Diabetic Foot Infections

 

Diabetic foot infection, defined as soft tissue or bone infection below the malleoli, is the most common complication of diabetes mellitus leading to hospitalization and the most frequent cause of nontraumatic lower extremity amputation. Diabetic foot infections are diagnosed clinically based on the presence of at least two classic findings of inflammation or purulence. Infections are classified as mild, moderate, or severe. Most diabetic foot infections are polymicrobial. The most common pathogens are aerobic gram-positive cocci, mainly Staphylococcus species. Osteomyelitis is a serious complication of diabetic foot infection that increases the likelihood of surgical intervention. Treatment is based on the extent and severity of the infection and comorbid conditions. Mild infections are treated with oral antibiotics, wound care, and pressure off-loading in the outpatient setting. Selected patients with moderate infections and all patients with severe infections should be hospitalized, given intravenous antibiotics, and evaluated for possible surgical intervention. Peripheral arterial disease is present in up to 40% of patients with diabetic foot infections, making evaluation of the vascular supply critical. All patients with diabetes should undergo a systematic foot examination at least once a year, and more frequently if risk factors for diabetic foot ulcers exist. Preventive measures include patient education on proper foot care, glycemic and blood pressure control, smoking cessation, use of prescription footwear, intensive care from a podiatrist, and evaluation for surgical interventions as indicated.

Diabetic foot infections, which are infections of the soft tissue or bone below the malleoli, are a common clinical problem. Most infections occur in a site of skin trauma or ulceration. The estimated lifetime risk of a person with diabetes mellitus developing a foot ulcer is 15% to 25%, with an annual incidence of 3% to 10%.1 Major predisposing factors are peripheral neuropathy, peripheral arterial disease, and impaired immunity. More than one-half of nontraumatic lower extremity amputations are related to diabetic foot infections, and 85% of all lower extremity amputations in patients with diabetes are preceded by an ulcer.2,3

The most common pathogens in diabetic foot infection are aerobic gram-positive cocci, mainly Staphylococcus species. Methicillin-resistant Staphylococcus aureus is present in 10% to 32% of diabetic infections and is associated with a higher rate of treatment failure in patients with diabetic foot infection.4 Moderate to severe infections and wounds previously treated with antibiotics are often polymicrobial, including gram-negative bacilli. Anaerobic pathogens are more commonly present in necrotic wounds and infections of the ischemic foot.

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SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

Diagnosis of diabetic foot infection is based on the presence of at least two classic findings of inflammation or purulence.

C

2, 5, 6

Magnetic resonance imaging is the most accurate imaging study in early osteomyelitis.

C

11, 15, 16

Surgical debridement and drainage of deep tissue abscesses and infections should be performed in a timely manner.

C

3032

All patients with diabetes should undergo a systematic foot examination at least once a year, and more frequently if risk factors for diabetic foot ulcers exist.

C

37


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort.

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

Diagnosis of diabetic foot infection is based on the presence of at least two classic findings of inflammation or purulence.

C

2, 5, 6

Magnetic resonance imaging is the most accurate imaging study in early osteomyelitis.

C

11, 15, 16

Surgical debridement and drainage of deep tissue abscesses and infections should be performed in a timely manner.

C

3032

All patients with diabetes should undergo a systematic foot examination at least once a year, and more frequently if risk factors for diabetic foot ulcers exist.

C

37


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort.

How Is Diabetic Foot Infection Diagnosed?

Diabetic foot infection is a clinical diagnosis based on the presence of at least two classic findings of inflammation or purulence.2,5,6

SUPPORTING EVIDENCE

Evaluation of a suspected diabetic foot infection should involve a thorough assessment of the wound, the limb, and the patient's overall health. Local signs of infection include redness, warmth, induration or swelling, pain or tenderness, and purulent secretions. Failure of a wound to heal in spite of proper treatment, and the presence of nonpurulent discharge, malodor, and necrotic or friable tissue also suggest infection.7

The Infectious Diseases Society of America and the International Working Group on the Diabetic Foot classify diabetic wounds as uninfected or infected, with mild, moderate, and severe grades of infection (Table 17). This classification system was prospectively validated in a longitudinal study of 1,666 patients and was found to reliably predict the need for hospitalization and limb amputation.5

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Table 1.

