wound management manual

WOUND MANAGEMENT MANUAL

2010

Tairawhiti District Health, Gisborne Hospital Updated May 2010

Last Updated: 2010 Page 1 of 80

Contents:

Principles of Wound Management Anatomy of the skin

3 4

Wound Healing

6

Factors that Affect Wound Healing 7

Hypergranulation 10

Nutrition and Wound Healing 11

Wound Management Wound Assessment Wound Bed Preparation

13 14 15

Negative Pressure Wound Therapy Wound Assessment and Treatment Form Guide to Completing Assessment Form

17 18 20

Wound Cleansing Agents 22

Product Selection for Shallow Wounds

24

Product Selection for Cavities and Sinuses 25

Product Information 26

Skin Tears 37

Management of Infected Wounds 40

Blister Management 49

Burns

51

Pressure Ulcers

64

Management of Skin Grafts and Donor Sites

74

References Useful Websites

78 80


Jenn Boyle, Clinical Nurse Specialist in Wound Management, and members of

the Wound Care Committee Tairawhiti District Health updated this edition

January 2010.

Our thanks to previous contributors

Pictures reproduced from Smith & Nephew “The Team System” 1990. Anatomical Chart Co., Stokie, Illinois. The skin

As this document is updated on a two yearly basis and often added to we

reference each section with full references at the end to the manual.


Principles of Wound Management In order to choose the wound care product and regime that will promote optimal healing, decisions must be made using a comprehensive approach.

• A comprehensive assessment of the patient as a whole person, not just the wound is necessary.

• Treat the underlying contributing factors e.g. relieve pressure; reduce oedema; improve circulation or nutrition; control diabetes; educate regarding smoking, hygiene and home safety.

• Treat a clinically infected wound with systemic antibiotics as prescribed.

NB Refer to the indications and management of clinically infected wounds and colonised wounds (See page 40).

Assess by:

• Determining the underlying pathophysiology that may have caused or contributed to the wound.

• Considering other factors that may impair healing.

• Considering the nutritional status of the patient.

• Completing a wound assessment form (See page 18-19).

Plan by:

• Selecting the product that will best treat the wound.

• Asking yourself “What am I trying to achieve here?” (See product selection guidelines pages 26-36).

• Referring to the product selection guideline sheet and the fact sheets about each product.

Implement by:

• Treating the underlying cause of the wound or the pressure.

• Using the product according to the manufacturer’s instructions.

• Recording on the Wound Assessment & Treatment Chart:

• Frequency of dressing procedure.

• Method of cleaning the wound.

• Primary dressing.

• Secondary dressing.

• Method of securing the dressing.

Evaluate by:

• Recording changes in appearance of wound, or amount of wound exudate.

• Determining whether the product is appropriate for the specific wound.

• Considering whether the product is appropriate if the wound is not progressing as anticipated.


Anatomy of the Skin The skin is divided into three distinct layers

• Epidermis

• Dermis

• Subcutaneous Tissue

Epidermis is the outer layer that is comprised of stratified, squamous keratinised epithelium. It is approximately 0.4mm thick and is avascular. It is supplied with nutrients by the dermal layer. Over a four-week period, the epithelium is continually being replaced as the outer cells are worn away. There are five layers of epidermis

• Stratum Corneum. This is the outer keratinised layer. It is composed of scaly, squamous plaques of dead flat cells

• Stratum Lucidum. This layer is a thin clear band of homogenous tissue found in areas where the epidermis is thicker (e.g. palms of the hands; soles of the feet). It can be from one to five cells thick.

• Stratum Granulosum is the middle layer and is made of layers of granular cells. These cells contain keratin.

• Stratum Spinosum. In this layer the cells are polygonal with tiny spines on their surfaces. As they migrate to the next layer, they become flat, lying parallel with the surface of the skin.

• Stratum Germinativum (Basale). A single layer of cylindrically shaped cells in contact with the dermis. It provides new cells to maintain the cells lost by abrasion from the outermost layer. These cells are constantly dividing and beginning on the journey toward the outer layer, where they eventually flake off.

Dermis. The second layer of the skin contains lymphatic and blood vessels, nerve endings, elastic and collagen proteins. The predominant cell type found in the dermis is fibroblast. It is these cells which synthesis collagen. The dermis supports the epidermis and is attached to the subcutaneous tissue. It is 0.5mm thick.

Subcutaneous Tissue. This is also referred to as hypodermis in some texts. It is the thickest part of the skin, composed of adipose and connective tissue as well as blood vessels. This layer provides a protective layer for the bone and muscle as well as insulation for the body.


Wound Healing

The healing process occurs in stages. Complete wound healing may take up to two years.

Wound: is basically the loss of continuity of the skin. It is the visible result of external or internal damage

Healing: is a complex mechanism by which the body repairs damaged tissue through a series of cellular and biochemical events (a cascade).

The stages of wound healing

STAGE PROCESS CLINICAL EFFECTS

Immediate (8-10

mins) • Vasoconstriction and activation of

endothelial cells, platelets and clotting cascade.

• Biochemical response: release of prostaglandins, serotonin & clotting factors.

• Homeostasis occurs with clot formation.

• Haemorrhage is controlled or reduced

Inflammatory (0-3 days)

• Histamine is released

• Increased blood supply to the area.

• Accumulation fluid in soft tissues.

• Pressure is exerted on sensory nerve endings.

• Neutrophils and macrophages begin phagocytosis.

• Erythema.

• Heat.

• Oedema.

• Discomfort.

• Impaired function.

• Cleansing of the wound bed and formation of crust or pus.

Proliferation (3-24 days) Granulation. Contraction Epithelialisation

• New blood vessels infiltrate the wound.

• Fibroblasts migrate to the scene and produce collagen.

• Fibroblasts transform into either myofibroblasts or fibrocytes

• Myofibroblasts pull the wound edges together.

• As new capillaries form, the clot is removed.

• Tissue appears granular (granulation tissue).

• Epithelial cells multiply and migrate over the surface.

• In wounds that heal by primary intention, stimulation of epithelial growth occurs concurrently with collagen synthesis.

• In wounds healing by secondary intention, epithelialisation will begin when the wound is filled with granulation tissue

• Red, granular and slightly uneven tissue.

• Collagen is a basic building protein & is a major component of granulation tissue

• Fibroblasts require an acid environment to manufacture collagen thus Vit C is essential at this stage of healing

• The size of the defect is reduced.

• A smooth marginal zone or islands of epithelium are seen in the wound.

Maturation (up to two years) Collagen remodelling Capillary regression

• Collagen increases in strength.

• There is a reduction in the number of vessels, so blood flow is reduced.

• Scar flattens and softens.

• The scar pales and itching subsides.


Factors That Can Delay Wound Healing

Systemic conditions

Disease Effect

• Age • Epidermal, dermal and subcutaneous thinning.

• Reduced collagen production

• Decreased adherence between epidermis and dermis

• Loss of elasticity

• Co-existing diseases

• Reduced/restricted mobility

• Poor nutrition

• Smoking • Reduced tissue perfusion

• Reduced oxygenation

• Inhibits epithelialisation, macrophage activity, and wound contraction.

• Renal disease • Raised urea delays granulation of the wound.

• Cardiovascular disorders

• Reduced tissue perfusion.

• Microscopic/macroscopic disease

• Venous stasis • Venous hypertension

• Oedema, skin changes, ulceration

• Bowel disease • Malabsorption and poor nutritional status.

• Possibly treated with anti-inflammatory and steroid therapy.

• Anaemia • Reduced O2 carrying capacity.

• Hepatic disease • Lower level of haemoglobin and increased blood toxicity.

• Diabetes Mellitus • Neuropathy (sensory, autonomic, motor)

• Ischemia with mico/macro vascular disease

• Infection decreased host response/resistance

• Reduced macrophage activity during inflammatory response (dampened inflammatory response)

• Malignancy • Compromised blood supply and necrosed tissues.

• Progressive growth and degeneration of tissues.

• Poor nutrition

• Chemotherapy and radiotherapy.

• Respiratory disorders • Reduced availability of O2 to tissues.

• Auto-immune disorders

• Retardation of anti-inflammatory stage. Reduction of leukocytes.

• Use of anti-inflammatory drugs.

• Nutrition See page 11 for more information

• Delays wound healing.

• Increased risk of infection.


Cause Effect

• Cytotoxic drugs • Interference with cell proliferation and reduce tensile strength.

• Radiotherapy • There is damage and disruption to cellular growth and reproduction.

• Nausea and vomiting may compromise nutritional status.

• Use of steroids • Suppress immunity to infection.

• Suppress multiplication of fibroblasts.

• Suppress collagen synthesis

• Non-steroidal anti-inflammatory drugs

• Suppress the inflammatory response by blocking prostaglandin synthesis.

• Penicillamine and Penicillin

• Penicillin releases Penicillamine, which reduces wound strength by preventing collagen cross-linking.

At the wound site:

Cause Effect

• Pressure, Shear & Friction

• See pages 64-73 for more information on pressure areas

• Reduced tissue perfusion, hypoxia and necrosis

• Poor blood supply • Blood supply is critical for tissue viability. Poor blood supply can result in impaired healing and tissue death.

• Dehydration • A dry wound bed delays migration of epithelial cells. A moist environment helps fragile cells maintain viability and facilitates migration.

• Decreased temperature

• A constant temperature of 370C promotes

macrophage and mitotic activity during granulation and epithelialisation. Cooling the wound may decrease the surface temperature by several degrees.

• Excess exudate • Excessive moisture causes maceration of the skin.

• Excess slough • Slough is made up of dead cells, which have accumulated in the exudate. As slough liquefies, it is easily removed. The aim of treatment is to moisten the wound bed and remove the dead cells.

• Necrotic tissue • The necrotic tissue may “hide” the extent of the wound.

• Unless the necrotic tissue is removed, the wound will continue to increase in size.

• Reduces wound contraction

• Delays proliferation phase of healing

• The presence of foreign bodies

• These can be both irritating and also harbour microorganisms.

• Recurrent trauma • Recurrent trauma (removal of a dressing that has adhered to the wound surface) disrupts the newly forming granulating tissue and may lead to renewed inflammatory response.


• Infection • Infection in the wound leads to devitalised tissue.

• Delays collagen synthesis and prevents epithelialisation.

• Localised infections can also lead to systemic infection, further compromising healing.

• (See section on treating infected wounds for management of this situation page 40-48).

Carville, K. 2005 David, 1986:38

Inappropriate wound management

Cause Effect

• Failure to select product based on assessment.

• This may result in selection of inappropriate treatment.

• Harsh swabbing rather than irrigation.

• Swabbing may damage granulation and frail epithelial cells.

• Use of chemicals to clean wounds.

• Causes toxicity in wound.

• Prolonged use of a product without evaluation.

• The products may not be appropriate for stage of wound healing.

Dealey,1994: 68-69


Hypergranulation Prolonged hypergranulation inhibits epithelial growth. The granulation tissue is more fragile and may force wound edges apart delaying healing and causing scarring. Hypergranulation affects all types of wounds, can be found in the following wounds:

• Stoma and drain sites

• Ulcers and incisional wounds

• Burns and skins grafts

ASSESSMENT

• Location -Extended above or beyond wound edges

• Colour -Dark red -Bluish discolouration -Light purple -Very pale

• Dehydrated or constantly wet

• Dull surface

• Bleed easily

• Prone to infection e.g.; diabetes

TREATMENT Treat the cause (s) -minimise local irritation Secure drainage tubes, reduce friction of dressings -manage exudate Promote moist not wet wound bed Step One: -Application of light pressure

Foam dressing firmly covered with hyperfix can help reduce the height of hypergranulation to that of the wound bed thus encouraging epithelial migration.

Step Two: -Steroid and antibacterial ointments

Treat local infection with the steroid inhibiting the wounds inflammatory response, requires charting by doctor e.g.; kenacomb- use for 4 days consecutively, stop for 4 days then reassess.

Another Option: -Removal of hypergranulation tissue

Last resort with silver nitrate sticks or diathermy or surgical excision. Silver nitrate may cause discomfort and necrosis if not used prudently.

Lay-Flurrie, K (2004) Rollins, H (2000)

Prevention involves


Nutrition and Wound Healing A balanced diet containing essential nutrients is needed for wound repair. The therapeutic role of nutrition in wound healing evolved from studies in patients with protein-energy malnutrition.

Malnutrition - causes delays in wound healing and increases the risk of wound infections. It can arise because of insufficient nutrient intake and can be the result, or cause of, drug interactions. This creates a competition for available nutrients in the malnourished patient with a wound. Malnutrition is common in hospital patients.

Protein Energy Malnutrition impairs wound healing, reduces the immune response and reduces the number of bacteria killed by leukocytes and macrophages. This results in increased susceptibility to infection morbidity and mortality. It has been shown that patients with adequate nutritional intake before surgery had better wound healing when compared with patients who had poor pre-operative nutritional intake.

Cell Energy - obtained from whole grains, sugar, honey, fruits and vegetables are used for cell proliferation and phagocytic activity. Cell energy is also obtained from fats in foods such as butter, oil, margarine, whole milk, nuts and seeds. Cells membranes are made from fatty acids. Linalenic and linoteic fatty acids regulate metabolism, circulation and inflammation. Studies indicate that nutritional support should begin soon after injury.

Carbohydrates/Glucose Provision of adequate energy is essential for optimal healing. Impaired glucose metabolism, as observed in Diabetes Mellitus reduces wound healing and enhances wound complication rates, which highlights the importance of optimal regulation of blood glucose levels in diabetic patients.

Lipids Essential for cell membrane and inflammatory mediators. After injury there is an enhanced requirement for essential fatty acids. Lipids have anti-inflammatory effects and could therefore influence wound healing.

Protein Lack of protein causes reduced wound breaking strength and increased wound infection rates.

Amino Acids Formed from protein obtained from whole grains, fish, meat, poultry, and milk. Amino acids are necessary for re-vascularisation, fibroblastic proliferation, collagen synthesis and lymphatic formation.

