Advances In Wound Care 2007 Rex Moulton-Barrett,MD

Advances In Wound Care 2007 Rex Moulton-Barrett,MD

Wound aspects Etiology Types: Acute/Chronic Patho-physiology
Treatment:Pain Ulceration Edema Exudate

Components of Normal Wound Healing
Coagulation process Inflammatory process Migratory/ Proliferative process Remodeling process A) Immediate to 2-5 days B) Hemostasis : Vasoconstriction , Platelet aggregation , Thromboplastin clot C) Inflammation: Vasodilation , Phagocytosis A) 2 days to 3 weeks B) Granulation: Fibroblasts lay collagen, Fills & new capillaries C) Contraction: Wound edges pull together to reduce defect D) Epithelialization: Crosses moist surface up to 3 cm Before discussing chronic wounds and chronic wound management, it may be important to review the healing process that occurs with acute wounds (surgical or traumatic). A) 3 weeks to 2 years B) New collagen forms which increases tensile strength C) Scar tissue is only 80 percent as strong as original tissue Injury: hours / days weeks

Chronic wound delayed healing
Repeated trauma Local tissue ischemia Necrotic tissue Heavy bacterial burden Tissue breakdown Chronic wound delayed healing Prolonged inflammation Stimulation of macrophage and neutrophils to wound bed Release of pro-inflammatory cytokines Degrades ECM impaired cell migration impaired connective tissue deposition Degrades growth factors While there is still much to learn, this model has been hypothesized to explain the chronic wound. Unlike the acute wound with normal healing, the chronic wound has a persistent pro-inflammatory stimulus. It may be one or several of the factors listed. Repetitive trauma Local tissue ischemia Necrotic tissue Heavy bacterial burden Tissue breakdown The inflammatory cells (neutrophils and macrophages) are drawn to the wound bed. The activated macrophages secrete the inflammatory cytokines Tumor Necrosis Factor-alpha (TNF-) and interlukin one-beta (IL-1). Tumor Necrosis Factor-alpha (TNF-) and interlukin one-beta (IL-1) increase the production of matrix MMPs and reduce the synthesis of TIMPs. (Tissue inhibitors of MMPs) The elevated MMPs degrades the extracellular matrix which impairs cell migration and connective tissue deposition. MMPs also degrade growth factors and their target cell receptors. This prevents the wound from entering the proliferative phase of healing and continues the vicious cycle of the chronic wound. Mast BA, Schultz GS. Interactions of cytokines, growth factors, and proteases in acute and chronic wounds. Wound Repair and Regeneration 1996;4: TNF and IL-1  Production MMPs and  TIMPs

Biochemical Differences
Healing wounds cell mitosis pro-inflammatory cytokines Matrix metalloproteinases Growth factors Cells capable of responding to healing signals Chronic wounds mitogenic activity pro-inflammatory cytokines MMPs Varied # growth factors Senescent cells To summarize the biochemical differences between healing wounds and chronic wounds: In healing wounds there is a high level of mitogenic activity. For example fluids collected from acute mastectomy wounds added to cell cultures stimulated DNA synthesis. In contrast fluid collected from chronic venous leg ulcers did not stimulate DNA. There is a distinct difference in the cytokine environment. In the healing wound there is a balance of pro-inflammatory cytokines and their natural inhibitors whereas in the chronic wounds there are increased levels of the pro-inflammatory cytokines. The pro-inflammatory cytokines also influence the levels of matrix metalloproteinases (MMP). Again in the healing wound there is a balance between MMPs and TIMPs however in the chronic wound MMPs levels are significantly elevated. Analysis of chronic wound fluids revealed a 116-fold higher level of protease activity as compared to mastectomy fluids. The high levels of MMPs also degrade various growth factors. The final point here is that while much research has been focused on the molecular environment there must also be consideration of the cells ability to respond to the molecular regulators. There is some interesting data demonstrating that the fibroblasts from venous leg ulcers present for more than 3 years grew more slowly and responded poorly when compared to venous ulcers present less than 3 years. This suggest that fibroblasts in ulcers that have been present for a long time may become senescent Schultz G, Mast B. Molecular Analysis of the Environment of Healing and Chronic Wounds: Cytokines, Proteases and Growth Factors. Wounds 1998;10:1F-9F

