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Topic 7. Leg ulcer

Venous anatomy of the lower extremity1) Deep venous system2) Supf. venous system GSV & SSV3) Perforating veins

Superficial Venous System

Greater saphenous vein (GSV) Ascends along the inner aspect of the calf and thigh Drains into the femoral vein, through the sapheno-femoral junction. Major tributaries: post. arch in the calf, posteromed. and anterolat. in the thigh, inf. epigastric in groin

Small Saphenous Vein (SSV)

Courses from the lateral ankle up the posterior calf Terminates in the popliteal fossa at the sapheno-popliteal junction (SPJ); Confluence with the

popliteal vein (PV) is variable.

Proximal portion lies between superficial & deep fascial layersPerforating veins

Connect supf. and deep veins Location:

- Proximal thigh - Hunterian- Distal thigh - Dodds- Knee - Boyds- Ankle/Calf - Cocketts

Incompetent perforators are often the source of venous stasisulcers at medial ankle

Physiology of the venous system

Perforating veins valvespermit unidirectional flow fromsupf. to deep venous sys.

2 major pumps:1) Cardiac2) Muscle (calf, thigh)

- Muscle contraction / systole pressure on deep veins blood flow toward the heart - Muscle relaxation / diastole Pressure falls in deep veins blood flows from superficial

to deep system due to pressure differences

The integrity of venous system depends on muscle function, valve competence, and patients veins

Leg ulcer (Ulcus Cruris)Ulcer, as it relates to skin, is defined as a discontinuity in normal layers thus leaving a void (open sores) on

the leg or foot that takes > 6 weeks to heal

The majority of vascular ulcers are chronic or recurrent.

affect 2-5% of the population Prevalence with age Presents as deep non-healing wounds on the lower leg, calf, foot and heel. The skin is thin and compromised prone to braking down even after minor trauma or ext. pressure. Often several small ulcers break out close by and soon fuse to form a large ulceration that spreads over

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Prognosis: People with leg ulcers have a poorer quality of life than age-matched controls because of pain,odor, and reduced mobility

Types Most common types include:1) Venous stasis ulcers2) Arterial (ischemic)3) Neurotrophic (DM)

Ulcers are typically classified by the appearance of theulcer, the ulcer location, and the way the borders and

surrounding skin of the ulcer look.

Overall causes

1. Venous hypertension2. Arterial disease Atherosclerosis: Buergers disease, Giant cell arteritis, PAN, Systemic sclerosis3. Small vessel disease DM, SLE, RA, Systemic sclerosis, Allergic vasculitis4. Abnormalities of blood Immune complex disease, Sickle cell anemia, Cryoglobulinaemia5. Neuropathy Diabetes mellitus, Leprosy, Syphilis, Syringomyelia, Peripheral neuropathy6. InfectionTropical ulcer, Tuberculosis, Deep fungal infections7. Tumor SCC, MM, Kaposis sarcoma, BCC8. Trauma Injury, Artifact, Iatrogenic

Ulcus Cruris Venosum

Venous stasis ulcers are a result of a poor functioning venous sys. leaky valves, obstructions, or

regurgitation disturbs the flow of blood from the lower extremities to heart blood collects in the lowerleg, damaging the tissues and causing wounds.

The risk to develop venous stasis ulcer with age.Etiology

1. Varicose veins result of pregnancy, obesity or hereditary factors.2. History of blood clots (phlebitis)3. History of trauma to the lower leg.4. Infla. diseases vasculitis, lupus, scleroderma or other rheumatological disease5. Infections6. Malignancies

Pathophysiology of venous leg ulcer

1. Fibrin Cuff theory: intra-capillary pressure exudation of plasmatic fluid and fibrinogen pericapillary fibrin cuff

oxygen and nutrient exchange are inhibited cellular degranulation

2. White cell trapping theory: pressure gradient b/w arteriolar and venular capillary blood flow blood cells adhere toendothelial cells leukocytes block and plug capillaries

Valves in the deep and communicating veins are incompetent calf muscle pump pushes blood into the

supf. veins venous hypertension enlarges the capillary bed White cells accumulate activated

(by hypoxic endothelial cells) releasing O2 free radicals and other toxic products which cause local tissuedestruction and ulceration.

