Diagnosis and Treatment of Venous Insufficiency and Varicose Veins

Transcription

1 Diagnosis and Treatment of Venous Insufficiency and Varicose Veins Joseph Conley, MD Scott and White Memorial Hospital Temple, TX September 22, 2012

2 Objectives Anatomy and Pathophysiology of venous insufficiency Common distribution patterns of venous insufficiency and varicose veins Current treatments and outcomes Impact upon patient management

3 Venous Anatomy Deep system: 90% Common femoral vein Femoral vein (SFV misnomer) Popliteal vein Paired tibial veins Posterior tibial Anterior tibial Peroneal Superficial system: 10% Greater saphenous vein Lesser saphenous vein Tributary veins Perforators Hunterian (upper thigh) Dodd s (lower thigh) Boyd (knee) Cockett (calf)

4 Venous Anatomy Deep system

5 Anatomy: superficial system

6 Superficial Deep connections Sapheno-femoral junction (GSV to CFV) Sapheno-popliteal junction (SSV to popliteal vein) Perforators (Tributary veins to deep system)

7 Perforators Connects superficial veins (usually tributaries) to deep venous system Competence involves valves and fascial gates Bi-directional flow is normal permits balance of pressure between superficial and deep systems. Major role in ulcer formation > 60 perforators /leg Hunterian Dodd Boyd Cockett

8 Superficial Deep connections Telangectasia Dermis Reticular vein Varicose vein Perforators Sup. fascia Deep fascia Deep vein

9 Valves Normal veins have regularly spaced valves which act as unidirectional dams that allow blood to move against gravity.

10 Impaired venous drainage Calf muscle pump dysfunction muscle wasting neuromuscular disease deep fasciotomies local vein valve failure within the muscle fascia sheath Venous obstruction DVT Mass artery Venous valvular incompetence Primary Secondary

11 Classification: Primary vs. Secondary Primary Intrinsic weakness of smooth muscle media layer of vein wall (hereditary, hormonal, endothelial damage) Intrinsic leakiness of valve Secondary Post thrombotic damage to valve leaflets

12 Vein wall weakness theory Primary defect in vein wall composition Increased collagen proliferation Disruption of smooth muscle organization Sagging of muscular grid

13 Vein wall weakness theory

14 Valvular incompetence theory 1628 by Sir William Harvey Too few valves or fragile valves One valve incompetent or damaged Reflux with expansion of vein Damage to adjacent valves

15 Valves Valve damage Incompetence with reversal of flow, pooling and venous hypertension.

16 Propagation of incompetence

17 Cellular Level Venous HTN Separation of endothelial cells ( leaky vessels ) Extravasation of fluid, proteins (fibrinogen), RBC s RBC s decompose releasing hemoglobin pigment Extravasated fibrinogen/fibrin coats capillaries, decreasing oxygen diffusion into tissue New vessels recruited Hyperpigmentation Tissue ischemia - ulceration

18 Evaluation of Venous Insufficiency Ambulatory venous pressure measurement Plethysmography Duplex ultrasound Descending venography

19 Ambulatory venous pressure Needle inserted dorsum of foot Pressures recorded during 10 tiptoe lifts AVP = lowest pressure during exercise Normal AVP < 30 mmhg with refill time of 18 secs With reflux, AVP increases and RT decreases Isolate superficial system with tourniquets

20 Ambulatory venous pressure Measurement with and without tourniquet. Incompetent superficial veins and competent deep veins

21 Venous occlusion plethysmography Measurement of variations in the size of an organ or body part on the basis of the amount of blood passing through or present in the part. Air/liquid plethysmography limb enclosed within an airtight chamber cuff applied to about 40mmHg (above venous, less than arterial pressure) after allowing venous pressure to reach 40 mmhg (volume stable), cuff is released and volume recorded slow return to pre-occlusion volume indicates low venous flow and underlying thrombus or insufficiency No anatomic info and large/cumbersome to use

22 Venous occlusion plethysmography Often also be performed by measuring while supine, after standing, after one tiptoe lift, and after 10 tiptoe lifts. Venous filling index (VFI) = rate of filling as a result of standing Venous volume (VV) = amount of blood in venous reservoir Ejection volume (EV) and Ejection fraction (EF) after one step Residual volume (RV) and RV fraction (RVF) as a result of 10 tiptoe lifts

23 Plethysmography Impedance plethysmography Strain gauge plethysmography

24 Duplex ultrasound: Confirm presence, patency and competence of venous system Deep system DVT, incompetence (valsalva or distal augmentation) Superficial system assessment Superficial thrombosis, incompetence, size, anatomy Trace major varicosities to source vessel (truncal or incompetent perforators Perforators Location, relationship to ulceration

25 Patient Positioning Supine with leg externally rotated for viewing CFV, SFV, PFV, GSV, popliteal, ATV, and distal PTV Prone or lateral for the popliteal, peroneal and proximal PTV, LSV and soleal veins Standing to access valve competency

26 Ultrasound Technique Augmentation - pressure (squeezing) applied to the leg below the transducer. The normal vein should show increased flow. Valvular competency - pressure applied above the transducer. Normal veins show less than 0.5 seconds of retrograde flow.