Wound Etiology Address the etiology
Mechanical Arterial Venous Neuropathic Malignancy Vasculitic Metabolic Address the etiology A comprehensive wound assessment starts with questions: What is the diagnosis or etiology of this wound? Why has the wound become chronic? Why has the wound healing rate slowed or stop completely? Most of us understand that quite often wounds become chronic due to a decrease in perfusion to the extremity or the wound bed. Possible causes of ischemia include pressure, friction, shear, arterial insufficiency and microcirculatory compromise as a result of uncontrolled diabetes or tissue edema to name just a few. Other contributing factors to the chronicity of wounds include, but are not limited to, the presence of malignancy or an inflammatory vasculitic processes. It is essential that these contributing factors are thoroughly investigated prior to initiation of wound management therapies. Once the etiology of the wound has been determined, all reasonable interventions should be undertaken to reestablish perfusion to the wound bed and optimize potential for wound closure.

Types of Ulcers & Pathophysiology
Diabetic: pressure(joint/bone)>neuropathic>ischemic>infective Venous Stasis: intercellular pressure>ischemia ( post-capillary ) Arterial: ischemia ( pre-capillary ) Pressure/Decubitus Sore: neuropathic>boney/joint pressure soft tissue infection is a secondary acute or chronic event joint infection and or osteomyelitis chronic secondary amyloidosis chronic Marjolin Ulcer: squamous cell carcinoma or sarcoma >3 yrs

Pressure Sore Staging National Pressure Ulcer Advisory Panel (NPUAP)
Stage 1 Nonblanchable erythema intact skin, discoloration of the skin, warmth, edema, induration, or hardnes ulcer defined area of persistent redness in lightly pigmented skin, in darker skin tones, persistent red, blue, or purple hues. Stage 2 Partial thickness skin loss involving epidermis, dermis, or both. ulcer is superficial with abrasion, blister, or shallow crater. Stage 3 Full thickness skin loss subcutaneous tissue that may extend to, but not through, underlying fascia. ulcer may have deep crater or undermining adjacent tissue. Stage Full thickness skin loss with, tissue necrosis, muscle, bone, or supporting structures (e.g., tendon, joint capsule) Undermining and sinus tracts

Diabetic Foot Ulcer DM: 10 Million USA today
Immunopathy, vasculopathy, neuropathy,erythrocyte hemopathy Misconception: small vessel disease Multidisciplinary approach: podiatry, vascular, plastics, physical therapy Neuropathy primary problem: small muscle contractures ( intrinsic minus ) Secondary ligament and tendon glycosation leads to shortening Secondary joint contracture: asensate pressure sore Treatment: restore balance and distribute load and protect surfaces Examples: midfoot ulcer: remove underlying metaphysis (118,000 lb/sq”) heel ulcer: Tendo achilles Z lengthening to 90 degrees Cuboid dislocation and Charcot Foot: requires internal fixation

Venous Stasis Ulcer Cause: intercellular & post-capillary stasis and edema Secondary causes: infection, dry wound, shearing forces Classic management: Zinc and compression Una Boot Rule out concomitant arterial ischemia Modern Work-up and treatment: Duplex u/s and cultures If significant venous reflux disease: end-venous ablation and venectomy Local treatment is a 4 component weekly: silver dressing 3 layer compression With or without absorbent dressing

Venous Stasis Ulcers & Compression
Circ-aid ( R:Allegra Medical ): Nonelastic, latex-free, 40 mmHg compression therapy system Uses interlocking Velcro® bands Washable and reusable Circ-aid vrs Una Boot: 45% faster , 38% cheaper than Una Boot Cir-aid: less surface shear and focal compression than 30mmHg stockings at 2 months 1/2 the edema remains a.c.t. similar stockings 67% of pts. With failed Una and stockings healed at 12 months

Ischemic and Post - Radiation Ulcers
Multidisciplinary approach Work-up arteriograms and duplex u/s digital toe pressures Primary treatment: revascularize arterial Secondary infections, osteomyelitis benefit from hyperbaric oxygen providing arterial supply adequate, ie toe pressures helpful

