Deep vein thrombosis


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Deep vein thrombosis

  1. 1. VENOUS THROMBOEMBOLISM Compositeterm for DVT &PE The presence of thrombus with in deep veinsis termed as deep vein thrombosis It is a life threatening condition that may leadto sudden death in the short term or longterm morbidity due to the development ofpost thrombotic limb and venous ulceration
  2. 2.  1846 virchow recognised association ofthrombus in leg and PE. 1916 J McLean ,a medical student discoveredheparin 1937 Heparin introduced to clinical practice. Last 25 years significant progress made in ourunderstanding of DVT.
  3. 3.  CLASSIFICATION :PROXIMAL DVT :thrombus formed in veinsabove the knee jt (femoral, iliac, popliteal)DISTAL DVT : those formed below the knee jt(calf veins)
  4. 4. Venous thrombosis are difficultto recognize clinically. Thedocumented cases probablyrepresent only tip of the IceBerg.SILENT KILLER
  5. 5.  M:F 1.2:1 Age more than 40 years. VT occur in more than 50% of patient’s havingorthopaedic surgical procedures. 10 to 20% of patient with idiopathic DVT have ordevelop cancer. 1/3rdto 1/4thpatient having proximal DVT maydevelop PE. About 10% of hospital deaths attributable to PE(from DVT)
  6. 6.  Calf vein - most common Ilio femoral - most symtomatic IVC - most lethal
  7. 7.  Blood clots occurring in people sitting at thecomputer for prolonged periods of time.AIR TRAVEL AND DVT Up to 1 out of 10 air line passengers develop smallasymptomatic blood clots. Due to hypoxia and reduced cabin pressure. VT occurs in patients regularly without any damagedto the blood vessels.
  8. 8. VTE Risk StratificationPatient Factors: Clinical Age Previous VTE Malignancy Advancing age Obesity Prolonged immobility Trauma Surgery (THR, TKR, HFS) Pregnancy/ postpartum Indwelling central venous catheter Thrombophilia Deficiency of anti-thrombin IIIProtein C or SContd...
  9. 9.  Paralysis of lower limbs Polycythaemia Paraproteinaemia PNH Antibody or lupus anticoagulant Medical illness◦ stroke◦ MI◦ CHF◦ pneumonia◦ COPD◦ infections◦ nephrotic syndrome◦ inflammatory bowel disease Oral contraceptives Varicose veins
  10. 10.  Pregnancy and postpartum period. Immoblisation longer than 3 days Major surgery in previous 4weeks Long air or car trips >4hrs in previous 4 weeks
  11. 11.  Predisposing Factors :1. Stasis2. Vascular damage3. Hyper coagulability Imbalance between thrombogenesis &thrombolytic agents
  12. 12. 1. Propagation2. Embolization3. Dissolution4. Organization & recanalisation ORGINDVT usually originates from veins of calfaround the valve cusps or with in solealplexus A minority of cases occurs directly in iliofemoral veins
  13. 13.  In practical terms the development of VT isbest understood as activation of coagulation inareas of reduced blood flow. Majority of calf vein thrombus dissolvecompletely. Only 20% progress proximally. Propagation occurs before embolisation.
  14. 14.  The process of adherence and organisation ofvenous thrombus does not begin until 5 to 10days after thrombus formation. This non adherent thrombus may propagate orembolise. Propagation or organisation of venousthrombus  destruction of valves & varyingdegree of venous outflow obstruction chronic venous insufficiency.
  15. 15. 1. Fatal PE2. Non-fatal PE3. Post-thrombotic syndrome Rate of fatal PE in gen population >65yrs is .003% In ortho pts (THR,TKR) it is 0.3% 10 fold increase in risk of having fatal PE
  16. 16.  Consequence of recanalisation of majorvenous thrombus Due to incompetence of valves Long term morbidity Causes chronic edema &venous ulcers
  17. 17.  Swelling/edemamost specific signunilateral Leg pain (50%)non specific Redness/erythemaover the thrombus Tenderness(75%)calf or along the involved veinsdoes not correlate size, site, extent Low grade pyrexia Signs and symptoms of PE
  18. 18.  Pain or discomfort in leg on forceful dorsiflexionof foot with knee straight Time honoured sign Present only in 10% of confirmed DVT Highly non-specific Present in 50%of cases with out DVT Misleading sign No longer used
  19. 19.  Pts with superficial thrombophlebitis with outcoexisting varicose veins & with no otheretiology (IV Catheter) are at high risk of havingDVT (40%) Pts with ST extending to sapheno-femoral jnare at high risk of associated DVT
  20. 20.  Painful blue inflammationPHLEGMASIA ALBA DOLENS Painful white inflammation Massive IVF thrombus with arterial spasm
  21. 21. In approximately 70% of patients with clinically suspectedDVT, alternate diagnoses are ultimately found as follows:ArthritisCellulitis, lymphangitisHematomaLymphedemaMuscle or soft tissue injuryNeurogenic painPostphlebitic syndromeProlonged immobilization or limb paralysisRuptured Baker cystStress fractures or other bony lesionsSuperficial thrombophlebitisVaricose veins
  22. 22. D-DIMER STUDY D-dimer fibrin fragments are present in fresh fibrin clots andfibrin dehydration products of cross linked fibrin. Monoclonal antibodies specific to D-dimer fragment are used todifferentiate fibrin specific clots from noncrosslinked fibrin andfrom fibrinogen. These specific attributes of the D-dimerantibodies account for their high sensitivity for venousthromboembolism. Elevated in any medical condition where clots form. Rised in trauma, recent surgery, haemorrhage, cancer andsepsis. It has high sensitivity and low specificity for VTE. Levels elevated in DVT for seven days. After clot organisation and adherence the levels decrease.
