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Venous diseases Zsolt Pécsvárady zspecs@chello.hu Pécs

Venous diseases Zsolt Pécsvárady zspecs@chello.hu Pécs. V . saphaena maga V . saphaena parva Main perfora tors Deep veins. I. Superficial thrombophlebitis Deep venous thrombosis and pulmonal embolisation III. Chronic venous insufficiency CVI. I. Superficial thrombophlebitis.

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Venous diseases Zsolt Pécsvárady zspecs@chello.hu Pécs

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  1. Venous diseases Zsolt Pécsvárady zspecs@chello.hu Pécs

  2. V. saphaena maga V. saphaena parva Main perforators Deep veins

  3. I. Superficial thrombophlebitis • Deep venous thrombosis • and pulmonal embolisation • III. Chronic venous insufficiency CVI

  4. I. Superficial thrombophlebitis • Varicophlebitis / -thrombosis • -Septic thrombophlebitis • - Catether phlebitis • Flebitis migrans: Unknown origin in different location. • Together with cancer, autoimmun or Buerger diseases. • - Mondor disease: Unknown origin with spontaneous healing. • associate with pancreas diseases. Hard, palpable veins. As these veins are not not flexible: stretching is painful It is a painful but not dangerous disease with quick recovery.

  5. II. Sign and symptoms of deep venous thrombosis- Oedema of dependent leg- Pain- Cyanosis- Shining skin- Superficial collateral veins- Acut developement of the symptoms- Pain to press of deep veins, muscles around them- „Cord” feeling of thrombotic vein- Dorsalflexion of calf can cause pain in the gastrocnemic muscles ( Homans-sign ) - Inflate of the BP meter (on both calves) can cause pain in the dependent leg (Lowenberg jel)

  6. Probability of DVT based on medical history and physical exminationClinical condition Score • active cancer 1 • plegia, plaster in the near past 1 • immobility or maior operation in the near past 1 • pressure sensitivity in the location of deep veins 1 • swelling of the whole leg 1 • >3 cm difference between the diameter of calves 1 • oedema 1 • collateral superficial veins 1 probability of other diagnosis -2High probability >3; medium probability 1-2; Low probability 0 (Wels és munkatársai Lancet 1997; 350-1795)

  7. Non invasive diagnosis of DVT CUS= compression ultrasound test Negative predictive value for proximal DVT is 98% for distal DVT is just 40% Low probability medium probabilityhigh probability 3-10% 15-30% >70% CUS negativ CUS negativ -D-dimer + D-dimer + D-dimer DVT can exclude DVT p value 3-5% DVT p value 20-30% without CUS repeat CUS repeat CUS

  8. Risk factors for DVT I. • major orthopedic surgery ( hip, knee ) • malignant disease • trauma, postoperative condition • DVT or PE in medical history • immobilization • heart attack, heart failure • stroke or paralysis • infections, sepsis

  9. Risk factors for DVT II. • Age older than 40 yrs • Obesity • Varicositas • Oral contraceptive, oestrogen treatment, gravidity • Thrombophylia APC resistency, Protein C and S, antithrombin III. insufficiency. fibrin és plasminogen disturbances, myeloproliferatíve diseases • Other serious diseases ( heart, lung, inflammatory bowel disease etc. )

  10. III. Chronic venous insufficiency C V I

  11. Etiology of Primary Insufficiency Heredity: most important risk factor „ Varicose veins are the result of poorly selecting one’s grandparents” Sir William Osler MD

  12. Epidemiology of CVI - Varicositas in Europe: 25,2% - CVI in Europe: 1,7 % - Venous ulcer: 1 %

  13. CVI = venous hypertension Causes: - reflux ( insufficiency of valves ) - occlusion ( thrombosis ) - disturbed lymphatic circulation - disturbed muscle pump function

  14. C.V.I. Izom- pumpa

  15. Physiology of Venous Return Pump Calf muscles provide the force Sinusoidal veins as chambers Valves Maintain unidirectional flow Foot to heart Superficial to deep

  16. Classification: C. E. A. P.

  17. C.E.A.P. - clinical state (C), - etiology (E), - anatomical localization (A), - pathophysiology (P)

  18. CEAP Clinical State 0 – No visible venous disease 1 – Teleangiectasia or reticular veins 2 – Varicose veins 3 – Edema 4 – Skin changes 5 – Healed ulcer 6 – Active ulcer

  19. Etiology (E): Congenital ( Ec) Primer ( Ep) Secundaer ( Es )

  20. Anatomy ( AS, AD, AP ) Superficial ( A S ) Deep ( A D ) Perforators ( A P )

  21. Pathopysiology( PR, PO, PRO ) reflux (PR) 81 %, occlusion ( PO) 2 %, combination of these 17 %, ** 3.5x risk ** of signs

  22. Patterns of Reflux • Truncal reflux • saphenous related • up to 5/6 of varicose veins • Non-truncal Reflux • at least 1/6 of varicose veins • Deep and perforator reflux • Not common alone but increases • with severity of disease

  23. Venous tests: • Percussion test ( reflux ) • Trendelenburg test ( reflux ) • - Perthes test ( occlusio )

  24. Continous wave ( CW ) Doppler in venous diagnosis Proximalis “A sound” Distalis “A sound” Normal venous flow 0 + Reflux + + Distal occlusion 0 0 animáció

  25. Photo-plethysmography ( reflux ) Refilling time

  26. Strain-gauge plethysmography ( Occlusion )

  27. Color duplex ultrasound ( IVUS ? ) Valsalva manover Compression tests

  28. Phlebography Ascendaló Descendaló Varicography MR Venography ?

  29. Conclusions • CVI results from venous hypertension usually related • to primary reflux in the superficial veins • - Heredity is primary risk factor • Multiparity increases chance of its expression • - Stigmata can vary • Depends on veins involved • Cosmetic to limb threatening • Most patiens have symptoms • - Disease occurs in patterns • Categorization most important first step

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