Acute wounds take less than 4 weeks to heal and have: • High mitogenic activity • Low levels pro-inflammatory cytokines • Decrease protease activity • Mitotically competent cells
Chronic wounds take longer than 4 weeks to heal and: • Become “Stunned & Stuck” in the inflammation stage • High levels of proinflammatory cytokines • Increase protease activity • Decreased mitogenic activity & senescent cells • Premature ageing of cells that results in impaied proliferation and their response to growth factors
- Compression therapy - Wound/skin Care – treat eczema - Self examination - Ambulation - exercise - Nutrition – weight loss - Elevate legs - Stop smoking - Calf & foot exercises - Moisturise - Treat the aetiology - Prevent recurrence – support groups
• No compression • Avoid mechanical/thermal trauma • Daily inspection • Foot wear, Podiatry care • Moisturises • Relief from pressure of clothing/shoes • Elevate head of bed • Consult with vascular surgeon
pressure injury prevention - Risk assessment -Waterlow or Braden score - Equipment – cushions, alternating mattress. Low air pulsation, foams, sheepskins - Turning regime – position pt - Nutrition/hydration - Hygiene – skin care - Manage incontinence - Prevent shearing and friction
Healing, Haemostasis, Day 1-4 post injury, Characterized by rubor, tumor, dolor, calor. Platelet aggregation and activation, Inflammation, Leukocyte migration, phagocytosis and mediator release, venule dilation, lymphatic blockade, exudative, Reconstitution, Day 4-42, Fibroblast proliferation stimulated by macrophage-released growth factors. Increased rate of collagen synthesis by fibroblasts. Granulation tissue and neovascularisation and a gain in tensile strength, Maturation, 6 wks-1 year, Intermolecular cross-linking of collagen via vitamin C-dependent hydroxylation characterized by increase in tensile strength. Type III collagen replaced with type I. The Scar flattens
Colonisation: • All chronic wounds are contaminated by bacteria. • Wound healing occurs in the presence of bacteria. • Certain bacteria appear to aid wound healing., Critically colonised, describes a state where ‘host defences are unable to maintain a healthy bacterial balance and bacteria are sufficient in number to delay healing but not cause a classical host reaction, such as heat, redness or swelling, Critically colonised wounds are typically treated with topical antimicrobials such as: treated honey & iodine., Infection:Infected wounds are characterized by: swelling, redness, discharge, and pain. Antibiotic treatment should be considered if the wound has a 2-3 cm ring of erythema or signs of cellulites.
Superficial partial thickness burns
venous leg ulcers, Assessment of Venous ulcer • History of DVT, valvular incompetence, previous ulcers, obesity • Peripheral oedema – leaking, haemosiderin pigmentation,dilated & tortuous superficial veins • Location – medial malleous, anterior to pretibial ulcer, lower 1/3 leg, uneven edges, ruddy granulation tissue, no necrotic tissue, maceration & puritis of surrounding skin • Foot pulses present
pressure ulcers, 4 Stages, Stage 1 • Intact skin with non-blanchable redness of a localised area usually over a bony prominence. • Darkly pigmented skin may not have visible blanching; its colour may differ from the surrounding area. • The area may be painful, firm, soft,, Stage 2 • Partial thickness loss of dermis presenting as a shallow, open wound with a red-pink wound bed, without slough. • May also present as an intact or open/ruptured serum-filled blister. • Presents as a shiny or dry, shallow ulcer without slough or bruising, Stage 3 • Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. • _Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunnelling., Stage 4 • Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed., Unstageable • Full thickness tissue loss in which the base of the PI is covered by slough (yellow, tan, grey, green or brown) and/or eschar (tan, brown or black) in the PI bed.
arterial leg ulcers, Assessment of arterial leg ulcer• History of: arteriosclerosis, advanced age, diabetes, hypertension, smoking • Thin, shiny, dry skin, thickened nails, absence of hair growth • Pallor Cool limb • Location: toes, over phalangeal heads, side or sole of foot • Deep punched out wound, necrotic tissue, deep pale base, pain at rest • May have neuropathy, diminished or absent foot/limb pulses
malegnincy, Wounds that fail to heal must be assessed for malegincy
Tier 1, GP's, Practice nurse & community nurses. No Referral necessary.
Tier 2, Specialized nurse practitioners, Located in community health centers across Canberra.
Tier 3, Specialist outpatient clinic locates @ the Canberra Hospital. Referral is necessary, from GP's & Nurse practitioners
Regular self examination
• Decreased dehydration and cell death (Neutrophils, macrophages, & fibroblast necessary for wound healing cannot thrive in a dry environment) • Increased angiogenesis • Enhanced autolytic debridement • Increased re-epithelialization (Dry crusted wounds decrease supply of blood and nutrients which thus results in a barrier to cell migration and slowing of epithelialization.) • Decreased pain (Moist wound bed insulates and protects nerve endings thereby reducing pain.)
cellulitits, emperical treatment: di / flucloxacillin