Transcript CHRONIC VENOUS INSUFFICIENCY

CHRONIC VENOUS
INSUFFICIENCY
(CVI)
CVI
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Occurs when the vein valves become dysfunctional and impairs venous blood
return.
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Affects up to 20% of adults.
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By age 50 ~40% of women and 20% of men have significant vein problems.
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More people lose work time from vein disorders then from artery disease. 1.
RISK FACTORS
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Advancing age
Family history of venous disease
Ligamentous laxity (eg, hernia, flat fleet)
Prolonged standing
Increased body mass index
Smoking
Sedentary lifestyle
Lower extremity trauma
Prior venous thrombosis (superficial or deep)
Arteriovenous shunt
Hereditary conditions
High estrogen states
Pregnancy 2.
PROGRESSION OF VEIN
DISEASE
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ASYMPTOMATIC
SUPERFICIAL VENOUS DILATATION
Telangiectasias (intradermal)
Reticular veins (subdermal)
PROGRESSION OF VEIN
DISEASE
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ASYMPTOMATIC VS SYMPTOMATIC
VARICOSE VEINS (subcutaneous)
PROGRESSION OF VEIN
DISEASE
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CHRONIC VENOUS INSUFFICIENCY
Leg edema
PROGRESSION OF VEIN
DISEASE
CHRONIC VENOUS INSUFFICIENCY
 Skin changes
Hyperpigmentation
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PROGRESSION OF VEIN
DISEASE
CHRONIC VENOUS INSUFFICIENCY
 Skin changes
Stasis dermatitis
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PROGRESSION OF VEIN
DISEASE
CHRONIC VENOUS INSUFFICIENCY
 Skin changes
Corona phlebectatica
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a. venous cups (veins)
b. telangiectasias
c. reticular veins
d. stasis spots (capillaries)
PROGRESSION OF VEIN
DISEASE
CHRONIC VENOUS INSUFFICIENCY
 Lipodermatosclerosis
a form of panniculitis just above the ankles.
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9.
PROGRESSION OF VEIN
DISEASE
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CHRONIC VENOUS INSUFFICIENCY
Venous stasis ulceration(s)
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.
EVALUATION
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CONSIDER A BIOPSY TO EVALUATE FOR
POSSIBLE MALIGNANCY VS INFECTIOUS OR
INFLAMMATORY PROCESS.
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DOPPLER ULTRASOUND - VENOUS.
CONSIDER ARTERIAL DOPPLER IF THERE IS
ANY CONCERN OF SIGNIFICANT ARTERIAL
OCCLUSIVE DISEASE.
EVALUATION
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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.
ANATOMY OF THE LOWER
EXTREMITY VENOUS SYSTEM
VIDEO SHOWING SIGNIFICANT
REFLUX DISEASE OF THE
GREAT SAPHENOUS VEIN
VENOUS INSUFFICIENCY WITH
COLOR FLOW
CLASSIFICATION VEIN DISEASE
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CEAP – an international consensus conference initiated the Clinical-Etiology-Anatomy-Pathophysiology
classification.
C 0 – no evidence of venous disease.
C 1 – telangiectasias/reticular veins.
C 2 – varicose veins.
C 3 – edema associated with vein disease.
C 4a – pigmentation or eczema.
C 4b – lipodermatosclerosis.
C 5 – healed venous ulcer.
C 6 – active venous ulcer.
E c – congenital
E p – primary venous disease.
E s – secondary venous disorder.
E n – not specified.
A s – superficial veins.
A d – deep veins.
A p – perforating veins.
A n – not specified.
P r – venous reflux.
P o – venous obstruction.
P n – not specified. 7.
MANAGEMENT OF CVI
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LEG ELEVATION – heart level for 30 minutes 3-4 times daily
improves micro-circulation reduces edema, and promotes
healing of venous ulcers.
4.
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EXERCISE – daily walking and simple ankle flexion exercises.
MANAGEMENT OF CVI
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Compression therapy
- avoid contraindications such as cellulitis
or significant arterial occlusive disease.
