New Dressings for Wound Management
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New Dressings for Wound Management
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New Dressings for Wound Management
- 1. NEW DRESSINGS FOR WOUND MANAGEMENT MAX BUSH, VMD DEPARTMENT OF SURGERY UPSTATE VETERINARY SPECIALTIES
- 2. OUTLINE • Introduction • Pathophysiology of wound healing • New management paradigms • Primary dressing materials • Honey • Calcium Alginate • Vacuum Assisted Closure (Negative Pressure Wound Therapy) • Summary
- 3. WOUND HEALING • Complex biologic process by which tissue attempts to restore function and structural integrity after injury • Organized into phases, which overlap
- 4. PHASES OF WOUND HEALING • Inflammatory • Removal of contaminants and dead/damaged tissue • Proliferative • Restoration of blood flow, ECM, and epithelium • Maturation (Remodeling) • Recovery of pre-wound strength
- 5. INFLAMMATORY PHASE • Begins at time of wounding • Tissue disruption • Coagulation cascade • Platelets adherence, aggregation, degranulation
- 6. • Neutrophils (24-48 hours) • Bactericidal: ROS • ECM breakdown • Phagocytosis of bacteria and debris • Cytokine release, prolonging inflammation Inflammatory Phase
- 7. PROLIFERATION PHASE • Days 4-12 (Duration variable) • Wound size, location, age, health • Predominant Cell Types • Fibroblasts, endothelial and epithelial cells • Capillary ingrowth, collagen production, wound contraction and coverage
- 10. REMODELING PHASE • Strengthening of collagen • Conversion of matrix from thin, weak tissue to more organized rigid framework. • Collagen synthesis complete by 4-5 weeks post injury – maturation can continue for 12-18 months. • Matrix strength improves as collagen is reabsorbed and redeposited along stress lines of the tissue. • week 1: 3% • week 3: 30% • week 12: 80%
- 11. IMPEDIMENTS TO HEALING • Local: • Mechanical factors • Wound perfusion • Tissue viability • Infection
- 12. WOUND ASSESSMENT • Location • Exudate • Infection Culture and Sensitivity • Stage Does the wound require additional debridement? • What is the goal of the bandage?
- 13. MOIST WOUND HEALING PARADIGM SHIFT • Wet to dry bandages • Non-selective mechanical debridement • Destroy epithelial cells • Can leave foreign material in the wound • Painful • Inefficient • Increase risk of nosocomial infections • Remove wound fluid • Reduce temperature
- 14. MOIST WOUND HEALING BENEFITS • Improves resistance to infection • Facilitates autolytic debridement • Selective • Preserves wound fluid • Autolytic enzymes • Growth factors • Systemic antibiotics
- 15. MOIST WOUND HEALING BENEFITS • Increases collagen synthesis and fibroblast proliferation • Hastens angiogenesis and wound contraction • Reduces pain • Reduces scarring • Faster healing
- 16. SELECTION OF A DRESSING • Dressing should match the characteristics of the wound: • Stage • Exudate level • Location • Patient temperament • Client compliance
- 18. HYDROGELS
- 19. HYDROCOLLOIDS • Biocompatible hydrophilic polymers Carboxymethycellulose • Powders, pastes, sheets • Absorbs exudate, conforms to wound • Can cause maceration if gel overlaps skin edges
- 20. CALCIUM ALGINATE • Derived from Algae • Non-occlusive, non-adhesive, highly absorptive • Forms viscous hydrogel • Can be inserted into deep cavitated wounds
- 21. CALCIUM ALGINATE • Moderate to heavy exudate • Many have silver ions to increase anti-microbial activity • Hemostatic capability; can be applied post operatively
- 22. HYDROFIBER
- 24. HONEY DRESSINGS
- 25. PHYSICAL/CHEMICAL CHARACTERISTICS • Sugar concentration • Osmotic effects • Acidification
- 26. DEBRIDEMENT • Osmotic effect pulls fluid into the wound from the interstitium • Facilitates conversion of plasminogen to plasmin
- 27. IMMUNOSTIMULATORY • Upregulation of • TNFa • IL-1B • IL-6 • TGF-a
- 28. ANTI-INFLAMMATORY • Phenolic compounds inhibit TNFa • Apalbumin inhibits phagocytosis by macrophages • Decrease inflammatory cells at the wound cells • Reductions in pain, edema, exudate, scarring
- 29. ANTIBIOSIS • Effective against MDR Staph, Enterococci, Pseudomonas • MOA • Osmotic desiccation • Acidity • Enzymatic activity • Plant factors
- 30. BIOACTIVITY • Methylglyoxal – cytotoxic chemical, water soluble • Maintains antibiotic efficacy above MIC even when diluted by wound fluids • Effective against MDR bacteria • MRSA • Coagulase-negative Staphylococci • VRE • ESBL-E coli • No resistance acquired
