Diabetic foot treatment

The pathogenesis of diabetic foot infection stems from three key factors neuropathy, angiopathy, and immunopathy. Aerobic gram-positive cocci, such as S. aureus and P-hemolytic streptococci, are the predominant pathogens in acutely infected diabetic foot ulcers. However, chronically infected wounds are subject to polymicrobial infection and require treatment with broad-spectrum antibiotics. 

The nonpharmacologic treatment of diabetic foot ulcers may include off-loading, chemical or surgical debridement of necrotic tissue, wound dressings, hyperbaric oxygen, vascular or orthopedic surgery, and the use of human skin equivalents.30... 

TABLE 70-6. Empirical Pharmacologic Treatment of Diabetic Foot Infection31... 

Tigecycline is not currently approved for the treatment of diabetic foot infections. 

Lipsky BA, Berendt AR, Deery G, et al. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis 2004 39 885-910. Livesley NJ, Chow AW. Pressure ulcers in elderly individuals. Clin Infect Dis 2002 35 1390-1396. 

Platelet-derived growth factor treatment of diabetic foot ulcers March 2002... 

The description given is typical of verrucas. Verrucas are plantar warts caused by the human papilloma virus affecting the sole of the foot in pressure areas. The lesion is pushed into the epidermis eventually forming a dry hard plaque with a small central black core, which comprises blood vessels. Preparations containing salicylic acid, which is a keratolytic agent, may be used as treatment. Diabetic patients should be referred. 

Complicated skin and skin structure infections (SSSIs) For the treatment of complicated SSSIs caused by S. aureus (methicillin-susceptible and -resistant strains). Streptococcus pyogenes, or Streptococcus agalactiae. It has not been studied in the treatment of diabetic foot and decubitus ulcers. 

B. Indications and nse Regranex Gel is indicated for the topical treatment of deep diabetic foot and leg ulcers that have an adequate blood supply. Patients with diabetes who develop chronic ulcers of the foot and leg are at higher risk for local and systemic infections and amputation. 

The patient is diagnosed with hyperosmolar non-ketotic (HONK) syndrome secondary to infection of a diabetic foot ulcer and the treatment plan is as follows ... 

Cavanagh PR, Lipsky BA, Bradbury AW and Botek G (2005) Treatment for diabetic foot ulcers. Lancet 366(9498) 1725-1735. 

Claudication and nonhealing foot ulcers are common in type 2 DM patients. Smoking cessation, correction of lipid abnormalities, and antiplatelet therapy are important strategies in treating claudicants. Pentoxifylline or cilostazol may he useful in selected patients. Revascularization is successful in selected patients. Local debridement and appropriate footwear and foot care are vitally important in the early treatment of foot lesions. In more advanced lesions, topical treatments may be of benefit. Diabetic foot care is an excellent example of the adage, an ounce of prevention is worth a pound of cure. ... 

Diabetic foot infections are managed with a comprehen- sive treatment approach that includes both proper wound care and antimicrobial therapy. Antimicrobial regimens for diabetic foot infections should include broad-spectrum coverage of staphylococci, streptococci, enteric gram-negative bacilli, and anaerobes. Outpatient therapy with oral antimicrobials should be used whenever possible. 

West NJ. Systemic antimicrobial treatment of foot infections in diabetic patients. Am J Health Syst Pharm 1995 52 1199-207. 

Grayson ML, Gibbons GW, Habershaw GM, et al. Use of ampiciflin-sulbactam versus imipenem-cilastatin in the treatment of Umb-threatening foot infections in diabetic patients. CUn Infect Dis 1994 18 683-693. Lipsky BA, Baker PD, Landon GC, et al. Antibiotic therapy for diabetic foot infections Comparison of two parenteral-to-oral regimens. Qin Infect Dis 1997 24 643-648. 

Second-generation cephalosporins generally have been displaced by third-generation agents. The oral second-generation cephalosporins can be used to treat respiratory tract infections, although they are inferior to amoxiciUin for treatment of peniciUin-resistant S. pneumoniae pneumonia and otitis media. Cefoxitin and cefotetan both are effective in situations where facultative gramnegative bacteria and anaerobes are involved e.g., intra-abdominal infections, pelvic inflammatory disease, and diabetic foot infection). 

H. influenzae, gonococci, and E. coli. It also is effective in the treatment of acute otitis media in children, sinusitis, animal or human bite wounds, cellulitis, and diabetic foot infections. The addition of clavulanate to ticarcillin (timentin) extends its spectrum to include aerobic gram-negative bacilli, S. aureus, and Bacteroides spp. There is no increased activity against Pseudomonas spp. 

Using plasma-generated NO for local treatment of ulcerous and necrotic tissues in patients with diabetes (diabetic foot ulcer) has been demonstrated by Shulutko, Antropova, and Kryuger (2004). Patients were selected for this study following 2 months of unsuccessful... 

Veves A, Sheehan P, Pham HT. A randomized, controlled trial of Promogran (a collagen/oxidized regenerated cellulose dressing) vs standard treatment in the management of diabetic foot ulcers. Arch Surg 2002 137 822-827. 

A diabetic foot nicer does not appear spontaneously there are multiple contributory factors and if these can be managed the incidence may be reduced. Unfortunately, the reahty often demands the selection of treatments from an ever increasing source, with the choice dependent on the specifics of the presenting nicer and the provision of optimum conditions for wound healing. Factors to be considered inclnde aetiopathogenesis, size, and depth of the nicer together with bacterial involvement. 

In this chapter we will focns on a modem treatment approach to diabetic foot problems with special emphasis on pharmacological therapies. 

The key treatment for diabetic foot wounds is often debridement in its many guises. Despite the plethora of treatment available their success can be limited if the wound is not sufficiently prepared. The process of debridement removes non-viable tissue and the products remaining from an abnormal, sustained inflammatory response. Increased protease levels and an imbalance of matrix metal-loproteinases and their tissue inhibitors [10] maintain the chronic wound state and their removal with associated hyperaemia will encourage an influx of the biological components of healing. The level of debridement used will depend on the aetiopathogenesis and the morphology of the ulcer. 

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