Remote ischemic conditioning involves the use of a blood pressure cuff or similar device to induce brief (3–5 min) episodes of limb ischemia. This, in turn, seems to activate a group of distress signals that has shown the potential ability to improve healing of the heart muscle and other organ systems. Until recently, this has not been tested in people with diabetic foot ulcers. The purpose of this review was to provide background on remote ischemic conditioning and recent data to potentially support its use as an adjunct to healing diabetic foot ulcers and other types of tissue loss. We believe that this inexpensive therapy has the potential to be deployed and incorporated into a variety of other therapies to prime patients for healing and to reduce morbidity in patients with this common, complex, and costly complication.
Foot complications are common in diabetic patients; foot ulcers are among the more serious consequences. These ulcers frequently become infected, and if not treated promptly and appropriately, diabetic foot infections can lead to septic gangrene and amputation. Foot infections may be classified as mild, moderate, or severe; this largely determines the approach to therapy. Staphylococcus aureus is the most common pathogen in these infections, and the increasing incidence of methicillin-resistant S aureus during the past two decades has further complicated antibiotic treatment. Chronic infections are often polymicrobial. Physiologic changes, and local and systemic inflammation, can affect the plasma and tissue pharmacokinetics of antimicrobial agents in diabetic patients, leading to impaired target-site penetration. Knowledge of the serum and tissue concentrations of antibiotics in diabetic patients is, therefore, important for choosing the optimal drug and dose. This article reviews the commonly used therapeutic options for treatment, including many newer antibiotics developed to target multidrug-resistant gram-positive bacteria, and includes available data relating specifically to the tissue penetration of these agents. (J Am Podiatr Med Assoc 100(1): 52–63, 2010)