Wound Care Module

7/25/2019 Wound Care Module

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WOUND CARE MODULE


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1Introduct ion ........................................................................................................................................................4

1.1 What is Wound Care?......................................................................................................................................4

1.2 What is a wound and what are the different types of wounds?.......................................................................4

1.3 Common types of wounds...............................................................................................................................4

2General overview of wounds ............................................................................................................................5

2.1 Complex and chronic wounds..........................................................................................................................52.1.1Acute wounds..........................................................................................................................................52.1.2Chronic wounds ......................................................................................................................................5

3Healing ................................................................................................................................................................6

3.1 How does the body heal? ................................................................................................................................6

3.2 Phases of Healing............................................................................................................................................63.2.1The inflammatory phase .........................................................................................................................63.2.2The proliferative phase............................................................................................................................63.2.3The maturation phase .............................................................................................................................7

3.3 Moist wound management...............................................................................................................................7

3.4 Control Factors Affecting Healing....................................................................................................................83.4.1Intrinsic factors ........................................................................................................................................8

3.4.1.1 Health status..............................................................................................................................83.4.1.2 Immune function ........................................................................................................................83.4.1.3 Diabetes.....................................................................................................................................83.4.1.4 Age factors.................................................................................................................................83.4.1.5 Body build ..................................................................................................................................83.4.1.6 Nutritional status ........................................................................................................................8

3.4.2Extrinsic factors.......................................................................................................................................93.4.2.1 Mechanical stress ......................................................................................................................9

3.4.2.2

Debris.........................................................................................................................................9

3.4.2.3

Temperature ..............................................................................................................................9

3.4.2.4 Desiccation ................................................................................................................................93.4.2.5 Maceration .................................................................................................................................93.4.2.6 Infection .....................................................................................................................................93.4.2.7 Chemical stress .........................................................................................................................93.4.2.8 Other factors ............................................................................................................................10

3.4.2.8.1 Systemic medications .........................................................................................................103.4.2.8.2 Lifestyle...............................................................................................................................103.4.2.8.2.1 Alcohol ............................................................................................................................103.4.2.8.2.2 Smoking..........................................................................................................................10

4Wounds .............................................................................................................................................................11

4.1

Chronic Wounds ............................................................................................................................................11

4.1.1Leg ulcers..............................................................................................................................................114.1.2Venous ulcers .......................................................................................................................................11

4.1.2.1 General features of venous ulcers...........................................................................................114.1.3Ischaemia, or arterial ulcers..................................................................................................................11

4.1.3.1 General features of arterial ulcers ...........................................................................................114.1.4Venous/Arterial (Mixed Ulcers) .............................................................................................................124.1.5Other causes of ulcers ..........................................................................................................................124.1.6The Diabetic ..........................................................................................................................................12

4.1.6.1 How does diabetes affect wound healing? ..............................................................................124.1.6.2 Risk factors in diabetes............................................................................................................13

4.1.6.2.1 Peripheral Vascular Disease ..............................................................................................134.1.6.2.2 Peripheral Neuropathy........................................................................................................13

4.1.6.2.3

Callus Formation.................................................................................................................13

4.1.6.2.4 Limited Joint Mobility ..........................................................................................................134.1.6.2.5 Bony Deformity ...................................................................................................................13

4.1.7Pressure Ulcers.....................................................................................................................................13


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4.1.7.1 Pressure ...................................................................................................................................134.1.7.2 Friction .....................................................................................................................................144.1.7.3 Shearing forces........................................................................................................................14

5Wound Dressings and Bandages...................................................................................................................15

5.1 Wound pharmaceuticals / Wound healing product classification ..................................................................15

5.2 Passive dressings..........................................................................................................................................155.2.1A modern inert dressing ........................................................................................................................155.2.2The non-absorbent passive dressings ..................................................................................................15

5.3 Interactive dressings......................................................................................................................................165.3.1Non-Absorbing dressings......................................................................................................................16

5.3.1.1 Film Dressings (for wounds with no to low exudate) ...............................................................165.3.2Absorbing dressings ............................................................................................................................17

5.3.2.1 Hydrocolloid dressings (for wounds with low to moderate exudate) .......................................175.3.2.2 Foam dressings (for wounds with medium to high exudate) ...................................................185.3.2.3 Alginate dressings (for wounds with medium to high exudate) ...............................................195.3.2.4 Hydrofibre dressings................................................................................................................205.3.2.5 Hydroactive dressings (for wounds with medium to high exudate) .........................................205.3.2.6 Hydrogels ( For dry or sloughy wounds ) .................................................................................21

5.3.3Miscellaneous dressings.......................................................................................................................22

5.3.3.1 Cadexomer Iodine Dressings (e.g. Iodosorb) ......................................................................225.3.3.2 Silver ........................................................................................................................................22

5.4 General rules for the topical use of antiseptics..............................................................................................22

5.5 Hypertonic Saline...........................................................................................................................................23

5.6 New burn dressings.......................................................................................................................................23

5.7 Keloid and Hypertrophic Scar Management ..................................................................................................24

5.8 Bandages.......................................................................................................................................................245.8.1Retention Bandages..............................................................................................................................245.8.2Support Bandages..................................................................................................................................245.8.3Compression Bandages........................................................................................................................24

5.8.3.1 High stretch compression bandages .......................................................................................255.8.3.2 Short stretch bandages............................................................................................................255.8.3.3 The hazards of compression bandages...................................................................................25

5.8.4Zinc paste bandages.............................................................................................................................26

6General rules ....................................................................................................................................................27

6.1 Acute wounds ................................................................................................................................................27

6.2 Chronic wounds.............................................................................................................................................27

6.3 Protocol for wound management of skin tears ..............................................................................................27

6.4 Difficult wounds (i.e. animal or insects bites).................................................................................................27

6.5 Post operative wounds ..................................................................................................................................28

6.6 Burns..............................................................................................................................................................28

7References........................................................................................................................................................29

ACKNOWLEDGEMENT

The development and production of the wound resources by Geoff Sussman, Director Wound Research Wound

Foundation of Australia is acknowledged.


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1 Introduction

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1.1

1.2

1.3

What is Wound Care?

Wound care is the provision of the appropriate environment for healing by both direct and indirectmethods together with the prevention of skin breakdown1. In other words wound care means morethan just putting a dressing onto a wound. It means looking into patients general health, lifestyle andfactors that might slow healing down.

What is a wound and what are the different types of wounds?

A wound is a physical injury to the body consisting of a laceration or breaking of the skin or mucousmembrane, or an opening made in the skin or a membrane of the body incidental to a surgicaloperation or procedure.

Wounds may be acute or chronic trauma resulting from an injury where, because of a number offactors, the injury does not heal. Acute wounds may be a planned or unplanned event, and healingtypically proceeds in an orderly and timely fashion. Examples of acute wounds include a cut, graze orburn. Examples of chronic wounds include leg ulcers, pressure wounds and diabetic wounds.

Common types of wounds

BLACK NECROTIC WOUNDYELLOW NECROTIC WOUNDWITH HIGH EXUDATE

YELLOW NECROTIC WOUNDWITH LOW EXUDATE

CAVITY WOUND WITH HIGHEXUDATE

EXUDATING WOUND WITH

SLOUGH AND CLINICAL SIGNS

OF INFECTION

SUPERFICIAL WOUND WITH

CLINICAL SIGNS OF INFECTION

SUPERFICIAL GRANULATING

WOUND WITH HIGH EXUDATE

SUPERFICIAL GRANULATING

WOUND WITH LOW EXUDATE

MALODOROUS WOUNDS

CAVITY WOUND WITH LOW

EXUDATE

EPITHELIALISING WOUNDS SKIN TEARS


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2.1

2 General overview of wounds

Complex and chronic wounds

A large proportion of wounds seen in clinical practice are chronic in nature. The epidemiologicalstudies indicate that one percent of the population has a chronic wound, and of that group sometwenty percent have had the wound for more than two years. More studies indicate that the level of

chronic wounds in older patients is considerably higher than that percentage

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.Chronic wounds may be classified into the following groups:

Leg ulcers

Pressure wounds

Post-operative wounds

Neoplasia (Cancer)

Chronic infected wounds

Diabetic wounds

The difficulty in the management of any chronic wound is that there is always an underlyingphysiological cause of the wound which must be treated, but many patients have multi-factorialissues and co-morbidities. For best results the basic cause of the problem must be addressed, andany negative factors altered.

