Presented by Natalie Scott 2012

1. Cellulitis Fungal Infection & Venous Eczema Presented by Natalie Scott 2012

2. Overview • Skin structure • Cellulitis eitiology, pathogens, symptoms • Tinea Pedis fungal infection and its potential risk factor for cellulitis • Treatment fungal infection • Venous Eczema and treatment • Summary: Holistic Assessment

3. Overview of structure of the skin Latin ‘Cellula’ (little cell) Greek ‘ itis’ (inflammation) Definition:Cellulitis Diffuse spreading acute bacterial infection of dermis & subcutaneous tissue (McCance et.al 2010)

4. Cellulitis: eitiology Normal skin provides effective barrier (1st line defence) pH 5.5 • Bacteria microbes - opportunistic gain entry through breaks in the skin e.g. trauma, insect bites, ulcers, burns, surgical incisions, IV catheters (all potential pathways) • Cellulitis associated inflammation occurs potentially dangerous affecting the skin layers, epidermis, dermis, subcutaneous tissue and spreading to the lymph and bloodstream

5. Cellulitis - Pathogens Staphylococcus Aureus can start from central localised infection & spread e.g. abscess Streptococci pyrogenes (Group A) Gram + (haemolytic) • Spreads up the leg rapidly & diffusely • Fever • > necrotising fasciitis (flesh eating bacterium) Pseudomonas spp. Bacteriodes spp. Hemophyllis spp

6. Cellulitis symptoms • Local heat - hot/warm. Swelling in the tissues surrounding wound • Redness – red streaking or broad areas of redness • Pain or tenderness • Swelling – rapid spreading ascent up lower leg. Tight glossy stretched appearance of the skin • Drainage or leakage of yellow clear fluid or pus from the skin • Flu like symptoms (CREST GUIDELINES 2005 ) Management of cellulitis in Adults

7. Cellulitis Condition spreads - Progress to lymph and blood stream • Fever > 38C • Malaise • Chills • Headache • Elevated white cell count & CRP • Abscess and tissue destruction (without intervention) • Life threatening – e.g. necrotising fasciitis (strep spp and anaerobes)

8. Cellulitis

9. Cellulitis with blisteringManagement protection /exudates

10. Possible Pre-disposing factors for cellulitis hospital admissions International Study (P.Koutika et.al. Infectious Diseases 1999) • Tinea Pedis 32% • Dry skin 68% • Diabetes Mellitus 50% • Hx cellulitis 48% • Peripheral vascular disease 40% • Trauma 32% • Saphenous harvest for CABG 27% • Current ulcers • Lymphoedema

12. Management of Cellulitis • Antibiotic regime – • Cellulitis - Dry skin – Keep dry Emollient helps re-establish skin integrity 50/50 soft white paraffin • Cellulitis Wet skin – Blistering. Control exudate with absorbent dressings (foams, alginates, hydrofibre, zetuvit). Control maceration

13. Management of Cellulitis • Pain - regular analgesia • Inflammation - Monitor area (mark with pen) • Rest– plenty of it • Exercise - Dorsiflexion and plantar foot exercises will aid drainage of oedema • Oedema – elevate limb • Patients with venous insufficiency history – compression bandage post acute stage (Hofman, 1998 & Van Onselen, 2001)

14. Tinea pedis ‘Athletes foot’15-25% population infected at any one time Caused by Parasitic fungi – Trichophyton dermaphyte • Webs between toes - warm moist environment plantar of the foot and bullous (blister) form • Inadequate hygiene /drying Infected - public amenities • Tinea pedis spp. (fungal) provides entry point for bacteria to invade the soft tissue through the broken skin, abrasions/wounds leading to infection – potential cellulitis

15. Tinea Pedis: symptoms • Appears “macerated” between toe webs (skin peeling) • Scales or flaking • Cracks or blisters • Itching or burning sensation in localised area • Redness & inflammation of the toes • Exposure of raw tissue

