Chronic Venous Insufficiency and Varicosity

every thing about venous insufficiency, its causes, pathophysiology, diagnosis and management.

1. Chronic Venous Insufficiency & varices Dr. Pezhman Kharazm Assistant Professor of Vascular Surgery G olestan University of Medical sciences

2. Today’s objectives To know anatomy of venous system To describe the physiology of venous system To know p athophysiology of CVI To diagnose Clinical Manifestations of CVI To name p ara clinic investigations in CVI To m anage patients with CVI

3. Lower extremity venous anatomy Cross sectional

4. Lower extremity venous anatomy L ongitudinal Small Saphenous Vein (S.S.V) Great Saphenous Vein (G.S.V) Perforating Veins (P.V)

5. Determinants of Venous Flow Direction Transmitted arterial pressure

6. Muscle Pump

7. Venous Insufficiency Insufficiency contributes to: Reflux

8. Reflux is the keyword of the CVI and occurs secondary to: Valvular incompetency

9. Valvular incompetency Types: Primary Secondary Causes: Primary Hereditary Senile Trauma Thrombosis AVF/AVM

10. C.V.I Risk Factors Advanced age .................. Height ......................... Pregnancy ....................

11. C.V.I Risk Factors (cont.) Obesity…………….. Smoking…………… Family history..........

12. C.V.I Risk Factors (cont .)   Prolonged standing.......... Female sex........

13. Pathophysiology: Everything starts with venous hypertension! But How?

14. Standing position + reflux = venous drainage problem Same inflow + less outflow = volume overload in venous system = venous hypertension

15. Pathophysiology V enous hypertension at first results in venous dilation for pooling more blood Clinical manifestation: Heaviness and warmness of the involved limb which resolves with limb elevation and upward massage.

16. Next step: S mall veins start to elongation and twisting in addition to dilation. Pathophysiology Clinical manifestation: Telangiectasia and reticular veins (grade 1) Varicosity (grade 2) Varicose veins are not present in all cases of chronic venous insufficiency

17. Next step: N o more pooling is possible: endothelial gapping and fluid extravasation occurs. Clinical manifestation: Edema

18. Next step: Intercellular gap enlargement allows larger molecules such as proteins and blood cells leave the vessel lumen. Clinical manifestation: Hyperpigmentation lipodermatosclerosis

19. And at last : Ulceration is the final result of this pathologic process.

20. Diagnostic Evaluation: History& physical examination: Consider risk factors Past medical history (DVT) D&H (IV. Drug abuse) Ph /E Detailed examination of the target limb

21. Physical Examination Adjuncts: Trendelenburg test Perthes test Inspection : Color Scar (GSV harvest) Edema Hyperpigmentation Ulcer Telangectasia , reticular & varicose veins Lipodermatosclerosis Auscultation : bruit Palpation : Warmness Pitting Thrill Distal pulses

22. Radiologic Studies: Purposes of the study: Detection of the existing thrombosis (S&D systems) Localization of the reflux point

23. After ruling out the thrombosis, localization of the “POINT OF REFLUX” is the key factor in CVI management.

24. Radiologic modalities: Detection of thrombosis: CT scan MRI Venography & IVUS Duplex Ultrasonography Localization of the reflux point: Venography & IVUS Duplex Ultrasonography

25. Duplex ultrasonography (DUS) is the most useful modality in diagnosis and management of the “CVI”

26. Principles of treatment Wound care Compression therapy Medical treatment Endovascular interventions Surgical treatments

27. Wound care Dressing Growth factors Skin grafts *** wound recurrence is inevitable, unless the venous hemodynamic is corrected

28. Compression *** Compression therapy is the mainstay of CVI management Elastic compression stockings ( 30-40 mm Hg for ulcers) Multilayer elastic wraps or dressings Pneumatic compression devices

29. Medical treatments Increasing venous wall strength (flavonoids, chest nut   oil) Increasing RBC flexibility (pentoxifylline) Decreasing blood coagulability (anti platelets and anticoagulants) ***Medications have a low grade of recommendation and only prescribed in conjunction with effective compression therapy

30. Interventions Purposes: Obstruction management Reflux elimination *** Failure of treatment and recurrence are the rule, unless these issues are taken into account

31. Obstruction management Endovascular management Surgical treatment

32. Reflux elimination Treatment is tailored based on point of reflux Superficial system reflux: Ablative Deep system reflux: Reconstructive Perforating vein reflux: Ablative

33. Superficial system reflux 1. Sapheno Femoral Junction (SFJ): Surgical ligation Stripping Chemical ablation Thermal ablation ( laser or radiofrequency)

34. Superficial system reflux 2. Sapheno Popliteal Junction (SPJ) Ligation Stripping ablation

35. Superficial system reflux Communicating veins & varicosities: (size dependent) Phlebectomy Sclerotherapy C utaneous laser

36. Deep system reflux Valve reconstruction Valve transplantation

37. Perforating vein reflux Ligation Cut SEPS

38. Summary Lower extremity venous system includes deep, superficial and perforating veins Cardiac pump, muscle contractions and venous valves are determinants of upward flow in venous system Reflux is the key factor in chronic venous insufficiency Edema, varicosity, hyperpigmentation and ulcer are clinical manifestations of CVI Compression therapy is the mainstay of management of CVI patients Elimination of the highest point of reflux is the key factor in successful treatment of CVI.

39. Thank You