Varicose veins .pptx

Varicose veins.

1. VARICOSE VEINS dr. mayank raj karn Resident 1 st year ( general surgery) 1

2. CONTENT 2

3. ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB Divided anatomically into The superficial venous system , located within the superficial tissues . T he deep venous system , beneath the deep fascia of the leg, accompanying the arterial tree . The superfcial veins drain into the deep system, either at junctions or via fascial P erforating veins . 3

4. DEEP VENOUS SYSTEM 4

5. 5

6. SUPERFICIAL VENOUS SYSTEM The superficial veins of the lower extremity form a network. The dorsal venous arch is continuous with T he Great Saphenous Vein (GSV) medially. T he Small Saphenous Vein (SSV) laterally. 6

7. GREAT SAPHENOUS VEIN 7

8. The GSV terminates into the S aphenofemoral junction , where it is joined by the confluence of T he superficial circumflex iliac veins, T he external pudendal veins, T he superficial epigastric veins . A scends in the superficial compartment and empties into the common femoral vein after entering the fossa ovalis . SFJ is approximately 2.5 cm below and lateral to the pubic tubercle. 8

9. SMALL SAPHENOUS VEIN 9

10. The SSV may extend cranially beyond the SPJ. Cranial extension of the SSV , which terminates by piercing the fascia in the posterior thigh to drain into the deep system. Giacomini vein , which communicates with the GSV system occasionally joining the GSV at or about the SFJ. 10

11. Perforating veins Connect the superficial venous system to the deep venous system by penetrating the fascial layers of the lower extremity . These perforators are also guarded by valves so that the blood flow is unidirectional, i.e . towards deep veins. Reversal of flow occurs due to incompetence of perforators which will lead to varicose veins. 11

12. Crockett perforators which connect the posterior arch and posterior tibial veins; Boyd perforators , which connect the great saphenous and gastrocnemius veins; Hunterian and Dodd perforators , which connect the great saphenous and superficial femoral veins. May or Kuster perforators ; Ankle 12

13. PHYSIOLOGY The venous pressure in a foot vein on standing is approximately 100 mmHg . To enable blood to be returned against gravity in the standing position a pressure gradient must exist between the veins in the leg and those in the chest . This gradient is created in two ways. The increase in thoracic volume during inspiration decreases intrathoracic pressure. T he pressure in the veins of the leg is increased by compression by the surrounding muscles (the ‘calf muscle pump’) and to a lesser extent the tone of the venous wall. 13

14. The net reduction in the pressure of the superficial system is dependent on T he presence of a pressure gradient between the leg and the thorax and A patent and compliant venous system containing competent valves. 14

15. VARICOSE VEINS They are dilated, tortuous, elongated veins in the leg . Epidemiology The adult prevalence of visible varicose veins is between 30% and 50 %. Gender: Higher prevalence in women than in men. Age : The prevalence of varicose veins increases with age . Ethnicity. Body mass and height. Pregnancy. Occupation and lifestyle factors: In smokers , in patients who suffer constipation and in those with occupations that involve prolonged standing. 15

16. AETIOPATHOGENESIS Aetiology Primary varicosities Congenital incompetence or absence of valves. Weakness or wasting of muscles—defective connective tissue and smooth muscle in the venous wall . Stretching of deep fascia. Inheritance (family history) with FOXC2 gene. Klippel-Trenaunay syndrome, avalvulia , Parkes-weber syndrome. 16

17. 2. Secondary varicosities Recurrent thrombophlebitis. Occupational—standing for long hours (traffic police, guards , sportsman). Obstruction to venous return like abdominal tumour , retroperitoneal fibrosis, lymphadenopathy, ascites, May– Thurner syndrome. Pregnancy (due to progesterone hormone), obesity, chronic constipation. AV malformations—congenital or acquired. Iliac vein thrombosis. Tricuspid valve incompetence. 17

18. An absence either a pressure gradient between the leg and the thorax and a patent and compliant venous system containing competent valves leads to , F urther vein wall damage, including loss of compliance, thickening, dilatation and valvular dysfunction. The development of all the clinical manifestations of Varicose veins can be ascribed to a blood flow driven inflammatory process. 18

19. Leukocytes are activated and marginalize . Adhesion to the endothelium is prompted by the expression of adhesion molecules, such as Intracellular Adhesion Molecule 1 (ICAM-1), Vascular Cell Adhesion Molecule 1(VCAM-1 ), L and P-selectins . D ysfunctional smooth muscle cell proliferation, collagen deposition. D ecreased elastin content and increased matrix metalloproteinases. These effects typically lead to loss of compliance, dilatation, elongation (causing tortuosity) and secondary valvular dysfunction. 19

