complex wound care in a nutshell · complex wound care in a nutshell k kaim cn wound management...

May 4, 2015 of 41 Kim Kaim, Wound Management Service

Complex Wound Care in a Nutshell

K Kaim CN Wound Management

Gold Coast University Hospital

HEIDI and TIME, the reasons behind why we fill in the wound care pathway ........................... 2!Physiology and function of the skin .............................................................................................. 3!

Function of Skin .......................................................................................................................... 3!Anatomy of Skin .......................................................................................................................... 3!

Hypodermis ................................................................................................................................ 3!Dermis ....................................................................................................................................... 3!Epidermis ................................................................................................................................... 4!

Physiology of Healing ................................................................................................................. 4!Haemostasis .............................................................................................................................. 4!Inflammation .............................................................................................................................. 4!Proliferation ................................................................................................................................ 5!Remodelling ............................................................................................................................... 5!

Assessment and management ....................................................................................................... 6!History .......................................................................................................................................... 6!Examination ................................................................................................................................. 8!

T is for TISSUE .......................................................................................................................... 9!I is for INFECTION / INFLAMMATION .................................................................................... 12!M is for MOISTURE ................................................................................................................. 15!E is for EDGES ........................................................................................................................ 16!

Investigation .............................................................................................................................. 17!Diagnosis ................................................................................................................................... 17!Implementation .......................................................................................................................... 18!

Collaboration ............................................................................................................................ 19!Getting Dressed ....................................................................................................................... 19!

Documentation .............................................................................................................................. 20!Using Photos ............................................................................................................................. 23!Privacy ........................................................................................................................................ 23!Improving Communication ....................................................................................................... 24!

Appendix A – Changes with Aging .............................................................................................. 25!Appendix B – Star Skin Tear Classification System .................................................................. 26!Appendix C – Pressure Ulcer Staging Guide .............................................................................. 29!Appendix D – Three Layer Tubigrip Application ........................................................................ 32!Appendix E – GCHHS Cleaning Procedure ................................................................................. 33!Appendix F – Dressing Selection Guide ..................................................................................... 38!References ..................................................................................................................................... 39!


HEIDI and TIME, the reasons behind why we fill in the wound care pathway Not all wounds are complex, just like not all patient’s presentations will be complex. However, the population we see in the hospitals is becoming more and more complex. People are living longer, with a myriad of medical complaints, which we need to be able to manage when they present to hospital. Managing the needs of the skin is no different from managing the needs of other organs like the heart or brain. The skin needs oxygen, hydration and nutrients, just like all other organs. And when it is deprived of these, like the heart, it does not function to it’s full potential. The problem is that we know, and the body knows, that damage to the skin is much less life threatening than damage to the heart or brain (or liver, or kidneys, or … you get the picture). So in times of crisis, where the body has limited resources (oxygen, nutrients), the body will shift focus away from the skin. And as clinicians, so do we. Look at our primary survey: ABCDE. We don’t even start to consider the function of the skin until E, and then it’s only for warmth. So we need to consciously shift our focus to helping the skin, to make sure that it is receiving the nutrients it needs to repair itself and optimally perform it’s function. Why do we do this? For chronic wounds, those wounds which do not heal in a timely manner, the benefits of performing a comprehensive assessment can be significant(1). There are many factors, systemic, regional, local and environmental, that can impair wound healing and increase the risk of an acute wound becoming a chronic wound(2). Where assessments are not performed correctly there is the risk of delayed healing and the potential for serious complications associated with living with a wound for a prolonged period of time(3). Not only are there risks associated with reduced skin barrier function, such as infection, but there is often pain, social isolation and a poorer quality of life(4, 5). There is also a clear economic impact. Delayed wound healing requires additional nursing and medical resources, higher costs of consumables in wound care, and potentially higher costs of hospital lengths of stay to treat complications(3). The ever-expanding market of dressing products only adds to worsen the situation when you combine a poor assessment with an inappropriate and expensive dressing selection(6). So how do we do this? According to the Australian Wound Management Association, the systematic assessment and collection of data should include(3, 7):

• initial assessment (patient history and systemic observations), • initial and ongoing assessment (wound bed and local area), • optional assessment (regional observations and investigations or assessments relevant to

wound location, aetiology or identification of other risk), and

• care planning (management plan, collaboration, documentation and evaluation).

Sounds a bit vague doesn’t it? Well it is. And that’s probably because the types of wounds are so diverse, and the range and inter dependency of systemic factors in any one individual are so complex, that assessment and management can not be


“standardized” or simplified(6). Instead we rely on prompts provided by the Wound Care Pathway (WCP) and Nurses’ critical thinking skills based on their knowledge of the physiology and function of the skin.

Physiology and function of the skin Function of Skin The skin is the body’s largest organ. In a 70kg person it weighs over 5kg and covers a surface area of almost 2m2. It performs the functions of(8, 9):

• Barrier to mechanical, chemical and physical insults

• Barrier to biological invasion • Moisture retention • Heat retention • Sensory perception (pain, heat, pressure,

vibration, itch) • Communication • Synthesis of vitamin D • Immune surveillance

The barrier function of the skin relies on a well hydrated epidermis. It is also this level of moisture in the stratum corneum that helps to regulate the pliability and elasticity of the skin(10).

Anatomy of Skin The skin has three layers, the thin epidermis which itself is composed of multiple layers, the thicker dermis and the hypodermis or what used to be referred to as “subcutaneous”. The skin is constantly remodeling itself based on external stimuli. Cells are produced in the basal layer of the epidermis and migrate to the outer layers to eventually flake off. This process takes about 28-30 days but is accelerated in diseases like psoriasis(9, 11). Aging, illness, medications and the effects of sunlight on skin also impact on the anatomy of the skin and how it responds to environmental stresses and trauma(12, 13). A table of age related changes and their clinical implications can be seen in Appendix A.

Hypodermis Made up of connective tissue and adipose tissue this layer provides a support framework allowing for attachment to bones and muscle. The adipose tissue in this layer improves it’s ability to provide thermal insulation and cushioning from traumatic forces as well as being a store of energy reserves(11, 14).

Dermis This is a layer of collagen and elastin that provides a support framework for nerve endings, blood vessels, lymphatic capillaries, sweat glands, sebaceous glands and hair follicles. It ranges from 0.5 to 5mm thick. It can be divided in to the papillary layer (the undulating interface with the epidermis) and reticular layer (deeper dermis, is more dense, houses blood supply and adnexals). The superficial venous plexus and deep venous plexus form a network of capillary beds responsible for heat regulation. Lymphatics follow the blood vessels, becoming larger as they go deeper. Innervation of the skin is via the autonomic nervous system affecting things like sweating


and flushing. Sensory fibres register painful stimuli and there are a number of nerve receptors (transducers) that register touch, pressure and vibration(9, 15).

Epidermis The epidermis ranges from 0.05 to 0.1mm thick depending on sex and anatomic location. The blood supply in the dermis does not pass the dermal/epidermal boundary so the epidermis is avascular. Instead, proteins and other nutrients are diffused through the thin basement membrane of the epidermis from the capillary beds of the dermis(9, 16).

Physiology of Healing When a wounding to the skin occurs the body immediately responds to attempt to restore the normal function. The response involves stopping the bleeding, cleaning up the area and fighting off infection, re-establishing a suitable blood supply to the area to be able to make repairs, and repairing the damage. The result is not the regeneration of normal skin but a repair in the form of a scar(17).

Haemostasis Immediately after the injury, the damaged blood and lymphatic vessels undergo vasoconstriction to slow or stop blood loss in the affected area. Under normal conditions platelets circulate freely, they do not interact with intact vasculature. But in an injury they come into contact with disturbed vasculature or extracellular matrix (ECM), this makes them adherent. Once they adhere they break open (degranulate) and release clotting factors and essential growth factors and cytokines. These cytokines attract leukocytes, fibroblasts and keratinocytes. Haemostasis is achieved by formation of a platelet-fibrin plug and the wound space fills with a fibrin clot. The clot provides temporary cover for the wound and acts as a provisional matrix that supports cell migration during healing(16, 18). The growth factors and cytokines released by the platelets are important triggers not only for hemostasis, but as important messages for the later phases of healing. The coagulation cascade is needed to initiate wound healing(16).

Inflammation Neutrophils quickly enter the wound site and begin removing foreign materials, bacteria, and damaged tissue. Other white blood cells and macrophages also begin to arrive. This point signals the initiation of the inflammatory phase. Neutrophil numbers peak after 1−2 days and, in the absence of infection or further damage, rapidly decline. Macrophages continue to increase until day 5, their numbers then decrease slowly as healing proceeds. A significant population of macrophages will still be present for the proliferation phase. The inflammatory phase must be temporary. If there is an infection or other inflammatory process, this retards wound healing(16, 18, 19).


Proliferation Once the inflammatory phase has produced a clean wound area, proliferation begins. This is the ‘repair’ phase of wound healing as new types of cells move in to start the processes of granulation and epithelialization. Granulation fills the base of the wound bed with a nutrient and oxygen rich environment for epithelialization (the migration of epithelial cells over the wound surface) to take place(16, 19). Granulation: Initially, ECM is deposited in an unorganised way. While the wound heals this matrix is continually degraded by proteolysis and resynthesized as needed. For example, for blood vessels to grow into the area (angiogenesis), capillary endothelial cells detach and, using proteases to dissect a pathway, migrate into the haphazard matrix. These capillary sprouts can grow up to a few millimeters per day and are what gives the granulating wound bed its red, ‘granular’ appearance(16, 18). As the granulation phase progresses, myofibroblasts grow across the wound, anchoring to the edges and start to contract, pulling the edges in and decreasing the wound area(18). Epithelialization: At the edges of the wound keratinocytes proliferate and produce daughter cells to migrate into the wound bed. Proteolytic action is required to dissect a pathway for keratinocyte migration, the same as for angiogenesis. If a scab is present the keratinocytes have to burrow underneath the scab and phagocytose and digest any debris they may encounter, not just the ECM. But in a moist environment, without a scab, the migration is easier and healing is accelerated. This discovery led to development of the concept of moist wound healing(18). While this new layer of cells is delicate, most modern wound dressings do not remove them when the dressing is changed. However, if a dressing is allowed to dry out or adhere to the wound, traumatic removal of the dressing may harm the delicate new epithelial layer(16). The process of re-epithelialization is complete when keratinocytes migrating from the wound margins reach each other and contact inhibition induces a cessation of migration. Because keratinocytes are located around adnexal structures, if the wound is superficial and these structures are intact the migration can occur from these sites. It is common to find ‘islands of epithelium’ in a large superficial wound. For full thickness wounds of the same size all of the migration must start at the wound edges, therefore re-epithelialization is slower(18).

