Version July 2025
INTRODUCTION —
Diabetic foot infections are associated with substantial morbidity and mortality [1]. Important risk factors for diabetic foot infections include neuropathy, peripheral vascular disease, and poor glycemic control.
The microbiology, clinical evaluation, and diagnosis 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 "Evaluation of the diabetic foot" and "Management of diabetic foot ulcers".)
Lower extremity cellulitis not involving the foot is discussed separately, as this condition is treated like lower extremity cellulitis in nondiabetic patients. (See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)
GUIDELINES —
In 2023, the Infectious Disease Society of America (IDSA) and the International Working Group on the Diabetic Foot (IWGDF) created joint intersociety guidelines for the diagnosis and management of diabetic foot infections [2]. Prior to 2023, IDSA and IWGDF each published separate guidelines [3,4].
The information reviewed in this topic is largely consistent with the 2023 guidelines. Links to these and other guidelines related to care of diabetes mellitus are found below. (See 'Society guideline links' below.)
DEFINITIONS —
The International Working Group on the Diabetic Foot (IWGDF) has defined a diabetic foot infection as infection of a foot wound located below the malleoli [2]. In many cases, the foot wound is an ulcer, but in some cases the site is not obvious (eg, dry cracked skin).
Diabetic foot infection may manifest in multiple forms:
●Skin and soft tissue infection due to a diabetic foot ulcer, with or without associated osteomyelitis.
●Skin and soft tissue infection in the absence of a foot ulcer, with or without associated osteomyelitis.
●Osteomyelitis underlying a diabetic foot ulcer, without evidence of overlying skin and soft tissue infection.
EPIDEMIOLOGY AND RISK FACTORS —
Diabetic foot infections are the most common cause of hospitalization in patients with diabetes and the most common cause of lower extremity amputations [2].
Specific risk factors for development of diabetic foot infections include peripheral neuropathy, peripheral artery disease, and poor glycemic control [2,5-11]. These conditions are discussed in detail separately. (See "Evaluation of the diabetic foot".)
Ulcers that are deep, chronic, recurrent, or due to trauma are particularly prone to development of infection.
PATHOGENESIS —
Diabetic foot infections are caused by microorganisms invading tissue following a break in the skin. The point of entry is often a diabetic foot ulcer or dry, cracked skin caused by diminished sweat secretion due to autonomic neuropathy [3,12].
Diabetic foot infections can spread contiguously, causing infection of subcutaneous tissues including fascia, tendons, muscles, joints, and bones [2,13,14]. Spread between deeper structures often occurs within the myofascial compartments of the foot, but severe infections may also spread between compartments (figure 1) [13].
Complications of diabetes predispose to infection (see "Susceptibility to infections in persons with diabetes mellitus"):
●Sensory neuropathy diminishes perception of pain and temperature, which makes many patients slow to recognize the presence of an injury or infection in their feet.
●Peripheral neuropathy may lead to changes in the shape of the foot (eg, Charcot osteoarthropathy, rocker-bottom deformity, claw toes), which create new points of pressure with weightbearing and shoewear.
●Peripheral artery disease impairs blood flow necessary for healing of ulcers and infections.
●Hyperglycemia impairs neutrophil function and reduces host defenses, as discussed separately.
MICROBIOLOGY —
Diabetic foot infections are often polymicrobial [15-19].
Common organisms — The microbiology of diabetic foot wounds varies depending on the type and severity of infection, and recent antibiotic exposure:
●Superficial diabetic foot infections (including infected ulcers) – In patients who reside in North America and Western Europe, aerobic gram-positive cocci (including Staphylococcus aureus, Streptococcus agalactiae, Streptococcus pyogenes, and coagulase-negative staphylococci) are the most common infecting organisms [2,18,19]. Gram-negative pathogens may predominate in patients living in subtropical regions of Africa and Asia [20-22].
A broader spectrum of organisms is possible in patients with recent antibiotic exposure.
