D Dermatological issues in lymphoedema and chronic oedema T · mised by impairment of the innate...
Transcript of D Dermatological issues in lymphoedema and chronic oedema T · mised by impairment of the innate...
Dermatology
27Journal of Community Nursing March/April 2013, volume 27, issue 2
Key words:
Skin care in lymphoedema and chronic
oedema
Function of the skin
Specific interventions
In order to understand lymphoedema
and chronic oedema skin breakdown
and thus consider the most appropriate
treatment options and strategies for
patient education, the normal function
and structure of the skin must be
understood.
This abridged version of the chapter
of the same name, from the
International Lymphoedema Framework
document, Best Practice for the
Management of Lymphoedema (2nd
ed.), outlines the skin conditions
commonly see in lymphoedema and
chronic oedema and offers
management strategies for these.
Mieke Flour, MD, Senior Staff DermatologyDepartment, University Hospital Leuven,Belgium, Head of out-patient clinics: chronicwounds, conservative phlebology,lymphoedema, compression andmultidisciplinary diabetic foot clinic
Article accepted for publication: October 2012
Dermatological issuesin lymphoedema andchronic oedema
Renewal of the stratum corneum is aconstant process, regulated by the actionof proteases. If the process is affected byan imbalance of proteases and proteaseinhibitors, the stratum corneum may thinand crack, potentially allowing the entryof irritants and allergens and makingskin barrier function less effective3. Inaddition, decreased levels of NMF,particularly urea, and the breakdown ofthe lipid lamellae, cause skin to dry as ineffect the ‘mortar’ holding the corneocyte‘bricks’ together, crumbles, leading togreater TEWL.
Over-hydration of the skin (occlusion,prolonged hydration) will lead to waterloss by enlarging and connecting theaqueous lacunae between the lipidlayers, making the barrier ‘leaky’2.
The effect of lymphoedema onthe skinChronic disturbance of lymph flowresults in chronic inflammation in theswollen body parts with enhancedactivity and proliferation of cellscontained in the epidermis, underlyingdermis (including vessels) and fat tissue.The clinical signs resulting from thesealterations are:
• thickening of the skin and of allunderlying tissues (fat, connectivetissue, fascia)
• hyperkeratosis
• papillomatosis
• hyperpigmentation
• fibrosis with loss of skin suppleness
• deepening of the skin folds
Papillomatosis: Papillomatosis producesfirm raised projections on the skin due todilation of lymphatic vessels and fibrosis,and may be accompanied by hyperker-atosis (Figure 2). Sometimes dilatedlymph vessels may form cystic ‘vesicles’leading to lymphorrhoea and fistulisa-tion following rupture.
Skin is actively maintained in home-ostasis by a dynamic repair response;after a disturbance, epidermal hyper-
The skin is the largest organ of thebody and has a number of func-tions:
• it provides a barrier to protect the bodyfrom the environment and infectionthrough its immune function
• it regulates temperature
• it detects sensations such as pressure,vibration and temperature
• it synthesises vitamin D
• it acts as an excretory organ
Skin varies in thickness in differentparts of the body; it is thinnest on the lipsand around the eyes, thickest on the solesof the feet. It is strong and flexible mainlydue to the subcutaneous tissue, elasticfibres and collagen in the dermis, thenumber and volume of which decline aswe age making the skin more fragile.
The ‘skin barrier’ is located in thestratum corneum, or upper layers of theepidermis (Figure 1). Normally, thisbarrier protects the underlying skin frompenetration by irritants and allergens andalso prevents trans-epidermal water loss(TEWL) from the body2. In healthy skin,the skin barrier functions effectively dueto its structure: corneocytes, whichcontain water and proteins includingnatural moisturising factor (NMF), arelaid down in a ‘brick’ formation heldtogether by ‘mortar’ comprising lipidlamellae. NMF contains urea, itself ahumectant and acids that maintain thelow pH of the skin.
The Editor would like to thank MEPLtd (London), for their kindpermission to reproduce the imagesin this article.
