Dr.Devasheesh

Introduction Ulceration is an established defect in an epithelial

surface On basis of etiology they can be

Neuropathic (most common) Venous Arterial Mixed (10%) (e.g. neuropathic–arterial, venous–arterial, etc)

Venous ulcers are the most severe and debilitating sequlaeof chronic venous insufficiency (CVI) and venous hypertension (HTN). They account for nearly 80% of all lower extremity ulcers.

Approximately 35% of patients afflicted with CVI will develop a venous ulcer before the age of 40 and nearly two thirds before the age of 65

Deep Veins Accompany axial arteries.

Run within the muscles

deep to the muscle fascia.

Superficial veins

• Lie in the subcutaneous tissue superficial to the muscle fascia.

• They have their own, well-developed muscle coat

• Long & short saphenousveins and their tributaries

Comunicating Veins “Perforators” Perforate the fascia

connecting the superficial & deep veins at certain points

Physiology Venous pressure in a foot vein on standing is approximately

100 mmHg To enable blood to be returned against gravity in the

standing position, an auxiliary pump in form of calf muscle pump is present

On calf muscles contraction, pressure within the calf compartment rises to 200–300 mmHg which compress the veins and the valves only allow blood to pass in the direction of the heart.

During muscle relaxation the pressure falls and blood from the superficial veins enters the deep veins through the perforating veins thus decreasing the pressure in superficial veins to around 30 mmHg.

Risk factors Advancing age Family history of venous disease Prolonged standing Increased body mass index Smoking Sedentary lifestyle Lower extremity trauma Prior venous thrombosis (superficial or deep) Arteriovenous shunt Hereditary conditions Pregnancy 2.

Etiology• AMBULATORY VENOUS HYPERTENSION

• Occurs when the vein valves become dysfunctional and impairs venous blood return.• Superficial venous reflux (long saphenous or short saphenous vein

reflux)

• Deep vein reflux (Primary or secondary to deep venous thrombosis

• Deep venous occlusion.

• Perforating vein reflux.

• Abnormal calf pump (Neurological/musculoskeletal)

• Congenital absence of deep veins (e.g. Klippel-Trenaunaysyndrome)

• Venous trauma (ligation of proximal vein).

Pathology Fibrin cuff theory:

widening of the pores between endothelial cells allows the passage of larger molecules out of the intravascular compartment into the tissues.

This allows the accumulation of fibrin around the capillaries of the dermis to form a cuff which acts as a barrier to oxygen and nutrient diffusion to interstitial tissues and cutaneous skin cells resulting in local tissue ischaemia and cell death which produces ulceration.

White cell trapping theory:Raised venous pressure reduces the capillary perfusion

pressure which causes trapping of white cells.Venous hypertension results in expression of

leukocyte adhesion molecules that permit adherence of leukocytes to the capillary endothelial cells.

The trapped cells become activated releasing proteolytic enzymes and oxygen free radicals which produce endothelial damage and tissue destruction and local ischaemia.

Other possible changes

• Suggested that the pericapillary cuffs might interfere with the diffusion of growth factors which are essential for skin and tissue repair

• Arteriovenous shunting

• All these factors work together and lead to formation of venous ulcer

Clinical Features The legs are

Oedematous, moist Ulceration classically occurs just above the medial malleolus

(gaiter area), where the skin is most vulnerable (may be bimallelolar and circumferential).

Gangrene is usually absent (base of the ulcer may be necrotic)

Foot is warm with normal pulses. Stigmata of venous disease are present

Varicose veins Venous eczema Haemosiderin deposition Lipodermatosclerosis Atrophie blanche.

Varicose veins-

C1: Telangiectasia (0.5-1 mm) Reticular veins (1-3 mm)

C2: Varicose veins (>3mm)

C3: Edema without Skin changes

C4a: pigmentation or eczema

C4b: lipodermatosclerosisor atrophie blanche

Lipodermatosclerosis (inverted champagne-bottle)

Atrophie blanche

C5: healed venous ulcer

C6: active venous ulcer

Venous UlcerPulses Present (difficult to palpate if

oedematous)

Skin perfusion Normal and warm

ABPI Normal

Ulcer location Medial malleolus (gaiter area)

Ulcer margin Large and irregular

Ulcer contents Yellow wet appearance

Ulcer drainage Moderate to large

Skin Signs of venous hypertension

Pruritus Yes

Oedema Moderate to severe

Painful

Investigation Routine investigations eg: full blood count,

erythrocyte sedimentation rate (C reactive protein) and sickle cell test

Early diagnostic studies include invasive measurements of ambulatory venous pressure (AVP) and venous recovery time (VRT)

80% incidence of venous ulceration if AVP of >80 mmHg

Plethysmography

evaluates venous function through the use of infrared light

provides a measurement of VRT

Investigation Venous Duplex Ultrasound

Gold standard for evaluation of venous function

Advantage that it can be used to evaluate individual venous segments targeting abnormal areas for treatment

Pneumatic pressure cuffs placed around the thigh, calf, and forefoot and ultrasound transducer positioned over the venous segment to be examined, just proximal to the cuff.

It is then inflated to a standard pressure for 3 seconds and then rapidly deflated. Ninety-five percent of normal venous valves close within 0.5 second.The presence of reflux for >0.5 second is considered abnormal.

Other investigations:

ABPI

Nerve conduction studies

Angiogram

Wound swab culture

Biopsy of ulcer edge

Management Conservative treatment:

Elevation of the legs at rest helps to reduce oedema, decrease exudates from ulcers and accelerate regression of skin changes.

EXERCISE – daily walking and simple ankle flexion exercises Graduated elastic compression which is highest at the ankle

and decreases proximally. Avoid in case of cellulitis

Unna boots :three layers

• rolled gauze bandage impregnated with calamine, zinc oxide, glycerin, sorbitol, gelatin, and magnesium aluminum silicate

• next layer consists of a 4-in-wide continuous gauze dressing

• followed by an outer layer of elastic wrap

Management Local measures

Clean base of the ulcer with saline

Curette the yellow fibrin eschar

Treat with metronidazole gel to reduce bacterial growth and odor.

Red dermatitic skin is treated with a medium- to high-potency corticosteroid ointment.

Cover with occlusive hydroactive dressing

Use of skin substitutes eg: Cultured epidermal cell grafts

Some ulcerations require grafting

Management Systemic therapy

Pentoxifylline, 400 mg three times daily administered with compression dressings

Zinc supplementation is occasionally beneficial

Use of antibiotics if accompanying cellulitis.

Stanozolol: fibrinolytic enhancing agent used in the treatment of preulcerative lipodermatosclerosis

Surgical measures Perforator Vein Ligation

Subfascial endoscopic perforator vein surgery (SEPS)

Superficial Venous Surgery

Stripping of saphenous vein

Perforator ligation

Deep Venous Valvular Reconstruction

Valve transplantation

Venous Stenting

Skin grafting: Done after treatment of underlying venous abnormality.

Reduces the healing time. Split skin mesh grafts.

Pinch grafts.

Full-thickness skin grafts.