- 31. NEGATIVE PRESSURE WOUND THERAPY • Uses suction to modify the wound environment • Macrostrain • Microstrain
- 32. NWPT THERAPY • Open cell foam sealed with adhesive, occlusive dressing • Helpful to use stoma-paste • Suction tubing is connected to canister, creating closed system
- 33. NWPT THERAPY • Application of subatmospheric pressure • Continuous or intermittent • Dressing is changed q3-4d • Standard pressure is -125mmHg
- 34. NEGATIVE PRESSURE WOUND THERAPY • Fluid removal • Physical tension • Microdeformation
- 35. VAC USES • Degloving • Chronic wounds • Severe abscess • Incisions with risk of dehiscence or infection • Traumatic wounds • Ulcers • Infected lacerations • Flaps and grafts
- 36. SUMMARY • Wide variety of wound dressings • Assess the wound • Match its needs • Moist Wound Healing • Speed wound healing • Reduce client cost • Improve patient outcomes
- 37. FURTHER INFORMATION • Moist Wound Healing: The New Standard of Care • Bonnie Grambow Campbell, Today’s Veterinary Practice July/August 2015 • Good article discussing MWH • Guidelines for dressing selection and timing of changes
- 38. QUESTIONS?
Editor's Notes
- Wounds are a frequent problem encountered in both general and specialty practice, and can be frustrating for patients, clients, and doctors. This lecture will review new strategies of managing open wounds, covering a change from the classic paradigm of wet-to-dry bandages to newer technologies and products which can help us achieve faster wound healing with less pain, less patient stress, and lower costs. Outline: Objectives: Provide a comprehensive review of new technology and materials to help us manage open wounds Discuss the advantages of these new products and also the new paradigm of moist wound healing
- Inflam: triggered by injured tissue, followed by removal of contaminants, and damaged/dead tissue Prolif: restoration of blood flow, components of ECM, and epithelium Maturation: reorganization of collagen and recovery of pre wound strength. acute vs chronic: those that do not progress through the normal phases of wound healing. Typically not beyond the inflammatory phase.
- Begins at time of wounding Tissue disruption initiates hemostasis and inflammation Coag cascade is started, thrombin is formed Thrombin is catalyst for fibrinogen to fibrin, activates platelets Platelets adhere to exposed subendothelial collagen of disrupted vessel wall, aggregate, degranulate. Platelet degranulation: release of alpha granules: PDGF, TGF-B, EGF, VEGF, FGF, attracts other cells required for healing to the local environment PDGF: neutrophils to remove bacteria TXA2, serotonin (activated platelets): initial vasoconstriction vasodilation: leukotrienes, prostaglandins, histamine, kinins
- Neutrophils arrive at the wound within 24-48 hours and begin debriding the wound, via bactericidal effects and degradation of the local ECM, which facilitates cell movement Neutrophil killing of bacteria is dependent upon high oxygen partial pressure within the wound, the conversion of oxygen to superoxide is dependent upon the PP. Hypoxia impairs resistance to infection Monocytes (48-96 hours) migrate and mature Macrophages become dominant cell population as neutrophils apoptose or are consumed by Macs secretion of signaling molecules for further stages secretion of MMPs, further debridement of the wound
- The Repair/constructive phase occurs between Days 4-12 Duration is variable: wound size, location, age, health Predominant cell types: Fibroblasts, endothelial cells, epithelial cells Capillary ingrowth, collagen production, wound contraction, wound coverage. goals of this phase: permanent closure, replacing of lost tissue angiogenesis begins with capillary sprouting from existing vasculature, in response to GF production by cells within and around wound bed (keratinocytes, macrophage, fibroblast, endothelial cells, platelets: VEGF) Resultant microvascular network provides O2, nutrients to developing granulation bed Fibroblasts migrate into wound and proliferate, synthesize collagen (III), GAGs, fibronectin skip: Collagen organized into triple helices post translation in the cell (remember?) Production and and post translational modification are dependent upon oxygen.