Glutamine is the most abundant amino acid in the body and is considered to be a major fuel for fibroblasts and immune cells.

Arginine - part of the urea cycle - causes increased collagen deposition.

Vitamins and Minerals

Vitamin A: - obtained from liver, eggs, yellow or dark green fruits and vegetables, whole milk and cod liver oil. Vitamin A is needed for epithelialisation and collagen synthesis.


Reverses the inhibitory effects of Corticosteroids, and can restore wound healing in diabetic animals. Aids the replacement of epithelial tissue, as well as being an antikeratinising agent. Over keratinisation will result in loss of normal lubrication, irritation, infection and sloughing, irritation, infection and sloughing. Since injury or stress leads to increased vitamin A requirements - recommend that supplement doses of vitamin A be given to severely injured patients.

Vitamin C - obtained from citrus fruits, kiwifruit, rock-melon, strawberries, tomatoes, and capsicum is essential for collagen synthesis, fibroblast production and reducing infection risks. It also contains an anti-oxidant that can combat free radical damage at the wound site. There is sufficient evidence that combination of injury or surgery with pre-existing marginal vitamin C status may impair wound healing. Deficiency of this induces a defect in wound healing, particularly a failure in collagen synthesis and cross-linking.

Vitamin B Vitamin B - complex - obtained from legumes; grains, nuts, meats, fish and poultry are necessary for lymphocyte function and antibody production. A co-factor in enzyme reaction in the metabolism of protein fats and carbohydrates.

Vitamin K Needed to enable blood clotting to take place.

Zinc Obtained from seafood, mushrooms, soybeans, sunflower seeds and organ meats is essential for cell mitosis and proliferation. Essential in humans. Deficiency causes reduced fibroblast function and collagen synthesis. Therefore overall wound strength is impaired and epithelialisation is delayed. Hospitalised patients are at high risk of developing zinc deficiency; therefore it is advisable to supplement them with additional zinc.

Trace Elements - such as copper and magnesium from seafood and nuts and chromium from whole grains are also essential for healing. Copper Increases the tensile strength of collagen. Iron Decreased levels from blood loss will decrease levels of oxygen to wound site

Carville, 2005 Stevens, 1997 23-24


Wound Management

Action Rationale

• An aseptic technique should always be used.

• Cleansing solutions must be warmed to body temperature before application.

• There is a significant increase in the mitotic activity when a stable wound bed temperature is maintained.

• When infection is suspected, a wound swab should be taken for bacterial culture after the wound has been cleaned with 0.9% sodium chloride solution.

• Cleansing the surface contamination of the wound and confirms a diagnosis of infection rather than colonisation. Refer to the management of infected wounds (page 40).

• Gentle wound irrigation is preferred to firm swabbing.

• Swabbing the wound surface may mechanically traumatise fragile tissue.

• Do not apply cotton wool or swabs that shed fibres directly against the raw surfaces

• Fibrous particles on the surface can create foreign body reactions, prolong the inflammatory process and increase the risk of wound infection.

• Forceful packing of cavities is to be avoided.

• This will exert excessive local pressure on the developing capillary loops, resulting in ischaemia and necrosis. In addition tightly packed dressings restrict the absorbent capacity of the dressing and create trauma and pain, both during insertion and during removal.

• Dressings should be replaced as soon as possible.

• To maintain wound temperature and prevent the wound from dehydration

• A drop in the wound temperature results in a drop in leukocytes

Carville, K. 2005 Flanagan, 1997:52

The wound care products should:

• Maintain a moist environment within the wound surface.

• Allow gaseous exchange of O2, CO2 and water vapour.

• Provide thermal insulation to the wound surface.

• Be impermeable to microorganisms.

• Be free of particles and toxic wound.

• Be non-adherent. i.e. allow removal without causing trauma during the dressing change.

• Remove excess exudate and toxic compounds.

• Adhesive tape should have just enough adhesion to hold dressings in place. Strong adhesives may damage delicate skin if the dressing needs to be changed repeatedly.

Carville, K., 2005


Wound Assessment Following a general or holistic assessment of the patient a thorough assessment of the wound is made.

This must include:

• Type of Wound – acute, chronic

• Type of Healing – primary, secondary

• Tissue Loss – superficial, partial, full.

• Clinical Appearance – necrotic, sloughy, granulation, epithealiating, infected

• Wound Location

• Measurement Dimensions

• Exudate – type, amount, colour consistency, odour

• Surrounding Skin – oedema, cellulitis, dry, wet

• Pain – cause, general, local

• Wound Infection – see page 40

• Psychosocial Implications – quality of life, body image, self esteem.

Modes of wound healing

• Wounds that heal by primary intention. Clean surgical wounds, or minor lacerations with skin edges in apposition heal by primary intention. Very little granulation tissue is produced. Within 10-14 days the re-epithelialisation is normally complete. However, it may take some months for the tissues to regain their tensile strength.

• Delayed Primary Healing. This occurs when the wound is infected or contains foreign bodies. In this instance the wound requires intensive cleaning prior to closure. See section on wound cleansing and irrigation for more details.

• Wounds that heal by secondary intention. This occurs in open wounds with significant tissue loss. Pressure sores, leg ulcers and some surgically made wounds, e.g. fasciotomy or abscess incisions fall into this category.

Carville, K., 2005.


Wound Bed Preparation

Wound bed preparation can assist with the early identification and management of problems in chronic wounds and promote healing. A framework has been set up to assist with wound bed assessment and management using

the acronym TIME.

TIME Acronym:

T = Tissue, non viable-viable or deficit

I = Infection and inflammation

M = Moisture imbalance

E = Edge of wound, non advancing or undermined

T = Tissue, non viable-viable or deficit The wound is assessed for non viable tissue. Wound debridement is the optimal goal. By removing cellular burden the normal wound healing process is stimulated and the risk of infection reduced. Debridement involves different methods of removing non viable tissue with the goal of exposing viable tissue. A comprehensive assessment needs to be completed in order to determine the appropriateness of debridement the best method of debridement. It may be necessary to repeat debridement. Types of Debridement Surgical or sharp debridement It is performed by medical personnel under aseptic conditions, and in an appropriate environment. This technique is often used when there is extensive tissue loss or infection, the wound bed needs to be prepared for grafting or the client is compromised. Conservative Sharp Wound Debridement (CSWD) This is the removal of loose avascular tissue and should be done so without pain or bleeding. It should be performed by a trained RN whom is aware of the contraindications. Enzymatic debridement It is the use of topical enzymes to breakdown necrotic, blood clots and fibrous tissue. There is only one product available in New Zealand, Iruxol (Smith & Nephew) which is a collagenase. This is rarely used and requires a consultant’s signature of approval. Mechanical Debridement This can be achieved with wet to dry dressings and irrigation under pressure. Disadvantage can be painful and damaging to healthy tissue. Autolytic Debridement This is achieved with hydrating products or moisture retentive dressings which assist the bodies own enzymes to liquefy non viable tissue. Occlusive dressings should not to be used on infected wounds. Biological or parasitic debridement This is the application of sterile maggots (Greenbottle fly) that debride non viable tissue. This is rarely used in New Zealand.


I = Infection and inflammation Refer to section: Management of Infected wounds pg 40. If critically colonized the following dressings are recommended for restoring bacterial balance: Cadexomer iodine (Iodosorb sheet or paste) PovIdone iodine impregnated tulle gras (Inadine) Silver impregnated dressings (Acticoat absorbent and Acticoat).

M = Maintaining Moisture Balance Moist wound healing has been demonstrated to promote epithelisation. Too much moisture can cause maceration and deterioration of the wound and surrounding skin. A dry wound bed needs to be hydrated. The goal is to promote the optimal moisture balance. The cause of the moisture imbalance should be determined and managed appropriately e.g. heart failure contributing to lower leg oedema This can also be assisted by selecting the appropriate dressing e.g. a shallow granulating highly exudating wound requires an absorbent dressing such as a foam (Allevyn) A dry wound may require a hydrogel and a moisture retentive dressing such as a film. (refer to Product Selection guides and exudate levels).

E = Edge of wound, non advancing or undermined

This can be caused by a dry wound in which case the wound requires rehydration. The wound may require debriding if the wound margins has debris \ scabs. Hypergranulation can impede epithelisation as epithelial cell only migrate across flat surfaces. Refer to section on Management of Hypergranulation. Rolled or undermined edges may indicate a bacterial imbalance and management with an appropriate antimicrobial dressing maybe necessary. Depending on the assessment different aspects of the TIME framework are focused on. An action may have an impact on more than one aspect of the TIME framework. If the focus is

on T e.g. removing necrotic tissue this could also impact on I as bacterial burden is reduced. Wound bed preparation is used in conjunction with a holistic assessment of the patient. Carville, K., 2005. EWMA Position Document. 2004.


Negative Pressure Wound Therapy Devices

These devices promote vacuum assisted wound closure. Topical negative pressure (TNP) applies non compressive mechanical forces to the arterioles to dilate and increase blood flow. The negative pressure is created by positioning a suction tube into either foam or gauze positioned the latter to fill the wound and connecting this to a pump, the wound/ packing and drain is occluded by a film dressing to create suction. NPWT Manufacturers contraindications for application:

• Necrotic tissue or eschar

• Use over exposed organs, blood vessels or tendons (a non adherent dressing may reduce the risk).

• Malignancy in the wound

• Non enteric or unexplored fistula

• Caution to be used with patients whom have difficult wound haemostasis/ active bleeding and patients whom are taking anticoagulants. Post surgery delaying application of NPWT for 24hours may reduce the risk of haemorrhage. Monitor tubing for signs of bleeding and stop if occurs. A non adherent dressing may reduce the risk of bleeding at dressing changes.

(If NPWT is applied outside manufacturer’s contraindications they should be done with caution, under close clinical supervision usually in hospital and will be the responsibility of the lead clinician)

Objectives for use of Topical Negative Pressure and endpoint: NPWT should be used if it provides the most clinically and cost effective method of achieving wound objectives/goals. The wound needs regular evaluation to determine that the objective for using NPWT is being met. When the objective is achieved NPWT is stopped or if the objective determined is not being met within an acceptable time frame (e.g. one week) or is unacceptable to the patient or has caused complications.

• Manage excessive exudate because of affect on skin integrity and quality of life.

Stop when level of exudate can be managed by conventional dressing

• Promote rapid improvement in wound bed (e.g. prior to surgical closure and skin grafting)

Stop when there is 100% healthy granulation tissue with minimal tissue deficit

• Improve vascularity of wound bed and/or promote granulation tissue.

Stop when the wound bed preparation can be better managed clinically and cost effectively with conventional dressing.

• Stabilizing wound graft or flap or used to aid care and rehabilitation (e.g. dehisced surgical wounds, open amputation sites, graft fixation )

• Promote healing when conventional dressings are not working

Stop when there has been no improvement in the wound after three applications

• NPT can be applied to an infected wound as it can aid in the reduction of bacteria in the wound bed, prevent contamination and promote cell proliferation thru mechanical stretching of the cells. If it is critically colonized it should be managed with the appropriate antibiotic in conjunction with NPWT therapy. In an acute infection the dressing needs to be changed every 12- 24 hours and continuous therapy is recommended until the infection is resolved.

Stop if the wound continues to deteriorate

Carville, K., 2005. EWMA Position Document, 2007.


Wound Assessment and Treatment Form

Patient Label

WOUND SIZE It its recommended that wounds are measured regularly - refer to guidelines.

WOUND SURFACE WOUND TYPE % Score <25% <50% <75% <100%

1 2 3 4

Pressure sore Ulcer Burn Trauma LOCATION:

�

�

�

Surgical Wound Other (Specify)

�

�

ALLERGIES (Related to Wound Care)

DATE

TIME

WOUND CONDITION % SCORE (enter appropriate score)

NECROTIC (BLACK) %

SLOUGH (YELLOW) %

GRANULATION (RED) %

EPITHELIAL (PINK)

SUTURED / CLIPS

EXUDATE (Amount)

NONE

LIGHT

MODERATE

HEAVY

EXUDATE (Type)

BLOOD

PURULENT

SEROUS FLUID

OTHER (Specify)

SURROUNDING SKIN

HEALTHY

FRAGILE

INFLAMMATION

OEDEMA

WET

DRY


Wound Assessment and Treatment Form (cont)

DATE

TIME

PAIN (Score 1-10)

CLINICAL SIGNS OF INFECTION

PAIN

REDNESS

ODOUR

SWAB TO LAB

TREATMENT PLAN PRIMARY DRESSING - please specify

SECONDARY DRESSING - please specify

CARE OF SURROUNDING SKIN - please specify

SECURING METHOD

FREQUENCY OF DRESSING CHANGE

SIGNATURE OF NURSE

DESIGNATION


GUIDE TO ASSESSING WOUND AND COMPLETING ASSESSMENT FORM

WOUND SIZE

Measurements should be completed weekly and recorded. The following methods can be used: Measure dimensions with a ruler, maximum length, and breath of the wound. Trace the wound margins carefully on a piece of transparent material using a fine permanent marker pen. Fluid volume measurement, cover wound with a transparent film e.g. Opsite, inject sterile saline into cavity and record volume. This method should not be used to measure fistulas. Probing wounds for depth measurements requires caution to prevent trauma. Photography provides visual progress of a wound. Date and file all measurements.

It is important to note that in the early stages of wound healing, it is quite

normal for a wound size to enlarge as devitalised tissue is removed.

WOUND CONDITION Four categories exist according to the appearance of the tissue in the wound bed. They are Black (Necrotic), Yellow (Slough), Red (Granulation), Pink (epithelialisation). Always treat the most severely affected area first.

PERCENTAGE OF TOTAL WOUND FLOOR WITH SPECIFIC CONDITION Estimate the % of the wound, which is: (a) healthy granulation, (b) thick slough, (c) necrotic tissue, using the following categories: Score 25 % (up to a quarter) 1 50 % (up to half) 2 75 % (up to ¾) 3 100 % (almost total) 4 e.g.: healthy granulation < 25% score 1 slough < 75 % score 3 necrotic tissue < 25 % score 1 This wound has some necrotic and a small healthy area but is mainly sloughy. If a debriding agent is being used this gives some indication of its effectiveness over time.


