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By : Saad Gharaibeh Anwar Al-Kassar Samah Telfah Abd-elsalam Sleman Venous Thrombo-embolism (VTE) 1.

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Presentation on theme: "By : Saad Gharaibeh Anwar Al-Kassar Samah Telfah Abd-elsalam Sleman Venous Thrombo-embolism (VTE) 1."— Presentation transcript:

1 By : Saad Gharaibeh Anwar Al-Kassar Samah Telfah Abd-elsalam Sleman Venous Thrombo-embolism (VTE) 1

2 2 General definition : A disease state that results from blood clot formation within a vein Epidemiology : - Females more than males - Incidence of a first VT is 1.92 : 1000 /year  Incidence increases with age rule of 10s : In children = 1 : 100,000 / year In young adults = 1 : 10,000 /year In middle-aged = 1 : 1000 /year In elderly = 1 : 100 / year - recurrence rate = 3–10% per year.

3 Pathogenesis : Virchow’s triad 3

4 4 VTE risk factors : previous VTE

5 Risk factors of recurrence : 5

6 6 Presentation of VTE : 1- DVT (60%) 2- PE (35%) 3- other sites

7 Deep Vein Thrombosis (DVT) 7 Keep in mind : ( major risk factors ) 1.Hypercoagulable state (look for family hx) 2.Blood stasis (immobility) look for occupation or recent orthopedic surgery

8 8

9 Categories : 9 A- Upper extremity DVT Higher risk to develop Pulmonary Embolism (PE) B- Lower Extremity DVT More Common than DVT of upper extremity and divided into : 1- Proximal vein thrombosis : In which thrombosis involves the popliteal, femoral, or iliac veins 2- Distal (calf) vein thrombosis : In which thrombi remain confined to the deep calf veins N.B : proximal is more serious than distal …

10 DVT may be occlusive or non occlusive and the later being more serious because the clot haven’t established an inflammatory reaction from the vessel wall yet to stabilize itself so its more likely to propagate with the floating stream of venous blood (embolism ). The classical features of DVT relate to occlusive thrombus. Most pts who die from PE have non-occlusive thrombus and the leg is normal on clinical examination. 10

11 11 Presentation : 1- swelling – pitting Edema and it’s the most specific 2- leg pain in 50% of patients 3- Tenderness – in 75% of patients 4- Warmth or Erythema of skin over the area of thrombosis 5- Cyanosis – severe obstruction 6- May be the clinical symptoms of pulmonary embolism as the primary manifestation. In 10% of patients with confirmed DVT. (other : Varicose Viens, lipodermatosclerosis, ulceration)

12 12

13 History : 13  Age : increased risk with age  Previous attacks  any risk factors (HF, recent surgery, prolonged bed rest)  females : pregnancy, OCP, HRT, recurrent fetal loss in the second or third trimester  Family hx  Review of associated signs and symptoms

14 Examination : 14 extremities : - unilateral swelling with a difference in calf diameters(find a reference point to measure and compare bilaterally –eg:10cm below tibial tuberosity or mid point from tibial tunirosity to medial malulous ), warmth, tenderness, erythema, superficial venous dilation. - discoloration. - Tenderness on deep palpation of the calf muscles (suggestive only) Homan's sign: It has fallen out of favor because a positive sign does not indicate DVT and a negative sign does not rule it out. A positive sign is present when there is pain in the calf on forceful and abrupt dorsiflexion of the patient's foot at the ankle while the knee is extended.

15 15 Homan's sign

16 16  When you suspect DVT, only about 17-32 % actually have it  So.. The clinical manifestations are not enough and you need further investigations to confirm it as DVT

17 Investigations : 17 A) Labs : 1) Blood Tests ( Complete Blood Count(CBC), platelets count, Protein C and protein S levels, Antithrombin levels, Factor V Leiden mutation 2) Coagulation studies (PT, aPTT) 3) Liver function test (LFT), kidney function test (KFT) 4) Urinalysis. 5) D-dimer (more than 500 ng/ml) (FDP) : a small protein fragment present in the blood after a blood clot is degraded by fibrinolysisblood clotfibrinolysis

18 Proteins C and S Proteins C and S, work as a natural anticoagulant system Activated protein C (APC) inactivating proteins Factor V a and Factor VIII aFactor V aFactor VIII a Genatic or Acuired deficiencies Multiple mechanisms and/or drugs can lead to acquired deficiencies of these proteins: oral anticoagulation, liver disease, lupus erythematosus, nephrotic syndrome, pregnancy

19 19

20 20 ➢ (B) Imaging : 1- contrast venography (gold standard) : venogram is an x-ray test that involves injecting x-ray contrast material (dye) into a vein to shows how blood flows through the veins. The dye has to be injected constantly via a catheter, making it an invasive procedure

21 21 -Highly accurate but invasive

22 2- U/S :Doppler ultrasound. -We look for non-compressibility of the vein by the probe (handle) of U/S <<which means there is thrombus. -This test works mainly for popliteal and femoral veins 22

23 23 Normal US (Veins Compressed)

24 24 Uncompressed vein

25 25 CT venography showing bilateral deep venous thrombosis. 3-CT venography

26 26

27 27 Treatment : 1- drugs ( Anticoagulants, Thrombolytic agents ) 2- surgery ( Thrombectomy, Filters ) 3- prophylaxis ( Compression stockings )

28 Drugs Anticoagulants : 28 1-Heparin & Warfarin 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. INR is useful for guiding the management of patients with known DVT who are on warfarin

29 29 2- thrombolytic agents : (Streptokinase, alteplase, reteplase). Thrombolytic therapy does not prevent - Clot propagation, -Rethrombosis, -Subsequent embolization.

30 30 Prophylaxis + with anticoagulent therapy pts. Should be encoraged to walk  compression stocking :


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