Assessment – Systemic Factors
Medications Tissue oxygenation Concomitant disease Age Body build Stress Nutrition One of the challenging aspects of wound care is to identify all of the potential barriers to wound closure. There are variety of systemic factors to be considered: Age - As we age there is a decrease in the density of collagen, fewer fibroblasts, fragmentation of elastin fibers and a decreased number of mast cells. Bodybuild - While we often think of the very thin person at risk, the obese patient may also be at risk due to the decreased vascularity in adipose tissue. Stress - The major stressors to be considered are psychological stress, pain and noise. The proposed mechanism is thought to be the stimulation of the sympathetic nervous system and the outflow of vasoactive substances resulting in vasoconstriction. Nutrition - Impaired wound healing is is usually associated with protein-calorie malnutrition as opposed to a single depleted nutrient. Medication - A variety of medications have the potential to effect healing, however the ones most noted are steroids. This is credited to the anti-inflammatory action which interrupts phases of wound healing. Tissue oxygenation - Lack of adequate tissue oxygen interferes with the deposition of collagen and the phagocytic activity of WBCs. Concomitant Disease - Conditions such a Diabetes, Renal Failure, Peripheral vascular Disease and Autoimmune Disease can have a significant impact on a patient’s ability to heal.

Assessment – Local Factors
Perfusion Mechanical stressors Edema Wound temperature Cytotoxic agents Necrotic tissue Bacterial burden Desiccation Excess exudate In addition to systemic factors, there are local factors that can be barriers to wound closure. Adequate perfusion is an essential criteria for healing. Local tissue ischemia is a factor frequently associated with chronic wounds Mechanical stressors - inadequate reduction in pressure, friction and shear. Edema - increased fluid in the interstitial space can interfere with the diffusion of oxygen, which is essential for collagen synthesis, and contributes to the amount of exudate. This can be a major factor in patients with Chronic Venous Insufficiency and is the rationale for using compression therapy. Wound temperature - changes in temperature can cause capillary constriction which in turn may cause decreased perfusion, reduced phagocytic activity and altered cellular mitosis. Cytotoxic agents - can have a detrimental effect on cells necessary to support healing, for example fibroblasts. The primary focus of this lecture is to address the following local factors that may contribute to impair wound healing. Devitalized tissue - the presence of necrotic tissue in the wound bed significantly impairs healing. Bacterial balance - while it is normal for all wounds to have bacteria we are learning a great deal about the importance of bacterial balance on wound healing. The appropriate level of moisture is also essential. As discussed earlier chronic wound fluid may have a number of deleterious effects on the healing process and need to be wicked away and yet optimal cellular division and migration only occur in a moist environment. If the wound is allowed to dry out this will contribute to delayed healing.

TIME Principles of Wound Bed Preparation Wound bed preparation accelerates healing
Tissue non viable or deficient Infection or inflammation Edge of wound non advancing or undermined Moisture imbalance Defective matrix and cell debris High bacterial counts or prolonged inflammation Desiccation or excess fluid Non-migrating keratinocytes Non-responsive wound cells Debridement The International Advisory Panel on Wound Bed Preparation offered the TIME principles for wound management, an excellent tool for recognizing and managing the barriers to healing. The barriers are observed as: Tissue nonviable or deficient Infection or inflammation Moisture imbalance Edge of Wound non advancing or undermined. The model addresses proposed pathophysiology, clinical actions of the TIME principles and the effect of that action on the wound. Debridement may be episodic or continuous. Various methods of debridement will be discussed later in the presentation. Infection or inflammation may be addressed with topical or systemic antimicrobial/anti-inflammatory agents. Moisture balance can be achieved by either adding moisture to a dry wound with a dressing such as a hydrogel. Absorptive dressing may the appropriate choice for wounds with moderate to large amounts of exudate. Compression therapy may reduce chronic wound fluid associated with edema among patients with venous insufficiency. For the non-advancing wound edge, interventions include addressing the cause and implementing corrective measures: biological agents, skin grafts, debridement and/or adjunct therapies. Antimicrobials Dressings compression Biological agents Adjunct Therapies Debridement Restore wound base and ECM proteins Low bacterial counts and controlled inflammation Restore cell migration, maceration avoided Stimulate keratinocyte migration

Suction Vac 0.15 mm pore, 125 mmHg suction:
Increased angiogenesis, VEGF, nitric oxide? Increased vessels,granulation: up to 5x’s Decreased exudate, hypoxia Dressing changes/2 days, but costly rental 76 in Jan 2005