EXUDATE - Amount and Type Assess the type, colour, amount, consistency and odour of wound exudate. Under normal circumstances wound exudate should decrease as healing progresses. Controlling exudate is of primary concern in dressing selection. Observe for changes that may indicate infection.

SURROUNDING TISSUE Visual inspection of surrounding skin is important and can indicate much about the ‘health’ of the wound. Note the colour, warmth, capillary return and general status of the surrounding skin to revel such abnormalities as oedema, eczema, cellulitis (inflammation of tissue around a lesion, characterised by redness, swelling), maceration and dryness, fragile skin (especially in elderly or as a result of steroid therapy). Local oedema and redness is to be expected during the early acute inflammatory response stage of healing, but prolonged response can indicate problems: e.g. infection, hypoxia or venous insufficiency.

PAIN AT DRESSING CHANGE Assessment of the type, duration, frequency and location and possible source of the pain should be included and managed. Patients have very different pain thresholds and abilities to cope. Ask this question to find out the patients perception of their pain and whether the pain is getting better or worse with treatment. Ask patient to rate pain level.

0 1 2 3 4 5 6 7 8 9 10 |______|______|______|______|_______|______|______|______|______|_______|

↑↑↑↑ ↑↑↑↑ I have no pain at all

My pain is as bad as it could get

INFECTION It is important to distinguish between infection and colonisation of a wound. The following signs and symptoms can indicate wound infection: Local spreading cellulitis, localised swelling, purulent or foul smelling

exudate, local pain, non healing wound. Systemic fever, leucocytosis, lymphadenitis. Wound culture and sensitivity is indicated for a wound that is displaying clinical signs of infection.

ALLERGIES In relation to wound care e.g. adhesives, dressings, antibiotics

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body w

ash b

efo

re

surg

ical pro

cedure

.

•

Do n

ot

use w

ith P

ovid

one

Iodin

e a

s inte

raction o

ccurs

.

•

Eff

ective a

gain

st

a w

ide r

ang

e o

f g

ram

+ve t

o –

ve b

acte

ria.

•

Low

toxic

ity t

o g

ranula

tion t

issue.

•

Skin

sensitiv

ity o

ccurs

.

•

Antiseptic a

ctivity r

educed b

y

blo

od o

r org

anic

conta

min

ation.

•

Ineff

ective a

gain

st

virus a

nd

fung

i.

•

Conta

min

ation b

y P

seudom

onas

aeru

gin

osia

may o

ccur.

Povid

one I

odin

e

Lim

ited u

se

•

Antiseptic

•

Availa

ble

in lotions,

cre

am

s,

oin

tments

and I

mpre

gnate

d g

auze

(Inadin

e).

•

Eff

ective a

gain

st

bacte

ria,

spore

s,

fung

i and v

iruses.

•

Inactivate

d b

y b

ody f

luid

s

•

Suppre

sses lym

phocytic

response.

•

Skin

sensitiv

ity m

ay o

ccur.

•

Toxic

to f

ibro

bla

sts

.

•

Ris

k o

f syste

mic

absorp

tion

when u

sed in larg

e w

ounds f

or

exte

nded p

eriods.

Hydro

gen P

ero

xid

e

Not R

ecom

mended

•

Weak a

ntiseptic –

convert

s t

o

oxyg

en a

nd w

ate

r w

hen c

om

es

into

conta

ct

with c

ata

lase,

an

enzym

e f

ound in b

lood a

nd

most

tissues.

•

The b

ubblin

g e

ffect

can a

id

mechanic

al debridem

ent.

•

May h

ave a

germ

icid

al eff

ect

ag

ain

st

anaero

bic

bacte

ria

because o

f O

2 r

ele

ase.

•

Eff

erv

escent

action c

an lift

new

ly

form

ed e

pitheliu

m.

•

Cyto

toxic

eff

ect

on f

ibro

bla

sts

.

•

Oxyg

en e

mbolu

s a

nd s

urg

ical

em

physem

a f

ollo

win

g irr

igation

under

pre

ssure

or

into

clo

sed

cavitie

s h

as o

ccurr

ed.

•

Can d

issolv

e c

lots

and c

ause

ble

edin

g.

Last

Update

d:

2010

P

age 2

3 o

f 80

Acetic A

cid

Lim

ited u

se

•

Acid

ic s

olu

tion t

hat

low

ers

pH

of

wound e

nvironm

ent.

•

There

is n

o d

ilution o

f acetic a

cid

th

at

is t

oxic

to b

acte

ria w

ithout

bein

g t

oxic

to f

ibro

bla

sts

.

•

Eff

ective a

gain

st

Pseudom

onas

aeru

gin

osa.

•

Toxic

to f

ibro

bla

sts

.

•

Not

isoto

nic

or

haem

oly

tic.

•

Not

to b

e u

sed t

o irr

igate

menin

ges,

bra

in

or

ear

dru

m.

•

May c

ause p

ain

in w

ound.

•

May irr

itate

surr

ound s

kin

s.

Sodiu

m H

ypochlo

rite

i.e.

Eusol, M

ilton,

Dakin

’s

solu

tion

Not re

com

mended

•

Hypochlo

rite

solu

tions a

re h

ighly

re

active c

hem

ical com

pounds

havin

g

•

Germ

icid

al, d

eodorisin

g

•

Ble

achin

g p

ropert

ies.

•

Not

safe

concentr

ation f

or

use in

wound c

are

.

•

Dis

infe

ction o

f in

anim

ate

obje

cts

. •

Rapid

ly inactivate

d b

y b

lood p

lus o

rganic

m

att

er.

•

Toxic

to f

ibro

bla

sts

and p

revents

colla

gen s

ynth

eses.

•

Eff

ects

leucocyte

mig

ration a

nd

endoth

elia

l cells

.

•

Occlu

des m

icro

circula

tion p

erm

anently.

•

Hig

hly

irr

itant

•

Causes O

edem

a.

•

Dis

solv

es c

lots

and m

ay c

ause b

leedin

g.

•

Sta

ble

2-3

weeks o

nly

.

•

Has little e

ffect

on e

schar.

•

Can lead t

o h

epatic/

renal fa

ilure

if

absorb

ed.

�

Solu

tions u

sed in w

ound h

ealin

g m

ust

not

be d

etr

imenta

l to

the w

ound h

ealin

g.

�

Antiseptics m

ay k

ill m

icro

org

anis

ms c

ausin

g infe

ction b

ut

they a

lso d

am

ag

e a

nd d

estr

oy h

ealthy c

ells

necessary

to h

ealin

g.

�

Challe

ng

e:

Only

put

in t

he w

ound w

hat

you w

ould

put

in y

our

eye.

C

arv

ille, K

., 2

005.

18

Last

Update

d:

2010

P

age 2

4 o

f 80

SHALLOW

WOUNDS P

roduct sele

ction g

uid

e

Necro

tic (Bla

ck)

Slo

ughy (Yellow

) Gra

nula

ting (Red)

Epithelialisin

g (pin

k)

WO

UN

D

DE

SC

RIP

TIO

N

AIM

OF

TR

EA

TM

EN

T

EX

UD

AT

E

LE

VE

L

PR

IMA

RY

DR

ES

SIN

G

SE

CO

ND

AR

Y D

RE

SS

ING

Infe

cte

d: G

reen

As a general rule

change daily

•

Cle

ar

infe

ction.

•

Deslo

ugh.

•

Absorb

exudate

.

NB if sig

ns o

f in

fection p

resent ta

ke s

wab a

nd

assess for sig

ns o

f genera

l sepsis

.

None

Modera

te

Heavy

Hydro

gel

Alg

inate

or

Foam

Alg

inate

or

Foam

Non a

dhere

nt F

ilm

Foam

or

non-a

dhere

nt com

bin

e

Foam

or

Non-a

dhere

nt com

bin

e

Necro

tic: Bla

ck

Surgical Debridement

prn

Change 1-3 days

•

Re-h

ydra

tion a

nd d

ebridem

ent of

tissue.

•

Surg

ical debridem

ent re

com

mended.

Low

Modera

te

Heavy

Hydro

gel or

Hydro

collo

id

Hydro

collo

id o

r F

oam

Foam

or

Alg

inate

Film

Non-a

dhere

nt com

bin

e

Foam

or

non-a

dhere

nt com

bin

e

Slo

ughy: Yellow

Change 1-3 days as

required

•

Rem

ove s

lough a

nd a

bsorb

exudate

. Low

Modera

te

Heavy

Hydro

gel or

Hydro

collo

id

Alg

inate

or

Hydro

collo

id

Alg

inate

or

Foam

Thin

Hydro

collo

id o

r film

Hydro

collo

id o

r N

on-a

dhere

nt

com

bin

e

Non-a

dhere

nt com

bin

e/f

oam

Gra

nula

ting: Red

Change 1-7 days as

required

•

Main

tain

mois

t environm

ent.

•

Absorb

exudate

.

•

Pro

mote

epithelia

lisation.

Low

Modera

te

Heavy

Hydro

gel or

Hydro

collo

id

Alg

inate

or

Foam

Alg

inate

or

Foam

Film

or

Hydro

collo

id

Non-a

dhere

nt com

bin

e

Non-a

dhere

nt com

bin

e

epithelialisin

g: Pin

k

Change 4-7 days

•

Main

tain

mois

t environm

ent.

•

Avoid

tra

um

atisation.

E

xtr

a thin

Hydro

collo

id

or

Film

or

Hypafix

Last

Update

d:

2010

P

age 2

5 o

f 80

CAVIT

IES A

ND S

INUSES

Pro

duct Sele

ction G

uid

e

Necro

tic (Bla

ck)

Slo

ughy (Yellow

) Gra

nula

ting (Red)

Epithelialisin

g (pin

k)

WO

UN

D D

ES

CR

IPT

ION

A

IM O

F T

RE

AT

ME

NT

E

XU

DA

TE

LE

VE

L

PR

IMA

RY

D

RE

SS

ING

S

EC

ON

DA

RY

DR

ES

SIN

G

None

Hydro

gel

Film

M

odera

te

Alg

inate

Rope

Com

bin

e +

Film

C

om

bin

e +

Hypafix

Infe

cte

d: G

reen

As a general rule change daily

•

Cle

ar

infe

ction.

•

Deslo

ugh.

•

Absorb

exudate

.

NB if sig

ns o

f in

fection p

resent ta

ke s

wab a

nd

assess for sig

ns o

f genera

l sepsis

.

Heavy

Alg

inate

Rope

Com

bin

e +

Film

C

om

bin

e +

Hypafix

Low

Hydro

gel

F

ilm o

r H

ydro

collo

ids

Modera

te

Alg

inate

Rope

Foam

or

Hydro

collo

id

Necro

tic: Bla

ck

Surgical Debridement prn

Change 1-3 days

•

Rehydra

tion a

nd d

ebridem

ent of

tissue.

•

Surg

ical debridem

ent re

com

mended.

Heavy

Alg

inate

rope

Foam

or

non-a

dhere

nt com

bin

e

Low

Hydro

gel or

Hydro

collo

id

Non-a

dhere

nt dre

ssin

g/f

ilm

Modera

te

Alg

inate

Rope

Non-a

dhere

nt com

bin

e/f

oam

Slo

ughy: Yellow

Change 1-3 days as required

•

Rem

ove s

lough a

nd a

bsorb

exudate

.

Heavy

Alg

inate

Rope

Non-a

dhere

nt com

bin

e/f

oam

Low

Hydro

gel

F

oam

or

Hydro

collo

id

M

odera

te

Alg

inate

Rope

N

on-a

dhere

nt com

bin

e o

r H

ydro

collo

id

Gra

nula

ting: Red

Change 1-7 days as required

•

Main

tain

mois

t environm

ent.

•

Absorb

exudate

.

•

Pro

mote

epithelia

lisation.

Heavy

Alg

inate

Rope

Non-a

dhere

nt com

bin

e o

r fo

am


Product Information

Non-Adherent - Dry

Stock: Melolin, Melolite, Exudry –Smith and Nephew Telpha - Kendall

Non-stock item:

Indications for use • Minor lacerations or healing by primary intention. • Protective dressing

• Secondary dressing. Melolin is the preferred dressing over Hydrogels

Advantages • Low adherent contact layer prevents shedding of fibres into wound

• If exudate is minimal, it will provide sufficient absorbency and prevent sticking to the wound bed

• Exudry has an anti shear layer and is highly absorbent

Disadvantages • Not suitable for heavily exudating wounds except exudry • Can be traumatic to remove. • May require soaking.

Change

Frequency

• Daily or depending on exudate.


Non-Adherent- tulle gras or paraffin gauze

Stock: Jelonet (soft paraffin, open mesh) Smith & Nephew. Cuticerin (fine mesh, contains wool wax) – Smith & Nephew.

Non-stock item: Adaptic – Johnson & Johnson

Indications for use • Simple grazes. Minor burns, Skin grafts • Superficial skin loss. • Temporary dressing

Advantages • Retain some moisture by covering wound bed with paraffin. • Less adherence with fine mesh products.

Disadvantages • Does not absorb exudate • Requires secondary dressing • Can shed fibres into wound. • Can cause allergy. Some contain lanolin or wool wax.

• Care required when removing as granulation tissue can grow through dressing especially Jelonet.

Change

Frequency

• Daily to alternate days.


Non-Adherent- Island dressings

Stock: Primapore (Melolin/ hyperfix) (Smith & Nephew.) Opsite post-op (melolin/film) (Smith & Nephew.

Non-stock item: Airstrip (Smith & Nephew) Cutifilm (Beiersdorf)

Indications for use • Surgical wounds • Minor lacerations/grazes • Protection once wound healed

Advantages • Low adherent contact layer prevents shedding of fibres into wound

• If exudate is minimal, it will provide sufficient absorbency and prevent sticking to the wound bed

• Conforms to body shape • Waterproof option.

