The International Working Group on the Diabetic Foot (IWGDF) has published evidence‐based guidelines on the prevention and management of diabetic foot disease since 1999. This guideline is on the diagnosis and treatment of foot infection in persons with diabetes and updates the 2015 IWGDF infection guideline. On the basis of patient, intervention, comparison, outcomes (PICOs) developed by the infection committee, in conjunction with internal and external reviewers and consultants, and on systematic reviews the committee conducted on the diagnosis of infection (new) and treatment of infection (updated from 2015), we offer 27 recommendations. These cover various aspects of diagnosing soft tissue and bone infection, including the classification scheme for diagnosing infection and its severity. Of note, we have updated this scheme for the first time since we developed it 15 years ago. We also review the microbiology of diabetic foot infections, including how to collect samples and to process them to identify causative pathogens. Finally, we discuss the approach to treating diabetic foot infections, including selecting appropriate empiric and definitive antimicrobial therapy for soft tissue and for bone infections, when and how to approach surgical treatment, and which adjunctive treatments we think are or are not useful for the infectious aspects of diabetic foot problems. For this version of the guideline, we also updated four tables and one figure from the 2016 guideline. We think that following the principles of diagnosing and treating diabetic foot infections outlined in this guideline can help clinicians to provide better care for these patients.

Recommendations Classification/diagnosis Diabetic foot infection must be diagnosed clinically, based on the presence of local or systemic signs or symptoms of inflammation (strong; low). Assess the severity of any diabetic foot infection using the Infectious Diseases Society of America/International Working Group on the Diabetic Foot classification scheme (strong; moderate). Osteomyelitis For an infected open wound, perform a probe‐to‐bone test; in a patient at low risk for osteomyelitis, a negative test largely rules out the diagnosis, while in a high‐risk patient, a positive test is largely diagnostic (strong; high). Markedly elevated serum inflammatory markers, especially erythrocyte sedimentation rate, are suggestive of osteomyelitis in suspected cases (weak; moderate). A definite diagnosis of bone infection usually requires positive results on microbiological (and, optimally, histological) examinations of an aseptically obtained bone sample, but this is usually required only when the diagnosis is in doubt or determining the causative pathogen's antibiotic susceptibility is crucial (strong; moderate). A probable diagnosis of bone infection is reasonable if there are positive results on a combination of diagnostic tests, such as probe‐to‐bone, serum inflammatory markers, plain X‐ray, magnetic resonance imaging (MRI) or radionuclide scanning (strong; weak). Avoid using results of soft tissue or sinus tract specimens for selecting antibiotic therapy for osteomyelitis as they do not accurately reflect bone culture results (strong; moderate). Obtain plain X‐rays of the foot in all cases of non‐superficial diabetic foot infection (strong; low). Use MRI when an advanced imaging test is needed for diagnosing diabetic foot osteomyelitis (strong; moderate). When MRI is not available or contraindicated, consider a white blood cell‐labelled radionuclide scan, or possibly single‐photon emission computed tomography (CT) and CT (SPECT/CT) or fluorine‐18‐fluorodeoxyglucose positron emission tomography/CT scans (weak; moderate). Assessing severity At initial evaluation of any infected foot, obtain vital signs and appropriate blood tests, debride the wound and probe and assess the depth and extent of the infection to establish its severity (strong; moderate). At initial evaluation, assess arterial perfusion and decide whether and when further vascular assessment or revascularization is needed (strong; low). Microbiological considerations Obtain cultures, preferably of a tissue specimen rather than a swab, of infected wounds to determine the causative microorganisms and their antibiotic sensitivity (strong; high). Do not obtain repeat cultures unless the patient is not clinically responding to treatment, or occasionally for infection control surveillance of resistant pathogens (strong; low). Send collected specimens to the microbiology laboratory promptly, in sterile transport containers, accompanied by clinical information on the type of specimen and location of the wound (strong; low). Surgical treatment Consult...

OBJECTIVE -Thiazolidinediones (TZDs), a class of insulin-sensitizing agents used clinically to treat type 2 diabetes, are also antiatherogenic. This study was designed to elucidate the relationship between the antiatherogenic and antidiabetic effects of pioglitazone, a TZD, in type 2 diabetic patients. RESEARCH DESIGN AND METHODS -A total of 136Japanese type 2 diabetic patients were included and divided into two groups: the pioglitazone-treated group (30 mg daily for 3 months) (n ϭ 70) and the untreated control group (n ϭ 66). The changes in glycolipid metabolism as well as plasma high-sensitivity C-reactive protein (CRP), leptin, adiponectin, and pulse wave velocity (PWV) were monitored to analyze the relationship between the antiatherogenic and antidiabetic effects of pioglitazone.RESULTS -The pioglitazone treatment significantly reduced hyperglycemia, hyperinsulinemia, and HbA 1c levels and increased plasma adiponectin concentrations relative to the control group (P Ͻ 0.01). It also significantly decreased CRP and PWV (P Ͻ 0.01). The antiatherogenic effect was observed in both the nonresponders showing Ͻ1% of reduction in HbA 1c (n ϭ 30) and responders showing Ͼ1% of reduction (n ϭ 40). ANCOVA revealed that treatment with pioglitazone was associated with a low CRP and PWV, independent of the changes in parameters related to glucose metabolism.CONCLUSIONS -This study represents the first demonstration of the antiatherogenic effect of pioglitazone in both nonresponders and responders with respect to its antidiabetic effect and suggests that pioglitazone can exert its antiatherogenic effect independently of its antidiabetic effect. Diabetes Care 26:2493-2499, 2003T ype 2 diabetes contributes to the risk of developing atherosclerotic diseases such as coronary heart disease and stroke and coronary restenosis after angioplasty or stenting (1-4). Therefore, it is of clinical importance to evaluate and treat cardiovascular complications in type 2 diabetic patients beyond glycemic control.Peroxisome proliferator-activated receptor-␥ (PPAR-␥) is a member of the nuclear receptor superfamily that, when activated by insulin sensitizers of the thiazolidinedione (TZD) class, including troglitazone, pioglitazone, and rosiglitazone, regulates a host of target genes (5,6). In humans with and animal models of insulin resistance and type 2 diabetes, TZDs can improve hyperglycemia and hyperinsulinemia and are currently used to manage type 2 diabetes (7). PPAR-␥ occurs abundantly in adipocytes where it regulates adipocyte differentiation (8), but it is also expressed in all major cell types participating in vascular injury, namely, endothelial cells, vascular smooth muscle cells (VSMCs), and macrophages (9,10). PPAR-␥ regulates the recruitment of monocytes to endothelial cells (11), modulates the inflammatory response in monocytes/macrophages and VSMCs (12-14), and inhibits macrophage foam cell formation and VSMCs proliferation and migration (13)(14)(15). In experimental models of atherosclerosis, ligandactivated PPAR-␥ prevents t...

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