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Basic plastic surgery techniques and principles: Chronic wound management


In the sixth part of our series, Aroushka L James and explain Ardeshir Bayat the management and treatment of chronic wounds

Visit any hospital in any country and many patients are likely to have chronic non-healing wounds. For example, in the United Kingdom the cost to the NHS of treating these patients is vast-estimated at £1000m ($1700m €1400m) a year.w1Of course, this estimate does not take into account the effect on the patient's quality of life.

The healing process

Healing is a highly complex process. The ordered sequence of events can be described as four key stages-thrombus formation, inflammation, cell proliferation and repair of the matrix, and epithelialisation and remodelling of scar tissue.w2

In a chronic wound, this order has become deranged, disrupting the sequence at one or several of the stages.w3 This may be because of defective remodelling of the extra cellular matrix, failure to re-epithelialise, or prolonged inflammation.w4

Types of chronic wound

Pressure ulcers

Pressure ulcers are a potentially avoidable type of chronic wound. They occur when soft tissue is compressed between a bony prominence and an external surface for a prolonged period of time producing a localised area of tissue necrosis. Intervention should be taken at the first signs of redness over a bony prominence or slightest skin break. But to prevent this from happening in a hospital setting, medical staff should implement a turning schedule to avoid prolonged compression.


KARI LOUTNATMAA/SPL


MRSAA under a microscope


Venous ulcers

Venous ulcers are the result of sustained venous hypertension in the superficial veins. Hypertension in the superficial veins occurs when valves in the deep perforating veins become incompetent or it may occur after a deep vein thrombosis. The increased pressure in the veins causes extravasation of fibrinogen, which leads to deposition of fibrin around the vessel. This in turn results in poor oxygenation of the surrounding skin.w5

Treatment of venous ulcers must include ongoing management of the venous hypertension if the ulcer is to resolve. Failure to manage this adequately contributes to the high recurrence rate of venous ulcers.

Arterial ulcers

Arterial ulcers occur as a result of arterial disease. They arise when inadequate perfusion of skin and subcutaneous tissue at rest (arterial insufficiency) leads to cell death.w6 Because arterial disease is usually always progressive, arterial ulcers are also usually progressive. This means clinicians should diagnose and treat arterial insufficiency as soon as possible to avoid further tissue loss. Dressings aim to keep the wound bed moist to prevent additional necrosis. However, treatment of arterial wounds is largely unbeneficial until an adequate blood supply is achieved.

Diabetic ulcers

Diabetic ulcers commonly occur on the feet due to peripheral neuropathy and peripheral vascular disease, which both lead to a lack of protective sensation, and so a minor wound may lead to an ulcer. To avoid diabetic ulcers, doctors should treat vascular disease, recommend appropriate footwear, and implement strict diabetic control.

Assessment and management

Achieving a healed wound is not as simple as many people expect. Wound care is becoming a multidisciplinary collaboration between the patient, general ­practitioner, district nurse, dietician, physiotherapist, and hospital staff. A chronic wound can be incredibly disfiguring, malodorous, and detrimental to quality of life. Clinicians should be aware of the psychological impact of scarring, and some patients may require the services of body image counsellors. Education, support, and selection of treatment affordable to the patient aid compliance and are more likely to result in a healed wound. If patients' needs are considered and taken into account, whether the wound completely resolves or not, the treatment will have been a success.

Continuous wound assessment and good observation allows clinicians to ascertain whether the wound management is effective, and allows them to monitor for complications. The most advanced techniques in wound care will fail if they are not applied appropriately, and this ultimately relies on the observation and how this is recorded.

Wound history

Clinicians should ask the following questions:

  • What are the causes? Can they be removed? For example, if a foreign body such as glass is present in the wound this delays healing and needs to be removed
  • How long has the wound been there? Commonly wounds fail to heal if the treatment is incorrect
  • Has the correct diagnosis of the wound been made? Often a lack of experience leads to misdiagnosis of the wound state and hence incorrect treatment
  • Have there been previous non-healing wounds? What treatments were used? Were they successful?
  • Is the wound recurrent? Causes of recurrence should be sought and addressed.

Wound examination

Recording wound characteristics allows the clinician to assess the effectiveness of treatment and minimise complications. They can then adapt the management plan to suit the changing wound state. The following information should be recorded in patients' notes.

Location

Wound location gives clues about the cause of the wound-for example, pressure ulcers are commonly found in sacral regions-but also the type of dressing that may be required.

Wound mapping

By tracing the margin of the wound on to acetate and measuring the depth with a sterile ruler, the clinician can make an estimation of the area and volume of the wound.