Classification of Diabetic Foot Infection

Clinical manifestation of infectionIWGDF grade/IDSA classification

No systemic or local signs of infection

1 (uninfected)

Local infection* involving only the skin or subcutaneous tissue (without involvement of deeper tissues and without signs of a systemic inflammatory response syndrome†); any erythema present extends > 0.5 to ≤ 2 cm around the wound

2 (mild infection)

Local infection* with erythema > 2 cm around the wound, or involving structures deeper than skin and subcutaneous tissues (e.g., abscess, osteomyelitis, septic arthritis, fasciitis) and no signs of a systemic inflammatory response syndrome†

3 (moderate infection)

Local infection* with signs of a systemic inflammatory response syndrome†

4 (severe infection)


IDSA = Infectious Diseases Society of America; IWGDF = International Working Group on the Diabetic Foot.

*—Local infection is defined as the presence of at least two of the following: local swelling or induration, erythema > 0.5 cm around the ulcer in any direction, local tenderness or pain, local warmth, and purulent discharge. Other causes of inflammatory response of the skin (e.g., trauma, gout, acute Charcot neuroarthropathy, fracture, thrombosis, venous stasis) should be excluded.

†—Systemic inflammatory response syndrome is defined as the presence of at least two of the following: temperature > 100.4°F (38°C) or < 96.8°F (36°C); heart rate > 90 beats per minute; respiratory rate > 20 breaths per minute or partial pressure of arterial carbon dioxide < 32 mm Hg; white blood cell count > 12,000 per μL (12.00 × 109per L) or < 4,000 per μL (4.00 × 109per L) or ≥ 10% immature band forms.

Adapted with permission from Lipsky BA, Peters EJ, Senneville E, et al. Expert opinion on the management of infections in the diabetic foot. Diabetes Metab Res Rev. 2012;28(suppl 1):164.

Table 1.

Classification of Diabetic Foot Infection

Clinical manifestation of infectionIWGDF grade/IDSA classification

No systemic or local signs of infection

1 (uninfected)

Local infection* involving only the skin or subcutaneous tissue (without involvement of deeper tissues and without signs of a systemic inflammatory response syndrome†); any erythema present extends > 0.5 to ≤ 2 cm around the wound

2 (mild infection)

Local infection* with erythema > 2 cm around the wound, or involving structures deeper than skin and subcutaneous tissues (e.g., abscess, osteomyelitis, septic arthritis, fasciitis) and no signs of a systemic inflammatory response syndrome†

3 (moderate infection)

Local infection* with signs of a systemic inflammatory response syndrome†

4 (severe infection)


IDSA = Infectious Diseases Society of America; IWGDF = International Working Group on the Diabetic Foot.

*—Local infection is defined as the presence of at least two of the following: local swelling or induration, erythema > 0.5 cm around the ulcer in any direction, local tenderness or pain, local warmth, and purulent discharge. Other causes of inflammatory response of the skin (e.g., trauma, gout, acute Charcot neuroarthropathy, fracture, thrombosis, venous stasis) should be excluded.

†—Systemic inflammatory response syndrome is defined as the presence of at least two of the following: temperature > 100.4°F (38°C) or < 96.8°F (36°C); heart rate > 90 beats per minute; respiratory rate > 20 breaths per minute or partial pressure of arterial carbon dioxide < 32 mm Hg; white blood cell count > 12,000 per μL (12.00 × 109per L) or < 4,000 per μL (4.00 × 109per L) or ≥ 10% immature band forms.

Adapted with permission from Lipsky BA, Peters EJ, Senneville E, et al. Expert opinion on the management of infections in the diabetic foot. Diabetes Metab Res Rev. 2012;28(suppl 1):164.

Wounds should be inspected carefully, debrided of devitalized and necrotic tissue, and probed during evaluation. Cultures of superficial swabs are discouraged because these often yield contaminants. Curettage from the base of an appropriately debrided ulcer or deep tissue specimens obtained by biopsy yield true pathogens and more accurate results.8

How Is Diabetic Foot Osteomyelitis Diagnosed?

The definitive method for diagnosing osteomyelitis is a bone biopsy with histopathology consistent with bone infection or a positive result on bone culture.9 Because these methods are not widely available, physicians should rely on a combination of clinical, radiographic, and laboratory findings.