KCI: Education See whp1.swf

T Debridement What to debride ? Why debride ?
Tissue Debridement The first step in Wound Bed Preparation is to remove the necrotic tissue. This process is important for several reasons: 1. Devitalized tissue (eschar and slough) in the wound bed will reduce the ability of the clinician to adequately assess the depth of the wound, condition of the tissue and surrounding structures. 2. It may mask signs of infection and serve as a medium for the proliferation of bacteria. 3. The presence of necrotic tissue is a physical barrier to healing and necrotic tissue supports significant bacterial growth which may result in excessive amounts of proteases which can have a very negative effect on healing. Why debride ? Enhanced wound assessment Decrease infection potential/extent Increase granulation epithelialization What to debride ? Slough-moist yellow, tan or gray non-viable tissue Eschar-dry, leathery

Debridement Methods Surgical: excise
Mechanical: adherance,sheer, irrigate Autolytic: topical Enzymatic: topical Biological: topical When thinking about wound bed preparation there are five methods of debridement: surgical, mechanical, autolytic, enzymatic and biological (larvae). Biological, although returning as an option, is not as commonly used as the others. Therefore this presentation will focus on surgical, mechanical, autolytic and enzymatic debridement. While there are advantages and disadvantages for each method, there are also clinical indications for each method. It is important to considers the patient’s overall condition and the goals of care when selecting a debridement method. While there are advantages and disadvantages for each method, there are also clinically appropriate indications for each method. It is important to consider the patient’s overall condition and the goals for care when selecting the method of debridement.

Surgical Debridement Scalpel Scissors Curet Laser Hydro-Scapel
U/S Hydro Surgical debridement is defined as the use of instruments to remove non-viable tissue from the wound bed. Traditionally, surgical debridement has been synonymous with sharp debridement and thus we think of scalpels, scissors and curettes. However today the use of laser to remove necrotic tissue is gaining popularity and hydro-surgical debridement is a relatively new method of surgical debridement. The primary indication for surgical debridement is for the removal of thick adherent eschar and devitalized tissue in large ulcers or wounds. Generally there must be a clear demarcation between the viable and non-viable tissue. After surgical debridement wounds may appear to be larger, however the increase in wound volume is just the result of removing the necrotic tissue from the wound. Recommended for removal of thick, adherent eschar and devitalized tissue in large wounds

Mechanical Debridement
Definition - The removal of foreign material and dead or damaged tissue by the use of physical forces. Methods Irrigation Wet-to-dry dressings Hydrotherapy: Whirlpool Suction Vac Mechanical debridement is defined as the removal of foreign material and dead or damaged tissue by the use of physical forces. The methods often thought of in this category are hydrotherapy and irrigation. However, wet-to-dry dressings are also considered mechanical debridement.

Mechanical Debridement Considerations
Aggressive debridement Wet-to-dry dressing may be painful Trauma to capillaries can cause bleeding Skin maceration may occur Dressing changes may be time-consuming

Autolytic Debridement
The process by which the wound bed utilizes phagocytic cells and proteolytic enzymes to remove debris This process can be promoted and enhanced by maintaining a moist wound environment Autolytic debridement is defined as the process by which the wound bed utilizes phagocytic cells and proteolytic enzymes to remove debris. Maintaining a moist wound bed helps to promote and enhance autolytic debridement. The process of autolytic debridement results in liquification of necrotic tissue and can result in significant wound fluid and this is a consideration when selecting the appropriate dressing. It is important to remember that when using occlusive dressings there will be an accumulation of wound fluids that have a tan opaque appearance. This is an anticipated normal occurrence (point out picture on slide).

Autolytic Debridement Considerations
Less aggressive debridement Slower than other methods Easy to perform Little or no discomfort Performed in any setting Contraindication: infection

Autolytic Debridement
This is an example of autolytic debridement, using a transparent film dressing.

Enzymatic Debridement
The use of topically applied chemical agents to stimulate the breakdown of necrotic tissue Common Topical Agents Papain-Urea Papain-Urea-Chlorophyllin Collagenase Over the years enzymatic agents have been used to debride necrotic tissue from the wound bed and have become a well established practice among wound care providers. Enzymatic debridement is defined as the use of proteolytic substances, applied topically to the wound, to stimulate the breakdown of necrotic tissue. Enzymatic debriders use chemical agents which are biologically capable of degrading eschar, protein and other nucleic acids. There are several preparations on the market for example Collagenase and Papain-Urea.