- characterized grossly by development of a granulation bed capillary bed, fibroblasts, macrophages, and ground substances At wound edge, epithelial cells proliferate and migrate into the wound. Migration continues until contact inhibition. Proliferation continues to regenerate normal epidermal thickness Fibroblast recruitment decreases and the existing fibroblasts are transformed into Myofibroblasts form focal adhesions which provide adequate mechanical leverage to enable wound contraction.
- Fibroblast function changes in response to mechanical loading Fibroblasts are stimulated by TGF-B to differentiate into myofibroblasts only in a loaded or stiff matrix. Therefore, as tension at the wound edge decreases secondary to collagen deposition, myofibroblasts regress, and collagen synthesis is progressively decreased.
- This depends on the gradual conversion from Fibrin and fibronection produced by hemostasis to GAG and PG produced by fibroblasts. Collagen contents change from 30% type III in granulation tissue to 10% in the final scar. The type III is a thinner, more heavily glycosylated fibril arranged in parallel, making it weak.
- In wounds under tension (crossing joint), fibroblasts persist and continue to produce collagen, leading to abnormal healing, contracture, scar formation, potential abnormal function wound perfusion: - maintaing perfusion is essential for oxygen delivery - multiple factors impede oxygenation: large inter capillary distances, vasoconstriction, -important to focus on maintaining perfusion, avoiding vasoconstriction (hypothermia, pain) necrotic tissue, bacterial burden, and foreign materials inhibit healing, and should be removed via sharp surgical debridement maintenance of wound moisture, avoiding desiccation infection: idea is to tip the balance of the bacteria-host defense equilibrium in favor of the host - identify high risk cases, proper wound classification, appropriate timing of administration of prophylactic Abx (30min to 1 hour of surgery), usually single dose sufficient, proper patient prep, adequate perfusion
- All wounds should be thoroughly examined on ER, and covered Sterile lube, shave, copious lavage, A 20ml syringe with an 18g catheter or needle delivers appropriate pressure Sterile saline or tap water is acceptable for initial decontamination of dirty wounds gentle blunt probing to look for pockets, communication with the abdominal or thoracic cavity Sedation or analgesia may be indicated Sterile instruments and gloves Goal of bandage is to assist in wound bed preparation via autolytic debridement, infection control, wound protection, and healing enhancement For all of these we prefer a bandage that promotes moist wound healing.
- No longer the standard of care Dry bandages adhere to wound surface and create nonselective tissue debridement Destroy epithelial cells and inhibit epithelialization Can leave foreign material in wound Painful, Require more intense wound care – sedation needed to change bandage Inefficient - What is cost of frequent changes, materials Can increase chances of nosocomial infection and transmission Remove wound fluid Reduce the temperature of the wound
- Neutrophils are available at the wound and not trapped in scabs moist wounds facilitate autolytic debridement by trapping enzymes that are endogenously produced Selective debridement a moist wound environment preserves growth factors and other substances that promote cell growth and proliferation within the wound fluid
- moist wound healing increases the synthesis of collagen and the proliferation of fibroblasts moist wound healing hastens angiogenesis and wound contraction The hard crust over the wound bed is removed, by eliminating these barriers keratinocyte distance and travel time across the wound is reduced moist wound healing reduces wound pain in most patients moist wounds often have less scarring after healing takes place moist wounds heal 2-3 times faster than dry wounds it decreases the intensity and length of the inflammatory phase, speeds the proliferative phase
- Adaptic gauze Use for primarily closed surgical incisions Superficial abrasions Wounds that have already entered proliferative phase, have good granulation bed Also very useful in covering skin graft sites Need to be changed after 2 days generally, as they can dry out and stick to wound surface
- Water or glycerin-based amorphous gels, impregnated gauze, or sheet dressings. Hydrogels are hydrophilic, insoluble dressings made primarily from synthetic polymers. Hydrogels help maintain a moist wound environment that promotes debridement, granulation tissue, and epithelialization. Because of their high water content, they do not absorb large amounts of exudate; so they should be reserved for less exudative wounds or can be used to rehydrate dry wound beds. They are nonadherent and provide some pain relief. Sheet dressings should be cut to the size of the open wound to prevent maceration of the skin at the wound edges. Hydrogel may be used to promote autolytic debridement during the inflammatory stage of wound healing and can also be used over granulation tissue to promote epithelialization and contraction.