MANAGEMENT OF CVI –
COMPRESSION THERAPY
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Compression bandages – elastic or non-elastic
with single or multi-layers.
MANAGEMENT OF CVI –
COMPRESSION STOCKINGS
MANAGEMENT OF CVI –
COMPRESSION STOCKINGS
CLASS
PRESSURE
LEVEL OF
SUPPORT
INDICATIO
N
CEAP
OTC
<15 mmHg
Minimal
Asymptomatic,
comfort only.
0, 1
I
15-20 mmHg
Mild
Minor varicosities, tired
aching legs, minor
swelling.
1, 2, 3
II
20-30 mmHg
Moderate
Moderate to severe
varicosities, moderate
swelling,phlebitis,
following ablation.
3, 4
III
30-40 mmHg
Firm
Severe varicosities,
swelling, management
of ulcerations, following
DVT, post surgery.
4, 5, 6
IV
>40 mmHg
Extra firm
Lymphedema.
NA
4.
MANAGEMENT OF CVI
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PNEUMATIC COMPRESSION THERAPY
CHRONIC VENOUS
INSUFFICIENCY VERSUS
LYMPHEDEMA
MANAGEMENT OF CVI MEDICATIONS
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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.
MANAGEMENT OF CVI – SKIN
CARE
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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.
MANAGEMENT OF CVI –
VENOUS STASIS ULCERS
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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 nonhealing ulcers (e.g. Apligraf, Dermagraft).
Skin grafting – an option for non-healing ulcers.
4.
MANAGEMENT OF CVI –
VENOUS STASIS ULCERS
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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.
MANAGEMENT OF CVI –
ABLATION THERAPY
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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.
Radiofrequency versus laser endovenous
ablation therapy.
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MANAGEMENT OF CVI –
RADIOFREQUENCY ENDOVENOUS
ABLATION THERAPY
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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.
Superficial veins include – Great Saphenous
Vein, Small Saphenous, and incompetent
perforator veins.
5.
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MANAGEMENT OF CVI
MANAGEMENT OF CVI
MANAGEMENT OF CVI –
RADIOFREQUENCY ENDOVENOUS
ABLATION THERAPY
MANAGEMENT OF CVI –
RADIOFREQUENCY ENDOVENOUS
ABLATION THERAPY
MANAGEMENT OF CVI –
RADIOFREQUENCY ENDOVENOUS
ABLATION THERAPY
MANAGEMENT OF CVI –
RADIOFREQUENCY ENDOVENOUS
ABLATION THERAPY
MANAGEMENT OF CVI –
RADIOFREQUENCY ENDOVENOUS
ABLATION THERAPY
MANAGEMENT OF CVI –
RADIOFREQUENCY
ENDOVENOUS ABLATION
THERAPY
MANAGEMENT OF CVI –
RADIOFREQUENCY ENDOVENOUS
ABLATION THERAPY
MANAGEMENT OF CVI –
RADIOFREQUENCY
ENDOVENOUS ABLATION
THERAPY
BEFORE
AFTER
MANAGEMENT OF CVI –
ENDOVENOUS LASER
ABLATION THERAPY
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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.
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MANAGEMENT OF CVI –
ENDOVENOUS LASER ABLATION
THERAPY
MANAGEMENT OF CVI –
MECHANICAL ABLATION
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Physical destruction of a vein with its partial or
complete removal.
- Vein ligation/stripping
- Stab phlebectomy
- Powered phlebectomy
- Open or endoscopic perforator ligation.
MANAGEMENT OF CVI – STAB
PHLEBECTOMY
MANAGEMENT OF CVI – VEIN
STRIPPING/LIGATION
MANAGEMENT OF CVI SCLEROTHERAPY
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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.
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MANAGEMENT OF CVI SCLEROTHERAPY
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DETERGENT AGENTS
- Sodium tetradecyl sulfate
- Polidocanol
OSMOTIC AGENTS
- Hypertonic saline
- Glycerin
MANAGEMENT OF CVI SCLEROTHERAPY
REFERENCES
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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.
QUESTIONS