Varicose or gravitational disorders
The largest group of patients with skin lesions of the legs suffer from disorders of venous drainage. The venous circulation of the legs has been likened to a pump which will work satisfactorily only if the valves in the deep veins and the communicating veins between the deep and superficial plexuses are intact, and the muscles of the leg active. Failure of any part of the pump leads to venous insufficiency which results in increased pressure in the venules particularly on walking and standing. The rise in pressure causes hypertrophy of the capillary walls which in turn interferes with the passage of metabolites and blood gases.
Venous insufficiency is caused by:
(i) Obstruction of the deep veins by phlebothrombosis.
(ii) Valvular incompetence after phlebothrombosis.
(iii) Primary valvular incompetence due to congenital absence of valves. (This condition is often hereditary and is associated with varicose veins.)
By far the commonest cause is the post-thrombotic state after childbirth, the patient usually is a middle-aged woman who has had several children and who is overweight. Thrombosis in the deep veins also follows surgical operations, injury to the leg and prolonged bed rest.
Since the deep veins may be grossly damaged without the formation of varicose veins it is incorrect to attribute the complications of venous insufficiency to varicose veins, alone and a preferable and more correct name for the condition is gravitational or stasis syndrome.
The complications of venous insufficiency are:
(i) Pigmentation. This occurs along the line of varicose veins and around the ankles. Raised capillary pressure forces red cells into the surrounding tissue where the haemoglobin is turned into haemosiderin. Melanin pigmentation may occur where there has been erythema from thrombophlebitis or eczema.
(ii) Eczema. Often eczema starts in an area of pigmentation. Erythema and scaling appear and may remain localised and persistent for years. Sudden exacerbation of the eczematous area is often accompanied by a generalised eczematous eruption on the face and forearms. Though infection and local applications may precipitate such a phase some form of auto allergy may be the correct explanation for the onset of gravitational eczema.
(iii) Atrophie blanche. White scars often linked together in a network occur on the ankles in patients with venous insufficiency. They resemble scars left by ulceration but are a result of slow necrosis. They occur frequently with blockage of the iliac veins or inferior vena cava.
(iv) Oedema. When standing, the normal individual is always on the verge of oedema of the legs. Any rise in venous pressure will cause increased filtration through capillary walls and increase of tissue fluids. In the early stages this may be unnoticed as it collects around the tendo Achilles. Organisation of oedema gives rise to induration and fibrosis which fixes the joints. This limits movement of muscles and adds to the failure of the muscle pump.
Ulceration. A leg suffering from venous insufficiency is liable to ulceration. This occurs usually after a minor injury, such as an abrasion or a bruise which precipitates necrosis of the skin and subcutis. The diagnosis is usually simple since pigmentation, varicosities, induration and oedema are likely to suggest the gravitational origin.
Avascular ulcers due to arterial insufficiency can be distinguished by a history of claudication and absence of pulsation in peripheral arteries. Essential investigations of any leg ulcer should include a Wassermann reaction, urine examination to exclude diabetes and blood pressure estimation since leg ulcers may occur as a complication of hypertension. A high proportion of patients with chronic leg ulcers develop an iron deficiency anaemia which adds to the tissue malnutrition. In the absence of evidence of venous insufficiency other less common causes of leg ulcers such as blood dyscrasias, rheumatoid arthritis or scleroderma should be sought.
A number of confused elderly patients develop superficial ulceration of the legs from postural oedema by sitting in a chair day and night. The syndrome of ‘arm-chair legs’.
Treatment of gravitational eczema and ulcer
Control of venous hypertension and the removal of oedema by restoration of the venous pump is the primary aim.
An elastic pressure bandage should be applied daily from toes to knee before the patient arises from bed. The bandage should enclose the whole ankle including the heel. If oedema is persistent around the tendoachilles massage and extra padding with polythene foam Bisgaard treatment (see appendix) may be necessary. If there is gross oedema oral diuretics may also be useful. With the bandage on, walking should be encouraged as walking is good for legs, it is standing which is harmful. The movement of the muscles beneath the elastic support massages fluid up the leg and the increased arterial blood flow and movement of the ankle joint previously fixed by pain and disuse are all beneficial. We see many patients in whom crepe bandages have been prescribed but these do not give sufficient support and are valueless. Elastic stockings are also less effective than elastic bandages and should be reserved for maintenance of support when the ulcer or eczema has healed. Almost as important as firm elastic pressure is weight reduction in the obese and, though frequently difficult to achieve, its value should be impressed on the patient. Many of the elderly are deficient in protein, iron, ascorbic acid and folate and correction of these factors will accelerate recovery. Claims for speedy healing by the giving of zinc sulphate 200 mg t.d.s. have been made. This is justifiable if zinc deficiency exists but in our hands the results have not been impressive.