Colour

Colour of the wound bed gives an indication of the phase of healingw7

  • red or purple indicates granulation tissue
  • yellow is fibrous tissue or necrotic slough
  • black is eschar or necrotic tissue
  • pink or purple means re-epithelialisation has begun.

Odour

Malodorous wounds are commonly associated with infection. Malodour can also be due to poor hygiene or from a dressing that has not been changed regularly. It is important to note change in characteristics of the smell, especially if it has become much stronger. Necrotic tissues give off an offensive repulsive odour, and anaerobes typically produce a distinctive acrid or putrid odour.

Infection

Infection is the single most important cause of delayed healing.w8 The presence of bacteria in the wound, however, does not indicate infection or that it will impair healing. Studies suggest that low numbers of certain bacteria stimulate healing.w9 But when the number of bacteria becomes too great, the healing process becomes impaired. The continuous presence of virulent bacteria can lead to massive continued inflammatory response that contributes to host injury.w10 Signs of infection should be looked for at each dressing change. These include redness, tenderness, warmth, odour, discharge, and swelling. Typically, Pseudomonas gives a blue-green hue to the wound bed, and anaerobes give a dull appearance. Wounds with a gelatinous texture that bleed easily sare also likely to be infected.

Topical antimicrobial agents are available for local infection. But their use should be weighed up against the risks, allergic reactions, and potential slowing of wound healing. Prolonged use of topical antimicrobials is not advised. If the infection has spread beyond the wound margin or the ulcer probes the bone, systemic antibiotics should be used.

Methicillin resistant Staphylococcus aureus (MRSA) is commonly found in ulcers. Its presence in wounds rarely leads to death, but cross infection into an immunocompromised patient can be fatal. Clinicians should screen for this pathogen in chronic wounds by culturing wound swabs for bacteria, and routinely include this in the management plan.


EAMONN McNULTY/SPL


A necrotic,ulcerated foot


Exudate

The volume of exudate is difficult to measure. A rough estimate should be recorded-no exudate, moderate, or excessive.

The type can be described as

  • Serous-clear fluid without blood pus or debris
  • Serosanguinous-thin, watery pale red to pink fluid
  • Sanguinous-bloody, bright red
  • Purulent-thick, cloudy, yellow, or tan.w6

Stage

Staging by clinical examination and assessment allows the clinician to record and evaluate the extent of tissue loss. It also will indicate the appropriate dressing type or whether the wound needs packing. Staging is limited, is unable to show the wound's progression over time, and should not be recorded in isolation. Staging is a valuable tool in wound assessment.

Pain

The patient may feel temporary pain ­during debridement or dressing changes, although excessive pain at this time should prompt re-assessment of wound care products or technique. Continuous pain is a cause for concern and should be investigated. It is usually due to infection or unsuccessful treatment of the underlying cause, such as ischaemia. Wound pain can be treated with analgesia or support of the tissue during dressing changes.

General patient assessment

General patient assessment can help to avoid a delay in healing. A wound that is poorly vascularised or flooded with oedema will not heal.w11 The resultant poor oxygenation leads to impaired leucocyte activity, decreased production of collagen, and decreased epithelialisation.w3 Wounds of the lower limb are particularly susceptible to poor blood supply.w8

One important cause of non-healing wounds is patient immobility and this should be assessed as pressure ulcers may occur. The Waterlow risk assessment score is a ­useful tool to assess risk of pressure ulcer development.

An often overlooked, easily treatable cause of non-healing is poor nutrition. Low dietary protein will result in delayed formation of granulation tissue, and vitamin C deficiency inhibits collagen synthesis.

Poorly controlled metabolic disorders such as diabetes mellitus are associated with poor wound healing.w12 Measures to control blood glucose are therefore included in the management plan. Glucocorticoids, non-steroidal anti-inflammatory agents, and immunosuppressive drugs all have well documented anti-inflammatory effects that may slow healing.

The patient's anxiety should be appreciated when assessing. Research has shown that increased anxiety is associated with delayed healing.w12 If anxiety is suspected, doctors have a duty to determine why and try to resolve it.

Wound investigations

Biopsies are not usually done on all wounds, but a longstanding non-healing wound must be biopsied, as the underlying cause could be a skin malignancy.

Goal setting

The purpose of the wound and general assessment is to set a goal for healing the wound. Goal setting allows both clinicians and patient to assess how the wound is progressing and guides decision making in its treatment. The goal should be realistic; unrealistic goals lead to patient dissatisfaction. It may not be a healed wound, but may be getting the patient mobile again, reducing the unpleasant symptoms such as pain or odour, or explaining the delayed healing in an immunocompromised patient.