It must be understood that some patients may never heal due to the basic pathophysiology of thedisease process and our inability to alter some or all of the major factors influencing the non-healingof the wound. However, even in the most extreme cases, good wound care can be a great help inminimising the worst effects of such chronic wounds.

2.1.1 Acute wounds

Acute wounds may show some of the following characteristics:

higher risk of infection due to debris contaminating the wound

inflammation occurs

may heal by primary intention

may require antiseptic use

2.1.2 Chronic wounds

Chronic wounds may show the following characteristics:

lower risk of infection

symptom of underlying condition

heal by secondary intention

may be sloughy and moist, or dry and scabby.


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3.1

3.2

3 Healing

How does the body heal?

There are three phases of wound healing

inflammatory (destructive)

proliferative (regenerative)

maturation (reparative)

During all of these phases there are a number of cells that are essential to the process of the healingincluding platelets, neutrophils, macrophages and fibroblasts.

Some of the cells which you may think are only present for one particular phase of the healingprocess are there from the very beginning of the wound, through to the ultimate healing of the wound.

The critical thing is that the phases of healing are a continuum. Each phase continues in a steadyprocess merging with the next phase. In fact, one wound may be in more than one phase at onetime.

Phases of Healing

3.2.1 The inf lammatory phase

The inflammatory phase is normally the shortest, and is manifest at the beginning of the wound itselfwhere a wound is either surgically created, caused by trauma or some other reason. There will bebleeding, and a clot will develop to induce haemostasis (clotting). The tissue around the wound mayoften be red, hot, sore and swollen. This does not indicate infection, it is merely the inflammatoryprocess itself and, consequently, it is not always necessary to apply topical antiseptics or topicalantibiotics. Wound exudate is often copious during the inflammatory phase. It is not a passivecomponent of the healing process, but serves to nourish the tissues and to flush out necrotic tissueand foreign debris from the wound. The inflammatory phase uses the exudate as a support mediumfor enzymes, antibodies and the various cells necessary for wound cleansing. Exudate also contains

a number of growth factors produced by the body which are critical in the promotion of healing. If theinflammatory phase is impaired, wound healing may be slowed or halted. The continued presence offoreign material, necrotic tissue, excessive antimicrobial use or other continued disruption of thewound can result in prolonged inflammation thereby preventing the onset of proliferation andmaturation. In turn, this may lead to fibrosed tissue. Some of the factors that will affect theinflammatory phase include continued tissue destruction due to pressure not being relieved, drynessand desiccation, poor blood supply, clinical infection, or thermal shock during the inflammatoryphase. The most important cells are the platelets whose task is not only haemostasis, but also theproduction of a growth factor which is important in stimulating the healing process.

During this phase the destruction of non-viable tissue and bacteria occurs. Neutrophils are involvedin phagocytosis (killing) of bacteria as well as aiding in the extra-cellular release of protease - an

enzyme used by the body for the destruction of necrotic tissue. The macrophages that are involved inphagocytosis of micro-organisms and necrotic tissue also release a growth factor important in thehealing cascade.

3.2.2 The proli ferative phase

During this phase the new vascular bed is formed by angio-genesis. Capillary buds are formed whichlink up with the existing capillary network and allow oxygenated blood to provide a lush bed ofcapillary vessels. During the proliferative phase collagen is deposited by the fibroblasts. Collagen isthe essential framework for the connective tissue which will eventually fill the wound. Fibroblasts alsosynthesise proteoglycans, or ground substance. It is collagen and ground substance which form thescaffolding for wound repair. Collagen is laid down in a wound over a period of weeks, after which

time no new collagen is produced. The fibroblasts produce enzymes which help break down thecollagen.

The collagen then realigns itself by cross-linking, resulting in tensile strength in the wound. There area number of elements essential for collagen production and deposition including vitamin C, oxygen,


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3.3

iron and zinc. A deficiency in these nutrients could lead to the development of a weakly bondedmatrix, and ultimately to dehiscence of the wound.

During the proliferative phase, wound contraction occurs. This is an action of the myofibroblasts,contractile cells which pull the wound margins together. Contraction and granulation are theprocesses by which the wound becomes smaller. During the latter stage of the proliferative phase,epithelialisation occurs. This involves the growth of the epidermal cells over the surface of thegranulation tissue, a process which is completed most efficiently in a moist, clean environment.

3.2.3 The maturation phase

The maturation phase is the final stage of healing. During this stage the fibroblasts decrease innumber, vascularisation decreases, and the tensile strength of the wound increases. Maturation isthe most misunderstood phase of healing. It is assumed that a wound is healing once the epitheliumhas closed the surface of the wound. Tensile strength of the wound may in fact take quite aconsiderable time to develop, and in some patients it can take up to twelve months. It is oftenincorrect to view a re-ephithelialised wound and think that the wound is totally healed beneath thesurface. The lack of tensile strength in a wound will increase the risk of breakdown that may berelated to tension of the tissue below the surface.

Moist wound management

Knowledge and understanding of wounds, tissue and healing have grown rapidly over the past 40years, resulting in a major change in the method of wound management. There has been a growingawareness that traditional wound-care products do little to aid healing, and in many cases actuallydelay it.

Traditional theory has always been that wounds should be kept clean and dry so that a scab mayform over the wound, the wounds should be exposed to the air and sunlight as much as possible,and where tissue loss is present, the wound should be packed to prevent surface closure before thecavity is filled, and then the wound should be covered with a dry dressing.

The clear disadvantages of these principles are that the scab, which is made up of the dehydratedexudate and dying dermis, is a physical barrier to healing, which is then delayed because the

epidermal cells cannot move through the scab formed. This may ultimately lead to a poor cosmeticresult, even scarring. Exposure to the air reduces the surface temperature of the wound causingperipheral vasoconstriction affecting the flow of blood to the wound which further delays healing. Thisreduced blood flow will also effect the supply of oxygen, nutrition and other factors to the wound. Airexposure will also cause the wound to desiccate and form a scab.

Where a wound is packed with dry gauze, the quality of healing is impaired due to adhesion of thematerial to the surface of the wound, causing it to dry out. Equally, covering the wound with a drydressing that adheres to the wound may traumatize the wound surface on removal. Wounds coveredby an occlusive dressing do not form a scab, so epidermal cells are able to move rapidly over thesurface of the dermis through the exudate which collects at the wound/dressing interface. Theapplication of a totally occlusive or semi-permeable dressing to the wound can also prevent

secondary damage as a result of dehydration.Dr George D Winter, in his work Formation of the scab and the rate of epithelialization of superficialwounds in the skin of young domestic pigs'(Nature, 1962)3was able to demonstrate scientifically thedifference between wounds of a similar nature when healing was open to the air, and when healingwas under occlusive dressing. Winter's work was to inflict artificial wounds on young domestic pigs,with fifty percent of the wounds occluded and fifty percent of the wounds open to the air. They werereviewed on a regular basis, and samples taken of both types of wounds which were then examinedmicroscopically. The experiment showed that the wounds healing under moist conditions healed fiftypercent faster than the wounds healing under dry conditions, open to the air. Winters work has sinceformed the basis of the principles of modern moist wound management. Many subsequent studieshave confirmed the theory that wounds heal faster in a moist environment compared to a dry

environment.Moist wound healing also simplifies cleaning by assisting with the autolytic debridement of wounds. Itfacilitates wound cleansing, since the wound exudate is part of the healing cascade, and also


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3.4

protects granulation and encourages epithelialization. Exudate has now been shown to carry anumber of growth factors essential to the healing of wounds.