Remodelling Now that the wound is closed over and the immediate repairs to the skin are complete, the body has time (up to 2 years actually) to remodel the tissue. Proteolysis continues in this phase, degrading the existing ECM and resynthesizing and cross-linking the new matrix to achieve greater wound strength(16, 18). However, even after months of remodeling, the tensile strength of the repaired skin will not achieve more than 80% of the strength of non-wounded skin(18, 19). The resultant scar tissue is brittle and less elastic than normal skin. Hair follicles and sweat glands do not grow back. Scar tissue is unattractive but it achieves the need of the body to restore skin barrier function and prevent the ingress of bacteria(18).


Assessment and management Years ago, cleverer people than I could see patterns emerging where if certain things were done there would be better wound healing outcomes, like the “moist wound healing” mentioned above. They pulled all these ideas together and wrapped mnemonics around them to make them easier to remember. Two mnemonics that work well together are HEIDI and TIME. These stand for History, Examination, Investigation, Diagnosis and Implementation (HEIDI) and Tissue, Inflammation, Moisture and Edges (TIME). Each of these are represented on the front page of the WCP. The rest of this document will go into more detail about each of these.

History It is important that your assessment considers the WHOLE patient, not just the HOLE in the patient(2). Start by considering what systemic factors might impact on wound healing or impact on your plan. Then look at regional symptoms that will need to also be managed to improve wound healing.

o Systemic ! Disease processes ! Behavioral ! Social

o Regional ! Circulation ! Infection ! Oedema

This is certainly not comprehensive, but to give you an idea of what some of these things might look like:

Systemic Impact on ability to heal plan

Medical Poor circulation – how will the nutrients get to the skin, how will waste/oedema be taken away? Poor oxygenation – how much oxygen is making it to the skin? Metabolic – what impact does diabetes have on wound healing? Auto-immune – for reasons not yet fully understood the body attacks it’s own organs, including the skin and supporting structures.

immune compromised - will not show typical signs of infection, do you watch for other signs or use a topical antimicrobial prophylactically? impaired sensation – can not feel if compression is too tight.

Surgical/ Iatrogenic

Alteration to lymph system such as in lymph node removal for Cancer – can lead to oedema Previous scar tissue – such as from radiation or burns – structure is different to normal skin and slower to heal, can be the source of malignancy Gate changes – amputation will change gate, causing abnormal

working around surgical sites – applying a VAC around ex-fix pins managing exudate from a stoma or fistula


pressures in other areas of the foot, potential for further ulceration in those new areas.

Nutrition Not eating well – often related to age Vegetarian

expect delay – higher protein and caloric intake is required for wound healing

Social Not mobile – pressure related tissue damage, poor calf muscle pump Poor housing or income – poor environmental controls can impact on healing Smoking – reduced oxygen to skin

on feet all day – off-loading? Venous return? cost - can not afford dressings

Medications Corticosteroids Anti-inflammatories Anti-coagulents

Warfarin – would you debride?

Allergies Adhesives Iodine Chlorhexadine

Regional Impact on ability to heal plan

Oedema oedema makes it difficult for adequate distribution of nutrients to feed the skin

Can it be managed?

Pulses indicates ability of nutrients to get to the area

Present? Not present? Do you need to collaborate?

Atrophy, no hair, thin shiney skin

Often associated with lack of pulses, may indicate poor arterial supply, possible claudication pain

Requires collaboration with Vascular as a minimum – do not debride

Haemosiderin staining, varicose veins, ankle flair, etc…

Often associated with oedema or an inverted champagne bottle appearance, may indicate poor venous return

Requires collaboration with Vascular as a minimum

Dry cracked skin Less resilient, increases risk of infection

non-soap cleaning, water intake?, humidity (air conditioning), moisturize

Charcot deformity Changes to gate, potential for ulceration

Requires collaboration with podiatry as a minimum

Contractures May be putting constant pressure onto certain areas or increasing build up of moisture in creases.

Redistribute pressure as able. Manage moisture. Collaborate with occupational therapist and/or physiotherapist

The information we get from the patient’s history gives us a list of items that may result in impaired healing or the potential for skin breakdown. We need to plan to mitigate the impact of as many as we can; ie education on quitting smoking, refer to specialist, or choosing more affordable dressings. There is very limited area for your systemic observations on the WCP. These will most likely need to go into EMR. However you can record the Allergies:


And from their social history you can record any home support they might have.

Your regional assessments such as pulses, sensation, ABPI and (if you can fit them) some descriptions can go into the regional area:

Examination This is where we start to look at the wound (finally!). Again, we are trying to restore the normal function of the skin and support the underlying physiological processes. TIME is very useful here as it focuses our thinking onto those areas that will support wound healing and also gives us a framework to start selecting dressings from. But before we get stuck into TIME, we need to record the size and location of the wound. Serial size measurements need to be recorded as they indicate whether or not a wound is healing; one source recommends that a wound should be at least 30% smaller (surface area) by week 4(20) to be considered on a healing trajectory.

The location of the wound will also impact on determining a diagnosis (if we don’t have one) and contribute to the plan. If there are multiple wounds they can be identified by numbering them, or you can complete separate WCPs for distinctly different regions or wound types.


T is for TISSUE Epithelial Granulating Slough Necrotic

The image above is trying to convey that if the wound is greater than 50% granulating and epithelial, consider protection as your aim. If it falls to the slough and necrotic side then consider debridement. Tissue types tend to be described by colour. Pink is for epithelial, red for granulating, yellow for slough and black for eschar. Also consider other descriptors that may be helpful, these four alone do not always give you a good picture of what’s happening in the wound. The wound in the photo on the right could be described as 90% eschar and 10% granulation tissue. But that could also pertain to a crusty dry scab, and this is really wet; it’s actually coagulated blood from under a blood blister. So maybe rather than saying eschar it could be recorded as wet eschar or even clotted blood firmly adhered to the wound bed. Photos are a great way to record a wound, but even with a photo a good description can be very helpful. The epithelial and granulating tissue types are considered viable. These are alive and doing well. Slough and eschar are not viable, they do not have a blood supply to support healing and they are not alive. It is dead material and it needs to go. The presence of non-viable tissue and debris (foreign bodies/old dressing product/sutures)(21):

• provides a focus for infection • prolongs the inflammatory phase • mechanically obstructs contraction • impedes re-epithelialization • masks underlying fluid collections or

abscesses • makes it difficult to evaluate wound

depth Debridement is the act of removing devitalized tissues from the wound bed. The act of debriding the wound bed not only improves the tissue in the wound bed but it also has a positive impact on inflammation (restores functional extracellular matrix proteins), moisture (reduces exudate) and edges (encourages migration) – the other three components of TIME. A number of things need to be considered before debriding (22):

• Patient preference - including pain

Non Viable

Viable

Epithelial

Granulating

Slough

Necrotic

Debride

Protect


tolerance (plus they might not like maggots) • Skill of the clinician – use your team, get others involved if needed • Risk management – is there a chance you could do more harm than good, is there training

you can do to improve your skills, and again, is there someone who can assist you? • Environmental factors – things like lighting, posture, PPE and risk for contamination of the

environment or further contamination of the wound • Resources - make sure you have everything you need

before you get started. In some areas you may be limited in your options.

• Contraindications - these include propensity to bleed, presence of underlying structures and lack of adequate blood supply.

On the WCP there is an area on the right for you to record your wound tissue observations. I would also like to suggest estimating a percentage coverage. This will help to demonstrate why you’ve chosen to either debride or protect. There is no space for it but you can write next to the tissue description. If debridement is required you need to determine the best method. Most often as Nurses we make use of autolytic and mechanical debridement (the vigorous use of a surgisponge is considered mechanical debridement). But you need to be sure that debridement – whatever the chosen method – is safe. When not to Debride Debridement is not always the preferred option for all wounds. In the case of the necrotic heel or toe in the patient with poor arterial flow. If the area is dry, leave it. It will eventually mummify and auto-amputate. Trying to moisten or remove the tissue is only likely to introduce new ways for microbial invasion that the body is not able to fight(23). Also, for the palliative patient where care is supportive, again if it is dry and not causing any pain, leave it(24). Fungating wounds are challenging in that they produce copious amounts of exudate and odour but are highly vascular. Attempts to debride may cause catastrophic bleeding, however leaving it causes further damage to the surrounding skin from maceration and stress to the patient from the odour(25). Cleaning with something like Prontosan helps to reduce the bioburden, which in turn reduces the exudate and the odour(26). Table 1: Debridement methods Type Mechanisms of action Advantages Disadvantages Who/where

Autolytic

Uses the body’s own enzymes and moisture to rehydrate, soften and liquefy hard eschar and slough using occlusive or semi-occlusive dressings and/or antimicrobial products to create a balanced moist wound environment either by donating or absorbing moisture

Can be used for pre-debridement, when there is a small amount of non-viable tissue !Also suitable for wounds where other forms of debridement are inappropriate

Can be used for maintenance debridement

The process is slow, increasing potential for infection !and maceration

Can be done by both generalist and specialist

Biosurgical

Larvae of the green bottle fly are used to remove necrotic and devitalised tissue from the wound. Larvae are also able to ingest pathogenic organisms in the wound.

Highly selective and rapid

Costs are higher than autolytic debridement, but treatment is short once in place !Not suitable for all patients or wounds

Can be applied by generalist or specialist practitioner with training. Closed bag method reduces skill level required and can be left for 4-5 days


Type Mechanisms of action Advantages Disadvantages Who/where

Hydrosurgical Removal of dead tissue using a high energy saline beam as a cutting implement

Short treatment time and selective. Capable of removing most if not all devitalised tissue from the !wound bed

Requires specialist equipment. There is potential for aerosol spread and it is associated with higher costs

Must be carried out by a specialist practitioner with relevant training. Can be used in a variety of settings

Mechanical

Traditional method involves using wet to dry gauze that dries and adheres to the top layer of the wound bed, which is !‘pulled’ away when the dressing is removed

Newer methods are more selective, faster and relatively pain-free !

