Phòng khám chuyên khoa da li�u - Thạc s� bác s� Hu�nh Văn Quang

Ulcers

Ulcers

Leg ulcers

Leg ulcers: background

Skin heals more slowly below the knee. If the arterial circulation, the venous circulation or the natural aversion to trauma that is associated with normal sensation is impaired, then the skin may not heal at all. This results in the development of a chronic ulcer at sites of trauma.

Disruption to the arterial circulation may occur due to large vessel disease such as thrombosis or embolus or small vessel disease such as vasculitis. Venous insufficiency is due to valvular incompetence and may be due to varicose veins or post-thrombotic recanalisation of veins. Sensory impairment may be due to peripheral neuropathy or central nervous system disease. Approximately 70% of leg ulcers have a purely venous origin, 15% have a purely arterial origin and 10 % have a mixed aetiology.

Skin biopsy from the healing edge of an ulcer does not impair healing and can be a very useful procedure. Basal cell carcinomas and squamous cell carcinomas occurring below the knee frequently lack the classical morphological features that skin cancers have elsewhere on the body. Any atypical, chronic ulcer should be biopsied to exclude skin cancer or other diseases such as pyoderma gangrenosum or opportunistic infection. This is particularly relevant in immunocompromised patients.

Wound healing involves three phases: inflammation, granulation and re-epithelialisation. A healing wound has different requirements during these three phases. Being able to identify which phase a wound is in and tailoring the treatment to that phase of healing is the cornerstone of leg ulcer treatment. The predominant colour of the wound can be used as a simple guide to wound stage, see Table 1.

The goal of treatment is to heal the ulcer, but this may not always be possible. Many patients live in harmony with their leg ulcer, their dressings and their attending carers for many years and failure to heal an ulcer does not mean that the treatment has failed to help the patient.

Venous ulcers

Venous ulcers affect 2% of the population over the age of 80 and cost the Australian community hundreds of millions of dollars each year. They occur on either the medial or lateral malleolus in people with deep, or superficial and deep, venous valvular incompetence. Superficial venous incompetence is associated with varicose veins, and alone is generally insufficient to produce leg ulceration. Patients with leg ulcers usually have associated incompetence of perforating veins connecting the deep and superficial veins of the legs. Deep venous incompetence usually occurs as a delayed complication of deep vein thrombosis.

In the community, 50% of venous ulcers heal within 9 months, while 20% persist for more than 2 years and 8% for more than 5 years. By comparison, in specialist ulcer clinics 70% of small ulcers will be healed within 3 months. Once an ulcer has healed, two-thirds of patients will develop recurrent episodes of ulceration.

The aim of treatment is to heal the ulcer or, if that is not possible, to minimise the morbidity of the ulcer and the associated dressing changes. The main morbidity of the ulcer comes from pain, excessive exudate, malodour and the risk of recurrent cellulitis. In addition, ankle oedema, aching legs, gravitational dermatitis, allergic contact dermatitis and lipodermatosclerosis may all complicate venous insufficiency and may be associated with leg ulcers.

First-line therapy consists of correction of venous stasis, with conservative measures and physical therapies (see below) or with corrective vascular surgery. Wound dressings, surgical debridement or skin grafts are used to promote wound healing. Management of complications, eg infection or dermatitis, can also assist wound healing.

Once the ulcer is healed, the secondary aim is prevention of further ulceration, as without intervention over two-thirds will subsequently relapse.

Compression bandages – Compression bandages and stockings are the single most important therapy for leg ulcers. Below knee compression bandages or graduated compression stockings are required in all cases, to reverse and prevent oedema and thereby promote healing of the ulcer. These are to be worn whenever the patient is upright. Patients should be encouraged to exercise whilst wearing their compression bandages or stockings. Unless surgical correction of the venous incompetence is possible, they will need to be worn for life, in order to prevent development of new ulcers in the future.

It is vital to establish that the patient has palpable pedal pulses prior to providing compression. If a Doppler stethoscope is available the ratio of the systolic blood pressure at the ankle to that in the arm, the ankle brachial index (ABI) should be measured. If the pulses are absent or the ratio of systolic blood pressures in the ankle to the arm is less than 0.8, then the patient should be referred to a vascular surgeon for assessment regarding angioplasty or bypass surgery. Care is required in interpreting Doppler pressures in patients with diabetes mellitus with arterial calcification, as this can produce falsely high readings.

Graduated compression stockings require individual fitting. All other therapies and dressings are secondary adjuncts to compression bandaging. The degree of compression achievable varies greatly between the bandages. In general, the greater the compression achievable the quicker the healing. Where possible, ‘around the clock’ compression should be advocated, although many patients prefer to remove them at night.