The most accurate diagnostic imaging study is magnetic resonance imaging.1012 The probe-to-bone test also has high sensitivity and specificity in outpatient settings.

SUPPORTING EVIDENCE

Infection of the bone is a serious complication of diabetic foot infection that increases the risk of treatment failure and lower extremity amputation. Diabetic foot osteomyelitis may be present in up to 20% of mild and moderate infections, and in 50% to 60% of severe infections.2,9

Physicians should suspect diabetic foot osteomyelitis in foot ulcers that are large (> 2 cm) or deep (> 3 mm), or that overlay a bony prominence; in chronic ulcers that do not heal in spite of appropriate wound care; and when bone is visible or palpable on probing.2

Plain radiography may help to assess for bone destruction and the presence of gas or a foreign body, but it has limited sensitivity for diabetic foot osteomyelitis, especially in the early stages of the condition. Depending on the timing of plain radiography and the severity of infection when radiography is performed, sensitivity ranges from 28% to 75%.13 Long-standing diabetic foot infections or ulcers are more likely to show underlying bony abnormalities because it takes weeks for bone infection to become radiographically apparent10 (Table 22,7,14).

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Table 2.

Common Radiographic Findings in Patients with Diabetic Foot Infections

Plain radiography

Periosteal reaction or elevation

Loss of cortex with bony erosion

Focal loss of trabecular pattern or marrow radiolucency

New bone formation

Bone sclerosis with or without erosion

Sequestrum: devitalized bone with radiodense appearance that has become separated from normal bone

Involucrum: a layer of new bone growth outside existing bone resulting from the stripping off of the periosteum and new bone growing from the periosteum

Cloacae: opening in involucrum or cortex through which sequestra or granulation tissue may be discharged

Magnetic resonance imaging

More specific changes

Low focal signal intensity on T1-weighted images

High focal signal on T2-weighted images

High bone marrow signal in short tau inversion recovery sequences

Less specific or secondary changes

Adjacent cutaneous ulcer

Adjacent soft tissue inflammation or edema

Cortical disruption

Sinus tract formation

Soft tissue mass


note: For both modalities, bony changes are often accompanied by contiguous soft tissue swelling.

Information from references 2, 7, and 12.

Table 2.

Common Radiographic Findings in Patients with Diabetic Foot Infections

Plain radiography

Periosteal reaction or elevation

Loss of cortex with bony erosion

Focal loss of trabecular pattern or marrow radiolucency

New bone formation

Bone sclerosis with or without erosion

Sequestrum: devitalized bone with radiodense appearance that has become separated from normal bone

Involucrum: a layer of new bone growth outside existing bone resulting from the stripping off of the periosteum and new bone growing from the periosteum

Cloacae: opening in involucrum or cortex through which sequestra or granulation tissue may be discharged

Magnetic resonance imaging

More specific changes

Low focal signal intensity on T1-weighted images

High focal signal on T2-weighted images

High bone marrow signal in short tau inversion recovery sequences

Less specific or secondary changes

Adjacent cutaneous ulcer

Adjacent soft tissue inflammation or edema

Cortical disruption

Sinus tract formation

Soft tissue mass


note: For both modalities, bony changes are often accompanied by contiguous soft tissue swelling.

Information from references 2, 7, and 12.

Triple phase technetium-99m methylene diphosphonate bone scan is more sensitive than plain radiography, with a sensitivity of about 90%, but it has a much lower specificity (46%). White blood cell scans are more specific than triple phase bone scan and may be useful when magnetic resonance imaging is not available or is contraindicated.1416

Magnetic resonance imaging is the most accurate imaging study in the diagnosis of osteomyelitis.1012 It is 90% sensitive and 80% specific.11 However, it may be of limited value in differentiating osteomyelitis from acute Charcot neuroarthropathy.17

Probe-to-bone testing (attempting to reach exposed bone with a metal probe) is an inexpensive diagnostic tool used to support the diagnosis of osteomyelitis. It should be performed after debridement of devitalized and necrotic tissue. A positive result on probe-to-bone testing (touching a hard or gritty bone surface) increases the likelihood of osteomyelitis in patients with high pretest probability. A negative result on probe-to-bone testing in patients with low pretest probability makes osteomyelitis unlikely but does not exclude the diagnosis.1820 A study of outpatients with diabetic foot ulcers found probe-to-bone testing to be 87% sensitive and 91% specific for osteomyelitis.19

What Is the Value of Blood Testing in the Diagnosis of Diabetic Foot Infections?