Collagenase Derived from Clostridium Hystoliticum Highly specific for peptide sequence found in collagen Less aggressive debridement Site of action – collagen fibers anchoring necrotic tissue to the wound bed 10Harper (1972) 11Boxer (1969) 12Varma (1973)

Papain-Urea Proteolytic enzyme derived papaya6 Urea is added as a denaturant6 Site of action – cysteine residues on protein8 Inactive against collagen6 6Falabella (1998) 8 Sherry and Fletcher (1962

Papain-Urea Mode of Action

Papain-Urea Chlorophyllin Contains Papain, Urea and Sodium Copper Chlorophyllin Sodium copper chlorophyllin is a Chlorophyll derivative Anti-agglutinin results in anti-Inflammatory action Reduces odor The third common enzymatic debriding agent is Papain-Urea with Chlorophyllin, which in addition to Papain and Urea, contains sodium copper chlorophyllin. Sodium copper chlorophyllin is a chlorophyll derivative, an anti-agglutinin, which may reduce inflammation in the wound. While proteolytic enzymes play an important role in debridement of necrotic tissue, it is believed that the tissue breakdown, from the use of these proteolytic enzymes, may result in agglutinated erythrocytes (depolymerized mucoproteins and mucopolysaccharides) in the wound, which can cause inflammation. The use of sodium copper chlorophyllin removes the products of digestions, and therefore may reduce inflammation. Chlorophyll is also known for it’s ability to reduce odor. 7Morrison J, Casali J (1957)

Enzymatic Debridement Considerations
Should be painless Less traumatic than surgical or mechanical debridement Easy dressing change Observe caution with infected wounds Consider the use of enzymatic debridement for individuals who: Cannot tolerate surgery long-term-care facility home care* *Agency for Healthcare Research and Quality (1994)

Autolytic, Collagenase, Papain-Urea-Chlorophyllin
Remember that the right method of debridement is a clinical decision that requires judgment of the clinician The right method is a clinical decision that requires judgment

I Bacterial Balance Control mechanism
Infection or inflammation Bacterial Balance Control mechanism Intact skin is a physical barrier pH is not conducive to bacterial growth Skin secretes fatty acids and antibacterial polypeptides Normal flora prevent pathogenic flora from establishing It is clear that while bacteria are present on intact skin, infection is rarely a problem. This is attributed to the mechanisms that are in place to control bacteria: The outer layer of the skin provides a physical barrier to invasion The slightly acidic pH of the skin is not conducive to bacterial growth The skin normally secretes fatty acids and antibacterial polypeptides that inhibit bacterial growth The presence of normal flora help to prevent potentially pathogenic bacteria from becoming established. The presence of a wound creates a portal of entry for bacteria. One of the most significant predisposing factors for a wound infection is inadequate blood supply. For example in pressure ulcers or ischemic leg ulcers

Risk Factors for Infection
Systemic Local Large wound area Increased wound depth Degree of chronicity Anatomic location (distal extremity, perineal) Presence of foreign bodies Necrotic tissue Mechanism of injury Degree of contamination Reduced perfusion Vascular disease Edema Malnutrition Diabetes mellitus Alcoholism Prior surgery or radiation Drugs e.g. corticosteroids Inherited immune defects

Bacterial Burden Contamination - Infection continuum Infection
Critically colonized Contamination Colonized Local Systemic Chronic wounds are known to exist along a bacterial continuum which ranges from contamination to infection. The challenge to the clinician lies in establishing where the wound is positioned on the continuum and what management strategies are appropriate at that particular point. Contamination refers to the presence non-replicating bacteria and is a normal condition in chronic wounds. The fact that wounds are contaminated does not contribute to impaired healing. Colonization is the presence of replicating bacteria without host reaction. All chronic wounds are contaminated and/or colonized. These wounds do not show signs of infection and colonization does not contribute to impaired healing. There is an evolving concept around the issue of criticaly colonized wounds. At this point in the continuum there no systemic signs, rather subtle local signs that there is a change in the equilibrium or an increasing bioburden that is contributing to delayed healing. Infection is considered present when the bacteria have invaded the tissue, are multiplying and causing a systemic host reaction and impaired healing. The challenge lies in identifying signs and symptoms of infection in the chronic wound and this will be discussed shortly.

