1. Venous Insufficiency: Nuts and Bolts
Harry Ma MD, PhD
Assistant Professor of Surgery
University of Oklahoma
Tulsa, Oklahoma
Department of Surgery

2. Disclosures
None

3. Outline and Objectives
Defining chronic venous disease
Clinical manifestations
Diagnostic evaluation
Treatment
Non-operative
Operative

4. Spectrum of Disease Spider veins (telangiectases) Reticular veins
Varicose veins
Edema
Chronic skin changes
Ulcers

5. Impact of CVD Most common form of vascular disorder
Chronic Venous Disease: 25 million people in US
Health care cost: $1 to 3 Billion dollars annually
Indirect cost: ~2 million work days lost annually
Depending upon definition and method of evaluation
2x the number of patients compared to CAD.
5X more than PAD
Significant impact on heal care cost usually related to complications such as venous disease

6. Definitions
Telangiectasias - are a confluence of dilated intradermal venules less than one millimeter in diameter.
Reticular veins - are dilated bluish subdermal veins, one to three millimeters in diameter. Usually tortuous.
Varicose veins - are subcutaneous dilated veins three millimeters or greater in size. They may involve the saphenous veins, saphenous tributaries, or nonsaphenous superficial leg veins.

7. Definitions of Skin Changes
Lipodermatosclerosis: localized chronic inflammation and fibrosis of the skin and subcutaneous tissue
Atrophie blanche: localized, often circular whitis and atrophic skin areas surrounded by dilated capillary spots and hyperpigmentation
Venous Ulcer: full thickness skin defect

8. CEAP classification
Clinical
Etiology
Anatomy
Pathophysiology

9. Clinical Classification
C0: no visible or palpable signs of venous disease.
C1: telangiectasies or reticular veins.
C2: varicose veins.
C3: edema.
C4a: pigmentation and eczema.
C4b: lipodermatosclerosis and atrophie blanche.
C5: healed venous ulcer.
C6: active venous ulcer.

10. Etiologic Classification
Ec: congenital (<5%)
Ep: primary (65-80%)
Es: secondary (postthrombotic 15-28%).

11. Valvular Dysfunction
Primary valvular dysfunction: weakness in leaflets or vessel wall
Secondary to previous DVT or phlebitis
Increases retrograde flow
Results in reflux
Increased hydrostatic pressure
Not just deep or superficial valves but perforators

12. Diagnostic Evaluation
Venous Duplex (New Gold Standard)
Phlebography or Venography (Old Gold Standard)
Air Plethysmography
Photophlethysmography
Venous pressure (hemodynamic gold standard)

13. Venous Duplex Can rule out thrombosis and obstruction
Quantify reflux in veins
Visualize anatomy

14. Venous Duplex Vast majority have superficial incompetence only.
Sensitivity 95 % for identifying the competence of the saphenofemoral and saphenopopliteal junctions.
Less sensitive for identifying incompetent perforators (40 to 60 percent)

15. Risk Factors for varicose veins
Morbid obesity
Advanced age
Sex/Hormonal changes
Family history/Genetics
History of DVT or phlebitis
Occupational risks

16. Clinical Manifestations
Veins are prone to thrombophlebitis
Common symptoms:
Pain
Swelling
Ulcerations
Skin changes
Cramping
Fatigue

17. Clinical Manifestations
Itching
Burning
Pain after standing
Relieved with leg elevation
Vague pain
Complications:
Ulceration
Bleeding
Skin changes

18. Patient Assessment History Examination Studies Venous Duplex
History of symptoms and onset
History of venous complications
Desire for treatment
Comorbidities
Rule out secondary cause including DVT and HEART Failure
Examination
Patient in general
Pedal pulses
Groins
Veins
Studies
Venous Duplex

19. Non-operative management
Leg elevation
Compression therapy
Treatment of ulcer: local wound care
NOT DIURETICS

20. Non-operative management
LEG ELEVATION – heart level for 30 minutes 3-4 times daily improves micro-circulation reduces edema, and promotes healing of venous ulcers.
EXERCISE – daily walking and simple ankle flexion exercises.

21. Compression Therapy Compression bandages Compression Stockings
Intermittent Pneumatic Compression
Contraindications
Active infection
Significant arterial occlusive disease
ABI <

22. Compression Stockings
CLASS
PRESSURE
STRENGTH
INDICATION
CEAP
OTC
< 15mmHG
Minimal
Minimal symptoms
0,1 I
15-20mmHg
Mild
Minor varicosities, minor edema
1,2,3 II
20-30mmHg
Moderate
Moderate varicosities, phlebitis, moderate edema, post-op ablation
3,4
III
30-40mmHg
Firm
Severe varicosities, active or history of ulcers, DVT
4,5,6 IV
>40mmHg
Extra Firm
Lymphedema
N/A

23. Compression Bandages Elastic In-elastic Types: ACE wrap Easier to use
Higher pressures at rest
Can cause pressure ulcers
Minimal increase in pressure when ambulatory
Types: Profore multi-layer wraps
High stiffness
Exert about 40mmHg
Can lose pressure quickly due to limb volume reduction
Difficult to apply
Better for ambulatory patients

24. Benefits of Compression
Increased ulcer healing
30-40mmHg compression resulted in 93% ulcer healing rate by 6 months
Prevention of recurrence with compliance: 29% recurrence at 5 years
Disadvantages: Compliance

25. Operative Management Ligation and Stripping Ablative therapy
Radiofrequency
Laser
Sclerotherapy

26. Ligation and Stripping
Traditional surgical approach
Reduced recurrence rates compared to high ligation alone

27. Ablation
Laser
Use a bare tipped optical fiber which applies laser light energy to the vein.
Therapy based on photothermolysis (light induced thermal damage).
Laser light heats the target tissue inducing thermal injury
Wavelength of light is chosen based on the target structure's chromophore
Radiofrequency
A high frequency alternating current resulting in energy that heats the adjacent vein walls to the probe which alters the protein structure of the vein effecting its closure

28. Complications of ablation
Nerve injury <2%
Skin injury <1%
Failure of closure <5%
Thrombotic complications <1%

29. Which is Better? Equivalent therapy Similar outcomes
Success rates >95% for both (N=159)
Improvement in QoL surveys and VVQ surveys
Cochrane review in 2014
13 randomized trials included
3081 patients total
Complication rates equivalent
Efficacy: equivalent for laser, RFA, foam sclerotherapy and ligation and stripping

30. Sclerosing Agents Hypertonic Saline Chromated glycerin
Nonchromated glycerin
Monoethanolamine oleate
Sotradecol (STS)
Polidocanol
Foam

31. Mechanism of action and use
Endothelial damage
Thrombosis
Resultant sclerosis and closure of the vein
For telangiectasias
Reticular veins
Perforator veins
More recently incompetent GSV

32. Ultrasound Guided Foam Sclerotherapy
First reported in 1995
Mixed with air or CO2
Bubble size of 100 µm or less
Ration of sclerosant to air or CO2 is usually 1:4

33. Limitations and complications
Large veins
Phlebitis 3-8%
Embolus (CVA)
Visual disturbance
DVT
Failure or recurrence
Anaphylaxis

34. Short term outcomes 1 year follow-up equivalent QoL improvement
72% success rate (vs 89% for EVLA)
Two year follow-up in patients with ulcers
85% healing rate

35. Long term outcomes 5-8 year follow-up of 285 patients
89% had improvement in QoL survey and AVSS
15% required repeat treatment

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