Disadvantages • Not suitable for highly exudating wounds • Not suitable for patients with known adhesive allergies • Some not waterproof.

Change

Frequency

• Up to 5 days, depending on exudate.


Non-Adherent- with antiseptic

Stock: Inadine (10% povodine iodine impregnated, fine mesh) (Johnson & Johnson.)

Non-stock item: Bactogras (0.5% Chlorhexadine, open mesh) (Smith & Nephew)

Indications for use • Anti microbial agent for prophylaxis and treatment of minor infections

Disadvantages • Not absorbent, requires a secondary dressing • Contraindicated for patients who are

pregnant/breastfeeding, children < 6years, Impaired renal function and iodine allergy.

• Prolonged use can delay healing

Change

Frequency

• Daily to 2 days for one week only. • Change when dressing turns white • If infection persists consider cadexomer iodine or silver

products or systemic antibiotics.


Hydrogels

Stock: Intrasite gel Solosite gel (contains preservative) (Smith & Nephew)

Non-stock Duoderm gel (Convatec)

Solugel (Johnson & Johnson)

Indications for

use • For rehydrating eschar and slough.

• Use in deep crater wounds with light exudate.

Advantages • Gels have soothing effect over exposed nerve endings, provide some pain relief.

• Rehydrates wound bed by creating a moist but not wet environment over the wound bed.

• Supports debridement.

• Fills in dead space and maintains intimate contact with wound surface.

• Provides absorption of some exudate.

• Easy to apply - may be applied by syringe into sinus.

• Easy to remove - irrigate with normal saline.

Disadvantages • Not recommended for wounds with moderate to heavy exudate.

• Requires a secondary dressing.

• Contra-indicated in superficial wounds.

Change

Frequency • Necrotic or sloughy wounds: daily.

• Granulating wounds: every three days.


Transparent Films

Stock: Op-site (Smith & Nephew)

Non-stock item: Tegaderm (3M)

Indications for use • Cover for areas subject to shearing and friction.


Advantages • Good adherence.

• Transparent - allows continual observation.

Disadvantages • Excessive exudate may accumulate under skin.

• Care required when removing, especially fragile skin.

Change

Frequency

• Up to 14 days.


Hydrocolloids

Stock: Comfeel Ulcer Plus Comfeel transparent (Coloplast distributed by Smith & Nephew)

Non-stock item: Duoderm (Convatec)

Restore Plus (Hollister)

Indications for use • Assists debridement by keeping the wound moisture in contact with the eschar.

• Granulating and epithelialising wounds with low to moderate amounts of exudate.

Advantages • Waterproof.

• Requires no secondary dressing. • Promotes the formation of granulation tissue. • Provides pain relief by keeping nerve endings moist. • Easy to use and comfortable.

Disadvantages • Not suitable for infected or dirty wounds.

• Do not use in wounds where muscle, tendon or bone is exposed.

• Moderate to excessive exudate may leak from site, thus during initial stages may require frequent dressing changes.

• Dressing breakdown can leave residue in the wound - which is time consuming to remove.

• Odour upon removal of dressing can be unpleasant. • Can cause over-granulation of wounds. • Dressings have a tendency to roll up and bunch.

Change

Frequency • A week or if leaks.


Alginates

Stock: AlgiSite M (Smith & Nephew) Seasorb ribbon (Coloplast distributed by Smith & Nephew)

Non-stock item: Kaltostat (Convatec)

Indications for use • For management of moderate to high levels of exudate.

• Haemostatic.

• Assists debridement of moist slough.

• Gel formation causes hydration of the wound. • Cavity wounds

Advantages • Can be used on infected wounds.

• Ropes presentation easy to apply to tunnelled and undermined sinus and cavity wounds.

• Effectively manages moderate to high levels of exudate. • Easy to use and comfortable.

Disadvantages • Requires a secondary dressing.

• Contra-indicated in wounds with low levels of exudate as there is a risk of drying the wound bed.

• Will not debride hard eschar.

Change

Frequency

• Infected or sloughy wounds: daily.

• Clean, exuding: Change when exudate strikes through outer dressing.


Foams

Stock: Allevyn: Adhesive and non-adhesive Allevyn Plus; Adhesive and non-adhesive Smith & Nephew

Allevyn Cavity Plus

Non-stock item: Lyofoam & Polymem (USL)

Indications for use • For management of heavy exudate.

• Deep cavity wounds as packing to manage exudate and prevent premature closure

Advantages • Can be used on infected wounds.

• Comfortable and conforms to shape of wound or cavity. • Effectively manages moderate to high levels of exudate. • Easily removed without causing trauma to wound bed.

• Can be used under compression bandages.

Disadvantages • Requires a secondary dressing.

• Contra-indicated in wounds with low levels of exudate as there is a risk of sticking to the wound bed.

• Will not debride hard eschar.

Change

Frequency • 1- 5 days depending on level of exudate.


Cadexomer Iodine

Stock: Iodosorb, Gel and paste (Smith & Nephew)

Indications for use • Provides sustained antimicrobial activity for up to 72 hours, effective in reducing bacterial burden.

Advantages

• Wide spectrum of activity including gram + and gram –

bacteria, including MRSA, fungi, protozoa and viruses. • Useful colour change to indicate need for dressing change • Facilitates debridement • Absorbs exudate

Disadvantages • Should not be used on patients with history of thyroid disorders

• Contraindicated for patients who are pregnant/breastfeeding, children < 12years. Impaired renal function and iodine allergy.

• Potential for interaction with lithium therefore co administration not recommended

• Prolonged use can delay healing

• Read manufacturers information carefully.

Change

Frequency

• Change when becomes saturated with wound fluid, indicted by loss of colour.


Silver Dressings

Stock:

Non Stock Item: Acticoat, Acticoat absorbent, Acticoat flexi, Allevyn Ag - Smith and Nephew,

Aquacel AG (Conva Tec),

Indications It is appropriate to use silver dressings when a wound is

for use: critically colonized or being treated for infection.

Advantages: A broad spectrum antimicrobial available in a variety of dressings types. Silver is effective against methicillin- resistant Staphylococcus aureus (MRSA and vancomycin-resistant Enterococuss (VRE).

Disadvantages: Silver dressings should be used with discretion as there is concern over developing resistance.

Cost, should be used at the discretion of the Unit manager

Use: Follow manufacturers instructions for all silver dressings. Acticoat needs to be moistened (not wet) with water to activate the

silver, it may be necessary to do this twice a day.

Change Refer to manufactures instructions.

Frequency: Important to monitor for infection and remove dressing if this occurs.


STAR SKIN TEAR CLASSIFICATION SYSTEM

STAR Skin Tear Classification System Guidelines 1. Control bleeding and clean the wound according to protocol. 2. Realign (if possible) any skin or flap. 3. Assess degree of tissue loss and skin or flap colour using the STAR

Classification System. 4. Assess the surrounding skin condition for fragility, swelling, discolouration

or bruising. 5. Assess the person, their wound and their healing environment as per

protocol. 6. If skin or flap colour is pale, dusky or darkened reassess in 24-48 hours or

at the first dressing change.

Star Classification System Category 1a

A skin tear where the edges can be realigned to the normal anatomical position (without undue stretching) and the skin

or flap colour is not pale, dusky or darkened

Category 1b

A skin tear where the edges can be realigned to the normal anatomical position (without undue stretching) and the skin

or flap colour is pale, dusky or darkened.

Category 2a

A skin tear where the edges cannot be realigned to the normal

anatomical position and the skin or flap colour is not pale, dusky or darkened.

Category 2b

A skin tear where the edges cannot be realigned to the normal

anatomical position and the skin or flap colour is pale, dusky or darkened.

Category 3 A skin tear where the skin flap is completely absent.

Last

Update

d:

2010

P

age 3

8 o

f 80

Last

Update

d:

2010

P

age 3

9 o

f 80


MANAGEMENT OF INFECTED WOUNDS

Foreword

Wound infection continues to be a challenging problem and represents a considerable healthcare burden. Early recognition along with prompt, appropriate and effective intervention are more important than ever in reducing its economic and health consequences, especially in the context of growing resistance to antibiotics. Professor Keith Harding An international consensus LONDON MEP 2008

Introduction

The development of a wound infection depends on the complex interplay of many factors. If the integrity and protective function of the skin is breached, large quantities of different cell types will enter the wound and initiate an inflammatory response. This may be characterised by the classic signs of redness, pain, swelling, raised temperature and fever. This process ultimately aims to restore homeostasis. One of the first actions in the management of a wound infection is that the wound should be assessed as to it being colonised or infected. The aim is to prevent the spread of infection because of the complications to the patient. A good tool is to use an infection continuum to assess the patients/clients response to infection and the ability of the immune system to respond (see next page for a sample of one).

Definitions

Contamination: the presence but not the multiplication of organisms on tissues. Contamination may be the precursor to colonisation, which in turn may be the precursor to infection.

Colonization: the presence and multiplication of organisms, with no ill effect to the host.

Critical Colonization: Critical colonization may be defined as increased bacterial burden (multiplication of organisms) within the wound that initiates the body’s immune response locally but systemically and results in delayed healing.

Infection: the deposition and multiplication of organisms in tissue with an associated host reaction. Healing is disrupted and wound tissues are damaged (local infection). Bacteria may produce problems nearby (spreading infection) or cause systemic illness (systemic infection)

Routes of Infection

Self-contamination: e.g. from skin or the gastro-intestinal tract

Airborne Contamination: e.g. dust, skin squames, water droplets

Contact: e.g. hands, clothing, equipment I


Pathogens commonly causing wound infections

Organism Source

Staphylococcus aureus and other Staphylococci

Skin

Streptococcus pyrogenes (Group A Strep) Human pathogen

Enterococcus Intestinal Tract

“Coliform” organisms e.g. E.coli, Klebsiella species, Enterobacter species, Proteus species

Intestinal Tract

Anaerobes e.g. Bacteroides fragilis, Clostridium species

Intestinal Tract

Pseudomonas aeruginosa Intestinal Tract, Environment

Continuum

The Infection Continuum

Kingsley A. (2001).


Local factors that increase the risk of infection

• Devitalised tissue in the wound promotes the colonisation of bacteria, especially anaerobes.

• Impaired local circulation favours bacterial growth.

• Wounds on the abdomen, thigh, calf or buttocks are the most susceptible to infection.

• Foreign bodies in a wound can be both irritating and also harbour micro-organisms.

• Haematomas or ‘dead spaces’ provide a suitable medium for bacterial growth.

Diagnosis of Wound Infection

Assessment of wounds for infection incorporates a full evaluation of the patient and should consider how immune status, comorbidities, wound aetiology/status and other factors will affect the risk, severity and likely signs of infection The classical signs of infection are not always present, particularly in patients with chronic wounds or diabetes mellitus The diagnosis of wound infection is based mainly on clinical judgment – appropriate investigations (e.g. microbiology of wound samples) can support and guide management. The way in which a clinical infection presents will depend on the nature of the pathogen. The infection may remain localised or it may spread via the lymphatic system or by direct extension through subcutaneous tissues and along fascial planes. When bacteria spread from a focus of infection in the general circulation, septicaemia may result. Diagnosis of wound infection is based on clinical criteria. The ‘host reaction’ may take a number of forms from classic signs of cellulitis to more subtle changes.


TRIGGERS FOR SUSPECTING WOUND INFECTION

ACUTE WOUNDS

e.g. surgical or traumatic wounds, or burns

Localized infection Spreading infection

■Classical signs and symptoms: – new or increasing pain – erythema – local warmth – swelling – purulent discharge ■Pyrexia – in surgical wounds, typically five to seven days post-surgery ■ Delayed (or stalled) healing ■ Abscess ■ Malodour

As for localized infection PLUS: ■ Further extension of erythema ■ Lymphangitis ■ Crepitus in soft tissues ■ Wound breakdown/dehiscence

Notes ■ Burns – also skin graft rejection; pain is not always a feature of infection in full thickness burns ■ Deep wounds – induration extension of the wound, unexplained increased white cell count or signs of sepsis may be signs of deep wound (i.e. subfascial) infection ■ Immunocompromised patients – signs and symptoms may be modified and less obvious

Sepsis – documented infection with pyrexia or hypothermia, tachycardia, tachypnoea, raised or depressed white blood cell count

Severe sepsis – sepsis and multiple organ dysfunction

Septic shock – sepsis and hypotension despite adequate volume resuscitation

Death

SYSTEM

IC

INFECTIO

N

(adapte

d fro

m 7

–9)

NB: Other sites of infection should be excluded before assuming that systemic

infection is related to wound infection

CHRONIC WOUNDS

e.g. diabetic foot ulcers, venous leg ulcers, arterial leg/foot ulcers or pressure ulcers

Localized infection Spreading infection

■ New, increased or altered pain* ■ Delayed (or stalled) healing* ■ Periwound oedema ■ Bleeding or friable (easily damaged) granulation tissue ■ Distinctive malodour or change in odour ■ Wound bed discoloration ■ Increased or altered/purulent exudate ■ Induration ■ Pocketing ■ Bridging

As for localized infection PLUS: ■ Wound breakdown* ■ Erythema extending from wound edge ■ Crepitus, warmth, induration or discoloration spreading into periwound area ■ Lymphangitis ■ Malaise or other non-specific deterioration in patient’s general condition

An international consensus LONDON MEP, (2008).


WOUND SWABBING

If the wound is thought to be infected then a wound swab should be taken to assist in identifying the infecting bacteria and then in selecting the most appropriate systemic antibiotics.

Steps in Taking a Swab for Culture Rationale

1. Irrigate wound with a gentle stream of normal saline at body temperature.

Removes surface contamination.

2. Moisten swab with transport media from swab transport container.

Organisms from the wound will adhere better to a moist swab rather than a dry swab.

3. Use a zigzag motion (Fig 1) across the wound, rotating the swab between the fingers. Sample the whole surface area o 2cm² if the area is large.

Allows a good representative area of the wound to be covered.

Figure 1: Swabbing wounds

4. Place the swab straight into the transport medium.

To prevent any organisms from dying.