Bacterial Burden Tissue bacterial levels > 105 have consistently resulted in impaired healing causing: Metabolic load Produces endotoxins and proteases It has been well documented that when bacterial levels reach greater than 105 there is a negative effect on healing. This has been seen in both the acute and chronic wound. 13Robson (1997) 14Dow (2001)

Bacterial balance Bacterial quantity Host resistance and virulence
Local perfusion immunosuppression Diabetes medications Adhesins cell capsules biofilms Antibiotic resistance Considering that bacteria are present in all chronic wounds there is a bacterial balance or equilibrium between host resistance and the quantity and virulence of bacteria. This balance must be maintained in order for wound healing to occur. A number of factors can tip the scale in either direction: Host resistance is an important variable in determining the risk for infection in chronic wounds. As previously mentioned there are a number of local and systemic factors that can impair healing. Perfusion is a factor that is associated with the pathophysiology of chronic wounds and an increased risk of wound infection Additionally, factors such as immunosuppression, diabetes, and medications can influence whether the bacteria present will lead to impaired healing. Virulence Factors that may tip the scale in favor of the bacteria include: Adhesins - which mediate cell adherence to the host Cell capsules - which prevent phagocytosis Biofilms - are an extracellular polysaccharide matrix in which the bacteria become embedded for protection. Antibiotic resistance - today one in four people with chronic wounds are receiving antibiotics and 60% have received a systemic antibiotic in the past six months. This prolific use of antibiotics is contributing to antimicrobial resistant strains of bacteria. 3Sibbald et al (2000) 12Dow (2001)

3 Rules for Topical Antimicrobial Agents
Do not use antibiotics that are used systemically – ability to breed resistant organisms (topical gentamiycin, tobramycin) Do not use agents that are common allergens (neomycin, gentamycin, amikacin, tobramycin, bacitracin, lanolin) Do not use agents that have high cellular toxicity in healable wounds (povidone iodine, chlorhexidine, hydrogen peroxide) 22Sibbald 2003

Topical Antimicrobials: Silver
Centuries of use Cytotoxicity associated with carriers not silver - ex. Silver nitrate, Silver sulfadiazine Traditional delivery required repeated applications due to binding with chlorine and proteins New silver dressings allow for continued silver release in to the dressing - up to 7 days Silver has been used for centuries for its antimicrobial activity. In fact, ancient Romans used it as a disinfectant for storage of water. More recently is was used by NASA to maintain water purity on the space shuttle. Reports of cytotoxicity with the use of silver preparations has been associated with the carriers and not the silver, The traditional delivery systems used with silver nitrate and silver sulfadiazine required repeated applications. The new technology allows for the consistent delivery of silver over time. Silver has a broad spectrum of activity including MRSA and VRE. There are no documented cases of bacterial resistance to silver and it is unlikely that resistance could occur due to the complex mechanisms by which the silver cation is toxic to the bacteria. These include binding to and disruption of bacterial DNA, respiratory enzymes and cell wall. 17Demling and DeSanti (2001)

Why Silver for Wound Bed Preparation?
Broad spectrum antimicrobial: yeasts, molds & bacteria, including MRSA Kills microbes on contact: inhibitiion cellular respiration denatures nucleic acids alters cell membrane permeability Does not induce resistance: if used at adequate levels Low mammalian cell toxicity Anti-inflammatory activity: delivery system dependent)

Nanocrystalline Silver
Decreased size of silver particles leads to increased proportion of surface atoms compared with internal atoms15 \ It is believed that the nanocrystalline structure is responsible for the rapid and long lasting action15 Magnification of normal Silver Magnification of Nanocrystalline Silver (< 1 micron) 17Demling and DeSanti (2001)

Evaluating Silver Products
Minimum bactericidal concentration (MBC) - amount of antimicrobial agent required to kill a given microbe MBC is represented by a log reduction of Stratton et al (1991) The silver required varies from 5ppm ppm for clinically relevant microbes Yin et al (1999) & Hall (1987) MBC of silver for MRSA = 60.5 ppm Calculated from Maple et al (1992) When evaluating silver products, one may benefit by understanding the minimum bactericidal concentration (MBC). MBC is the amount of antimicrobial agent required to kill a given microbe. MBC is represented by a log reduction of 3 – for example, decreasing the number of bacteria from 107 to 104.

