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3/24/17
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Wound ManagementJan RiceDirector
Jan Rice WoundCareServices0418367485
Wound healing is a series of interactive chemical and cellular responses in order to achieve skin closure
Another way or saying the same• Reactive• Regenerative • Remodelling
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Cell types required in the inflammatory include:
•Neutrophils•Monocytes•Macrophages Each type of leukocyte is
present in the blood in different proportions:neutrophil 50 -‐ 70 %eosinophil 2 -‐ 4 %basophil 0.5 -‐ 1 %lymphocyte 20 -‐ 40 %monocyte 3 -‐ 8 %
Cell types required in the proliferative include:
•Macrophages• Fibroblasts • Endothelial cells
http://www.pnas.org/content/103/13/F1.medium.gif
Cell types required in the epithelialisation phase include:
• Fibroblasts •Myofibroblasts• Endothelial cells• Epithelial cells
http://www.rejuvenal.info/images/Terminology/FibroblastImage.jpg
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Other requirements •Matrix components-‐proteins & proteoglycans• Biological factors–growth factors–proteinases and –cytokines
http://ethesis.helsinki.fi/julkaisut/mat/bioti/pg/jeltsch/images/cytokines.gif
Cell surface receptors
• Growth cell receptors• Integrin receptors
•Without a receptor to bind to, the soluble mediator is not ‘heard’ or responded to by the target cell
Transforming growth factor betaTGFß1, TGFß2
TGFß3
PlateletsFibroblastsMacrophages
Fibroblast chemotaxis and activationECM deposition↑Collagen synthesis↑TIMP synthesis↓MMP synthesisReduces Scarring↓Collagen↓Fibronectin
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Platelet derived growth factorPDGF-AA, PDGF-BB, vascular endothelial growth factor (VEGF)
PlateletsMacrophagesKeratinocytesFibroblasts
Activation of immune cells and fibroblastECM deposition↑Collagen synthesis↑ TIMP synthesis↓MMP synthesisAngiogenisis
Fibroblast growth factor
Acid FGF, Basic FGF, KGF
MacrophagesEndothelial cellsFibroblasts
AngiogenisisEndothelial cell activationKeratinocyteproliferation and migrationECM deposition
Insulin-‐like growth factorIGF-1, IGF-2, Insulin
LiverSkeletal muscleFibroblastsMacrophagesNeutrophils
KeratinocyteproliferationFibroblast proliferationEndothelial cell activationAngiogenisis↑Collagen
synthesisECM depositionCell metabolism
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Epidermal growth factor
EGF, HB-EGF, TGF, Amphiregulin, Betacellulin
KeratinocytesMacrophages
Keratinocyteproliferation and migrationECM deposition
Connective tissue factor
CTGF FibroblastsEndothelial cellsEpithelial cells
Mediates action of TGFß on collagen synthesis
Pro Inflammatory cytokine activityTNFa Macrophages PMN margination and cytotoxicity,
provides metabolic substrate
IL1 MacrophagesKeratinocytes
Fibroblast & keratinocytechemotaxis, collagen synthesis
IL2 T lymphocytes >fibroblast infiltration & metabolism
IL6 Macrophages, PMN’s, Fibroblasts
Fibroblast proliferation, hepatic acute-phase protein synthesis
IL8 MacrophagesFibroblasts
Macrophage and PMN chemotaxis, keratinocytematuration
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Anti-‐inflammatory cytokinesIL4 T lymphocytes
BasophilsMast cells
Inhibition of TNF, IL1 & IL6 production;; fibroblast proliferation, collagen synthesis
IL10 T lymphocytesMacrophagesKeratinicytes
Inhibition of TNF, IL1, IL6 production, inhibits macrophage and PMN activation
Proteases
• These are involved in the localized enzymatic breakdown of the extracellular matrix• This is a normal part of the repair process–Aiding normal wound debridement–Dissolution of the basement membrane– In growth of capillary buds–Turnover of the provisional matrix and tissue remodelling
Matrix metalloproteinases (MMP’s)
• Collagenases-‐degrade intact fibrillar collagen molecules• Gelatinases-‐ degrade damaged fibrillar collagen molecules• Stromelins-‐ degrade proteoglycans•Neutrophil elastase-‐degrades almost all types of protein molecules
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Tissue inhibitors of metalloproteinases(TIMP’S)
• These also constitute the normal environment within a healing wound
–It is all about the balance
Classification of wounds
• Wounds are generally classified as acute or chronic
• Chronic wounds are generally associated with physiological impairments that slow or prevent wound healing
• Wounds may be caused by a variety of mechanisms including acute injury to the skin (abrasion, puncture, crush), surgery and other aetiologies that cause initially intact skin to break down (eg, ischaemia, pressure).