- Biocompatible hydrophilic polymers, such as carboxmethycellulose, with gelatins or pectin. Available as powders, pastes, or sheets (most common) As a hydrocolloid absorbs wound exudate, it liquifies to form a viscous gel on the wound surface, This gel conforms to the wound bed and maintains a moist wound environment. Care should be taken with these bandages to ensure that the gel does not rest over skin surround the wound bed, as it can can masceration These are best used to minimally exudative wounds, and should be changed when the pad feels like a fluid filled blister, indicating that ithas received absorptive capacity When these dressings are changed, any gel left on the wound surface can be gently flushed away with saline
- alginate is a substance found in the cells walls of brown algae. When combined with calcium chloride, it forms calcium alginate, which is then spun and woven into soft, felt-like consistency fabric, in the form of rope, ribbon or flat sheets. The dressing can be classified as non-occlusive, non-adhesive, and absorb large amounts of fluid and in doing so, turns into a viscous hydrogel. The creates a sac-like pocket over the wound that retains moisture in the wound bed while preventing exudate from macerating the surrounding skin. The robe and ribbon forms can be inserted into wound cavities, even in the presence of heavy exudate. Capillary action along the small fibers of the wound wicks exudate away from the wound bed. The fibers swell and become gelatinous, trapping the fluid and bacteria within the dressing. The resulting gel is permeable to gas, allowing for oxygen diffusion to the wound bed.
- Absorb 20-30x their weight in exudate, useful for moderate to heavily exudative wounds. During the transformation from fibers to gel, dressing will release calcium, zinc or manganese into the wound bed, depending upon the composition of the dressing. Some variations contain silver ions to increase antimicrobial activity These dressings also have hemostatic capability, and can be applied post operatively to control minor oozing hemorrhage The dressings can remain in place much longer than traditional gauze, on theorder of days (3-4) due to their absorptive capacity and alternative MOA. In general my guideline is ~4 days, or earlier if moisture appears to reached the outer layers of the bandage, indicating exduate has exceeded capacity. This allows for less frequent dressing changes, less disturbance of the wound bed, fewer trips to the hospital, and fewer episodes of sedation or restraint This can be helpful in maintaining owner compliance and patient temperament. When the dressing is changed, it can be lifted from the wound bed as one piece of gel. Any residual material can then be easily flushed from the wound bed, with minimal patient discomfort. Fragments of alginate that remain in the wound bed are easily broken down into calcium and simple sugars, so there is minimal risk of left over bandage fragments causing foreign body reactions, granulomas, draining tracts.
- The are the next generation of hydrocolloid dressings Composed of sodium carboxymethycellulose, these dressings coming pads or ribbons of non-woven fibers Similar to regular hydrocolloids, these dressings will gel in the wound bed to create a moist wound environment, But the unique feature is that of vertical absorption through the pad, leading to minimal horizontal travel of fluid within the dressing This serves to draw excess exudate away from the wound bed, and prevents maceration of adjacent skin The absorptive capacity is high for these dressings, and they are designed for heavily exudative wounds It is important to not try and use these dressings on dry wounds, as they are designed to work via interaction with exudate They can be left in place for multiple days, depening upon the exudative status of the wound
- Particularly useful in wounds of the paw pads, with concerns about maceration and moist desquamation, pad sloughing, due to capability to wick and trap fluid
- Honey has been used as a therapeutic agent for thousands of years. It enjoyed relative popularity in everyday wound care until the advent of antibiotics in the early 20th century. Misuse of antibiotics, emergence of resistant bacteria and a trend towards naturopathy have all encouraged honey’s re-emergence as a broad spectrum antimicrobial Honey is composed predominantly of sugar and water, and is non toxic to human tissue Perhaps some of the resistance to more widespread adoption of honey in clinical practice is based upon uncertainty as to he source and quality of the honey. It should be emphasized that the therapeutic quality of honey varies based on several factors including the type of flower and climate. Medical grade honey is produced according to specifications, filtered, and gamma irradiated to ensure a uniform product.
