Diabetic Foot Infections

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Diabetic Foot Infections

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Compromise of the blood supply from microvascular disease, often in association with lack of sensation because of neuropathy, predisposes persons with diabetes mellitus to foot infections. These infections span the spectrum from simple, superficial cellulitis to chronic osteomyelitis.

The radiograph below demonstrates a foot lesion in a patient with diabetes.

Diabetic foot infections typically take one of the following forms:

Cellulitis

Deep-skin and soft-tissue infections

Acute osteomyelitis

Chronic osteomyelitis

Cellulitis

Tender, erythematous, nonraised skin lesions are present, sometimes with lymphangitis

Lymphangitis suggests group A streptococcal infection

Bullae are typical of Staphylococcus aureus infection, but occasionally occur with group A streptococci

· No ulcer or wound exudate is present

Deep-skin and soft-tissue infections

The patient may be acutely ill, with painful induration of the soft tissues in the extremity

Wound discharge is usually not present

In mixed infections that may involve anaerobes, crepitation may be noted over the afflicted area

Extreme pain and tenderness may indicate compartment syndrome or clostridial infection (ie, gas gangrene)

The tissues are not tense, and bullae may be present

Discharge, if present, is often foul

Acute osteomyelitis

Unless peripheral neuropathy is present, the patient has pain at the site of the involved bone

Usually, fever and regional adenopathy are absent

Chronic osteomyelitis

The patient’s temperature is usually less than 102°F

Discharge is commonly foul

No lymphangitis is observed

Pain may or may not be present, depending on the degree of peripheral neuropathy

Deep, penetrating ulcers and deep sinus tracts (diagnostic of chronic osteomyelitis) are usually located between the toes or on the plantar surface of the foot

The medial malleoli, shins, or heels are not usually sites of involvement

See Clinical Presentation for more detail.

Cellulitis

The WBC and ESR are slightly or moderately elevated, but these elevations are not diagnostic

Blood culture results are usually negative; if positive, they usually indicate the presence of group A or group B streptococci

Cultures of skin via aspiration or biopsy are generally unrewarding; aspiration of a sample from the leading edge of the erythematous border has a low yield (likely < 5%) but may be used if the likely organism must be identified on initial presentation

Skin and soft-tissue infections

The WBC and ESR are mildly or moderately elevated

If bullae are present, Gram stain and culture results from aspirated exudate from a bullous lesion may help identify the pathogen

Blood culture results may be positive

In suspected deep soft-tissue infection, plain radiography, CT, or MRI may be performed to evaluate for compartment syndrome or for gas or a foreign body in the deep tissues^[1]; excessive gas signifies a mixed aerobic-anaerobic infection, in contrast to gas gangrene (clostridial myonecrosis)

Gram stains and/or cultures of samples aspirated from deep-skin and soft-tissue infections may be used to identify the organism

Acute osteomyelitis

The WBC usually reveals leukocytosis, and the ESR is moderately or highly elevated^[2]

Blood culture results are usually negative; when positive, the findings most frequently indicate the presence of S aureus

For affected long bones, plain radiographic findings generally become abnormal after 10-14 days; soft-tissue swelling and periosteal elevation are the earliest signs

Bone scans are preferred to gallium or indium scans; bone-scan findings are positive within 24 hours

Bone biopsy is not necessary

Chronic osteomyelitis

The WBC is often within the reference range; the ESR is usually very highly elevated and may exceed 100 mm/hr^[2]; the platelet count is also often elevated

Blood culture results are usually negative

Plain radiographic findings are invariably abnormal

Bone scans are usually unnecessary unless diagnostic confusion exists with another disorder (eg, bone tumor); an MRI scan would also be helpful in such a situation

Bone biopsy performed under aseptic conditions in the operating room is the preferred way to identify the causative pathogen

Important pathogens include Bacteroides fragilis, E coli, Proteus mirabilis, and Klebsiella pneumoniae; Pseudomonas aeruginosa is usually not the causative organism

See Workup for more detail.

