are DVT or PE with contraindication to anticoagulation therapy prior hemorrhagic stroke Recent neurosurgical procedure or major surgery Multiple trauma Active internal bleeding Intracranial neoplasm Bleeding diathesis Pregnancy DVT or PE having complication with anticoagulation therapy Failure of anticoagulation therapy Free-floating iliofemoral or caval thrombus Relative indication Prior history of chronic pulmonary HTN Morbidly obese with BMI >55

41. Catheter Directed Intra-thrombus thrombolysis Placement of thrombolysis catheter within the clot . Rapid clearance of the DVT . SITE: IJV, contralateral CFV, popliteal, tibial vein . Thrombolytic drugs: streptokinase, alteplase , reteplase, and tenecteplase, urokinase . convert plasminogen to plasmin, which leads to the degradation of fibrin. Higher success in acute DVT , new onset DVT and upper limb DVT. < 10 days with 34% and > 10 days 19% 1 year patency 79% for complete lysis and 32% for partial lysis Overall one year patency is 60% Major bleeding -11% Mortality 0.4% Contraindicated in:Recent surgery, active or recent bleeding, bleeding diathesis, pregnancy and cerebral disease

42. VENOUS THROMBECTOMY In di cation s Phlegmasia alba dolens . Phlegmasia cerulea dolens with impending venous gangrene threatening to the patient’s life and limb . Failed or contraindicated anticoagulation and thrombolysis . If the patient has phlegmasia cerulea dolens, a fasciotomy of the calf compartments is first performed Useful in relatively young patient who has cause other than malignant dis orders for the DVT

43. An intraoperative completion venogram is obtained to determine if any residual thrombus or stenosis is present. Post op managed with limb elevation, calf exercise, compression stockings, antibioitc therapy, heparin for 5 days and warfarin for 6 months or life long . Good result if performed with in 7-10 days of event . Mortality rate is 1% . Intraoperative PE occurs in 20% . 10 yrs follow up patency 77% . Severe PCD and venous gangrene have poor outcome .

44. COMPLICATIONS OF DVT P ulmonary embolism . P ost -thrombotic syndrome occurs in 15% of patients with deep vein thrombosis (DVT). It presents with leg oedema, pain, nocturnal cramping, venous claudication, skin pigmentation, dermatitis and ulceratiaion (usually on the medial aspect of the lower leg).

45. High clinical pretest probability- DVT likely Doppler ultrasound Ultrasound positive for DVT Diagnoses of DVT confirmed Begin treatment Ultrasound negative for DVT D-Dmer test (if available and reliable) Otherwise skip to repeat ultrasound D-Dimer positive Repeat ultrasound in 1 week D-Dimer negative DVT ruled out Repeat ultrasound positive for DVT Diagnoses of DVT confirmed Begin treatment Suspect DVT Low clinical pretest probability- DVT likely Consider starting with D-dimer test first (if available and reliable ) Or skip to ultrasound D-dimer positive D-Dimer negative DVT ruled out Doppler ultrasound Ultrasound positive for DVT Diagnose of DVT confirmed Begin treatment Ultrasound negative for DVT DVT ruled out (c on si d er re p eat ultrasound if D-dimer not available)

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