The Editor would also like tothank the InternationalLymphoedema Framework forallowing publication of this abridgedchapter. The full document can befound at www.lympho.org
Figure 1: Schematic of the skin (ack. WPClipart)
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Dermatology
29Journal of Community Nursing March/April 2013, volume 27, issue 2
plasia and inflammation restore its prop-erties and integrity. In lympho edema, theskin’s protective role may be compro-mised by impairment of the innate andadaptive immunologic defence againstinfection and by perturbations of the skinbarrier. pH imbalance will delay barrierrecovery and facilitate inflammation andinfection4.
Innervation: Innervation of the skin medi-ates the sensations of heat, cold, itch,touch and pain, and co-regulates thefunctions of all types of small vessels andsweat glands. Peripheral neuropathymay thus directly and indirectly influ-ence blood and lymphatic flow, theformation of the protective mantle, recog-nition of and response to external noxes,including the capacity to modulate theimmune responsiveness of the epidermalcells. Paralysed limbs often develop
surfaces that touch, causing a moist,whitish exudate and itching. It can lead tothe development of cellulitis/erysipelas.
Folliculitis: Is the inflammation of the hairfollicles causing a red rash with pimplesor pustules, and is most commonly seenon hairy and/or occluded areas (head,trunk, buttocks, limbs). It may precedecellulitis/erysipelas. In some cases (i.e.irritant folliculitis), it caused by friction(compression treatment), or the applica-tion of occlusive substances such aspetrolatum topical preparations.
Contact dermatitis: When applying topicalmedication, skin care products, orthrough occupational exposure, peoplesuffering from chronic oedema (espe-cially in venous disease) andlymphoedema are at risk for the develop-ment of allergic or cumulative irritantcontact dermatitis. Signs may includeitchy or painful fissures, dessication,erythema and even vesicles, but predominantly lichenification andhyper keratosis. Contact dermatitis(Figure 5) is the result of an allergic or irri-tant reaction. It usually starts at the site ofcontact with the causative material, butmay spread. The skin becomes red, itchyand scaly, and may weep or crust.
Venous eczema: Also known as varicoseeczema or stasis dermatitis, usuallyoccurs on the lower legs, particularlyaround the ankles, and is associated with varicose veins (Figure 6). The skinbecomes pigmented, inflamed, scaly anditchy.
chronic oedema through the combinedeffects of hyperaemia, gravity, loss oflympho-venous pump and immobility.
Dry skin: Dry skin develops when alter-ations of the stratum corneum barrierlead to a loss of water, lipids or thenatural moisturising factor (NMF) of theepidermis. The wicking effect of band-ages may aggravate this, making the skinless pliable and elastic and prone tocracks and fissures. Dry skin may varyfrom slightly dry or flaky to rough andscaly. Barrier perturbation, mechanical
factors (scratching the itchy skin), andapplication of irritant substances furtherdelay recovery and lead to release of pro-inflammatory cytokines. In moreadvanced stages the skin may becomedull red, oozing, crusting, excoriated and presenting nummular lesions ofasteatotic eczema or irritant dermatitis.
Hyperkeratosis: Hyperkeratosis is causedby over-proliferation of the keratin layerand produces scaly brown or greypatches. It relates to mechanical trauma,for example, repeated low grade frictionand repetitive mechanical trauma insuboptimal footwear (open heels, ‘slip-pers’) and under compression bandagesat pressure sites. It must be distinguishedfrom acanthosis nigricans in endo -crinopathies like morbid obesity and themetabolic syndrome.
Lymphangiectasia: Lymphangiectasia orlymphangiomata, are soft, fluid-filledprojections caused by dilatation oflymphatic vessels (Figure 3). Lymphaticprotruding dilatations and cysts mayrupture under the mechanical burdens ofmanual drainage or compression band-aging, resulting in lymph leakage(lymphorrhoea) (Figure 4).