5. Complete relevant information on the laboratory specimen request form. State the site of the wound, the type of wound (e.g. ulcer or surgical wound), any antibiotic therapy, and the time and date of collection.

Different areas of the body or wound types have their own normal or expected flora. Tests may be decided on the basis of information given.

Re-Evaluate Regularly

■ Relate frequency of re-evaluation to the severity of the infection and condition of the patient ■ Are the wound and patient improving? ■ Is the wound starting to heal? ■ If not, re-evaluate the patient and wound and adjust management accordingly ■ Systematic monitoring and recording of symptoms is helpful in detecting improvement or deterioration. Consider use of an appropriate assessment tool. Serial clinical photographs or tracking changes in markers of inflammation (e.g. erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), white blood cell count) may be useful in registering subtle deterioration or improvement, especially in chronic wounds

1

2

3

4

5

6


Management of an Infected Wound When a wound is suspected or confirmed as being infected the consultant will decide the management of the wound.

The following principles may apply:

Practice Rationale

Facilitate wound drainage To prevent build up of fluid which may encourage bacterial growth and may contribute to wound maceration.

Cleanse the wound of organic debris mechanically or by irrigation

To prevent bacterial growth

Systemic antibiotics may be prescribed if there is evidence of infection

To clear the infection to promote wound healing. Use of topical antiseptics is controversial because of the possible harmful effects on wound healing.

Surgical excision of dead and devitalised tissue may be required in cases of severe infection e.g. necrotising fasciitis and synergistic gangrene.

To prevent further complications of infection and to promote wound healing.

Protection of wound with appropriate dressing.

To contain exudate and prevent contamination.

Aims of a treatment regime are to

• Promote normal immune function

• Increase blood flow

• Decrease oedema

• Remove necrotic debris

• Control pain

• Heal


Figure 2. Management of infected wounds

Redress with an

appropriate

dressing

Is there evidence of acute wound infection?

• Abscess

• Cellulitis

• Discharge

• Odour

• Wound breakdown

• Delayed healing • Discoloration

• Bridging/pocketing at the base of the wound

• Friable granulating tissue

No

Yes

Has a wound swab been taken?

No Take swab following protocol on page 44.

Have the results been seen by medical staff and systemic antibiotics prescribed?

Choose appropriate primary and secondary dressing

Document type of dressing and date of next change on treatment chart

Yes No

Redress with appropriate dressing

Bring results to the attention of medical staff

Yes

Redress with an appropriate dressing


Complications of Wound Infection

There are adverse consequences of wound infection

Organisms that have infected a wound compete with the cells involved in healing tissues for available nutrients and oxygen, healing is delayed and where bacterial toxins are involved these may have adverse local or systemic effects. Infection prolongs the inflammatory stage of healing as the cells combat the large numbers of bacteria. Systemic infection is often associated with pyrexia. Pyrexia causes an increase in the metabolic rate, thus increasing catabolism or tissue breakdown. Management of an infected wound must take in to account the aims of the treatment regime as a whole. Factors such as a patient’s resistance to infection, other disease processes, presence of necrotic or sloughy tissue, the cause of the wound and underlying pathology must be addressed and measures directed at increasing tissue viability.

Principles of Wound Management In order to choose the wound care product and regime that will promote optimal healing, decisions must be made using a comprehensive approach.

• A comprehensive assessment of the patient as a whole person, not just the wound is necessary.

• Treat the underlying contributing factors e.g. relieve pressure; reduce oedema; improve circulation or nutrition; control diabetes; educate regarding smoking, hygiene and home safety.

• Treat a clinically infected wound with systemic antibiotics as prescribed.

NB Refer to the indications and management of clinically infected wounds and colonised wounds (See page 40).

Assess by:

• Determining the underlying pathophysiology that may have caused or contributed to the wound.

• Considering other factors that may impair healing.

• Considering the nutritional status of the patient.

• Completing a wound assessment form (See page 18-19).

Plan by:

• Selecting the product that will best treat the wound.

• Asking yourself “What am I trying to achieve here?” (See product selection guidelines pages 26-36).

• Referring to the product selection guideline sheet and the fact sheets about each product.

Implement by:

• Treating the underlying cause of the wound or the pressure.

• Using the product according to the manufacturer’s instructions.

• Recording on the Wound Assessment & Treatment Chart:

• Frequency of dressing procedure.

• Method of cleaning the wound.

• Primary dressing.



• Method of securing the dressing.

Evaluate by:

• Recording changes in appearance of wound, or amount of wound exudate.

• Determining whether the product is appropriate for the specific wound.

• Considering whether the product is appropriate if the wound is not progressing as anticipated.

Principles of best practise: Wound infection in clinical practise. An international consensus (2008) LONDON:MEP ltd pp1-4 Available from www.mepltd.co.uk Smith & Nephew. (November 2008). New Zealand Wound Care Catalogue Pp16:Author:Auckland


Blister Management A blister is a wound of the epidermis with fluid collection under the skin.

Blisters are normally caused by a combination of friction and heat, and are often an external manifestation of an area of pressure. Generally there are three types/causes of blisters:

• Burns

• Pressure - including blisters that arise from incorrect application of adhesives

• Fractures

Best treatment of blisters is prevention

• Correct assessment of patient (Waterlow Score)

• Use of pressure relieving devices (i.e. Roho, AlphaXcell)

• Correctly fitting splints, crutches, casts

• Don’t apply adhesives, especially film dressings (Opsite) under tension .

If redness develops as a result of pressure, cover the area with a film dressing. This reduces the friction on the skin and will prevent a blister from developing. Burns normally form blisters. If a burn occurs, apply first aid principles, and cool the burn with cold water for ten minutes.

Blister Treatment Leave intact if no local sign of discomfort and allow physiological re-absorption of fluid. If broken or accidentally ruptured, manage as for stage II wound.

Stage II wound Superficial loss of skin integrity with damage to the epidermal and dermal layers of the skin. Erythema of surrounding tissue is evident, which may be hot, painful and oedematous. Low - moderate exudate may be present.

If the blister is causing pressure to underlying tissue, it is best to fully debride the blister, as the fluid in the blister will cause excessive pressure. This has the potential to become a pressure ulcer which will lead to a stage III or IV wound. Never debride blisters on the hands or soles of the feet due to horny layer of skin. The aim of debriding is to facilitate fast and effective removal of devitalised and infected tissue. (Carville, 1998)


Blisters are debrided using the conservative sharp wound debridement (CSWD), which is the conservative removal of loose, avascular tissue in a wound without pain or bleeding. Performed under aseptic conditions in the clinical setting, using sharp, sterile instruments (Carville, 1998).

• Flush the wound with NaCl before and following debridement.

• Exercise caution at the periphery of the wound.

• Cover with a calcium alginate (e.g. Algisite M) or a hydrofibre (Aquacell) and use an occlusive secondary dressing (Opsite or Comfeel transparent).

Rationale Calcium Alginate or Hydrofibre allows the absorption of serous fluid and forms a gel between wound and product (preventing adhesion). An occlusive dressing provides a seal to minimise the chances of infection and prevent on-going drainage of serous fluid by osmosis.

Fracture Blister Treatment NB This is provided underlying tissue are not affected by pressure from the fluid Leave all fracture blisters intact. If pressure under the blister increases, debride and treat for Stage II wound If the blister ruptures spontaneously, debride remaining tissue and cover as described above (Giordano, 1995).

Oedematous Blisters Cause by gross oedema in extremities. Aim of treatment is to control oedema by medical intervention and elevation of the affected limb(s). An absorbent, low cost dressing (e.g. Combi-pad) is preferred to expensive dressings (e.g. Foams).


Burns

This section on Burns is based on a summary from the New Zealand Guidelines group for ACC (2007). Evidence Based Best Practice Guideline: Management of Burns and Scalds in Primary Care. Wellington, New Zealand. Please refer to copy of guidelines for more in-depth information.

An electronic copy can be downloaded from: www.acc.co.nz or to get a printed copy phone ACC Stationary Order line 0800 222 070. If information is from a different source it will be referenced separately.

Definition A burn is tissue injury caused by heat, friction, extreme cold, electricity, radiation or chemicals. Burns usually break the skin and thus can cause infection, fluid loss and loss of temperature control. Deep burns can damage underlying tissues. Burns may also damage the respiratory system and the eyes. Burns are classified by the source, such as thermal, electrical or radiation burns. The depth also classifies them. The deeper the burn, the more severe it is.

Initial assessment and management of Burns and scalds First Aid (Care that should commence in the community)

• Ensure your own safety

• Stop the burning

• In electrical injuries, disconnect the person from the source of electricity

• Cool the burn, with running tap water (8-15 degrees Celsius) for at least 20 minutes (no ice). Irrigation of chemical burns should occur for one hour

-Avoid hypothermia: keep the person as warm as possible, consider turning the temperature up to 15 degrees Celsius (tepid)

-can be started up to three hours after injury

• Remove clothing and jewellery

• Cover the burn with cling film (layered not applied circumferentially) or a clean dry cloth (avoid topical treatments until the burn depth has been assessed).

• Administer analgesia

• Seek medical advice

Emergency management

� Paediatric burns care may be shared between surgeon and pediatrician

� Please refer to Trauma Nursing Core Course and for pediatrics refer to the Pediatric

Burns Pathway

• For major burns perform an ABCDEF primary survey and x-rays as indicated.

• Assess analgesic requirements

• Establish and record the cause of the burn, the exact mechanism and timing of the injury, other risk factors and what first aid has been given.

• Assess Burn size and depth (page 53)

• Give tetanus prophylactic if required.

• Be alert to the possibility of non accidental injury (Page 54)


• Decide on the level of care needed; is a specialist burns unit indicated (see referral criteria)?

A= Airway maintenance with cervical spine control B= Breathing C=Circulation with hemorrhage control D=Disability =neurological status E= Exposure + environmental control (remove jewelry and clothing examine the whole person. Keep the person warm hypothermia develops quickly especially in children F=Fluid resuscitation proportional to burn size. Consult pediatrician for children. Signs of inhalation injury: History of flame burns or burns in an enclosed space Full thickness or deep dermal burns to face, neck or upper torso Singed nasal hair Carbonaceous sputum or carbon particles in oropharynx Indications for intubation: Erythma or swelling of the oropharynx on direct visualization Change in voice with hoarseness or harsh cough Stidor, tachypnoea or dyspnoea Fluid Resuscitation

• Establish intravenous access with two large peripheral intravenous lines.

• Take full blood count, urea electrolytes, coagulation screen, amylase and carboxyhaemoglobin

• The main aim is to maintain tissue perfusion to the wound and prevent the burn deepening and to avoid hypoperfusion or oedema.

• Burns of >10% body surface area in children and >15% in adults warrant fluid resuscitation

• Give fluids:

• 24hour requirement:3-4ml crystalloid solution per kg per % burn

• Plus maintenance fluids for children

• Give half of the fluids over the first eight hours, the remainder over the next 16 hours.

Pain management Paracetamol and NSAIDs can be useful to manage background pain. Consider administering opioids for intermittent or procedural pain. Metabolic and electrolyte disturbances

• In initial stages, avoid over-cooling of burn (see first aid above). This could lead to hypothermia.

• Monitor fluid balance and blood results.

• Patients tolerating oral fluids and nutrition require increased calorie and protein intake. - Dietician referral required.

Electrical Burns: Small entry and exit wounds maybe associated with severe deep tissue damage. An electrocardiogram (ECG) should be carried out to detect arrythmias All electrical burns should be referred to a burns unit


Circumferential Burns. Burns of the circumference of a limb i.e. arm, leg, or the torso. These burns can affect circulation

• Monitor burns to ensure blood supply to skin. Eschar may occur 6 – 12 hours after burn.

• Monitor the colour, warmth, sensation, and movement (CWSM) regularly.

• Toes and fingers of the burnt limb must remain visible.

• Ensure dressings are not tight.

• If necessary, an escharotomy is performed. This is a surgical incision to enable blood flow distal to the eschar.

Burn Depth

• The depth of a burn should be reassessed two to three days after the initial assessment, preferably by the same clinician (burn depth is easier to assess after the initial oedema and inflammatory reaction has settled).

• Testing for pinprick sensation should be avoided.

• The extend and speed of capillary refill can be used as a clinical method of assessing burn depth

Classification of Burns based on Depth ANZBA Classification (2004):

Epidermal Burns e.g. UV light, very short flash Appearance: dry and red, painful, blanches with pressure and there are no blisters Sensation: maybe painful Healing time: seven days Scarring: no scarring. Superficial Dermal e.g. scald (spill or splash) short flash Appearance: pale pink with fine blistering blanches with pressure. Sensation: usually extremely painful Healing Time: within 14 days Scarring: cab have colour match defect. Low risk of hypertropic scarring Mid Dermal e.g. scald (spill), flame oil or grease Appearance: Dark pink with large blisters, capillary refill sluggish. Sensation: Maybe painful Healing time: 14 -21 days Scarring: moderate risk of hypertropic scarring. Deep Dermal e.g. Scald (spill), flame oil or grease Appearance: Blotchy red may blister, no capillary refill. In child maybe dark lobster red with mottling. Sensation: no sensation Healing time: over 21 days, grafting probably needed Scarring: High risk of scarring


Full Thickness e.g. Scald (immersion), flame, steam oil, or grease chemical high volt electricity Appearance: white waxy or charred, no blisters, no capillary refill. Maybe dark lobster red with mottling in a child. Sensation: No sensation Healing time: Does not heal spontaneously, grafting needed if greater than 1cm Scarring; will scar.

Distinguish between burns that will probably heal without skin grafting and those that will probably require grafting (deep dermal burns and full thickness). ****Burn Depth Assessment tables x2

Non Accidental burns

• Indicators of possible non accidental burns or scalds include the following:

• Delay in seeking help

• Historical accounts of injury differ over time

• History inconsistent with the injury presented or with the developmental capacity of the child

• Past abuse or family violence

• Glove and sock pattern scalds

• Scalds with clear cut immersion lines

• Symmetrical burns with uniform depth

• Other signs of physical abuse or neglect Other possible indicators of non accidental injury may include:

• Inappropriate behaviour/interaction of child or caregivers

• Restraint injuries on upper limbs If suspected refer to Social Worker.

