Chapter 123: Skin ulcers

An ulcer is a localised break in the epidermal tissue of the surface of the skin or mucous membrane as a result of trauma, pressure, infection; they are associated with an underlying pathology. This applies particularly to leg ulcers. Ulcers are commonly found on the legs and feet, on areas exposed to the sun, and over bony prominences on the sacrum and heels. They may be clean, sloughy or necrotic.

The national morbidity survey (UK) showed that 2–3 per 1000 patients per annum consulted their GP with ‘chronic ulcers of the skin’.

It is useful to keep in mind the various causes of ulcers (see TABLE 123.1). The commonest causes or types are venous and ischaemic ulcers of the leg, pressure ulcers (decubitus) and trauma. It is important not to misdiagnose malignant ulcers, including ‘Marjolin ulcer’, which is a squamous cell carcinoma (SCC) developing in unstable chronic scars or ulcers (e.g. burns, venous ulcers, tropical ulcers) of long-standing duration. Amelanotic melanoma is a specific trap.

History

A careful history helps determine the cause of the ulceration. Relevant history includes previous deep venous thrombosis or pulmonary embolism, diabetes, rheumatoid arthritis, inflammatory bowel disease, chronic skin ulcers and arterial insufficiency, including a history of intermittent claudication and ischaemic rest pain.

A drug history is important, considering especially beta blockers and ergotamine, which can compromise the arterial circulation, corticosteroids and NSAIDs, which affect healing, and nifedipine, which tends to aggravate ankle oedema.

Examination³

Any ulcer should be assessed for the following characteristics:

• site

• shape

• size

• edge—consider consistency

• floor

• base

• discharge

• surrounding skin:

  • – colour (? signs of inflammation)

  • – sensitivity

• mobility in relation to underlying tissue

• regional lymph nodes

Site of ulcer

Venous ulcers typically occur on the medial side of the leg in relation to incompetent perforating veins in the traditional gaiter area (see FIG. 123.1).

Ischaemic ulcers tend to occur on the lateral side and anterior part of the leg and the foot.

Trophic ulcers, which are associated with neuropathy, occur on parts subject to repeated pressure and trauma, such as the ball of the foot or the pulps of the fingers.

Postsolar keratoses

Solar-induced ulcers, such as SCCs and BCCs, occur on such parts exposed to the sun. It should be noted if the ulcer is related to old scars, including burns and chronic ulcers.

Size, shape and edge

The classic appearances of various ulcers are presented in FIGURE 123.2. These are general guidelines only. Infective ulcers due to Mycobacterium species and pressure injury tend to have an undermined edge while a trophic ulcer is punched out and typically round in surface shape. A raised firm ulcer edge may indicate malignancy.

Floor of the ulcer

The floor or base of the ulcer provides useful clinical information. A dry or extended base or necrotic eschar in the floor implies ischaemia. Venous ulcers on the other hand are often superficial and tend to have fibrinous exudate and ooze, sometimes purulent fluid.

Colour guide:

• black—necrosis, ischaemia

• yellow—slough

• red—granulation

• pink—epithelium

Investigations

The following should be considered, according to the clinical findings:⁴

• full blood count

• ESR/CRP

• random blood sugar/HbAIc (known diabetes)

• kidney function tests

• rheumatoid factor tests

• duplex Doppler ultrasound

• swab for specific organisms

• biopsy, especially if SCC suspected (be careful of biopsy if melanoma: amelanotic melanomas are a trap); also accurately identify an infective organism

The most common causes of lower limb ulceration are venous disease, arterial disease, mixed venous and arterial, and diabetes.

Differentiating between leg ulcers (85%) and foot ulcers (15%) is very important since they present two very different problems.³ According to the survey by Stacey, venous disease is present in two-thirds of leg ulcers, while arterial disease occurs in 28% (see TABLE 123.2). Ulceration on the foot frequently has an arterial aetiology (72%), with many of these patients also having diabetes, whereas venous disease is present in only 6%.⁵

The differential characteristics are presented in TABLE 123.3.

A general examination, including the leg, is very important. This includes examining the venous drainage (CHAPTER 66), the arterial pulses and the sensation of the leg, and checking for the presence of diabetes.

Appropriate investigations (if required) include:

• full blood count

• blood sugar

• duplex Doppler ultrasound for arterial circulation

To swab or not to swab

A routine ulcer swab is not considered to be of significant value. If specific organisms such as Mycobacterium ulcerans are suspected, then cultures are necessary. Biopsy is considered to be accurate.

