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  1. 1. DEEP VENOUS THROMBOSIS Prof. M.C.Bansal MBBS;MS. MICOG . FICOG. Founder Principal & Controller, Jhalawar Medical College & Hospital , Jhalawar. Ex Principal & controller , Mahatma Gandhi Medical College & Hospital, Sitapura , Jaipur.
  2. 2. Definition Deep venous thrombosis is the formation of a semisolid coagulum within flowing blood in any of the deep veins of the body, usually in the lower limb or Pelvic veins.
  3. 3. VEINS OF LOWER LIMB Superficial veins Deep veins Perforating veins Superficial veins includes great and small sephanous veins and their tributaries. They drain into deep veins through perforating veins. The greater saphenous vein joins the femoral vein at a fixed point in the groin 2.5 cm below and lateral to the pubic tubercle, and the lesser saphenous vein terminates at a variable site in the popliteal fossa. Blood passing up the superficial veins enters the deep veins at the saphenopopliteal and saphenofemoral junctions..
  4. 4. Superficial veins
  5. 5. Deep Calf Veins The deep veins of the lower limb arise from three pairs of venae commitantes, which accompany the three cruralarteries(anterior and posterior tibial and peroneal arteries) These six veins intercommunicate and join in the popliteal fossa to form the popliteal vein, which also receives the soleal and gastrocnemius veins. .
  6. 6. Deep veins
  7. 7. Perforating Veins Of leg Perforating veins- connect superficial veins with deep veins. Perforators- 1-adductor canal perforator, 2-below knee peforator, 3- medial perforator, 4-lateral perforator
  8. 8. Deep Veins of Thigh The popliteal vein passes up through the adductor hiatus to enter the subsartorial canal as the femoral vein, which receives the deep (profunda) femoral vein (or veins) in the femoral triangle before passing behind the inguinal ligament to become the external iliac vein.
  9. 9. Pelvic Veins (MAJOR )  The internal iliac vein joins with the external iliac vein in the pelvis to form the common iliac vein. The left common iliac vein passes behind the right common iliac artery to join the right common iliac vein on the right side of the abdominal aorta to form the inferior vena cava.
  10. 10. ETIOLOGY DVT usually originates in the lower extremity venous system ,starting at the calf vein and progressing proximally to involve popliteal ,femoral ,or iliac system. 80 -90 % pulmonary emboli originates here .
  11. 11. Virchow’s triad More than 100 years ago, Virchow described a triad of factors for the development of venous thrombosis- venous stasis, endothelial damage, and  hypercoagulable state
  12. 12. Venous stasis –Favoured by  Age---Incidence increases with advancing age  Obesity-- >BMI > is DVT  Prolonged bed rest (4 days or more)  A cast on the leg  Limb paralysis from stroke or spinal cord injury  Extended travel in a vehicle/Aeroplane
  13. 13. Hypercoagulability Surgery and trauma are responsible for up to 40% of all thromboembolic disease Malignancy Increased estrogen (due to a fall in protein ‘S) Increased estrogen occurs during as in pregnancy and HRT,OCP Taking women. Hyper coagulabilty status -Through out pregnancy— -the first three months postpartum, -after elective abortion, and  during treatment with oral contraceptive pills
  14. 14. Inherited disorders of coagulation  deficiencies of protein ‘S,  protein ‘C,’ and  antithrombin III.
  15. 15. Acquired disorders of coagulation nephrotic syndrome – results in urinary loss of antithrombin III, this diagnosis should be considered in children presenting with thromboembolic disease Antiphospholipid antibodies- accelerate coagulation and include the lupus anticoagulant and anticardiolipin antibodies.
  16. 16. >Inflammatory processes, such as • systemic lupus erythematosus (SLE) •sickle cell disease, •inflammatory bowel disease (IBD), also predispose to thrombosis, presumably due to hyper coagulability •
  17. 17. Endothelial Injury Trauma,  surgery, and  invasive procedure may disrupt venous integrity Iatrogenic causes of venous thrombosis are increasing due to the widespread use of central venous catheters, particularly subclavian and internal jugular lines. These lines are an important cause of upper extremity DVT, particularly in children . Femoral vein cannulation and Vene section for Iv therapy (prolong duration ) predispose for DVT
  18. 18. Clinical Pathophysiology -> An intimal defect often works sThe nidus works as a nidus for clot is Formation. -> initially a platelet aggregate, -ate develops . ->subsequently clotting factors through intrinsic and extrinsic pathway fibrin and red cells Cells form a mesh until the lumen clot occludes the vein. wall occludes.
  19. 19. When a clot forms on an intimal defect, the coagulation cascade promotes clot to growth proximally. Thrombus can extend from the superficial veins into the deep veins and after detachment passes through venacava, through the right heart and from which it can embolize to one or both the lungs via pulmonary arteries.