Leukocytosis and elevated erythrocyte sedimentation rate increase the risk of a diabetic foot infection, but their absence does not rule it out.

SUPPORTING EVIDENCE

In one multicenter study, investigators found that more than one-half of the patients admitted with acute diabetic foot infection had a normal leukocyte count, and 83.7% had a normal neutrophil count.21 The absence of leukocytosis, an absence of a left shift in a white blood cell differential, or lack of elevation of acute phase reactants does not exclude infection. An erythrocyte sedimentation rate greater than 70 mm per hour in combination with clinical suspicion has been shown to correlate with increased likelihood of osteomyelitis. Conversely, a normal erythrocyte sedimentation rate lessens the likelihood of osteomyelitis but does not exclude it.22

Erythrocyte sedimentation rate and C-reactive protein are helpful biochemical markers to monitor therapeutic response.10,11,1420,2224 Blood cultures should be obtained in patients with severe diabetic foot infections.

How Should Diabetic Foot Infections Be Treated?

Treatment of a diabetic foot infection is based on the extent and severity of the infection. No single antibiotic regimen is clearly superior to another. Mild infections should be treated with oral antibiotics in the outpatient setting. Selected patients with moderate infections and all patients with severe infections require hospitalization to receive parenteral antibiotics, surgical consultation, and additional evaluation.

SUPPORTING EVIDENCE

Care provided by a well-coordinated, multidisciplinary team has been shown to improve outcomes in diabetic foot infections.25,26 The National Institute for Health and Clinical Excellence guidelines on the inpatient management of diabetic foot problems recommend that each hospital have a care pathway carried out by a multidisciplinary team.16

Initial choice of empiric antibiotic is based on severity of infection and the likely pathogen (Table 32,7,27). Mild infections with no prior antibiotic therapy should be treated with one to two weeks of oral antibiotics that cover aerobic gram-positive pathogens.2729 Selected patients with moderate infections (patients with poor glycemic control or peripheral arterial disease, and patients who are unable to adhere to a treatment plan that includes antibiotic use, appropriate wound care, pressure off-loading, and return for close follow-up) and all patients with severe infections require hospital admission and treatment with broad-spectrum parenteral antibiotics. Surgical interventions may include incision and drainage of an abscess, extensive debridement of necrotic and devitalized tissue, resection, amputation, and revascularization, and should be performed in a timely manner.3032

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Table 3.

Suggested Antibiotics for Treatment of Diabetic Foot Infection

PathogenEmpiric antibioticActive against MRSA?Duration of initial therapyRenal dose adjustment?

Mild infection

1 to 2 weeks

Gram-positive cocci with or without MRSA

Amoxicillin/clavulanate (Augmentin)

No

Yes

Cefdinir (Omnicef)

No

Yes

Cephalexin (Keflex)

No

Yes

Clindamycin*

Yes

No

Dicloxacillin (Dynapen)

No

No

Doxycycline

Yes

No

Levofloxacin (Levaquin)

No

Yes

Linezolid (Zyvox)

Yes (use if high risk for MRSA)

No

Minocycline (Minocin)

Yes

Yes

Trimethoprim/sulfamethoxazole

Yes

Yes

Moderate to severe infection

2 to 3 weeks

Gram-positive cocci; gram-negative rods; anaerobes with or without multidrug-resistant organisms (e.g., MRSA, extended-spectrum beta-lactamase–producing strains, vancomycin-resistant enterococcus)

Ampicillin/sulbactam (Unasyn)

No

Yes

Cefoxitin

No

Yes

Ceftriaxone (Rocephin)

No

No

Clindamycin/fluoroquinolones

Somewhat

No/Yes

Daptomycin (Cubicin)

Yes

Yes

Ertapenem (Invanz)

No

Yes

Imipenem/cilastin (Primaxin)

No

Yes

Linezolid

Yes

No

Moxifloxacin (Avelox)

No

No

Piperacillin/tazobactam (Zosyn)

No

Yes

Ticarcillin/clavulanate (Timentin)

No

Yes

Tigecycline (Tygacil)

Yes

No

Vancomycin

Yes

Yes


MRSA = methicillin-resistant Staphylococcus aureus.