Patients should be encouraged to undertake beneficial practices such as walking (to promote calf muscle pump activity) while wearing compression stockings, ankle exercises, elevation of legs above the heart when resting or sleeping, and weight loss in obese patients.

Nutrition - Anaemia, malnutrition and zinc deficiency should be corrected. Zinc supplementation is not routinely required and should only be used in patients.

Corrective vascular surgery: it is not always feasible to perform corrective surgery, but where possible this should be promoted. In general, surgery is deferred until the ulcer has healed. Superficial vein surgery (ligation or sclerosis of the long and short saphenous systems, with or without communicating vein ligation or sclerosis) does not enhance healing of ulcers but has been shown to be of value in preventing recurrences when the deep circulation is competent. There does not seem to be any benefit when the deep veins are incompetent. Newer surgical techniques such as internal and external valvuloplasty show promise and are undergoing further evaluation.

Wound dressings - There are over one hundred different dressings currently available. No single dressing is suitable for all ulcers or for all three phases of wound healing. Dressings are chosen on an individual basis to reduce inflammation, protect and promote granulation, encourage re-epithelialisation, relieve pain, control or absorb exudate, provide haemostasis, remove slough, control odour, care for the surrounding skin or facilitate ulcer care. Dressings such as amorphous hydrogels, alginates and hydrocolloid paste and powder require a secondary dressing, eg film or nonadherent dressings for low exudating wounds and foam dressings for use over amorphous hydrogels and alginates. Dressings can be held in place with a good quality tape if the surrounding skin is good, or with a tubular bandage or a light-weight cohesive bandage if the skin is poor.

The choice of a wound dressing is based on the nature of the wound, the phase of wound healing, the presence or absence of infection, the level of exudate and the depth of the wound. The colour of the wound can also be used as an indicator of the phase of wound healing and aid in the choice of an appropriate dressing.

In general, dressings should be changed as infrequently as possible. Some hydrocolloid dressings can remain in place for 2 weeks at a time if the wound is clean. Exudate, ooze, leakage and malodour are the main reasons for changing dressings sooner. Suspected wound infection also warrants more frequent wound inspection.

Surgical debridement - The prevailing theory to explain why surgical debridement enhances wound healing is that it converts the ulcer from a chronic to an acute wound. This encourages inflammation and the production of cytokines within the tissue that lead to a recommencement of the healing cascade. It is used when there is eschar or slough in the base of the ulcer that is difficult to remove with dressings and chemical agents alone. In addition, surgical debridement is commonly required for preparation of the ulcer bed for grafting.

Skin grafts - Split skin grafting, pinch grafting, mesh grafting, cultured skin grafts or skin substitute dressings such as Apligraft or Dermograft have all been used to promote re-epithelialisation and healing of the ulcer. Grafting is normally reserved for cases that have failed to heal after 12 months of properly applied compression bandaging. Very large ulcers may justify early grafting. Grafting may be done on a day-patient basis. The wound bed needs to have good quality granulation tissue, and may require surgical debridement to remove slough and eschar. Swabs to exclude streptococcal infection should be performed prior to grafting.

Infection - It is not necessary to routinely swab ulcers. Swabs for bacterial microscopy and culture are only required if the ulcer is painful, rapidly increasing in size or surrounded by cellulitis or lymphangitis. Staphylococcus aureus is part of the normal flora of ulcers, and moderate counts do not delay wound healing and do not require treatment unless there is a surrounding cellulitis. Group A beta-haemolytic streptococci and Pseudomonas pyocyanea are significant and should be treated, as should heavy growths of Staphylococcus aureus.

Pseudomonas aeruginosa is very commonly a coloniser and almost impossible to eradicate. The use of a cadexomer iodine product (Iodosorb, Iodoflex) helps to reduce levels of bacteria, absorb exudate and remove slough and may stimulate cytokine production in the wound. Silver sulfadiazine 1% cream is also used in some pseudomonal colonised wounds.

Dermatitis - Acute dermatitis with itch, redness, weeping and scaling may complicate venous ulcers and further impair healing. Treatment with topical corticosteroids applied to affected areas up to the ulcer’s edge, but not into the ulcer, is advocated and does not delay healing, see Table2.

Arterial ulcers

Critical impairment of blood flow in the arteries of the legs may be due to thrombosis associated with arteriosclerosis, or less commonly, embolus or angiitis. The consequent lack of tissue oxygenation may lead to skin necrosis and ulceration. Many patients do not have isolated arterial disease, but have mixed venous and arterial disease. In these patients, lesser degrees of arterial impairment may prevent wound healing and exacerbate leg ulceration from other causes.

