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Leg Ulcer
- 2. Definition Focus on Leg Ulcers Epidemiology Aetiology Classification Differentiation Risk Factors Diagnosis Management Dressings Introduction
- 3. Definition A sore on the skin, or a mucous membrane, accompanied by the disintegration of tissue, the formation of pus etc. http://dictionary.reference.com/browse/ulcer A local defect, or excavation of the surface, of an organ or tissue, produced by the sloughing of necrotic inflammatory tissue http://medical-dictionary.thefreedictionary.com/ulcer
- 4. Chronic Ulceration of the Leg Course of Condition Long term (decades) relapsing history Cost of treatment in UK Approximately £600 million per annum Prevalence trend Increasing alongside obesity and comorbidities Impact on quality of life Similar scale to Diabetes and Arthritis Overview
- 5. Epidemiology 1% lifetime prevalence in developed countries 1.1 - 3% point prevalence Higher frequency in more elderly groups 80% treated in the community setting Intensive treatment can lead to healing Relapse rate up to 75%
- 6. Aetiology Often multifactorial Key underlying processes Decreased perfusion Progressive Atherosclerosis Arterial Embolus Venous Hypertension Infection Ischaemia decreased ability to fight infection
- 7. Classification Cause affects presentation and treatment Venous Stasis Varicose Neurotrophic Diabetic Arterial Ischaemic Decubitus
- 8. Differentiation Venous Stasis Neurotrophic Arterial Location Below Knee Medial Aspect Proximal to Medial Malleolus Unilateral or Bilateral Increased pressure points Trauma Feet: Heels, tips of toes Between toes Protrusion/Rubbing Nail Bed Base Erythematous +/- covered with yellow fibrous tissue +/- green or yellow discharge if infected Variable: Pink/Red or Brown/Black Yellow, Brown, Grey or Black Rarely Bleeds Borders Irregular Punched out Punched out Surroundings Discoloured Oedematous Calloused +/- oedema & erythema if infection/irritation Affected Population History of SVT/DVT Varicose Veins Oedema Diabetics Impaired sensation Poor Circulation
- 9. Risk Factors Poor circulation Venous insufficiency Disorders of clotting and circulation Neuropathies (Diabetes) Renal failure Hypertension (treated or untreated) Lymphoedema Inflammatory diseases Other medical conditions History of smoking Pressure Genetics Malignancy Infections Certain medications
- 10. Diagnosis History Taking: Rapidity of onset Preceding events Duration of ulceration Previous treatment Symptoms Relevant predisposing factors Family history Recent foreign travel Ambulatory status of patient Type of footwear worn Patient psychological status
- 11. Symptoms Venous Arterial Pain “Heaviness” Aching Swelling Itching Eczema Pigmentation Intermittent Claudication Pain •Severe •Persisting at rest •Worse at night Positional Variation •Erythema with limb dependent •Turning pale with elevation
- 12. Diagnosis Clinical Examination & Description: Position Colour Tenderness Temperature Shape Size Specifics: base edge depth discharge relationship to other structures lymph nodes state of local tissues, including pulses
- 13. Diagnosis Investigations: FBC Urine Dipstick Glucose, HbA1c Biopsy Duplex Ultrasonography Radiology
- 14. General Management Risk Reduction Controlling Risk Factors Medical Therapy Dressings Drainage & Desloughing Antibiotics Correction of Specific Abnormalities Surgical Therapy Revascularisation Venous Intervention Skin Grafts/Rotational Flaps Amputation and Rehabilitation
- 15. Specific Management Venous Ulcer Compression & Mobilisation Treatment of Associated Varicosities Neurotrophic - Diabetic Reduce Pressure Orthotics & Foot Care Glucose Control Visual Monitoring of At Risk Areas Arterial Endovascular or Vessel Replacement Therapy Rheologic Therapy
- 16. Venous Compression Types of dressings include: Moist to moist dressings Hydrogels/hydrocolloids Alginate dressings Collagen wound dressings Debriding agents Antimicrobial dressings Composite dressings Synthetic skin substitutes
- 17. Research Developments Low Intensity Ultrasonic Stimulation Intermittent Pneumatic Compression Hyperbaric Oxygen Therapy Injected LMWH Spray on Skin