Control Factors Affecting Healing

Most wounds heal readily whereas others are slow or remain unhealed for a considerable length oftime. There are a number of factors which affect the healing of a wound, and these factors are both

intrinsic and extrinsic.

3.4.1 Intrinsic factors

health status

immune function

diabetes

age factors

body build

nutritional status.

3.4.1.1 Health status

Good circulation, both arterial and venous, is essential for good wound healing. Anaemia, regardlessof type, reduces the capacity of the blood to provide oxygen to the tissues, since haemoglobintransports oxygen to the cells.

3.4.1.2 Immune function

Normal immune system function is required for the inflammatory phase of healing. A reduction inimmune function slows the cleansing of the wound bed and reduces the ability of the body to fightinvading pathogens (This is likely to be due to a reduction of the number and activity of the whiteblood cells).

3.4.1.3 Diabetes

Diabetes is one of the major problems for chronic wounds. Diabetics have a delayed capillaryresponse to injury, reduced cellular function at the injury site, and defects in collagen synthesis andwound strength. Hyperglycaemia (caused by reduced insulin availability and increased insulinresistance) appears to be a major predisposing factor in delaying healing in diabetic patients andincreasing the rate of infection.

3.4.1.4 Age factors

As we age our skin and tissues change. We lose the sensory cells, as well as the secretory cellswhich are so essential for the maintenance of skin moisture and flexibility. We lose the vasculaturewithin the skin, and hair follicles. The skin becomes thinner, dryer, and far more prone to destruction-

whether by physical or by chemical means.

3.4.1.5 Body build

Because of the adipose tissue being poorly vascularised, an obese patient will have a great deal oftrouble healing due to the inability to deliver oxygen and nutrients to the wound site. Underweightindividuals may also experience difficulties in the healing process.

3.4.1.6 Nutritional status

Nutrition is one of the most important factors in the healing of wounds. Proteins, carbohydrates, fats,vitamins, trace elements and fluids all play a vital role in wound repair. Research has shown thatamino acids (eg. Arginine), when given as a supplement, will improve the rate of wound healing.


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3.4.2 Extrinsic factors

mechanical stress

debris

temperature

desiccation / maceration

infection

chemical stress

other factors.

3.4.2.1 Mechanical stress

When a patient is immobile and pressure is exerted locally, especially over a bony prominence, formore than two hours, at a pressure exceeding 30 mm of mercury, localised microvascular ischaemiawill occur. This will ultimately lead to tissue destruction both at the surface and deeper into thewound-leading eventually to a pressure ulcer. Equally, shearing forces and friction occur when thetissue below the skin is forced to move while the skin itself is restrained by contact to a surface, such

as the bed sheet. This is particularly evident in the patients heels.3.4.2.2 Debris

Debris-whether slough, eschar, scab, wound dressing residue, gauze fibres or sutures- will impedewound healing. Their presence will prolong the inflammatory phase, as well as predisposing thewound to infection. Debris should be removed, either surgically or by the use of hydrogels, proteolyticenzymes or hydrocolloids.

3.4.2.3 Temperature

The optimum temperature for the growth of human cells is 37 degrees centigrade. It is thereforeessential to maintain the wound environment at body temperature. A drop in body temperature willlead to peripheral vasoconstriction- affecting the flow of blood through the wound- and it will markedly

reduce the activity of growth factors and proteases. Increased body temperature can lead tochanges at the wound site increasing the risk of cellular breakdown and limiting the healing process.

3.4.2.4 Desiccation

If a wound dries, healing is either delayed, or will cease. Exposed, dry wounds are more inflamed,painful, itchy, and have more scab material during the early stages of wound healing.

3.4.2.5 Maceration

Maceration may be due to incontinence, perspiration or excessive exudation. Maceration will causethe destruction of tissue and slow the healing process. It is essential to maintain the moistenvironment without excessive exudation.

3.4.2.6 InfectionAll wounds will have some level of bacterial colonisation, however, this does not mean that thewound is infected. The presence of erythema, discharge, fever, pain with elevated white blood cellcount, and sometimes odour, is evidence that the wound is infected. If clinical signs of infection arepresent, the use of systemic antibiotics is mandatory. If there are no clinical signs of infection there islittle reason to use either systemic or topical antibiotics. An exception to this may be the use of veryspecific topical antibiotics in very specific cases to reduce the level of bacteria in wounds ofcompromised patients (eg. the use of topical metronidazole in anaerobic colonised wounds).

3.4.2.7 Chemical stress

Iodine, peroxide, chlorhexidine, alcohols, hypochlorites and acetic acid are commonly used

antiseptics and cleansing agents. Use of these agents is often responsible for delayed healing, sincethey are non-selective in their activity and will kill healthy cells as well as bacteria. It is preferable toavoid the prolonged use of these products on a granulating wound. Even their use in infected woundsis somewhat dubious, as research has shown that although they may reduce the surface load of


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bacteria in an infected wound, they do not penetrate below the surface and therefore have no realeffect on the infection in the tissue itself4. They may be of use in dilute forms when applied to somechronic wounds and left in place for no more than five minutes and then washed off.

3.4.2.8 Other factors

3.4.2.8.1 Systemic medications

The effects of systemic medications on the healing wound vary greatly. We commonly see medicines

prescribed for a condition which is unrelated to the wound, but may have side effects which couldeither inhibit or stimulate healing. Medications can therefore be divided into two groups; thestimulatory drugs and the inhibitory drugs. The stimulatory drugs affect the inflammatory response,epithelialisation, fibroblast activity, fibrinolysis, and cell stimulation, whereas the inhibitorymedications affect tensile strength, cell activity, capillary proliferation, and fibroplasia.

3.4.2.8.2 Lifestyle

3.4.2.8.2.1 Alcohol

Excessive and/or chronic alcohol intake can lead to health problems affecting wound healing.Alcohol-induced digestive problems may lead to malnutrition and anaemia. Liver damage can result

in chronic disturbances due to a reduction in platelet levels, and subsequent circulatory damage thatmay reduce the blood flow that is required for wound healing.

3.4.2.8.2.2 Smoking

The adverse effects of smoking and the potentiation of cancer in various parts of the body have beenunderstood for many years. However, it is clear that the toxic constituents of smoking such asnicotine, carbon monoxide and cyanide have a dramatic and inhibiting effect on healing. Nicotine willdiminish red blood cells, fibroblasts and macrophages, and increase platelet adhesiveness. This willproduce cutaneous vasoconstriction. Carbon monoxide has an affinity for haemoglobin 200 timesgreater than that of oxygen. This will have a major effect on the oxygen-carrying capacity of the bloodand may potentially lead to ischaemia. Hydrogen cyanide inhibits the enzyme-systems necessary for

oxygen transport at the cellular level, as well as oxidative metabolism. Smoking can therefore be amajor cause of the non-healing of wounds.


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4.1

4 Wounds

Chronic Wounds

4.1.1 Leg ulcers

Leg ulcers have a number of different causes, including venous insufficiency, arterial disease,

diabetes mellitus, vascular complication of auto-immune disease (such as rheumatoid arthritis),malignant disease and trauma.

4.1.2 Venous ulcers

Venous ulcers result from the breakdown of the venous circulation of the leg, and are an associationof the inability of the leg to force the passage of blood through the various connecting veins via thebicuspid valves by muscular contraction. Deep veins are supported by thick connective tissue andtheir surrounding muscle masses. Superficial veins dilate easily under sustained back pressure.Communicating veins connect the two systems. Valves, usually bicuspid, are found in all threesystems and they may become damaged, thickened or may degenerate with age. Thrombosis cancause their destruction.

