1. Vascular disesases L. Yu. Ivashchuk.

2. The varicose veins is the disease which is characterized by nonreversible progressing changes in superficial, perforating and deep veins, and clinically manifests by the dilation of superficial veins of the inferior extremities VARICOSITY

3. Epidemiology Varicosity is the most widespread disease among the vascular pathology. Aproximately 20 % of male and 40 % of female population suffer from different forms of varicosity. 50 % of patients are the people before aged from 20 to 60, furthermore, 10-15 % of this pathology occurs in school children. The cost of treatment of varicosity in UK is 2000-4000 € consisting annually of 2 % of national budget of the country.

4. Etiology Hereditary factors (60 %) Congenital weakness of the vascular connective tissue, anatomical insufficiency of venous valves Endocrine factors Pubertal and climacteric age, pregnancy, labor Obesity Excess weight on 20 kg increases the risk of varicosity in 5 times. Mode of life Prolonged standing, hot environment, increased intraabdominal pressure, weightlifting varicosity is the consequence of the human vertical standing position

6. Factors of normal venous hemodynamic Venous vascular tonus Venous valves Muscular contractions Arterial pressure, arterio-venous fistulae Negative diaphragmatic pressure, breathing movements Arterial pulsation Intraabdominal pressure

7. Pathogenesis

8. Increased venous pressure Dilatation of superficial veins Valvular incompetence Intravascular stagnation of venous blood Sclerosis of venous wall and valves Dilatation of perforating veins Edema, extravasal exudation Dilatation of deep veins, venous microcirculatory congestion Lipodermatosclerosis, dermatitis, eczema, hyperpigmentation Trophic ulcer

9. CLINIC 60-80 % of varicosity represents only cosmetic disturbances “Heavy leg” sensation Edema Hyperpigmentation Lipodermatosclerosis (indurative cellulitis) Eczema Trophic ulcer

11. І stage – heavy sensation; ІI stage – transitory or persistent edema, lipodermatosclerosis, hyperpigmentation; ІII stage – trophic ulcer (open or healed). Classification

14. Anamnesis Objective examination General blood and urine analyses Coagulogram Functional tests for definition of the state of a valvular system of superficial, deep and perforating veins Dopplerography Colour-flow duplex imaging Phlebography Diagnostic

15. The cause of varicosity (the state of deep veins) The presence of saphenofemoral and saphenopopliteal reflux Localization of saphenopopliteal junction The valvular state of great and small saphenous veins The presence of perforating reflux and its localization AIM OF THE DIAGNOSTICS

18. Differential diagnosis Postthrombotic disease Arterio-venous fistulas Venous angiodysplasia

19. Treatment Conservative treatment Sclerosing therapy Surgery

20. MEDICAMENTAL TREATMENT Aim: Exclusion of the risk factors ( correction of job overload, diet ) Improving of the venous wall nutrition and venous outflow Correction of microcirculation, rheology and lymph outflow Arrest of inflammatory reaction Trophic changes sanation

21. Conservative treatment Elastic bandage Phlebotonics (detralex, phlebodia, venoplant, hincor-forte) Antiinflammatory therapy (diclofenac Na, mesulid, naclofen) Physiotherapy (darsonvalization, ultraviolet insolation in suberythematous doses, laser therapy) Local therapy (antiseptics, curiosin, treatment of dermatitis and eczema)

22. І – 18,4-21,2 mm Hg ІІ – 25,1-32,1 mm Hg ІІІ – 36,4-46,5 mm Hg ІV – more than 59 mm Hg Elastic bandage

23. THE TREATMENT OF TROPHIC ULCERS Exclusion of the risk factors ( correction of job overload, diet ) Elastic bandage Correction of microcirculation, rheology and lymph outflow (phlebodia, detralex – double doses, enzymes) Antiinflammatory therapy (diclofenac Na, mesulid, naclofen) Physiotherapy (darsonvalization, ultraviolet insolation in suberythematous doses, laser therapy) Local therapy (antiseptics, curiosin) Surgical treatment (subfascial ligation of perforative veins by Linton, endoscopic subfascial clipping of perforative veins )

24. SCLEROSING TREATMENT Reticular varicosity Teleangiectases Varicosity relapse (diameter of vein less 4 mm) Complications Early (urticaria, allergic reactions, pain syndrome) Late (thrombophlebites, skin necrosis) Fibrovein 0.5 %, varicocid

26. SURGERY Saphenectomy

27. SURGERY

28. THE CAUSES OF VARICOSITY RELAPCE Diagnosis mistakes Secondary varicosity, arterio-venous fistulae, proxymal compression by tumour, scars. Technical errors Unligated and unremoved the trunk of v. Saphena magna Missed double or triple trunk of v. Saphena Long stump of v. Saphena magna Missed varicose trunk of v. Saphena parva Unligated incompetent perforative veins The mistakes in postoperative period Early refuse of elastic compression Obesity Prolonged standing job Job overload Repeated pregnancies

29. CHRONIC ARTERIAL ISCHEMIA

30.  Atherosclerosis  Obliterating endarteritis (obliterative thromboangitis, thrombangiitis obliterans)  Aorto-arteritis (Takayashu arteritis )  Diabetes mellitus  Raynaud's disease  Group of hypersensitive angiites, autoimmune angiopathy (mixed cryoglobulinemia, arteritis as a result of collagenous diseases: nodular periarteritis, dermatomyositis, systemic scleroderma)  Acute and blunt trauma with artherothrombosis Peripheral arterial disease generally results from atherosclerotic occlusion of the lower-limb arteries.