20. CLASSIFCATION CEAP (Clinical– aEtiology –Anatomy–Pathophysiology ) For clinical classifcation : ● C0 : No signs of venous disease; ● C1 : Telangiectasia or reticular veins; ● C2 : Varicose veins; ● C3 : Eedema ; ● C4a : Pigmentation or eczema; ● C4b : LDS or atrophie blanche; ● C4c: Corona phlebectatica ● C5 : Healed venous ulcer; ● C6 : Active venous ulcer. 20 Clinical class can be further characterised as symptomatic (s), asymptomatic (a) or recurrent following previous successful treatment or healing (r), e.g. C2a, C2s, C6r .

21. 21

22. 22

23. 23

24. For aetiological classifcation : ● Ec : congenital; ● Ep : primary; ● Es : secondary (post-thrombotic); ● En : no venous cause identifed . For anatomical classifcation : ● As : superficial veins; ● Ap : perforator veins; ● Ad : deep veins; ● An : no venous location identifed . 24

25. For pathophysiological classifcation : ● Pr : reflux ; ● Po : obstruction; ● Pr,o : reflux and obstruction; ● Pn : no venous pathophysiology identifiable . 25

26. SYMPTOMS H eaviness , discomfort, and extremity fatigue. The discomforts usually relieved by leg elevation or elastic support. The pain is characteristically dull, is exacerbated in the afternoon, especially after periods of prolonged standing. Swelling Pruritus Patients may report cramping pain that occurs during or after exercise and is relieved with rest and leg elevation: Venous Claudication 26

27. SIGNS 27 Clinically obvious tortuous dilated subcutaneous veins. The distribution of varicosities may indicate which superfcial axis is defective M edial thigh and calf varicosities suggest GSV incompetence. P osterolateral calf varicosities are suggestive of SSV incompetence. Anterolateral thigh and calf varicosities may indicate isolated incompetence of the AAGSV.

28. 28

29. 29 Telangiectasia Reticular vein Saphena varix Corona phlebectatica (malleolar fare ) Oedema Eczema Pigmentation ( haemosiderosis ) Lipodermatosclerosis (LDS ) Atrophie blanche Venous ulcer

30. TESTS Brodie-Trendelenburg test Vein is emptied by elevation the limb and a tourniquet is tied just below the saphenofemoral junction (or using thumb, saphenofemoral junction is occluded). Patient is asked to stand quickly. Trendelenburg test I Tourniquet or thumb is released, rapid filling from above signifies saphenoemoral incompetence. Trendelenburg test II Tourniquet is not released . Filling of blood from below upwards rapidly can be observed within 30–60 seconds. It signifies perforator incompetence . 30

31. B) Fegan’s test The course of the great saphenous vein Is marked . The veins are emptied and the sites of known perforator area are palpated with a finger . The sites where perforators are incompetent and dilated a crescentic gap may be felt in the deep fascia. 31

32. C) Perthe’s test The affected lower limb is wrapped with elastic bandage and the patient is asked to walk around or exercise. Development of severe cramp like pain in the calf signifies DVT . D ) Modified Perthe’s test Tourniquet is tied just below the saphenofemoral junction without emptying the vein. Patient is allowed to have a brisk walk which precipitates bursting pain in the calf and also makes superficial veins more prominent . It signifies DVT. 32

33. E) Schwartz test In standing position, when lower part of the long saphenous vein in leg is tapped, impulse is felt at the saphenous junction or at the upper end of the visible part of the vein. It signifies continuous column of blood due to valvular incompetence . 33

34. F) Three tourniquet test To find out the site of incompetent perforator , three tourniquets are tied after emptying the vein.at S aphenofemoral junction. Above knee level. Another below knee level . Patient is asked to stand and looked for filling of veins and site of filling. Then tourniquets are released from below upwards , again to see for incompetent perforators. 34

35. G) Pratt’s test Esmarch bandage is applied to the leg from below upwards followed by a tourniquet at saphenofemoral junction. After that the bandage is released keeping the tourniquet in the same position to see the “blow outs” as perforators . H) Morrissey’s cough impulse test The leg is elevated and then the patient is asked to cough. If there is saphenofemoral incompetence, expansile impulse is felt at saphenous opening. 35