Arterial ulcers are most commonly located over the toes or on pretibial skin. The edges are sharply defined and the ulcer is punched out. In addition to the absence of peripheral pulses, the features on examination that suggest arterial disease include foot pallor, cyanosis, loss of hair, xerosis, venous guttering on elevation of the limb and positive Buerger’s test, showing delayed but exaggerated hyperaemia of the foot on dependency.

Measuring the ABI with a Doppler stethoscope will help to determine the severity of the arterial disease if the pulses are absent. The systolic blood pressure in the calf is measured with a Doppler ultrasound probe and compared to the blood pressure in the arm. If the ratio is less than 0.8, formal investigation of the arterial circulation is required; if the ratio is less than 0.5, the patient is likely to have rest pain and is at risk of arterial ischaemia and gangrene. If a Doppler ultrasound probe is not available, the patient should be referred for duplex Doppler ultrasound studies or angiography.

The aim of treatment is to promote healing of the ulcer and if that is not possible to prevent extension of the ulcer and alleviate morbidity. The main morbidity of the ulcer comes from pain, cellulitis and malodour.

Conservative measures - Patients should be encouraged to stop smoking, hyperlipidaemia should be corrected and antithrombotic therapy initiated with aspirin if appropriate. If the patient is anaemic or polycythemic, these conditions should be corrected and hypertension should be treated. For patients on beta-blockers, an alternative medication should be considered.

Surgical treatments - Correction of large artery disease, either by balloon angioplasty or vascular bypass surgery, is the treatment of choice whenever possible. Referral to a surgeon in this field is suggested. Alternatively, lumbar sympathectomy can be performed surgically or chemically. Sympathectomy leads to an increase in blood flow in dermal arterioles. Although the effects are relatively short lived, the increased blood flow may be sufficient to enable an ulcer to heal or alleviate symptoms. The morbidity of the procedure is minimal. If these treatments are unsuccessful, healing of the ulcer is unlikely and for palliation use:

           support rather than compressive bandaging, eg shaped support bandage or straight tubigrips

           dressings to promote wound healing,

           management of the pain, malodour and cellulitis that are common complications of arterial ulcers, see Table 3

           below knee amputation; a treatment of last resort and required when there is intractable pain, uncontrolled cellulitis and spreading (moist) gangrene.

Bandage and wound dressing tables

Neuropathic ulcers

Neuropathic ulcers are relatively rare. In developed countries they occur most commonly in association with diabetes mellitus, but leprosy is the most common cause on a worldwide basis. They may result from any disorder that disrupts the sensory nervous system. Common sites are pressure points such as the ball of the foot, the heel, toes and medial and lateral malleoli. If the gait is abnormal or the posture of the foot unusual, ulceration may occur at other pressure sites. Testing will reveal diminished or absent cutaneous sensation.

The primary aim of treatment is to prevent ulcers forming at vulnerable sites. Once ulceration has occurred, the aim is to promote healing and to identify other areas vulnerable to ulceration and protect them. First-line therapy consists of pressure distribution away from the ulcer (eg orthotics, prosthetics, casting) and bed rest. Additional treatments include dressings to promote wound healing, surgical debridement to remove eschar or chemical debridement to remove slough and skin grafting or flap surgery following surgical debridement, to close the ulcer in select cases. The role of hyperbaric oxygen chamber therapy is controversial.

Pyoderma gangrenosum

This is a noninfective, destructive, necrotising ulceration of the skin. A lymphocytic vasculitis may be seen histologically at the advancing border, but it is more common for the skin biopsy to reveal nonspecific histological changes. Neutrophils are the predominant inflammatory cell, and most of the treatments used in pyoderma gangrenosum specifically target neutrophil chemotaxis or function. The ulcers develop rapidly and have a distinctive blue, raised border. A zone of erythema surrounds the ulcer during phases of activity. The edge of the ulcer is commonly undermined. The base of the ulcer may contain granulation tissue or the ulcer may invade deeply, exposing muscle, tendon or periosteum.

Approximately 10 to 30% of cases are idiopathic, the remainder occurring in association with inflammatory bowel disease, inflammatory arthritis (seropositive rheumatoid arthritis and seronegative arthritis) and blood dyscrasias such as monoclonal gammopathy, myeloproliferative disease and leukaemia. Numerous other associations have been described in case reports, many of which are coincidental. The activity of the pyoderma gangrenosum does not always correlate with the activity of the associated disease.