- Honey assists in wound bed management to accelerate endogenous healing, by addressing the impediments to healing in chronic wounds: exudate, devitalized tissue, and bioburden. Physical/chemical characteristics: The sugar in honey serves as an alternative nutrient source for the bacteria, which results in production of lactic acid rather than the sulphur and ammonia compounds associated with the metabolism of protein. The osmotic effects of honey are similar to those of sugar dressings in the dessication of bacterial cells as the high sugar concentration yields a low water activity, inhibitory to bacterial growth. However, this effect is only transient as wound fluid quickly dilutes the honey to a level ineffective at preventing bacterial growth. The acidification of the wound bed promotes healing via modulating the oxygen-hemoglobin dissociation curve to favor oxygen release. Decreased ph also reduces the efficacy of proteases in the wound bed, moderating tissue destruction.
- Debridement: Honey encourages a moist wound environment, facilitating autolytic debridement. The osmotic effect of the honey constantly pulls fluid from the tissue, bathing the wound bed with beneficial lymph fluid that contains proteases to assist in debridement. The constant sluicing of the wound bed is believed to promote clearance of foreign material. Subwound circulation is adequate to prevent wound dehydration. Some theorize that an additional component of the debriding action of honey involves conversion of plasminogen into plasmin, facilitating fibrinolysis in the wound bed which helps to remove eschar. Honey inhibits the production of plasminogen activator inhibitor (PAI) by the macrophages.
- Immunostimulatory properties: Honey stimulates the immune system, upregulating the release of such cytokines as TNFa, IL-1B, and IL-6, and TGF-a. The upregulation of these cytokines is though to contribute to faster healing via increased keratinocyte activity and angiogenesis.
- Anti-inflammatory: While these pro-inflammatory cytokines can be dangerous if unchecked, they are essential in the cycle of wound healing, and appear to be kept in check by the anti-inflammatory properties of honey. The anti-inflammatory mechanism is not completely elucidated but may be related to the phenolic compounds in all honeys, shown to inhibit TNFa, but recent studies indicate that a bee derived protein, apalbumin, is found in a more potent glycated form in manuka honey. This protein inhibits phagocytosis by macrophages. Anti-inflammatory properties of honey decrease inflammatory cells at the wound site. This has been confirmed histologically. Reductions in inflammatory cells leads to reduction of pain, edema, and exudate. A further benefit is that the hypertrophic scarring associated with chronic inflammation is avoided. Numerous studies in people have documented patients feeling a soothing sensation, and multiple clinical trials report relief of dyspepsia, inflammatory ophthalmic conditions, skin ulcers, post operative tonsillectomy pain, and post radiation mucositis and dermatitis.
- Bioburden is also reduced via the anti-microbial properties of honey. Honey is of particular interest due to the efficacy against anti-biotic resistant strains of Staph, Enterococci, and Pseudomonas. The anti-microbial modes of action of honey include: osmotic dessication, acidic pH (3.2-4.5), enzymes such as glucose oxidase which produce hydrogen peroxide, and specific plant derived factors.
