LEG ULCERS
Venous ulcers
Leg ulcers are common in western societies and can have many causes (Table 23.12). Venous ulcers are the most common type in developed countries.
Venous ulcers are the result of sustained venous hypertension in the superficial veins, owing to incompetent valves in the deep or perforating veins or to previous deep vein thrombosis. The increased pressure causes extravasation of fibrinogen through the capillary walls, giving rise to perivascular fibrin deposition, which leads to poor oxygenation of the surrounding skin.
Venous ulcers are common in later life and cause a significant drain on healthcare budgets as they are often chronic and recurrent; they affect 1% of the population over the age of 70 years. They are most commonly found on the lower leg in a triangle above the ankles (Fig. 23.35), and are associated with:
venous eczema (p. 1330)
brown pigmentation from haemosiderin
varicose veins
lipodermatosclerosis (the combination of induration, reddish brown pigmentation and inflammation)
scarring white atrophy with telangiectasia (atrophie blanche).
Treatment
Table 23-12. Causes of leg ulceration
Venous hypertension
Arterial disease (e.g. atherosclerosis)
Neuropathic (e.g. diabetes, leprosy)
Neoplastic (e.g. squamous or basal cell carcinoma)
Vasculitis (e.g. rheumatoid arthritis, SLE, pyoderma gangrenosum)
Infection (e.g. ecthyma, tuberculosis, deep mycoses, tropical ulcer, syphilis, yaws)
Haematological (e.g. sickle cell disease, spherocytosis)
Drug (e.g. hydroxycarbamide (hydroxyurea))
Other (e.g. necrobiosis lipoidica, trauma, artefact)
High-compression bandaging (e.g. Unna boot or four-layer bandaging) and leg elevation are used to try to decrease the venous hypertension. Doppler studies should always be done before bandaging to exclude arterial disease. This treatment is best delivered in the community by appropriately trained nurses. 'Four-layer bandaging' is increasingly popular as this provides high levels of graduated compression (with pressures decreasing up the leg). The choice of ulcer dressing is less critical but one should be chosen to keep the ulcer moist and free of slough and exudate. Up to 80% of ulcers can be healed within 26 weeks. Slower healing rates occur in patients with decreased mobility and if the ulcers are very large, present for longer than 6 months or are bilateral. Diuretics are sometimes helpful to reduce the oedema. Antibiotics are necessary only for overt bacterial infection. Unusual fungal infection ('tinea incognito') is increasingly reported under compression bandaging.
Venous leg ulcers can be very painful so adequate analgesia should be given, including opiates if required. Underlying venous disease is best investigated with duplex ultrasound or plethysmography. Split-thickness skin grafting is used in resistant cases. Life-long support stockings (individually fitted) should be worn after healing as this lessens recurrence.
Surgery for purely superficial venous disease can occasionally be useful for ulcer healing but, in general, venous surgery is unhelpful.
Arterial ulcers
Arterial ulcers may present as punched-out, painful ulcers higher up the leg or on the feet. There may be a history of claudication, hypertension, angina or smoking. Clinically the leg may be cold and show pallor. Absent peripheral pulses, arterial bruits and loss of hair may be present. Doppler ultrasound studies will confirm arterial disease (p. 866) and digital subtraction angiography will further delineate the extent and site of the disease.
Treatment depends on keeping the ulcer clean and covered, adequate analgesia and vascular reconstruction if appropriate.
Neuropathic ulcers
Neuropathic ulcers tend to be seen over pressure areas of the feet, such as the metatarsal heads, owing to repeated trauma. These are most commonly seen in diabetics because of peripheral neuropathy. In developing countries leprosy is a common cause.
Treatment depends on keeping the ulcer clean and removing pressure or trauma from the affected area. Diabetics should pay particular attention to foot care and correctly fitting shoes with the help of a specialist podiatrist (p. 1130).
PRESSURE SORES (DECUBITUS ULCERS, BEDSORES)
These occur in the elderly, immobile, unconscious or paralysed patients. They are due to skin ischaemia from sustained pressure over a bony prominence, most commonly the heel and sacrum. Normal individuals feel the pain of continued pressure, and even during sleep, movement takes place to change position continually. Pressure sores may be graded:
Stage I: non-blanchable erythema of intact skin
Stage II: partial-thickness skin loss of epidermis/dermis (blister or shallow ulcer)
Stage III: full-thickness skin loss involving subcutaneous tissue but not fascia
Stage IV: full-thickness skin loss with involvement of muscle/bone/tendon/joint capsule.
There are numerous risk factors for development of pressure sores (Table 23.13).
The majority of pressure sores occur in hospital. Seventy per cent appear in the first 2 weeks of hospitalization, and 70% are in orthopaedic patients, especially those on traction. Between 20% and 30% of pressure sores occur in the community.
Table 23-13. Risk factors for the development of pressure sores
Prolonged immobility:
paraplegia
arthritis
severe physical disease
apathy
operation and postoperative states
plaster casts
intensive care
Decreased sensation:
coma, neurological disease, diabetes mellitus
drug-induced sleep
Vascular disease:
atherosclerosis, diabetes mellitus, scleroderma, vasculitis
Poor nutrition:
anaemia
hypoalbuminaemia
vitamin C or zinc deficiency
Eighty per cent of patients with deep ulcers involving the subcutaneous tissue die in the first 4 months.
The early sign of red/blue discoloration of the skin can lead rapidly to ulcers in 1-2 hours. Leaving patients on hard emergency room trolleys, or sitting them in chairs for prolonged periods, must be avoided.