Treatment

The principle behind wound treatment is to change the wound bed environment from a chronic to an acute wound, and so aid in healing. Falanga suggested several clinical targets12 for wound bed preparation to achieve the acutely healing wound bed state.

Removal of necrotic or fibrinous tissue to promote formation of granulation tissue

Simple cleansing and irrigation with sterile water or saline will remove the debris from the wound surface, remove excess exudates, and decrease bacterial burden by removing heavily contaminated slough.3

Removal of deeply imbedded debris, necrotic and fibrinous tissue and bacteria requires debridement. Debridement is removal of devitalised or decontaminated tissue, and immediately returns the wound bed environment from a chronic to an acute state. Chronic wounds will require ongoing debridement, as build up of non-viable tissue needs to be removed to promote formation of granulation tissue. Although debridement usually occurs naturally, artificial debridement accelerates healing.13 For types of debridement and their indications (see Table 3).

Some clinicians believe that a moist wound environment will hinder healing and promote infection, but studies show that moist wound environments can actually accelerate healing by as much as 50%.17 However wound fluid, especially that from chronic wounds, does have a negative effect on wound healing13 and should be controlled.

Dressings (see Table 4) can successfully control exudates as well as reduce and prevent infection, stimulate autolytic debridement, reduce wound pain, and stimulate the development of granulation tissue. Excessive exudate is often caused by infection and should be investigated and treated where possible.

Achieve a well vascularised wound bed

Clinicians should make every attempt to ensure that the wound is well vascularised. This may involve removal of local pressures such as a callus on the feet. In some cases the intervention of the vascular team may be required for Doppler assessment and surgical revascularization.

Decrease bacterial burden

If an organism is identified, the patient should receive antibiotics, as discussed earlier. Clinicians should also consider an underlying metabolic factors predisposing to infection, for example poor glycaemic control. Debridement is also used to reduce bacterial burden, as it is fast and effective.

Control oedema - compression bandaging

Oedema is often seen in the lower limbs of people whose superficial and deep veins have incompetent valves. Techniques used to reduce oedema include raising the affected area where possible and giving diuretics. Compression bandaging (see tables 5 and 6) uses different types of bandages to produce graduated compression in the treatment of venous ulcers.16

VAC Therapy

Controlled negative pressure is applied to the wound to create a hypoxic environment which stimulates angiogenesis, and promotes the formation of granulation tissue. The risk of excessive bacterial colonization of the wound bed is reduced as VAC therapy gets rid of wound fluid, thereby reducing the bacterial burden.5 The wound is fully occluded using adhesive tape with intermittent or continuous suction applied at approx 120-125mmHg. The pump is adjustable and can be programmed to the appropriate amount of negative therapy that needs to be applied. Machines are large and treatment is expensive, so use is not widespread.

Future Concepts

Growth factors and cytokines

Much research has focussed on the use of topical growth factors and cytokines, which control key cellular activities including cellular division and tissue repair. The early optimism for cytokine and growth factor directed therapy was followed by mixed clinical results.23 How to deliver the factors and how to avoid their inactivation by the hostile environment of the wound bed are current problems.

Skin substitutes

Cultured grafts of allogenic and autologous epidermal kertinocytes are thought to help chronic wounds which don't respond to conventional treatment.24

Gene transfer technology

By inserting genes into cells involved in the healing process, it may be possible to deliver specific therapeutic proteins into the wound site.25

Table A Schultz's definitions of bacterial involvement in the woundw2
Term Definition
Wound contamination Presence of non-replicating micro-organisms in the wound
Wound colonisation Presence of replicating micro-organisms adhering to the wound that do not cause injury to the host
Critical colonisation Presence of replicating micro-organisms leading to increased bacterial burden causing a delay in wound healing
Wound infection Presence of replicating micro-organisms in the wound causing injury to the host.