*—Consider a double disk diffusion test before using for MRSA.

Information from references 2, 7, and 27.

Table 3.

Suggested Antibiotics for Treatment of Diabetic Foot Infection

PathogenEmpiric antibioticActive against MRSA?Duration of initial therapyRenal dose adjustment?

Mild infection

1 to 2 weeks

Gram-positive cocci with or without MRSA

Amoxicillin/clavulanate (Augmentin)

No

Yes

Cefdinir (Omnicef)

No

Yes

Cephalexin (Keflex)

No

Yes

Clindamycin*

Yes

No

Dicloxacillin (Dynapen)

No

No

Doxycycline

Yes

No

Levofloxacin (Levaquin)

No

Yes

Linezolid (Zyvox)

Yes (use if high risk for MRSA)

No

Minocycline (Minocin)

Yes

Yes

Trimethoprim/sulfamethoxazole

Yes

Yes

Moderate to severe infection

2 to 3 weeks

Gram-positive cocci; gram-negative rods; anaerobes with or without multidrug-resistant organisms (e.g., MRSA, extended-spectrum beta-lactamase–producing strains, vancomycin-resistant enterococcus)

Ampicillin/sulbactam (Unasyn)

No

Yes

Cefoxitin

No

Yes

Ceftriaxone (Rocephin)

No

No

Clindamycin/fluoroquinolones

Somewhat

No/Yes

Daptomycin (Cubicin)

Yes

Yes

Ertapenem (Invanz)

No

Yes

Imipenem/cilastin (Primaxin)

No

Yes

Linezolid

Yes

No

Moxifloxacin (Avelox)

No

No

Piperacillin/tazobactam (Zosyn)

No

Yes

Ticarcillin/clavulanate (Timentin)

No

Yes

Tigecycline (Tygacil)

Yes

No

Vancomycin

Yes

Yes


MRSA = methicillin-resistant Staphylococcus aureus.

*—Consider a double disk diffusion test before using for MRSA.

Information from references 2, 7, and 27.

The suggested duration of antibiotics for moderate to severe soft tissue infections is two to three weeks. Traditionally, the duration of antibiotic therapy for diabetic foot osteomyelitis has been prolonged, but persons in whom the infected bone was surgically removed can be treated with a shorter course (Table 42).

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Table 4.

Suggested Route of Administration and Duration of Antibiotic Therapy for Diabetic Foot Osteomyelitis

Bone or joint infectionRoute of administrationDuration of therapy

No residual infected tissue (e.g., postamputation)

Parenteral or oral

2 to 5 days

Residual infected soft tissue (but not bone)

Parenteral or oral

1 to 3 weeks

Residual infected (but viable) bone

Initially parenteral, then consider oral

4 to 6 weeks

No surgery, or residual dead bone postoperatively

Initially parenteral, then consider oral

≥ 3 months


Adapted with permission from Lipsky BA, Berendt AR, Cornia PB, et al.; Infectious Diseases Society of America. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2012;54(12):e158.

Table 4.

Suggested Route of Administration and Duration of Antibiotic Therapy for Diabetic Foot Osteomyelitis

Bone or joint infectionRoute of administrationDuration of therapy

No residual infected tissue (e.g., postamputation)

Parenteral or oral

2 to 5 days

Residual infected soft tissue (but not bone)

Parenteral or oral

1 to 3 weeks

Residual infected (but viable) bone

Initially parenteral, then consider oral

4 to 6 weeks

No surgery, or residual dead bone postoperatively

Initially parenteral, then consider oral

≥ 3 months


Adapted with permission from Lipsky BA, Berendt AR, Cornia PB, et al.; Infectious Diseases Society of America. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2012;54(12):e158.

A recent systematic review of several randomized controlled and cohort studies by the International Working Group on the Diabetic Foot comparing different antibiotic regimens showed there was no one superior regimen, route of administration, or duration of treatment for diabetic foot infections.13 The Infectious Diseases Society of America guidelines on diabetic foot infection reached the same conclusion.2

Beyond the initial treatment phase, subsequent choice of antibiotics should be guided by the extent of infection, culture results, and the clinical response to empiric therapy (Figure 17). Physicians should also consider local antibiotic resistance patterns and the presence of multidrug-resistant organisms, renal and hepatic impairment, drug allergies, immunosuppression, patient compliance, and cost of treatment.6,12

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Approach to the Infected Diabetic Foot

Figure 1.