Measurement of ankle/brachial pressure index

To plan management of a leg ulcer, it is ideal to determine the blood flow with hand-held Doppler ultrasound. Measure ankle and brachial systolic pressures and then determine the ABI, which is the ankle pressure divided by the brachial pressure. Typical levels are:⁴

The ability to determine the cause of the ulceration and thus treat accordingly, especially with pressure dressings, has been a major advance in management. An ABI <0.8 warrants caution in applying any compression; <0.4 demands urgent referral.

General rule: Low compression 0.7–0.8; no compression <0.7.

Arterial (ischaemic) ulcers

Ischaemic ulcers are generally localised to the most peripheral areas below the ankle joint (see FIG. 123.3), such as the tips of the toes and the point of the heel, or to pressure points such as the heels, malleoli or head of the first metatarsal.

Clinical features

• Painful

• Punched out

• Minimal granulation tissue

Management is directed towards reperfusion.

Venous ulceration

Venous ulceration (synonyms: ‘varicose’, ‘stasis’ and ‘gravitational’ ulcers) accounts for the majority of leg ulcers. Chronic venous insufficiency is one of the most common medical problems in the elderly, with an estimated incidence of 5.9%.⁶

The problem is invariably secondary to deep venous thrombophlebitis. The subsequent chronic venous hypertension produces trophic changes such as hyperpigmentation (see FIG. 123.4), fibrotic thickening, induration and oedema. The end point of this process is ulceration, which affects 3% of those with varicose veins and 30% of those with trophic changes.⁷

Clinical features⁸

• Occur in same area as venous eczema

• Shallow (but can reach periosteum)

• More common medial than lateral

• Sometimes circumferential

• Granulating floor sometimes with surrounding inflammation—may be cellulitis

• Notoriously slow in healing without adequate compression

• Generally not tender but can be painful

• Associated pain is usually relieved by raising the leg

On examination, superficial varicosities are usually but not invariably present. Pitting oedema may be present early but with time fibrosis and firm induration develop. Other clinical features include dermatitis (eczema), punctate capillary proliferation, haemosiderin, hyperpigmentation and ‘atrophie blanche’ (porcelain white scar with rim of telangiectasia).⁸

Management (venous leg ulcers)

A major advance in the management of venous ulcers has been the finding that wounds heal better in an occluded or semi-occluded state.⁹ A moist environment also aids healing. The dressing will control the wound environment. The main treatment is graduated compression at 20–40 mmHg. See TABLE 123.4.

Principles of optimal management

• Explanation about the cause, and promotion of patient compliance

• Promoting clean granulation tissue to permit healing (see TABLE 123.4)

• Meticulous cleansing and dressing (avoid soaps and sensitising preparations)

• Prevention and control of infection—antibiotics indicated only if cellulitis (cephalexin or erythromycin): if infection is confirmed NOT where inflammation is present (as in most venous ulcers)

• Firm elastic compression bandage—use a minimal stretch bandage from base of toes to just below the knee. The degree of compression depends on the blood flow and is proportional to it

• Bed rest with elevation (if severe, 45–60 minutes twice a day and at night): ensure legs are elevated higher than the heart

• Encourage early ambulation and exercise

• Appropriate modification of lifestyle including weight reduction, smoking cessation (NB)

• Good nutrition includes a healthy balanced diet with ample protein and complex carbohydrates

• Be aware of drugs that can adversely affect healing (see TABLE 123.5)

Note: Firm compression is the single most important factor in the healing of venous ulcers.^2,7 Options include elastic stockings, elastic bandages, zinc paste bandages (Unna’s boots) and legging orthoses.¹¹

Cleansing/debridement agents

There are many cleansing agents, including:

• N saline, surfactants e.g. QV wash and warm tap water

As a rule, avoid antiseptics, which destroy cells, although cadexomer iodine, which is a slow-release form of iodine, is non-toxic to tissues, reduces bacterial load and clears odorous slough. However, wash off iodine solution after 5 minutes. Iodosorb is a low-dose iodine dressing appropriate for infected, contaminated wounds, particularly a diabetic wound. A good combination is normal saline cleansing followed by IntraSite Gel for debridement, covered with a foam dressing. Strong salt dressings (e.g. Mesalt or Curasalt) are very good for cleaning contaminated, infected wounds and hypergranulation but need changing daily and to be covered by a very absorbent overlying dressing.