Non-selective and traditional methods are potentially harmful Requires frequent dressing changes and can be very painful for the patient

Can be done by both generalist and specialist

Sharp

Removal of dead or devitalised tissue using a scalpel, scissors and/or forceps to just above the viable tissue level. This does not result in total debridement of all non-viable tissue and can be undertaken in conjunction with other therapies (eg autolysis)

Selective and quick. No analgesia is required normally

Clinicians need to be able to distinguish tissue types and understand anatomy as the procedure carries the risk of damage to blood vessels, nerves and tendons

Can be done at the patient’s bedside or in clinic by a skilled practitioner with specialist training

Surgical

Excision or wider resection of non-viable tissue, including the removal of healthy tissue from the wound margins, until a healthy bleeding wound bed is achieved

Selective and is best used on large areas where rapid removal is required

It can be painful for the patient and anaesthetic is normally required !It can be associated with higher costs

Must be performed in the operating theatre by a surgeon, podiatrist or specialist nurses following training

Ultrasonic

Devices deliver ultrasound either in direct contact with the wound bed or via an atomised solution (mist). Most devices include a built-in irrigation system and are supplied with a variety of probes for different wound types

Immediate and selective. It can be used for excisional debridement and/or maintenance debridement over several sessions

Availability issues due to higher costs and requirement for specialist equipment !Requires longer set up and clean up time (involving sterilisation of hand pieces) than sharp debridement.

Must be carried out by competent practitioner with specialist training in a variety of settings

Table copied from Debridement Made Easy(27) At the very bottom of the area where you recorded the tissue types there is a section for debridement. Select the type or write in the blank space to the right. For example, I will often put in Autolytic if I’m using the dressings to debride or None if it is not suitable for debriding.


I is for INFECTION / INFLAMMATION

This image shows the progression from normal inflammation (where the wound is contaminated with opportunistic and transient pathogens) to systemic infection. Below each phase are the actions you can consider for each phase. They are cumulative: so for a wound that appears critically colonized you would want to clean, debride and use a topical antimicrobial. Infection is the outcome of the dynamic interactions that take place between a host and a potential pathogen where the host defense strategies are successfully evaded and there is a negative impact on the host(28). Complex interactions leading to infection are not yet completely understood but have been grouped into 3 broad areas: Contamination

• All wounds will have a transient collection of micro-organisms. When the host’s defenses are adequate and the conditions are not in favour of the micro-organism, they will not multiply and wound healing is not delayed.

Colonisation

• Microbial species are able to successfully grow and replicate but do not progress further to damage the host. Wound healing may be delayed.

Infection

• The level of microbial growth and replication overwhelms the host’s defenses leading to cellular injury and host immunological reactions. Wound may deteriorate.

The image shown above, the infection continuum arrow, is a modified version of the one in “The Microbiology of Wounds” by Percival & Dowd (29). They expand this spread from colonization to infection into 6 stages: Table 2: Stages of microbial invasion Contamination or Transient Stage

This is where bacteria are entering an area and assessing its suitability for colonization. They may have come from surrounding areas on the patient (endogenous) or from the environment or healthcare worker (exogenous). These bacteria are still in a free floating or ‘planktonic’ stage and are vulnerable to eradication.

Clean

Debride

Topical Antimicrobial

Systemic Medications


Colonization Stage 1—Reversible Adhesion

If the bacteria decide that this is a suitable location to grow it will start to attach itself to the host cells using whatever adhesion options it has. This is called reversible adhesion because it is still possible to remove these bacteria with low levels of sheer force (eg saline rinses) and they are also still very susceptible to antimicrobial agents and host defenses. As time goes on the adhesion forces become stronger and the bacteria start to produce extracellular substances to make the area more suitable, thus starting the development of the biofilm. Early colonizing bacteria are typically Staphylococcus and beta hemolytic Streptococci.

Colonization Stage 2—Irreversible Adhesion

At this point the biofilm is now starting to alter the conditions in the wound, making it more difficult for the host defenses and antibiotics to get to the bacteria hiding in it. It is still possible to remove but with a greater amount of force required. This new biofilm encourages other bacteria to join the community. As the community grows and numbers of bacteria increase micro-colonies form and areas of the biofilm become hypoxic, thus creating a suitable environment for anaerobic bacteria as well.

Critical Colonization Stage—Climax Community or “Biofilm”

From a clinical perspective, this is where the wound is sufficiently colonized to exert it’s effects on the wound and prevent healing. From a microbiological point of view it is the critical mass of bacteria that has formed a viable colony but has not yet obtained high enough numbers to invade surrounding tissues (cause infection). There is no set number as different combinations of pathogens and host defenses mean this threshold will vary.

Local Infection Stage Once the colony is mature, growth will continue exponentially and bacteria will be able to use this safe colony as a staging area to invade local tissues. A local wound infection will present clinically with redness (erythema), excessive pain, swelling, heat generation, wound breakdown and increased local temperature. Other more subtle clinical signs of infection have included alteration in exudate, friable granulation tissue that bleeds easily, malodor, and discolored granulation tissue. Reported granulation tissue discolouration has included yellow, green, or blue when bacteria such as Pseudomonas aeruginosa, Streptococci, and Bacteroides fragilis have been cultured.

Systemic Infection Stage

If the biofilm is not disturbed with appropriate wound bed preparation techniques, appropriate dressing management and the use of topical antimicrobials the colony will continue to produce invading bacteria which can lead to bacteria getting into the bloodstream (bacteremia) leading to sepsis or septicemia (multiplication of bacteria in the blood and toxin production), potential organ failure, and in extreme cases, death.

Cleaning, debriding and appropriate use of antimicrobial dressings all help to reduce bioburden and reduce the establishment of a biofilm. Researchers are still unclear how long it takes a biofilm to form. There are many variables including strain of bacteria and it’s adhesion methods, host defenses and type of material being adhered to (ie skin vs implant). There are in-vitro studies (controlled environment, in a lab/not on a live subject) that indicate Staphylococcus aureus can create a biofilm within 2-3 hours and other studies on pig models that have established biofilms within 48 hours(30, 31). The theories behind why these bacteria form biofilms are also varied(32). Biofilms may be created for protection from host defenses, colonization of a nutrient-rich area and/or utilization of the cooperative benefits of a community(32). The biofilm is known to enhance communal protection from phagocytosis by polymorphonuclear leukocytes (PMNs). This means that once the hardier species have started to establish a biofilm the more sensitive species will have a safe place to attach and grow. It may even make these sensitive species appear to be ‘resistant’. Once the oxygen starts to be depleted the anaerobes can also join the community. This synergy between aerobic and anaerobic bacteria has been documented to increase the severity of an infection(33, 34).


The site the bacteria choose to colonize may be nutrient rich, but the bacteria still need to be able to unlock those nutrients including glycoproteins, sugars, and proteins. In order to do this numerous enzymes are required, ranging from proteases to glycosidases. Having a community of bacteria with a range of different enzymatic properties means that more nutrients can be ‘unlocked’ which would benefit the community as a whole(29). By creating communities where different bacteria inhabit niche micro-habitats best suited for their survival, and where the bacteria cooperate to meet their collective metabolic requirements, the biofilm is more likely to succeed. If we do not remove the biofilm, then the wound is less likely to heal(29, 35). How do we know it’s infected? Identifying the difference between inflammation and infection can be tricky. Generally speaking, erythema, warmth, exudate and pain can be associated with both. In a person who is immunocompromised or has a reduced immune response for another reason (such as in the feet of people with diabetes) there may be no local sign that infection is present; the first signs could be rigors or pain at regional lymph nodes(36, 37). Chronic and acute wounds are also assessed differently because in acute wounds we have the window of the first 48 hours where we have an expectation of what the ‘normal’ wound healing will look like. We expect that for the acute wound, after 48 hours there should be a reduction in erythema, warmth, exudate and pain and if these do not reduce, or if they get worse, there may be a local infection. For chronic wounds Sibbald et al(38) recommend two mnemonics to help remember what to look for and to also differentiate between superficial and deep bacterial burden. The difference being that superficial bacterial burden may respond to topical antimicrobials whereas deep infections usually require the use of systemic medications. For superficial infection, think of NERDS:

• Nonhealing wounds • Exudative wounds • Red and bleeding wound surface granulation tissue (friable) • Debris (yellow or black necrotic tissue) on the wound surface • Smell or unpleasant odour from the wound.

For deep infection, think of STONES:

• Size is bigger • Temperature increased • Os [probe to or exposed bone] • New or satellite areas of breakdown • Exudate, erythema, edema • Smell

Record your finding in the WCP, just under where you recorded tissue types. There is a small amount of space if you have other findings you would like recorded (ie immunocompromised).


M is for MOISTURE

An imbalance in moisture results in:

• Desiccation - slows epithelial cell migration • Maceration – damage to wound margin

The aim is to restore epithelial cell migration through the management of exudate and its underlying causes(39). At the edges of the wound keratinocytes proliferate and produce daughter cells to migrate into the wound bed. If a scab is present proteases have to break down and clear a path for the keratinocytes to burrow underneath the scab. But in a moist environment, without a scab, the migration is easier and healing is accelerated. This discovery led to development of the concept of moist wound healing(18). While this new layer of cells is delicate, most modern wound dressings do not remove them when the dressing is changed. However, if a dressing is allowed to dry out or adhere to the wound, traumatic removal of the dressing may harm the delicate new epithelial layer(16). Moisture in a wound can be modified directly or indirectly(40):

• Direct o The use of absorbent or moisture-balancing dressings o The use of compression and/or elevation to eliminate fluid from the wound site o The use of Topical Negative Pressure (TNP) with devises such as the VAC -

Vacuum Assisted Closure • Indirect

o Control of infection or bacterial load o Control of oedema by systemic therapy such as the treatment of heart failure o Use of immunosuppression or steroids to control inflammatory exudate from

wounds such as pyoderma gangrenousum, vasculitic or rheumatoid ulcers General observations about dressings:

• Dressing that contribute to wound moisture include TenderWet, hydrogels, Honey, Iodosorb Paste and other “Wet” dressings.