Once the diagnosis has been confirmed, infectious ulceration excluded (usually by biopsy and culture of tissue) and the presence of any associated conditions determined by extensive screening tests, the aims of treatment are to provide pain relief, to heal the ulcer and to prevent the development of new lesions. Many medications have been used to treat pyoderma gangrenosum. In general, the treatment target is the neutrophilic infiltrate, and these medications have in common, actions that inhibit neutrophil chemotaxis or function. As many of the treatments are immunomodulatory, the importance of prior exclusion of infection, particularly atypical or opportunistic infection, is emphasised.

New lesions can be provoked by minor trauma, including skin pricks, and minor surgery. Attempts at skin grafting commonly fail for this reason, and the skin graft donor site may also develop pyoderma gangrenosum. Similarly, limb amputation may be associated with the development of pyoderma gangrenosum in the stump.

The choice of therapy depends on the patient’s state of health, the severity of the pain associated with the ulceration, the size and depth of the ulcer and whether the ulceration is actively extending or not. First-line therapy consists of corticosteroids. Topical corticosteroids provide pain relief and may encourage healing.

very potent topical corticosteroids under an occlusive dressing (hydrocolloid or occlusive film).

Intralesional corticosteroids may prevent extension and encourage healing. Initially, use

triamcinolone acetonide 10mg/mL OR betamethasone acetate/sodium phosphate 5.7mg/mL, injected into the active border of the lesion.

If this is not successful, use

triamcinolone 40mg/mL, injected into the active border of the lesion.

Oral corticosteroids are often combined with topical therapy. Use

prednisolone 1 to 3mg/kg orally, daily.

Second-line therapy consists of azathioprine, with or without prednisolone. There is a delay of 3 to 4 weeks in the onset of action of azathioprine. Use

azathioprine 1 to 2mg/kg orally, daily.

Alternatively, one or more of the following agents may be used either alone or in combination with prednisolone or azathioprine.

dapsone 100 to 200mg OR colchicine 1 to 2g OR minocycline 100 to 200mg OR sulfasalazine 4 to 6g orally, daily.

Additional pain relief measures include wound dressings (sheet and amorphous hydrogels, polyurethane foam, hydrocolloid) and oral analgesics. If the ulcer is rapidly extending or deeply undermined, immobilisation using a plaster of Paris backslab and bed rest is recommended, but caution is required to avoid freezing of the neighbouring joint. Active treatment of the underlying disease process is always advisable. However, the activity of the pyoderma does not always mirror the activity of the associated disease.

If the above treatment is not successful, further management should be conducted in conjunction with a tertiary referral centre, with access to agents such as cyclosporin, pulsed methylprednisolone (0.5 to 1g), clofazimine 200 to 400mg per day and other cytotoxic therapy. Hyperbaric oxygen chamber therapy has been used, but its role is controversial.

Therapy is continued until complete healing of the ulcer has occurred. This may take a number of months. Recurrent ulceration may occur on cessation of the medication in a proportion of patients, who will then require long-term maintenance therapy.

Diabetic foot ulcers

Patients with diabetes mellitus are prone to infectious diseases, neurological disease and both large vessel and small vessel vascular disease. In addition, while patients with diabetes mellitus are not especially prone to venous disease, it is common in the community. Thus, diabetic ulcers are commonly multifactorial and an assessment of the relative importance of the different factors contributing to each ulcer is required. The site of the ulcer is the one of the most important aetiological indicators. Infection should be looked for and treated according to the antibiotic sensitivities of the organisms cultured, see Diabetic foot infections. A skin biopsy for culture may occasionally be required to exclude opportunistic infections. Evidence of any correctable large vessel disease should be sought and corrected initially, and clinicians should be aware that arteriography may be needed, as Doppler ultrasonography may underestimate large vessel disease in the hardened arteriosclerotic vessels of patients with diabetes mellitus.

Prevention is the key to management of diabetic ulcers and good foot care is essential in the context of neuropathy. Patients with diabetes mellitus should have their feet examined regularly as part of their routine medical assessment. They should be encouraged to inspect their feet frequently, treat coincidental infections such as tinea pay attention to small injuries and abrasions and look after their footwear. Special shoe inserts, prostheses and footwear designed to minimise trauma and evenly distribute the weight away from pressure points can be arranged through podiatrists.

Once ulceration has occurred, the principles of management are the same as for other arterial or neuropathic ulcers, but there should be a lower threshold for swabbing the wounds to exclude concurrent infection, particularly opportunistic infections.