  20. 20. Opposing the coagulation cascade is the endogenous fibrinolytic system. After the clot organizes or dissolves, most veins will recanalize in several weeks. Residual clots retract as fibroblasts and capillary development lead to intimal thickening.  Venous hypertension and residual clot may destroy valves, leading to the postphlebitic syndrome, which develops within 5-10 years
  21. 21. Edema, sclerosis, and ulceration characterize this syndrome, which develops in 40-80% of patients with DVT.  patients also can suffer exacerbations of swelling and pain, probably as a result of venous dilatation and hypertension Pulmonary embolism (PE) is a serious complication of DVT. Many episodes of pulmonary embolism go unrecognized, and at least 40% of patients with DVT have clinically silent PE.
  22. 22. An Organised Clot (c) Thrombus ( T)
  23. 23. Presentation and Physical Examination Calf pain or tenderness, or both in one or both the lower limbs Swelling with pitting edema 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
  24. 24. DVT Both Legs
  25. 25. DVT—Left Leg
  26. 26. Venous thrombosis---causing venous gangrene
  27. 27. Palpate distal pulses and evaluate capillary refill to assess limb perfusion. Move and palpate all joints to detect acute arthritis or other joint pathology. Homan’s test: pain in the posterior calf or knee with forced dorsi flexion of the foot.
  28. 28. Moses Test: tenderness over calf muscles on squeezing the muscles from side to side. Not done now for the fear of embolism Bilateral DVT is common, up to 30% of all cases of DVT. Bilateral DVT should be differentiated from other systemic edema, such as hypo protienaemia, renal failure and heart failure etc.
  29. 29. Many patients report as they develop respiratory symptoms of PE so search for signs of PE such as plueritic chest pain, haemoptysis,tachycardia (common),tachypnea and central cynosis.
  30. 30. Pelvic vein thrombisis
  31. 31. venography gold standard” modality for the diagnosis of DVT Advantages Venography is also useful if the patient has a high clinical probability of thrombosis and a negative ultrasound,  it is also valuable in symptomatic patients with a history of prior thrombosis in whom the ultrasound is non-diagnostic.
  32. 32. side effects phlebitis anaphylaxis
  33. 33. RADIOACTIVE FIBRINOGEN TEST A fibrinogen uptake test is a test that was used to detect deep vein thrombosis. Radioactive labeled fibrinogen (I-131, I- 125) is given which is incorporated in the thrombus. The thrombus can then be detected by scintigraphy.
  34. 34. Plethysmography Plethysmography measures change in lower extremity volume in response to certain stimuli. Impedance phlebography, or impedance plethysmography (IPG), is a non- invasive medical test that measures small changes in electrical resistance of the calf. These measurements reflect blood volume changes, and can indirectly indicate the presence or absence of venous thrombosis. This procedure provides an alternative to venography, which is invasive and requires a great deal of skill to execute adequately and interpret accurately.
  35. 35. Ultrasonography color-flow Duplex scanning is the imaging test of choice for patients with suspected DVT inexpensive,  noninvasive, widely available Ultrasound can also distinguish other causes of leg swelling, such as tumor, popliteal cyst, abscess, aneurysm, or hematoma.     
  36. 36. Colour Dropller –Aeroes showing DVT
  37. 37. clinical limitations expensive 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
  38. 38. Magnetic Resonance Imaging It detects limb, pelvis, and pulmonary thrombi and is 97% sensitive and 95% specific for DVT.  It distinguishes a mature from an immature clot.  MRI is safe in all stages of pregnancy.
  39. 39. DIFFERENTIAL DIAGNOSIS o Cellulitis o Thrombophlebitis o Arthritis o Asymmetric peripheral edema secondary to CHF, liver disease, renal failure, or nephrotic syndrome o Lymphangitis o Extrinsic compression of iliac vein secondary to tumor, hematoma, or abscess o Hematoma o Lymphoedema
  40. 40. 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
  41. 41. Management Using the pretest probability score calculated from the Wells Clinical Prediction rule, patients are classified into 3 risk groups—high, moderate, or low. The results from duplex ultrasound are incorporated as follows: If the patient is at high or moderate risk and the duplex ultrasound study is positive, treat for DVT.
  42. 42. If the patient is at high risk but the ultrasound study was negative, the patient still has a significant probability of DVT If the duplex study is negative and the patient is low risk, DVT has been ruled out. • When discordance exists between the pretest probability and the duplex study result, further evaluation is required.
  43. 43. a venogram is done to rule out a calf vein DVT surveillance with repeat clinical evaluation and ultrasound in 1 week. results of a D-dimer assay to guide management
  44. 44. EMERGENCY DEPARTMANT CARE The primary objectives of the treatment of DVT are to prevent pulmonary embolism, reduce morbidity, and  prevent or minimize the risk of developing the postphlebitic syndrome.
  45. 45. LINE OF MANAGEMENT Anticoagulation Thrombolytic therapy for DVT Surgery for DVT Filters for DVT Compression stockings
  46. 46. Anticoagulation Heparin prevents extension of the thrombus Heparin's anticoagulant effect is related directly to its activation of antithrombin III. Antithrombin III, the body's primary anticoagulant, inactivates thrombin and inhibits the activity of activated factor X in the coagulation process.