Maceration: In deep skin folds, occludedskin sites, and around areas with lymphleakage, the skin frequently becomes wetand macerated, loosing its defenceagainst infection, and allowing easypenetration of applied substances/aller-gens. An over-hydrated epidermis ismore susceptible to blistering and break-down.
Infection: Occur because the skin iscompromised due to a break in the skin,blockage or malfunctioning of drainageroutes and lymph node alterations. Inter-triginous infections may be caused byyeast, microbes, and fungi. Fungal infec-tion occurs in skin creases and on skin
Figure 2: Papillomatosis
Figure 3: Lymphangiectasia
Figure 4: Lymphorrhoea with associated maceration
Figure 5: Contact dermatitis
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Ulceration: Ulceration is unusual inprimary lymphoedema patients; in mostcases it is to be attributed to trauma orcomorbidities/underlying diseases. It isimportant to establish the underlyingcause because it determines treatmentand whether compression is appropriate.
Lymphangiosarcoma: In the most severecases of lymphoedema, lymphangiosar-coma, a rare form of lymphatic cancer(Stewart-Treves syndrome) can develop.It mainly occurs in patients who havebeen treated for breast cancer withmastectomy and/or radiotherapy. Thesarcoma first appears as a reddish orpurplish discoloration or as a bruisedarea that does not change colour. Itprogresses to an ulcer with crusting, andeventually to extensive necrosis of theskin and subcutaneous tissue. It canmetastasise widely.
Skin careMaintenance of skin integrity and carefulmanagement of skin problems in patientswith lymphoedema are important tominimise the risk of infection. The general principles of skin care
include:
• washing daily, using pH neutralsoap, natural soap or a soapsubstitute, drying thoroughly
• if skin folds are present, ensuring thatthey are clean and dry, monitoringthe affected and unaffected skin forcuts, abrasions or insect bites
• applying emollients
• avoiding scented products
• using vegetable-based products ratherthan those containing petrolatum ormineral oils in tropical climates
The aim is to preserve skin barrierfunction through washing and the use ofemollients5. Ordinary true soaps have an
with a potent topical corticosteroid inointment form, and should be reviewedafter seven days. Treatment shouldcontinue for three to four weeks, duringwhich time the strength of the steroid andamount applied are gradually reduced.
Venous eczema: Adequate compressiontreatment is expected to reverse thesecondary skin changes seen in venousinsufficiency including venous eczema.Treatment is with topical corticosteroidsin ointment form for seven days,followed by a moderate corticosteroid.
Lymphangiectasia: Treatment is compres-sion with lymphoedema compressionbandaging (LCB). If there is no responseto initial compression or the lymphang-iectasia are very large, contain chyle orcause lymphorrhoea, the patient shouldbe referred immediately to a lympho -edema practitioner.
Lymphorrhoea: The patient may requiremedical review to determine the under-lying cause. The surrounding skinshould be protected with emollient and non-adherent absorbent dressingsshould be applied to the weeping skin.Lymphoedema compression bandagingwill reduce the underlying lympho -edema, but needs to be changedfrequently to avoid maceration of theskin. Frequency will be determined bystrikethrough and the rate of swellingreduction. In the palliative situation, lightbandaging may be more appropriate. Ifthere is no improvement after six weeksof treatment, the patient should bereferred to the lymphoedema service.
Folliculitis: Swabs should be taken forculture if there is any exudate or an open wound. An antiseptic wash/lotionshould be used after washing and emol-lient applied.