Pressure ulcers

Pressure ulcers are also known as bedsores or decubitus ulcers. They are produced by unrelieved compression of skin between a bony prominence and an external surface for a prolonged period of time. Pressure ulcers most commonly occur over the sacrum, ischial tuberosity, greater trochanters, heels and lateral malleoli. They develop in people who are confined to a bed or a chair for long periods, mainly in hospitals, homes and nursing homes. Intermittent relief of pressure minimises damage. Shearing forces applied to the skin enhance vascular occlusion and contribute to the size and grade of pressure ulcers. Friction forces reduce the amount of pressure required to produce ulcers. Moisture from perspiration or incontinence also reduces skin resistance to ulceration.

In addition to immobility, the development of pressure ulcers is enhanced by poor circulation, smoking, poor nutrition and old age. Medications such as analgesics and sedatives may also reduce sensation and mobility, while antihypertensive agents may reduce tissue perfusion.

The incidence of pressure ulcers among hospitalised patients in an acute care setting varies between 1% and 5%, while the prevalence varies between 3% and 14%. Among patients with spinal injuries, the prevalence ranges from 20% to 30%. Elderly patients with femur fractures and critical care patients are also high-risk groups.

Preventive measures in persons at risk have been shown to significantly reduce the incidence of pressure sores. Risk assessment tools such as the Norton scale and Braden scale incorporate the ulcer grade (see below), nutritional and mental status of the patient, levels of patient activity and mobility as well as incontinence.

Pressure ulcers are graded or staged to classify the degree of tissue damage. Debridement of eschar may be required for full assessment. The national pressure ulcer advisory panel (NPUAP) has classified pressure ulcers into four stages:

The term closed pressure sore has been used to describe ischaemic necrosis of the subcutis without skin ulceration.

Effective treatment of pressure ulcers incorporates the management of the patient as well as the ulcer. Management of the patient requires attention to their nutrition, provision of pain relief, identification and treatment of depression, and frequent turning to prevent the development of a second ulcer.

Pressure care should be practiced while in bed or sitting in chairs to direct pressure away from the ulcer. Positioning devices, prostheses, support surfaces, water, air or gel mattresses and even plaster of Paris casts may be required, depending on the ulcer site. Debridement of eschar, necrotic tissue or adherent slough should be performed and saline irrigation carried out at each dressing change. Surgical debridement is favoured for large ulcers and thick eschars and in the presence of infection. Dressings (film, hydrocolloid and hydroactive) can be used to enhance autolytic debridement. Ulcer dressings should be selected to provide a moist wound bed, while keeping the surrounding skin dry. The dressing should also control exudate without desiccating the ulcer bed. When present, wound dead spaces should be eliminated by loose packing.

Surgical repair should be considered for patients with clear stage III and IV ulcers unresponsive to conservative management. Procedures include excision with primary closure, skin grafting, musculocutaneous flaps and free flaps. Careful patient selection is critical to achieving a good postoperative outcome.

Bacterial colonisation and wound infection need to be distinguished. All stage II, III and IV ulcers are colonised by bacteria. Superficial swabs are not recommended for diagnosis of infection, as they only detect surface colonisation. When a culture is required, aspiration of fluid through a needle inserted into the tissue or a punch biopsy of the ulcer bed for quantitative tissue culture is recommended. Healing may be impaired if bacterial levels of colonisation exceed 100 000 organisms per gram of tissue or if the patient has osteomyelitis. Regular cleansing and debridement are adequate to prevent colonisation progressing to clinical infection. If a clean ulcer fails to show signs of healing after 2 weeks or continues to have heavy exudate after 2 to 4 weeks, culture of a tissue sample should be performed or a 2 week empirical trial of topical or oral antibiotics could be considered.

Foul odour usually indicates infection or colonisation with anaerobic bacteria and requires culture and treatment with oral antibiotics, although topical metronidazole may be effective for malodour due to colonisation. Bacteraemia may complicate pressure ulcers and is often polymicrobial. This may be complicated by sepsis, endocarditis and even death.

Nonhealing, chronic pressure ulcers may be associated with osteomyelitis either by direct extension or haematogenous spread, and technetium labelled bone scans may be required for diagnosis. Chronic ulcers may be complicated by squamous cell carcimona (SCC), akin to the development of Marjolin-type development of SCC in burn scars. These SCCs often behave aggressively, with a greater than 50% metastatic rate reported.

Sinus tracts may develop in apparently superficial ulcers and communicate with joint spaces or even deep viscera. Sinugrams and surgical exploration are usually indicated when sinuses are detected.

Adjunctive therapies such as electrotherapy, hyperbaric oxygen therapy, ultrasound, topical cytokine growth factors, sugar, honey, vitamins, zinc, and infra-red, ultraviolet and laser irradiation have all been tried, but cannot be routinely recommended at this stage on the basis of currently available evidence.

• < Trước
• Tiếp tục >