1. الجامعة السورية الدولية الخاصة للعلوم و التكنولوجيا M.A.Kubtan1 كلية الطب البشري قسم الجـراحـة الدكــتـور عاصم قبطان MD – FRCS www.surgi-guide.com 1 st lecture

2. Peripheral Vascular Disease M.A.Kubtan2

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16. Continue Contraceptive hormonal therapy M.A.Kubtan16

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20. Clinical Features VVs rarely cause sever symptoms. Aching in the veins at the end of the day after prolonged standing. Ankle swelling. Itching. Bleeding. Superficial thrombophlebitis. Eczema. Lipodermatosclerosis. Ulceration. M.A.Kubtan20

21. M.A.Kubtan21 Lipodermatosclerosis Eczema Ulceration Lipodermatosclerosis Ulceration

22. Signs of varicose veins The termination of long and short saphenous veins must be palpated. The presence of dilated trunk can be rolled back and forth. Percussion over the VVs may elicit an impulse tap by the fingers. A large VVs in the groin ( saphena varix ) may be visible. Gentle palpation during coughing may elicite a cough thrill. M.A.Kubtan22

23. M.A.Kubtan23 Saphena varix

24. M.A.Kubtan24 A torniquet test Trendilenburg test

25. Investigation Tourniquet test. Standared doppler examination. Duplex ultrasound imaging. Varicography. Venography. M.A.Kubtan25

26. M.A.Kubtan26 Duplex ultrasound imaging

27. M.A.Kubtan27 VVs connecting long and short SV Varicogram Perforator joining long SV to deep veins

28. M.A.Kubtan28 Venogram

29. Management of patients with varicose veins  Prevention ( avoid lengthy standing ).  Supportive measures (encourage exercises).  Elastic stockings ( lower pressure 30, higher pressure 12 ).  Sclerotherapy.  Ultrasound-guided foam sclerotherapy.  Surgery ( stripping of long or short saphenous vein,avulsion of varicose tributaries, ligation of perforators ). M.A.Kubtan29

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32. M.A.Kubtan32 Avulsion

33. Alternative technique Radiofrequency ablation ( using radiofrequency to destroy the endothelial lining ). Laser to cause endothelial damage. Endovenous laser ablation. M.A.Kubtan33

34. M.A.Kubtan34 Radiofrequency ablation

35. M.A.Kubtan35 Laser treatment for spider veins

36. Complication of VVs surgery Bruising. Sensory nerve injury ( saphenous nerve, sural nerve ). Recurrence. M.A.Kubtan36

37. الجامعة السورية الدولية الخاصة للعلوم و التكنولوجيا M.A.Kubtan37 كلية الطب البشري قسم الجـراحـة الدكــتـور عاصم قبطان MD – FRCS www.surgi-guide.com 2 nd lecture

38. M.A.Kubtan38 Venous thrombosis

39. Venous thrombus Is the formation of a semi-solid coagulum within flowing blood in the venous system. Venous thrombosis of the deep veins of the legs is complicated by the immediate risk of pulmonary embolus and sudden death. Subsequently, patients are at risk of developing a post thrombotic limb and venous ulceration. M.A.Kubtan39

40. Aetiology Virchow triad Changes in the vessel wall ( endothelial damage ). Stasis, which diminished blood flow through the veins. Coagulability of blood ( thrombophilia ). M.A.Kubtan40

41. Risk factors for venous thromboembolisim Patients factors : Age. Obesity. Varicose veins. Immobility. Pregnancy. Puerperium. High-dose oestrogen therapy. Previous deep vein thrombosis. Pulmonary embolism. Thrombophilia. M.A.Kubtan41

42. Continue Disease or surgical procedure : Trauma or surgery of pelvis, hip and lower limb. Malignancy, pelvic and abdominal metastasis Heart failure. Recent myocardial infarction. Paralysis of lower limb(s). Infection. Dehydration. M.A.Kubtan42

43. Continue Other risk factors Inflammatory bowel disease. Nephrotic syndrome. Polycythemia. Paroxismal nocturnal haemoglobinuria antibody or Lupus Anticoagulant. Behcet,s disease. Homocystinaemia. M.A.Kubtan43

44. M.A.Kubtan44 Clinical Pathology A thrombus often develops in the soleal veins of the calf. A. Initially as a primary platelet thrombus ( aggregate ). B. Coralline thrombus. C. Occluding thrombus. D. Consecutive clot to the next venous tributary.

