Venous diseases. - Presentation

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Venous diseases.

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..

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Venous diseases.






Presentation on theme: "Venous diseases."— Presentation transcript:

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.