●Deep or chronically infected ulcers - Ulcers that are deep (ie, involve ligaments, tendons, joint capsules, deep fascia, or bone) or chronically infected are more likely to have polymicrobial infection. In addition to the organisms seen in superficial infections, additional pathogens may include enterococci, Enterobacterales, Pseudomonas aeruginosa, and anaerobes.
●Wounds with extensive local inflammation, necrosis, malodorous drainage, or gangrene – In addition to the above pathogens, anaerobic organisms are often present (eg, anaerobic streptococci, Bacteroides spp, Clostridium spp) [23-27]. (See 'Anaerobic organisms' below.)
Risk of specific organisms — Specific organisms that are not always covered by empiric treatment regimens should be considered based on individual risk factors and geography. [28].
Resistant Staphylococcus aureus — Methicillin-resistant S. aureus (MRSA) is a common pathogen in diabetic foot infections in certain parts of the world, including the United States. Previous MRSA infection or known colonization are major risk factors for its presence. Other risks include hemodialysis and residence in a long-term care facility (table 1). (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology", section on 'Risk factors'.)
Diabetic patients with chronic foot wounds who receive repeated and prolonged courses of antibiotics have developed vancomycin-intermediate S. aureus infections in rare case reports. (See "Staphylococcus aureus bacteremia with reduced susceptibility to vancomycin".)
Pseudomonas aeruginosa — P. aeruginosa is a common organism in diabetic foot infections in regions with warm climates [22]. As an example, P. aeruginosa was the most common isolate, found in 20 percent of initial cultures in a study of 434 patients with infected diabetic foot ulcers in Northern India [29]. Macerated ulcers, foot soaking, and other exposure to water or moist environments also increase the risk of involvement with P. aeruginosa.
In temperate climates and in the absence of the preceding exposures, P. aeruginosa is a relatively uncommon pathogen [30]. In a study of 292 patients hospitalized with diabetic foot infections without osteomyelitis at five urban medical centers across the United States, the prevalence of P. aeruginosa was only 9 percent and was associated with immunocompromise or recent antibiotic exposure [31].
The role of Pseudomonas as a pathogen is often hard to assess in clinical practice. As an example, when P. aeruginosa was isolated from participants of clinical studies of diabetic foot infections, most patients improved on antibiotic regimens that did not cover Pseudomonas, suggesting that it was not the primary pathogenic organism [32,33].
Other resistant gram-negative rods — Gram-negative bacilli that express an extended-spectrum beta-lactamase (ESBL) or carbapenem-resistance are increasing in prevalence worldwide, including in diabetic foot infections [22,34,35]. The prevalence of gram-negative resistance varies by country and hospital, and is more common among patients with prolonged hospital stays, prolonged catheterization, prior antibiotic use, or residence in a long-term care facility. (See "Extended-spectrum beta-lactamases", section on 'Epidemiology' and "Carbapenem-resistant E. coli, K. pneumoniae, and other Enterobacterales (CRE)", section on 'Risk factors'.)
Anaerobic organisms — The role of anaerobes in diabetic foot infections remains unclear due to a lack of standard collection, transportation, and culture techniques in published studies [18,24,36]. Some have found a high prevalence of anaerobes in samples taken from diabetic foot infections, especially necrotic, deep, or severe infections.
Empiric antibiotic regimens for moderate to severe infections include anaerobic coverage.
CLINICAL MANIFESTATIONS
Spectrum of involvement — Diabetic foot infections can present as localized superficial skin infection or as deeper infection, involving fascia, bone, joints, and the bloodstream.
In many cases, the underlying cause of infection is usually obvious in patients with severe neuropathy, vascular deficiency, trauma, paronychia, or pre-existing skin fissures or cracked skin [37].
Skin and soft tissue infection — Skin and soft tissue infections in diabetic patients often present with the cardinal manifestations of inflammation (erythema, warmth, swelling, and tenderness) and/or the presence of pus in an ulcer [15]. (See 'Diagnosis of infection' below.)
However, local manifestations of infection are not evident in all cases. In patients with severe peripheral artery disease, warmth and erythema may be absent. Patients with peripheral neuropathy can have minimal pain and tenderness. In such instances, infection may progress to involve deeper tissue before the patient notices the infection or seeks clinical attention.