The venous pressure also forces fibrinogen and 2-macroglobulinout through the capillary walls

macromolecules trap growth and repair factors so that minor traumatic wounds cannot be repaired andan ulcer develops.

http://www.foot-pain-explained.com/peripheral_circulation.htmlhttp://www.foot-pain-explained.com/peripheral_circulation.html

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Characteristics

These types of ulcers are found on the inner part ofthe lower leg usually just above the ankle.

Can occur either on one or both legs and each leg mayhave more than one ulceration.

Can range from painless to extremely painful (may berelieved by elevation of leg)

Clinical presentation The patient generally has a swollen leg and may feel

burning or itching.

There may also be a rash, redness, brown discolorationor dry, scaly skin.

The tissue surrounding these ulcers may exhibit signs of stasis dermatitis.The ulcer is characterized by:

Moist granulating base which oozes venous blood when manipulated Irregular, well defined borders Erythematous or hyper pigmented skin Teleangiectatic vein

Clinical classification of chronic lower extremity venous disease

Class 0 No visible or palpable signs of venous disease

Class 1 Telangiectasias, Reticular veins, Malleolar flare

Class 2 Varicose veins

Class 3 Edema w/o skin changes

Class 4 Skin changes ascribed to venous disease pigmentation, venous eczema,

lipodermatosclerosis

Class 5 Skin changes as defined above with healed ulceration

Class 6 Skin changes as defined above with active ulceration

Therapy of the venous ulcer

Compression therapy elastic bandages, pelotta Surgery varicose vein treatment, incompetent Perforator vein ligation Skin grafting partial or full thickness

Arterial Ulcer

Arterial (ischemic) ulceration result from an inadequate blood supply due to: Advanced age Arterial occlusive disease / atherosclerosis DM Thrombangiitis HTN Vasculitis Trauma Pyoderma gangrenosum Cigarette smoking / nicotine-vasoconstriction, carbon monoxide (damages the endo.!)

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Characteristics of arterial ulcersPresent almost anywhere on the leg usually distally and on the dorsum of the foot or toes, around lateral

malleolus, or at sites subjected to trauma or rubbing of footwear.

Wound may be superficial or deep. Margins are even, sharply demarcated, and punched out. Wound beds may be pale, gray or yellow with no evidence of new tissue growth With manipulation (such as debriding) these ulcers bleed very little or not at all Cellulitis or necrosis may be present

Clinical presentation

Pain, with exercise, at night, or during rest, is often the most distinguishing characteristic of aa. ulcers.

characteristic findings of chr. ischemia include:

Atrophic appearing skin (shiny, thin, dry) pale and cold skin absent pulses Delayed capillary return time Loss of digital and pedal hair

Fontaine classificationPeripheral artery disease may be asymptomatic orsymptomatic and the spectrum of symptoms is

classified according to the Fontaine classification.

This classification is not usually used ineveryday clinical practice, but it is useful

for research purposes

Embolic occlusion

Sudden obstruction in the arterial flow to the extremity due to an embolism or thrombosis

Pain/sudden, great intensity Pallor - caused by ischemia Pulse deficit helps determining the site Coldness Paralysis

Summary of diff. b/w leg ulcer types

Venous Arterial

Localization Superior to the medial malleolus Anterior tibial surface

any bony prominence of foot-toes, heelsArterial

circulation

Normal pulses or absent pulses

Ulcer appearance irregular border sharply demarcated margins

Surrounding areas Edema, Erythema, Stasis, Pigmentation Pale and waxy, shinny texture

skin atrophy, Pale and cold, hair loss

Class Symptoms

I No symptoms

II Claudication but no rest pain

1. intermittent, moderate claudication2. intermittent, severe claudication

III Pain at rest and night, but no tissueinvolvement

IV Pain and ulceration1. with local inflammation2. with widespread inflammation