Publications by authors named "R G Sibbald"

Debridement, a mainstay of nursing clinical practice, refers to the removal of dead or unhealthy tissue from a wound to facilitate healing. Debridement is one component of the concept of wound bed preparation that has long guided the approach to wound management. The ability of a wound to heal must be determined prior to the initiation of any method of debridement.

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Rosacea is a chronic inflammatory skin condition that affects over 5% of individuals worldwide. Its clinical presentation is characterized by an array of features, including erythema, papules and pustules, phymatous changes, telangiectasia, and ocular manifestations. Specifically, the multifaceted manifestation of erythema varies widely in intensity and distribution.

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Chronic wounds place a heavy burden on healthcare systems and markedly reduce the ability of patients to engage in activities of daily living. One major factor contributing to impaired wound healing is bacterial bioburden. With the rise in antibiotic resistance and the slowdown in antibiotic development pipelines, alternative antimicrobial strategies are important.

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The standard treatment for patients with confirmed Venous Leg Ulcers (VLUs) is compression therapy to improve the function of the calf muscle pump. There is a significant cohort of patients who are unable to tolerate optimal compression therapy or indeed any level of compression therapy. In addition, there is a cohort of patients who can tolerate compression whose ulcers show little or no evidence of healing.

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Introduction: Pemphigus vulgaris (PV) is a rare intraepidermal blistering disease that is potentially life-threatening due to risk of infection and failure of skin barrier function. The identification of biomarkers has the potential to provide diagnostic utility and identify new therapeutic targets. The objective of this systematic review is to identify all potentially relevant PV biomarkers, categorize them, and identify trends to determine the involvement of T-cell-mediated, B-cell-1mediated, and innate immune-mediated pathways in PV pathogenesis.

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