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Diagnosing and treating unusual aetiologies of lower leg ulcers

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VOL: 101, ISSUE: 04, PAGE NO: 44

Brenda King, ONC, RN, DN, MMed Sci, is tissue viability nurse, Sheffield Community, Sheffield

Neoplasm

All ulcers in this group require urgent referral to the appropriate specialty. Most will need excision and possible skin grafting.

Basal cell carcinoma: This is a common, slow-growing and locally destructive tumour thought to arise from a subset of the basal cells in the epidermis. Initially it presents as a reddish, dome-shaped nodule. As it expands the central area ulcerates, leaving a raised, rolled border, which may be mistaken for over-granulation.

Basal cell carcinoma rarely involves deep tissue, except at sites of chronic inflammation. It is characterised by a translucent pearly appearance (Fig 1). Lesions tend not to be scaly as they do not produce keratin, but occasionally there is mild crusting and oozing.

Variants of basal cell carcinoma include nodular carcinoma, cystic carcinoma, pigmented basal cell carcinoma, rodent ulcers and sclerosing carcinoma, which have different appearances.

Squamous cell carcinoma: This is an aggressive, malignant tumour derived from keratinocytes. It commonly occurs on damaged skin or old scars and appears as opaque, skin-coloured, fleshy papules, nodules or plaque, which are often scaly due to the keratin production.

They may be eroded or nodular and often have a friable surface, which bleeds easily. A primary squamous cell carcinoma presenting as ulceration has been described as squamous cell carcinoma per primam (Negus, 1995).

Squamous cell carcinoma can invade chronic ulcers, causing them to undergo malignant changes (Marjolin’s ulcer), although this is uncommon (Browse et al, 1988).

Squamous cell carcinoma can be recognised by significant changes to the wound bed, followed by a rapid deterioration, which can indicate it is well established. Taylor (1998) argued that biopsies should be undertaken on chronic ulcers.

Malignant melanoma: This is a malignant growth of pigment cells, arising in 70 per cent of cases from normal skin and in 30 per cent from moles. Certain forms of this condition give rise to a wound, which will be fragile, have an inflamed border and may bleed or discharge. Its history is of a lesion with a mole-type appearance. It can be confused with Kaposi’s sarcoma.

Kaposi’s sarcoma: This arises from the blood vessels in the skin. The lesions are usually small and multiple, appearing as purple to dark brown plaques or nodules, which can ulcerate.

Metabolic causes

Necrobiosis lipoidica diabeticorum: These lesions (Fig 2) are seen on the anterior surface of the lower legs of patients with diabetes, although they may predate the development of diabetes by several years.

They are atrophic, red or yellowish depressed areas with marked telangiectasia (visible blood vessels coursing through them), and are thought to result from fat necrosis and infection.

Histological examination reveals a central area of altered and damaged collagen in the mid-dermis, surrounded by inflammatory cells. These lesions are usually asymptomatic except for cosmetic problems, but can ulcerate, usually as a result of trauma, and be very slow to heal.

Diabetes and ischaemia: Patients with diabetes may present with venous ulceration but should also be screened for arterial disease because of their compromised microcirculation. Atherosclerosis occurs at a faster rate and to a greater extent in these patients, primarily in vessels below the knee. However, it is also possible for the small vessels to be compromised when foot pulses are palpable and the ankle brachial pressure index (ABPI) is relatively normal.

This may be due to the formation of microthrombi, resulting from infection, cholesterol emboli, hypertension drugs that reduce blood flow, such as vasopressors, and atherosclerosis with thrombosis formation.

Patients with diabetes may also have increased hypercoagulation, resulting in increased blood viscosity, which impairs blood flow through the microcirculation.

Diabetes and neuropathy: A high proportion of patients with diabetes have sensory, motor and/or autonomic neuropathy, which may cause foot ulcers or bandage pressure damage due to the patient’s inability to feel pain.

Physical and traumatic causes

Injection scleropathy: This technique is now performed infrequently, but involved injecting dilated superficial varicose veins with a sclerosing agent to obliterate the vessel. The procedure carried a risk of extravasation and ulceration. However, ulcers have resulted from the extravasation of medicinal drugs injected into veins in the legs.

Drug abuse: An increasing cause of lower leg ulcers results from people who misuse drugs resorting to injecting. Ulcers may develop due to:

- Underlying venous hypertension that has resulted from damage caused by injecting into the venous system;

- Lymphoedema secondary to deep venous damage in the groin or damage to the lymphatic system due to infection;

- Attempting to inject into the subcutaneous tissue when vessel access is impossible;

- The use of drug ‘bulkers’ such as talcum powder or gravy browning, which damage the tissues;

- Infection of injection sites.

Bandage damage: Fig 3 shows an illustration of a patient with significant damage resulting from an inappropriately applied bandage system. The patient, who had good arterial circulation, experienced gross gravitational oedema.

Following bandaging, bed rest and elevation, there was a dramatic reduction in the oedema and a subsequent reduction in the limb circumference, leaving a very vulnerable limb.

However, the limb was not reassessed after the oedema had been reduced. This demonstrates the importance of limb measurement, which should take into consideration the calf and not just the ankle circumference.

Dermatitis artefacta: Factitious ulcers or wounds caused by self-harm may be bizarre in location and appearance as they are inflicted by agents such as rubber bands around the ankle (Negus, 1995). Although rare, any unusually shaped wounds should be considered suspicious.

