1. Wounds
1.1. Types
1.1.1. Healing
1.1.1.1. Haemostasis
1.1.1.1.1. Day 1-4 post injury, Characterized by rubor, tumor, dolor, calor. Platelet aggregation and activation
1.1.1.2. Inflammation
1.1.1.2.1. Leukocyte migration, phagocytosis and mediator release, venule dilation, lymphatic blockade, exudative
1.1.1.3. Reconstitution
1.1.1.3.1. 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
1.1.1.4. Maturation
1.1.1.4.1. 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
1.1.2. Colonisation: • All chronic wounds are contaminated by bacteria. • Wound healing occurs in the presence of bacteria. • Certain bacteria appear to aid wound healing.
1.1.2.1. 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.
1.1.2.2. 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.
1.2. Causes
1.2.1. Trauma
1.2.2. Superficial partial thickness burns
1.2.3. venous leg ulcers
1.2.3.1. 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
1.2.4. pressure ulcers
1.2.4.1. 4 Stages
1.2.4.1.1. 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,
1.2.4.1.2. 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
1.2.4.1.3. 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.
1.2.4.1.4. 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.
1.2.4.1.5. 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.
1.2.5. arterial leg ulcers
1.2.5.1. 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
1.2.6. diabetes associated
1.2.7. malegnincy
1.2.7.1. Wounds that fail to heal must be assessed for malegincy
2. Management
2.1. Services
2.1.1. Tier 1, GP's, Practice nurse & community nurses. No Referral necessary.
2.1.2. Tier 2, Specialized nurse practitioners, Located in community health centers across Canberra.
2.1.3. Tier 3, Specialist outpatient clinic locates @ the Canberra Hospital. Referral is necessary, from GP's & Nurse practitioners
2.2. prevention
2.2.1. Regular self examination
2.2.2. Education
2.2.3. Personal hygine
3. treatment
3.1. Acute
3.1.1. 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
3.2. Chronic
3.2.1. 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
3.3. Venous
3.3.1. - 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
3.4. Arterial
3.4.1. • 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
3.5. Pressure
3.5.1. 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
4. Treatment principles
4.1. Moist wound healing theory, proposes that a balance must be struck between excessive wound fluid, particularly in chronic wounds which can cause maceration of the periwound skin destroying some of the beneficial processes occurring in the wound, and a wound surface exposed to air which then forms a dry, hard scab that can delay healing
4.1.1. • 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.)
5. Treatment Agents
5.1. Oral antibiotics
5.1.1. cellulitits, emperical treatment: di / flucloxacillin