Algorithmic approach to the assessment and treatment of diabetic foot infections.

Adapted with permission from Lipsky BA, Peters EJ, Senneville E, et al. Expert opinion on the management of infections in the diabetic foot. Diabetes Metab Res Rev. 2012;28(suppl 1):164.

Approach to the Infected Diabetic Foot


Figure 1.

Algorithmic approach to the assessment and treatment of diabetic foot infections.

Adapted with permission from Lipsky BA, Peters EJ, Senneville E, et al. Expert opinion on the management of infections in the diabetic foot. Diabetes Metab Res Rev. 2012;28(suppl 1):164.

What Is the Role of Peripheral Arterial Disease in Diabetic Foot Infections?

Peripheral arterial disease is an independent risk factor for diabetic foot infections and is the most important predictor of the outcome of diabetic foot ulceration.33

SUPPORTING EVIDENCE

Peripheral arterial disease is present in up to 40% of patients with diabetic foot infections.34 In spite of advancements in medical and surgical therapies, the risks of amputation and the five-year mortality rate after amputation remain high.35 Evaluation of the vascular supply is critical in the treatment of diabetic foot infection. Examination should include the color and temperature of the skin, palpation of peripheral pulses, and signs of arterial insufficiency, including skin and nail atrophy. An ankle-brachial index below 0.9 indicates occlusive arterial disease; an index below 0.5 is consistent with significant peripheral arterial disease.33 Additional evaluation that includes toe blood pressure measurement, transcutaneous pressure of oxygen, or arterial Doppler examination may be warranted. Computed tomography angiography and magnetic resonance angiography are most useful in patients who are candidates for revascularization.36

Prevention

All patients with diabetes should undergo a systematic foot examination at least once a year, and more frequently if risk factors for diabetic foot ulcers exist (Table 5).37 Appropriate preventive measures include patient education about proper foot care, glycemic and blood pressure control, smoking cessation, use of prescription footwear, intensive podiatric care, and evaluation for surgical interventions as indicated.

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Table 5.

Risk Classification System of the ADA Task Force of the Foot Care Interest Group

Risk categoryDefinitionTreatment recommendationsSuggested follow-up

0

No loss of protective sensation, no peripheral arterial disease, no deformity

Consider patient education on foot care, including information on appropriate footwear

Annually (by primary care physician and/or specialist)

1

Loss of protective sensation with or without deformity

Consider prophylactic surgery if deformity cannot be safely accommodated in shoes

Every 3 to 6 months (by primary care physician or specialist)

Continue patient education

Consider the use of prescriptive or accommodative footwear

2

Peripheral arterial disease with or without loss of protective sensation

Consider the use of accommodative footwear

Every 2 to 3 months (by specialist)

Consider a vascular consultation for combined follow-up

3

History of ulcer or amputation

Consider patient education on foot care

Every 1 to 2 months (by specialist)

Consider vascular consultation for combined follow-up if peripheral arterial disease is present


ADA = American Diabetes Association.

Adapted with permission from Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the Foot Care Interest Group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care. 2008;31(8):1684.

Table 5.

Risk Classification System of the ADA Task Force of the Foot Care Interest Group

Risk categoryDefinitionTreatment recommendationsSuggested follow-up

0

No loss of protective sensation, no peripheral arterial disease, no deformity

Consider patient education on foot care, including information on appropriate footwear

Annually (by primary care physician and/or specialist)

1

Loss of protective sensation with or without deformity

Consider prophylactic surgery if deformity cannot be safely accommodated in shoes

Every 3 to 6 months (by primary care physician or specialist)

Continue patient education

Consider the use of prescriptive or accommodative footwear

2

Peripheral arterial disease with or without loss of protective sensation

Consider the use of accommodative footwear

Every 2 to 3 months (by specialist)

Consider a vascular consultation for combined follow-up

3

History of ulcer or amputation

Consider patient education on foot care

Every 1 to 2 months (by specialist)

Consider vascular consultation for combined follow-up if peripheral arterial disease is present


ADA = American Diabetes Association.

Adapted with permission from Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the Foot Care Interest Group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care. 2008;31(8):1684.