Hydrogels such as IntraSite Gel, which have been found to be effective at debridement (including black necrotic areas), have generally replaced enzyme dressings.

Lymphoedema¹²

This is not pitting oedema but a reduction in the function of the lymph vessels to drain extracellular fluid.

Primary lymphoedema is caused either by malformation of the lymph vessels or by damage from bacteria, fungi, parasites, insects, chemicals, radiotherapy or surgery. Secondary lymphoedema is caused by primary malignancy or intralymphatic propagation of a tumour. Lymphoedema results in major changes to the skin such as thickening of the skin, build-up of scale and keratin and worsening hyperkeratosis, producing a warty appearance.

Wounds are common in lymphoedema. They are managed by treating the wound environment with appropriate dressing, but the main treatment is significant compression with either specially developed garments or inelastic bandages. Difficult cases should be referred to a specialist lymphoedema clinic.

A simple clinical test for determining a lymphoedema component in a swelling of the lower leg is the Stemmer’s sign test. This test is performed by lifting and pinching the skin at the dorsum of the second toe on each foot. A positive Stemmer’s sign results when the skin cannot be lifted and pinched together. The test is negative for lymphoedema when the skin can be pinched and lifted. A positive Stemmer’s sign always indicates lymphoedema, but a negative sign does not always rule out lymphoedema.

Wound dressing^9,13

There are six main types of modern wound dressings: films, hydrogels, hydrocolloids, alginates, foams and hydroactives (foam-like)—all expensive. Films, hydrogels and hydrocolloids increase the wound moisture whereas alginates and foams absorb exudate. The more traditional dressings such as tulle gras, non-adherent pad dressings and saline soaks have little use. A lightweight cohesive bandage or a lightweight tubular bandage can be used to hold non-adherent dressings in place.

General rules:¹⁰

• allow 2–3 cm of dressing greater than the wound

• place one-third above and two-thirds below the wound

• remove when ‘strike-through’ occurs

• remove with care in older patients

• remove under the shower if necessary

• when in doubt, DO NOT HARM: use foam and gel combinations

Medicated occlusive bandages

There are several suitable occlusive paste bandages for ambulant patients, which ideally should be left on for 7–14 days. These contain zinc oxide. Examples include Flexi-Dress, Gelocast and Zipzoc (which are zinc paste bandages with no preservatives).

Patch testing for an allergic response should be performed for a few days beforehand.

Bandages

Bandages have two main uses:

• retention: to keep a dressing in place

• compression: to assist venous return

High-stretch compression bandages are best. Method of application:

• spiral application from toes with figure 8 around ankles, then spiral to knee

• 50% overlap

• constant tension provides graduated compression (Laplace’s Law)

Pitfalls and other factors to be considered

• Treat the primary cause by surgery or other means (e.g. varicose veins, vascular insufficiency).

• If oedema, elevate legs and prescribe diuretics. An ulcer will not heal in the presence of significant ankle oedema.

• Clarify the cause of oedema, which may be due to medication e.g. calcium channel blockers.

• Be careful of allergy to local applications (e.g. zinc).

• Be careful of irritation from local applications (e.g. antibiotics). Antibiotic-impregnated dressings are not generally recommended.

• Avoid heavy packing of the wound.

• Consider grafting (pinch skin or split thickness).

• Consider oxpentifylline (Trental 400) for chronic occlusive arterial disease and venous disease.⁸

Post-healing and prevention of ulcers

• Encourage preventive measures, such as regular walking, good nutrition, no smoking, elevation of leg when resting, great care to avoid trauma.

• Apply emollients for varicose eczema.

• Wear a compression-grade elastic stocking for varicose ulcers (e.g. Jobst Fast-Fit, Jobst Venoscan).

A recommended treatment routine for a leg ulcer is presented in TABLE 123.6. It is desirable (for the outpatient) to leave the dressings and bandages in place for 1 week, perhaps 2 weeks, depending on the state of the dressing.

Principles of management for chronic ulcers are summarised in TABLE 123.7.

Decubitus ulcer (pressure injury)

Pressure injuries tend to occur in immobile patients, especially those who are unconscious, paralysed or debilitated. The cause is skin ischaemia from sustained pressure over a bony area, particularly the heels, sacrum, hips and buttocks. Poor general health, including anaemia, is a predisposing factor.