Treatment of diabetic foot infections varies by type, as follows:

Cellulitis – Most responsive to antibiotics

Deep skin and soft-tissue infections – Usually curable, but additional debridement is usually indicated

Acute osteomyelitis – Infecting microorganisms and the likelihood of successful treatment with antimicrobial therapy are essentially the same as in patients without diabetes

Chronic osteomyelitis – Surgical debridement is essential, in addition to antibiotics; amputation may be necessary

See Treatment and Medication for more detail.

Foot infections are the most common problems in persons with diabetes. These individuals are predisposed to foot infections because of a compromised vascular supply secondary to diabetes. Local trauma and/or pressure (often in association with lack of sensation because of neuropathy), in addition to microvascular disease, may result in various diabetic foot infections that run the spectrum from simple, superficial cellulitis to chronic osteomyelitis.

The radiograph below demonstrates a foot lesion in a patient with diabetes.

Infections in patients with diabetes are difficult to treat because these individuals have impaired microvascular circulation, which limits the access of phagocytic cells to the infected area and results in a poor concentration of antibiotics in the infected tissues. In addition, diabetic individuals can not only have a combined infection involving bone and soft tissue called fetid foot, a severe and extensive, chronic soft-tissue and bone infection that causes a foul exudate, but they may also have peripheral vascular disease that involves the large vessels, as well as microvascular and capillary disease that results in peripheral vascular disease with gangrene.^{[3, 4, 5, 6, 7]}

Except for chronic osteomyelitis, infections in patients with diabetes are caused by the same microorganisms that can infect the extremities of persons without diabetes. Gas gangrene is conspicuous because of its low incidence in patients with diabetes, but deep-skin and soft-tissue infections, which are due to gas-producing organisms, frequently occur in patients with these infections.

In general, foot infections in persons with diabetes become more severe and take longer to cure than do equivalent infections in persons without diabetes.

Staging in diabetic foot infections is applicable only in cases of chronic osteomyelitis that require surgery.

Go to Type 1 Diabetes Mellitus,Type 2 Diabetes Mellitus, and Diabetic Ulcers to see more complete information on these topics.

In chronic osteomyelitis, a sequestrum and involucrum form; these represent islands of infected bone. Bone fragments that are isolated have no blood supply.

Bacteremia may accompany cellulitis, skin or soft-tissue infections, and/or acute osteomyelitis, but this is not a complication per se. If chronic osteomyelitis is left untreated for years, it may lead to complications such as amyloidosis or squamous cell carcinoma at the site of drainage through the skin. Bacteremia and septic shock rarely, if ever, occur as a result of chronic osteomyelitis.

Research indicates that when present in Staphylococcus aureus, the prophage ROSA-like inhibits the bacterium from infecting diabetic foot ulcers and also prevents S aureus from replicating inside osteoblasts, diminishing cell damage to these lesions.^[8]

Diabetes mellitus is a disorder that primarily affects the microvascular circulation. In the extremities, microvascular disease due to “sugar-coated capillaries” limits the blood supply to the superficial and deep structures. Pressure due to ill-fitting shoes or trauma further compromises the local blood supply at the microvascular level, predisposing the patient to infection, which may involve the skin, soft tissues, bone, or all of these combined.

Diabetes also accelerates macrovascular disease, which is evident clinically as accelerating atherosclerosis and/or peripheral vascular disease. Most diabetic foot infections occur in the setting of good dorsalis pedis pulses; this finding indicates that the primary problem in diabetic foot infections is microvascular compromise.

Impaired microvascular circulation hinders white blood cell migration into the area of infection and limits the ability of antibiotics to reach the site of infection in an effective concentration. Diabetic neuropathy may be encountered in conjunction with vasculopathy. This may allow for incidental trauma that goes unrecognized (eg, blistering, penetrating foreign body). Go to Diabetic Neuropathy for more complete information on this topic.

