Dr shweta S Phadke CHRONIC VENOUS INSUFFICIENCY CVI CVI Occurs when the vein valves become dysfunctional and impairs venous blood return Affects up to 20 of adults By age 50 40 of women and 20 of men have significant vein problems ID: 623148
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Slide1
Venous diseases.
Dr.
shweta
S.
Phadke
.Slide2
CHRONIC VENOUS INSUFFICIENCY
(CVI)Slide3
CVI
Occurs when the vein valves become dysfunctional and impairs venous blood return.
Affects up to 20% of adults.
By age 50 ~40% of women and 20% of men have significant vein problems.
More people lose work time from vein disorders then from artery disease.
1.Slide4
RISK FACTORS
Advancing age
Family history of venous diseaseLigamentous laxity (eg, hernia, flat fleet)
Prolonged standingIncreased body mass indexSmokingSedentary lifestyleLower extremity traumaPrior venous thrombosis (superficial or deep)Arteriovenous shuntHereditary conditions
High estrogen statesPregnancy 2.Slide5
PROGRESSION OF VEIN DISEASE
ASYMPTOMATIC
SUPERFICIAL VENOUS DILATATION
Telangiectasias (intradermal)
Reticular veins (subdermal)Slide6
PROGRESSION OF VEIN DISEASE
ASYMPTOMATIC VS SYMPTOMATIC
VARICOSE VEINS (subcutaneous)Slide7
PROGRESSION OF VEIN DISEASE
CHRONIC VENOUS INSUFFICIENCY
Leg edemaSlide8
PROGRESSION OF VEIN DISEASE
CHRONIC VENOUS INSUFFICIENCY
Skin changes HyperpigmentationSlide9
PROGRESSION OF VEIN DISEASE
CHRONIC VENOUS INSUFFICIENCY
Skin changes Stasis dermatitisSlide10
PROGRESSION OF VEIN DISEASE
CHRONIC VENOUS INSUFFICIENCY
Skin changes
Corona phlebectatica a.
v enous cups (veins)
b. telangiectasias c
. reticular veins
d
. stasis spots (capillaries)Slide11
PROGRESSION OF VEIN DISEASE
CHRONIC VENOUS INSUFFICIENCY
Lipodermatosclerosis a form of panniculitis just above the ankles.
9.Slide12
PROGRESSION OF VEIN DISEASE
CHRONIC VENOUS INSUFFICIENCY
Venous stasis ulceration(s)Slide13
EVALUATION
CHARACTERISTICS
VENOUS
ARTERIAL
APPEARANCE
Irregular, dark pigmentation, sometimes fibrotic, granulation, usually shallow.
Irregular, smooth edge, minimum to no granulation, usually deep with a punched out appearance.
LOCATION
Distal lower leg, medial malleolus.
Distal lower leg/feet/toes, lateral malleolus, anterior tibial area.
PEDAL PULSES
Usually present.
May be diminished or absent.
PAIN
May be present. Usually improves with leg elevation.
Usually painful especially with leg elevation.
DRAINAGE
Moderate to large.
Minimal to none.
TEMPERATURE
May be increased.
May be decreased.
SKIN CHANGES
Flaking, dry, hyperpigmented.
Thin, shiny, hairless, yellow nails.
3.Slide14
EVALUATION
VENOUS DOPPLER ULTRASOUND
Evaluate for deep and superficial venous
thrombosis. Evaluate for incompetent veins with significant reflux disease. Evaluate for incompetent perforating veins and tributaries.Slide15
MANAGEMENT OF CVI
LEG ELEVATION
– above heart level for 30 minutes 3-4 times daily improves micro-circulation reduces edema, and promotes healing of venous ulcers.4.
EXERCISE – daily walking and simple ankle flexion exercises.Slide16
MANAGEMENT OF CVI
Compression therapy
- avoid contraindications such as cellulitis
or significant arterial occlusive disease. Slide17
MANAGEMENT OF CVI – COMPRESSION THERAPY
Compression bandages – elastic or non-elastic with single or multi-layers.Slide18
MANAGEMENT OF CVI – COMPRESSION STOCKINGSSlide19
MANAGEMENT OF CVI - MEDICATIONS
Diuretics – one of the most inappropriate treatments.
Aspirin – may accelerate the healing of chronic ulcers.
Pentoxifylline – more effective for complete or partial ulcer healing then placebo.Stanozolol – an anabolic steroid that stimulates fibrinolysis and improves lipodermatosclerosis and possibly ulcer healing.Escin (horseshoe chestnut) – 50mg twice daily reduces leg volume and edema. It stimulates the release of F series prostaglandins which induce venoconstriction, decreasing the permeability of vessel walls to low molecular proteins, water, and electrolytes. Hydroxyethylrutoside, Sulodexide, Prostacyclin Analogues – not available in the United States.
4.Slide20
MANAGEMENT OF CVI – SKIN CARE
Skin cleansing – wash with a mild non-soap cleanser (e.g. Dove, Olay, Caress).
Emollients – provides a film of oil to lubricate the skin (e.g. Vaseline, Lubriderm, Aveeno).
Barrier preparations – physically block chemical irritants and moisture.(e.g. Zinc oxide, Vaseline). Topical corticosteroids – often used to treat stasis dermatitis. 4.Slide21
MANAGEMENT OF CVI – VENOUS STASIS ULCERS
Surgical debridement – used to remove devitalized tissue.