The classification of pressure injuries is based on the level of tissue damage and depths of the wound:

• Stage 1: non-blanching erythema

• Stage 2: partial thickness (superficial) ulceration

• Stage 3: full thickness ulceration

• Stage 4: deep full thickness—skin loss with extensive tissue loss

Unstageable: deep tissue injury.

Clinical features

• Preliminary area of fixed erythema at pressure site

• Relatively sudden onset of necrosis and ulceration

• Ulcer undermined at edges

• Possible rapid extension of ulcers

• Necrotic slough in base

Prevention

• Good nursing care including turning patient every 2 hours

• Regular skin examinations by the nursing and medical staff

• Special care of pressure areas, including gentle handling

• Special beds, mattresses (e.g. air-filled ripple) and sheepskin to relieve pressure areas

• Good nutrition and hygiene

• Control of urinary and faecal incontinence

• Avoid the donut cushion

• Avoid soaps

Treatment¹³

The most important principle is early intervention including relief of pressure, friction and shear. Use above prevention measures, plus:

• clean base with warm water or saline solution and a surfactant (applied gently via a syringe)

• general guidelines for dressings:

  • – deep ulcers—alginates (e.g. Algisite M, Kaltostat)

  • – shallow ulcers—hydrocolloids (e.g. DuoDERM, CGF)

  • – dry or necrotic ulcers—hydrogels (e.g. IntraSite, Purolin gel)

  • – heavy exudative ulcers—foams (e.g. Lyofoam, Lyofoam extra, Allevyn, Cutinova Cavity)

• give vitamin C, 500 mg bd

• give antibiotics for spreading cellulitis (otherwise of little use)

• for non-healing large pressure wounds, apply negative pressure therapy

• review patient’s nutritional status as it impacts on both formation of pressure injury and slow healing

• healing is usually satisfactory but, if not, surgical intervention with debridement of necrotic tissue and skin grafting may be necessary; this is very effective if the patient can cope

Undressing wounds

Removal of dressings from ulcerated wounds is very important. The contact layer should be removed slowly to prevent detachment of fragile epithelial surface cells and trauma to healthy granulation tissue.¹⁵

Role of honey

Honey has been advocated for centuries for healing ulcers. A particular type, Medihoney, is marketed. It provides moist healing and has antibacterial properties. Care has to be taken with over-moisturisation and maceration. Its role is still somewhat controversial as is the application of sugar, cromoglycate powder, maggots and hyperbaric oxygen.

Trophic ulcers

Trophic ulcers are due to neuropathy causing loss of sensation (invariably diabetic) and usually follow an injury of which the patient was unaware (see FIG. 123.5).

A feature is a deep, punched-out lesion (similar to ischaemic ulcers) over pressure points. A common site is the ball of the foot under the first metatarsal head, but the heel or a bunion may also be affected.

The ulcers may extend to the bone and into joints. They are prone to secondary infection.

Treatment is based on controlling the diabetes and clearing infection with appropriate antibiotics, but referral for surgical management is usually essential.

Mycobacterium ulcerans (Buruli ulcer)

Buruli ulcer (also known as a Bairnsdale or Daintree ulcer) is caused by Mycobacterium ulcerans and usually begins as a painless papule or nodule that forms a necrotic ulcer over weeks to months. An undermined edge is a classic feature.

It occurs in specific geographic locations, namely coastal Victoria, Far North Queensland and the tropical regions of Central and West Africa.

There is a current epidemic in coastal Victoria, where possums are believed to be a reservoir. All age groups may be affected, including children.

Early referral to an infectious diseases unit is recommended, with 8 to 12 weeks of oral antibiotics (usually rifampicin and clarithomycin) required, along with specialist wound care. Surgical debridement of the ulcer may also be necessary.

These self-inflicted ulcerated or erosive skin lesions have a psychological basis.

Dermatitis artefacta

In this condition, patients deny self-trauma and may have deep-seated psychological problems, or they may be malingering or manipulative for secondary gain.

Neurotic excoriations

These lesions, which are usually identical to the artefactual lesions, are caused by patients who admit to scratching, picking or digging at their skin (FIG. 123.6). It occurs at times of stress and treatment is seldom successful. Treatment consists of counselling with CBT, a trial of antidepressants and topical antipruritics such as:

• coal tar solution (liquor picis carbonis) and menthol in sorbolene cream

• or

• menthol (0.5%) or phenol (1.0%) in aqueous cream

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Pressure sores (bed sores)