  23. 23.  Current evidence strongly supports the use of a D-dimer assay in the clinical algorithm of suspectedDVT.A negative D-dimer assay R/O DVT in patientswith low-to-moderate risk (Wells DVT score <2).All patients with positive D-dimer assay and allpatient with a moderate-to-high risk of DVT ( WellsDVT score >=2) require a diagnostic study.
  24. 24.  Protein S, protein C, anticromin III, factor V Leyden,prothrombin 20210A mutation, antiphospholipidantibodies and homocysteine levels can be measured. investigations for these abnormalities are primarilyindicated when DVT is diagnosed in patients younger that35 years or when venous thrombosis is detected inunusual sites.
  25. 25. CONTRAST VENOGRAPHY Gold standard for DVT. Used when other test are inconclusive. It is either contra indicated or non diagnostic in as many as 20-25%of patients. Drawbacks : Allergic reactions, contrast induced DVT, technicalproblems, inter observer variability and lack of availability. It is replaced by non invasive studies as initial diagnostic test.
  26. 26.  Combination of real – time ultrasonographicimaging with Doppler flow studies. Sensitivity for proximal DVT is 97% for calfveins is 73%. Overall specificity is 95%. Helpful to differentiate from haematoma,baker cyst, abscess and other causes of legpain and edema.
  27. 27.  Primary disadvantage : Inherent inaccuracy indiagnosis of calf vein thrombosis.Those proximal to the inguinal ligament are alsodifficult to visualize. Non occluding thrombi may bedifficult to detect.Not able to differentiate to old and new clots inpatients with acute recurrent DVT.Depends on experience of radiologist
  28. 28.  Based on recording changes in blood volume of anextremity, which are directly related to venous outflow. Sensitive and specific for proximal vein thrombosis. Cannot differentiate between thrombotic occlusion andextra vascular compression of the vein. Insensitive for calf vein thrombosis, non-occludingproximal DVT and ileofemoral DVT.
  29. 29.  Increasingly used. Accuracy approaches to that of contrast venograghy. Diagnostic test of choice for suspected iliac vein & IVCthrombosis. 2nd&3rdtrimester of pregnancy (gravid uterus altersdoppler flow characteristics). In suspected calf vein thrombosis it is more sensitivethan other non invasive study. Expense, lack of general availability and technical issueslimit its use.
  30. 30.  Used for pelvis vein thrombosis.NUCLEAR MEDICINE IMAGING STUDIES I125labeled fibrinogen. Takes longer than 24 hrs. No longer used.
  31. 31. PRIMARY OBJECTIVES1. To prevent PE.2. Reduce morbidity.3. Prevent or minimize risk of developing the postphleticsyndrome.SURGICAL TREATMENT1. Indicated when anticoagulant therapy is ineffective, unsafe orcontraindicated.2. Major surgical procedures : clot removal and partialinterruption of IVC to prevent PE.
  32. 32.  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 IF vein thrombosiswhen limb viability is at risk.FILTERS FOR DVT First suggested by Trousseau in 1868. Today introducing intracaval devices percutaneosly and floatingthem into position with fluoroscopy is the procedure of choicefor filter placement.
  33. 33.  Severe hemorrhage complications ofanticoagulant therapy. Absolute contra indications to anticoagulation. Failure of anticoagulation such us new orrecurrent VTE or PE.
  34. 34.  Bed rest Affected limb is elevated above the level of heart. Anticoagulant prevent thrombus propagation andallow the endogenous lytic system to operate Pain relief.