Osteomyelitis — Diabetic patients with osteomyelitis often present with no symptoms other than soft tissue infection or chronic ulcer [38-43].
In some patients, visible bone or a sinus tract is present on examination, which is highly suggestive of osteomyelitis. However, a chronic ulcer or soft tissue infection may be the only clue to underlying osteomyelitis in other patients [17,38]. In such cases, additional studies are necessary to either exclude or confirm the presence of osteomyelitis, as discussed below. (See 'Diagnosis of underlying osteomyelitis' below.)
Osteomyelitis in patients with diabetes may also present as a "sausage" toe, with erythema and nonpitting edema that obliterates the normal contour of the digit [44].
DIAGNOSIS —
The evaluation of a patient with a suspected diabetic foot infection involves three key components: (1) determining the extent and severity of infection, (2) assessing the microbial etiology, and (3) identifying underlying factors that predispose to and promote infection.
Initial evaluation — A detailed history and physical examination are basic components of the initial evaluation.
●History – The clinical history should focus on proximate causes such as recent trauma or new shoewear, the duration of current lesion(s), associated systemic symptoms, and prior treatment, if any.
Patients should be questioned about symptoms suggestive of neuropathy and peripheral vascular disease. The adequacy of blood glucose control should be assessed. (See "Evaluation of the diabetic foot", section on 'History'.)
●Physical examination – All patients suspected to have a diabetic foot infection should undergo a physical examination that includes a skin examination (loss of skin appendages, cracked thickened skin, bunions, toenails), neurologic evaluation to document the extent of sensory loss, and vascular evaluation for the presence and severity of arterial and/or venous insufficiency (table 2). (See "Evaluation of the diabetic foot".)
Diagnosis of infection — The diagnosis of a diabetic foot infection is primarily based on physical examination. An ulcer is not a necessary component of a diabetic foot infection, as described above. (See 'Definitions' above.)
Physical examination — As part of the complete physical examination, focal evaluation of diabetic foot infection should assess the following:
●Classic signs of soft tissue infection – Classic manifestations of soft tissue infection include erythema, warmth, tenderness, edema, and induration. In the setting of an ulcer, purulent discharge is another indicator of infection.
Patients with diabetes may present with blunted signs of infection due to peripheral vascular disease and neuropathy, as described above. (See 'Skin and soft tissue infection' above.)
●Extent of infection – Examination should note the location of infection and wounds, extent and depth of infection (eg, involving skin, subcutaneous tissue, muscles, tendons), whether bone is grossly visible, presence of sinus tracks, evidence of foreign material (eg, foreign body, soil), and the presence of tissue necrosis. If bone is not visible, palpation by probing (the “probe-to-bone” test) may help evaluate for underlying osteomyelitis, as described below. (See '"Probe-to-bone" test' below.)
Systemic symptoms (eg, fever, chills, leukocytosis) are uncommon and may indicate severe and potentially limb- or life-threatening infection, including necrotizing infection [2]. Other signs of necrotizing infection include bullae, soft tissue gas, dusky or blue-gray skin discoloration, a foul odor, and rapid progression of illness. Gangrene, severe ischemia, or tissue necrosis are additional indicators of a potentially limb-threatening infection (table 3). (See "Necrotizing soft tissue infections", section on 'Clinical manifestations'.)
If osteomyelitis is suspected, imaging and additional evaluation can provide additional information, as discussed below. (See 'Diagnosis of underlying osteomyelitis' below.)
A few studies have evaluated the use of novel examination techniques to detect soft tissue infection, such as digital photographic foot imaging and infrared thermography. We agree with expert guidelines that these tools are unlikely to provide additional benefit beyond the physical examination [2].
Classifying the infection — There are multiple different classification and scoring systems for diabetic foot infections [2,3,45,46]. Classifying the infection allows consistent and accurate communication among clinicians when discussing individual cases.