4.1.2.1 General features of venous ulcers

They are most often found in the lower 1/3 of leg (in the gaiter area) are usually irregular in shape,may not be painful, and oedema is often present. The skin is often stained around the ulcer area dueto haemosiderin deposition. Part of the underlying cause is past fractures or trauma with a possiblesilent deep vein thrombosis (DVT). Skin changes such as eczema and atrophy blanche (whitestippled scars on the skin) are often present, and ankle flare, distended small veins on the medialaspect of the foot are seen and there is a history of varicose veins. The main feature is a lack ofvenous return caused by a malfunction of the valve system either in the deep or the peripheralsystem. There is often a history of obesity, past DVT, and/or poor mobility resulting in venous stasis.Venous leg ulcers are usually painless, irregular in shape, and may have copious exudate.

The treatment for Venous Incompetence includes surgery in some cases, however, the main stay oftreatment is the application of compression therapy- toe to knee 30-40mmHg at ankle. It is, however,essential to exclude arterial involvement. Exercise should be encouraged and occupational factorssuch as long periods of standing which leads to venous stasis, should be avoided.

4.1.3 Ischaemia, or arterial ulcers

The death of skin automatically follows occlusion of its arterial blood supply unless this occlusion isgradual enough to allow a collateral blood supply to be established. Atheroma (thickening) is themost common cause of arterial ulcers of an ischaemic nature. The loss of arterial circulation may bedue to extramural strangulation. Scar tissue or other factors may cause strangulation of thearterioles, or fibrosis resulting from longstanding, chronic oedema. Chronic infection may also

obstruct arterial flow. Arterial ulcers can result from mural and intramural changes to the vesselwalls:

Mural changes: Atherosclerosis, or plaque formation reduces the blood flow until thrombosis,embolism or infection cause complete closure.

Intramural changes: Occlusion of small vessels by changes in blood viscosity, plateletadhesiveness or fibrinogenesis, (especially in small painful ulcers of the feet and ankles).

4.1.3.1 General features of arterial ulcers

Arterial ulcers are very painful, especially at night. This is as marked in small ulcers as in largerulcers. Their edges are sharply defined, and the ulcer is 'punched out'. The base is often coveredwith slough, which may deepen to bare the tendons. There is often a history of intermittent

claudication (pain on exercise), dependent foot (dusky foot) white on elevation, a history of peripheralvascular disease, lower Ankle Brachial Index (ABI), weak/absent pulses, and sluggish/poor capillaryrefill.


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The ulcer site is usually below the ankles to toes. The skin is often shiny and friable. Uncontrolleddiabetes and smoking are significant factors causing arterial insufficiency. Healing is often slow andmay depend on the control of the underlying cause.

Some examples of arterial ulcers are

traumatic ulcers on the shin and ankles

ulcers following fractures

ulcers caused by ill-fitting callipers or braces

post-burn ulcers

those caused by intra-lesional injections (in an area with an already impoverished blood supply).

Treatment of arterial ulcer may involve a surgical intervention - angioplasty, stenting, bypass, graftingand ultimately amputation. Pain control is an important aspect of the management of arterial ulcers.

4.1.4 Venous/Arterial (Mixed Ulcers)

It is important to note that between 10 percent and 15 percent of leg ulcers are of mixed aetiology.These ulcers are often hard to heal due to associated oedema, cellulitis, thrombophlebitis, diabetes

or underlying vascular disease, rheumatoid diseases especially in bed-ridden patients, and generalconditions of the skin in elderly patients which are often associated with malnourishment.

4.1.5 Other causes of ulcers

In addition to the more common forms of ulceration, there are a number of less familiar causes.Vasculitic ulcers may develop as a result of other medical conditions, such as those that effect theimmune system (eg. rheumatoid arthritis, lupus and polyarthritis).

Infections of the skin can produce ulcers especially if necrotising bacteria are involved. Otherpotential causes of ulcers are:

Haematological problems such as thalassemia or leukaemia.

Polycythaemia and skin conditions like pyoderma gangrenosum and epidermolysis bullosa.

Some ulcers may be as a result of neoplasia (cancer) which may develop into non-healingulcers. The most common of these are squamous cell and basal cell carcinomas.

Ulcers may also form in patients with lymphoedema, caused by a reduction in the function of thelymph vessels to drain extracellular fluid. The resultant oedema will place the patient at risk ofulcer development as a result of minor trauma and by the hyperkerototic nature of the skin.

4.1.6 The Diabetic

The prevalence of diabetes in Australia is on the rise with estimates of 3 to 4 percent of the

population currently having diabetes

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. The trend is of concern as the number of people diagnosedwith diabetes, as of 2006, is 1925 people every week6.

This constitutes a very large number of people in this country and many health professionals will beconfronted by patients with the problem of diabetic foot ulcers. Many diabetics may have a small andminor skin breakdown which they may not consider important however, due to their disease, theseminor wounds have the potential of becoming serious.

4.1.6.1 How does diabetes affect wound healing?

Patients with diabetes are prone to have:

Impaired inflammatory response

Association of atherosclerosis (small vessel disease)

Damaged nerves which diminish pain sensation and nerve response

Up to a five fold risk of infection.


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4.1.6.2 Risk factors in diabetes

4.1.6.2.1 Peripheral Vascular Disease

A major consequence of diabetes is the damage to both macro-vascular and micro-vascular systems.The resultant reduction in perfusion will contribute to the development of ulcers and also to a delay inwound healing.

4.1.6.2.2 Peripheral Neuropathy

The lack of feeling or diabetic peripheral sensory neuropathy is the major risk factor for footulceration. The fact that the diabetic patient is unable to detect even minor injuries or discomfort inthe feet will often place the patient at risk of developing a small wound. Due to the lack of sensation,the patient is unaware of the tissue damage and the wound will progress and only be noticed when itis larger in size. The other indicator may be the presence of odour which may indicate an infectedwound. In addition to sensory neuropathies there may be autonomic and motor neuropathies present.

4.1.6.2.3 Callus Formation

The development of excess callus will elevate plantar dynamic pressure and when combined withperipheral neuropathy, may lead to ulcer development.

4.1.6.2.4 Limi ted Joint Mobil ity

This will increase foot pressures and therefore increase the risk of ulcer development.

4.1.6.2.5 Bony Deformity

Deformities of the ankle, feet, bunions and toes will all increase the risk of ulcers forming.

4.1.7 Pressure Ulcers

Pressure ulcers are the most preventable of all of the chronic wounds. Pressure wounds may be assimple as the blister most of us may have experienced over the years from footwear, to the extensivepressure sores experienced by patients suffering from mobility decreasing conditions.

It has been estimated that between six to twelve percent of all patients treated in hospital develop apressure wound, but sadly, this number increases to about 30 percent in the elderly7.

A pressure wound develops when the capillary blood flow to the skin and tissue over a bonyprominence is decreased for a sufficient period of time.

The capillary pressure in the arterial blood system is some 32mm of mercury. It therefore requires apressure of only about 30mm of mercury to restrict the arterial blood flow. The consequence of thisrestricted blood supply is a reduction in oxygen supply and nutrition to the tissue, accompanied bythe problem of waste products not being removed from the site.

The result of this is hypoxia, tissue acidosis, increased capillary permeability- which allowsintravascular fluid to escape causing oedema, and cell death.

The main causes of pressure wounds are

pressure

friction

shear

4.1.7.1 Pressure

Direct pressure on tissue over a bony prominence in excess of 30mm of mercury will cause

ischaemia in the surrounding tissue. This will occur not only from a patient being in bed, but also on atrolley or sitting in a chair. The extent of tissue damage will depend on the intensity of the pressure,and the length of time the pressure remains unrelieved. The tissue can tolerate pressure for short


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periods of time; however, even low pressure over a long period of time will have some detrimentaleffect.