45. M.A.Kubtan45 Methode of propagation in phlebothrombosis a) With thrombus formation at each entering tributary. b) Clotting mass in an extensive length of vein propagated clot.

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47. Pulmonary embolism The embolus arising from the lower leg veins becomes detached, passes through the large veins of the limb and vena cava. Through the right heart ( heart occlusion ). Lodges in the pulmonary arteries. Massive pulmonary embolus (total occlusion of pulmonary trunk). Partial pulmonary embolus affecting Rt or Lt pulmonary arteries. Recurrent micro emboli. Pyramidal shape infarcts. M.A.Kubtan47

48. Clinical Symptoms of DVT The most common presentation of DVT is : No symptoms. Pain in the calf muscles. Swelling in the calf muscles. May present with sudden symptoms of pulmonary embolism (pleuritic chest pain, haemoptysis, shortness of breath ). Bilateral DVT are relatively common occurring in 30% M.A.Kubtan48

49. Clinical signs of Iliac femoral vein thrombosis Swelling involving the whole length of lower limb. Phlegmasia alba dolens. Phlegmasia cerulia dolens. Venous gangrene. M.A.Kubtan49

50. Phlegmasia alba dolens PAD When the thrombosis involves only major deep venous channels of the extremity sparing collateral veins. The venous drainage is decreased but still present. These phases are reversible if proper measures are taken. M.A.Kubtan50

51. Phlegmasia cerulia dolens PCD The thrombosis extends to collateral veins, resulting in venous congestions with massive fluid sequestration and more significant edema. Without established gangrene. These phases are reversible if proper measures are taken. M.A.Kubtan51

52. Physical signs of DVT May be absent or ephermeral. Mild pitting oedema of the ankle. Dilated surface veins. Stiff calf and tenderness over the course of deep veins. Homans sign ( resistance of calf muscles to forcible dorsiflexion ) might be misleading. Low grade pyrexia may be present, especially in a patient who is having repeated pulmonary emboli. Patient may develop signs of cyanosis and dyspnoea, raised neck veins, split second heart sound, pleural rub in PE. M.A.Kubtan52

53. A foot with venous gangrene. The gangrene is symmetrical involving all the toes. There is no clear – cut edge and there is marked oedema of the foot. M.A.Kubtan53

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55. Investigation M.A.Kubtan55 Early Diagnosis of DVT D-dimer is a fibrin degradation product (FDP ). D-dimer is a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis. D-dimer measurment if withen normal range it rules out the diagnosis of DVT or Pulmonary embolus and there is no indication for further investigation. If raised, a duplex ultrasound examination of the DVT. Ascending venography ( now rarely required ).

56. Transverse section of duplex scan of vein containing a thrombus M.A.Kubtan 56

57. An ascending venogram of DVT seen as filling defects ( arrows ) with contrast passing around the thrombus M.A.Kubtan57

58. Diagnosis of pulmonary embolus Ventilation-perfusion scanning, which mismatched defect. Computerised tomography CT. Pulmonary angiography ( rarely required ). M.A.Kubtan58

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60. Ventilation – perfusion lung scan showing unmatched filling defects on the perfusion scan. (a) Ventilation, (b) Perfusion. M.A.Kubtan60

61. CT scan showing pulmonary emboli as a filling defects in the pulmonary artery. M.A.Kubtan61

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64. The differential diagnosis of DVT Ruptured Baker,s cyst. Calf muscle haematoma. Ruptured plantaris muscle. Thrombosed popliteal aneurysm. Arterial ischaemia. M.A.Kubtan64

65. Classification of risky patients Low risk : young, minor illnesses, who are to undergo 30 min or less surgery. Moderate risk : over the age of 40,or those with debilitating illness who are to undergo major surgery. High risk : those who are over the age of 40, who have serious accompanying medical condition ( stroke, MI, past history of DVT, known malignant disease ). M.A.Kubtan65