• Dressings that conserve moisture (stop if from evaporating away and/or handle a small amount of exudate) include films and hydrocolloids.

• Moderate amounts of exudate can be managed by hydrofibres, alginates, foams, simple dressings (like melolin if changed frequently) and dressings which contain these items as one of its components. An example of a combination dressing is the Aquacel Surgical, which has a hydrofibre interface and a hydrocolloid adhesive backing.

• High amounts of exudate need either much more frequent changes of simpler dressings (such as combine) or use of high absorbency dressings such as Zetuvit or Drymax.

Too Dry: Presence of eschar, slower ‘2-stage’ healing

Too Wet: Maceration and excoriation damages periwound skin and slows healing

Just right: Warm, moist wound healing

Manage Moisture

Contribute/Conserve Moisture


Alternatively incontinence aids (with the elastic trimmed off) can be secured to the exuding area. Products like blueys/pinkies and improperly secured incontinence aids can be trip hazards so please use these carefully.

• Other options. There are some dressings which will allow the exudate to pass through to a secondary dressings so that the primary dressing does not have to get changed as often as the cheaper secondary dressing but still provide the benefits of the longer wear time for the primary dressing (examples are mepilex transfer, aquacel, tulle gras, and silicone interface dressings). Exudate management systems involving hydrocolloid seals and plastic bags are also an option. Topical negative pressure therapy can also be considered.

When recording moisture in the WCP, consider also adding descriptions if it is discoloured (ie bright yellow or green) and to describe it’s consistency (ie serous, thin, thick, custardy, chunky).

E is for EDGES

Wound edges that are: • rolled • at a different level to the wound bed • undermined

do not allow for the migration of keratinocytes across the wound bed. Addressing the underlying cause should be the answer, but debridement or the use of adjunctive therapies may need to be considered. The aim is to encourage keratinocyte migration and wound contraction; this will be seen as an advancing wound edge and reduction in wound bed size(21). The edges really are the final indicator to let you know that everything else you did with T, I, and M is working or not. The other thing to remember is that these edges, and the periwound skin, need to be protected during the course of the wound treatment. Things like excess moisture and increased bioburden levels can affect the periwound skin. The use of adhesives can cause damage from their frequent removal or may trigger an allergic response. Products used to debride necrotic tissue can be just as ready to break down the healthy tissue so care must be taken. The use of moisturizers/emollients and an adequate intake of water, daily, help to give the skin resilience(41). Simple periwound skin protection can be obtained by using barrier wipes, creams or sprays(26). In some cases (TNPT and exudate management bags) hydrocolloid dressings and pastes need to be used to ensure adequate protection.


Investigation Do we have enough information to understand the underlying problem (diagnosis) and create a comprehensive management plan, or do we need more? Examples of investigations we can do at the beside are things like checking for the presence of pulses and sensation. Get into the practice (on healthy patients) of finding brachial, dorsalis pedis, posterior tibial and popliteal pulses. We don’t tend to use these often so don’t get much practice. Also, having, and knowing how to use, a monofilament pen or tuning fork to determine sensation perception is very useful. Marking on the WCP is a simple “+” or “-“, but as usual, you can be more descriptive. Also, for the patient with diabetes it may also be beneficial to mark the location of callouses (often with a Δ – then refer to the podiatrist!). Other investigations undertaken by the doctors include pathology and medical imaging. You can always recommend investigations be done when discussing your patient with the doctor. For example, in a wound with bone on view, it is reasonable to recommend imaging for osteomyelitis. In legs with signs of arterial or venous disease, it is reasonable to recommend an ABPI. For the wound bed that is friable, has an odd or pearly texture, especially where the patient has a history of skin cancers, it is reasonable to recommend a biopsy. The doctor may or may not wish to include this in their plan, but at least you have brought attention to a potential problem. Remember to use your SBAR communication skills when making these recommendations.

Diagnosis We understand a diagnosis to be the identification of a disease or medical condition by examination of the signs, symptoms and any tests performed(42). If a person comes into hospital with chest pain the medical staff will look at all the signs and symptoms, run investigations, and eventually come up with a diagnosis for the cause of the chest pain; Myocardial infarct or Ischaemic Heart Disease, for example. There is then a set treatment protocol that includes anti-coagulants, vasodilators, blood pressure modification and cholesterol reducing drugs if needed, and a certain set of observations at regular intervals. The person may go on to see other allied health professionals to assist with reconditioning, long term strategies for healthy heart maintenance, social workers and home help to improve independence, and potentially surgical interventions to remove the cause of the infarction. This all makes perfect sense. So why is it that when a person comes in with an infected ulcer (which is just a symptom) they do not undergo the same process? “Ulcer” or “Chronic Wound” is not a diagnosis, but rather the manifestation of an underlying disease process(43). So if we give the person antibiotics and a wound dressing, then discharge them home when the infection settles … it’s like giving the person with chest pain oxycodone and then sending them home when the pain settles. We’re just addressing a symptom, not the cause. We need an accurate diagnosis to identify comorbidities and complications that may contribute to delayed healing and to drive appropriate treatment(42). Some diagnoses are obvious, like when the patient hits their arm on the rollator and gets a skin tear. This is a skin tear (preferably with appropriate category) secondary to trauma. We can usually put a diagnosis to the acute wounds and some chronic wounds like pressure injuries. However, other chronic wounds that are not healing with optimum treatment may either have no diagnosis, or the wrong one. Let’s have another look at the woman who hit her arm on the rollator. The wound is cleaned, edges re-apposed, and dressing with compression applied. After a few months the woman is seen again, she still has a small area that appears to heal, then gets a bit crusty and starts bleeding again. The area is slightly raised compared to the surrounding skin. Is the diagnosis of skin tear still appropriate? Or should there be further investigations to determine what is happening at the cellular level to stop this wound completely healing? This is where we need to collect as much information and discuss the need for further investigations and possibly referral with the treating team.


Some examples of wound diagnoses are: • Skin Tear (category 1a, 1b, 2a, 2b or 3 as per the STAR classification system – see

Appendix B) • Pressure Injury (stage I, II, III, IV, mucosal, unstageable, or suspected deep tissue injury as

per the NPUAP classification system – see Appendix C) • Surgical • Diabetic Foot Ulcer • Venous Ulcer • Arterial Ulcer • Mixed Venous/Arterial Ulcer • Cancer (SCC, BCC, solar keratosis, melanoma, and many others) • Vasculitis • Pyoderma Gangrenosum • Too many dermatological conditions to mention!

The important thing to remember is that we need to know what it is to be able to create the most appropriate care plan. Failure to correctly diagnose a wound type may result in failed management and wasted resources. Interventions based on accurate diagnosis delivers benefits to patients, healthcare systems and society(44). Let’s look at the person with chest pain that we sent home. What’s going to happen? Is the pain going to come back? Get worse? This patient is likely to re-present to hospital time and time again with the same symptoms, or worse. The underlying condition (whatever is causing the infarct) is not likely to improve by itself and will generally follow a deteriorating course. So now let’s look at a person with an infected ulcer. It’s been there a while, the antibiotics reduce the redness and swelling and the wound appears to start healing, but it has done this before, and will do it again. Why? We have no diagnosis so we don’t know why. Because we have not treated the cause we have wasted time and resources and the person with the wound has to continue to live with it and bear the costs, everyday. What if the diagnosis of the wound is a squamous cell carcinoma or peripheral venous disease? We need a diagnosis to ensure the wound is adequately managed and all contributory factors are addressed(42, 43). As our society continues to age, and lifestyle diseases continue to increase, the problem of pressure injuries and diabetic ulcers is growing. These and other common types of chronic wounds will require accurate and concise diagnosis and appropriate treatment as part of holistic care(20). Once you have a diagnosis, write it on the WCP.

Implementation Once you have collected your history, done your examination, completed any other investigations and determined the wound diagnosis, you will be ready to put together your comprehensive wound care plan. In all of these previous steps you will have identified risks to healing or other things that will impact on healing or your care plan. For example: History • Smoking

• Heart Failure with Fluid overload

• Loss of 10kg in the last 2 months

• Education to quit smoking • The treating team will be managing the fluid overload, but

the condition will impact on any plans for compression: compression shifts the fluid from the legs back into circulation, which will exacerbate the fluid overload problem.

• Refer to dietician for nutritional support in light of the extra requirements needed for wound healing

Examination >50% slough High exudate Oedema Varicose veins, ankle flair, haemosiderin staining Palpable dorsalis pedis, warm feet.

• debride • Manage moisture, prevent periwound maceration • Manage oedema


Investigation ABPI: Left leg 1, Right leg 1.1 Long duration of ulcer (6 years) and ‘lumpy’ tissue in part of the wound base

• Legs will tolerate compression but there is still the problem of fluid shifts. Start with single layer tubigrip and slowly increase layers if tolerated (see Appendix D)

• Discuss with the treating team the need to rule out Marjolin’s ulcer via biospy.

Diagnosis ?Venous Leg Ulcer Discuss with the treating team the need to refer to Vascular for a diagnosis and plan for compression.

Collaboration Communication and collaboration in wound care is essential. Gottrup(45) refers to a study done in one hospital in Copenhagen where they found in the majority of cases that:

• Chronic wounds were not having diagnostic examinations • Venous leg ulcers were not receiving compression therapy • Patients with foot ulcers were not being assessed for Diabetes Mellitus • Patients with pressure ulcers were not having off-loading treatment

Why? Did they not have a diagnosis or were the people looking after these patients missing the necessary skills? Gottrup proposes that to remedy this and provide optimum care for the complex wound care patient, care needs to be delivered by teams, and not individuals. Who are the collaborators that make up these teams? We mentioned the patient’s treating team, specialists and allied health above. What about the patient and their family/carers or other support in the home? Are they in a nursing home? For the complex, chronic wound, evidence tells us that we need a coordinated, multidisciplinary care team, including participation from at-home caregivers and the patient, for optimum results. Specialist-lead advanced care is needed when there is evidence of ischemia, inability to comply with wound-care regimens, suspected malignancy, and peripheral arterial disease(46). This is best supplemented with a member of the allied health care team (for example, occupational therapist, physical therapist, podiatrist, dietitian, social worker and so on)(20). How do you know when to refer? Whenever you are in doubt regarding etiology, suspected malignancy, evidence of ischemia or wounds that do not demonstrate an adequate response to treatment(46). By getting the right people involved we can allow for earlier diagnosis, better management, and may reduce the cost of treating wounds(46). With the level of complexity in the patients we see, accurate wound diagnosis and development of successful treatments plans can be quite challenging(20). But it can be equally rewarding.