27 Gray scale imaging Identifies abnormal tissues Linear transducer 5 MHz or greater depending on density of patient tissues Patency evaluated in transverse plane every 2 cm by compressing vessel of interest with transducer.

28 Doppler spectral analysis Doppler carrier frequencies should be 3.5 MHz or greater Angle of insonation <60 degrees Where flow disturbance is noted, proximal, mid and distal images should be documented Color doppler aids in visualizing perforators

29 Deep System: DVT dx Loss of compressiblity Direct visualization of thrombus: Chronic clot generally appears more echogenic, involves venous collaterals, and wall thickening Acute clot is typically less echogenic and involves a larger vein diameter. Altered doppler flow dynamics: Loss of respiratory phasicity Absence of color flow Loss of augmentation of flow with calf compression

30 Deep System Evaluation without compression with compression

31 Noncompressible Acute DVT without compression with compression

32 Noncompressible Chronic DVT without compression with compression

33

34

35 US Criteria: GSV Insufficiency Diameter > 4 mm Expansion in upright position Reflux: duplex and color flow reversal Traceable to visible varicose vein

36 GSV Fascia CFA

37 GSV Dilatation Normal Incompetent

38 GSV Positional Expansion Supine Standing

39 Reflux: Color Doppler

40 Reflux: Spectral Doppler Response to Valsalva Competent vein Incompetent vein

41 Reflux grading by US Grade Reflux duration Normal < 0.5 sec Moderate sec Severe > 1 sec

42 Perforator

43 Descending Venography Contrast injected into the iliac vein from IJ or contralateral approach Reflux into leg observed fluorosopically Kistner Classification Grade 0 Competence No reflux below CFV Grade 1 Minimal Incompetence Reflux to Upper Thigh Grade 2 Mild Incompetence Reflux to Distal Thigh Grade 3 Moderate Incompetence Reflux to Knee Grade 4 Severe Incompetence Reflux to Calf

44 Descending Venogram: deep system Reflux Grade: (venographic) 0 = reflux; 1 = prox thigh; 2 = dist thigh; 3 = knee; 4 = calf

45 How common is venous insufficiency? Varicose veins are thought to affect 30-60% adult population Female:Male = 2-4:1 Prevalence increases as population ages Post-thrombotic syndrome seen in 21 to 88% of patients with DVT (600,000 each year in US)

46 Varicose Veins Age Prevalence Women: % 41% 72% Men: % 24% 43%

47 Predisposing factors Heredity: positive family history = 2x risk Female gender: hormonal effects Pregnancy: hormonal effects + increased blood volume + pelvic venous compression Age: loss of vessel wall elasticity and recoil Obesity Occupation: standing vs. mobile

48 Why treat varicose veins? If untreated, the natural history of venous insufficiency is inexorable progression of disease over time. The process advances from cosmetic concerns, to pain and discomfort, to swelling/bleeding/clotting, and ultimately to frank skin ulceration

49 Venous stasis ulcer

50 CEAP classification of venous insufficiency clinical signs (C) etiology (E) anatomical distribution (A) physiopathology (P) Class 0 Class 1 Class 2 Class 3 Class 4 Class 5 Class 6 No visible or palpable signs of CVI Telangiectatic or reticular veins Varicose veins Edema Skin changes due to chronic venous insufficiency Skin changes with healed ulceration Skin changes with active ulceration

51 Reversing the cycle Valve incompetency Interrupt refluxing segment Reflux Reversal of venous HTN Venous HTN and vein distension Vein detumescence Valve ring contraction Valve ring expansion Improved valve competency Additional incompetent valves

52 Indications for Rx Cosmetic Pain/heaviness Fatigue Superficial thrombophlebitis Bleeding Ankle hyperpigmentation Lipodermatosclerosis Venous stasis ulcer