  35. 35.  Initial bolus 7500 to 10000 IU followed bycontinuous in infusion to 1000 to 1500 IU/hr. Infusion rate adjusted so that aPTT is approxtwice the control value Every 6 hrs aPTT monitered till therapeuticrange is reached Duration :5 days Discontinue when platelet count <75,000
  36. 36.  Effective and better than conventional heparin. Different preparations available. Administered SC in fixed doses once or twicedaily. Duration -7 to 14 days Anticoagulant effect by inhibiting the activatedfactor X. Hemorrhagic complications doesn’t occur
  37. 37.  LMWHs are individual, distinct compoundsthat exhibit unique physical, pharmacokineticand pharmacodynamic profiles LMWHs exhibit distinct non-antithrombin III-mediated effects, including unique tissuefactor pathway inhibition and von Willebrandfactor release profiles.
  38. 38.  Currently four LMWH are available.EnoxaparinTinazaparinDalteparinNadroparin Only enoxaparin and tinazaparin areapproved by FDA for DVT prophylaxis.
  39. 39.  To be taken along with heparin for initial 4 to5days. Dose adj to maintain prothrombin time at INR2.0 to3.0 Continued for 3 to6 months for pts with acuteidiopathic DVT For recurrent DVT/PE low intensity warfarincontinued indefinitely maintaining INR 1.5 to2.0
  40. 40.  Early administrationa) Prompt resolution of symptomsb) Accelerate clot lysisc) Preserve venous valvesd) Decrease the potential for developing post-phlebitic syndrome
  41. 41.  Does not prevent clot propagation orrethrombosis. Heparin and oral anti coagulant therapy mustfollow a course of thrombolysis. Haemorraghic complications reduced byregionally administering with flouroscopiccontrol. Streptokinase,urokinase,tPA (alteplase)
  42. 42.  Lepirudin or aragatroban Used when heparin is contra indicated due toHIT(heparin induced thombocytopenia)
  43. 43.  LOW RISK: young pts ,minor illness, surgerylasting <30 mt with no risk factors MODERATE RISK: >40yrs with deblitatingillness undergoing major surgery but no riskfactors HIGH RISK: >40 yrs with serious medicalcondition undergoing major surgery withadditional risk factors
  44. 44.  YES - Overall reduction in DVT and PE is by 40%to 60%
  45. 45.  Three pronged approach Designed to address stasis & coagulation Usually combination of therapiesI. EARLY MOVT & REHABLITATIONII. MECHANICAL METHODSlower extremity exercisesgraded compression stockings
  46. 46. intermittent pneumatic compression devicesCPMIII PHARMACOLOGICAL PROPHYLAXISa) ASPIRINeasy to administerlow costfew bleeding complications
  47. 47.  Most commonly used Takes 36 hrs to start action Started day before surgery Low doses are usedLOW MOLECULAR WT HEPARIN More effective than conventional Lesser bleeding
  48. 48.  Low molecular wt heparinoid For pts with HITFondaparinux Synthetic pentasaccharide
  49. 49.  Graduated compression stockings Exercise Avoid alcohol &sleeping tabletsHIGH RISK PATIENTS LMWH ,single dose SC before the flight
  50. 50.  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 importantin upper limb
  51. 51.  Early - ProgressionPulmonaryembolism Paradoxicalembolism Acutecompartment syndrome venous gangrene Late - Rec DVT, Post phlebitic syndrome
  52. 52.  Special group of pts very high risk for DVT & may reach up to 60 to 80% without 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 mostcommon cause for emergency readmission anddeath in joint replacement pts
  53. 53.  •Pre-op Immobilization (stasis)•Trigger of tissue factorreamed products (THR)tissue debris ,fat  activation ofcoagulation• Distortion of Femoral and Poplietal viensretraction,twisting,manipulation –damage to vessel wall•Prolonged post-op Immobilization.
  54. 54.  THR, TKR Hip fracture surgery Spine surgery [ malignancy, neurological deficit]
  55. 55.  Although thromboprophylaxis is routinely givento patients who undergo major orthopedicsurgery, it is usually stopped at discharge. Coagulation cascade remains abnormal upto 4weeks. Risk of propagation of the DVT, and PE,remains active during this period. Patients undergoing THA TKA or HFS receiveThromboprophylaxis with LMWH Fondaparinuxor VKA for a minimum of ten days. [can be cont.for 4 – 5 wks]
  56. 56.  Not an uncommon condition in clinical practice DVT OCCURS ONLY IN POST-OP PATIENTS’ IS A MYTH Awareness is most important for early diagnosis Prompt treatment can prevent lethal complications Diagnosis can be made using noninvasive methods Long term follow up is necessary to identify patientswho develop chronic venous insufficiency.