4.1.7.2 Friction

Friction occurs when the top layers of skin are worn away by continued rubbing against an externalsurface. This can manifest itself in a simple blister or tissue oedema, or an open pressure wound.This can be caused by ill-fitting footwear, or even bed linen.

4.1.7.3 Shearing forcesShear is when the skin remains in place, usually unable to move against the surface it is in contactwith, while the underlying bone and tissue are forced to move. This force will contribute to thedestruction of microvasculature in a manner similar to direct pressure. This type of pressure injury isseen in patients left sitting up in bed or on a chair, while gravity causes the patient to slide down withthe skin adhering to the bed linen or the surface of the chair.


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5.1

5.2

5 Wound Dressings and Bandages

Wound pharmaceuticals / Wound healing product classification

The history of the development and use of dressings has seen an evolution through many centuriesfrom inert and passive products such as gauze, lint and fibre products to a dazzling range of modernmoist wound dressings.

The range of dressings increases every year and is often a source of confusion when attempting todifferentiate between both similar and different dressings. The simplest way of classifying dressingsis by their functionality.

Wound products can be divided into two broad groups:

Passive products

Interactive products

Within these two groups, the passive dressings can be sub-classified into absorbing and non-absorbing dressings whereas the interactive dressings can be sub-classified as absorbing, non-absorbing and moisture donating. The interactive group has six different dressing types.

Turner8has defined the following as the properties of the ideal wound dressing:

Remove excessive exudate from the wound without allowing the wound to dry out therebymaintaining a moist environment

Allow gaseous exchange so that oxygen, water vapour and CO2may pass in and out of thedressing

Be thermally insulating so as to maintain the wound core temperature at approximately 37degrees C

Be impermeable to micro-organisms in order to minimise contamination of the wound fromoutside the wound itself

Be free from either particulate or toxic contamination

Be non-traumatic and not adhere to the wound, so that at dressing change it will not damagegranulating tissue.

Passive dressings

For many years the products used were of the 'passive' or the 'plug and conceal' concept andincluded gauze, lint, non-stick dressings, and tulle dressings. Passive dressings fulfil very few of theproperties of an ideal dressing and have very limited (if any) use as a primary dressing, however,some are useful as secondary dressings.

In addition to gauze, lint and cotton dressings, other simple modified absorbent pads covered with a

perforated plastic film to prevent adhering to a wound (such products include Melolin, Cutilin andTelfa) are used both as primary and secondary dressings. They are used in minor and lowexudating wounds.

5.2.1 A modern inert dressing

Exudry and Mesorb are examples of products with a highly absorbent pad and a non-stick, non-shear surface. They can be used as a secondary dressing over moderate to highly exudating woundsand over hydrocolloid paste, cadexomer iodine, alginate and other primary dressings.

5.2.2 The non-absorbent passive dressings

The non-absorbent passive dressings such as paraffin gauze (tulle) dressings, are among theearliest modern dressings. Many variations have been developed over the years by changing theloading of paraffin in the base. In general, these dressings produce a waterproof paraffin cover over


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5.3

the wound which may lead to maceration in that water vapour and exudation may not pass throughand so become trapped within the wound. These products:

are permeable to bacteria

are known to adhere to the wound causing trauma on removal

require a secondary dressing.

Their use is limited to simple, clean, superficial wounds and minor burns. They are also used as a

primary dressing over skin grafts. There are modern alternative dressings composed of syntheticfibres tightly meshed and impregnated with materials that allow moisture to pass through and thusminimise any maceration of the wound and tissues. Examples include Adaptic, Cuticerin andAtrauman.

Interactive dressings

These dressings help to control the micro-environment by combining with the exudate to form eithera hydrophilic gel, or by means of semipermeable membranes, controlling the flow of exudate from thewound into the dressing. They may also stimulate activity in the healing cascade and speed up thehealing process.

There are six classes of interactive dressings which are classified according to their functionality.

5.3.1 Non-Absorbing dressings

5.3.1.1 Film Dressings (for wounds with no to low exudate)

These dressings consist of a thin, poly-urethane membrane coated with a layer of acrylic adhesiveand:

are waterproof

are gas/vapour permeable

are flexible

protect from shear, friction, chemicals and microbes

are transparent

spread tension forces.

They are particularly useful in superficial, clean wounds and in the prevention of breakdown and pre-ulcers in pressure wounds. They are also used as a post operative dressing over sutures and toreduce sub-tissue tension over a closed sutured wound after removal of the sutures or clips. Filmdressings should not be used for infected wounds.

BRAND MANUFACTURER TYPE

Opsite Smith & Nephew Plain film, Island Film

Flexigrid

Flexi Fix {continuous rolls}

IV 3000 {high MVTR*}

Post-op {island dressing}

Tegaderm 3 M Plain film

HP* {high MVTR}with absorbent pad

island dressing


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Biofilm Johnson & Johnson Plain film

Polyskin II

Aqua Protect

Hydrofilm

Tyco

Beiersdorf

Hartmann

Plain film

MR* {high MVTR}

Plain film

Island Film

Plain film

*MVTR = Moisture Vapour Transmission Rate ie. the level of passage of water vapour or exudatethrough the surface of the dressing.

*HP = Holding Power

*MR = Moisture Responsive

5.3.2 Absorbing dressings

5.3.2.1 Hydrocolloid dressings (for wounds with low to moderate exudate)

Hydrocolloids are a combination of polymers held in a fine suspension, and often containpolysaccharides, proteins and adhesives. When placed on a wound the polymers combine with theexudate and form a soft, moist gel-like mass. They also encourage autolysis to aid in the removal ofslough from a wound.

They:

are flexible and waterproof

provide a physical barrier

form a gel with exudate

aid in debriding

need no secondary dressing

are available in a thin form (transparent).

The early forms of hydrocolloids are occlusive, so as to make them impermeable to gases and watervapour. They do, however, act as a barrier to external bacteria and are waterproof enabling thepatient to shower. The thin, transparent hydrocolloids have a polyurethane film backing, are non-occlusive, thereby allowing the passage of water vapour and gases.

Hydrocolloids should be applied over the wound with at least 3-4 cm extra product greater than thesize of the wound. The skin should be dry and free from creams, ointments or oil to ensure goodadhesion. The dressing should be placed 1/3 above the wound and 2/3 below the wound, as this willprolong the wear time of the dressing. The dressing can remain in place for up to 7 days with removal

dependent on the level of exudate and when strikethrough has occurred (i.e. the exudate hasmigrated to the edge of the dressing).

Hydrocolloid products are used in low to moderately exudating wounds- including ulcers, donor sites(after haemostasis) and granulating wounds. They may also be used in conjunction with a paste orpowder form. The paste or powder is used in a deeper ulcer or cavity. These convert to the samehydrophilic gel and are covered with the normal hydrocolloid wafer.

BRAND MANUFACTURER TYPE

Comfeel Ulcer Dressing

Comfeel Paste

Comfeel Powder

Coloplast Multiple Sizes

Tube

Pack


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Comfeel PlusTransparent

Multiple Sizes

DuoDerm CGF

DuoDerm Border

DuoDerm ExtraThin

DuoDerm Paste

ConvaTec Multiple Sizes

Multiple Shapes and Sizes


Tube

Replicare Smith & Nephew Multiple Sizes

Ultec Tyco Multiple Shapes and Sizes

Hydrocoll

Hydrocoll Thin

Hartmann Multile Sizes

Multiple Sizes

Tegasorb

Tegasorb Thin

3M Multiple Shapes and Sizes


5.3.2.2 Foam dressings (for wounds with medium to high exudate)

These products are soft, open-celled hydrophobic/ hydrophilic non-adherent dressings that may besingle or multiple layered and meet many of the properties of an ideal dressing.

They:

allow the passage of exudate through the non-adherent surface to be absorbed in the mainbody of the product

are absorbent

maintain a moist environment

are thermally insulating

are cushioning

are non-adherent

are non-residual.