Enzymatic agents – used to break down necrotic tissue (e.g. Santyl).
Growth factors – synthesized by many cell types such as platelets, neutrophils, and epithelial cells (e.g. Regranex).Bioengineered tissue – used for a variety of non-healing ulcers (e.g. Apligraf, Dermagraft).Skin grafting – an option for non-healing ulcers. 4.Slide22
MANAGEMENT OF CVI – VENOUS STASIS ULCERS
Dressings – depend upon the ulcer characteristics, frequency of dressing changes, and cost.
-Occlusive dressings may be fully occlusive (impermeable to gases and liquids) or semi-impermeable (impermeable to liquids and partially permeable to gases and water vapor).
It stimulates collagen synthesis, angiogenesis, and speeds reepithelialization. -Low adherent gauze dressings – frequent changes but inexpensive. -Hydrogels and alginate dressings are highly absorbent to handle heavily exudative ulcers, while hydrocolloids can help with wound debridement and skin protection.
-Silver can be incorporated if the ulcer is infected. 4.Slide23
MANAGEMENT OF CVI – ABLATION THERAPY
Indications – patients with persistent signs/symptoms of venous disease after a minimum of 3 months of medical therapy (e.g. compression) and documented reflux (e.g. >0.5 seconds of reflux GSV).
Absolute contraindications – acute DVT or phlebitis and pregnancy.
5,6.Radiofrequency versus laser endovenous ablation therapy.Slide24
MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY
Radiofrequency devices – generate a high frequency alternating current for which the energy heats the adjacent vein walls to the probe which alters the protein structure of the vein effecting its closure.
5.
Superficial veins include – Great Saphenous Vein, Small Saphenous, and incompetent perforator veins.Slide25
MANAGEMENT OF CVI – ENDOVENOUS LASER ABLATION THERAPY
Lasers emit a single, coherent wavelength of light. Laser therapy of venous structures is based upon the concept of selective photothermolysis (ie, selective thermal confinement of light induced damage). Vein wall injury is mediated directly by absorption of photon energy by the vein wall and indirectly by thermal convection from steam bubbles, and from heated blood.
Superficial veins include – Great Saphenous Vein, Small Saphenous Vein, incompetent perforator veins, telangiectasias and reticular veins.
6.Slide26
MANAGEMENT OF CVI – MECHANICAL ABLATION
Physical destruction of a vein with its partial or complete removal.
- Vein ligation/stripping
- Stab phlebectomy - Powered phlebectomy - Open or endoscopic perforator ligation.Slide27
MANAGEMENT OF CVI - SCLEROTHERAPY
Chemical irritants injected to close unwanted veins. Preparations include liquid and foam. It is used primarily in the treatment of telangiectasias, reticular veins, and small varicose veins.
These substances cause endothelial damage by their actions as either osmotic or detergent agents. Osmotic agents achieve their effect by dehydrating endothelial cells through osmosis. Detergents are surface active agents which damage the endothelium by interfering with cell membrane lipids.
8.Slide28
REFERENCES
2012 Vascular Disease Foundation. 8206 Leesburg Pike, suite 301, Vienna Virginia 22187.
Alguire PC, Scovell S. Overview and medical management of lower extremity chronic venous disease. 2012 UpToDate.
Venous stasis and arterial ulcer comparison. February 1, 2009. http://www.lhsc.on.ca/Health_Professionals/Wound_Care/venous.htm.Alguire PC, Mathes BM. Medical management of lower extremity chronic venous disease. 2012 UpToDate.
Scovell S. Radiofrequency ablation for the treatment of lower extremity chronic venous disease. 2012 UpToDate.
Ihnat DM. Endovenous laser ablation for the treatment of lower extremity chronic venous disease. 2012 UpToDate.Collins KA. Classification of lower extremity chronic venous disorders. 2012 UpToDate.Greenberg DL, Scovell S. Liquid and foam sclerotherapy techniques for the treatment of lower extremity veins. 2012 UpToDate.
Alguire PC, Mathes BM. Pathophysiology of chronic venous disease. 2012 UpToDate.Slide29
QUESTIONSSlide30
Leg Pain Has a Differential Diagnosis
Spinal canal stenosis
Peripheral neuropathy
Peripheral nerve painHerniated disc impinging on sciatic nerve Osteoarthritis of the hip or knee
Venous claudicationSymptomatic Baker’s cyst
Chronic compartment syndromeMuscle spasms or crampsRestless leg syndrome
Also see Table 3 of
Hirsch AT, et al.
J Am Coll Cardiol.
2006;47:e1-e192.Slide31
Differential Diagnosis of
Common Foot Ulcers
Neuropathic Ulcer
Neuroischemic Ulcer
Painless
Painful
Normal pulses
Absent pulses
Typically punches-out appearance
Irregular margins
Often located on sole or edge of foot or metatarsal head
Commonly located on toes
Presence of calluses
Calluses absent or infrequent
Loss of sensation, reflexes, and vibration sense
Variable sensory findings
Increase in blood flow
(arteriovenous shunting)
Decrease in blood flow
Dilated veins
Collapsed veins
Dry, warm foot
Cold foot
Bone deformities
No bony deformities
Red appearance
Pale, cyanotic
Reprinted with permission from Dormandy JA, Rutherford RB.
J Vasc Surg
. 2000;31:S1-S296.