31. ATHEROSCLEROSIS OBLITERANS Atherosclerosis obliterans of the inferior extremities is a widespread disease, with a specific lesion of arteries of elastic and muscular-elastic types as a focal growth of connecting tissue with a lipid infiltration of intima. It results in disturbances of a circulation in tissues.

32. Epidemiology Symptomless peripheral arterial disease is very common, with a prevalence on non-invasive testing of up to 25 % in men older than 50 years. Population surveys have reported a prevalence of intermittent claudication between 1 % and 7 % for men aged 50-75 years. Symptomatic peripheral arterial disease is two to five times more common in men than in women. The incidence of chronic critical ischaemia is around 50- 100 per 100000 per year, which translates to about 20000 patients presenting per year in the UK.

33. Natural course As a result of the generalised nature of the arterial disease, patients with intermittent claudication have a mortality rate 2-3 times higher than age-matched, sex-matched controls. Men with intermittent claudication have 5-year cumulative mortality rates of around 15 %. 70 % of patients dye in 5-year period after the amputation. Among prognostic factors which associate with increasing of mortality, consider the severity of lower- limb ischaemia, presence of coronary or cerebrovascular disease, hypertension, and diabetes mellitus.

34. Natural course Critical ischaemia is associated with a high rate of death and limb loss. Very poor outcomes have been reported for patients with chronic critical ischaemia treated conservatively. In one report of more than 100 patients with critical ischaemia, unsuitable for reconstruction, only 28 % of patients were alive without amputation at 1 year.

35. Etiology (risk factors) Smoking Obesity Hyperlipidemia Diabetes mellitus Hypertension

36. Risk factors Low density lipoproteins modification Damage of endothelium Increase of lipid peroxidation Increase of inflammatory mediators Block of creation and biologic properties of NO Monocyte and macrophag activation IL-1, IL-6, growth factors release Migration and proliferation of smooth muscle cells in intima Exudation, proliferation, fibrosis, calcinosis

37. Arterial stenosis Collateral compensation Decreasing of intravascular pressure Microcirculatory disturbances Tissue acidosisCapillary atony Hypoxia Arterio-venous fistula Increase of blood coagulation EdemaPain Trophic changes Necrosis and gangrene Pathogenesis

38. І stage – complete compensation (coldness, fatigue, paresthesias); ІІ stage –functional circulatory insufficiency (a leading sign - intermittent claudication); II A st. - intermittent claudication 200-500 m II B st. - intermittent claudication less than 200 m ІІІ stage – ischemia of extremity at rest (a leading sign – rest or night pain); III A st. - ankle pressure less than 50 mm Hg III B st. - ankle pressure less than 30 mm Hg ІV stage – considerably expressed destruction of tissues of the distal parts of extremity (ulcers, necrosis, gangrene). Classification (according to A. Fountain, 1954)

39. Symptomatology and clinical course Coldness Intermittent claudication Color changes of skin Impaired pulsation Trophic changes Edema Ulceration and gangrene

44. Lerishe’s syndrome Absence of pulsation Intermittent claudication Impotence

45. Severe pain at rest Ulceration or gangrene A low ankle arterial pressure (<50 mm hg) Permanent sitting position for pain relief Ortostatic edema of lower leg. Patients with critical ischaemia inevitably require amputation if treated conservatively, whereas more than 25 % of those with subcritical ischaemia retain the leg without intervention. Critical ischaemia

46. Diagnostic Complaints, anamnesis Examination of extremities. Palpation, auscultation of vessels. Coagulogram. Biochemical analysis of blood (cholesterol, triglycerides, lipids). Rheovasography. Dopplerography of vessels. Arteriography.

47. Duplex imaging

48. Measurement of the sphygmomanometer cuff pressure at which blood flow becomes detectable by doppler in the posterior tibial artery and dorsalis pedis artery gives a valuable guide to the severity of arterial disease. Readings are commonly expressed as the ankle/brachial pressure index (ABPI). This index allows comparison between patients and, more importantly, sequential recordings can monitor disease progress. Intermittent claudication is commonly associated with an ABPI of between 0.5 and 0.9. Critical ischaemia is usually associated with an ankle pressure of less than 50 mm Hg. Doppler ankle pressure

50. Traditionally, surgical or endovascular intervention has been considered only after intra-arterial angiography. By means of digital subtraction, high-quality images are obtained and small volumes of contrast are required. However, angiography is an invasive procedure, associated with complications, and bed rest is required after the procedure. Common practice in some vascular units is now to plan angioplasty and even peripheral revascularisation on the basis of duplex imaging alone. Intraoperative angiography may be useful to visualise calf arteries in patients with severe proximal disease since the flow in these vessels is difficult to detect with duplex. Angiography

55. Magnetic resonance angiography Spiral computed tomographic angiography Newer imaging methods

56. Magnetic resonance angiography Spiral computed tomographic angiography Newer imaging methods

57. Differential diagnosis Endarteritis obliterans Ishioradiculitis Diabetic angiopathy Nonspecific aorto-arteriitis

58. Complications Arterial thrombosis Aneurysm Gangrene

59. Arterial thrombosis

60. Aneurysm Pulsating elastic formation with systolic murmur over it

61. Gangrene

62. Conservative therapy The goal of the treatment of obliterating endarteriitis consists of the renewal or improvement of capillary circulation. This problem could be solved by: 1) improving of blood rheology; 2) improving of peripheral macrohemodynamics, particularly by reducing of the arterio-venous dumping of blood (thus the application of spasmolytics is categorically contraindicated); 3) normalization of interaction between endothelium and formed elements of blood. Prostaglandins Antiaggregants Stimulators of metabolism Stimulators of rheology

63. Surgery Endarterectomy

64. Surgery Autovenous bypass

65. Surgery Prosthetic graft repairing

66. Surgery Plastic of deep femoral artery