Foams are mainly used in moderately to heavily exudating wounds- including ulcers, donor sites andminor burns, and they act as a secondary dressing, particularly as a covering with the use ofamorphous hydrogels. In addition to standard and waterproof foams there is also a charcoal-impregnated version, Lyofoam C, as well as shaped cavity devices which may be inserted into

cavity wounds or gaping surgical wounds.

BRAND TYPE MANUFACTURER

Allevyn Sheet

Allevyn Island

Allevyn Adhesive

Allevyn Cavity

Multiple layer

Multiple layer waterproof

Multiple layer waterproof andadhesive

Dual layer cavity insert

Smith & Nephew

Cavicare Conforming Foam Smith & Nephew

Curafoam Single layer Kendall


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Hydrasorb Single layer Kendall

Lyofoam

LyofoamAdhesive

Lyofoam Extra

Lyofoam C

Permafoam

Mepilex

Mepilex Thin

Dual layer

Dual layer waterproof

Multiple layer

Dual layer combination with

charcoal

Multiple layer

Multiple layer

Thin Multiple layer

Aaxis Pacific

Aaxis Pacific

Aaxis Pacific

Aaxis Pacific

Hartmann

Molnlycke

Molnlycke

5.3.2.3 Alginate dressings (for wounds with medium to high exudate)

Alginates are the calcium or sodium/calcium salts of alginic acid, composed of manuronic andguluronic acids obtained from seaweed. When applied to a wound, the sodium salts present in the

wound exchange with the calcium in the alginate to form sodium alginate which is a hydrophilic gel.This gel has the ability to absorb exudate into itself while maintaining a moist environment at theinterface between the dressing and the tissue.

Alginate dressings:

are highly absorbent

form a gel with exudate

create a moist interface

are easily removed

are haemostatic.

Alginates are used on donor sites, bleeding sites, exudating leg ulcers and cavities. They are notconsidered to be of value in low exudating wounds or dry wounds with eschar.

They come in a number of different forms, including sheets, packing rope and in combination withcharcoal for exudating malodorous wounds.

Sheet alginates should be cut to the shape of the wound, placed on the wound and covered with asuitable secondary dressing (eg. foam and non-stick dressings). They should then be held in placewith a cohesive or tubular bandage. If the wound is highly exudating then an outer absorbent padmay be added. In the case of a moist cavity wound, the rope or packing ribbon is gently placed intothe cavity taking care not to pack the material tightly into the space. In general, alginates should bechanged when they have fully converted to a gel, this will vary from 1 to 3 days depending on the

level of exudate in the wound. When used on a donor site, the material is placed over the area afterskin harvesting and covered with a film or a foam dressing, which can remain in place for up to 7days.


Algoderm

Kaltostat

Carboflex(withcharcoal)

Surface sheet {firm gel}

Cavity Rope {firm gel}

Surface sheet{firm gel}

Cavity rope {firm gel}

Surface sheet

Johnson & Johnson

Convatec

Comfeel Alginate Cavity Rope {soft gel} Coloplast


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Comfeel Seasorbsoft


Curasorb Surface sheet {firm gel}


Tyco

Sorbsan Surface sheet {soft gel}

Cavity rope {soft gel}

Unomedical

Tegagen HI

Algisite M




3-M

Smith & Nephew

5.3.2.4 Hydrofibre dressings

Hydrofibre dressings have some of the properties of alginates in that they are a fibre rope or dressingthat forms a firm gel in contact with fluid.

They:

are composed of a synthetic fibrous mat

form a firm gel in contact with exudate

are highly absorbent

have no lateral wickingprotects peri-skin

An example of this product is Aquacel.

5.3.2.5 Hydroactive dressings (for wounds with medium to high exudate)

These multi-layered highly absorbent polymer dressings with a surface adhesive and a waterproofouter layer are similar to hydrocolloids, however, instead of forming a gel in contact with exudate, thefluid is trapped within the product itself, to maintain a moist environment.

Hydroactive dressings are:

highly absorbent polymer dressings

waterproof

expandable

non-residual

semi-permeable.

Hydroactive dressings are indicated for use in highly exudating surface and cavity wounds includingleg ulcers, pressure wounds and minor burns. They are particularly useful over joints such as elbows,knees, fingers and toes due to their ability to expand and contract without causing constriction.Hydroactive dressings are not indicated for dry or lightly exudating wounds.


Cutinova Hydro

Allevyn Thin

AllevynCompression

Allevyn plus Cavity

Surface sheet thick

Surface sheet thin

Surface sheet non-adhesive

Cavity dressing

Smith & Nephew


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Tielle Surface sheet Johnson & Johnson

Biatane Surface sheet

Cavity dressing

Coloplast

PolyMem Surface sheet Ferris

5.3.2.6 Hydrogels ( For dry or sloughy wounds )

Hydrogels are a group of complex organic polymers having a high water content ranging between 30to 90 percent. This broad class of polymers swells extensively in water, but does not dissolve inwater. They have the properties of both rehydrating dry tissue, and absorbing certain amounts of fluidinto themselves. They are provided as either amorphous gels or sheet gels. These products are usedto help re-hydrate sloughy wounds and necrotic tissue to aid in the autolytic debridement of wounds.They are also used in the management of burns, including sunburn, scalds and other partialthickness burns. Amorphous hydrogels have also been used in the management of chicken pox and

shingles, applied to the eruptions three to four times a day. They provide a moist environment andrelieve the discomfort of the lesion, and also reduce the probability of scarring.

Hydrogels are also available in sheet form consisting of a cross-linked polymer and water held in abacking. These products are particularly useful in the management of burns, and also to aid theremoval of necrotic tissue in pressure wounds.


DuoDERM Gel Amorphous non-preserved Convatec

Safgel Amorphous preserved Convatec

Intrasite gel Amorphous non-preserved Smith & Nephew

Intrasite gelconformable

Impregnated amorphous Smith & Nephew

Solosite Amorphous preserved Smith & Nephew

Curafil gel Amorphous preserved Tyco

Curafil Impregnatedgauze

Curagel

Impregnated amorphous Sheet Gel Tyco

Purilon gel Amorphous non-preserved Coloplast

Solugel

Nu-gel

AquaClear

Amorphous both preserved and nonpreserved

Sheet Gel

Sheet Gel adhesive and non-adhesive

Johnson &Johnson

Johnson &Johnson

Hartmann


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5.3.3 Miscellaneous dressings

There is a small number of specialised dressings for use in particular wound types.

5.3.3.1 Cadexomer Iodine Dressings (e.g. Iodosorb)

This is a non-toxic iodophor that combines iodine with a polysaccharide polymer. When applied to thewound, the exudate combines with the polymer and is absorbed at the same time as the iodine isreleased- over a period of 72 hours at a low strength.

Cadexomer Iodine was developed in the 1980s and consists of cadexomer polysaccharide polymerand iodine 0.9%. The iodine is cross-linked into the structure of the polymer. Upon contact with awound, this dressing:

is absorbent forms a gel with exudate

releases iodine as gel forms

pulses iodine at 0.1% (not cytotoxic)

is used for sloughy/ infected wounds, diabetic wounds, chronic, slow healing wounds

may stimulate growth factors.

5.3.3.2 SilverSilver has been used for many years, and has proven antimicrobial activity. It is broad spectrum andinactivates almost all known bacteria, including methicillin-resistant staphylococcus aureus (MRSA)and vancomycin-resistant enterococci (VRE). No cases of bacterial resistance have beendocumented9,10. Silver has been used in the treatment of burns as a silver sulfadiazine cream, andthis cream has also been applied to some wounds. The difficulty in applying a cream to a mucoussurface is that it will cause the development of mucilaginous slough. The development of a range ofmodern silver dressings overcomes this difficulty by delivering varying levels of silver directly from thedressing. The base dressings include hydrocolloids, alginates, tulles, hydroactives, foams, gels andpolyethylene mats. The amount of silver and the method of action vary greatly between thesedressings. Some release silver into the wound and some maintain the silver within the dressing and

kill bacteria as they are absorbed into the dressing.