We favor the 2023 International Working Group on the Diabetic Foot (IWGDF) and Infectious Diseases Society of America (IDSA) joint clinical classification scheme [2]. The IWGDF/IDSA classify diabetic foot changes as uninfected, mild, moderate, and severe based on the extent of inflammatory findings, the tissue depth involved, and the presence of signs of systemic toxicity; osteomyelitis is considered a subcategory of moderate or severe infections.
The IWGDF/IDSA classification system has been clinically validated and predicts the need for amputation or hospitalization in patients with diabetic foot infections [2,5,47].
Role of wound cultures — Because microorganisms colonize lower extremity wounds regardless of the presence of a true infection, cultures should be performed only in selected patients. If the clinical suspicion for infection is low, samples from the wound should not be submitted for culture.
In patients with mild infection in whom there is low suspicion for resistant organisms (table 1), wound culture is generally unnecessary. However, if purulent drainage from an abscess is present, obtaining samples of pus for Gram stain and culture may be helpful.
For moderate and severe infections or when concern for multidrug-resistant organisms is high, wound culture helps to guide antibiotic therapy. The preferred method for specimen collection is aspirating an abscess or curettage from an ulcer base following superficial debridement of necrotic tissue.
Superficial swabs of ulcers are not appropriate because organisms cultured from superficial swabs are not reliable for predicting the pathogens responsible for infection [2,48-51]. (See "Osteomyelitis in the absence of hardware: Approach to diagnosis in adults".)
Diagnosis of underlying osteomyelitis — The possibility of osteomyelitis should be considered in diabetic patients with deep soft tissue infection and in patients with chronic ulcers, particularly those overlying bony prominences that do not heal after several weeks of wound care and off-loading.
General approach — Definitive diagnosis of osteomyelitis requires isolation of bacteria or fungus from a sterilely obtained bone biopsy sample with histologic evidence of inflammation and osteonecrosis [3,45]. (See 'Bone biopsy' below.)
Before bone samples are obtained, a presumptive diagnosis of osteomyelitis can be made if certain clinical features are present [38-41]:
●Visible bone.
●A positive "probe-to-bone" test [42,43,52]. The ability to touch bone by probing the wound (ie, “the probe-to-bone test") is further discussed below. (See '"Probe-to-bone" test' below.)
●Sinus tract. We agree with other experts who believe the presence of a sinus tract is pathognomonic of chronic osteomyelitis.
Other clinical findings that increase the likelihood of osteomyelitis include an ulcer larger than 2 cm2 or an ulcer duration longer than several weeks despite appropriate care [40,41].
A plain x-ray or magnetic resonance imaging (MRI) with findings consistent with osteomyelitis markedly increase the probability of osteomyelitis in patients with compatible clinical findings. (See 'Imaging studies' below.)
Laboratory findings that suggest osteomyelitis include elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). (See 'Inflammatory markers (eg, ESR, CRP)' below.)
Specific tests
"Probe-to-bone" test — If possible, probing to bone with a sterile blunt metal tool should be included in the initial assessment of diabetic patients with infected or chronic nonhealing foot ulcers. [17,39,40].
The procedure involves gently inserting a sterile blunt metal probe into the wound. A positive result consists of detection of a hard, gritty surface. Although it is easy to perform, proper training is necessary because incorrect technique provides unreliable results [2].
The probe-to-bone test can be used as a screening tool in conjunction with the patient's pretest probability for osteomyelitis to determine whether additional tests (such as radiographic imaging or bone biopsy) are needed for diagnosis of diabetic foot osteomyelitis [53].
The reliability of the probe-to-bone test may vary by the ulcer location and the expertise of the clinician performing the test [42,43]. In a systematic review evaluating the performance of the probe-to-bone test (using bone histopathology or culture as the reference standard), the pooled sensitivity and specificity for the test were 87 and 83 percent, respectively [54].
Inflammatory markers (eg, ESR, CRP) — The value of inflammatory markers in the diagnosis and management of diabetic foot infections is uncertain. Most studies have evaluated the ability of these tests to differentiate soft tissue infection from osteomyelitis [2]. No inflammatory marker should be used in isolation to confirm or rule out the presence of osteomyelitis.
