Showing papers on "Chronic wound published in 2005"

A review of the microbiology, antibiotic usage and resistance in chronic skin wounds

Abstract: Chronic leg and foot wounds represent an increasing burden to healthcare systems as the age of the population increases. The deep dermal tissues of all chronic wounds harbour microorganisms, however, the precise interaction between microbes in the wounds and impaired healing is unknown. With regard to antibiotic therapy, there is a lack of evidence concerning its effectiveness, optimal regimens or clinical indications for treatment. Despite this lack of evidence, antibiotics are frequently a feature of the management of chronic wounds and these patients receive significantly more antibiotic prescriptions (both systemic and topical) than age and sex-matched patients. Current guidelines for antibiotic prescribing for such wounds are often based on expert opinion rather than scientific fact and may present difficulties in interpretation and implementation to the clinician. Although the increasing prevalence of antibiotic resistance is widely recognized, the relationships between antibiotic resistance, chronic wound microbiology and rationales for antibiotic therapy have yet to be determined. This review discusses the role of microbes in chronic wounds from a clinical perspective with particular focus on the occurrence of bacteria and their impact on such wounds. The evidence and role of antibiotics in the treatment of such wounds are outlined and current practice of antibiotic usage for chronic wounds in the primary care setting described. The implications of antibiotic usage with regard to antibiotic resistance are also considered.

Arginine supplementation and wound healing.

Abstract: Modern advances in nutritional therapies have led to the specific use of arginine supplementation for protein synthesis, cell signaling through the production of nitric oxide, and cell proliferation through its metabolism to ornithine and to polyamines. Arginine is classified as a nonessential amino acid that becomes a conditionally essential substrate in stressed adults. Arginine has been shown to enhance wound strength and collagen deposition in artificial incisional wounds in rodents and humans. A role for dietary intervention in the form of arginine supplementation has been proposed to normalize or enhance wound healing in humans. Although this hypothesis is frequently discussed, the therapeutic effect of arginine supplementation on chronic wound healing in humans is still undetermined and requires further objective evidence. Well-designed clinical trials are required to determine whether arginine supplementation is effective in enhancing healing of acute and chronic wounds in humans and how much arginine is recommended to meet metabolic needs during the phases of wound healing.

Proteases and the diabetic foot syndrome: mechanisms and therapeutic implications.

Abstract: The diabetic foot syndrome represents a major problem in the health care of diabetic patients. Understanding the molecular basis of this disease is an important step toward a rational treatment. Due to the systemic character of diabetes, disturbances in several basic cell functions appear to contribute to impaired wound healing. Many essential processes of normal wound healing are regulated in large part by growth factors and proteases, and changes of their expression and activity are relevant for the pathogenesis of the chronic wound. This review summarizes the current status of research on diabetic foot syndrome and describes new implications for the treatment of this syndrome. The diabetic foot syndrome is clearly one of the most important complications of diabetes. It not only occurs as a typical complication in the late stages of diabetes but also in patients with newly diagnosed diabetes (1). Despite the postulations of the St. Vincent Declaration that within 5 years the amputation rate has to be reduced by 50%, there are ∼30,000 amputations reported each year in Germany due to the diabetic foot syndrome (2–6). Greater success in reducing the diabetic foot syndrome can be achieved using structured diagnosis, classification, and therapy of diabetes (7–12). For example, chronically elevated blood glucose levels result in reduced leukocyte function and cell malnutrition, which contribute to a high rate of wound infection and associated healing problems (13,14). Due to the systemic effects of diabetes, not only do cellular abnormalities exist but interactions of growth factors and other mediators of wound healing are also impaired (15,16). Thus, understanding the cellular and molecular abnormalities that contribute to the diabetic foot syndrome will enable the rational development of treatments that will reduce the incidence and severity of this major complication of diabetes. The physiological …

Infection and the chronic wound: a focus on silver.