Burns Transfer Criteria Criteria for referral

• Burns greater than 10% Total Body Surface Area (TBSA). (See page 58 for Lund and Browder chart for estimating TBSA).

• Burns of special area – face, hands, feet, genitalia, perineum and major joints.

• Full thickness burns greater than 5% TBSA.

• Electrical burns.

• Chemical burns.

• Burns with associated inhalation injury.

• Circumferential burns of the limbs or chest.

• Burns at the extremes of age – children and the elderly.

• Burn injury in those with pre-existing medical or physiological disorders, which could complicate management, prolong recovery or increase mortality.

• Any burn patient with associated trauma. Severely burned patients are usually transferred to Waikato Hospital Burn’s Unit. Referral by telephone requires Consultant to on call registrar of burns unit. Transfer between services is facilitated by prompt assessment, medical photographs. Jane Widdowson CNE Burns, Plastics and Maxillofacial Surgery, Health Waikato


Preparation of the patient for transfer

• Endotracheal intubation should be considered/ performed prior to transfer.

• Administer 100% humidified oxygen.

• IV access is established and fluid commenced.

• If transfer is within 6 hours of burn, apply glad wrap or other instructions given by accepting registrar or consultant. Do not apply SSD cream

• Avoid hypothermia. Keep pt warm. Do not leave patient lying in wet sheets.

• Administer analgesic IV only.

• Fax completed burns assessment form with patient details to burns unit (Form available from ED and digital photos).

• Use aseptic technique to clean the burn with saline

• Remove loose skin with sterile scissors Jane Widdowson CNE Burns, Plastics and Maxillofacial Surgery, Health Waikato

If the patient is to be treated at Tairawhiti District Health Board, the principles of managing burns relate to assessment for and treatment of:

Management of Epidermal Burns or Scalds

These patients are not normally admitted. Consider referral to District Nurse or Paediatric Outreach Nurses. A protective dressing or moisturising cream can be used for comfort in epidermal burns and scalds. Review epidermal burns or scalds after 48hours. If the skin is broken change to a moist wound healing product.

Management of superficial and mid and deep dermal burns or scalds

• Not usually admitted consider referral to District Nurses or Pediatric Outreach Nurses

• Use aseptic technique to clean the burn with saline

• Remove loose skin with sterile scissors

• Products with an antimicrobial action should be used on all burns for the first 72hours (three days) after burn injury to prevent infection.

• Acticoat is the preferred product or can use silver sulphadiazine cream (SSD cream).

• After 3 days if there is no infection consider changing to a product that provides re epithelialisation by moist wound healing e.g. film, foam, hydrocolloids.

Nanocrystalline silver (Acticoat) is the preferred dressing for initial management of burns due to the fact it reduces the time it takes for the burn to epithelise, reduced dressing changes and trauma of dressing changes associated with the application and removal of SSD cream. It reduced the requirement for grafting and long term scar management and length of time in hospital thus making it a cost effective dressing with better client outcomes (Cuttle et al 2007). In addition to the latter it has also be shown to reduce the incidence of infection (Fong & Fowler,

2005). It has also been recommended for use because the slow release of silver is less likely to produce a toxic effect that has been associated with the use of SSD cream. (Atiyeh et al ,

2007). References: Fong, J., and Fowler, B. (2005). A silver coated dressing reduces the early burn wound cellulitis and associated costs of inpatient treatment: Comparative patient care audits. Burns 31 562-567 Cuttle, L., Naidu S., Mill, J., Hoskins, W., Das, K., & Kimble, M. (2007). A retrospective cohort study of Acticaot versus Silvavine in a paediatric population. Burns 33 701-70. Atiyeh, B., Costagliola, M., Hayek,S., & Dibo, S. (2007). Effect of silver on burn wound infection control and healing: Review of literature Burns 33 139-148


Management of Blisters: Preferably leave small blisters intact unless likely to burst or interfere with joint movement. If necessary drain fluid by snipping a hole in the blister. Note: a deroofed blister can be more painful than an intact blister.

Review of superficial and mid dermal burns: Daily for the first three days by lifting the edge of the acticoat dressing then subsequently every three days. Consider referral to District Nurses, Paediatric Outreach Nurses.

Infection Regular monitoring is important as infection can delay healing, increase scarring and potentially cause systemic infection.

• Swab the wound

• Use nanocrystylline silver (Acticoat)

• Antibiotic cover.

• Ensure tetanus toxoid has been given.

• Daily reassessment of healing must be carried out.

Healing wounds Education re protection from sun, sunscreen or protective clothing should be worn. Daily moisturisers and non drying non perfumed soap should be used to protect the skin after burn injury and may also be helpful for pruritis.

Prevention of Contractures

• Involve scar management service and physiotherapy re positioning of burnt limb and range of movement and exercises to maintain normal function.

• Physiotherapist should assess movement with the burns dressing removed.

Scarring

• Often scarring is inevitable following burns that involve the deep dermal layers even with grafting.

• Children and those with dark skin pigmentation are often at higher risk for developing scarring. Since scarring can take an average of 18 months to mature and often gets worse before it improves it is crucial that patient and family are educated and involved early to achieve the best possible outcome.

• Scarring can result in long term functional disability and changes in appearance both of which are an indication for specialist care.

• Any burns that are unlikely to heal within 21days without grafting should be referred to a burns service for scar management by day 10-14. Contact Burns and Scar Management Service Ext 8096

• At three weeks the healed area may appear flat and supple however scarring may still eventuate. A referral to scar management is advised to monitor progress.

• A person presenting with scarring some months after a burn should still be referred for specialist opinion.

• Scar Management may also involve the use of pressure garments, silicone, contact media and moisturizers to flatten and soften scars as well as splinting to prevent or correct contractures (Rob Heath, Smith and Nephew Scar Management 2009).


Psychological consequences of a burns injury

• Monitor people for signs of stress or depression.

• Recognize and treat pre existing disorders and co morbidities (including alcohol and drug dependence) associated with post traumatic stress disorder (PTSD).

• Refer people with acute or chronic PTSD for specialist mental health management.

• Be aware of increases risk of sleep disorders after burn injuries. Support groups: www.burnsupport.org.nz www.burns.org.nz

References:

New Zealand Guidelines group for ACC. (2007). Evidence Based Best Practice Guideline: Management of Burns and Scalds in Primary Care. Wellington, New Zealand. An electronic copy can be downloaded from: www.acc.co.nz or to get a printed copy phone ACC Stationary Orderline 0800 222 070.


Dressing Application

To ensure appropriate and effective use of Nanocrystalline Silver Acticoat in the

management of burn wounds.

1. Definitions

Nanocrystalline Silver Acticoat ™ - antimicrobial barrier dressing that contains nanocrystalline silver. Consists of layers of rayon which are sandwiched between layers of silver-coated, low adherent, polyethylene net. Indicated for use as an anti-microbial barrier over partial and full thickness wounds (burns) as prophylactic or when infection is present. (Silver ion activity lasts for up to 3 days, Acticoat ™ 7 also available – silver activity lasts up to 7 days dependent on exudate levels.)

2. Competency required Decision to use Acticoat should be by medical staff or delegated to an appropriately skilled senior nurse. Product application and ongoing care is by nursing staff who have received education and training in its use.

3. Contraindication/precautions

Patients allergic to silver, patients undergoing MRI scans, do not use with oil based products, avoid contact with electrodes.

4. Equipment

Dressing pack, Dressing saline, Debriding set, gloves, Acticoat™ dressings Sterile Water for irrigation, +/- hyperfix Secondary dressings – gauze roll, crepe, surginet etc

Method – Initial outer dressing change and ongoing management

Process Rationale

Explain procedure to patient Gain informed consent

Assess need for analgesia and administer as prescribed

Burns debridement is painful, some patients may also experience stinging on application of Acticoat

Cleanse wound and surrounding skin using saline + soap and water.

Decontaminate, reduce risk of infection

Assess burn wound depth pg 53

Depth diagnosis important to direct ongoing management

Debride loose skin and blisters pg 49-50

This skin is non-viable

Cut the Acticoat to the shape/size of the wound. Moisten the Acticoat with sterile water either by pouring onto the dressing or by submerging into gallipot. (DO NOT USE SALINE) Wring out excess water Apply Acticoat to wound – it does not matter which way up

Prevent maceration of surrounding skin Activates the release of the silver ions Saline will formulate silver chloride which will affect the availability of silver to the wound.


Key point – secondary dressings: Acticoat must be kept moist to continue to release silver ions onto wound bed. Choices of secondary dressings include: Hyperfix keep moist by showering and or use of saline given to you by nurse. Pat dry with clean towel or sterile gauze. Application four times a day or when necessary to keep moist to touch.

Final dressing layer options: Gamgee/gauze roll. Change secondary dressing when there is strike though.

Crepe bandage, surginet etc to secure

To keep Acticoat moist For padding and or to absorb exudate.

Document wound assessment and ongoing dressing management in clinical notes. A portion of the primary Acticoat dressing should be inspected to determine whether further moistening is required. Waikato DHB predominantly uses Acticoat – 3 day version therefore full dressing change and wound review is required at this time. When Acticoat is removed, staining or the periwound skin and/or the wound bed may be seen. This is transient.

Antimicrobial activity ceases if Acticoat is dry

5. References

Application Guidelines Acticoat and Acticoat 7. Smith & Nephew product brochure. Ovington, L., G. (2004). The truth about silver. Ostomy Wound Management. 50 (9a).

Jane Widdowson CNL Burns, Plastics and Maxillofacial Surgery, Health Waikato


Application of SSD Cream

• Apply SSD cream 3-5mm thick for 3-4 days.

• Cover SSD cream with Paranet gauze, combine and fix with loose bandage.

• Daily shower or bath using copious amounts of water to remove dead tissue and SSD cream. Requires adequate pain relief especially with children

• Wounds must be reassessed daily for first three days.

• If healing well, treat as a superficial burn. Note: SDD cream needs to be cleaned off daily as it builds up an eschar and on non infected wounds shouldn’t be applied longer than 7 days as it may delay healing.

Facial burns:

• Do not apply SSD cream to facial areas as it causes tattooing or staining of the skin.

• Clip of trim singed hair

• Debride blisters and loose skin (Pg 49-50)

• Apply olive or paraffin oil 1-2 hourly. There is no need to cover burns with a dressing.

• If the burn is severe enough to warrant admission, do not use pillow on bed, elevate the head of the bed 30 ° instead. Use of the pillow can cause contractures.

• Daily showering with use of Dermaveen bath oil to remove crusts.

Ears: deep burns to the external ear predispose the auricular cartilage to chondritis and necrosis resulting in late ear deformities and tissue loss.

• Avoid pressure on the auricle no pillows

• Cleanse as above and apply topical application usually SSD due to conformability

• Remove excess exudate from ear canal as required. Placing a jelonet plug in the ear canal may help prevent accumulation.

• Consult surgeon before debriding blisters.

Lips: Keep lubricated with white soft paraffin/Vaseline Avoid prematurely removing crusts as lips tear and bleed easily

Eyes: (including eyelids or singed lashes) Manage as per ophthalmologist Rx if corneal damage is present. Regular eye toilets using saline and gauze Apply artificial tears or prescribed ointment as directed (reduces corneal drying and infection)

Beards: Usually it is difficult to shave a beard on a conscious patient. The aim is to minimize the build up of exudate/crust and thus avoid infection. Shave if possible (preferably while under general anesthetic) Wash and remove crustings /exudate regularly

Hands

• Avoid restricting the movement of fingers as this may decrease function.

• Apply acticoat and hyperfix (length wise on fingers to avoid constriction)

• Cover foot in SSD cream. Place inside sterile plastic bag and elevate.

Feet

• Apply acticoat and hyperfix (length wise on fingers to avoid constriction)

• Place Paranet gauze between the toes to prevent them adhering (and healing) to each other.

• Cover foot in SSD cream. Place inside sterile plastic bag and elevate. Jane Widdowson (2009) CNE Burns, Plastics and Maxillofacial Surgery, Health Waikato


CHART FOR ESTIMATING SEVERITY OF BURN WOUNDS

Name: ______________________________ Ward ______________

NHI No: _____________________________ Date: ______________

RELATIVE PERCENTAGE OF BODY SURFACE AREA

AFFECTED BY GROWTH

AREA AGE 0 1yrs 5yrs 10yrs 15yrs ADULT

A = ½ of Head 9½ 8½ 6½ 5½ 4½ 3½

B = ½ of one thigh

2¾ 3¼ 4 4½ 4½ 4¾

C = ½ of one leg 2½ 2½ 2¾ 3 3¼ 3½

LUND & BOWDER CHARTS

B

A

C

B B B

C C C

SUPERFICIAL DEEP

Region % Head Neck Ant. Trunk Post. Trunk Rt Arm Lft Arm Buttocks Genitalia Rt Leg Total Burn


Patient Guidelines

Caring For Burns Using Acticoat What is acticoat? Acticoat is a special silver dressing that when moistened will form a protective barrier helping to prevent bacteria from entering your wound.

While Healing:

1. If you have acticoat silver on your wound this dressing can stay on for three days. The wound will be reviewed daily by gently lifting an edge of the dressing up.

2. To activate the silver in the dressing it must be keep moist (not wet) by using water not

saline.

3. You will be given a supply of water or alternatively if you are on town supply you may shower. Pat dry with gauze or a clean towel. This will need to be done every four hours or when necessary.

4. If soaked in water for over five minutes, the dressing will become soggy and increase the risk of infection.

5. Avoid activities that may cause injury to the wound, or lead to bleeding or infection.

For example: digging in the sand, swimming, gardening, mechanical repairs.

6. If the wound becomes red and hot with an increase in pain fluid or swelling

beneath the dressing or blisters form, contact your nurse or see your GP.