Lymphoedema

This is caused by failure of the lymphatic drainage system. Treatment should aim to address the underlying problem with intensive decongestion therapy, exercise programmes and compression garments.

Infection

Tuberculosis: Tuberculous ulcers are characterised by an irregular bluish and friable undermined edge. They are generally multiple and the patient usually shows evidence of pulmonary or skeletal tuberculosis. Tuberculous ulceration of the calf has been named erythema induratum scrofulosorum, or Bazin’s disease. This was a rare condition in the UK, although the incidence of tuberculosis is now rising markedly.

Leprosy: This is due to chronic infection caused by Mycobacterium leprae. Infection is spread through respiratory droplets from the nasal mucosa. It occurs primarily in tropical countries.

Tropical ulcers: Tropical ulcers exclude the bacteria mentioned above, but anaerobes, coliform and Pseudomonas are commonly isolated. The ulcers are usually singular but may be multiple and have raised, well-defined edges. Predisposing factors include malnutrition, chronic anaemia and poor sanitary conditions.

Filarial infections: Filarial infections such as Wuchereria bancrofti and Onchocerca volvulus are mostly associated with the development of lymphoedema. Larvae enter through the bite of an infected mosquito and then settle in the lymphatic system, principally in the groin and axilla.

Haematological ulcers

These may occur as a result of the following conditions:

- Cooley’s anaemia or thalassaemia (abnormality of the protein part of haemaglobin);

- Cryoproteins;

- Myeloid metaplasia;

- Thrombocythaemia;

- Polycythaemia;

- Haemolytic anaemia;

- Sickle cell anaemia, which causes small painful lesions similar to ischaemic or vasculitic ulcers.

Vasculitis: Vasculitis, the inflammation of blood vessels, describes a host of conditions with multiple causes and consequences, depending on the vessels involved. Some are idiopathic, such as Behçet’s disease and microscopic polyangiitis.

Patients present with non-specific symptoms of malaise, weight loss and fever, with joint and muscle pains, and skin lesions.

Vasculitis can also be secondary to other diseases and factors such as viral, bacterial or abnormal drug reactions (hypersensitivity vasculitis). The inflammation of the vessels results in necrosis (Fig 4), so it is important to understand its pathophysiology.

Connective tissue disorders

This describes a group of conditions characterised by multisystem involvement and abnormal immunological features such as auto-antibodies and immune complex deposition.

Many have overlapping and variable clinical features, and the aetiology is unknown or incompletely understood. The key feature is inflammation, which gives rise to problems with the microcirculation and possible ulceration.

Systemic lupus: This autoimmune disease causes inflammation throughout many systems of the body. It can cause vasculitis, venous and arterial thrombosis, and Raynaud’s.

Raynaud’s: This presents as episodic ischaemia of the digits, manifesting as a triphasic colour change of pallor, cyanosis and rubor.

It is defined in three ways:

- Raynaud’s phenomenon - cold-related digital vasospasm;

- Raynaud’s syndrome - with an associated disorder;

- Raynaud’s disease - no associated disorder.

As many as 50 per cent of patients with vasospasm have an associated disease such as connective tissue disorder or atherosclerosis, or a metabolic disease such as hypothyroidism and malignancy (Belch and Zurier, 1995).

Systemic sclerosis: This is a chronic disorder characterised by inflammation, fibrosis and degenerative changes in the blood vessels, skin, synovium, skeletal muscles and certain internal organs.

A significant component is thickening of the skin (scleroderma) due to excessive accumulation of connective tissue, causing the skin over bony prominences to stretch tightly or to ulcerate at sites such as the shoulders and ankles.

Rheumatoid arthritis One of the most common and significant connective tissue diseases is rheumatoid arthritis. Approximately five per cent of people with rheumatoid arthritis, especially women, develop a leg ulcer (Klippel and Dieppe, 1994).

Causes may include:

- Venous stasis due to immobility of the ankle;

- Trauma or pressure on thin skin due to systemic steroid therapy;

- Co-existing conditions such as diabetes or arterial disease;

- Systemic vasculitis, with occlusion of small vessels.

Immunological ulcers

Pyoderma gangraenosum: This is an acute, necrotising, cutaneous ulceration, which may occur in the course of gastrointestinal disease, rheumatoid arthritis or myeloma. The ulcer presents with a deep reddish active border, and has a necrotic and ulcerated centre.

A halo of erythema surrounds the lesion, which is often extremely painful. Management of this condition involves specialist attention and treatment with anti-inflammatory drugs.

Hypertensive ulcers: These painful ulcers, situated on the posterior surface of the lower legs, occur in patients with severe hypertension (Martorell, 1950) that is due to embolisation of athero-sclerotic debris in the small skin vessels.

Conclusion: Leg ulcer management is based on the identification of the underlying aetiology. The most common cause is a disturbance in the haemodynamics of venous return from the lower legs, leading to venous hypertension. Some of the rarer causes of leg ulceration have been identified.

The assessing practitioner must be aware of the possibility of other causes and of co-existing diseases that would affect the treatment choice, especially as the incidence of rarer causes may increase.

The number of patients with venous disorders will still be seen, but some other conditions may need excluding or treating before compression therapy is used to treat venous hypertension.

This paper is the fifth in a six-part series on leg ulcers that first appeared in Journal of Wound Care in October 2004 (13: 9, 394-396). The final paper will be published in the Nursing Times Wound Care supplement on 19 April. It will focus on providing optimum treatment, and on working with patients and carers to meet their clinical and social needs.

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