Silver Product Type Trade name Manufacturer

High Density Polyethylenedressings

Acticoat Smith & Nephew

Foam Dressing Avance Aaxis Pacific

Alginate Dressing Acticoat Absorbent Smith & Nephew

Hydrocolloid Dressing Contreet H Coloplast

Hydroactive Dressing Contreet Coloplast

Hydrofibre Dressing Aquacel Ag Convatec

Tulle Dressing AtraumanAg Hartmann

5.4 General rules for the topical use of antiseptics

The role of topical antiseptics in chronic wounds is not as clear as in the case of acute wounds.There is a group of patients with long standing, non-healing leg ulcers. There are some clinicians

who believe that one of the reasons for non-healing of these wounds is the presence of largenumbers of colonised bacteria, especially in those patients who may be malnourished, diabetic orimmuno-compromised. In some of these patients, the use of a short course of dilute topical


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antiseptics may help reduce the surface flora and speed the process of wound healing. The decisionshould be made for the individual patient, taking into account all of the benefits and risks.

WOUND TYPE MANAGEMENT

CUT/LACERATION

Clean the area with water or saline. If there is any contamination, use asurfactant antiseptic (eg. Savlon or Povidone Iodine scrub) to remove

any foreign material that may be a focus for infection. Apply anantiseptic around the area and cover with a simple dressing (eg. a filmdressing).

GRAZE Due to the presence in most grazes of dirt, gravel and other material,scrub the area with a surfactant antiseptic eg. Savlon or PovidoneIodine scrub.

Apply an antiseptic around the wound and cover with either a filmdressing or an island film dressing.

BURN Most minor burns do not require the use of a topical antiseptic. Their

use will depend on the depth of the burn and if there is damaged andnecrotic tissue present. If there is, then the use of SSD cream isconsidered appropriate in the early management. If the burn is minorand there is little tissue damage (eg. minor blisters) then apply anamorphous or sheet hydrogel.

CHRONICWOUNDS

eg. Leg Ulcersand Pressure

Ulcers

If the level of colonised bacteria is high, the short term use of PovidoneIodine Solution is the most effective antiseptic to use. Therecommendation is to use a low strength (eg. 1%) solution and to applyfor 3 to 5 minutes and then wash the product off. Within this time theproduct will have significantly reduced the numbers of surface bacteria.

The other option is the use of Iodosorb being non-toxic.

5.5

5.6

Hypertonic Saline

Hypergranulation is generally treated with topical silver nitrate or copper sulphate. An alternative andless toxic method is the application of a hypertonic saline dressing. These are applied to thehypergranulation and covered with a simple secondary dressing and a compression bandage. Thedressing is changed daily. Examples of this dressing are Mesalt and Curasalt.

New burn dressings

Once the burn has settled down and any necrotic tissue removed by autolysis, an additional modalitymay be used. The use of retention tape dressings, for example Fixomull and Hypafix, applieddirectly over a minor burn is also a possibility. Such a protocol was introduced by the Burns Unit atRoyal Perth Hospital and is now in general use.

The tape, once applied, remains in place for seven days at a time. It is removed by dissolving theadhesive in a fixed oil or citrus oil, allowing the tape to be easily removed without damaging the newepithelium. These retention tapes are permeable, allow exudate to flow through their surface, areflexible and although not waterproof may be washed after the first 48 hours of application and theywill dry and remain in place.

It is also important to cover the dressing with a cohesive bandage to apply some compression to the

skin.


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5.7

5.8

Keloid and Hypertrophic Scar Management

A topical method for treatment of keloid and hypertrophic scars is the use of a silicone dressing. Thedressing is applied to the scar initially for 4 hours and then progressively increasing the contact to 24hours. The scar may gradually reduce in depth and colour. This will however, be a slow processrequiring application for six months or more. Examples of this type of dressing are Cica Care andMepiform.

Bandages

The use of material to bind a wound is as ancient as medicine itself. Techniques and material havechanged little over the centuries, but in the past fifteen years there has been an explosion in the typeof bandages available.

When choosing and applying a bandage it is important to differentiate between the traditional and theritual on one hand, and what is best and most cost effective for the patient on the other.

The bandage may be needed for keeping a dressing in place, supporting an injured joint or assistingvenous return.

5.8.1 Retention Bandages

The role of retention bandages is effectively to hold a dressing in place. They are of particular usewhere a patient has very fine and very fragile skin that is easily damaged if the dressing was held inplace with any type of adhesive tape or other adhesive product. For many years, cotton crepebandages have been used to hold dressings in place for this purpose. However, today there are anumber of more effective and appropriate bandages that may be used to hold a dressing in place.

The first is the lightweight conforming cohesive bandage. This type of bandage is a lightweight crepecoated with a thin latex. As a result of this coating the bandage sticks to itself but not to skin, hair orclothing. You only require a very small length to hold the dressing in place, compared with using acomplete roll of a standard crepe bandage. This type of bandage comes in widths that areappropriate for fingers and toes and also for limbs and larger sizes for the head. The other mainadvantage is that the same amount is not required to hold the dressing in place compared with using

a standard crepe bandage. This makes this type of bandage less bulky and very cost effective.Examples of this type of bandage are Handigauze Cohesive, Easy Fix Cohesive and Hospifix.

The other type of product is the elasticised tubular bandage available in a light weight form that maybe cut to the required size and placed over the dressing, again holding it in place. An example is TubiFast.

5.8.2 Support Bandages

Support Bandages are of a heavier construction and are made from both natural and synthetic fibres.They achieve their stretch by the use of high twist yarns and the heavier construction. The main roleof strong support bandages is the support of joints in strains and also in the management of muscular

injuries. Strong support bandages can be used singularly or in combination to restrict movement, tohelp reduce some of the oedema and act as a mechanism of support following soft tissue injury. Theexamples of this type of bandage are the heavy duty crepe bandage such as Elastocrepe andHandycrepe, and the heavier weight cohesive bandage (eg. Coban, Coplus, Handygrip).Also, single layers of the heavier weight tubular bandage may also be used for this purpose (eg. TubiGrip, Handyplast Tubular or Tensogrip).

5.8.3 Compression Bandages

The action of these bandages is to provide pressure firm enough to compress the pathologicallydistended veins, thus enabling the valves to remain tightly against the wall of the vessel, increasingvelocity of the venous blood stream and normalising the returned flow of blood to the heart.

Accumulated fluid and waste products are removed from the affected tissue by the accelerated rateof flow resulting from application of a pressure bandage.


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Effective therapeutic compression starts with a sub-bandage pressure of 18 mm of mercury at theankle. Anything giving a lower value may be appropriate for support, but is not consideredappropriate in the treatment of venous leg ulcers.

The primary aim of compression is to reduce pressure in the superficial veins in order to encouragevenous return to the heart. This is performed by increasing the velocity of flow in the deep veins anddiscouraging oedema by reducing the pressure difference between the capillaries and the tissues.The most effective method is to apply graduated compression from the toes to the knee. The highest

pressure should be exerted at the ankle, gradually falling to 50 percent at the knee. Anti-embolicstockings should only be used for the prevention of deep vein thrombosis in hospitalised patients.They provide a pressure of between 12mm and 18mm of mercury.

Compression bandages are divided into two types: high stretch compression and shortstretch.

5.8.3.1 High stretch compression bandages

These bandages have an extension from 130 percent to 200 percent, high elasticity, medium to highresting pressure, and medium to high working pressure. They exert their effects superficially, workingin combination with the muscles. They are indicated for venous oedema and the management ofvenous ulcers and may be left in place for 24 hours. Examples include Tensopress, Setopress,Surepress and Eloflex.