7. The nurse will remove the dressing after 3 days and review the wound and reapply an appropriate dressing.

8. Acticoat may cause a silver glitter effect on your wound or some mild staining on the

surrounding skin. This is nothing to worry about it is just the silver released from the dressing (and only lasts a short time) Once your wound has healed the slight grey silvery appearance may remain for a short period of time.

References: Smith and Nephew (2005). A Patients Guide to Acticoat.


Management of Burn Wounds at TDH

Cool Burn. Give appropriate analgesia pg. Obtain history Assess depth of burn pg 53

Superficial/ mid dermal

Nanocrystalline silver dressing (eg acticoat pg 36) Blister and oedema management pg 49-50 Pain relief pg 52 Facial burns pg 60

Deep dermal/full thickness

Is the burn area > than 1cm wide

Yes

No

Antimicrobial dressing (eg acticoat SSD cream pg 36 & 60) Pain relief pg 52 Daily review Note:1

Day 3 reassessment

Reassess burn depth pg 53. Is it significantly worse (likely to be full thickness)?

Apply nanocrystalline silver (acticoat) Review within 72 hours Monitor for signs of infection pg 43

Yes

No

Days 5-7: Change to moist wound healing product pg 16

Refer to

Regional

Burns Unit see

referral criteria

pg 54 or

surgeon for

grafting Note 2

Days 10-14 Is healing likely within seven days

No Note 2

Yes

Continue with dressings

Is healing progressing

Yes

Continue with dressings as above Monitor for signs of infection pg 42-43

Healed consider rehabilitation needs pg 56.

Pg numbers refer to additional detail in Wound Care Manual

Note 1: consider referral to Physio pg 54 Paediatric Outreach Nurses/Social Worker/District Nurse Burns and Scar Management Service pg 56

Note 2: Continue with acticoat dressing until surgery

Full Thickness


PRESSURE ULCERS

The EPUAP (European Pressure Ulcer Advisory Panel 1999) defines pressure ulcers as "…an area of localised damage to the skin and underlying tissue caused by pressure, shear or friction and or a combination of these”. Pressure ulcers can occur on any part of the body, but are commonly found in areas with bony prominences, also termed pressure points. The term pressure ulcer is synonymous with decubitus ulcer, bed sore, pressure sores and

pressure areas. Pressure is a perpendicular force applied vertically to the skin’s

surface (Bliss 1993). This loading force compresses tissues, restricts the microcirculatory blood vessels, reduces oxygen and nutrient supply to the tissues and interrupts lymphatic drainage (Polliack et al 1997) leading to tissue death. Such lesions tend to be round and neater than those caused by shear or friction (Hampton & Collins 2004, and Dealey 1999). Localised pressure can result in damage from high pressure for short intense periods or from lower pressure for prolonged periods (Bell 2005). If the pressure is of sufficient intensity, or applied for a sufficiently long period of time, erythema may be present. Erythema that does not fade over time, after the removal of pressure is considered to be a pressure ulcer.

Factors which cause pressure ulcers

1. Extrinsic Factors

Pressure

• Pressure is the most significant factor causing tissue damage

• This can vary between patients, depending on vessel structure, adipose deposits over bony prominences, B/P & general health status..

• The blood pressure at the arterial end of the capillaries is approximately 32 mmHg, while at the venous end this drops to10 mmHg.

• The average mean capillary pressure equals about 17 mm Hg and any external pressures exceeding this will cause capillary obstruction.

• Tissues that are dependent on these capillaries are deprived of their blood supply. Eventually the ischaemic tissues will die.

• Ischaemia results if pressure exerted is greater than capillary pressure causing occlusion of the capillaries & microcirculation.

Friction

• Damage to the skin and underlying tissues can also occur from friction and shearing. Friction occurs when there is rubbing against resistant surfaces. Friction most commonly occurs when heels and elbows rub against the sheets. It also occurs during over vigorous rubbing of the skin. Friction causes the abrasion of the epithelial surface.

Shearing

• Shearing forces occur when the skin is dragged or slides over another surface. Most commonly this occurs when patients are positioned in the semi-Fowler’s (i.e. the bed head is raised at an angle higher that 30

0, and slide down the bed. Shearing forces will

traumatise the underlying tissues and blood vessels.


Risk assessment and predisposing factors There are a number of predisposing factors that increase the susceptibility to develop pressure ulcers. There are also a number of risk assessment scales available. In this organisation, we have chosen to use the Waterlow (2005) Pressure Ulcer Prevention/Treatment Scoring System*. The predisposing factors for skin breakdown are incorporated into this system.

Build/weight for height. This includes the underweight and obese patient, who may be nutritionally compromised, and/or immobile.

Continence. Incontinent patients at risk of damage from shearing and friction. Moisture pre-disposes the skin to pressure ulcers because of the effects of maceration and excoriation.

Skin type. Broken skin is already compromised and at risk of further damage. In addition, patients who have very dry skin are at increased risk of damage by shearing and friction. Furthermore, those with peripheral vascular disease have compromised circulation.

Mobility. Immobility is a major cause of sustained pressure. Lack of activity itself reduces venous return, thus allowing oedema to occur.

Age. As adults age, the loss of subcutaneous fat, reduced skin elasticity and gradual breakdown of the body’s repairs mechanisms, thus placing the older adult at risk.

Appetite. Poor nutritional status impairs wound healing, reduces the immune response and reduces the number of bacteria killed by leukocytes and macrophages.

Tissue malnutrition. Poor tissue perfusion, e.g. from peripheral vascular disease delays healing as essential nutrients are not transported to tissues and toxic cellular material accumulates. Patients with multi-organ failure or terminal cachexia become malnourished due to reduced absorption of nutrients.

Neurological defects. Patients who have neuropathy due to diseases such as Diabetes Mellitus, or impaired function through CVA or paraplegia have additional risk of pressure ulcer development because of sensory loss.

Major surgery/trauma. During surgery patients are immobilised for long periods of time, especially on hard theatre surfaces. Patients require reassessment at regular intervals to ensure appropriate prevention treatment.

Medications. Wound healing is delayed in patients who are receiving cytotoxic drugs, steroids, anti-inflammatory medications or who are receiving long term Penicillin.


Pressure Ulcer Prevention The aim of pressure ulcer management is prevention.

Action Rationale

Assess every patient on admission. To identify the patient at risk of developing Pressure ulcers.

The risk assessment tool approved by TDH is the Waterlow Pressure Ulcer Risk Assessment tool. The Waterlow Score is a supplement to clinical judgement. The assessment and score are recorded in the nursing assessment form.

To maintain consistency in assessment by using an agreed system.

Patients should be classified in one of the following categories:

< 10 Not at risk 10+ At risk 15+ High risk

20+ Very high risk

Reassessment should occur following a significant clinical event (e.g. theatre or a prolonged procedure) or change in patient condition and at regular intervals.

Inspect skin of the “at risk” patient at least daily and then after a significant event. Document skin changes. If any changes occur refer to the protocols for Treatment of Pressure Ulcers.

Do not rub any area at risk.

Rubbing causes maceration and degeneration of subcutaneous tissues, especially in the elderly.

Wash areas at risk only if the patient is incontinent or sweating profusely. Use mild soap. Ensure that all soap is rinsed off and that the area is patted dry.

To maintain skin integrity and prevent the formation of sores. Excessive use of soap can be harmful to the skin. Thorough gentle drying of the skin promotes comfort and discourages the growth of micro-organisms.

Use moisturiser if the skin is very dry.

Dry skin cracks allow entry of micro-organisms.

Use barrier creams only when indicated.

Barrier creams prevent damage to the epidermis. However they are occlusive and prevent moisture exchange from the skin.

If frequent soiling occurs action should be taken to control the source of moisture e.g. continence management.

Tensile strength of skin is impaired when there is frequent or excessive contact with moisture Skin becomes macerated Ulceration occurs with friction or shearing of the skin when moisture is present.

Use talcum powder sparingly. Gently rub it in and remove excess from bed.

Excess talcum powder will form small balls once it dampens, thus creating friction and pressure objects.


Action Rationale

Keep the linen wrinkle-free and dry at all times.

Remove crumbs, hairpins and other hard objects from the bed promptly.

In especially debilitated patients a small hard object can create ulceration in a very short time.

Avoid dragging or scraping the patient’s bottom when transferring in and out of chair, bed or commode.

The bed and commode should be the same height as the chair.

For easier and safer transfer.

Diet and fluid of “at risk” patients should be monitored. Consider also those ‘nil by mouth’ pre-op or on limited intake following major surgery.

A fluid or nutrition deficit compromises skin integrity.

Educate the patient to shift position, to pull or push up regularly and to examine the vulnerable areas.

After discharge the patient may be self-caring and possibly still vulnerable to sores. To encourage the patient to participate in their own care.

Initiate a mobility programme for the patient. Call on the physiotherapist or occupational therapist as appropriate.

Patients may need management of long-term compromised immobility.

Where possible relieve the pressure over areas vulnerable to tissue breakdown. Use appropriate pressure relieving devices (see Fig.1). If necessary, turn the patient at least two-hourly and record the position on the relevant charts.

To reduce pressure where possible. Use of inappropriate aids may increase pressure to vulnerable areas.

Avoid pressure on bony prominences. Pressure is the most significant factor causing tissue damage.

Foam wedges may be used to maintain position, but doughnut devices to be avoided.

Doughnut devices tend to pinpoint, rather than relieve pressure.

Raise the bed no higher than the lowest elevation (30

0).

Raising the bed to a higher degree increases the likelihood of shearing.

Specialist support surfaces should be used as part of an overall plan.


Waterlow Risk Assessment Tool DATE DATE DATE DATE DATE

BUILD/WEIGHT FOR HEIGHT

WT (kg)

BMI =

HT (m2)

BMI Average (20 - 24.9) = 0

Above average (25 - 29.9) = 1

Obese > 30 = 2

Below average < 20 = 3

SEX/AGE

Male = 1

Female = 2

14 - 49 = 1

50 - 64 = 2

65 - 74 = 3

75 - 80 = 4

81+ = 5

SKIN TYPE & VISUAL RISK AREAS

Healthy = 0

Tissue paper = 1

Dry = 1

Oedematous = 1

Clammy, pyrexia = 1

Discoloured Pressure ulcer Grade 1 = 2

Broken/spots Pressure ulcer Grade 2, 3, or 4 = 3

CONTINENCE

Complete continence/catheterised = 0

Urine incontinence = 1

Faecal incontinence = 2

Urinary & faecal (double) incontinence = 3

MOBILITY

Fully mobile = 0

Restless/fidgety = 1

Apathetic = 2

Restricted = 3

Bed-bound (eg traction) = 4

Chair-bound (eg wheelchair) = 5

SPECIAL RISKS

MEDICATION

Cytotoxics, long term/high dose steroids, anti-inflammatory = 4

(Maximum score of 4 for one or more in this category)

TISSUE MALNUTRITION

Terminal Cachexia = 8

Multiple Organ Failure = 8

Single organ failure (resp, renal, cardiac) = 5

Peripheral vascular disease = 5

Anaemia (HB < 80) = 2

Smoking = 1

NEUROLOGICAL DEFICIT

Diabetes, MS, CVA = 4-6

Motor/Sensory

Paraplegia

(Maximum score of 6 in this category)

MAJOR SURGERY OR TRAUMA

Orthopaedic/Spinal = 5

* On table > 2 hrs = 5

* On table > 6 hrs = 8 *Scores can be discounted after 48 hrs provided pt recovering normally

TOTALS

ASSESSORS INITIALS

Refer to dietician if unintended weight loss with decreased appetite.

Circle score. Each category may have more than one score. Add total. Revised Waterlow 2005. TDH 2010

GUIDE: 10+ AT RISK 15+ HIGH RISK 20+ VERY HIGH RISK.

Weight =

Height =


WATERLOW-PRESSURE ULCER PREVENTION REMEMBER TISSUE DAMAGE MAY START PRIOR TO ADMISSION, IN CASUALTY.

A SEATED PATENT IS AT RISK. ASSESSMENT (See Over). IF THE PATIENT FALLS INTO ANY OF THE

RISK CATEGORIES, THEN PREVENTATIVE NURSING IS REQUIRED, A COMBINATION OF GOOD

NURSING TECHNIQUES AND PREVENTATIVE AIDS WILL BE NECESSARY.

ALL ACTION MUST BE DOCUMENTED.

PREVENTION

PRESSURE REDUCING AIDS

WOUND GUIDELINES

Special

Mattresses/beds:

10+ Overlays or specialist foam mattresses. 15+ Alternating pressure overlays, mattresses and bed systems. 20+ Bed systems. Fluidised bead, low air loss and alternating pressure mattresses. Note: preventative aids cover a wide spectrum of specialist features. Efficacy should be judged, if possible, on the basis of independent evidence.

Assessment: Odour, exudate, Measure/photograph, position.

WOUND CLASSIFICATION - EPUAP

Cushions: No person should sit in a wheelchair without some form of cushioning. If nothing else is available-use the persons own pillow. (consider infection risk). 10+ 100mm foam cushion 15+ specialist gel and/or foam cushion 20+ specialist cushion, adjustable to individual person.

GRADE 1

GRADE 2

Discolouration of intact skin not affected by light finger pressure (non blanching erythema) Partial thickness skin loss or damage involving epidermis and/or dermis. The pressure ulcer is superficial and presents clinically as an abrasion, blister or shallow crater.

Bed Clothing:

NURSING CARE

General

Pain

Nutrition

Patient Handling

Patient Comfort Aids

Operating

Table/Theatre/

A & E Trolley

Skin Care

Avoid plastic draw sheets, inco pads and tightly tucked in sheet/sheet covers, especially when using specialist bed and mattress overlay systems. Use duvet-plus vapour permeable membrane. HANDWASHING, frequent changes of position, lying, sitting, use of pillows. Appropriate pain control. High protein, vitamins and minerals Correct lifting technique-hoists-monkey poles, transfer devices. Real sheepskin-bed cradle. 100mm (4ins) cover plus adequate protection. General hygiene. NO rubbing, cover with an appropriate dressing.