We typically obtain these tests in three different situations:
●If we are uncertain whether an infection is present (for example, in a nonhealing ulcer without signs of soft tissue infection).
●To help differentiate osteomyelitis from soft tissue infection if the examination is equivocal.
●For monitoring response to therapy in patients with confirmed osteomyelitis [55].
Performance characteristics of these tests vary:
●Erythrocyte sedimentation rate (ESR) – The ESR may help differentiate osteomyelitis from soft tissue infection [2,17,40,56,57]. In one study, the finding of an ESR ≥70 mm/hr was found to increase the clinical probability that osteomyelitis is present, with a sensitivity of 81 percent and specificity of 80 percent [40]. Cut-off values predictive of osteomyelitis have ranged from >43 to ≥70mm/hr in different studies.
It is important to note that the ESR can be elevated for reasons other than infection, including kidney disease and anemia.
●C-reactive protein (CRP) – Compared with ESR, CRP increases more rapidly with infection and falls faster with resolution of infection. It may be more useful than ESR for differentiating infection from noninfection and for following response to therapy [2,55,56,58].
In one large-scale single-center study, a CRP ≥80 mg/L combined with an ESR >60 mm/hr had a high positive predictive value of predicting biopsy-confirmed osteomyelitis, but CRP or ESR alone had suboptimal sensitivity and specificity [56].
●Procalcitonin – The value of obtaining procalcitonin levels is uncertain based on limited data [2,55,58-60] .This test is not always readily available, and further investigation is needed to determine the clinical utility and role of this assay.
More information about inflammatory markers is available separately. (See "Acute phase reactants".)
Imaging studies — The most common imaging studies used in the diagnosis of diabetic foot infections are plain X-rays and MRI (table 4 and figure 2). Other studies are sometimes performed, such as ultrasound, computed tomography (CT) scan, and nuclear imaging (eg, positron emission tomography [PET] scans, bone scans, tagged white blood cell scans), and are discussed separately. (See "Imaging studies for osteomyelitis".)
We obtain plain X-rays in all patients with suspected osteomyelitis. If osteomyelitis is suspected despite a negative plain X-ray, we obtain an MRI for further evaluation. Additionally, for patients undergoing surgical intervention for diabetic foot infection, we obtain formal vascular evaluation.
Of note, imaging modalities often have difficulty distinguishing osteomyelitis from neuropathic osteoarthropathy (eg, Charcot foot) [2].
●Plain X-rays – If interpreted by an experienced reader, findings on plain X-rays can strongly suggest the presence of osteomyelitis and may also identify gas in tissues or foreign bodies.
Findings characteristic of osteomyelitis include cortical erosion, periosteal reaction, mixed lucency, and sclerosis (table 5) [2,3,40,61-63]. If such findings are present, the likelihood of osteomyelitis is high, particularly when coupled with typical physical exam findings and elevated inflammatory markers [64]. However, conventional radiography may be insufficient to distinguish osteomyelitis from other processes such as Charcot arthropathy and fracture [2,65].
In patients with negative X-rays and ongoing suspicion of osteomyelitis, repeating plain X-rays in two to three weeks or obtaining an MRI can be helpful. The sensitivity of plain X-rays is especially poor for detection of acute or early osteomyelitis; bony changes on plain X-rays typically lag two weeks behind onset of osteomyelitis. (See "Imaging studies for osteomyelitis".)
Plain X-rays remain advantageous over more expensive imaging studies such as MRI because they are widely available, less expensive, and are useful for establishing baseline imaging and monitoring response to therapy.
●MRI – MRI is highly sensitive and specific for osteomyelitis and is superior to plain X-rays and other common imaging studies (table 4) [2,3,40,41,45,66].
