Despite the great increase in our understanding of the pathology of leg ulcers, their management is still largely “art”.
Consequently there are numerous treatments, each with their enthusiastic advocates.
There are, however, basic concepts which are helpful in management.
As about 95% of leg ulcers are of the “venous” or gravitational variety these will be considered first.
Pathology of venous ulcers
The skin Ulcers arise because the skin dies from inadequate provision of nutrients and oxygen. This occurs as a consequence of
(a) oedema in the subcutaneous tissues with poor lymphatic and capillary drainage and
(b) the extravascular accumulation of fibrinous material that has leaked from the blood vessels.
The result is a rigid cuff around the capillaries, preventing diffusion through the wall, and fibrosis of the surrounding tissues.
The blood vessels
Arterial perfusion of the leg is usually normal or increased, but stasis occurs in the venules.
The lack of venous drainage is a consequence of incompetent valves between the superficial veins and the deeper large veins on which the calf muscle “pump” acts.
In the normal leg there is a superficial low pressure venous system and deep high pressure veins.
If the blood flow from superficial to deep veins is reversed then the pressure in the superficial veins may increase to a level that prevents venous drainage, Vancose veins with “back pressure” causing stasis and oedema.
Incompetent valves
Incompetent valves leading to gravitational ulcers may be preceded by:
(1) deep vein thrombosis associated with pregnancy or, less commonly, leg injury, immobilisation, or infarctions in the past
(2) primary long saphenous vein insufficiency
(3) familial venous valve incompetence that presents at an earlier stage there is a familial predisposition in half of all patients with leg ulcers
(4) deep venous obstruction. Who gets ulcers?
Mainly women get ulcers 2% of those over 80 have venous ulcers as a long term consequence of the factors listed above.
Leg ulcers are more likely to occur and are more severe in obese people.
Clinical changes
Oedema and fibrinous exudate often lead to fibrosis of the subcutaneous tissues, which may be associated with localised loss of pigment and dilated capillary loops, an appearance known as “atrophic blanche”.
This occurs around the ankle with oedema and dilated tortuous superficial veins proximally and can lead to “champagne bottle legs”, the bottle, of course, being inverted.
Ulceration often occurs for the first time after a trivial injury.
Lymphoedema results from obliteration of the superficial lymphatics, with associated fibrosis.
There is often hypertrophy of the overlying epidermis with a “polypoid” appearance, also known as lipodermatosclerosis. Venous ulcers occur around the ankles, commonly over the medial malleolus.
The margin is usually well defined with a shelving edge, and a slough may be present.
There may also be surrounding eczematous changes. Venous ulcers are not usually painful but arterial ulcers are.
It is important to check the pulses in the leg and foot as compression bandaging of a leg with impaired blood flow can cause ischaemia and necrosis.
Treatment
When new epidermis can grow across an ulcer it will, and the aim is to produce an environment in which this can take place.
To this end several measures can be taken:
(1) Oedema may be reduced by means of:
(a) diuretics;
(b) keeping the legs elevated when sitting;
(c) avoiding standing as far as possible;
(d) raising the heels slightly from time to time helps venous return by the “calf muscle pump”;
(e) applying compression bandages to create a pressure gradient towards the thigh.
(2) Exudate and slough should be removed. Lotions can be used to clean the ulcer and as compresses 0·9% saline solution, sodium hypochlorite solution, Eusol, or 5% hydrogen peroxide.
There is some evidence that antiseptic solutions and chlorinated solutions (such as sodium hypochlorite and Eusol) delay collagen production and cause inflammation.
Enzyme preparations may help by “digesting” the slough.
To prevent the formation of granulation tissue use silver nitrate 0·25% compresses, a silver nitrate “stick” for more exuberant tissue, and curettage, if necessary.
(3) The dressings applied to the ulcer can consist of:
(a) simple non-stick, paraffin gauze dressings an allergy may develop to those with an antibiotic;
(b) wet compresses with saline or silver nitrate solutions for exudative lesions;
(c) silver sulfadiazine (Flamazine) or hydrogen peroxide creams (Hioxyl); and
(d) absorbent dressings, consisting of hydrocolloid patches or powder, which are helpful for smaller ulcers.