Local applications to gravitational eczema
In principle, local treatment is the same as it is to eczematous eruptions elsewhere but even more care than usual should be taken to avoid sensitisation to medicaments. Zinc paste B.N.F. as a simple protective with the addition of coal tar 1 per cent if itching is not rapidly relieved is all that is necessary in the mild case. The paste should be covered with Tubegauze and an elastic bandage applied over this. If skin damage by scratching is a marked feature an occlusive bandage of ichthammol or coal tar left in position for a week gives good results. Acute exudative eruptions are an indication for topical steroid lotion or ointment without added antibiotic or antiseptic. If the eczema on the primary site can be controlled quickly the risk of generalised spread of the eruption is reduced. Where possible the patient should remain ambulant and only if severe weeping of the skin and gross oedema of the leg are not controllable than bed rest becomes necessary. Exercises in bed to prevent further phlebothrombosis should be carried out.
Local treatment of leg ulcers
Wet dressings of 1/4 strength sodium hypochlorite solution are as effective as any other local application and the risk of contact sensitivity is minimal. If steroid applications are used for the treatment of surrounding eczema, care should be taken to prevent any entering the ulcer cavity. Steroids cause vaso-constriction and delay healing. Epithelialisation will not start while sloughs remain in an ulcer. The clearance of sloughs may be hastened by the use of a malic acid preparation Aserbine cream, applied twice daily to the ulcer. We have found a layer of zinc paste applied around the ulcer necessary to prevent irritation of the adjacent skin. When there is a clean granulating surface non adherent rayon squares, Johnsons NA or a proprietary honey and cod liver oil tulle (M and M tulle, Malam Laboratories, Manchester) can be left in position for 3 days at a time. It is a mistake to disturb the epithelialising ulcer more frequently.
The healing time of extensive granulating areas can be shortened by the use of multiple small skin grafts applied under paraffin gauze and left in position for 10 days. This simple procedure, using the thigh as a donor area and carried out under local anaesthesia, is safe, effective and does not require plastic surgical skill. Severely infected ulcers should be treated by systemic antibiotics though the exception is when the infecting organism is Bacillus pyocyaneus which can be controlled by polybactrin (Polymixin bacitracin) or locally applied colistin.
Whatever local treatment is used elastic bandages are essential. In the few patients who will not cooperate an adhesive elastic bandage (Elastoplast) can be substituted. Skin irritation can be avoided by applying a calamine impregnated bandage beneath or applying adhesive bandage with the resin surface outwards. When the ulcer has healed the majority of patients still need elastic support, possibly only elastic stockings, and weight reduction must be maintained. To avoid recurrent ulceration surgical treatment, either by ligation or injection of perforating veins around the malleoli or the stripping of varicose veins must be considered but careful investigation and possible venography are advisable before surgery is embarked upon.
Necrosis of the skin of the leg from anoxia occurs in patients with peripheral arterial disease, frequently a complication of diabetes. There is usually a history of claudication in the calf muscles. The ulcers which are usually higher up the leg than venous ulcers are covered by a dry, hard slough. The skin of the foot is shiny, the toes are likely to be cold and blue or with a dull erythema and no pulsation can be felt in the peripheral vessels.
Treatment. It is important to recognise the arterial insufficiency as elastic bandages are contra-indicated. Exercises, control of diabetes if present, systemic antibiotics and bed rest may permit slow healing to take place. Eventually amputation of the limb may be necessary if reconstructive arterial surgery is not possible.
Livedo reticularis (Marbled skin)
There is considerable individual variation in the vascular supply of the skin of the face and limbs and in particular its response to heat and cold.
This is an exaggeration of the normal vascular pattern seen on the limbs in children and young adults. Islands of white skin are surrounded by a bluish, pink network where the blood flow is more sluggish. This network of vessels can be made permanently visible by prolonged exposure to heat from the fire or hot water bottle which gives rise to erythema and pigmentation (erythema ab igne). After puberty many girls develop cold blue swelling of the lower third of the legs (erythrocyanosis crurum) associated with a liability to chilblains. A similar bluish response of the hands and feet to cold is termed acrocyanosis.
Chilblains are caused by exposure of susceptible individuals to cold; not only must the extremities be cooled but chilling of the whole body is an important factor. Chilblains are dusky red, itchy swellings which occur mainly on the fingers and toes but can extend up the backs of the legs and occasionally occur on areas such as the buttocks, the nose and ears. The swelling and burning are a result of the active hyperaemia which follows a period of spasm of the small arterioles induced by cold.
Treatment. The best simple preventive measures are designed to prevent body chilling. Sedentary workers in cold surroundings are more liable to suffer from chilblains than active, out-of-door workers exposed to much lower temperatures. Adequate heating of offices, shops and schools, physical exercise and the wearing of warm clothing are of more value than drugs. Exposure of the chilblain areas to intensive ultraviolet light just before the winter has been shown to prevent chilblains by increasing the skin blood flow for some months, but we have found this an unreliable method of treatment. When chilblains have developed inunction of the following gives symptomatic relief, Balsam of Peru and camphor 3 per cent of each in lanolin and soft paraffin equal parts. Calcium and calciferol which have long been used are ineffective but some relief may be obtained by the use of vasodilator drugs such as nicotinic acid 100 mg or dibenyline (Phenoxybenzamine) 10 mg twice daily.