Classification cont.• Surgical wounds are a controlled form of trauma created in
the operating room environment• Classified according to the degree of bacterial load or
contamination of the surgical wound.• The categories, clean, clean-‐contaminated, contaminated,
and dirty are used to predict the risk of surgical wound infection which can impact wound healing.
• The majority of clean and clean-‐contaminated wounds are closed primarily at the completion of the surgery. Contaminated and dirty wounds (eg, faecal contamination, debridement for wound infection) are typically packed open and allowed to heal by delayed primary intention or secondary intention
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Tensile strength• The tensile strength of a wound is a measurement of its load capacity per unit area.
• The bursting strength of a wound is the force required to break a wound regardless of its dimension
• It varies with skin thickness• Peak tensile strength of a wound occurs approximately 60days after injury
• A healed wound only reaches approximately 80% of the tensile strength of unwounded skin
In order for the nurse to know if the wound is healing –an assessment must
be conducted
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Wound assessment
• Begin by examining the wound itself in terms of
• C – colour of tissue• D – depth of wound• E – exudate volume
• Measure wound and note other characteristics
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Begin by examining the wound itself in terms of
T-‐ tissue within the woundI-‐ inflammation or presence of infectionM-‐moisture –balance –wet /dryE – exudate volume/type
Measure wound and note other characteristics
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Other wound characteristics that you would assess
–Presence of undermining or tracking–Effects of previous treatments–Current dressing frequency and proposed frequency
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Wound tissue descriptor
• Necrotic tissue—eschar or slough• Granulation tissue• Hypergranulation tissue• Epithelium• Macerated tissue
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Dry hard black-‐almost no erythema, nil odour, ‘quiet’ DO NOT HYDRATE!!! Keep dry
Soft, boggy, offensive black often with peri wound maceration—have someone debride but usually after a few days of antibiotics-‐if you debride without antibiotic coverage there is often uncontrolled bleeding
Necrotic eschar
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Infected wounds-‐containing necrotic tissue of fluid
These wounds have thick purulent exudate often brown/red in colour or green
– requires systemic antibiotic therapy, exudate control and safe topical therapy
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Sloughy wounds
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The drier yellow/brown tissue if not able to be debrided requires rehydration to assist autolyticdebridement
The moist creamy yellow wet tissue requires an antimicrobial that will help to manage exudate
Clinicians must however be able to identify other yellow tissue…..
• Tendon• Bone-‐creamy / white• Fat / Subcutaneous tissue
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Granulating woundsThis tissue should be almost level with the perimeter of the wound and not bleed easily when cleansed
This tissue requires some moisture but not too much and it requires a dressing that will protect
Poor quality granulation tissue
• Can present as pale tissue with irregular tissue and copious exudate and non healing edges• This tissue often requires an antimicrobial, very good cleansing and exudate management and peri wound protection
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Hypergranulation tissue• Bleeds easily and raised above side edges of wound
• May also present as loose ‘bubbles’ of tissue within deeper wounds
• Sometimes described as ‘Jelly like’ tissue
• Flattens when pressed for short length of time– The aim here is to control exudate, apply direct pressure and consider antimicrobials
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Epithelialising tissue • This represents the wound in the final stages of healing, it may be transparent and pearly pink • Young epithelium wrinkles when pressed and has a matt finish appearance with minimal exudate
-‐requires some hydration and protection, particularly against friction and shear
Delayed wound healing• There is usually not a single primary factor that contributes to impaired wound healing
• There are multiple, smaller contributing issues that can disrupt the process.
• As examples,-‐local tissue ischemia and neuropathy can impair chemotaxis during the haemostasis and inflammatory stages
• Tissue necrosis and infection alter the balance of inflammation and compete for oxygen.
• Uncontrolled periwound oedema and wound instability disrupt myofibroblast activity, and collagen deposition and cross-‐linking
I am not here to tell you about what a wound requires
You all know-‐Protein, Vitamin C, Zinc, Iron and carbohydrates
I want to discuss specific wound types that may have additional nutritional needs however just to recap.......