Table B Types of wound investigation
Investigation Description
Punch biopsy Cylindrical portion of tissue removed via a needle and sent for histological examination
Incision biopsy Transverse section of healthy skin and wound bed are taken for histological comparison
Doppler assessment If peripheral pulses cannot be felt, Doppler ultrasound imaging can be used to assess arterial circulation in that area
Bacterial swab Swabs of the wound bed are taken to detect and identify pathogens
Urinalysis Checking for glycosuria and a full blood count to detect anaemia and blood dyscrasias

Table 3. Types of Debridement and their indications
Type of Debridement Description Indication Advantages Disadvantages
Autolytic Automatic process involving macrophages & endogenous proteolytic enzymes that liquefy & spontaneously separates necrotic tissue Occurs naturally in most people -Causes least amount of pain
Most cost effective
- free
-Slow
-There is a high risk of infection
Surgical Removal of necrotic & non-viable tissue using a sterile scalpel -Large wound area
-Widespread infection
-Fast
-Most effective
-Immediately converts chronic wound bed environment into an acute one
-Painful
-Expensive
-Can cause bleeding
-Risk of damage to tendons
Enzymatic autolytic Application of topical exogenous enzymes to wound surface where they act in unison with endogenous enzymes. Removal of eschar from large wounds where surgical techniques are not appropriate - Can be applied to very large areas
- Useful for difficult areas such as those overlying tendons on the ankle
-Produces excessive amounts of exudates
-Local irritation to surrounding skin
Mechanical Simplest form is use of wet to dry dressings but irrigation & whirlpool techniques are also used to physically remove debris for the wound Necrotic wounds at the inflammatory phase Reduces bacterial burden -Expensive
-Nurse time intensive cannot be used on granulation tissue
-Bleeding and pain on removal
Larval Sterile larvae of Lucidia Sericata fly are placed in the wound they produce powerful enzymes that break down dead tissue without harming healthy host tissue14 Large areas of necrotic tissue -Enzymes combat clinical infection15 Larvae can die in excess exudates

Table 4. The Role of Dressings on Different Wound Types.
Wound appearance/Characteristic Description Management aim Dressing choice Dressing description
Necrotic Dead, devitalized tissue. This tissue can become dehydrated in a hospital ward or centrally heated room, as it drys out it shrinks and darkens until it becomes olive green or black and hard & dry to touch. This hard necrotic tissue inhibits autolysis20 Keep the necrotic tissue moist therefore assisting autolysis 1ary: Apply wet soaks via gauze
Or
cotton wool
Or
Intrasite gel 2ary: Melolin
Or
Opsite flexigrid
Saline or water soaked gauze or cotton wool
Hydrogel Dressing inert to normal biological processes. Permeable to metabolites. Provide high concentration of water 70-90% contained in insoluble polymers.
Perforated plastic film dressing. Provides barrier to prevent evaporation of moisture.
Moisture Vapour Permeable Adhesive Film Dressing
Sloughy Mixture of dead white cells, dead bacteria, rehydrated necrotic tissue and fibrinous tissue A thick layer can build up quickly and it has been shown that slough can predispose to infection21 Control exudates and remove slough fluid from wound 1ary: either as a dressing Iodosorb
Or
a paste Iodoflex applied to gauze
2ary: Melolin Opsite flexigrid
Dressing contains polysaccharide beads that absorb moisture and progressively move bacteria and cellular debris away form the surface of the wound. Also contains iodine that confers antibacterial properties
Granulating Complex combination of newly formed vascular tissues and fibroblasts Protect angiogenesis and promote wound healing 1ary: Iodosorb Large cavities: Allevyn cavity wound dressing
Heavily exudative: Algisite*M
Or
Allevyn adhesive
Highly absorbent dressing containing foam chips in a soft flexible pouch. The surface contains perforations to allow entry of exudates.
Calcium-alginate fibre dressing derived from algenic acid extracted from seaweed, creates a hydrophilic gel in the presence of exudates. Also contains high concentrations of calcium ions which are used by clotting factors in the clotting cascade, thus stabilising bleeding21
Hydrocellualr dressing- self-adhesive dressing that holds liquid within its microscopic structure
Epitheliasing Wound bed that has completed proliferation and is level with the surface, where epithelial tissue will begin to migrate over the wound surface Protect fragile tissue Algisite*M Replicare Layer of hydrocolloid (liquid absorbing particles in an elastic, self-adhesive mass), covered on the upper side by a semi-permeable polyurethane film22. Slightly absorbent major class of wound healing dressings. Dressings are occlusive providing an anaerobic environment that promotes angiogenesis.
Malodorous Unpleasant smell associated with wound exudates or poor hygiene21 Reduce unpleasant odour 1ary: Carboflex
2ary: Allevyn adhesive
Dressing contains activated charcoal that has the ability to absorb odour. May also contain silver ions that destroy bacteria21.