The microbiologic features of diabetic foot infections vary according to the tissue infected. In patients with diabetes, superficial skin infections, such as cellulitis, are caused by the same organisms as those in healthy hosts, namely group A streptococci and S aureus. In unusual epidemiologic circumstances, however, organisms such as Pasteurella multocida (eg, from dog or cat bites or scratches) may be noted and should always be considered. Group B streptococcal cellulitis is uncommon in healthy hosts but not uncommon in patients with diabetes. In diabetic individuals, group B streptococci may cause urinary tract infections and catheter-associated bacteriuria in addition to cellulitis, skin and/or soft-tissue infections, and chronic osteomyelitis. Such infections may be complicated by bacteremia.

Furthermore, as previously mentioned, deep soft-tissue infections in diabetic persons can be associated with gas-producing, gram-negative bacilli. Clinically, these infections appear as necrotizing fasciitis, compartment syndrome, or myositis. Gas gangrene is uncommon in persons with diabetes.

Acute osteomyelitis usually occurs as a result of foot trauma in an individual with diabetes. The distribution of organisms is the same as that in an individual without diabetes who has acute osteomyelitis. In chronic osteomyelitis, however, the pathogens include group A and group B streptococci, aerobic gram-negative bacilli, and Bacteroides fragilis.

Other pathogens implicated in chronic osteomyelitis in patients with diabetes include B fragilis, Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae.

Pseudomonas aeruginosa is generally not a pathogen in chronic osteomyelitis in these individuals. Although P aeruginosa is frequently cultured from samples obtained from a draining sinus tract or deep penetrating ulcers in patients with diabetes, these organisms are superficial colonizers and are generally not the cause of the bone infection.

Because Pseudomonas organisms are water-borne, superficial ulcers may be contaminated by bacteria in wet socks or dressings. To the authors’ knowledge, however, no well-documented cases of biopsy-proven P aeruginosa infection have been reported in patients with chronic osteomyelitis.

Fetid foot represents a combined deep-skin and soft-tissue infection caused by pathogens involved in chronic osteomyelitis.

Globally, diabetic foot infections are the most common skeletal and soft-tissue infections in patients with diabetes. The incidence of diabetic foot infections is similar to that of diabetes in various ethnic groups and most frequently affect elderly patients. There are no significant differences between the sexes.

Mortality is not common, except in unusual circumstances. The mortality risk is highest in patients with chronic osteomyelitis and in those with acute necrotizing soft-tissue infections.

A prospective cohort study by Lynar et al indicated that in patients with diabetic foot infections, the mortality risk is increased in those who are undergoing hemodialysis or of older age. The 1-year, cumulative mortality risk in patients receiving hemodialysis was determined to be 24.5%.^[9]

The prognosis for cases of cellulitis, skin and/or soft-tissue infections, and acute osteomyelitis depends on the adequacy of antimicrobial therapy and surgical debridement. For cases of chronic osteomyelitis, the prognosis is directly related to the vascular supply in the affected limb and the adequacy of surgical debridement.

In a German study, nearly 250 patients with diabetic foot ulcers were evaluated and followed over time. Major adverse risk factors for long-term limb salvage included the presence of significant peripheral artery disease and renal insufficiency.^[10]

A study by Chammas et al indicated that ischemic heart disease is the primary cause of premature death in patients with diabetic foot ulcer, finding it to be the major source of mortality on postmortem examination in 62.5% of 243 diabetic foot ulcer patients. The study also found that in patients with diabetic foot ulcer, the mean age of death from ischemic heart disease, as derived from postmortem examination, was 5 years below that of controls. Patients with neuropathic foot ulcers were determined to have the highest risk of premature death from ischemic heart disease.^[11]

A study by Chen et al indicated that following hospital treatment for diabetic foot ulcer, invasive systemic infection associated with the ulcer (DFU-ISI) is an important late complication that increases mortality risk. In the study’s patients, methicillin-resistant Staphylococcus aureus (MRSA) gave rise to 57% of the ISIs. Using Cox regression modeling, the investigators found that complicated ulcer healing and the presence of MRSA in the initial ulcer culture predicted the development of DFU-ISIs (hazard ratios of 3.812 and 2.030, respectively), with the hazard ratio for mortality risk in association with DFU-ISIs being 1.987.^[12]

Patients with diabetes must be careful to avoid foot trauma and to properly care for their feet to minimize the possibility of infection. In addition, they must understand that chronic osteomyelitis cannot be cured with antibiotics alone and that adequate surgical debridement is necessary.