Abstract: Wound healing failure often represents the interaction of a complex series of abnormalities in the wound bed and the host’s responses to tissue injury. These may be considered the pathways to wound healing failure and are the focus of wound assessment and treatment. Factors that contribute to chronic wound healing failure include infection, any condition that produces abnormal blood flow and hypoxia, cellular failure, and trauma. Correcting one of these common pathways frequently improves the other pathways and significantly aids in wound healing. Although bacteria are present on intact skin, infection is rarely a problem because of the mechanisms that are in place to control bacteria. The outer layer of the skin, for example, provides a physical barrier to invasion. The skin’s surface is not normally conducive to bacterial growth because it has a slightly acidic pH and it secretes fatty acids and other antibacterial polypeptides. The normal flora on the skin’s surface helps prevent potentially pathogenic bacteria from becoming established. However, once this protective barrier is lost and the skin has an open wound, the subcutaneous and deeper tissues are at risk from the potential adverse effects of bacteria and other microorganisms. The presence of a wound, in essence, creates a portal of entry for these organisms. An increased bacterial burden on the surface of a wound and in wounded tissue increases the metabolic requirements of the wound and of the host’s response to that heavy bacterial load. Bacteria produce endotoxins, exotoxins, proteases, and local tissue injury. In some cases, as in gas gangrene caused by Clostridium species, bacteria produce systemic effects that are ultimately responsible for the death of the host. The presence of a bacterial burden in a wound stimulates a proinflammatory environment; the presence of bacteria induces the in-migration of monocytes, macrophages, and leukocytes—all of which initially act in an appropriate fashion but later produce a response that is exaggerated and deleterious. This is evidenced by the fact that wounds associated with a heavy bacterial burden often show healing failure. An increased bacterial burden in a wound can also affect tissue oxygen availability. Leukocytes are needed in the wound bed to kill phagocytic bacteria—by mechanisms that involve an oxydated burst and the consumption of significant amounts of molecular oxygen. In severely malperfused wounds, this increased oxygen consumption by inflammatory cells can act as a sump, ‘‘stealing’’ oxygen required for basic wound metabolism. In addition, the white blood cells’ inflammatory response—needed to kill bacteria—increases the release of damaging oxygen free radicals. The increased production of enzymes and the release of toxins can also facilitate an induced cellular failure. Bioburden may be defined as the metabolic load imposed by bacteria in the wound bed. Bacteria will compete with normal cells for available oxygen and nutrients. In addition, bacteria and bacterial products, such as endotoxins and metalloproteinases, can cause disturbances in all phases of wound healing.

Proteases and pH in chronic wounds.

Abstract: Research into the chronic wound environment has led to an improved understanding of the molecular and cellular processes occurring at the wound bed, culminating in the concept of wound bed preparation. This paper discusses the role of proteases and pH in wound healing, and proposes that pH may influence healing outcomes.

Wound chronicity and fibroblast senescence--implications for treatment.

Abstract: A proportion of chronic wounds fail to heal in response to standard therapy. For venous leg ulcers, a correlation exists between longer duration before treatment initiation and poor healing response to compression therapy. Differences identified between the healing wound microenvironment and that of the non healing chronic wound suggests that many potential mechanisms exist to impair healing. One contributory mechanism may be inhibition of fibroblast proliferation and induction of a stress-induced premature senescence phenotype by the continuing inflammation found in chronic wounds. Senescent fibroblasts exhibit an extracellular matrix degradative phenotype that contributes to wound chronicity. Accumulation of greater than 15% senescent fibroblasts has been described as a threshold beyond which wounds become hard to heal. The ratio of senescent : non senescent cells is therefore critical to determining response to treatment, and adjunctive therapies that modulate this ratio in favour of non senescent cells are likely to enhance therapeutic healing rates. A number of tissue-engineered dermal replacements contain non senescent fibroblasts and can donate cells to the wound environment additional to releasing growth factors and reversing the antiproliferative activity of chronic wound exudate. Recognition of the role of fibroblast senescence in wound chronicity may allow for identification of those wounds that will respond positively to these products.

Cellular senescence mechanisms in chronic wound healing.