GRADE 3

GRADE 4

Dressing Guide:

IF TREATMENT IS

REQUIRED, FIRST

REMOVE PRESSURE

Full thickness skin loss involving damage of subcutaneous tissue but not extending to the underlying fascia. The pressure ulcer presents clinically as a deep crater with or without undermining of adjacent tissue. Full thickness skin loss with extensive destruction and necrosis extending to underlying tissue. Use local dressings formulary and/or www.worldwidewounds


Fig.1 Pressure area: Flowchart for selection of equipment category A-E. Reprinted from Shipperley, T. (1998).Journal of Wound Care 7(6).

Water score

<10

No risk.

Reassess regularly

Waterlow score

10-14

Can patient

turn with

no/minimal

assistance?

yes Is patient in

bed <19

hours each

day A

Waterlow score

15-19

no

Is patient’s

skin intact?

no

Is patient free

from erythema

on pressure

area?

B yes yes

yes

no

Waterlow score

20 or more

Is patient in

bed <14

hours per

day?

Is patient’s

skin intact?

yes yes

no

C

Is patient in

bed <19 hours

per day?

yes

Is patient’s

pressure damage

less severe than

Grade III?

yes

D

no

E

A =Low risk: Pressure reduction (TheraRest,

prima, standard hospital linen, no mackintosh)

B/C= Medium Risk: Static overlays (gel pads)

Static replacement mattresses ( Roho, AtmosAir)

dynamic mattress overly (Elite 5000, Alpha

Xcell). One hospital sheet only.

D/E= Very High Risk: Dynamic replacement

mattresses (Nimbus) or Rental


Table 1 Pressure Ulcer Classification (Grading System). (European Pressure Ulcer Advisory Panel 1999)

Grade I

Non-blanching of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness can also used as indicators, particularly on individuals with darker skin.

Grade II Partial thickness skin loss involving epidermis and/or dermis. The ulcer is superficial and presents as an abrasion or blister.

Grade III Full thickness skin loss involving damage or necrosis of subcutaneous tissues that may extend down to but not through underlying fascia.

Grade IV Extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures with or without full thickness skin loss.

Table 1: Staging of pressure ulcers.

NB Accurate staging of a pressure ulcer is not possible when necrotic tissue is present. Superficial Pressure Ulcers may develop into deeper ulcers if pressure is unrelieved. The reddened area of a Stage I pressure ulcer may be indicative of deep tissue damage.


Ulcer Classification (Grading System).


Pressure Ulcer Treatment

Action Rationale

1. Any patient presenting with a pressure sore should have a comprehensive history and examination (See protocol for prevention of Pressure Ulcers).

The aetiology and underlying or related pathophysiology, as well as the wound itself, must be assessed in order to provide the most appropriate treatment.

2. If patients are admitted to TDH with an existing ulcer a referral to the community team is necessary.

To facilitate assessment of living arrangement that may have caused/ exacerbated pressure.

3. Assess the size, shape and condition of the wound using the TDH Wound Assessment form.

4. Use a pressure sore grading system as indicated in Table 1.

To provide cross-disciplinary uniformity of diagnosis.

5. Select wound care product based on wound assessment and TDH product selection guidelines.

6. Continue to consider changes to nutritional needs as patient’s condition changes.

Extra protein, Vitamin C and fluid intake to promote healing.

7. Pressure ulcers should be gently irrigated at each dressing change.

To minimise bacterial colonisation. Mechanical force (through swabbing) can cause damage to fragile granulating tissue and epithelial cells.

8. Use warmed Normal Saline to clean wounds.

Antiseptic agents are non-selective and cytotoxic to healthy tissue.

7. Necrotic tissue should be debrided. Autolytic debridement is inappropriate if the pressure ulcer is infected. Refer to Wound Resource Nurse or surgeon to review wound

While autolytic debridement is effective, speed is important to prevent the wound infection worsening to generalised septicaemia.

8. Follow guidelines for wound care management based on patient’s condition and aims of treatment.

To maximise care and create an environment to optimise wound healing.

9. Pressure relief or reduction should be used to avoid direct pressure on already damaged tissue.

Unrelieved pressure/friction/shear will continue to cause tissue damage.


Management of Skin Graft and Donor Sites

Skin grafting is a fundamental technique used to provide a cover over a defect. In order to achieve the best possible outcome, the ideal donor skin should match the skin being replaced as closely as possible in texture and hair-bearing qualities, providing a good cosmetic result and creating minimal donor site deformity.

Management of Skin Grafts Skin transplanted from one location to another on the same individual is termed an autogenous graft or autograft. There are 3 main skin graft techniques.

1. Full thickness Skin Graft (FTSG) Is the term used where the entire thickness at the dermis is included. It offers more durable coverage and more sensation than a split skin graft. Usually recommended for areas where cosmetic appearance is important e.g. face.

2. Split Skin Graft (STSG) Is the term used if less than the entire thickness at the dermis is included. Split Skin Grafts have a much broader range at application, heal quicker but are more fragile.

Uses: a) Resurfacing of large wound b) Line Cavities c) Resurfacing of muscle flaps d) To promote healing of large burns

3. Composite Grafts Combination of skin fat, skin cartilage – dermis and fat e.g. 3 dimensional areas such as the nose.

Aims of Skin Graft Site Wound Management The main principles are: 1. To maintain and provide uniform tension/pressure over the entire graft site to promote

adherence of the graft to the wound bed. 2. To immobilise the graft and prevent friction and shearing forces which will destroy fragile

capillaries growing into the newly placed graft.

Dressing of Skin Graft Initial post op dressings from theatre are left undisturbed for approx 5 days unless there is considerable pain, odour or other signs of a complication. In Ward setting: initial dressing is taken down by the surgeon or unless specific orders given.


In Outpatient setting: initial dressing is taken down by the surgeon Tie over bolster gauze dressings are used and sutured in place when wound has irregular contours and it is difficult to secure a dressing: e.g.: hose. VAC dressings maybe applied to graft sites. Follow clinical guidelines for VAC application and management.

Dressings

• Primary Dressing: Is non-adherent, semi-occlusive and absorbent. Paraffin gauze dressing such as Jelonet cut to size is moulded over the graft site. This is used to allow fluid to escape from beneath the grafted skin.

• Secondary dressing comprises of additional adequate soft padding and light bandaging.

• The use of cast or splint may be used when grafting over mobile surfaces e.g. elbow.

• When removing any dressing material from graft site. Material should be moistened with saline solution to reduce adherence of material to the graft site.

• The dressing must be removed very carefully to prevent lifting of the graft from the underlying wound bed.

• Regular analgesia should be administered as charted. After 7-10 days any remaining sutures are removed.

Donor Sites A donor site is an area of skin that is used to provide a split-thickness skin graft, comprised of epidermis and varying thicknesses of dermis. The healing of donor site wounds is primarily through re-epithelialisation of the raw, exposed dermis. The donor site produces more fluid than other superficial wounds. Epithelial cells in the hair follicles, sebaceous and sweat glands migrate across the surface of the donor site and form a new layer of epithelium. This process is completed in 10-21 days. The age and general health of the patient, and the site, size and depth of the tissue excised affect the healing rate.

Aim of Donor Sites Management The main principle is to protect the area from dehydration and further mechanical trauma. Drying out may cause dressing material to adhere to the wound surface and become incorporated into the granulation tissue. An ideal donor site dressing should reduce pain, be easy to apply, minimise leakage of exudate, promote rapid infection-free healing, and require minimal nursing. The faster a donor site can heal, the less risk there is of contamination, wound infection and hospitalisation.


Dressing of Donor Sites

• The choice of dressing should not inhibit the patient’s mobility. The choice of dressing is an alginate because of its haemostatic properties and absorbency. The primary dressing should have a 5% margin overlap of the donor site, especially on limbs where exudate tends to soak downward.

• Fixation of the primary dressing should be securely done with hyperfix. A skin care preparation painted on the surrounding skin will protect the skin from adhesive and help the tape stay in place. Reinforcement of gamgee, bandaged on can be changed as required if strike through dictates.

• The primary dressing ideally should be left in place for 14 days then removed by soaking with cooking oil the night prior to removal. This will enable the dressing to be spontaneously removed without trauma to the newly epitheliazed skin.

• Regular analgesia should be administered as charted. The patient needs to be reassured about wound odour at the donor site, which can be embarrassing and offensive. Explain that this is due to stale blood or exudate trapped within the dressing. It can be reduced by appropriate product selection for an outer dressing (e.g. a carbon alginate) if necessary.

• Observe and act on signs of excessive bleeding, signs and symptom of infection (excessive pain not relieved by analgesia, raised temperature, offensive wound odour or exudate).

If infection is present:

• Remove the dressing before the agreed date only if it is grossly contaminated

• Assess donor site and review the initial contact dressing.

• If local infection is present, change primary contact dressing to an anti –microbial product.

• Inadine can be used as a low adherent wound contact dressing. The secondary dressing can be secured with Hypafix. The donor site should be redressed daily for four days using Inadine.

• If there is no improvement the site should be reassessed and another antimicrobial dressing could be applied, e.g. Acticoat 7.

• The decision to introduce a silver dressing requires input from nurse unit manager and/or wound care specialist nurse and medical staff. On going wound care management with silver dressings should be undertaken with full knowledge of the product and how to use it (refer to product instructions).

• Inadine should not be used on patients who are sensitive to iodine or povidone-iodine.

• The management of local infection should be based on accurate diagnosis and consideration of patients individual needs.


After Care

• Ensure the patient has appropriate after care advice. The majority of donor sites should heal with minimal scaring, good mobility and no impairment of sensation. The wound should be protected from extremes of temperature, trauma and sun exposure and skin should be moisturized with non-perfumed, water base cream or oil to keep the donor site scar soft and supple.

• Total sun block (Factor 25 or higher) should be used if the newly healed donor site is likely to be exposed to direct sunlight.


References An international consensus, (2008).Principles of best practise: Wound infection in clinical practise. LONDON:MEP. Available from www.mepltd.co.uk Carville, K. (1998). Wound care manual. (3

rd Edition). Australia: Silver Chain Foundation.

Carville, K. (2005). Wound Care Manual. (5

th Edition). Australia: Silver : Chain Foundation.

Dealey, C. (1994). The Care of Wounds. Great Britain: Blackwell Science. Donovan S. (1988). Wound infection and wound swabbing. Professional Nurse 13(11); 757-759. Dunford C. (1999). Hypergranulation tissue. Journal of Wound Care 8 (10) pg 506 European Pressure Ulcer Advisory Panel Guidelines. (1998). Available on line: www.epuap.org

EWMA position Document (2004). Wound Bed Preparation in practice. Available online www.epuap.org EWMA Position Document, (2007).Topical negative pressure in wound management. Retrieved from www.ewma.org/english/english.htm Faller, N., Lawrence, K., Morgan, B., & Keller, B. (1995). Using the nursing process to solve a problem: Post-op tape blisters. Ostomy Wound Management 41(1) pp68-70 Flanagan, M. (1997). Access to clinical education: Wound Management. Edinburgh: Churchill Livingstone. Fowler, A., & Dempsey, A. (1998). Split-thickness skin graft donor sites. Journal of Wound Care 7(8); 399-402. Giordano, C., & Koval, K. (1995). Journal of Orthopaedic Trauma 2, pp171-176. Golbal Wound Academy. Available online: www.globalwoundacademy.com Harris, A. Rolstad, B. (1994). Hypergranulation tissue: a nontraumatic method of Management. Ostomy wound Management 40 (5) 20-2, 24, 26-30 Juniper, H. (1992). Hamilton Base Hospital - Wound care. Hamilton, Vic.: Hamilton-base hospital Kingsley, A. (2001). A proactive approach to wound infection. Nursing standard 30(15) Lawrence, J.C. (1993).Wound infection. Journal of Wound Care. 2(5);150-153. Lay-Flurrie, K. (2004). Wound management to encourage granulation and epithelialisation. Professional nurse papers. 19 (4).


Morris, J., Dowlen, S., Cullen, B. (1994). Early clinical experience with topical collagen in vascular wound care. Wound, ostomy and continence nurse society. Retrieved from www.woundheal.com Morrison, M.J. (1992). A Colour Guide to the Nursing Management of Wounds. Mosby, London, UK. National Pressure Ulcer Advisory Panel (1992/98). Pressure Ulcer Guidelines. Available on: www.npuap.org.

Payne, R., & Martin, M. (1993). Defining and classifying skin tears: Need for a common language; a critique and revision of the Payne-Martin Classification system for skin tears. Ostomy Wound Management, 39(5), 16-20.

Rollins, H. (2000). Hypergranulation at gastrostomy sites. Journal of wound care 9 (3) p 127. Shipperley, T. (1998). Guidelines for pressure sore prevention and management. Journal of Wound Care 7(6); 309-311. Smith&Nephew. (2005). New Zealand Wound Care Catalogue. Steven, W. (1997). Nutrition and wound healing. Nursing Times 93, No.30, 23 July:1-6 Waterlow, J. (2005). Pressure Ulcer Prevention Manual. Avalible online: www.judy-waterlow.co.uk

Acknowledgements

In addition to the reference list, information regarding product selection compiled from:

Capital Coast. Clinical Policy and Procedures Manual, Wound Management

Peach, S. Wound Healing: Self -directed learning package Waikato Hospital

Smith & Nephew Website. Http://www.snwmn.com/wound

Turner, K, Wound Care Specialist Nurse, Tairawhiti District Health

EMSB Course Manual 1996

Jane Widdowson CNL Burns, Plastics and Maxillofacial Surgery, Health Waikato


Useful Websites http://www.medscape.com http://www.smithandnephew.com http://www.healthline.com http://www.neutrogena.co.nz http://www.woundcarecentre.net http://www.woundsource.com http://www.acrymed.com http://surgical-tutor.org.uk http://www.bmj.com http://www.solutions.3m.com http://www.nzwcs.org.nz http://www.woundcare.com http://www.wound.com http://www.journalofwoundcare.com

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