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
Table 123.2Causes of chronic ulceration of the leg and foot5 ||Download (.pdf) Table 123.2 Causes of chronic ulceration of the leg and foot5
| ||% |
|The leg |
|Venous disease ||52 |
|Mixed venous and arterial disease ||15 |
|Arterial disease ||13 |
|Others ||20 |
|The foot |
|Arterial disease ||72 |
|Mixed venous and arterial disease ||2 |
|Venous disease ||4 |
|Others ||22 |
The differential characteristics are presented in TABLE 123.3.
Table 123.3Comparison of typical features of venous and arterial ulceration of the leg ||Download (.pdf) Table 123.3 Comparison of typical features of venous and arterial ulceration of the leg
| ||Venous ||Arterial |
|Site || |
Around ankle and lower third of leg (gaiter area)
Just above medial and lateral malleoli
Distal to ankle
Over pressure points on toes, side of foot, metatarsal heads
|Pain ||Nil to mild ||Usually moderate to severe |
|Oedema ||Pitting oedema usually present ||Usually absent |
|Ulcer features || |
Ooze + + +
Often deep, involving deep fascia
|Associated limb features || |
Leg warm, red, oedematous
Diminished or absent peripheral pulses
Thin, shiny, dry skin
|History || |
Peripheral vascular disease—claudication, rest pain
|ABI ||>0.9 ||<0.5–0.7 |
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:
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
|Normal range ||0.91−1.3 |
|Normal ||>0.9 (venous ulcer) |
|Ischaemic ||<0.5 (arterial ulcer) |
|Claudicant ||0.5−0.9 (mixed arterial− venous ulcer, significant ischaemia if <0.8) |
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.
Ischaemic ‘arterial’ ulcers in an elderly woman with a long history of intermittent claudication and a recent history of nocturnal ischaemic rest pain in the feet. The ulcers healed after reconstruction for arterial obstruction.
Photo courtesy Terry Devine
Management is directed towards reperfusion.
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
Venous ulceration in an elderly patient with postphlebitic varicose ‘eczema’. Venous pigmentation, dermatitis, atrophy and calcification of the subcutaneous tissues are present.
Photo courtesy Terry Devine
Occur in same area as venous eczema
Shallow (but can reach periosteum)
More common medial than lateral
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.
Table 123.4Wound management principles ||Download (.pdf) Table 123.4 Wound management principles
|The good ||The bad |
|Hydration ||Dryness |
|Washing with water or saline ||Excess antiseptics |
|Insulation protection ||Exposure to air |
| ||Scabs, crust, slough |
|Compression (venous) ||Dry dressings |
|Hydrogel ||Gauze packing |
|Foams ||Tulles |
|Minimal changes ||Oedema/lymphoedema |
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)
Table 123.5Drugs that can hamper healing10 ||Download (.pdf) Table 123.5 Drugs that can hamper healing10
|Cytotoxic agents |
|Beta blockers |
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
There are many cleansing agents, including:
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.
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.
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.
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 have two main uses:
High-stretch compression bandages are best. Method of application:
spiral application from toes with figure 8 around ankles, then spiral to knee
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.
Table 123.6A recommended leg ulcer treatment method ||Download (.pdf) Table 123.6 A recommended leg ulcer treatment method
|Clean with normal saline |
If slough, apply IntraSite Gel
Dressing: non-adherent e.g. Allevyn; Melolin
Occlusive paste bandage—e.g. zinc oxide (7–14 days), from base of toe to just below knee, plus compression bandage
Compression bandage (e.g. Eloflex) to just below knee
Consider Tubigrip stockinette cover
Principles of management for chronic ulcers are summarised in TABLE 123.7.
Table 123.7Principles of management of chronic ulcers14 ||Download (.pdf) Table 123.7 Principles of management of chronic ulcers14
|Ulcer type ||Major management principles |
|Venous ||Control venous insufficiency: |
|Arterial ||Vascular assessment for surgical intervention |
|Mixed venous/arterial ||Vascular assessment for surgical intervention |
|Pressure ||Eliminate or reduce pressure |
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.
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
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
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
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
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 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).
Neuropathic ulcer under the third metatarsal of the right foot in a patient with diabetes
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.
DERMATITIS ARTEFACTA AND NEUROTIC EXCORIATIONS
These self-inflicted ulcerated or erosive skin lesions have a psychological basis.
In this condition, patients deny self-trauma and may have deep-seated psychological problems, or they may be malingering or manipulative for secondary gain.
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:
Neurotic excoriations (neurodermatitis) seen on three of four extremities. The fourth extremity is a prosthetic leg.16
Principles of treatment10
Occluded and moist wounds heal faster.
Maintain moist wound environment.
Control exudate and debris (remove excess—leave enough to allow cellular regeneration).
Insulate and protect.