- 18. Summary Common Condition Increasing Prevalence Expensive to Treat Diagnosis History, Examination, Investigation Treatment Dependent on Differentiation Long, Relapsing Process Positive New Developments
- 19. References http://my.clevelandclinic.org/heart/disorders/vascular/legfoot http:// www.gpnotebook.co.uk/simplepage.cfm?ID =395968533 http://emedicine.medscape.com/article/1298345-overview#a
Editor's Notes
- While normal wounds heal because of epidermal division and migration within a neovascularized mesh of granulation tissue, resulting in a cover of new skin, chronic wounds typically show inadequate repair due to: Decreased perfusion: either inflow or outflow – most commonly from Venous hypertension valvular incompetence = a failure of the valves in the veins of the leg that causes congestion and slowing of blood circulation in the veins increased afterload at capillary beds
- Neurotrophic: nerve damage loss of sensation & changes in sweat gland ++ risk of callouses, cracks, injury loss of awareness
- Venous Stasis Ulcers Location Base: The base of an ulcer usually consists of granulation tissue or slough. Fluid drainage can be significant. The redness of the granulation tissue is proportional to the underlying vascularity of the ulcer site (and therefore of the ulcer's ability to heal) Borders: It may even feel warm or hot. The skin may appear shiny and tight, depending on the amount of edema (swelling). Often have flat sloping edge: indicates that epithelium is growing in from the ulcer edge in an attempt to heal it. Usually only seen in superficial ulcers. Surroundings: skin around the ulcer is red-blue (due to haemosiderin deposition) and almost transparent. Who is affected Account for 80 to 90% of all leg ulcers. Neurotrophic Location on body Base: Variable, depending on the patient's circulation - solid brown or grey dead tissue suggests full-thickness skin death Punched-out (square-cut) edge: this indicates that there has been the rapid death of a whole thickness of skin without the body making much attempt to repair of the defect. This type of ulcer is often caused by pressure on an insensitive area of skin. Examples include diabetes, syphilis, any other peripheral neuropathies. Arterial (ischemic) Ulcers Location Nail bed where aggressive toenail cutting digging in Appearance Base: no granulation tissue is often present in ischaemic ulcers - in this case structures such as tendons may lie bare in the base of the ulcer Borders:
- Poor circulation (often caused by arteriosclerosis) Venous insufficiency Neuropathies Mainly diabetes but also tabes dorsalis – syphillis, spina bifida, leprosy) Lymphoedema (a build up of fluid that causes swelling in the legs or feet) Inflammatory diseases including vasculitis, lupus, scleroderma or other rheumatological conditions Other medical conditions (such as high cholesterol, heart disease, haemolytic anaemias, sickle cell anaemia, bowel disorders = pyoderma gangrenosum UC) Pressure (caused by lying in one position too long, ill fitting shoes) Genetics (ulcers may be hereditary) Malignancy (usually SCC but also Bowen’s disease – SCC in situ/Marjolin’s ulcer – rare aggressive SCC associated with areas of chronic damage e.g. burn wounds)
- As classification affects treatment ++ importance of correct differentiation rapidity of onset: arterial >> venous preceding events, e.g. trauma or surgery at the site of the ulcer(1) duration of ulceration; gives an indication of chronicity and likelihood of successful treatment relevant predisposing factors venous disease: varicose veins, deep vein thrombosis in past, phlebitis, previous fractures, trauma or surgery arterial disease: ischaemic heart disease, transient ischaemic attacks of cerebrovascular events, peripheral vascular disease, cigarette smoking, hypertension, hypercholesterolaemia (1) diabetes mellitus, rheumatoid arthritis family history e.g. venous disease, diabetes mellitus recent foreign travel; may be suggestive of rare infective aetiologies ambulatory status of patient type of footwear worn patient psychological status; likely compliance with treatment
- Arterial ulcers are typically very painful, especially at night. The patient may instinctively dangle his/her foot over the side of the bed to get pain relief.