Cellulitis/erysipelasPatients with lymphoedema are atincreased risk of acute cellulitis/erysipelas, an infection of the skin andsubcutaneous tissues. The cause of mostepisodes is believed to be Group Ahaemolytic streptococci.Symptoms are variable. Episodes may
come on over minutes, grumble overseveral weeks or be preceded by systemicupset. Symptoms include pain, swelling,warmth, redness, lymphangitis,lymphadenitis and sometimes blisteringof the affected part (Figure 7). More severecases have a greater degree of systemicupset, for example, chills, rigor, high
alkaline pH of 9-10, so should be avoidedbecause they dry the skin; natural or pHneutral soap can be used. Synthetic deter-gents (‘soap-free soap’), have a pH of5.5-7 to minimise skin barrier disruption.Body wash emulsion systems combine asyndet with moisturisers or emollients.Lipid-free cleansers may contain glycerinand other emollients, while cleansingcreams contain waxes and mineral oil.Moisturisers should be used aftercleansing the skin in order to replace thelipid film barrier that has been disruptedby washing. Emollients re-establish the skin’s
protective lipid layer, preventing furtherwater loss and protecting the skin frombacteria and irritants. In general, oint-ments, which contain little or no water,are better skin hydrators than creams,which are better than lotions. The bestmethod of emollient application isunknown. Some practitioners recom-mend applying them using strokes in thedirection of hair growth to preventblockage of hair follicles and folliculitis.Others recommend applying emollientsby stroking towards the trunk toencourage lymph drainage.
Skin care regimensSkin conditions that can occur in patientswith lymphoedema require carefulmanagement. They may occur simulta-neously and require combinations ofregimens. The general principles of skincare apply to all conditions and where anintervention has proved unsuccessful,the patient should be referred as appro-priate .
Intact skin/dry skin: Apply emollientstwice daily to aid rehydration. If heels aredeeply cracked, emollients and hydro-colloid dressings may help.
Hyperkeratosis: Frictional and mechanicalcauses such as footwear, bandages,rubbing and scratching need to beaddressed. Emollients with low watercontent are recommended. Lympho -edema compression bandaging (LCB)reduces the underlying lymphoedemaand improves skin condition.
Papillomatosis: May be reversible withadequate compression, although if itdoes not improve after one month, referto a lymphoedema service.
Contact dermatitis: Avoid causative irri-tants and allergens and restore epidermalbarrier function. Acute episodes ofcontact allergic dermatitis are treated
Figure 6: Venous eczema
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STARRING:STARRING:
THE DRY SKIN RESTORER RESTORES & REHYDRATES
LOWEST COST IN CLASS3
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PRODUCT INFORMATION Balneum Cream Active Ingredient: Urea 5 %, Ceramide 3. Indication: For the symptomatic relief of dry and very dry skin conditions. Dosage and Administration: Using clean hands, apply the cream to the skin twice daily. Consult package leaflet for method of administration. Contraindications, Warnings, etc: Contraindications: Patients with known hypersensitivity to any of the ingredients, soya or peanut.Precautions: For external use only. Do not use on broken or inflamed skin. Caution should be exercised with concomitant use of some medicated topicals. If the condition worsens on usage or if patients experience side effects, discontinue use and consult a Health Care Professional. Adverse Effects: Very few side effects have been reported; typically local skin reactions. Legal Category: Class 1 Medical Device. NHS Cost: (excluding VAT, Pump dispenser containing 50g - £2.85, Pump dispenser containing 500g - £9.97. CE marking held by: Almirall Hermal GmbH, Scholtzstrasse 3, 21465 Reinbek, Germany. Further information is available from: Almirall Limited, 1 The Square, Stockley Park, Uxbridge, Middlesex UB11 1TD, UK. Tel: (0) 207 160 2500. Fax: (0) 208 7563 888. Email: [email protected]. Date of Revision: 1/2013Item code: UKSOY1554
Adverse events should be reported. Reporting forms and information can be found at www.mhra.gov.uk/yellowcard. Adverse events should also be reported to Almirall Ltd.