In the wound care pathway you can record who referrals were sent to, you can also add in the date the referral was sent. Alternatively, where patient’s have an appointment with a specialist, you can write the date of the appointment next to the specialist.

Getting Dressed There is usually a lot to consider, you’re probably taking a dressing off, as well as putting one on. You need to make sure your work area is clean so that you’re not introducing new bugs to the wound. What supplies will you need? How will you keep your work area as clean as possible? When putting the plan together, consider using the framework: Cleaning Does it need cleaning? Should it get wet? How should it be cleaned

and with what solutions? (Appendix E – Cleaning Protocol) Emollient It has been shown that moisturizing improves the barrier function of the

skin and skin resilience(10, 47). The use of barrier creams or sprays can


also protect periwound skin from damage caused by exudate, other body fluids or adhesives(48, 49).

Primary dressing This is the dressing that manages the moisture and microbial balance at the wound surface. (see Appendix F for a dressing guide)

Secondary dressing This may be needed to hold the dressing in place and/or for excess exudate management. Consider the effect of adhesives on the skin and any skin allergies. (see Appendix F for a dressing guide)

Retention/compression Retention dressings tend to be used in preference to adhesives on vulnerable skin. Compression is used primarily for oedema and scar management.

Frequency Based on the recommendations of the manufacturer, however clinical judgment must be applied to each individual’s circumstance.

In the WCP there is a section for cleaning and debriding, but I usually write the details of the dressing plan in the wound plan/products area as well, because there is more space for detailed information.

Documentation What is documentation? Within Queensland Health we have many ways in which we can record interactions with a patient. There are care pathways, care plans, paper records, electronic records, photographs, discharge plans, emails, letters, observation charts, handover sheets, SMS … it’s information overload. All of these pieces of information, together, are meant to provide a record of care for each person seen by the hospital. And while there are plenty of reports to say that nurses all over the world are producing poor documentation there are none to state exactly what format good documentation should take. In fact, the reports even contradict themselves. For example: it is generally accepted that good documentation will show an accurate, chronological record of events, it is also generally accepted that good documentation will clearly show observation-intervention-outcome. The problem being that observation, intervention and outcome do not necessarily happen exactly one time slot after another and linking up outcomes to interventions can take some searching in a patient record which contains an accurate, chronological record of events(50). So why do we keep all these records? The aim of clinical recordkeeping is to(51):

• help to improve accountability • show how decisions related to patient care were made • support the delivery of services • support effective clinical judgments and decisions • support patient care and communications • make continuity of care easier • provide documentary evidence of services delivered • promote better communication and sharing of information between members of the multi-

professional healthcare team • help to identify risks, and enable early detection of complications


• support clinical audits, research, allocation of resources and performance planning • help to address complaints or legal processes

As clinicians, documentation isn’t just a time consuming nuisance(52) that is “something we have to do” it’s also a great tool to promote proactive care and risk management(53). We use the historical documentation to determine if there has been improvement or deterioration, or if there are potential risks, and we use this information to modify the plan of care if necessary. A study in the UK showed that poor documentation contributed to the failure to identify when patients were deteriorating(50). But rather than embrace this tool as a means of improving patient care it is more often thought of as just a way to address nurse accountability(50). Points to remember when completing documentation Although there is not a specific guide or plan to follow for every nursing situation there are some points to remember which will improve the quality of your clinical documentation(51):

• Handwriting needs to be legible. The use of electronic records has helped with this but not all communications are typed. If it can’t be read then not only is it not useful as a tool for managing patient care, but it won’t help you in court either.

• All entries should be identified with name and title as well as be signed. EMR makes this easy as each entry is tagged by your login – do not share your login or use someone else’s login to write up your notes.

• All entries should show date and time. Again, EMR puts a date/time stamp on each entry but we need to remember to put it on any hand-written communications, this includes letters.

• Be accurate and clear. Records should be factual and not include unnecessary abbreviations, jargon, meaningless phrases or irrelevant speculation. Remember to use quantifiable data when you can(54), “looks good” and “normal” are not quantifiable. BTW, it is not appropriate to use text-speak, but like OMG you should know that ;-> Consider that the people reading this will not just be the next nurse on duty but may have very varied backgrounds (possibly including legal personnel and research assistants) and use language accordingly.

• Be concise and relevant. You will need to use your professional judgment to decide what is relevant. Tools and frameworks can help with this but context is also important. For example, if a person talks about how cold it is lately you would not necessarily record this, but if they explain that they have no heating, drafts through the floor, sleep on a cot and have no blankets this is a potential health and healing risk that needs to be addressed, so you would write about it and include your referral to the social worker.

• You should record details of any assessments undertaken, and provide clear evidence supporting plans of care or treatments chosen. If during your assessment you find a new issue then write in both the issue and steps taken to address it (Problem > Intervention). Equally, if you put in place a new plan you need to write about why (Assessment > Intervention)(54).

• You must not alter or destroy any records. If you need to alter an entry you have made draw a single line through the original, write up the changes, and initial the error. The original entry must still be readable as changes where the original information has been obliterated may be seen as a cover-up(53). EMR does not allow you to obliterate data.

• You should not falsify records. You may say A-DUH, but this is easier to get caught out with than you think. Especially where there are tick and flick forms involved. Don’t tick yes to “pedal pulses palpable” when the person is a bilateral below knee amputee.

• Get patients involved, if it is appropriate. Patients can be asked to keep diaries about their blood sugar levels, pain levels, or whatever is relevant, these can all form a part of their care documentation.


• Records should be readable when photocopied or scanned. Quite a lot gets scanned into EMR and there is still a need for documents to be photocopied for things like inter-hospital transfers and coroner investigations.

Remember, the information recorded is for you and your colleagues to use to ensure completeness of care for your patients. Legal-eeze There are also a few things to consider from a legal standpoint:

• Tone. Ensure all wording is professional. Communication which is seen to be derogatory or written in such a way as to humiliate / anger / prejudice may be considered slanderous in a court of law. As an example, “Patient arrived at 1330 for an 1100 appointment”, not “Patient couldn’t be bothered to arrive on time”. Reference to other staff or the organization in this manner can also result in a defamation suit(53).

• Timely. Notes written some time after the service was given are subject to recall errors(53). Documentation is often seen as less important than patient cares and is therefore left to last in the shift and then hurried because we run out of time. This can lead to a lack of relevant information being recorded(52).

• Missing information/illegible. Where there is a lack of information to make a legal ruling it may come down to patient recollection. Pt is more likely to remember the occasion but might not remember education, cautions, risks(53). Illegible – falls back to recollection(53).

• Abbr. I’d like to say no abbreviations but they are almost part of the natural language of health (Pt BIBA c/o SOB, etc…). Minimize what abbreviations are used, ensure that they are considered universally known and not just specific to your specialty, and if in doubt, spell it out(53).

The record you write today could be used in an investigation in years to come. It may be the primary source of information in deciding the outcome of an investigation(50). “The test of a good clinical record – Will this clinical record tell the whole story in a year?(53)” Queensland Health’s “Good Clinical Documentation Guide” is worth a read. Barriers In the literature there are a number of reasons given to explain why documentation is not optimal. These include:

• Rapid patient turnover(50) and plethora of ‘mandatory forms’ means too much paperwork to be completed.

• Lack of time(52). With more patients, higher acuity, broader range of responsibilities and minimal staffing nurses are spread thin.

• Documentation is seen as being “less important” than patient care(52). • Belief that you don’t need to document the obvious(50). Things that seem so fundamental

to care they shouldn’t need to be written still do! If it’s not written, it’s not done, and this may be seen as neglect.

The creation of care plans, pathways, observation forms and other standard forms are intended to ensure important information is not missed and that treatment is guided by protocols. Data collection forms also try to display trends in such a way as to make it easier and quicker to identify changes. But are they all necessary for every patient? Also, nurses are very resourceful and we come up with many ways to make things easier/quicker. We may have a standard entry that says “meds as charted, cares as documented in care plan”. Is this good documentation? Think about the barriers in your area and what could be done remove these barriers and improve your documentation.


Tools The notes you write are not just for good patient care and legal reasons but these are also notes to yourself, to help you jog your own memory later(54). So you need to write these in a format that makes sense to you. There are a number of general formats you could adopt such as SOAP (subjective, objective, assessment, plan) and ADPIE (assess, diagnose, plan, implement, evaluate)(52) and more wound specific ones like HEIDI and TIME which we have been talking about in this document that are the basis for the Queensland Health form, the Wound Care Pathway. And finally, sometimes it works best to work chronologically – this is basically just recalling the steps taken from the start of the episode of care to the end. This may best be used when focused on a specific task by considering the steps completed in the task and making a reporting framework from them. For example, when writing about a dressing change you would use the headings cleaning, emollient, primary dressing, secondary dressing, compression or retention and other/frequency as this is the order of application. There is no single tool or strategy that fits all needs, is comprehensive and is lightning fast to complete. It’s a matter of keeping in mind the purpose of the documentation and working out what format best suits your nursing/writing style.

Using Photos Wound photography is a whole education session in itself. Consent, storage, privacy, as well as the actual taking of the photo all need to be considered. But the main points for us to remember are:

• Ensure consent • Consider privacy and dignity • Have something in the photo to use as a scale reference • Upload photos into a specific “clinical photograph” document type in EMR • Do not use personal phones or anything that is not secured • Date and sign photos just like all other documentation

Privacy Privacy and confidentiality are paramount in health care (again, this takes up an entire education session in itself). Privacy must be considered in relation to documentation, including photographs (as mentioned above), emails and other correspondence. Some tips when writing your notes include:

• Do not refer to patients, other than your patient, by name. So if Mr Jones in bed 30 rang the buzzer because your patient’s breathing sounded funny you would just refer to him as the patient in bed 30.

• Do not share/take home patient information. This is one of the reasons why you do not use your own phone to take photographs. Documentation can only be shared with other health professionals in the course of treatment IF the patient consents. There are some other instances but it is best to refer any requests to your Nurse Unit Manager.