  47. 47. Heparin is a heterogeneous mixture of polysaccharide fragments with varying molecular weights but with similar biological activity. The larger fragments primarily interact with antithrombin III to inhibit thrombin.  The low molecular weight fragments exert their anticoagulant effect by inhibiting the activity of activated factor X. The hemorrhagic complications attributed to heparin are thought to arise from the larger higher molecular weight fragments.
  48. 48. The optimal regimen for the treatment of DVT is anticoagulation with heparin or a LMWH followed by full anticoagulation with oral warfarin for 3-6 months Warfarin therapy is overlapped with heparin for 4-5 days until the INR is therapeutically elevated to between 2-3.
  49. 49. After an initial bolus of 100 U/kg, a constant maintenance infusion of 20 U/kg is initiated. The aPTT is checked 6 hours after the bolus and adjusted accordingly. . The aPTT is repeated every 6 hours until 2 successive aPTTs are therapeutic. Thereafter, the aPTT is monitored every 24 hours as well as the hematocrit and platelet count.
  50. 50. Advantages of Low-Molecular-Weight Heparin Over Standard Unfractionated Heparin Superior bioavailability Superior or equivalent safety and efficacy Subcutaneous once- or twice-daily dosing Less phlebotomy (no monitoring/no intravenous line) Less thrombocytopenia Results are Earlier
  51. 51. At the present time, 3 LMWH preparations, Enoxaparin, Dalteparin, and Ardeparin
  52. 52. warfarin  Interferes with hepatic synthesis of vitamin K- dependent coagulation factors Dose must be individualized and adjusted to maintain INR between 2-3 Oral dose 2-10 mg/day caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis.
  53. 53. Duration of anticoagulation in patients with deep vein thrombosis Transient cause and no other risk factors: 3 months Idiopathic: 3-6 months Ongoing risk for example, malignancy: 6 - 12 months Recurrent pulmonary embolism or deep vein thrombosis: 6-12 months Patients with high risk of recurrent thrombosis : indefinite duration.
  54. 54. COMPLICATIONS Acute pulmonary embolism  Hemorrhagic complications Chronic venous insufficiency
  55. 55. Thrombolytic therapy for DVT Streptokinase Urokinase Advantages prompt resolution of symptoms, prevention of pulmonary embolism, restoration of normal venous circulation, preservation of venous valvular function, and prevention of postphlebitic syndrome. Heparin therapy and oral anticoagulant therapy always must follow a course of thrombolytics.
  56. 56. Thrombolytic therapy is not effective once the thrombus is adherent and begins to organize The hemorrhagic complications of thrombolytic therapy are formidable (about 3 times higher), including the small but potentially fatal risk of intracerebral hemorrhage.
  57. 57. Surgery for DVT Indications  when anticoagulant therapy is ineffective  or unsafe,  contraindicated. The major surgical procedures for DVT are clot removal (venous thrombectomy),femoral vein ligation and partial interruption of the inferior vena cava (insertion of inferior venacava filters) to prevent pulmonary embolism.
  58. 58. Filters for DVT Indications for insertion of an inferior vena cava filter Pulmonary embolism with contraindication to anticoagulation Recurrent pulmonary embolism despite adequate anticoagulation
  59. 59. Deep vein thrombosis with contraindication to anticoagulation Deep vein thrombosis in patients with pre-existing pulmonary hypertension Free floating thrombus in proximal vein Failure of existing filter device Post pulmonary embolectomy
  60. 60. Inferior vena cava filters reduce the rate of pulmonary embolism but have no effect on the other complications of deep vein thrombosis. Thrombolysis should be considered in patients with major proximal vein thrombosis and threatened venous infarction
  61. 61. Clot Filter in IVC
  62. 62. Compression stockings (routinely recommended
  63. 63. Prognosis All patients with proximal vein DVT are at long- term risk of developing chronic venous insufficiency. About 20% of untreated proximal (above the calf) DVTs progress to pulmonary emboli, and 10-20% of these are fatal. With aggressive anticoagulant therapy, the mortality is decreased 5- to 10-fold. DVT confined to the calf virtually never causes clinically significant emboli and thus does not require anticoagulation
  64. 64. PROPHYLAXIS Identify any patient who is at risk. Prevent dehydration. During operation avoid prolonged calf compression. Passive leg exercises should be encouraged whilst patient on bed. Foot end of bed should be elevated to increase venous return.
  65. 65. VTE in pregnancy
  66. 66. Diagnosis
  67. 67. D-DIMER
  68. 68. Compression ultrasonography
  69. 69. CT Pulmonary angiography vs. V/Q scan
  70. 70. CT Pulmonary angiography vs. V/Q scan
  71. 71. Treatment of VTE during pregnancy
  72. 72. Treatment of VTE during pregnancy
  73. 73. Treatment of VTE during pregnancy
  74. 74. Treatment of VTE during pregnancy
  75. 75. Treatment of VTE during pregnancy
  76. 76. Anticougulant therapy during labour and delivery
  77. 77. Anticougulant therapy during labour and delivery
  78. 78. Thrombolytic therapy
  79. 79. Vena cava filters
  80. 80. Prevention of VTE in pregnant women with previousVTE
  81. 81. stesis of bloosd flow---Pelvi congestion syndrome ---prone to get thrombosed