Data Sources: A PubMed search was completed in Clinical Queries using the terms diabetic, foot, and infections. The search included meta-analyses, randomized controlled trials, clinical trials, reviews, expert opinions, and guidelines. We also searched the Cochrane database, Clinical Evidence, and Essential Evidence Plus. Search dates: February 1, 2012, to November 30, 2012.

The Authors

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FASSIL W. GEMECHU, MD, is a staff physician and assistant professor in the Department of Family Medicine at MetroHealth Medical Center in Cleveland, Ohio....

FNU SEEMANT, MD, is a fellow in primary care sports medicine in the University Orthopedic Center at the State University of New York at Buffalo. At the time this article was written, he was a fellow in the Department of Family Medicine at MetroHealth Medical Center.

CATHERINE A. CURLEY, MD, is division director in the Division of Hospital Medicine and an assistant professor of medicine at MetroHealth Medical Center.

Address correspondence to Fassil W. Gemechu, MD, MetroHealth Medical Center, 4229 Pearl Rd., Cleveland, OH 44109 (e-mail: fgemechu@metrohealth.org). Reprints are not available from the authors.

Author disclosure: No relevant financial affiliations.

REFERENCES

show all references

1. Reiber GE, Vileikyte L, Boyko EJ, et al. Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Diabetes Care. 1999;22(1):157–162....

2. Lipsky BA, Berendt AR, Cornia PB, et al.; Infectious Diseases Society of America. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2012;54(12):e132–e173.

3. Boulton AJ, Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The global burden of diabetic foot disease. Lancet. 2005;366(9498):1719–1724.

4. Vardakas KZ, Horianopoulou M, Falagas ME. Factors associated with treatment failure in patients with diabetic foot infections: an analysis of data from randomized controlled trials. Diabetes Res Clin Pract. 2008;80(3):344–351.

5. Lavery LA, Armstrong DG, Murdoch DP, Peters EJ, Lipsky BA. Validation of the Infectious Diseases Society of America's diabetic foot classification system. Clin Infect Dis. 2007;44(4):562–565.

6. Daum RS. Clinical practice. Skin and soft-tissue infections caused by methicillin-resistant Staphylococcus aureus [published correction appears in N Engl J Med. 2007;357(13):1357]. N Engl J Med. 2007;357(4):380–390.

7. Lipsky BA, Peters EJ, Senneville E, et al. Expert opinion on the management of infections in the diabetic foot. Diabetes Metab Res Rev. 2012;28(suppl 1):163–178.

8. Mutluoglu M, Uzun G, Turhan V, Gorenek L, Ay H, Lipsky BA. How reliable are cultures of specimens from superficial swabs compared with those of deep tissue in patients with diabetic foot ulcers? J Diabetes Complications. 2012;26(3):225–229.

9. Berendt AR, Peters EJ, Bakker K, et al. Diabetic foot osteomyelitis: a progress report on diagnosis and a systematic review of treatment. Diabetes Metab Res Rev. 2008;24(suppl 1):S145–S161.

10. Dinh MT, Abad CL, Safdar N. Diagnostic accuracy of the physical examination and imaging tests for osteomyelitis underlying diabetic foot ulcers: meta-analysis. Clin Infect Dis. 2008;47(4):519–527.

11. Kapoor A, Page S, Lavalley M, Gale DR, Felson DT. Magnetic resonance imaging for diagnosing foot osteomyelitis: a meta-analysis. Arch Intern Med. 2007;167(2):125–132.

12. Liu C, Bayer A, Cosgrove SE, et al.; Infectious Diseases Society of America. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children [published correction appears in Clin Infect Dis. 2011;53(3):319]. Clin Infect Dis. 2011;52(3):e18–e55.

13. Peters EJ, Lipsky BA, Berendt AR, et al. A systematic review of the effectiveness of interventions in the management of infection in the diabetic foot. Diabetes Metab Res Rev. 2012;28(suppl 1):142–162.

14. Teh J, Berendt T, Lipsky BA. Rational imaging. Investigating suspected bone infection in the diabetic foot. BMJ. 2009;339:b4690.

15. Capriotti G, Chianelli M, Signore A. Nuclear medicine imaging of diabetic foot infection: results of meta-analysis. Nucl Med Commun. 2006;27(10):757–764.