Abstract: Wound healing normally proceeds in a timely, sequential manner and can be broken down into four phases: inflammation, granulation, re-epithelialization, and tissue remodeling (see Table 1) When this process is interrupted, a chronic wound is produced. Chronic wounds have been defined as wounds that have failed to return to functional and anatomical integrity in a timely fashion, or wounds that have proceeded through the repair process without a normal functional end result. The vast majority of chronic wounds fall into one of three categories: pressure sores, diabetic ulcers, and venous ulcers. Although these wounds all have very different etiologies, chronic wound development invariably stems from three factors; the cellular and systemic effects of aging, repeated ischemia–reperfusion injury, and bacterial contamination resulting in an inflammatory response. The majority of chronic wounds respond well to conventional treatments; however, in a small population of chronic wound patients (estimated to be anywhere from 15 to 20% of all chronic wound sufferers) healing does not occur despite the best care. Although there are many theories regarding the etiology of nonhealing chronic wounds, there are also similarities that are fairly consistent. Typically nonhealing wounds display decreased growth factors (EGF, KGF, PDGF, and IGF), decreased keratinocyte migration, increased reactive oxygen species (ROS), increased tissue proteases, and microbial contamination. Aged skin is more susceptible to developing chronic wounds than younger skin, possibly due to cellular senescence. In culture, most cells will only replicate a certain number of times before they become senescent, a phenotype characterized by enlargement and spreading of the cells, an accumulation of lipofuscine, expression of senescence associated b-galactosidase (SA-b-gal), and an increase in polynucleation. These cells are cell cycle arrested in G1, but are still metabolically active. Senescence in culture is frequently associated with shortening of the telomeres during repeated cell divisions eventually leading to cell cycle arrest, and is also known as replicative senescence. Cell divisions in culture can be increased artificially through the expression of telomerase, which rescues the cell through the addition of telomeric sequences during cell division. In the chronic wound, replicative senescence is often mimicked, yet is not associated with telomere length. Factors that can cause a cell to develop a senescent phenotype include oxidative stress, activated oncogene supressor proteins, and cyclin-dependent kinase (cdk) inhibitors. In the chronic wound environment, ROS attack DNA, causing an accumulation of lipofuscin (which is undegradable by the cell) and DNA damage-induced cell cycle arrest.

Silver absorption and antibacterial efficacy of silver dressings.

Abstract: Objective: To evaluate the patterns of silver release from selected sustained silver-release dressings and the protective role of proteins in wound exudate and wound scale. The bactericidal action of silver in chronic wound therapy is also examined. Method: Sequential microbiological examination of wound swabs from seven patients with chronic wounds and sampling of wound exudate and wound scale. Silver content was measured using atomic absorption spectrometry. The ability of Contreet Foam to absorb exudate and release silver was studied in punch biopsy wounds in a rodent model. Results: Silver accumulation in wound exudate correlated well with its viscosity and protein content. Silver bound to wound scale and debris was approximately proportional to the silver ion release from dressings. Bacterial burden was controlled, but not eliminated, following chronic silver therapy. Conclusion: Silver dressings (Acticoat-7, Actisorb Silver, Contreet Foam, Aquacel Ag and Flamazine) were found to be safe for use in c...

Effect of chronic wound exudates and MMP-2/-9 inhibitor on angiogenesis in vitro.

Abstract: BACKGROUND New evidence suggests that matrix metalloproteinases (MMPs) may facilitate angiogenesis as well as function to generate angiogenesis inhibitors. In this study, the angiogenic effect of wound exudates from patients with venous insufficiency ulcers was examined in an in vitro angiogenesis model with and without synthetic MMP-2/-9 inhibitor. METHODS Wound exudates were obtained from 20 patients with venous insufficiency ulcers and 20 control patients with donor-site wounds after skin grafting for burns. In the angiogenesis model, suramin (20 microg/ml) was used in five wells without wound fluid as negative control, and vascular endothelial growth factor (1 microg/ml) was used in five other wells as positive control. Chronic wound fluids were analyzed without and with a synthetic MMP-2/-9 inhibitor with a concentration of 2 microM and 20 microM in the medium. The total length of tubules was calculated by map reader. Statistical analysis was performed using the Mann-Whitney test. The level of significance was considered to be p < 0.05. RESULTS Chronic ulcer exudates inhibited angiogenesis significantly (490 +/- 130 microm) compared with acute wound fluids (1740 +/- 320 microm; p < 0.05). In wells with chronic wound exudates and high concentrations of MMP-2/-9 inhibitor, angiogenesis was stimulated significantly (870 +/- 220 microm, p < 0.05). CONCLUSIONS In this model, reduced angiogenesis might be due to an antiangiogenic effect of MMP-2 and MMP-9. MMP-2/-9 inhibition results in a stimulation of angiogenesis and might be an approach for the treatment of patients with chronic wounds and reduced angiogenesis.