Table 5. Types of Bandage.
Class 1 Class 2 Class 3 Class 3a Class 3b Class 3c Class 3d
Conforming stretch Light support Compression light (1417mmHg) Moderate (18-24mmHg) high (25-35mmHg) extra (36-60mmHg)

Table 6. Types of Compression.
One layer A short stretch class 2 bandage with or without a primary dressing over the wound.
Two layer A layer of absorbent protective bandage plus a spirally applied class 3c bandage.
Three layer A layer of absorbent protective bandage plus a spirally applied class 3c bandage, plus a retaining bandage.
Four layer Absorbant protective bandage, plus a conforming bandage, plus a class 3a bandage in a figure of eight, plus a spirally applied bandage

Aroushka L James third year medical student

Email: Aroushka.james@stud.man.ac.uk

Ardeshir Bayat honorary lecturer and specalist registrar in plastic and reconstructive surgery University of Manchester

Email: Ardeshir.bayat@man.ac.uk

References

  1. Leaper DJ, Harding KJ ed. Wounds: Biology and Management. Oxford: Oxford University press. 1998;191.
  2. Schultz GS, Sibbald RG, Falang V et al. Wound bed preparation: A systematic approach to wound management. Wound Repair and Regeneration. 2003;11(2):1-27.
  3. Sibbald RG, Williamson D, Orsted HL et al. Preparing the wound bed - Debridement, Bacterial balance and Moisture balance. Ostomy Wound Management. 2000;46(11):14-35.
  4. Cook H, Davies KJ, Harding KG, Thomas DW. Defective extra cellular matrix reorganisation by chronic wound fibroblast is associated with alterations in TIMP-1, TIMP-2 and MMP-2 activity. Journal of Investigative Dermatology. 2000;115:225-33.
  5. Bryant RA ed. Acute and Chronic Wounds: Nursing Management. Missouri:Mosby 2000;96.
  6. Cotran RS, Kumar V, Collins T, editors. Pathological Basis of Disease, 6th edn. Pennsylvania: W.B Saunders comp 1999;110.
  7. Miller M. The role of infection in wound healing. Community Nurse. 1996;2(7):33-5.
  8. Dow G, Browne A, Sibbald RG. Infection in chronic wounds: controversies in diagnosis and treatment. Ostomy Wound Management. 1999;45:23-40.
  9. Krasner D ed. Chronic wound care: A Clinical Source Book for Healthcare Professionals, 2ed. Wayne Pa: Health management publications inc. 1997;152-157, 158.
  10. Sykes MT, Godsey JB. Vascular evaluation of the diabetic foot. Clinics in Podiatric Medicine & Surgery. 1998;15(a):49-83.
  11. Cole-King A. Harding KG. Psychological factors and delayed healing in chronic wounds. Psychosomatic Medicine. 2001;63(2):216-20.
  12. Falanga V. classification for wound bed preparation and stimulation of chronic wounds. Wound Repair and Regeneration. 2000;8(5):347-52.
  13. Steed DL, Donohoe D, Webster MW, Lindsley L. Effect of extensive debridement and treatment on the healing of diabetic foot ulcers. Journal of the American College of Surgeons. 1996;183(1):61-4,
  14. Krasner D, Cooling M, Hyder T et al. Sterile versus Non-sterile wound care: An Interactive Monograph for Healthcare Professionals. Toronto, Canada; Dumex medical surgical products 1998.
  15. Eltringham L. Mupiricon resistance and methicilin resistant staphylococcus aureus (MRSA). Journal Hospital Infections. 1997;35:1-8.
  16. Eaglestein WH, Falanga V. Chronic wounds. Surgical Clinics of North America. 1997;77(3):693.
  17. Geronemus RG, Robins P. The effect of two new dressings on epidermal wound healing. Journal of Dermatological Surgery. 1982;8:850-2.
  18. Http://www.worldwidewounds.com/1997/july/thomas-guide/dress-select.html.
  19. Collins F, Hampton S, White R ed. A-Z Dictionary of Wound Care. Mark Allen Publishing Ltd. Wiltshire 2002;1,9,52,71.
  20. Http://wound2.snwmd-us.com/UK/Product.asp?NodeId=526.
  21. Mendez-Eastman S. When wounds won't heal. RN. 1998;61(1):20-3.
  22. Clarke M, Kumar P, eds. Clinical Medicine 4thed. London. Harcourt publishers ltd. 1999;20:1185.
  23. Rumalla VK. Borah GL. Cytokines, growth factors, and plastic surgery. Plastic & Reconstructive Surgery. 2001;108(3):719-33.
  24. Eaglestein WH, Falanga V. Tissue engineering and the development of Alpigraf a human skin equivalent. Advanced Wound Care. 1998;11(l4):1-8.
  25. Eming SA, Kreig T, Smola H. Treatment of chronic wounds: state of the art and future concepts. Cells Tissues Organs 2002;172:105-117.
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