- Sometimes the floor of the ulcer will provide extra information about the nature of the ulcer: wash-leather appearance is seen in syphilitic ulcers bluish unhealthy granulation tissue seen in tuberculosis ulcers The edge of the ulcer provides important information about the pathophysiology of the ulcer: undermined ulcer: this is seen when an infection at an ulcer site affects the subcutaneous tissues more than the skin. This occurs in tuberculosis ulcers. rolled edge: this occurs where there is slow growth of tissue at the ulcer edge and the peripheral tissue becomes heaped-up. This is classically seen in a rodent ulcer (basal cell carcinoma). everted edge: in this case the tissue at the edge of the ulcer is growing so fast that it overlapse the normal skin as it 'spills out' of the ulcer site. An everted edge is seen in carcinomata. Depth Defined either: height: in millimetres anatomically: which structures are visible Discharge This may be: serous (normal healing), sanguinous (bloody), purulent (pus/nfective) Always take a bacteriological swab of an ulcer. It may be appropriate to remove overlying scabs to facilitate proper examination of the ulcer. Relation especially deep to it. Ascertain whether the ulcer is adherent to deep structures. Check for: enlargement, tenderness Assess: local blood supply, local nerve supply, for evidence of previously healed ulcers, - if cannot feel pulses then use Doppler
- Treatment of chronic wounds, is futile if underlying disease is not addressed – investigations help to clarify the nature of any contributory factors investigations: FBC to exclude anaemia, to look for underlying inflammatory states, infections, immune function, and vitamin, protein, electrolyte deficiencies dipstix urine to exclude diabetes mellitus Glucose – assess diabetic control biopsy edge of ulcer if suspicion of malignancy or aetiology is still unknown. No indication that biopsy increases the risk of spread. USS duplex – dvt, assessment of arterial blood flow radiology: if suspicion of spread of infection from deeper focus – angiography to visualise extremity vessels
- Risk Reduction: Quit smoking, Manage BP and Diabetes, Lose Weight, Exercise, Self Examination Medical: correct dressings, frequently changed. ensure adequate drainage and desloughing: slough inhibits the functioning of granulation tissue, drainage should be encouraged by surgical or chemical desloughing of ulcer base All chronic wounds need to be debrided to convert them into an acute wound to allow for the normal wound healing cycle to resume. In addition, a formal debridement removes the biofilm that has been built up during the chronic phase. The colonized bacteria are removed and cytoprotective cytokines are secreted to start the inflammatory phase of wound healing. This is also necessary prior to skin grafting where used to ensure a clean base for healing 3. antibiotics are only indicated for infected ulcers in which: there is evidence of spread around the margin e.g. a cellulitic rim or there may be ongoing systemic infection e.g. syphilis, tuberculosis 4. correction of specific abnormalities e.g.: malnutrition, myxoedema, excessive steroid use Surgical options: revascularization and/or coverage of the wound, Vein stripping or junction disconnection eg saphenofemoral or saphenopopliteal by ligation of incompetent venous perforators – veins which allow communication between superficial and deep veins The rate of wound healing for those treated with surgery is not significantly higher than that of patients who are treated conservatively, but the resultant diminished rate of wound recurrence is a benefit.[8] Ligation of superficial venous perforators has been shown to reduce the 4-year recurrence rate of vascular ulcers, from 56% in ulcers treated by compression alone to 31% in ulcers treated by compression plus surgery (P < .01).[15] (3) For large deficits or prolonged ulcers with little evidence of healing, further surgical intervention may be indicated e.g. skin grafts and rotational flaps (Often, the wound bed is not suitable for grafting or a structure such as a bone or tendon is exposed. Under these circumstances, consider pedicled or free flaps). (4) primary amputation and rehabilitation.
- Decubitus Ulcers: similar to neurotrophic as the mobility impaired patient is more likely to have impaired sensation/ability to monitor themselves – bed/mattress, schedule for turning, partial mobilisation Rheologic Therapy: Medical therapy aimed at improving circulation Rx e.g. pentoxyfylline to decrease blood viscosity – off licence use in venous leg ulcers where compression not working Musculotrophic vasodilators eg Naftidrofuryl – peripheral vasodilator Calcium channel blockers e.g. nifedipine, diltiazem – arterial vasodilation – don’t work on venous smooth muscle
- High compression products for management of gross varices, post-thrombotic venous insufficiency, venous leg ulcers, and gross oedema in average-sized limbs. Assist the return of pooled blood to the circulation Expert knowledge of the elastic properties of the products and experience in the technique of providing careful graduated compression. Incorrect application can lead to uneven and inadequate pressures or to hazardous levels of pressure. In particular, injudicious use of compression in limbs with arterial disease has been reported to cause severe skin and tissue necrosis (in some instances calling for amputation). Doppler testing is required before treatment with compression. Venous ulcers are treated with compression of the leg to minimize edema or swelling. Compression treatments include wearing compression stockings, multi-layer compression wraps, or wrapping an ACE bandage or dressing from the toes or foot to the area below the knee. The type of dressing prescribed for ulcers is determined by the type of ulcer and the appearance at the base of the ulcer. Increased use of interactive and active dressings