36. 36

37. INVESTIGATIONS Venous Doppler Doppler test: When a hand held Doppler ( continuous wave 8 MHz flow detector) is kept at SFJ, typical audible , ‘ whoosh signal’ >0.5 sec while performing Valsalva manoeuvre is the sign of reflux at SFJ . 2. Duplex scan First and best modality to assess for the normal function and presence of venous insufficiency of the lower extremities. Here high resolution B mode ultrasound imaging and Doppler ultrasound is used ). Examination is done in standing, lying down position and with valsalva manoeuvre . 37

38. The aim of the duplex scan in a patient with varicose veins is to establish T he presence of reflux in the deep and superfcial venous system ; T he exact distribution and extent of reflux in the superficial venous system including afected junctions and perforators; T he presence of obstruction in the deep venous system; 38

39. The suitability of the incompetent superficial veins for the different treatments available(based upon diameter, extent, tortuosity,saphena varix ); The presence of thrombus within the superficial veins ; An indication of a pelvic source of reflux or obstruction. 39

40. 40

41. 41

42. 3. Phlebography and Venography It is a noninvasive method which measures volume changes in the leg . It gives functional information on venous volume changes and calf muscle pump insufficiency. 42

43. 4. Transabdominal and Transvaginal Duplex 5. Magnetic Resonance and Computed Tomography Venous Imaging Done to investigate Pelvic and iliac veins. 43

44. Management Conservative treatment Lifestyle modification Elastic compression stocking application Limb elevation Unna boots Pneumatic compression method , provide dynamic sequential compression. These methods reduce the AVP , reduce transcapillary fluid leakage by increasing SC pressure and improve cutaneous microcirculation . 44

45. 2. Endothermal ablation The gold standard treatment Marginally safer, have extremely high technical efficacy , offer superior quality of life post procedure (with a rapid recovery) E quivalent improvements in quality of life in the longer term . 45

46. Treatment device is inserted into the incompetent axial vein percutaneously. The vein is surrounded by tumescent local anaesthetic solution . This compresses the vein onto the treatment device, emptying it of blood . It also hydro-dissects tissues such as nerves away from the zone of injury . The treatment device then produces thermal energy that destroys the structure of the vein, resulting in permanent occlusion. 46

47. Two broad technologies Laser Ablation Radiofrequency Ablation 47

48. 3. Non-endothermal , non-tumescent ablation Sclerotherapy The direct contact with detergent causes cellular death and initiates an infammatory response, A iming to result in thrombosis, fibrosis and obliteration (sclerosis). 48

49. Ultrasound-guided foam sclerotherapy The effcacy of UGFS is significantly worse than for endothermal ablation, leading to High reintervention rates, and the rates of complications Such as phlebitis and pigmentation can be high. 49

50. b. Catheter-directed sclerotherapy and mechanochemical ablation 50

51. B. Endovenous glue 51

52. 4. Open surgery Saphenofemoral ligation and great saphenous stripping S uperficial circumflex, superficial external pudendal , superficial epigastric vein. A flush SFJ ligation is then performed ( Trendelenburg operation) and the GSV retrogradely stripped to around the knee. 52

53. 53

54. B. Saphenopopliteal junction ligation and small saphenous stripping Stripping of the small saphenous vein is done from ankle below upwards after passing stripper from above downwards. 54

55. C . Phlebectomy ( Stab Avulsion) Performed following treatment of junctional incompetence and axial vein reflux. A s a sole treatment in patients with isolated tributary incompetence , or possibly in very early axial reflux. 55

56. D. Perforator ligation Subfascial ligation of Cockett and Dodd Linton’s vertical approach 56

57. 57

58. Recurrent varicose veins Approximately 10–20% of patients who present to hospital with varicose veins have had previous intervention . Significant clinical recurrence 5–10 years following varicose vein surgery occurs in 10–35% of patients. Causes of recurrence include N eovascularisation , R eflux in the residual axial vein, I nadequate initial surgery and N ew junctional reflux 58

59. Recurrence is more common following SSV surgery than following GSV surgery. I n patients with high body mass index. W hile stripping of the incompetent axial vein reduces recurrence rates . Recurrent varicose veins often have an atypical distribution and duplex assessment is mandatory. 59

60. REFERENCES Bailey and love’s short practice of surgery 28 th edition. Sabiston textbook of surgery 21 st edition. 60

61. 61 THANK YOU..