5.8.3.2 Short stretch bandages

These have an extension of 30 percent to 90 percent, low elasticity, low to slight resting pressure, buthigh to very high working pressure. They exert their main effects deep within the limb and areindicated for venous oedema and lymphoedema. These may be left in place for 24 hours. Examplesof this type of bandage are Comprilan, Lastolan and Tensolan.

Application methods include the simple spiral method which is performed by applying the bandagewith a figure eight at the ankle, and continuing up the limb in a spiral application covering 50% of thepreviously bandaged area. The application is generally undertaken with the high stretch type ofbandage.

A continuous figure eight method of application is performed by overlapping as the bandage is woundup the leg so that it is applied in one direction and then in the opposite direction, producing a Vshape in the bandage. This method is used particularly with the low stretch compression bandages.

A development in bandaging has been the introduction of the Charing Cross 4 layer system. Thiscombines an orthopaedic wool, crepe, elastic and cohesive bandage in multiple layers. This achieves40 mm of mercury at the ankle, graduating to 17 mm of mercury at the knee. A number of publishedstudies have shown good healing rates in 12 weeks with this particular system 11. The commercialbrands of this type of bandage system are Profore, Profore Lite, Pro-guide and Veno-4.

If it has been clearly demonstrated by Doppler and/or Duplex scanning that a true venous pathologyexists, compression bandaging is then used in combination with management of the wound byappropriate dressings, using either a high or low stretch compression bandage.

Where there is some indication of minimal arterial involvement, compression is provided by the useof a straight tubular bandage. Where more significant arterial disease is present, no compression isapplied over the dressing.

5.8.3.3 The hazards of compression bandages

Care must be exercised when applying compression bandages to ensure that there is adequatearterial blood flow. The application of compression can cause skin necrosis, trauma, ulceration, oreven amputation (which may result from damage caused by lack of arterial blood in the area).

An alternate method of applying graduated pressure to the leg is through the use of compressionstockings. Stockings may be used as part of the treatment of venous leg ulcers, as an ongoingmanagement modality of venous disease, and/or for the prevention of venous stasis.

The use of compression stockings both as a preventive measure and anti-embolic stocking tominimise the risks of venous stasis is common. The difficulty is that there is considerable confusion


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as to the appropriate type of stocking to use and the level of compression necessary for besttreatment.

Anti-embolic stockings may also be used alone or in conjunction with systemic medication (eg. LowMolecular Weight Heparin) for the prevention of Deep Vein Thrombosis in patients undergoingsurgery. The stockings are worn by non-ambulatory patients in hospital pre and post surgery to helpprevent DVTs.

It should be noted that anti-embolic stockings are not suitable for the treatment or management of

venous disease.

Compression stockings have a major role to play in the prevention of venous stasis, should also beworn when travelling long distances to minimise oedema and thrombosis development.

5.8.4 Zinc paste bandages

Zinc has been used in medicine for hundreds of years, even though very little published data of itspharmacology is available. Zinc is an important trace element in many functions of the body. Inwound healing it is essential for cell proliferation and tissue regeneration, and is also involved incollagen synthesis and epithelialisation.

There are a number of commercial zinc paste bandages available on the Australian market. These

include: Zincaband and Steripaste of Seton, Viscopaste and ZipZoc of Smith and Nephew,Flexidress of Convatec, and Gelocast of BSN Medical.

The bandage can be applied to the limb, as a patch over the wound or as a full length bandage. Awater-based zinc paste bandage with no preservatives is beneficial in the management of chronicvenous leg ulcers, particularly where venous eczema is present and when used in conjunction withappropriate compression bandaging.


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6.1

6 General rules

Acute wounds

Assess and identify

Clean and decontaminate

Stop the bleeding (alginates/ pressure)

Wound closure (closure strips/ film dressings)

Dressing film, island film or island dressing

Bandage (simple cohesive).

6.2

6.3

6.4

Chronic wounds

Confirm underlying cause ie. venous / arterial etc

Dressing dependent on wound type and the level of exudate

If true venous-pathology exists, graduated compression should be used.

Protocol for wound management of skin tears

Clean the wound with water or saline. If there is contamination, use a surfactant wash product(eg. QV Wash) to help remove any debris.

If bleeding, apply gentle pressure with a piece of gauze padding (ensure that the gauze doesnot stick as this may result in further tearing), if unsuccessful then apply a haemostatic alginatedressing (eg. Kaltostat) to aid in haemostasis.

If there is major separation of the skin edges, apply an elastic sterile strip, preferably 3-4mm inwidth to several parts of the skin tear to hold the skin flap in place.

Apply a low strength povidone iodine solution to the wound, leave in place for 3 minutes andthen wash off.

Apply a small amount of an amorphous hydrogel (eg. IntraSite Gel) to the wound.

Cover with a foam dressing (eg. Lyofoam, Allevyn, Mepilex).

Hold in place with a light weight cohesive bandage.

This system is left in place for 4 to 5 days at which time the dressing is removed, the wound cleanedand the system replaced. After the next 4 5 days the dressing is removed and replaced with apatch of non-preserved zinc paste bandage (eg. Gelocast, Steripaste, ZipZoc). This is thencovered with foam and held in place with a lightweight cohesive bandage (eg. Handygauze cohesive

) and left in place for seven days. Upon removal the wound should be healed. If not, then repeatthe zinc paste patch dressing system for a further seven days.

Difficult wounds (i.e. animal or insects bites)

Assess and identify

Plan treatment

Clean

Dress as appropriate

NB. May need systemic antibiotics, infection may be due to atypical micro-organisms.


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6.5

6.6 Burns

Post operative wounds

Assess

Dress over sutures with a film or thin hydrocolloid.

If exudating use an island dressing.

For an open cavity wound, use alginates and/or foam. Use film dressings over the incision once sutures are removed.

For sunburn, apply cold water then amorphous hydrogels.

For simple burns and scalds of partial thickness, apply cold running water for 10-15 minutesthen hydrogels (either sheet or amorphous), or retention tape (eg. Fixomull or Hypafix).

The final aspect of wound care is a plan for management. Once the wound is healed, it is important

to investigate and examine the intrinsic and extrinsic factors. Once identified, try to alterenvironmental aspects such as nutrition, exercise, use of compression stockings, and environmentalissues such as standing for long periods of time leading to venous stasis. These actions may wellprevent redevelopment of the wound or the development of new ones.


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7 References

1. Sussman G, Wound Management: How to treat. Australian Doctor 30 November 2001:S1-S8

2. Nelzen O, Bergqvist D, Lindhagen A. The prevalence of chronic lower-limb ulceration has beenunder estimated: results of a validated population questionnaire. British Journal of Surgery

1996;83:255-258

3. Winter, G. Formation of the scab and the rate of epithelization of superficial wounds in the skin ofthe young domestic pig. Nature 1962;193: 293-4

4. Drosou, A. Antiseptics on wounds an area of controversy. Wounds 2003 15(5):149-166

5. Australian Institute of Health and Welfare 2002. Diabetes: Australian facts 2002. AIHW Cat. No.CVD 20 (Diabetes Series No.3). Canberra: AIHW.

6. Diabetes Australia press release 16th May 2006)

7. Bennett G, Leigh IH. Pressure ulcers: prevalence, aetiology and treatment modalities: a review,American Journal of Surgery 1994,167(1a):25S-30S (correct)

8. Turner, T D. Products and their Development in Wound Management, Plastic Surgery Journal1979 75-84

9. Thomas S, McCubbin P. A comparison of the antimicrobial effects of four silver-containingdressings on three organisms. Journal of Wound Care.2003 Mar;12(3):101-7

10. Lansdown ABG. Silver 1: its antibacterial properties and mechanism of action, Journal of WoundCare 2002,11(4):125-130

11. Moffatt CJ, Dickson D. The Charing Cross High Compression Four Layer Bandage System,Journal of Wound Care (1993) 2(2): 91-94.
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Wound Care Module