rather than passive dressings that cover and absorb. Interactive hydrocolloid dressings provide moisture and a controlled microenvironment for growth of new tissue. Wide range of properties helping to control exudate, encourage epithelial cell migration, liquefy eschar and lyse fibrin to allow easier debridement and manage infection These dressings are also believed to provide symptomatic relief, such as decreased pain and pruritus. Active dressings deliver substances such as growth factors, which are important in the healing cascade. Topically applied growth factors are meant to assist the chronic wound with establishing healthy granulation tissue or epidermal cell function for improved healing. Platelet-derived growth factor has been shown to reduce the size of chronic ulcers by up to 70%, as compared to 17% for placebo, probably via acceleration of provisional wound matrix deposition. Epidermal growth factor supplementation was associated with healing of 8 of 9 wounds in which therapy had previously failed. Chronic wounds may be associated with active infection, such as cellulitis. Additionally, an occasional chronic wound may be the nidus for bacteremia and sepsis. In these cases, administer systemic antibiotics. Alternatively, the wound itself may be infected, without systemic effects. Dressing changes alone usually lower the bacterial load, regardless of the type.[9] Silver sulfadiazine has been shown to almost universally reduce the bacterial load to levels acceptable for wound closure. It is a broad-spectrum antibiotic and does not cause pain, as has been noted with mafenide acetate (Sulfamylon). However, penetration of eschar is questionable with this antibiotic. Saline-dampened gauze dressing changes also reduce the bacterial load in the large majority of wounds, but not as effectively as silver sulfadiazine. Povidone-iodine solution (Betadine) has also been used as a topical antibiotic and is largely successful at reducing bacterial counts. However, a widely held belief is that this solution also kills granulation tissue, which significantly impairs healing of these wounds.
- The use of low-intensity ultrasonic stimulation of venous ulcers has shown a significant improvement in the rate of wound healing from 29% in a control group to 63% in the experimental group. This increased rate of healing is thought to be mediated by stimulation of signal-transduction pathways directly involved in angiogenesis, leukocyte adhesion, and growth factor production.[10] The results of a Cochrane Database of Systematic Reviews study found that intermittent pneumatic compression (IPC) may increase healing compared with no compression in the treatment of venous leg ulcers and limb swelling due to lymphedema. Further trials are needed to determine whether IPC increases healing when used in conjunction with bandage treatment or if it can be used as an alternative to compression bandages.[11] Even though hyperbaric oxygen therapy is considered an important adjunct in wound healing, it is always important to revisit the evidence in the literature. The authors of a recent Cochrane summary reviewed relevant trials and concluded that in people with foot ulcers due to diabetes, hyperbaric oxygen therapy significantly improves ulcer healing in the short term but not in the long term. More studies are needed to properly evaluate hyperbaric oxygen therapy in patients with chronic wounds.[12] Investigations have highlighted the possibility of using injected low molecular weight heparin to speed healing in neurotrophic ulcers in the setting of occlusive peripheral artery disease. The rationale for this therapy is to improve the microcirculation of the healing wound by thinning the blood and increasing the flow of capillary flow of blood to the injured tissues. Data published by Kalani et al show 67% wound healing in patients treated with dalteparin compared to 47% healing in individuals treated with placebo.[13] This medication also showed benefit in a lower rate of amputation, from 19% amputation rate in the placebo group to 5% rate of amputation in the dalteparin group.[13] Oral therapies under investigation reportedly decrease the symptoms of chronic venous insufficiency but remain experimental at this time.[14] “Spray on skin to help leg ulcers,” The Daily Telegraph headlines, reporting that scientists have developed a skin spray consisting of a “soup of skin cells and proteins” that can be used to treat venous leg ulcers. The new spray (HP802-247) consisted of a combination of donated skin cells and proteins. It contains keratinocytes, which are the main cell type in the outer layer of the skin, and fibroblasts, a cell type found in connective tissue. The results from the trial were promising. They are likely to lead to further trials testing the safety and effectiveness in larger numbers of people with venous ulcers. The potential value of this spray is that it could treat those people whose skin will not heal with conventional treatment (such as compression bandages and dressings), and for whom the only alternative option could be skin graft. The study was conducted by researchers from the University of Miami and other institutions in the US and was funded by Healthpoint Biotherapeutics, a biotech company that specialises in wound care products. The study was published in the peer-reviewed medical journal The Lancet. This was a phase 2 randomised controlled trial that compared different concentrations and dosing frequencies of a new treatment for venous leg ulcers, called HP802-247. These cells had been grown in the laboratory and were originally derived from newborn foreskin samples (removed during circumcision). This was a phase 2 trial that aimed to see whether the new treatment was effective and safe, and to find out the best dose to use. If the results of phase 2 trials are positive (as these trial results were) they will usually be followed by larger phase 