Use of the PUSH tool to measure venous ulcer healing

Abstract: Currently, no instrument is available to provide an accurate and simple method of monitoring venous ulcer healing in clinical practice. The Pressure Ulcer Scale for Healing (PUSH) tool was developed and validated to monitor the healing of pressure ulcers. During a 2-month study involving 27 venous ulcer patients visiting a chronic wound clinic of a major university, the feasibility of using the PUSH tool to monitor healing was evaluated. The patients were assessed by two Wound Ostomy Continence Nurses using the PUSH tool, where 0 = healed and 17 = worst possible score. The mean score at the initial clinic visit was 12. One month and 2 months later, the mean scores were 9 and 8, respectively. Of the 27 participating patients, 23 had a decrease in their PUSH score over the 2-month period of the study; four of the 23 patients had PUSH scores of zero after 2 months because their venous ulcers had healed. One ulcer did not change and three ulcers worsened and their PUSH scores increased. Based on this study, the PUSH tool appears to be an effective way to monitor healing trends in venous ulcers as well as pressure ulcers.

Approach to infected skin ulcers.

Abstract: OBJECTIVE To review the diagnosis and management of infected chronic skin ulcers. SOURCES OF INFORMATION Cochrane database, MEDLINE, and Google were searched for clinical practice guidelines (CPGs) for wound care. Most recommendations found in the CPGs had level II or III evidence. Expert and consensus opinion from the Canadian Chronic Wound Advisory Board and the International Wound Bed Preparation Advisory Board were also used. MAIN MESSAGE Bacteria in skin ulcers act along a continuum from contamination through colonization and critical colonization to infection. Critical colonization is not always associated with overt signs of infection but can result in failure to heal, poor-quality granulation tissue, increased wound friability, and increased drainage. Good-quality swab samples should be an adjunct to clinical acumen, not a primary strategy for diagnosis. Iodine and silver-based dressings, topical antibiotics, and systemic antibiotics can be helpful. CONCLUSION Diagnosis of chronic wound infection is based on clinical signs and a holistic approach to patients. More research into assessment and treatment of skin ulcer infection is needed.

The lived experience of having a chronic wound: a phenomenologic study.

Abstract: Though millions of American elders suffer from chronic non-healing wounds, relatively little research has been done on the wound experience. The purpose of this descriptive phenomenologic study was to describe the lived experience of having a chronic wound.

Role of the wet-to-dry phase of cleansing in preparing the chronic wound bed for dressing application

Abstract: The wet-to-dry phase is a method of cleansing that acts as an alternative to rinsing prior to the application of a modern wound dressing. Debris, exudate and pathogens are removed from the wound, reducing itching and inflammation.

A review of studies that examine the impact of infection on the normal wound-healing process.

Abstract: Wound infection disrupts the normal healing process, although to what extent is not proven. This review explores controversies in the literature surrounding the bacterial load of the chronic wound and its impact, if any, on this process.

Using honey to heal a chronic wound in a patient with epidermolysis bullosa.

Abstract: This case study details the healing of a chronic wound (20years' duration) in a patient with dystrophic epidermolysis bullosa (EB). Many different dressings and creams had been used, and on occasions the wound began to heal but never progressed to closure. A honey impregnated dressing was used and the wound healed in 15 weeks. A brief overview of the dystrophic form of EB is given and some evidence for the efficacy of honey is presented.

Established and current procedures in wound healing

Abstract: Most chronic wounds are caused by arterial or venous vascular disease. Wound care is an interdisciplinary task and economic challenge. Numerous new wound dressings and treatment methods have been introduced recently. Basic research has enhanced our understanding of stimulation and inhibition of wound healing. Well-constructed clinical studies have shown some traditional approaches to be effective and others, less so. Successful wound healing requires treatment of the underlying disease as well as correction of local factors that may delay healing. The choice of dressings must be based on continuous re-assessment of the wound. Modern approaches for the most common types of chronic wounds, as well as options such as vacuum treatment and tissue-engineered skin are presented along with information on latest rules for reimbursement for wound care in Germany.