Management
Prevention
Prevention is better than cure. Specialist 'tissue-viability nurses' help identify at-risk patients and train other medical staff. Several risk-assessment tools have been devised for the immobile patient based on the known risk factors. The 'Norton scale' and Waterlow Pressure Sore Risk Assessment (Box 23.4) are two such validated systems which produce a numerical score, enabling staff to identify those at most risk.
Treatment
Bed rest with pillows and fleeces to keep pressure off bony areas (e.g. sacrum and heels) and prevent friction.
Air-filled cushions for patients in wheelchairs.
Special pressure-relieving mattresses and beds.
Regular turning but avoid pressure on hips.
Ensure adequate nutrition.
Non-irritant occlusive moist dressings (e.g. hydrocolloid).
Adequate analgesia (may need opiates).
Plastic surgery (debridement and grafting in selected cases).
Treatment of underlying condition.
Box 23.4 Pressure sore risk-assessment tools
Norton Scale for Pressure Sores
Physical Neurology Activity Mobility Incontinence
4 Good 4 Alert 4 Ambulant 4 Full 4 None
3 Fair 3 Apathetic 3 Walks with help 3 Slightly 3 Occasionally
2 Poor 2 Confused 2 Not bound 2 Limited* 2 Usually
1 Very poor 1 Stupor 1 Bedfast 1 Very limited
Immobile 1 Double
Waterlow Pressure Sore Risk Assessment
Build/weight for height Visual skin type Continence Mobility Sex Age Appetite
Average 0 Healthy 0 Complete 0 Fully mobile 0 Male 1 Average 0
Above average 2 Tissue paper 1 Occasionally incontinent 1 Restricted/difficult 1 Female 2 Poor 1
Below average 3 Dry 1 14-18 1 Anorectic 2
Oedematous
Clammy
Discoloured 1
1
2 Catheter/incontinent of faeces 2 Restless/fidgety
Apathetic 2
3 50-64
65-75
75-80 2
3
4
Broken/spot 3 Doubly incontinent 3 Inert/traction 4 81+ 5
Special risk factors Assessment value
1. Poor nutrition; e.g. terminal cachexia 8 At risk 10
2. Sensory deprivation, e.g. diabetes, paraplegia, cerebrovascular accident 6 High risk 15
3. High-dose anti-inflammatory or steroids in use 3 Very high risk 20
4. Smoking 10+ per day 1
5. Orthopaedic surgery/fracture below waist 3
*Norton Scale for Pressure Sores. Low scores carry a high risk
VASCULITIS (see also p. 581)
Vasculitis is the term applied to an inflammatory disorder of blood vessels which causes endothelial damage. Cutaneous vasculitis (confirmed by skin biopsy) may be an isolated problem but occasionally is associated with vasculitis in other organs. The most commonly used classification is based on the size of blood vessel involved (see Tables 10.18 and 10.19).
The cutaneous features are of haemorrhagic papules, pustules, nodules or plaques which may erode and ulcerate. These purpuric lesions do not blanche with pressure. Occasionally a fixed livedo reticularis pattern may appear which does not disappear on warming. Pyrexia and arthralgia are common associations even in the absence of significant systemic involvement. Other clinical features depend on the underlying cause.
The most common cutaneous vasculitis affects small vessels and is called leucocytoclastic vasculitis (LCV) or angiitis. This usually appears on the lower legs as a symmetrical palpable purpura. It is rarely associated with systemic involvement. This can be caused by drugs (15%), infection (15%), inflammatory disease (10%), malignant disease (< 5%) but often no cause is found (55-60%). Extensive investigations are probably best reserved for those with persistent lesions or associated signs and symptoms. Whilst LCV often settles spontaneously, treatment with analgesia, support stockings, dapsone or prednisolone may be needed to control the pain and to heal up any ulceration. Urticarial vasculitis is discussed on page 1335.
LYMPHATICS
Lymphoedema
Lymphoedema refers to a chronic non-pitting oedema due to lymphatic insufficiency. It is most commonly seen affecting the legs and tends to progress with age. The legs can become enormous and prevent wearing of normal shoes. Chronic disease may cause a secondary 'cobblestone' thickening of the skin. Lymphoedema can be primary (and present early in life) owing to an inherited deficiency of lymphatic vessels (e.g. Milroy's disease) or can be secondary because of obstruction of lymphatic vessels (e.g. filarial infection or malignant disease).
Treatment is with compression stockings and physical massage. If there is recurrent cellulitis, long-term antibiotics are advisable as each episode of cellulitis will further damage the lymph vessels. Surgery should be avoided.
Lymphangioma circumscriptum
Lymphangioma circumscriptum is a rare hamartoma of lymphatic tissue. It usually presents in childhood with multiple small vesicles in the skin which weep lymphatic fluid and sometimes blood. They reflect deeper vessel involvement so surgery should be avoided. Cryotherapy or CO2 laser treatment may help the superficial lesions.
FURTHER READING
Cullum N et al. (2003) Pressure sores. Clinical Evidence 9: 2167-2176.
Fiorentino DF (2003) Cutaneous vasculitis. Journal of the American Academy of Dermatology 48: 311-340.
Health Technology Assessment Programme - Systematic Reviews of Wound Care Management (1999) Vol. 3, No. 17 (parts I and II); (2000) Vol. 4, No. 21; (2001) Vol. 5 No. 9. London: Department of Health. Online. Available: http://www.ncchta.org.
Topham EJ et al. (2002) Chronic lower limb oedema. Clinical Medicine 2: 28-31.
Valencia IC et al. Chronic venous insufficiency and venous leg ulceration (2001) Journal of the American Academy of Dermatology 44: 401-421.
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