Case Study Day • Day 20 10 year old venous leg ulcers • Treated: silver nanocrystal therapy previously treated: compression and SSD

Topical Antimicrobials Cadexomer Iodine
Iodine is a well known antimicrobial agent 0.9% iodine is carried in polysaccharide beads Provides sustained release iodine:non- cytotoxic concentration High rate of absorption from exudating ulcers No documented cases of bacterial resistance Iodine is a well recognized antimicrobial agent. The routine use of iodine in chronic wound care has been an area of much controversy. The cadexomer iodine preparation being discussed here has different characteristics. The polysaccharide beads contain the 0.9% iodine and as fluid is absorbed iodine is slowly released. The product is very absorbent and useful with highly exudative wounds.

Recommendations for Wound Bed Prep
Colonized Critically colonized INFECTION Contaminated Impaired healing Thorough cleansing Debridement if needed Exudate management Consider topical antimicrobials Silver Cadexomer iodine gel dressing Systemic antibiotics Recommendations for wound bed preparation are similar to those for the heavily colonized wound, the additional consideration is for systemic antibiotics. If there is cellulitis and/or systemic signs of infection then systemic antibiotics are indicated. As rule of thumb when wounds are presently with strictly local signs of infection then local or topical therapy is often adequate and it there are systemic signs then systemic therapy is indicated. Even when treating with systemic antibiotics, it may be wise to continue topical therapy because there is no vascular supply (for delivery of systemic antibiotics) to necrotic tissue. Additionally, for a wound on an ischemic lower extremity, systemic antibiotics may not be well delivered to the wound.

M Exudate Management 1960’s: Moist Wound Environment Dr. George Winter
moisture Exudate Management 1960’s: Moist Wound Environment Dr. George Winter Improved Collagen synthesis & granulation tissue Faster Cell migration and epithelial resurfacing Prevention of scabs, crusts, and eschar The concept of moist wound healing is not new, in fact, it is rooted in scientific evidence. The early work of George Winters demonstrated the effects of moist wound healing. These included: Improved collagen synthesis and granulation tissue formation Cellular migration and epithelial resurfacing occurred faster. A moist wound environment prevents the development of scabs, crusts and eschar.

Moist Wound Environment
Additional benefits Faster healing Capacity for autolysis Decreased rates of infection Reduced wound trauma Decreased pain Fewer dressing changes Cost effective Additional benefits of a moist wound environment include: Decreased healing time Capacity for autolysis Decreased rates of infection Reduced wound trauma Decreased pain Fewer dressing changes Cost effectiveness - When defined as total cost of care to achieve desired outcome and not just cost of dressing. It is the evidence of improved healing and the benefits that have influenced the development of advance wound therapies.

Moisture Imbalance - Dry
Desiccation slows epithelial migration Painful and uncomfortable for the patient Delays normal healing process Acts as a source of infection Longer treatment time Increased cost

Moisture Imbalance - Wet
Maceration of peri-wound skin Chronic wound fluid issues

Exudate from a Chronic Wound
Different from acute wound Imbalance of growth factors and pro-inflammatory cytokines Excessively high levels of proteases Degrades ECM and selectively inhibits proliferating cells 21Enoch and Harding, 2003

Breakdown of Necrotic tissue (debridement)
Exudate Management Chronic wound fluid Bacterial burden Breakdown of Necrotic tissue (debridement) Edema Microbial management Increased exudate is usually associated with other chronic issues and exudate management should begin with consideration of these issues. As previously discussed when the bacterial colonization increases there is an increase in the amount of drainage. Intervention should manage the microbial load in the wound environment Edema, particularly in the lower extremities, contributes to an increased amount of exudate and can be significantly reduced with compression therapy. The breakdown of necrotic tissue also contributes to increased amounts of exudate. A comprehensive approach to exudate management will include interventions to address the underlying factors as well as maintaining an optimally moist wound environment by choosing the appropriate topical dressings. The term moist wound environment refers to maintaining an optimal level of moisture that allows for cell migration and does not allow the wound bed to dry out or to stay wet. Compression Dressing selection

Chronic Wound Fluid - Edema
Ankle-Brachial index & compression < High Reduced None Compression therapy is recognized as the mainstay in treating venous leg ulcers. When considering exudate management compression therapy may play an important role in decreasing exudate. Ankle-Brachial Index (ABI) is the parameter used to identify the appropriate level of compression. When the ABI is multilayer high compression systems are generally well tolerated. For the patient with mixed disease and an ABI between reduced pressure compression therapy is more appropriate. For the patient with an ABI of 0.5 or less compression therapy is considered contraindicated.