53 Classification of Varicose veins with Sources and Patterns of Reflux

54 Classification of varicose veins Type Class Size Color I Telangectasia/spiders mm Red II Venulectasia 1-2 mm Violet III Reticular veins 2-4 mm Blue IV Nonsaphenous varicose Saphenous varicose 3-8 mm Blue 7-8 mm Blue V

55 Spectrum of varicose veins I and III: Spiders and reticular veins II: Venulectasia

56 Spectrum of varicose veins V: Saphenous tributaries IV: Tributary v.v.

57 GSV reflux with loop circuit

58 1 Tributary incompetence

59 1 Tributary incompetence

60 Anterolateral tributary

61 Posteromedial tributary

62 Giacomini/Short Saphenous Incompetence

63 Perforator incompetence

64 Neovascularity

65 Treatment

66 Treatment Compression hose use Regular exercise Avoid prolonged sitting or standing Elevate legs

67 Classification: Large versus Small Small Large Reticular varicosities Telangiectasias Truncal (GSV,SSV) Tributary branches Perforators Sclerotherapy Surgical Stripping/Ligation or Sclerotherapy or Endovenous Ablation

68 Specific treatments targeted to specific levels of reflux Tributary branch reflux: Ambulatory (Stab, Micro) phlebectomy Sclerotherapy Trivex

69 Treatments for Saphenous Vein Reflux

70 Surgical Vein Stripping

71 GSV Stripping 94% clinical success General anesthesia Average 4 days return to activity Average 12 days to return to work

72 Endovenous Thermal Ablation

73 Endovenous Thermal Ablation Endovenous application of heat to thermally denature vein wall collagen and promote contraction, fibrosis, occlusion, and atrophy of the target vein segment. Applicable to GSV, SSV, major tributary trunks. Varicose veins below source of reflux spontaneously decompress and detumesce.

74 ETA Equipment Laser

75 ETA: Thermal device positioning cm below the SF junction GSV Femoral vein

76 ETA : Tumescent anesthesia 0.2% lidocaine GSV Provides: 1. Anesthesia 2. Thermal barrier 3. Compression of vein around laser = improved heat transfer

77 Mechanism of Laser Action Transmural thermal damage through direct contact Predominantly fibrotic, not thrombotic, closure

78 RF ablation (Closure) VNUS Medical Technologies, Inc Analogous procedure, different heating apparatus

79 RF ablation (Closure) 6 or 8 French RFA probe degrees Celsius 2-4 cm/min pull-back speed

80 EVLT compared to RFA Both procedures 98% technical success Both procedures 90-93% success at 2 years EVLT is technically 4X faster to perform than RFA RFA has less immediate post procedural discomfort.

81 ETA Outcomes 98% technical success 85-93% persistent success at 2 years Long-term outcomes pending Likely less neovascular recurrence due to less tissue disruption

82 ETA of Trib/GSV Laser

83 ETA: Pre and Post

84 Ultrasound-guided Sclerotherapy Direct injection of incompetent perforator with high concentration/foamed sclerosant Real-time US visualization during vein cannulation and injection

85 Ultrasound-guided Sclerotherapy Needle

86 Target veins for Sclerotherapy US-Guided Sclerotherapy (Foam) Tributaries ie. Anterior and posterior accessory saphenous veins Truncal vessels: GSV/SSV/GIACOMINI Perforators Failed segments of endothermal ablation Failed segments of sclero treated veins

87 Foam Sclerotherapy

88 Ultrasound Guided Sclerotherapy

89 US-guided Sclerotherapy Extends sclerorx applications to larger deeper veins: Saphenous veins, major tributary trunks, perforators Intravenous needle placement confirmed, minimal risk of arterial injection Synergistic with foam technique

90 Sclerotherapy Results Before After Photos courtesy of Steven Zimmet, MD, FACPh

91 Modern vein treatments: Before and After

92 Tributary Foam Sclerotherapy Pre Post

93 Trib/GSV ETA 2 weeks post EVLT Trib GSV

94 Giacomini-LSV complex ETA

95 Sclerotherapy of telangectasia Pre 2 weeks post

96 ETA with adjunctive sclerorx Pre 4 mo post EVLT

97 Tributary ETA: early effect 10 days

98 Tributary ETA: pre and post 4 mo

99 LSV ETA with adjunctive ScleroRx 4 mo

100 US ScleroRx of GSV and branches Before Photos courtesy of Steven Zimmet, MD, FACPh After

101 Conclusion Venous insufficiency is a source of significant morbity Ultrasound plays a vital role in the evaluation of venous insufficiency. There have been major advances in the treatment of varicose veins and venous insufficiency