- Bioactivity: There is some evidence that honey also reduces biofilms. The bacteriocidal active is mediated by H2o2 in vitro but when in the presence of tissue, much of this action is negated, as catalase (found in blood, and wound exudate) inactivates this chemical. The specific antibacterial agent in Manuka honey is theorized to be methylglyoxal, a cytotoxic chemical, formed by spontaneous conversion in ripened honey from its precursor substance dihydroxyacetone, found in manuka nectar. MG is a small, water soluble molecule that diffuses easily, which is though to contribute to the efficacy of Honey in treating infections even in the presence of a biofilm. The methyglyoxal concentration in Manuka honey gives it antibacterial activity equivalent to 12-16% phenol, even in the face of dilution in a wound bed, the potency would remain enough to continue to inhibit bacterial growth. In these tests several resistant strains of bacteria were tested and found to be susceptible to Honey, including, various species of Streptococci, and a range of anaerobes. methicillin-resistant Staphylococcus aureus (MRSA) various coagulase-negative Staphylococci, vancomycin-resistant Enterococci (VRE) Acinetobacter baumannii (including 5 pan-resistant strains), extended-spectrum beta-lactamase (ESBL)-producing strains of Escherichia coli, Klebsiella species, and Enterobacter species. P. aeruginosa Long term resistance training experiment have been conducted to investigate the concern of developing honey-resistant mutants, but so far no studies have detected resistance or increases in the MIC. Conversely, a side-by-side experiment investigating resistance to honey versus antibiotics in naïve P. aeruginosa and S. aureus, showed rapid induction of ciprofloxacin, oxacillin, and tetracycline resistant phenotypes.
- Negative pressure wound therapy uses the VAC system to modify the wound environment in a very different manner from moist wound healing, instead using macrostrain and microstrain. Macrostrain is the visible stretch that occurs when negative pressure contracts the foam which reduces the wound size by drawing the wound edges together, evenly distributing negative pressure, and removing exudate and infectious material. Microstrain is the microdeformation at the cellular level, which leads the cells to stretch by reducing edema, promoting perfusion, and promoting granulation tissue formation by facilitating cell migration and proliferation.18 The generation of microstrain at the wound is dependent upon the ability of the tissue interface to transfer pressure to the tissue. These strains can affect the existing vascular structures in a wound bed and induce angiogenesis
- The dressing used for the technique is an open-cell foam, which is sealed with an adhevise occlusive transparent dressing to keep the vacuum seal at the wound site. Especially with our haired patients, It is often helpful to use a stoma-paste, or other type of sealant at the edges of the dressing to ensure a tight seal.l The technique used in applying negative wound pressure includes a dressing or filler material which is fitted to the contours of the wound and then covered with a nonadherent dressing film. Three types of fillers are normally used: foams which are cut to fill open cavity wounds; open-weave cotton gauze; or layers of nonwoven polyester joined by a silicone elastomeric.27 The filler is then sealed with a transparent film. A drainage tube is fixed to the dressing through an opening in the transparent film which runs to a canister on the side of the vacuum pump. This results in a closed wound in which circulation is increased and all excess fluids are removed,24 creating a moist healing environment and reducing edema. Once the dressing is completely sealed at both ends, the vacuum pump is set to either produce a continuous or intermittent pressure that varies between -125 mm Hg and -75 mm Hg, depending on material used and the patient’s tolerance.27
- Through application of subatmospheric pressure at the wound using a sealed wound dressing connected to a vacuum pump.23 Fluid is drawn out from the wound by the continuous vacuum and blood flow is increased at the area The vacuum pressure can be applied continuously or intermittently depending on the type of wound treated and the clinical objectives of the practitioner, and the dressing is changed every 3-4 days. Standard treatment in usually with a pressure of -125 mm HG; however, other studies have suggested different values, since some patients experience pain and ischemia. The earlier generations of suctions units had limited options, the first generation of KCI pumps allowed only 1 pressre setting that would be applied continuously, however newer devices can be set to different pressure and set to cycle. It is likely that no 1 ideal pressure exists for all wounds, and, the pressure should be altered according to the wound type and tissue composition.
- Negative pressure wound therapy works by a mechanism that includes fluid removal, physical tesnsion that draws the wound together, microdeformation, and moist wound healing Its application provides a quick wound bed preparation to optimize healing conditions, then the acceleration in wound healing comes about from the alteration of the microvascular blood flow in the wound edge. Sterile healing environment Reduction of edema Increased wound perfusion Increased/faster granulation tissue Decreased bacterial load Overall faster wound healing