Dressing Selection Factors
Amount of exudate Anatomical location Presence of dead space (depth, undermining, tunneling) Condition of surrounding skin Caregiver ability Healable vs. non-healable wound Cost Choosing a topical dressing is a decision that should be based on several factors, including the amount of exudate, anatomical location, presence of dead space, condition of surrounding skin, caregiver ability, whether healing is expected and cost.

Small Amount of Exudate
B Determining the most appropriate topical dressing is based on the wound assessment including the amount of exudate present, the appearance of the wound bed and the depth of the wound. Picture A - is an anterior shin wound that started as a traumatic injury and has failed to improve. One factor that may be contributing is that the wound has been allowed to dry out and presently has no drainage. Picture B - are vasculitic ulcers that are also very dry. Both of these wounds would be appropriate for a hydrogel to help moisten and soften Picture C - this is tissue injury secondary to pressure, moisture, friction and shear. There are several dressing choices and it would also depend on the patients level of activity. One might consider a hydrocolloid or a hydrogel to maintain an optimal level of moisture necessary for cell migration Picture D - is a dehisced surgical wound that is clean with minimal drainage. Consider those 3 factors for choosing a dressing: 1. Appearance of the wound bed… clean 2. Amount of drainage… minimal 3. Depth of the wound… full-thickness. This wound needs to be kept moist and the cavity needs to be filled. Obviously the wafer type dressing don’t meet that need. A hydrogel impregnated gauze would be an appropriate choice. C D

Moderate Amount of Exudate
These wounds have more drainage and while quantifying drainage is a very subjective criteria these would generally be considered to have moderate exudate. Picture A - Is a leg ulcer. The exudate is causing periwound irritation. Zinc based barrier ointments have proven to be helpful in protecting the periwound skin. This wound could be effectively managed with a foam dressing. Picture B - is a DFU that is being sharp debrided and has low to moderate amounts of exudate. An alginate dressing could provide absorption and help to fill the wound cavity. Picture C - is a dehisced surgical wound that is clean yet having a significant amount of serrous drainage. This should raise a question as to why a wound that appears relatively healthy is continuing to drain and not improving. Could there be a bacterial burden? An alginate dressing would be appropriate here. Picture D - is a leg ulcer with exposed tendon. It is important to recognize that while the wound may be draining moderate, it is important to maintain a moist environment for the tendon and in this case it may be necessary to use a hydrogel. Selecting topical therapy requires consideration of all aspects of the wound.

Large Amount of Exudate
These wound have heavy amount of exudate. Determining the appropriate dressing requires assessing the underlying cause of the exudate and addressing the cause as well as providing an absorbent dressing. Picture A - is a VLU that has sloughy tissue as well as a heavy bactertial burden. Picture B - is a full thickness pressure ulcer that also has necrotic tissue and bacterial burden. In order to manage the exudate both of these wound will need interventions to remove the necrotic tissue and reduce the bacterial burden. A B

Managing Moisture Imbalance
Exudate amount None Small Moderate Large Films Hydrogel Hydrocolloid Alginate Foams Specialty Absorbent Suction Vac With a small amount of exudate it may be necessary to use hydrogels which will add moisture to the wound environment. Hydocolloids may also be used to maintain a moist wound environment in partial thickness wounds. As the amount of exudate increases it becomes necessary to use a topical dressing capable of absorbing exudate and foams are a good choice for wounds with moderate to large amounts of exudate. Alginate dressing are also appropriate for wound with moderate to large amouns of exudate. It may be necessary to use a specialty absorptive product as the secondary or cover dressing.

Edge of Wound Non-advancing or Undermined
Cells not capable of responding to healing signals Hyper-proliferation of epidermal cells occurs at the wound margins Epidermis fails to migrate across the wound

Useful teaching resources
Wound Care Information Network KCI Smith & Nephew

Advances In Wound Care 2007 Rex Moulton-Barrett,MD

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