Patients who are unwilling to undergo the surgical procedure must understand the long-term complications of chronic osteomyelitis. They should be advised that if the infection is not adequately treated with sufficient surgical debridement and/or amputation, systemic complications, including bacteremia and/or systemic infection, amyloidosis, and squamous cell carcinoma at the affected site, may occur over time.

Long-term suppressive therapy may decrease the incidence of septic complications, but it does not affect the long-term complications, which may include amyloidosis or squamous cell carcinoma at the drainage site.

For patient education information, see the Diabetes Center, as well as Diabetic Foot Care.

Tan PL, Teh J. MRI of the diabetic foot: differentiation of infection from neuropathic change. Br J Radiol. 2007 Nov. 80(959):939-48. [Medline]. [Full Text].

Malabu UH, Al-Rubeaan KA, Al-Derewish M. Diabetic foot osteomyelitis: usefulness of erythrocyte sedimentation rate in its diagnosis. West Afr J Med. 2007 Apr-Jun. 26(2):113-6. [Medline].

Lipsky BA, Armstrong DG, Citron DM, Tice AD, Morgenstern DE, Abramson MA. Ertapenem versus piperacillin/tazobactam for diabetic foot infections (SIDESTEP): prospective, randomised, controlled, double-blinded, multicentre trial. Lancet. 2005 Nov 12. 366(9498):1695-703. [Medline].

Lipsky BA, Giordano P, Choudhri S, Song J. Treating diabetic foot infections with sequential intravenous to oral moxifloxacin compared with piperacillin-tazobactam/amoxicillin-clavulanate. J Antimicrob Chemother. 2007 Aug. 60(2):370-6. [Medline]. [Full Text].

Lipsky BA, Stoutenburgh U. Daptomycin for treating infected diabetic foot ulcers: evidence from a randomized, controlled trial comparing daptomycin with vancomycin or semi-synthetic penicillins for complicated skin and skin-structure infections. J Antimicrob Chemother. 2005 Feb. 55(2):240-5. [Medline]. [Full Text].

Stein GE, Schooley S, Peloquin CA, Missavage A, Havlichek DH. Linezolid tissue penetration and serum activity against strains of methicillin-resistant Staphylococcus aureus with reduced vancomycin susceptibility in diabetic patients with foot infections. J Antimicrob Chemother. 2007 Oct. 60(4):819-23. [Medline]. [Full Text].

Wang S, Cunha BA, Hamid NS, Amato BM, Feuerman M, Malone B. Metronidazole single versus multiple daily dosing in serious intraabdominal/pelvic and diabetic foot infections. J Chemother. 2007 Aug. 19(4):410-6. [Medline].

Rasigade JP, Dunyach-Remy C, Sapin A, et al. A Prophage in Diabetic Foot Ulcer-Colonizing Staphylococcus aureus Impairs Invasiveness by Limiting Intracellular Growth. J Infect Dis. 2016 Nov 15. 214 (10):1605-8. [Medline].

Lynar SA, Robinson CH, Boutlis CS, Commons RJ. Risk factors for mortality in patients with diabetic foot infections: a prospective cohort study. Intern Med J. 2018 Dec 4. [Medline].

Morbach S, Furchert H, Gröblinghoff U, Hoffmeier H, Kersten K, Klauke GT, et al. Long-Term Prognosis of Diabetic Foot Patients and Their Limbs: Amputation and death over the course of a decade. Diabetes Care. 2012 Jul 18. [Medline].