A more serious reaction to cold is that of Raynaud’s phenomenon. The manifestations are due to arteriolar vasoconstriction of the vessels of the fingers and, less commonly, the toes, nose and ears. The fingers become cold, dead white for a period of several minutes to several hours. When the spasm of the vessel diminishes, the fingers become blue, hot and painful. Whilst this response to cold may persist with little structural change for many years, in some patients the symptoms denote the onset of a chronic systemic disease, systemic sclerosis of scleroderma, now recognised as one of the auto-immune diseases. The condition, which is more common in women than in men, involves the connective tissue of the whole body and severe irreversible changes take place in the dermis, kidney, lung, heart and gastro-intestinal tract. After the initial Raynaud’s phenomenon the fingers become stiffened with binding down of the dermis to the deeper tissues and gradual tapering and atrophy of the finger tips which is called acrosclerosis. This stage may last many years before systemic organs appear to be involved. The face and mouth are frequently affected and this gives rise to a characteristic facies with a shrunken mouth and beak nose. Telangiectases appear also on the face and hands. Dysphagia is complained of when the oesophagus is involved, though x-ray changes may be found even without symptoms. The course is progressively downhill with acute episodes of gangrene of the extremities associated with ulceration and calcification. No curative treatment exists for systemic sclerosis but sympathectomy is of some value in Raynaud’s disease not associated with scleroderma.
Localised scleroderma or morphoea
This is histologically due to a similar change in the dermal collagen to the systemic disease but is a harmless disorder. Circumscribed patches of hardened ivory coloured skin with a violaceous border appear usually on the trunk though occasionally segmental or nerve distribution is seen. Local injection of steroids or the application of steroid ointment under polythene have been used but give disappointingly poor results but spontaneous resolution occurs in a considerable number of patients. Closely allied to localised scleroderma is another disorder known as lichen sclerosus et atrophicus. This differs only in that the lesions are usually smaller and there is frequent involvement of the vulva in women.
Pressure sores develop in bedridden patients if they are left lying inert bearing their weight for hours on the same bony areas. Thus a patient lying on his back develops pressures sores over the sacrum, the backs of the heels and the scapulae. Constant pressure on these points impairs the blood supply to the skin and subcutaneous tissues so that they develop a localised gangrene. If the patient is in a state of collapse, so that the normal blood supply to the skin is already reduced, such lesions can form very rapidly; for example someone who collapses unattended at home and lies unconscious on a hard floor for about 12 hours before being found, may already be developing sores on the points of pressure.
Maceration of the skin in the incontinent patient makes the development of bedsores more probable. In some skin diseases such as pemphigus in which large areas of skin become eroded as part of the disease process, bedsores are extremely difficult to prevent.
Once formed, bedsores are very difficult to heal and every possible preventive measure should be adopted from the start of the patient’s illness. In a very ill patient who is needing a lot of attention and may have to be somewhat immobilised for transfusion of fluids it is only too easy to give insufficient attention to the pressure areas until it is too late. The patient should be moved or encouraged to move, or to lie for 2 hours on one side then for 2 hours on the other. If the patient’s general condition allows, even though the skin may be severely diseased, he should be got out of bed and sat in a chair for an hour or two each day to take pressure off the heels and sacrum. The very ill patient who cannot be got out of bed can be nursed on a ripple mattress which by varied inflation alters the points bearing weight. Possibly even better than the ripple mattress is a sheepskin of which a synthetic type is available which is very easy to clean. When the patient has to sit up, an inflatable air ring takes pressure off the sacrum but sometimes defeats its object by making it difficult for the patient to move himself. Also in the sitting patient padded rings should be bound on the heels to lift them off the bed or an oblong block of foam rubber or polythene 4-6 inches thick can be cut to extend from the knee to the ankle and placed under calves so that the heels are elevated off the bed.
The traditional practice of rubbing the back with spirit—which is in any case of doubtful value—is out of the question in cases of generalised skin disease. Talc powder dusted over the back and into the underlying areas of the bed absorbs sweat and reduces friction. The incontinent patient presents an additional difficulty and obviously the draw sheet should be changed whenever soiled so that the skin does not become macerated. The application of an oily cream B.P. to the back and buttocks twice daily also helps to waterproof the skin and prevent maceration. If these precautions are meticulously observed pressure sores should not develop.
Unfortunately occasionally patients have already developed pressure scores at home before they come under nursing care. In such cases the first line of treatment is removal of pressure from the sore by the methods already detailed.
The multitude of ideas on what is the best application for the established pressure sore indicates that none is of outstanding value and suggests that most are virtually useless. We have found cod-liver oil and honey tulle (M & M tulle) to be a sure, comfortable and satisfactory application. If the ulcer is deep it can be packed with the tulle; if shallow applied once daily. The healing of any ulcer depends at least as much on the patient’s general condition as on local applications. Large bedsores produce toxaemia which can lead to death and always depress blood formation causing anaemia. Improvement in the underlying disease, correction of anaemia with blood transfusion if necessary, maintenance of an adequate diet and vitamin supplements are all valuable moves in the battle against an established bedsore.