• If you need to carry results, charts or other patient documentation from one location to another ensure that you keep it covered so that patient information is not revealed.

• If you are completing notes in a public area (ie. Computer visible to public) discuss this with your team leader to work out options for maintaining patient privacy.


Improving Communication How can we improve wound communication? A lot of the information in the documentation section above relates to your EMR documentation. Which is incredibly important, as we have discussed. But how many of you have time to go back through all the EMR entries of all your patients since the last time you saw them? Handover is where you probably get most of your information, highlighting the importance for a good systematic handover plan. But for skin and wounds, how much detail do you cover? Not much more than “needs PAC @ x-time” and “Dressing to right shoulder due tomorrow”. And to keep handover concise that is what you want. So you need to put as much detail as you can into the bedside Wound Care Pathway. The front page of the wound care pathway is incredibly important; it shows the reasoning behind your plan as well as the details of your plan. By looking at the front page you can quickly see that the wound is a (Diagnosis) Stage 3 Pressure Injury, for example, that you are allergic to iodine (so we won’t be using Iodosorb), where the wound is (so where to keep pressure off), etc… Also, when it comes time for discharge you can quickly look at the care plan and see who you need to call (Community Nursing Agency) to get them to resume/increase services instead of trying to find the information somewhere in EMR. Also, by looking at the referrals you can see what referrals were made and follow up to see if they were done and what recommendations they made. For example, if a Vascular or Plastics referral was done and the patient was seen – what is their recommendation for wound care? You will need to look this up in EMR but at least you can narrow your search. Then you can create a new wound care plan with their recommendations and you can even note under referrals the date the patient was seen or when their next r/v is with that team. The plan that is written on the front of the WCP is the plan that should be followed on the remaining pages of that WCP. And a plan needs to be given time to have a chance to take effect. On the front page of the WCP there is also a date at the bottom for the next planned review – this is not the next dressing change. Let’s look at a patient with a highly exuding, critically colonised venous leg ulcer. You may have put a plan in place to use 3 layer Tubigrip for compression and Sorbact for the bioburden. You have scheduled it for daily dressing changes due to the very high level of exudate and choice of antimicrobial. You would expect that in about a week this should have settled. Therefore, your dressing changes are daily but your review is not for one week. If the next person comes in and changes the plan at the next dressing change – how do you know if the last plan had any effect? Let’s look at this scenario for comparison: a doctor prescribes BD Cephtriaxone, the first dose is given. When the patient is due for the second dose another doctor decides, no, we’ll use Doxycycline OD. Then, when the next dose is due another doctor comes in and says, no, let’s go for Flucloxacillin QID. They’re all suitable for use in skin infections, but do we do this? No! So why would we do it in wound care? Yes, there will always be multiple viable plans for the one wound, but we have to pick what appears to be the ‘best’ plan and stick with it for enough time to objectively (ie change in size) and subjectively (ie change in exudate levels) assess the plan’s performance. Do situations change – of course they do! But we need to effectively communicate reasons for change. This could be a change in patient status, new observation in the wound or limb, reaction to selected dressings, pain, etc… Clearly document the reason for the change of plan and the new plan. I have found there is very limited space to do this within the pages of the WCP so I tend to “cease” the current WCP and create a new one where I can fully record the observations and wound care plan where there is space to do so - on the front page.


Appendix A – Changes with Aging Physiologic change Pathologic change Clinical significance Thinning of epidermis and dermis Increased vulnerability to

mechanical trauma, especially shearing and friction

Increased incidence of skin tears

Flattening of dermal papillae Increased risk of blister formation

Increased susceptibility to infection

Slowdown in turnover rate of epidermis; decrease in ratio of proliferative-to-differentiated keratinocytes

Delayed cellular migration and proliferation.

Increased time to re-epithelialization.

Decreased wound contraction Longer healing times after injury or surgery

Decrease in elastin fibres Loss of elasticity Lax skin and wrinkling, with loss of self-esteem and/or depression

Decrease in vascularity and supporting structures in dermis

Fragile, easily broken blood vessels.

Skin easily bruised (senile purpura)

Decreased wound capillary growth

Increased risk of wound dehiscence

Decrease in vascular plexus, blunted capillary loops

Loss of thermoregulatory ability

Hypothermia, heat stroke

Changes in and loss of collagen and elastin fibres

Decreased tensile strength, lower layers more susceptible to injury

Increased risk of pressure damage to elderly skin, decubitus ulcers

Delayed collagen remodeling Longer healing times after injury or surgery

Impaired immune response Impaired inflammatory response

Impaired wound healing

Impaired delayed hypersensitivity reaction

Increased risk of severe injury from irritants

Decreased production of cytokines

Impaired immune function

Decrease in number of Langerhans cells

Increased susceptibility to photocarcinogenesis, false-negative delayed hypersensitivity tests

Impaired neurologic responses Reduced sensation Increased risk of thermal or other accidental injury

Decreased skin thickness Loss of cushioning and support

Increased risk of pressure damage, decubitus ulcers Increased susceptibility to skin tears, bruising

Decreased vitamin D precursor production

Osteoperosis and bone fractures

Atrophy of sweat glands Decreased sweating Less ability to thrermoregulate, hypothermia Dry skin, xerosis

Reduced stratum corneum lipids Decreased ability to retain water

Variable response to topical medications, altered sensitivity to irritants

Structural changes in stratum corneum

Altered barrier function Variable response to topical medications, altered sensitivity to irritants

Reduced movement of water from dermis to epidermis

Reduced epidermal hydration Dry skin, xerosis

Decrease in melanocytes Loss of ability to tan, greater susceptibility to solar radiation

Cutaneous neoplasms

Greying hair Loss of self-esteem Copied from Farage et al (2009)(55)


Appendix B – 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 Category 1b Category 2a Category 2b Category 3 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.

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.

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.

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.

A skin tear where the skin flap is completely absent.

Skin Tear Audit Research (STAR). Silver Chain Nursing Association and School of Nursing and Midwifery, Curtin University of Technology. Revised 4/2/2010.

STAR Skin Tear Classification System

STAR Skin Tear Classification System Glossary

x Skin Tear: “a traumatic wound occurring principally on the extremities of older adults, as a result of friction alone or shearing and friction forces which separate the epidermis from the dermis (partial thickness wound) or which separate both the epidermis and the dermis from underlying structures (full thickness wound)”1.

x Pale, dusky or darkened skin or flap colour: when compared to the individual’s ‘normal’ surrounding skin, may indicate

ischaemia or the presence of haematoma, which may affect skin or flap viability. x Ischaemia: inadequate tissue perfusion as evidenced by pale, dusky or darkened tissue. x Haematoma: a collection of blood or clot under the flap or realigned skin. x Realign: to replace the skin or flap into the normal anatomical position without undue stretching. x Linear skin tear: a skin split or the skin splitting in a straight line. x Flap skin tear: a segment of skin or skin and underlying tissue that is separated from the underlying structures. References:

1 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.

2 Photographs courtesy of the Skin Tear Audit Research (STAR) photographic library, Silver Chain Nursing Association and School of Nursing and Midwifery, Curtin University of Technology.

3 Carville, K., Lewin, G., Newall, N., Haslehurst, P., Michael, R., Santamaria, N., & Roberts, P. (2007). STAR: A consensus for skin tear classification. Primary Intention, 15(1), 18-28.

STAR Tool G 4/2/2010


Appendix C – Pressure Ulcer Staging Guide

Category/Stage I: Non-blanchable redness of intact skin Intact skin with non-blanchable erythema of a localized area usually over a bony prominence. Discoloration of the skin, warmth, edema, hardness or pain may also be present. Darkly pigmented skin may not have visible blanching. Further description: The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue. Category/Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons.

Category/Stage II: Partial thickness skin loss or blister Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum- filled or sero-sanginous filled blister. Further description: Presents as a shiny or dry shallow ulcer without slough or bruising. This category/stage should not be used to describe skin tears, tape burns, incontinence associated dermatitis, maceration or excoriation.


Category/Stage III: Full thickness skin loss (fat visible) Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Some slough may be present. May include undermining and tunneling. Further description: The depth of a Category/Stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and Category/Stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep Category/Stage III pressure ulcers. Bone/tendon is not visible or directly palpable.

Category/Stage IV: Full thickness tissue loss (muscle/bone visible) Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present. Often include undermining and tunneling. Further description: The depth of a Category/Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Category/Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis or osteitis likely to occur. Exposed bone/muscle is visible or directly palpable.

Unstageable/ Unclassified: Full thickness skin or tissue loss – depth unknown Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Further description: Until enough slough and/or eschar are removed to expose the base of the wound, the true depth cannot be determined; but it will be either a Category/Stage III or IV. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as “the body’s natural (biological) cover” and should not be removed.


Suspected Deep Tissue Injury-depth unknown Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. Further description: The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with treatment. Information from The Australian Wound Management Association (AWMA) Pan Pacific Guideline Development Steering Committee and the European Pressure Ulcer Advisory Panel / National Pressure Ulcer Advisory Panel.(56, 57)


Appendix D – Three Layer Tubigrip Application


Appendix E – GCHHS Cleaning Procedure

Document ID PRO0096

Wound Cleansing Gold Coast Hospital and Health Service

1 Purpose The aim of wound cleansing is to remove and reduce the number of colonised pathogens in the wound base. It does this by removing surface contaminants, bacteria and remnants of previous dressings from the wound surface and its surrounding skin. Wound cleansing involves the selection and use of a solution, with or without pressure, to mechanically dislodge debris and pathogens.

2 Scope This procedure relates to all staff directly engaged in the care of wounds. Thorough wound cleansing should precede any wound assessment.

Compliance with this procedure is mandatory.

3 Procedure for Wound Cleansing Prior to cleansing a wound:

x Provide adequate pain relief x Wash hands and put on appropriate personal protective

equipment (PPE) x Ensure patient’s privacy

During wound cleansing:

x Continually assess patient’s comfort. Certain solutions and techniques may be more painful than others and you may need to change.

x Be aware of your positioning and your environment so as not to cause harm/discomfort to yourself or your patient.

