Magnet therapy: opening the debate.
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Biomedical subjects
Publications and source records attributed to Keith F Cutting.
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Infection in chronic wounds presents a major clinical challenge and is a cause of high morbidity rates. Much attention has been dedicated to identifying and managing this problem since the publication of the first article on chronic wound infection criteria in 1994. To illustrate how alteration in wound bioburden impacts pathology, the Wound Infection Continuum has been devised and subsequently modified. One stage in this continuum, critical colonization, is putatively described as a pivotal phase that occurs without inducing an overt host response. Critical colonization suggests that the concept is currently better explained from a microbiological than from a clinical perspective. The status of critically colonized wounds may change in one of several ways: 1) deteriorate to clinical infection, 2) remain in a critically colonized state, or 3) improve following appropriate intervention. Research to clearly define the term and clarify the role of bioburden in the chronic wound is needed to help clinicians recognize and implement appropriate treatment.
The accurate identification of wound infection provides a clinical challenge to those involved in patient care and would appear to have not kept pace with other developments in the field of wound care. Attempts have been made to improve on the situation but diverse opinions together with lack of consensus prevail. The literature on infection criteria was reviewed and a set of criteria were collated; a number of criteria at the time were described as subtle in nature and have undergone validation studies. This article suggests a new perspective on the clinical identification of wound infection--ie, the signs of infection are closely associated with the wound type. Infection criteria for six wound types are explored and presented. This approach is intended for consideration together with the results of an impending Delphi study that will raise awareness of this issue, promote discussion, and lead to validation of an accurate set of clinical criteria.
Clinical criteria for the identification of wound infection are regularly based on a list created by Cutting and Harding (1994). This list was established from empirical data generated in a large, multidisciplinary clinical practice, and is now widely accepted as a seminal article in wound care. Both Cutting (1998) and Gardner et al (2001) have conducted validation exercises on these wound infection criteria, based on the assumption that the criteria broadly apply to most wound types. Although many of the original criteria do apply across the spectrum of wound types, the major categories of wounds should be considered separately to avoid the possibility of overlooking the presence of infection. The focus of this article is a review of the published literature on wound infection criteria for acute and surgical wounds, diabetic foot ulcers, venous and arterial leg ulcers, pressure ulcers and burns. All known criteria for each wound type are presented, as well as an outline of the ongoing research project to refine the criteria by wound type using a Delphi panel technique. No attempt has been made to correlate visual signs and symptoms with microbiological sampling techniques. It is clear that there are subtle variations between infection criteria for wound types and that these should be recognized if treatment is to be given appropriately and promptly, and morbidity avoided.
Wound exudate is all too often perceived as a clinical management problem. While this can be the case, it should be recognized that exudate does fulfill an important function in the healing process. Gradual acceptance of the benefits of moist wound healing, combined with the current goals of the 'ideal' moist environment, focuses attention on the role of exudate. This review is intended to define the components and functions of 'normal' exudate and differentiate it from abnormal exudate.
Maceration, caused by prolonged exposure to moisture, can complicate the healing of wounds, especially chronic ones. This paper--the first of three reviewing the literature on its aetiology and management--looks at how maceration occurs.
Excessive wound exudate or other bodily fluids, such as urine or sweat, can cause skin maceration to occur around a wound, which may delay healing and lead to other complications. This paper examines means of preventing maceration while ensuring a moist wound-healing environment and looks at management techniques if the condition develops.
In the course of managing exuding wounds, particularly chronic wounds, failure to deal adequately with exudate can lead to exposure of the peri-wound skin to exudate and hence damage. This results in maceration of the skin and wound bed. Maceration is a largely under-recognized problem and one of the causes of delayed wound healing. Previous articles have focused on the nature and causes of maceration. This article describes a wide variety of wounds and skin conditions in which maceration might be present, or develop, during treatment, together with some strategies for avoiding maceration and the evidence base supporting them. It is only by becoming familiar with the various presentations of maceration, and with prophylactic treatment measures, that practitioners can avoid the increased costs and morbidity associated with it.