Chammas NK, Hill RL, Edmonds ME. Increased Mortality in Diabetic Foot Ulcer Patients: The Significance of Ulcer Type. J Diabetes Res. 2016. 2016:2879809. [Medline]. [Full Text].

Chen SY, Giurini JM, Karchmer AW. Invasive Systemic Infection After Hospital Treatment for Diabetic Foot Ulcer: Risk of Occurrence and Effect on Survival. Clin Infect Dis. 2017 Feb 1. 64 (3):326-334. [Medline].

Nelson A, Wright-Hughes A, Backhouse MR, et al. CODIFI (Concordance in Diabetic Foot Ulcer Infection): a cross-sectional study of wound swab versus tissue sampling in infected diabetic foot ulcers in England. BMJ Open. 2018 Jan 31. 8 (1):e019437. [Medline]. [Full Text].

[Guideline] Hingorani A, LaMuraglia GM, Henke P, Meissner MH, Loretz L, Zinszer KM, et al. The management of diabetic foot: A clinical practice guideline by the Society for Vascular Surgery in collaboration with the American Podiatric Medical Association and the Society for Vascular Medicine. J Vasc Surg. 2016 Feb. 63 (2 Suppl):3S-21S. [Medline].

Matos M, Mendes R, Silva AB, Sousa N. Physical activity and exercise on diabetic foot related outcomes: a systematic review. Diabetes Res Clin Pract. 2018 Feb 22. [Medline].

Hwang YG, Lee JW, Park KH, Han SH. Allogeneic keratinocyte for intractable chronic diabetic foot ulcers: a prospective observational study. Int Wound J. 2019 Jan 2. [Medline].

[Guideline] Tucker ME. New guidelines stress need for diabetic foot ulcer offloading. Medscape Medical News. 2014 Dec 26. [Full Text].

Snyder RJ, Frykberg RG, Rogers LC, Applewhite AJ, Bell D, Bohn G. The management of diabetic foot ulcers through optimal off-loading: building consensus guidelines and practical recommendations to improve outcomes. J Am Podiatr Med Assoc. 2014 Nov. 104(6):555-67. [Medline].

Rogers LC, Frykberg RG, Armstrong DG, et al. The Charcot foot in diabetes. Diabetes Care. 2011 Sep. 34(9):2123-9. [Medline].

Lipsky BA, Berendt AR, Cornia PB, et al. 2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2012 Jun. 54(12):e132-73. [Medline].

Tucker M. Short-Course Antibiotics Good in Diabetic Foot Osteomyelitis. Medscape Medical News. 2014 Nov 26. [Full Text].

Tone A, Nguyen S, Devemy F, Topolinski H, Valette M, Cazaubiel M, et al. Six- Versus Twelve-Week Antibiotic Therapy for Nonsurgically Treated Diabetic Foot Osteomyelitis: A Multicenter Open-Label Controlled Randomized Study. Diabetes Care. 2014 Nov 20. [Medline].

[Guideline] Allahabadi S, Haroun KB, Musher DM, Lipsky BA, Barshes NR. Consensus on surgical aspects of managing osteomyelitis in the diabetic foot. Diabet Foot Ankle. 2016. 7:30079. [Medline]. [Full Text].

US Food and Drug Administration. FDA Drug Safety Communication: Serious CNS reactions possible when linezolid (Zyvox®) is given to patients taking certain psychiatric medications. Available at http://www.fda.gov/Drugs/DrugSafety/ucm265305.htm. Accessed: July 27, 2011.

Lázaro-Martínez J, Aragón-Sánchez J, García-Morales E. Antibiotics versus conservative surgery for treating diabetic foot osteomyelitis. A randomized comparative trial. Diabetes Care. 2013 Oct 15. [Medline].

Nainggolan L. Antibiotics First Choice for Diabetic Foot Osteomyelitis. Medscape Medical News. 2013 Oct 24. [Full Text].

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern Society for Clinical Investigation