After wound cleansing:

x Appropriately dispose of contaminated waste x Towel dry surrounding tissue; pat the skin as opposed

to rubbing it x Apply moisturisers as appropriate x Dress wound prior to returning patient to bed x Remove PPE and wash hands

Custodian/Review Officer: CNC Wound Care Team Version no: 5 Applicable To: All GCHHS employees Approval Date: 12/02/2014 Effective Date: 25/02/2014 Next Review Date: 06/02/2017 Authority: Nicole Morley, Nurse Practitioner Vascular Approving Officer: Title: General Manager, Specialty and Procedural Services Name: Dr Lance Le Ray Signature Date: . Supersedes: GCDPRO0096v4 Key Words: Wound Accreditation References: EQuIP National and other criteria and standards

Version No.: 5.0; Effective From: 25/02/2014 Page 1 of 4

pro0096v5 QHEPS ID: pro0096ep

Printed copies are uncontrolled

Gold Coast Hospital and Health Service Procedure: Wound Cleansing

3.1 Solutions for use in wound cleansing Potable tap water. This is water which has been deemed suitable for drinking. If it has not been deemed suitable for drinking it should not be used. Potable tap water can be used on adults with lacerations and post-operative wounds, children with simple lacerations, and chronic wounds in adults. If potable water is not available boiled and cooled water is an acceptable substitute. Potable water has been shown to not cause harm or increase the risk of infection in these wounds. Normal saline. This is present within the hospital system as a 0.9% solution of sodium chloride in water. This can be used on patients deemed unsuitable to be washed with potable water either due to their immune status or for mobility reasons. Normal saline has been shown to not harm healing wound tissues. Normal saline should be warmed to body temperature prior to use. Prontosan. This is a solution of 0.1% Polyhexamethylene biguanide (PHMB), an antimicrobial agent and 0.1% Betaine, a surfactant. This can be used on any wounds where the patient has not shown a previous sensitivity to the product. The solution has been shown to effectively kill the planktonic bacteria in the wound and to also break up the denatured proteins which form biofilms. Betaine has also been reported to have a role in disrupting cell-to-cell communications in biofilms, reducing their pathogenicity. 1% Povidone-Iodine. Povidone-iodine is an antimicrobial solution. It can be used on any surface wounds where the patient has not shown a previous sensitivity to iodine. There is evidence to support its use as an irrigation solution but it has been shown to be ineffective when used as a soak. 3.2 Irrigation pressures appropriate for wound cleansing Showering. Shower pressure is sufficient to dislodge surface debris and can be used in conjunction with disposable washcloths or a Surgisponge to provide additional mechanical force to remove loose debris and old dressing materials. Showering may also give patients a feeling of well-being and cleanliness. Irrigation. 13 PSI of pressure is achievable by using a 20-30ml syringe with an 18g cannula or vial access cannula. This level of pressure has been shown to dislodge debris on the wound without causing harm to healing tissues. This method is appropriate for patients who can not be moved to a shower due to equipment (ie ICU) or comfort reasons (ie extreme pain on movement) or for immune-compromised patients. The use of sterile gauze squares may provide additional mechanical force to remove loose debris and old dressing materials. Soaking. Soaking is only suitable when using Prontosan. It allows the product time to break up the biofilm. Irrigate the wound first to remove loose debris, and then apply the solution to a sterile gauze and place in the wound bed. Leave in place for 15 minutes. The wound may also be cleaned with Prontosan-soaked sterile gauze squares to provide additional mechanical force to remove loose debris and old dressing materials. 4 Supporting /Relating Documents

Authorising Policy and Standard/s:

x Australian Wound Management Association

http://www.awma.com.au/awma/index.php




http://www.awma.com.au/awma/index.php


Procedures, Guidelines, Protocols

x Personal Protective Equipment GCDPRO0460

http://qheps.goldcoast.health.qld.gov.au/gldcoast/polproc/Inf/PRO0702ep.pdf

x Hand Hygiene and Handcare PRO0459


Forms and templates

� Nil

5 Definition of terms

Term Definition Source See also Prontosan This is a solution of 0.1%

Polyhexamethylene biguanide (PHMB), an antimicrobial agent and 0.1% Betaine, a surfactant.

Bradbury & Fletcher, 2011, 'Prontosan® made easy', Wounds International, 2, 2, pp. s25-s30,

6 References and Suggested Reading Bradbury & Fletcher, 2011, 'Prontosan® made easy', Wounds International, 2, 2, pp. s25-s30,

Cutting, K 2010, 'Addressing the challenge of wound cleansing in the modern era', British Journal Of Nursing, 19, 11, p. S24

Joanna Briggs Institute, 2006, ‘Solutions, techniques and pressure in wound cleansing ‘, Best Practice, 10, 2, pp. 1-4

7 Consultation Key stakeholders who developed/reviewed this version are:

x Nicola Morley Nurse Practitioner (GCUH) x Kim Kaim, CN Wound Management (GCUH)

8 Procedure Development/Revision and Approval History Version No

Developed/Modified by

Content authorised by

Approved by Date of Effect

Last Reviewed

4 Cheryl Frank Cheryl Frank Nurse Practice Committee

Ged Williams ED Nursing & Midwifery

24/09/2010 06/02/2014

5 Kim Kaim CN Wound Management

Nicola Morley Nurse Practitioner (Vascular)

General Manager, Specialty and Procedural Services

25/02/2014

8.1 This version supersedes/replaces:

x Wound Cleansing, Document ID GCDPRO0096v4







9 Audit Strategy

Level of risk Medium Audit strategy Infection control data collection Audit tool attached No Audit date Annually Audit responsibility CNC wound management Key Elements / Indicators / Outcomes

Reduction in wound infections Improved patient outcomes Efficient use of hospital resources

10 Appendices (nil)





Appendix F – Dressing Selection Guide None to Low Low to Moderate Moderate to High High to Very High Epithelial

Film Interface Simple dressing

Foam Hydrocolloid

High Absorbent High Absorbent

Antimicrobial/interface Antimicrobial/simple

Antimicrobial/interface Antimicrobial/Foam

Medicated bandage Medicated bandage

Granulating

Film Hydrogel

Interface Foam Hydrocolloid

Alginate Hydrofibre

High Absorbent

Povidone-Iodine Enzymatic Gel

Antimicrobial /Foam Antimicrobial/interface

Cadexomer-Iodine Antimicrobial/Alginate Antimicrobial/Hydrofibre

Antimicrobial/interface

Slough

Hydrogel

Foam

Alginate Hydrofibre

High Absorbent

Enzymatic Gel Cadexomer-Iodine

Enzymatic Gel Cadexomer-Iodine Antimicrobial/Foam Curasalt (Curity)

Antimicrobial/Alginate Cadexomer-Iodine Mesalt

Antimicrobial/interface

Necrotic Hydrogel Hydroactive

Hydrocolloid Foam Alginate

High Absorbent

Povidone-Iodine Antimicrobial/Hydroactive

Cadexomer-Iodine Cadexomer-Iodine Antimicrobial/Foam Antimicrobial/Alginate

Antimicrobial

This table has been modified from those used in the NHS Current products (subject to change) Generic Brand Generic Brand Film Tegaderm

Opsite Medicated Bandage ZipZok

Interface Jelonet Antimicrobial/ Interface Bactigras Sorbact Acticoat

Simple Primapore Compose

Antimicrobial/Simple Kendall AMD island dressing

Hydrogel Solosite Antimicrobial/ Hydrogel Hypergel (also consider enzymatic gels)

Hydrocolloid Comfeel Duoderm

High Absorbent Combine Zetuvit Incontinence Aid

Enzymatic Gel

Flamminal Hydro Honey

Cadexomer-Iodine Iodosorb Paste Iodosorb Powder

Foam Allevyn Mepilex (for delicate skin only)

Antimicrobial/Foam Kendall AMD Foam Allevyn Ag Mepilex Ag (for delicate skin only)

Alginate Kaltostat Antimicrobial/ Alginate Silvercel Hydrofibre Aquacel Antimicrobial/ Hydrofibre Aquacel Ag Not categorised above: Skin Protector

! Cavilon ! Menalind ! White paraffin !

Cavity ! Alginate ! Hydrofibre

Bleeding ! Ca Alginate

Malodorous

! Charcoal

Wound Closure ! Steristrips !

Irrigation ! Prontosan

Hypergranulation

! Foam


References 1.! Fletcher,!J.,!Wound&assessment&and&the&TIME&framework.!British!Journal!of!Nursing,!

2007.!16(8):!p.!462A4.!2.! Harding,!K.,!et!al.,!Evolution&or&Revolution?&Adapting&to&complexity&in&wound&

management.!International!Wound!Journal,!2007.!4$Suppl.$2(2):!p.!1A12.!3.! GreatrexAWhite,!S.!and!H.!Moxey,!Wound&assessment&tools&and&nurses'&needs:&an&

evaluation&study.!International!Wound!Journal,!2013.!4.! Cook,!L.,!Wound&assessment:&exploring&competency&and&current&practice.!British!Journal!

of!Community!Nursing,!2011:!p.!S34A40.!5.! Moffatt,!C.,!et!al.,!Psychosocial&factors&and&delayed&healing,!in!Position&Document:&HardF

toFheal&wounds:&a&holistic&approach,!European!Wound!Management!Association,!Editor!2008,!MEP!Ltd:!London.!p.!10A14.!

6.! Cooper,!D.M.,!Human&wound&assessment:&status&report&and&implications&for&clinicians.!AACN!Clinical!Issues!in!Critical!Care!Nursing,!1990.!1(3):!p.!553A565.!

7.! Australian!Wound!Mangement!Association,!Standards&for&Wound&Management.!2nd!ed2010:!Australian!Wound!Mangement!Association.!31.!

8.! Flour,!M.!The&pathophysiology&of&vulnerable&skin.!World!Wide!Wounds!2009!![cited!2011!October!18];!Available!from:!http://www.worldwidewounds.com/2009/September/Flour/vulnerable-skin-1.html.!

9.! McGrath,!J.A.!and!J.!Uitto,!Anatomy&and&Organization&of&Human&Skin,!in!Rook's&Textbook&of&Dermatology,!T.!Burns,!et!al.,!Editors.!2010,!WileyABlackwell:!Oxford,!UK.!p.!3.1A3.53.!

10.! Watkins,!P.,!Using&emollients&to&restore&and&maintain&skin&integrity.!Nursing!Standard,!2008.!22(41):!p.!51A57.!

