leg ulcer management in patients with chronic oedema - Wounds ...

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Reviewlikely that patients with co-existingoedema and leg ulcers, eitheras a result of trauma or venousdisease, will be encounteredfrequently in practice.This article aims to promoterecognition of chronic oedemaand lymphoedema in patientswith leg ulceration, and willdiscuss what implications thediagnosis of chronic oedema willhave on the management of thepatient with leg ulcers.The lymphatic systemThe lymphatic system has animportant role in maintainingfluid balance. It carries fluid, fatsand proteins back to the generalcirculation from the tissues thatwould otherwise accumulateas oedema. It also providesan important immunologicalfunction (Levick and Mortimer,2003), carrying immune cellssuch as lymphocytes andmacrophages to the lymphnodes (Mortimer, 2000).Circulating blood carries fluidand nutrients to the bodytissues. As blood passesthrough the capillaries, fluidleaks out through the semipermeablewalls (filtration) andinto the interstitial space thatlies between the capillary walland the tissues.The exchange of nutrients,wastes, fluid, electrolytes, andproteins from the vascular andlymphatic systems and tissuecells occurs through this space.In this area, pressure may below and attract fluid into thetissue, or an increase in tissuepressure forces fluid into theinitial lymphatics and capillaries.It is in the interstitial fluid spacethat the forces resulting inoedema come into effect.Evidence has shown that themajority of interstitial fluid isreturned to the blood circulationvia the lymphatic system andnot, as initially thought, byabsorption directly into venouscapillaries (Mortimer andLevick, 2004). The absorptionof interstitial fluid is the crucialrole of the lymphatic system inmaintaining fluid balance. Whenthe lymphatic system is unableto maintain this role, oedemaoccurs.LymphoedemaLymphoedema is defined asswelling of a limb or part ofthe body due to failure of thelymphatic system. It resultsprimarily when the lymphdrainage system fails toadequately drain fluid from theinterstitial spaces. This failureleads to an accumulation offluid and proteins in the tissues,resulting in swelling or oedema.It can affect any part of the bodybut usually affects the limbs and/or the adjacent quadrant of thebody (Board and Harlow, 2002).Lymphoedema is classified asprimary or secondary. Primarylymphoedema is due to anintrinsic abnormality of thelymphatic system. It may becaused by insufficient numbersof lymphatic collectors (resultingin aplasia or hypoplasia). Itmay result from an abnormalityof the lymphatic vessels suchas hyperplasia or valvularincompetence (Mortimer, 1998).It may be congenital (present atbirth but not hereditary), or candevelop at puberty or any agethereafter.Secondary lymphoedema isdue to damage or long-termoverload of the lymphaticsystem by extrinsic factorsincluding:8Cancer treatment, e.g.surgery and/or radiotherapy8Recurrent infection8Trauma8Parasitic infection8Obstruction by tumour8Immobility8Venous disease, which will bedescribed now in more detail.Lymphovenous oedemaLymphovenous oedemaoccurs when chronic venousdisease associated with deepvein thrombosis, venoushypertension and chronic legulceration influences capillarypermeability and increasescapillary filtration rates.Venous hypertension is causedby failure of the calf musclepump to return blood back upthe leg. Incompetent valvesin the deep, perforating orsuperficial veins lead to thebackflow of blood and theveins elongate and becometortuous. The resulting increasein pressure leads to leakageof blood particles and fluidinto the tissues. This is usuallycompensated for by a healthylymphatic system.However, a sustained increasein capillary filtration leads toan overload of the lymphaticsystem, which will ultimatelyresult in oedema. Thus, acombined lymphatic andvenous oedema results;lymphovenous oedema. Aslymphatic drainage becomesfurther compromised,lymphostatic fibrosis begins toWound Essentials • Volume 2 • 2007 47
Reviewa swollen foot or toes, increasedexudate from an ulcer site or apoorly healing wound may besigns that oedema is not beingadequately controlled (Figure 3).Figure 2. Ulceration and maceration of the surrounding skin and oedema around theulcer.Figure 3. Swollen toes (Courtesy of St. Giles Hospice).develop leading to a chronicoedema (Green and Mason,2006).Table 1Visible signs of long-term oedema in the lower limb8Positive Stemmer’s sign (Figure 6)8Dry, flaky skin8Skin creases around the ankles and toes (Figure 7)8Hyperkeratosis (Figure 7)8Lymphangioma8Papillomatosis8Increased subcutaneous fat.Chronic oedema ischaracterised as a longstandingoedema that hasbeen present for at least threemonths and does not reduceon elevation of the affectedpart of the body (Green andMason, 2006). With continuedfluid accumulation, skin andtissue changes occur (Table1). Chronic oedema has beenshown to affect a significantnumber of patients with legulceration (Moffatt et al, 2004).In such patients, impairedlymphatic drainage may beidentified around the ulcer siteby the presence of oedema andlocalised swelling at the ulceredge (Figure 2). The presence ofRecognising chronic oedemaA thorough assessment of thepatient will help to identify riskfactors for the development ofchronic oedema and aid in itsdiagnosis. A careful history andexamination should be carriedout to include:8General medical history,including identification ofconditions that may affectthe outcome of treatmentsuch as a history of venousinsufficiency, deep veinthrombosis and cardiachistory8Limb volume measurement toassess the degree of swelling8Assessment of the skin andtissues to identify changesassociated with chronicoedema, noting factors thatmight affect the outcome oftreatment, such as repeatedepisodes of cellulitis, fungalinfections, papillomatosis,and skin allergies, such asdermatitis8Psychosocial assessment todetermine the impact of theswelling on the patient8Circulatory assessment— ankle brachial pressureindex (ABPI) or toe brachialpressure index (TBPI). AnABPI must be calculated toexclude significant arterialdisease. An ABPI must begreater than 0.8 before highcompression can be applied.If below 0.8 refer for furthervascular investigations(Stevens, 2004) beforeundergoing compressiontherapy.48 Wound Essentials • Volume 2 • 2007
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