3 trials. What did the research involve? Between 2009 and 2011 this study enrolled adult patients being treated for venous leg ulcers in outpatient clinics at 28 centres in the US and Canada. To be eligible patients had to have venous insufficiency confirmed by an ultrasound scan, and to have up to three venous leg ulcers. At least one of the ulcers had to measure between 2cm squared and 12cm squared and served as the target ulcer for treatment. The ulcer had to have been present for between six and 104 weeks. They excluded people with poorly controlled diabetes or other medical conditions that could affect the integrity of the skin. A total of 228 participants were randomly assigned to one of five treatment groups: five million cells per ml every seven days (45 patients) five million cells per ml every 14 days (44 patients) half a million cells per ml every seven days (43 patients) half a million cells per ml every 14 days (46 patients) control solution (no skin cells) every seven days (50 patients) Both researchers and patients were not aware of the dose or frequency they were receiving (the trial was double blinded). To enable this, patients assigned to treatment every 14 days (either concentration) also received control spray on the intervening weeks so all patients received a treatment every seven days. All five groups also received four-layer compression bandage treatment for their ulcers. Bandages were applied over the spray and changed weekly. Patients had weekly assessments of their ulcer for 12 weeks, or until the wound was no longer draining fluid and had developed a new covering of skin without need for dressing. Complete wound closures were confirmed after two additional weeks of compression. The main outcome of interest was the mean (average) percentage change in wound area at the end of 12 weeks. What were the basic results? A total of 205 patients (90%) completed treatment, but all 228 patients were included in the analyses. The HP802-247 spray improved the main outcome of interest. Patients who had received the treatment had significantly greater mean reduction in wound area than those who received the control spray alone. The greatest benefit was observed with the lower dose of half a million cells per ml given every 14 days, which gave a statistically significant 16% greater reduction in wound area than control (95% confidence interval 5.56 to 26.41%). The results of the other treatment groups were: half a million cells per ml every seven days: a non-significant 9% improvement compared with control five million cells per ml every seven days: a significant 12% improvement compared with control five million cells per ml every 14 days: a non-significant 8% improvement compared with control By week 12 of the trial 70% of people who received half a million cells per ml every 14 days had wound healing, compared with 46% in the control group. There was no difference in the rate of adverse effects between the groups. How did the researchers interpret the results? The researchers conclude that venous leg ulcers can be healed, without the need of skin graft, with a spray formulation of keratinocytes and fibroblasts at an optimum dose of half a million cells per ml every 14 days. Conclusion These are promising results from a well-designed phase 2 trial that has investigated the use of a new spray treatment to heal venous leg ulcers. The study found the best results with a dose of HP802-247 spray of half a million cells per ml every 14 days, which gave a 16% improvement in wound area compared with control spray. The other three doses gave between 8 and 12% improvements compared with control, but only the five million cells per ml every seven days dose was statistically significant. There were also no adverse effects of treatment. The results suggest that this treatment may help ulcers to heal, without the need for skin grafts, which is sometimes the only option for chronic ulcers that will not heal with supportive care alone. However, the researchers do acknowledge that this trial only included people with a wound area less than 12cm squared, which they say represents about 80% of all venous leg ulcers, but a smaller proportion of chronic venous leg ulcers that will not heal with supportive care alone. They also say that only including people whose ulcer had been present for less than two years meant that they included a potentially more responsive population in their trial. This means that the current trial results may not apply to people with chronic venous leg ulcers, and the effectiveness of this treatment for larger and more persistent ulcers has yet to be examined. The results of this phase 2 trial are likely to lead to larger phase 3 trials to further investigate the effectiveness and safety of the treatment. It should be remembered that, although this treatment may help the skin to heal, unfortunately it will not be able to cure the underlying problem of venous insufficiency (where blood pools in the legs as a result of incompetence of the valves in the veins of the legs), which caused the ulcers to develop. Often, even when a venous ulcer heals, another will develop. The common way of healing current venous ulcers, and preventing venous ulcers from recurring, is to use compression stockings (usually prescribed by the treating health professional) to improve the flow of blood back up the legs, in addition to taking care of the skin and addressing other lifestyle factors that may worsen the problem (such as smoking and obesity). Read more about how to reduce the risk of developing venous ulcers. In this trial all patients received standard compression bandage treatment. If further clinical trials demonstrate the success and safety of this treatment for venous ulcers, and it is eventually approved as a treatment, it is still likely to be used alongside such standard supportive care treatments for venous ulcers and venous insufficiency.