11.! Bianchi,!J.!and!J.!Cameron,!Assessment&of&skin&integrity&in&the&elderly&1.!British!Journal!of!Community!Nursing,!2008.!13(3):!p.!S26.!

12.! Thomas,!D.R.!and!N.M.!Burkemper,!Aging&skin&and&wound&healing.!Clinics!in!Geriatric!Medicine,!2013.!29(2):!p.!xiAxx.!

13.! Nazarko,!L.,!Wound&Care&Series:&Part&one:&Consequences&of&ageing&and&illness&on&skin.!Nursing!and!Residential!Care,!2005.!7(6):!p.!255A257.!

14.! Benbow,!M.,!Maintaining&skin&integrity&and&preventing&pressure&damage.!Nursing!and!Residential!Care,!2009.!11(9):!p.!443.!

15.! McGrath,!J.A.!and!J.!Uitto,!Chapter&3.&Anatomy&and&Organization&of&Human&Skin,!in!Rook's&Textbook&of&Dermatology,!T.!Burns,!et!al.,!Editors.!2010,!WileyABlackwell:!Oxford,!UK.!

16.! StreckerAMcGraw,!M.K.,!T.R.!Jones,!and!D.G.!Baer,!Soft&tissue&wounds&and&principles&of&healing.!Emergency!medicine!clinics!of!North!America,!2007.!25(1):!p.!1A22.!

17.! O'Toole,!E.A.!and!J.E.!Mellerio,!Wound&Healing,!in!Rook's&Textbook&of&Dermatology,!T.!Burns,!et!al.,!Editors.!2010,!WileyABlackwell:!Oxford,!UK.!p.!14.1A14.27.!

18.! Moore,!K.,!Cell&Biology&of&Normal&and&Impaired&Healing,!in!Microbiology&of&Wounds,!S.!Percival!and!K.!Cutting,!Editors.!2010,!CRC!Press:!Boca!Raton,!Fla.!p.!151A186.!

19.! Hermans,!M.H.E.!and!T.!Treadwell,!An&Introduction&to&Wounds,!in!Microbiology&of&Wounds,!S.!Percival!and!K.!Cutting,!Editors.!2010,!CRC!Press:!Boca!Raton,!Fla.!p.!83A134.!

20.! Sibbald,!R.G.,!et!al.,!Special&considerations&in&wound&bed&preparation&2011:&an&update.!World!Council!of!Enterostomal!Therapists!Journal,!2012.!32(2):!p.!10A30.!

21.! Dowsett,!C.!and!E.!Ayello,!TIME&principles&of&chronic&wound&bed&preparation&and&treatment.!British!Journal!of!Nursing,!2004.!13(15):!p.!S16.!

22.! O'Brien,!M.,!Debridement:&ethical,&legal&and&practical&considerations.!Wound!Care,!2003.!March:!p.!23A25.!

23.! unkown,!Debridement&in&wound&care.!Wound!Essentials,!2011.!6:!p.!88A89.!


24.! Anderson,!I.,!Debridement&methods&in&wound&care.!Nursing!Standard,!2006.!20(24):!p.!65A72.!

25.! Benbow,!M.,!Fungating&malignant&wounds&and&their&management.!Journal!of!Community!Nursing,!2009.!23(11):!p.!12.!

26.! Bradbury,!S.!and!J.!Fletcher,!Prontosan&made&easy.!Wounds!International,!2011.!2(2):!p.!s25As30.!

27.! Vowden,!K.!and!P.!Vowden,!Debridement&made&easy.!Wounds!UK,!2011.!7(4):!p.!1A4.!28.! Cooper,!R.A.,!Understanding&Wound&Infection,!in!European&Wound&Management&

Association&(EWMA)&Position&Document:&Identifiying&Criteria&for&Wound&Infection,!S.!Caine,!et!al.,!Editors.!2005,!MEP!Ltd:!London.!

29.! Percival,!S.L.!and!S.E.!Dowd,!Chapter&6.&The&Microbiology&of&Wounds,!in!Microbiology&of&Wounds,!S.!Percival!and!K.!Cutting,!Editors.!2010,!CRC!Press:!Boca!Raton,!Fla.!

30.! Liesse!Iyamba,!J.M.,!et!al.,!Study&of&the&formation&of&a&biofilm&by&clinical&strains&of&Staphylococcus&aureus.!Biofouling,!2011.!27(8):!p.!811A821.!

31.! Davis,!S.C.,!et!al.,!Microscopic&and&physiologic&evidence&for&biofilmFassociated&wound&colonization&in&vivo.!Wound!Repair!And!Regeneration,!2008.!16(1):!p.!23A29.!

32.! Jefferson,!K.K.,!What&drives&bacteria&to&produce&a&biofilm?!FEMS!Microbiology!Letters,!2004.!236(2):!p.!163A173.!

33.! Mastropaolo,!M.D.,!et!al.,!Synergy&in&polymicrobial&infections&in&a&mouse&model&of&type&2&diabetes.!Infection!And!Immunity,!2005.!73(9):!p.!6055A6063.!

34.! Pollock,!A.V.,!Wound&infection:&synergy&between&aerobic&and&anaerobic&bacteria.!Annals!Of!The!Royal!College!Of!Surgeons!Of!England,!1980.!62(3):!p.!243A244.!

35.! Fazli,!M.,!et!al.,!Nonrandom&distribution&of&Pseudomonas&aeruginosa&and&Staphylococcus&aureus&in&chronic&wounds.!Journal!Of!Clinical!Microbiology,!2009.!47(12):!p.!4084A4089.!

36.! Richard,!J.AL.,!J.AP.!Lavigne,!and!A.!Sotto,!Diabetes&and&foot&infection:&more&than&double&trouble.!Diabetes/Metabolism!Research!and!Reviews,!2012.!28:!p.!46A53.!

37.! Edmonds,!M.,!A.V.M.!Foster,!and!P.!Vowden,!Wound&bed&preparation&for&diabetic&foot&ulcers,!in!European&Wound&Management&Association&(EWMA)&Position&Document:&Wound&Bed&Preparation&in&Practice2004,!MEP!Ltd:!London.!

38.! Sibbald,!R.G.,!K.!Woo,!and!E.A.!Ayello,!Increased&bacterial&burden&and&infection:&the&story&of&NERDS&and&STONES.!Advances!in!Skin!&!Wound!Care,!2006.!19(8):!p.!447A461.!

39.! Dowsett,!C.,!Moisture&in&wound&healing:&exudate&management.!British!Journal!of!Community!Nursing,!2011:!p.!S6As12.!

40.! Vowden,!K.!and!P.!Vowden.!Wound&Bed&Preparation.!2002;!Available!from:!http://www.worldwidewounds.com/2002/april/Vowden/Wound-Bed-Preparation.html.!

41.! Carville,!K.,!Wound&Care&Manual.!5th!ed2007,!Osborn!Park,!WA:!Silver!Chain!Nursing!Association.!

42.! World!Union!of!Wound!Healing!Societies!(WUWHS),!Principles&of&best&practice:&Diagnostics&and&wounds.&A&consensus&document.2008,!London:!MEP!Ltd.!

43.! Casey,!G.,!Chronic&wound&healing:&Leg&ulcers.!Kai!Tiaki!Nursing!New!Zealand,!2011.!17(11):!p.!24A29.!

44.! Inernational!consensus,!Making&the&case&for&cost&effective&wound&management.!Wounds!International,!2013.!

45.! Gottrup,!F.,!A&specialised&wound&care&concept:&The&multiFdisciplinary&approach.!The!Chronical,!2009.!26(Spring!2009):!p.!5A6.!

46.! Optimal&Care&of&Chronic,&NonFHealing,&Lower&Extremity&Wounds:&A&Review&of&Clinical&Evidence&and&Guidelines,!2013,!Canadian!Agency!for!Drugs!and!Technologies!in!Health.!

47.! Carville,!K.,!et!al.,!The&effectiveness&of&a&twiceFdaily&skinFmoisturising&regimen&for&reducing&the&incidence&of&skin&tears.!International!Wound!Journal,!2014.!11(4):!p.!446A453.!


48.! Bianchi,!J.,!Protecting&the&integrity&of&the&periwound&skin.!Wound!Essentials,!2012.!1:!p.!58A64.!

49.! Corcoran,!E.!and!S.!Woodward,!IncontinenceFassociated&dermatitis&in&the&elderly:&treatment&options.!British!Journal!Of!Nursing,!2013.!22(8):!p.!450A457.!

50.! Prideaux,!A.,!Issues&in&nursing&documentation&and&recordFkeeping&practice.!British!Journal!Of!Nursing,!2011.!20(22):!p.!1450A1454.!

51.! Nursing!and!Midwifery!Council,!Record&keeping&guidance&for&nurses&and&midwives,!N.a.M.!Council,!Editor!2010,!Nursing!and!Midwifery!Council:!London.!p.!10.!

52.! Blair,!W.!and!B.!Smith,!Nursing&documentation:&frameworks&and&barriers.!Contemporary!Nurse,!2012.!41(2):!p.!160A168.!

53.! Queensland!Health,!Good&clinical&documentation&F&Its&importance&from&a&legal&perspective,!Q.!Health,!Editor!2013,!Queensland!Health:!Brisbane.!p.!2.!

54.! Campos,!N.K.,!The&legalities&of&nursing&documentation.!Nursing,!2010.!40(1):!p.!SS7.!55.! Farage,!M.A.,!et!al.,!Clinical&implications&of&aging&skin:&cutaneous&disorders&in&the&elderly.!

American!Journal!Of!Clinical!Dermatology,!2009.!10(2):!p.!73A86.!56.! The!Australian!Wound!Management!Association!(AWMA)!Pan!Pacific!Guideline!

Development!Steering!Committee,!Pan&Pacific&Clinical&Practice&Guideline&for&the&Prevention&and&Management&of&Pressure&Injury.2012,!Osborne!Park,!WA:!Cambridge!Media.!

57.! European!Pressure!Ulcer!Advisory!Panel!and!National!Pressure!Ulcer!Advisory!Panel,!Treatment&of&pressure&ulcers:&Quick&Reference&Guide2009,!Washington!DC:!National!Pressure!Ulcer!Advisory!Panel.!

!