Overview of diabetic infections of the lower extremities

INTRODUCTION

Diabetic foot infections are associated with substantial morbidity and mortality [1]. Important factors for development of diabetic foot infections include neuropathy, peripheral vascular disease, and hyperglycemia. In the setting of sensory neuropathy there is diminished perception of pain and temperature, so delays in injury presentation are common. Autonomic neuropathy can cause diminished sweat secretion resulting in dry, cracked skin, facilitating microorganism entry, while motor neuropathy can lead to foot deformities. Peripheral arterial disease can lead to impaired blood supply needed for healing of ulcers and infections. Hyperglycemia impairs neutrophil function and reduces host defenses. Trauma in patients with one or more of these risk factors precipitates development of wounds that can be slow to heal and predispose to secondary infection.

The microbiology, clinical evaluation, diagnosis and management of diabetic foot infections will be reviewed here. The general evaluation of the diabetic foot and management of uninfected diabetic foot lesions are discussed separately. (See "Management of diabetic foot lesions" and "Evaluation of the diabetic foot".)

MICROBIOLOGY

Most diabetic foot infections are polymicrobial, with up to five or seven different specific organisms involved. The microbiology of diabetic foot wounds is variable depending on the extent of involvement [2-5]:

• Superficial diabetic foot infections (including cellulitis and infected ulcers in antibiotic naïve individuals) are likely to be due to aerobic gram-positive cocci (including S. aureus, S. agalactiae, S. pyogenes, and coagulase-negative staphylococci). Methicillin-resistant S. aureus should be presumed and empiric antibiotic treatment should include activity against this organism, particularly for patients who are severely ill at the time of presentation.
• Ulcers that are deep, chronically infected, and/or previously treated with antibiotics are more likely to be polymicrobial. Such wounds may involve the above organisms in addition to enterococci, Enterobacteriaceae, Pseudomonas aeruginosa, and anaerobes.
• Wounds with extensive local inflammation, necrosis, or gangrene with signs of systemic toxicity should be presumed to have anaerobic organisms in addition to the above pathogens. Potential pathogens include anaerobic streptococci, Bacteroides species, and Clostridium species [6-10].

It is also important to note that diabetic patients with chronic foot wounds who receive repeated and prolonged courses of antibiotics represent an important risk group for development of vancomycin-intermediate Staphylococcus aureus infections. (See "Vancomycin-intermediate and vancomycin-resistant Staphylococcus aureus infections".)