1. Puschmann M et al. Measurements of Skin Hydration after a Single Application. Data on file, Almirall Ltd 2000.
2. Balneum Cream Product Information, January 2013.3. British National Formulary 64. September 2012: 730-731
Job code: UKSOY1650. Date of preparation: February 2013
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32 Journal of Community Nursing March/April 2013, volume 27, issue 2
fever, headache and vomiting. In rarecases, these symptoms may be indicativeof necrotising fasciitis. The focus of the infection may be tinea
pedis, venous eczema, ulceration, in-growing toe nails, scratches from plantsor pets, or insect bites. Box 1 outlines theprinciples involved in the managementof acute cellulitis/erysipelas at home orin hospital.It is essential that patients with
cellulitis/erysipelas, who are managed athome, are monitored closely, ideally by thegeneral practitioner. Prompt treatment isessential to prevent further damage thatcan predispose to recurrent attacks.
Criteria for hospital admissionThe patient should be admitted tohospital if they show:
• signs of septicaemia (hypotension,tachycardia, severe pyrexia,confusion or vomiting)
• continuing or deteriorating systemicsigns, with or without deterioratinglocal signs, after 48 hours of oralantibiotics
• unresolving or deteriorating localsigns, with or without systemic signs,despite trials of first and second lineoral antibiotics
Conclusion
Lymphoedema and chronic oedema canhave have a major impact on skin func-tion. While some of the conditions arerelatively easy to manage, others, such ascellulitis, can present an emergency situ-ation.Prevention of course, is key, and
community practitioners are ideallyplaced to work with patients and theirfamily to implement prevention andearly management strategies.
References 1. Cork MJ. (1997) The importance of skin barrierfunction. J Derm Treat. 8: S7-13
2. Proksch E, Brandner JM, Jensen JM. (2008) Theskin: an indispensable barrier. Exp Dermatol. 17;12: 1063-72
3. Flour M. (2009) The pathophysiology of vulner-able skin. World Wide Wounds. http://www.worldwidewounds.com/2009/September/Flour/vulnerable-skin-1.html
4. Schmid-Wendtner MH, Korting HC. (2006) ThepH of the skin surface and its impact on thebarrier function. Skin Pharmacol Physio. 19; 6: 296-302
5. Korting HC, Kober M, Mueller M, et al. (1987)Influence of repeated washings with soap andsynthetic detergents on pH and resident flora ofthe skin of forehead and forearm. Results of across-over trial in healthy probationers. ActaDerm Venereol. 67; 1: 41-7
Figure 7: Cellulitis
Box 1: Guidelines for the management of cellulitis/erysipelas inlymphoedema6
Exclude:
• Other infections, for example, those with a systemic component
• Venous eczema, contact dermatitis, intertrigo, microtrauma and fungal infection
• Acute deep vein thrombosis
• Thrombophlebitis
• Acute lipodermatosclerosis
• lymphangiosarcoma (Stewart-Treves syndrome)
Swab any exudate or likely source of infection, for example, cuts or breaks in theskin
Before starting antibiotics establish:
• The extent and severity of the rash – mark and date the edge of the erythema
• Presence and location of any swollen and painful regional lymph nodes
• Degree of systemic upset
• Erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) and white cellcount
Start antibiotics as soon as possible, taking into account swab results and bacterialsensitivities when appropriate.
• During bed rest, elevate the limb, administer appropriate analgesia (forexample, paracetamol or non-steroidal anti-inflammatory drugs (NSAID),increase fluid intake
• Avoid simple lymphatic drainage (SLD) and manual lymphatic drainage (MLD)
• If tolerated, continue compression at a reduced level or switch fromcompression garments to reduced pressure LCB
• Avoid long periods without compression
• Recommence usual compression and levels of activity once pain andinflammation are sufficiently reduced for the patient to tolerate
• Educate patient/carer – symptoms, when to seek medical attention, risk factors,antibiotics ‘in case’, prophylaxis if indicated
Reflection Points
1. How relevant is skin care oflymphoedema patients to yourpractice?2. After reading this article, wouldyou explore or change your practice?In what ways would you do this?3. How can simple skin care alleviateor prevent some of the lymphoedema-associated conditions discussed inthe article?
6. Partsch H. (2003) Understanding the patho-physiological effects of compression. In:European Wound Management Association(EWMA). Position Document: Understandingcompression therapy. MEP Ltd, London
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