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Fat
• Most concentrated form of kilocalories
• Transports fat soluble vitamins-‐A, D, E, K
• Provides insulation under the skin and padding to bony prominences
• Essential component of cellular membranes
Protein and amino acids
• Protein is the only nutrient containing nitrogen
• Protein is important for tissue perfusion, preservation of immune function, repair and synthesis of enzymes, cell replication and collagen and connective tissue synthesis
• During periods of stress arginine and glutamine become conditionally essential
L-‐Arginine
• Composed of 32% nitrogen and shown to increase the concentration of hydroxyproline, an indicator of collagen deposition and protein
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Vitamins and minerals• Ascorbic acid is a cofactor with iron during hydroxylation of proline and lysine in the production of collagen
• Vitamin A increases collagen formation and promotes epithelialisation
• Vitamin E an antioxidant• Zinc-‐cofactor for collagen formation, enhances metabolism of protein, liberates Vitamin A from storage in the liver and assists in immune function
Vitamins and minerals cont..
• Copper essential for collagen cross-‐linking• Zinc and copper compete for the same binding site on albumin –so careful with supplementation
Water
• The transport medium for moving nutrients to the cells and removing waste products
• Fluids are solvents for minerals, vitamins, amino acids, glucose, and other small molecules, thus enabling them to diffuse into and out of cells
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Scientific research
• There is little scientific evidence between nutrition, nutritional intervention and wound healing yet nobody would argue against the importance of adequate nutrition to preserve skin viability and promote tissue repair
Full thickness burn
Burns• Energy requirements can increase by 100% in the presence of sever burns
• The hypermetabolism is accompanied by exaggerated protein catabolism and increased nitrogen excretion
• Protein is also lost through the burn wound exudate
• Management of the burn is about early excision and grafting and so early attention to nutrition requirements also means a more successful surgical outcome
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Skin tears
Skin tears
• The skin is less elastic, has limited subcutaneous fat, is more susceptible to medication reactions and is prone to shear and friction forces resulting in these painful trauma wounds
• In order to fight the potential infection in these wounds the elderly require protein, calories and adequate hydration
Leg ulcers
Venous Arterial
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Venous leg ulcers
• Unless managed well these can leak copious volumes of exudate
• The skin is virtually washed away so epithelialisation can be delayed
• These patients require diets high in protein, and zinc with fluid replacement
Arterial ulcers
• These can be seen in those with diabetes, hyperlipidaemia, hypercholesterolaemia, and smokers
• Clearly managing the underlying abnormality and then encouraging a diet high in protein to build new tissue and iron to aid oxygen delivery is required
Lymphoedema
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Lymphoedema
• These patients lose excessive fluid volumes and this fluid is rich in protein and other electrolytes
• Careful replacement of these elements is required in order to reduce excess which can tax the kidneys and aggravate fluid retention
• Too little protein in itself may cause oedema so the balance and careful assessment of the wound and its healing is needed
Pressure injuries
Pressure injuries
• Whilst a simple stage 1 or 2 may require tweeking of the diet a stage 3 and 4 and suspected deep tissue injury will require huge changes to protein, zinc, Vitamin C and fluid intake
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Diabetic foot wounds
Bullous Pemphigoid
• These blisters contain protein and in order to aid rapid repair, skin growth and reduction in infection
Infected wounds are extremely demanding on nutritional
requirements 8 times more common in Vitamin C-‐deficient patients than in those with normal Vitamin C levels
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Polypharmacy
• Drug treatment may contribute to loss of appetite, nausea, diarrohea, weight changes, taste alterations, decrease in saliva secretion, modifications in lipid profile, alterations in electrolyte balance, and changes in glucose metabolism
Malignancy
• Exudate• Rapidly multiplying cells• Infection
Dermatitis
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Obesity Obesity is linked with more infections, delayed wound healing and greater incidence of wound dehiscence
The other spectrum
• Unintentional weight loss greater than 5% of total body weight over 3 months is considered significant
What questions to ask the nurse about the wound
• Is there less inflammation • Is there less slough • Is there more granulation tissue• Is there skin growing at the edges and/or across the granulation tissue
• Has the volume of exudate eased off • Has the malodour reduced
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Resources
• Series 12 technical documents of the National Pressure ulcer advisory Group for the study of pressure ulcers and chronic wounds (Logroño 2011)
• www.ewma.org• www.woundsinternational.com• www.awma.com.au• www.worldwidewounds• www.woundinfection-‐institute.com
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