[Effect of vacuum-assisted closure on the expression of proto-oncogenes and its significance during wound healing].

Abstract: OBJECTIVE To study the effects of VAC on starting the process of wound healing and decreasing apoptosis. METHODS To examine the variations in expression of proto-oncogenes c-myc, c-jun and Bcl-2 in pig wound model with acute full-thickness skin defect and human chronic wounds by immunohistochemistry, calculate the numbers of expressive positive cells and the labelling index (LI), and observe the process of wound healing. RESULTS (1) In pig experiment, the wound in experimental group was very clean and without obvious exudates, many neoepiderm and granulation tissue rapidly appeared or formed after 6 days, and healed completely by the 25th day. On the contrary, in the wound of control group, more exudates and blood crust could be seen and fewer neoepiderm and granulation tissue appeared after 6 days and was healed by 30th day. Immediately after the wound was created, the expression of c-myc, c-jun and Bcl-2 was lower and mainly situated in nucleus or cytoplasma of the basilar cells. After the wound was created in control group, or after starting the VAC treatment in experimental group, their expression rapidly and obviously increased, the distribution of the positive cells also became enlarged, but the amount of expression decreased rapidly after the expressive peak have reached. In the successive 12 days following the wound was created, the expression of c-myc, c-jun and Bcl-2 in the experimental group was constantly higher than that of the control group. (2) In human chronic wounds, there wasn't obvious secretions and more healthy granulation tissue was rapidly formed after VAC treatment. The expression of c-jun was mainly located in cytoplasma of basilar cells of epithelium, dermal fibroblasts and inflammatory cells, and the positive cell and labelling index obviously decreased. The expression of c-myc and Bcl-2 was mainly in cytoplasma of basilar cells, but the amount of expression and the labelling index became obviously increased after VAC treatment. CONCLUSIONS VAC could rapidly start the healing course of the pig' s acute skin wound and human chronic wound, decrease apoptosis of the reparative cells, so as to accelerate wound healing.

Treatment of a venous leg ulcer with a honey alginate dressing.

Abstract: The management of chronic wounds such as venous ulcers is a common and long-term issue with the aging population. Non-standard treatment that is both medically and financially effective needs to be identified. Honey has been used for its healing properties for centuries and has been used to successfully heal wounds including pressure-ulcers in our care facility. However, there is not much evidence for its use in treating venous ulcers. To this end, I trialed the use of a honey-impregnated alginate dressing on a man who had a long-standing history of venous ulcers on his leg with the aim of evaluating the effectiveness of honey as an alternative treatment to the current wound management therapies. The honey seemed to act as an effective antibacterial, anti-inflammatory and deodorizing dressing, with total healing of the ulcer achieved. This result, together with past successes with the use of honey alginate on ulcerated wounds, has led to this product becoming mainstream in the treatment of chronic wounds within our care facility.

Wound Microbiology and the Use of Antibacterial Agents

Abstract: Cutaneous wound healing is a well-orchestrated cascade of events. These events lead to repair when the underlying dermis is compromised, while alternatively leading to regeneration when only the epidermis is injured. This process, should it occur in a timely fashion, is termed “acute wound healing” typically with restoration of skin integrity occurring a period of days to weeks. Classically, acute wound healing is considered to occur in three overlapping phases termed the inflammatory, proliferative, and remodeling phases, respectively (1). Conversely, when this process is disrupted and healing is prolonged, delayed or does not occur, the wound is termed a “chronic wound” (2). An exact time does not exist when acute wound healing becomes chronic but is rather dependent upon variables such as patient age and comorbid conditions and wound related variables such as the location of the wound, the size, depth and shape of the wound, or by what method the wound was created.

Choosing the right prescribing options in wound debridement

Abstract: Wound debridement is an effective way of promoting healing in a chronic wound. There are a number of debridement options, some of which require the prescription of desloughing agents. There are other options which require additional skills, such as sharp debridement. The different options for wound debridement and the factors which influence the choice of which agent to use, e.g. cost, clinical effectiveness and clinical competence, will all be discussed in this article.