MRI is generally unnecessary if the plain radiograph is consistent with osteomyelitis. Reasons for obtaining an MRI include the following:
•Uncertainty about osteomyelitis when plain X-rays are indeterminate or negative
•Concern of a deep abscess
•To guide surgical intervention
MRI findings of osteomyelitis include cortical destruction, bone marrow edema, and soft tissue inflammation. Bone marrow edema is the earliest MRI finding of osteomyelitis but is also present in other infective and noninfective conditions (including reactive to adjacent soft tissue infection). Bone marrow edema in the absence of other MRI features of osteomyelitis should not be taken to confirm the presence of osteomyelitis. (See "Imaging studies for osteomyelitis".)
It can be challenging to distinguish a diabetic foot with Charcot arthropathy from concomitant infection on MRI. The presence of sinus tracts, fluid collections with thick rim or diffuse enhancement, and extensive adjacent marrow abnormality are concerning for Charcot with superimposed osteomyelitis [67]. In cases of severe Charcot arthropathy, definitive radiographic exclusion of osteomyelitis may not be possible. Preliminary data suggest that techniques such as diffusion-weighted MRI, dynamic contrast-enhanced MRI (DCE-MRI), or 18F-FDG PET/CT may more effectively differentiate Charcot arthropathy from osteomyelitis [68-71].
●Other studies – Other imaging studies often used in patients with suspected diabetic foot osteomyelitis include CT and nuclear studies (eg, bone scans, tagged white blood cell scans, PET). These studies are discussed in detail separately. (See "Imaging studies for osteomyelitis", section on 'Imaging modalities'.)
Bone biopsy — Bone biopsy is the only definitive way to confirm osteomyelitis and to guide antibiotic therapy.
If feasible, bone biopsy for both histopathology and culture should be obtained. Ideally, bone biopsy is obtained prior to initiation of antibiotics, but many patients require antibiotic therapy for soft tissue infection. Bone biopsies can be obtained either intraoperatively during surgical debridement or by percutaneous route.
Bone biopsy is particularly helpful in the following circumstances [3]:
●Diagnostic uncertainty
●Failure of empiric antibiotic therapy with concern for antibiotic-resistant organism
●Mid- or hindfoot lesions that could lead to high-level amputations if inadequately treated
Bone cultures provide valuable information to guide antibiotic therapy [72,73]. In a study of 305 patients with diabetic foot infection and osteomyelitis, culture results altered antibiotic selection in 87 percent of patients, regimens were narrowed in 62 percent and were broadened in 9 percent, and Methicillin-resistant S. aureus (MRSA) coverage was often discontinued based on culture results [72]. In a systematic review of 11 studies, bone biopsy was found to be positive in 84 percent of patients with diabetic foot osteomyelitis [74].
Bone biopsy is not always routinely available or practical. In such instances, a presumptive diagnosis of osteomyelitis is based on clinical and radiographic assessment.
More detailed discussion of bone biopsy is found separately. (See "Osteomyelitis in the absence of hardware: Approach to diagnosis in adults", section on 'Bone biopsy as gold standard'.)
DIFFERENTIAL DIAGNOSIS —
Noninfectious conditions that cause inflammatory changes in the skin of the lower extremities can mimic an infection. Additionally, infection may coexist with these conditions.
●Diabetic neuroarthropathy (Charcot arthropathy) – The onset of Charcot arthropathy may be acute or subacute. Patients characteristically present with sudden onset of unilateral warmth, redness, and edema over the foot or ankle, often with history of minor trauma [75]. Alternatively, in some cases, Charcot arthropathy presents insidiously with swelling over months or years [76,77].
Differentiating diabetic neuroarthropathy from diabetic foot infection is often difficult. Clues to infection include the presence of an ulcer, fever, leukocytosis, or elevated inflammatory markers. Imaging may be unable to differentiate these conditions. Joint aspiration or bone biopsy is sometimes necessary. (See "Diabetic neuroarthropathy".)
●Venous stasis – Venous stasis is often bilateral, mostly involves the calves rather than the foot, and systemic or laboratory signs of infection are absent. (See "Clinical manifestations of lower extremity chronic venous disorders".)