(4) Paste bandages, impregnated with zinc oxide and antiseptics or ichthammol, help to keep dressings in place and provide protection.
They may, however, traumatise the skin, and allergic reactions to their constituents are not uncommon.
(5) Treatment of infection is less often necessary than is commonly supposed.
All ulcers are colonised by bacteria to some extent, usually coincidental staphylococci.
A purulent exudate is an indication for a broad spectrum antibiotic and a swab for bacteriology.
Erythema, oedema, and tenderness around the ulcers suggest a beta haemolytic streptococcal infection, which will require long term antibiotic treatment.
Dyes can be painted on the edge of the ulcer, where they fix to the bacterial wall as well as the patient’s skin.
In Scotland bright red eosin is traditionally used, while in the south a blue dye, gentian violet, is favoured.
Systemic antibiotics have little effect on ulcers but are indicated if there is surrounding cellulitis.
A swab for culture and sensitivity helps to keep track of organisms colonising the area.
(6) Surrounding eczematous changes should be treated. Use topical steroids, not more than medium strength, avoiding the ulcer itself.
Ichthammol 1% in 15% zinc oxide and white soft paraffin or Ichthopaste bandages can be used as a protective layer, and topical antibiotics can be used if necessary.
It is important to remember that any of the commonly used topical preparations can cause an allergic reaction: neomycin, lanolin, formaldehyde, tars, Chinaform (the “C” of many proprietary steroids).
(7) Skin grafting can be very effective.
There must be a healthy viable base for the graft, with an adequate blood supply; natural re-epithelialisation from the edges of the ulcer is a good indication that a graft will be supported. Pinch grafts or partial thickness grafts can be used.
Any clinical infection, particularly with pseudomonal organisms, should be treated.
(8) Maintaining general health, with adequate nutrition and weight reduction, is important.
(9) Corrective surgery for associated venous abnormalities.
Arterial ulcers
Ulcers on the leg also occur as a result of:
(a) atherosclerosis with poor peripheral circulation, particularly in older patients;
(b) vasculitis affecting the larger subcutaneous arteries; and
(c) aterial obstruction in macroglobulinaemia, cryoglobulinaemia, polycythaemia, and “collagen” disease, particularly rheumatoid arthritis.
Arterial ulcers are sharply defined and accompanied by pain, which may be very severe, especially at night.
The leg, especially the pretibial area, is affected rather than the ankle.
In patients with hypertension a very tender ulcer can develop posteriorly (Martorelli’s ulcer).
As mentioned above, compression bandaging will make arterial ulcers worse and may lead to ischaemia of the leg.
Diagnosis
The differing presentation of arterial and venous ulcers helps in distinguishing between them, but some degree of aterial insufficiency often complicates venous ulcers.
Phlebography and Doppler ultrasound may help in detecting venous incompetence and arterial obstruction, which can sometimes be treated surgically.
Ulcers on the leg may also occur secondary to other diseases, because of infection, in malignant disease, and after trauma.
Secondary ulcers
Ulcers occur in diabetes, in periarteritis nodosa, and in vasculitis.
Pyoderma gangrenosum, a chronic necrotic ulcer with surrounding induration, may occur in association with ulcerative colitis or rheumatoid vasculitis.
Infections
Infections that cause ulcers include staphylococcal or streptococcal infections, tuberculosis (which is rare in the United Kingdom but may be seen in recent immigrants), and anthrax.
Malignant diseases
Squamous cell carcinoma may present as an ulcer or, rarely, develop in a pre-existing ulcer.
Basal cell carcinoma and melanoma may develop into ulcers, as may Kaposi’s sarcoma.
Trauma
Patients with diabetic or other types of neuropathy are at risk of developing trophic ulcers.
Rarely they may be self induced “dermatitis artefacta”.