66. Prevention and prophylaxis Mechanical approach. Pharmacological approach. M.A.Kubtan66

67. Mechanical approach Lower limbs elevation. Graduated elastic compression stockings. External pneumatic compression pump. M.A.Kubtan67

68. M.A.Kubtan68 Anti – embolism thigh compression stockings Anti embolic knee compression stockings

69. External pneumatic compression M.A.Kubtan69

70. Pharmacological approach More effective than mechanical method in reducing the risk of thrombosis. They carry an increased risk of bleeding. Most patients at risk should start on low molecular weight Heparin given subcutaneously. The amount of given heparin based on the patients body weight. This treatment does not require PTT monitoring,and has reduced risk of developing thrombocytopenia. It can be given once daily and has lower risk of bleeding. M.A.Kubtan70

71. Treatment of a deep vein thrombosis Intravenous sodium heparin by heparin pump after loading dose and PTT monitoring. Subcutaneous low molecular heparin without PTT monitoring. Rapid oral anticoagulation with warfarin. Warfarin given loading dose for 3 days after measuring prothrombin time. Complete bed rest followed by ambulation. M.A.Kubtan71

72. Thrombolysis of DVT By using streptokinase or uorokinase. Should be considered in patients with an iliac vein thrombosis if they are seen in the early stages. When the limb is extremely swollen. M.A.Kubtan72

73. Invasive approach to DVT Rarely carried out in Iliac and femoral vein thrombosis In case of patient with the risk of developing venous gangrene. In patient developing phlegmasia cerulia dolen. If it,s been performed it should be accopmpanid by arterio-venous fistula at the PT level. Trans venous stent deployment. Greenfield umbrella. M.A.Kubtan73

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75. Treatment of pulmonary embolus Multiple and recurrent micro emboli's can be treated by anticoagulation and observation. Those with sever onset who develop sever heart strain and shortness of breath indicates the need for fibrinolytic treatment. Surgical pulmonary embolectomy may not save the patient from his or her fate. M.A.Kubtan75

76. Superfacial thrombophlebitis Implies a major inflammatory component. Common causes include external trauma especially to VVs. Venopuncture and infusion of hyperosmolor solution and drugs. Thrombo angitisobliterance ( Buerger disease) M.A.Kubtan76

77. الجامعة السورية الدولية الخاصة للعلوم و التكنولوجيا M.A.Kubtan77 كلية الطب البشري قسم الجـراحـة الدكــتـور عاصم قبطان MD – FRCS www.surgi-guide.com 3rd lecture

78. Leg Ulceration Venous disease is responsible for 60 – 70% of legs ulcers. Arterial iscaemic ulcers. Rheumatoid ulcers. Traumatic ulcers. Neuropathic ulcers ( Squamous cell carcinoma and Basal cell carcinoma ). M.A.Kubtan78

79. Aetiology of ulceration Ambulatory venous hypertension regarded as the cause of ulceration. The venous hypertension may be the result of primary valve incompetence. Incompetence of the perforating veins. Obstruction of deep veins. M.A.Kubtan79

80. Clinical features A venous ulcer has gently sloping edge and the base contains granulation tissue. Any elevation of the ulcer edge should indicate the need for biopsy. Venous ulcer of the leg usually develop in the skin of the gaiter region, which is rich in perforators. M.A.Kubtan80

81. Continue The majority ob venous ulcers develop on the medial side of the calf. Ulcers associated with lesser saphenous incompetence often develop on the lateral side of the leg. Ulcer can develop on any part of the calf skin in patients with post DVT syndrome. Venous ulcer rarely develop on the foot or into the upper calf. Almost all venous ulcers have surounding lipodermatosclerosis. M.A.Kubtan81

82. M.A.Kubtan82 Venous ulcer at the gaiter areaMarjolin ulcer arising from venous ulcer

83. Investigation Duplex scan. Full blood count. ESR. CRP. Sickle cell test. Bipedal ascending phlebography ( detection of DVT ). M.A.Kubtan83

84. Management Elevation of legs. Bandaging ( Elastic compression bandage ). Excision and grafting. Biological dressing.( amniotic membrane ). Skin graft. M.A.Kubtan84

85. Congenital anomalies Aplasia. Hypoplasia. Duplication. Persistance of vestigeal vessels. M.A.Kubtan85

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