●Deep vein thrombosis (DVT) – DVT usually manifests with erythema, warmth, tenderness, and edema of the calf, as opposed to the foot. Ultrasound confirms the diagnosis of DVT. (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)
●Crystal-associated arthritis – The joints of the toes are often involved in crystal-induced arthritis, and fever and leukocytosis can be present in both conditions. Joint aspiration is necessary to differentiate septic arthritis from crystal-induced arthritis. (See "Gout: Clinical manifestations and diagnosis" and "Calcium pyrophosphate crystal deposition (CPPD) disease: Clinical manifestations and diagnosis".)
●Fracture and other trauma-associated injuries – Because patients with diabetic neuropathy lack sensation, fractures may not initially be noticed. Plain X-ray can diagnosis fracture. (See "Forefoot pain in adults: Evaluation, diagnosis, and select management of common causes".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Diabetes mellitus in adults".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword[s] of interest.)
●(See "Patient education: Diabetes and infections (The Basics)".)
SUMMARY AND RECOMMENDATIONS
●Definitions – Diabetic foot infection if defined as soft tissue infection and/or osteomyelitis of the foot. A diabetic foot ulcer is a common component. (See 'Definitions' above.)
●Epidemiology – Diabetic foot infections are the most common cause of hospitalization in patients with diabetes and the most common cause of lower extremity amputations. (See 'Epidemiology and risk factors' above.)
●Microbiology – Staphylococcus aureus and beta-hemolytic streptococci are the most common pathogens. (See 'Common organisms' above.)
In patients with deep, chronic, or necrotic infection, aerobic gram-negative bacilli (eg, E. coli, Pseudomonas spp) and anaerobes are also common.
Methicillin-resistant S. aureus (MRSA) is more prevalent in certain regions and patient populations (eg, the United States) (table 1), and Pseudomonas spp may be more common in humid, tropical regions. (See 'Resistant Staphylococcus aureus' above and 'Pseudomonas aeruginosa' above.)
●Clinical manifestations – Soft tissue infection manifests as cellulitis or deeper infection, including abscess.
Osteomyelitis is often painless. Visible bone, a sinus tract, or sausage toe are highly suggestive of osteomyelitis. (See 'Clinical manifestations' above.)
●Diagnosis
•Soft tissue infection – Physical examination is the primary method of diagnosis. In addition to overlying warmth and erythema, the depth of infection should be assessed. (See 'Physical examination' above.)
The IWGDF/IDSA classification scheme categorizes the infection as mild, moderate, or severe, which ultimately guides treatment (table 6). (See 'Classifying the infection' above and "Diabetic foot infections, including osteomyelitis: Treatment".)
Imaging (eg, MRI) is often unnecessary but may be of value in determining the extent of infection.
Superficial wound cultures are not appropriate due to colonization, but cultures from abscess fluid or deep tissue are helpful to guide therapy in moderate to severe infection. (See 'Role of wound cultures' above.)
•Osteomyelitis – Osteomyelitis should be considered in diabetic patients with deep soft tissue infection and in patients with chronic ulcers that do not heal after several weeks of wound care. (See 'General approach' above.)
Definitive diagnosis requires isolation of an organism from a sterilely obtained bone biopsy sample with histologic evidence of infection. Before bone samples are obtained, a presumptive diagnosis can be made if the patient has visible bone, a positive “probe-to-bone” test, or a sinus tract. (See 'Bone biopsy' above and '"Probe-to-bone" test' above.)
We obtain plain X-rays in all patients with suspected osteomyelitis. If necessary, we obtain MRI for further evaluation to aid diagnosis or define the extent of infection. (See 'Imaging studies' above.)
Inflammatory markers (eg, erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) may be helpful if diagnostic uncertainty remains; however, their clinical value is uncertain. (See 'Inflammatory markers (eg, ESR, CRP)' above.)
●Differential diagnosis – Numerous conditions can mimic diabetic foot infection, including diabetic neuroarthropathy (Charcot arthropathy), venous stasis, deep venous thrombosis, crystal-associated arthritis, and fracture. (See 'Differential diagnosis' above.)