Effects of Wenshen Jianpi Recipe on chronic wound healing in rats

Abstract: OBJECTIVE To study the effects of Wenshen Jianpi Recipe (WSJPR, a traditional Chinese medicine for warming kidney and invigorating spleen) on chronic wound healing and the mechanism. METHODS Ninety-six SD rats were randomly divided into 4 groups, with 24 rats in each group, and back wound was made in the rats. For rats in 3 of the 4 groups, hydrocortisone injection was administered to induce chronic wound. Rats in 2 of the 3 groups were treated with WSJPR and Xinpukang Granules (XPKG) respectively, and the rats in the other group were untreated. The rats in the fourth group were taken as control. The wound healing time and the width of new epidermis were observed, and the histomorphological changes and cell cycle of the granulation tissue, and the protein expressions of epidermal growth factor (EGF), transforming growth factor-beta(1) (TGF-beta(1)) and fibronectin (FN) in the granulation tissue were tested with immunohistochemical technique and flow cytometry. RESULTS The wound healing time of the WSJPR-treated and XPKG-treated groups was (17.0+/-1.9) and (18.8+/-1.9) d respectively, much shorter than that of the untreated and control groups (P<0.05). On the 14th experiment day, the width of new epidermis of the WSJPR-treated and XPKG-treated groups was (3.73+/-0.19) and (3.21+/-0.15) mm respectively, much wider than that of the untreated and control groups (P<0.05). The numbers of angiogenesis, fibroblasts and cells in the S phase in WSJPR-treated and XPKG-treated groups were much higher than those in the untreated and control groups (P<0.05). Compared with the untreated and control groups, the protein expressions of EGF, TGF-beta(1) and FN in WSJPR-treated and XPKG-treated groups were higher (P<0.05). CONCLUSION WSJPR can enhance the wound healing. It was likely through accelerating the cell proliferation and up-regulating the expressions of EGF, TGF-beta(1) and FN.

The Clinical Study of Recombinant Human Basic Fibroblast Growth Factor in Stimulating the Wound Surface Healing

Abstract: Objective To observe the effects of recombinant human basic fibroblast growth factor(rh-bFGF)on the burning, supplying skin area for operation,and chronic wound surface and to study the medication methodsMethods One hudred and sixty three patients were divided into burning,supplying skin,chronic wound surface groups according to the classification of wound surfaceThe patients were treated with routine methodsExperimental groups were treated by rh-bFGF and nothing was used to the control groupsThe contrast method of the first and second groups were randomly auto-contrast and of the third group was comparing the effects between before and after the treatment in one individual The time of healing of wound surface and the change of blood routine,urine routine,hepatic and renal function were examinedResults After the treatment with rh-bFGF,the healing time of supplying skin area and chronic wound surface was shortened obviouslyEspecially in the wound surface of deepⅡdegree burning and partial thick supplying skin area,the healing time was shortened 3 to 5 days compared with the control groupThe average effective percent of rh-bFGF was 913% and no side effect was foundConclusion The rh-bFGF can stimulate the healing of burn,injured skin,and chronic wound surfaceThis effect is more significant in deep Ⅱdegree burning,severe injured skin(partial thick supplying skin area),and the chronic wound surface

Estrogen and wound healing

Abstract: Cutaneous wound healing is a complex process encompassing a number of overlapping events including inflammatory cell recruitment,matrix deposition,epithelialization and the formation of a mature scar.The effects of aging on the cutaneous wound healing process are profound,and the resulting acute and chronic wound morbidity imposes a substantaial social and financial burden on health services.The skin appears to act as an end-organ target for estrogenic action.Estrogens clearly have an important function in many components of human skin including the epidermis,dermis,vasculature,hair follicle and the sebaceuous gland etc.In recent years the effects of topical estrogen on cutaneous wound healing in healthy elderly men and women have been investigated. Hence,estrogen has significant roles in cutaneous wound healing.This review provides a survey of the literature that is available regarding the involvement and influence of estrogens on the various phases of cutaneous repairinflammation,proliferation and remodelling.However,studies on estrogen action in skin were limited.Further understanding of the complex interaction between estrogen and wound healing in the elderly is needed.Clinically our aim should be to restore the integrity and function of wounded tissue as rapidly as possible after injury and it is generally believed that a better understanding of the effects of estrogens on wound healing could lead to improved care of cutaneous wounds.