16. Tinea Pedis • Common portal of entry is toe web maceration

17. Athletes FootTinea Pedis

18. Tinea PedisTreatment (anti-fungal creams/tabs) • Lamisil (Terbinafine) (86% cure rate at 6 wks) • Azoles: Miconazole & Clotrimazole (53% cure) • Apply to dried skin (weave gauze around toes) Oral tabs • Fluconazole & Terbinafine Antibiotics for co-existing bacterial infection Continue tx till 1 – 2 weeks after fungal infection resolved

19. Other common skin conditionsVenous Eczema • Skin is starved of nutrients and O2 (malnourished) -becomes dry, rough to touch, flaky and itchy • Caused by extravasations of irritating proteolytic and other metabolic waste products • Treatment (hit hard initially)Steroids, emollients & compression therapy.

20. Venous eczema:requiresurgent Doppler)Treat with steroid cream/zinc/emollients and compression

21. Steroid ClassificationNZ DermNet • Class 1:Dermol 600 x more potent than hydrocortisone (very potent) • Class 2: Betnovate/Locoid/Elecon 100 -150 x more potent than hydrocortisone (potent) • Class 3: Eunovate cream, kenacomb cream/ung 25 x more potent than hydrocortisone (mod potent) • Class 4: Hydrocortisone 0.5-2.5% found in Lemnis fatty cream, pimafucort, DP lotion HC1% mildly potent

22. Application of steroid creamhttp://dermnetnz.org/treatments/fingertipunits.html Fingertip unit: (describes amount of cream squeezed from tube) Adult Male: 0.5g Adult female: 0.4g One leg apply 6 fingertip units One foot apply 2 fingertip units e.g. Female applies cream 1x daily to 1 leg = 1 leg x 6 fingertip units x 0.4 = 2.4g daily x 7 =16.8g per week

23. Assessment • Differential diagnosis: cellulitis or inflammation This is common source of diagnostic confusion with redness alone – spreading erythema more accurate indicator of infection when accompanied with raised temp or increased pain levels) • Elderly, obese or chronic oedematous legs can have significant erythema (usually not hot to touch & is symmetrical)

24. ConclusionThorough Wound/Skin Assessment Need a good assessment tool History taking- medical status looking for the underlying cause e.g. Physical assessment – thorough examination of the limb, foot examination Plan –manage infection, pain, manage venous insufficiency, wound management, wound measurement (Note: 30% reduction in wound size at 4 weeks the wound will be healed at 12 weeks) Referral? To specialist

25. Questions

26. References Eagle M (2007). Understanding Cellulitis of the lower limb. Wound Essentials 2 Dermnet NZ Fingertip unit http://dermnetnz.org/treatments/fingertip units.html Semel JD, Goldin H, (1996) Association of athletes foot with cellulitis of the lower extremities: diagnostic value of bacterial cultures of ipsilateral interdigital space samples. Clinical Infectious Diseases 23 pp1162-1164 http://dermatology.jwatch.org/egi/content/full/1997/301/1 Wiley On Line Library (2009) Diabetic Medicine Vol 26 Issue 5 http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2009.02722.x/pdf

27. References Roujeau, J., Sigurgeirsson, B., Korting, H., Helmut, K., & Paul, C. (2004). Chronic Dermatomycoses of the Foot as Risk Factors for Acute Bacterial Cellulitis of the Leg: A Case-controlled Study. Dermatology,209, 301-307. Retrieved from, http://content.karger.com/produktedb/produkte.asp?DO1=10.1159/000080853 Vanhooteghem, O., Szepetiuk, G., Paurobally, D., & Heureux, F. (2011). Chronic interdigital dermatophyic infection: a common lesion associated with potentially severe consequences. Diabetes Research Clinical Practice, 91(1), 23-5. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21035887 Al Hasan, M., Fitzgerald, S.M., Saoudian, M., & Krishnasamy, G. (2004).Dermatology for the practicing allergist: Tinea pedis and its complications.Clinical and Molecular Allergy,2(5). Retrieved from, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC419368/