16. Tan T, Shaw EJ, Siddiqui F, Kandaswamy P, Barry PW, Baker M; Guideline Development Group. Inpatient management of diabetic foot problems: summary of NICE guidance. BMJ. 2011;342:d1280.

17. Botek G, Anderson MA, Taylor R. Charcot neuroarthropathy: an often overlooked complication of diabetes. Cleve Clin J Med. 2010;77(9):593–599.

18. Aragón-Sánchez J, Lipsky BA, Lázaro-Martínez JL. Diagnosing diabetic foot osteomyelitis: is the combination of probe-to-bone test and plain radiography sufficient for high-risk inpatients? Diabet Med. 2011;28(2):191–194.

19. Lavery LA, Armstrong DG, Peters EJ, Lipsky BA. Probe-to-bone test for diagnosing diabetic foot osteomyelitis: reliable or relic? Diabetes Care. 2007;30(2):270–274.

20. Morales Lozano R, González Fernández ML, Martinez Hernández D, Beneit Montesinos JV, Guisado Jiménez S, Gonzalez Jurado MA. Validating the probe-to-bone test and other tests for diagnosing chronic osteomyelitis in the diabetic foot. Diabetes Care. 2010;33(10):2140–2145.

21. Armstrong DG, Perales TA, Murff RT, et al. Value of white clood cell count with differential in the acute diabetic infection. J Am Podiatr Med Assoc. 1996;36(5):224–227.

22. Butalia S, Palda VA, Sargeant RJ, Detsky AS, Mourad O. Does this patient with diabetes have osteomyelitis of the lower extremity? JAMA. 2008;299(7):806–813.

23. Kaleta JL, Fleischli JW, Reilly CH. The diagnosis of osteomyelitis in diabetes using erythrocyte sedimentation rate: a pilot study. J Am Podiatr Med Assoc. 2001;91(9):445–450.

24. Fleischer AE, Didyk AA, Woods JB, Burns SE, Wrobel JS, Armstrong DG. Combined clinical and laboratory testing improves diagnostic accuracy for osteomyelitis in the diabetic foot. J Foot Ankle Surg. 2009;48(1):39–46.

25. Sanders LJ, Robbins JM, Edmonds ME. History of the team approach to amputation prevention: pioneers and milestones. J Vasc Surg. 2010;52(3 suppl):3S–16S.

26. Aydin K, Isildak M, Karakaya J, Gürlek A. Change in amputation predictors in diabetic foot disease: effect of multidisciplinary approach. Endocrine. 2010;38(1):87–92.

27. Kosinski MA, Lipsky BA. Current medical management of diabetic foot infections. Expert Rev Anti Infect Ther. 2010;8(11):1293–1305.

28. Bakker K, Apelqvist J, Schaper NC; International Working Group on Diabetic Foot Editorial Board. Practical guidelines on the management and prevention of the diabetic foot 2011. Diabetes Metab Res Rev. 2012;28(suppl 1):225–231.

29. Bader MS, Brooks A. Medical management of diabetic foot infections. Postgrad Med. 2012;124(2):102–113.

30. Aragón-Sánchez J. Seminar review: a review of the basis of surgical treatment of diabetic foot infections. Int J Low Extrem Wounds. 2011;10(1):33–65.

31. Wieman TJ. Principles of management: the diabetic foot. Am J Surg. 2005;190(2):295–299.

32. Aragón-Sánchez J. Treatment of diabetic foot osteomyelitis: a surgical critique. Int J Low Extrem Wounds. 2010;9(1):37–59.

33. Schaper NC, Andros G, Apelqvist J, et al. Diagnosis and treatment of peripheral arterial disease in diabetic patients with a foot ulcer. A progress report of the International Working Group on the Diabetic Foot. Diabetes Metab Res Rev. 2012;28(suppl 1):218–224.

34. Prompers L, Schaper N, Apelqvist J, et al. Prediction of outcome in individuals with diabetic foot ulcers: focus on the differences between individuals with and without peripheral arterial disease. The EURODIALE study. Diabetologia. 2008;51(5):747–755.

35. Armstrong DG, Wrobel J, Robbins JM. Guest editorial: are diabetes-related wounds and amputations worse than cancer? Int Wound J. 2007;4(4):286–287.

36. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/ Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients with Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation. 2006;113(11):e463–e654.

37. Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the Foot Care Interest Group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care. 2008;31(8):1679–1685.


 

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