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* No [[Adjuvant therapy|adjunctive therapy]] has been proven to improve [[infection]] resolution, but for selected [[diabetic foot]] [[wounds]] that are slow to [[wound healing|heal]], [[physicians]] might consider using bioengineered [[skin]] equivalents, [[growth factors]], [[G-CSF|granulocyte colony-stimulating factors]], [[hyperbaric oxygen]] [[therapy]], or negative [[pressure]] [[wound]] [[therapy]].
* No [[Adjuvant therapy|adjunctive therapy]] has been proven to improve [[infection]] resolution, but for selected [[diabetic foot]] [[wounds]] that are slow to [[wound healing|heal]], [[physicians]] might consider using bioengineered [[skin]] equivalents, [[growth factors]], [[G-CSF|granulocyte colony-stimulating factors]], [[hyperbaric oxygen]] [[therapy]], or negative [[pressure]] [[wound]] [[therapy]].
*[[Becaplermin]] is a [[human]] [[platelet]]-derived [[growth factor]] (also known as [[Becaplermin|Regranex gel]]) can be used for [[neuropathy|neuropathic]] [[diabetic foot]] [[ulcers]]. It can augment [[wound healing]] by causing [[chemotaxis]] and [[Mitosis|mitogenesis]] of [[Cell (biology)|cells]] such as [[neutrophils]], [[fibroblasts]], and [[monocytes]].<ref name="pmid9589248">{{cite journal| author=Wieman TJ, Smiell JM, Su Y| title=Efficacy and safety of a topical gel formulation of recombinant human platelet-derived growth factor-BB (becaplermin) in patients with chronic neuropathic diabetic ulcers. A phase III randomized placebo-controlled double-blind study. | journal=Diabetes Care | year= 1998 | volume= 21 | issue= 5 | pages= 822-7 | pmid=9589248 | doi=10.2337/diacare.21.5.822 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9589248  }} </ref>
*[[Becaplermin]] is a [[human]] [[platelet]]-derived [[growth factor]] (also known as [[Becaplermin|Regranex gel]]) can be used for [[neuropathy|neuropathic]] [[diabetic foot]] [[ulcers]]. It can augment [[wound healing]] by causing [[chemotaxis]] and [[Mitosis|mitogenesis]] of [[Cell (biology)|cells]] such as [[neutrophils]], [[fibroblasts]], and [[monocytes]].<ref name="pmid9589248">{{cite journal| author=Wieman TJ, Smiell JM, Su Y| title=Efficacy and safety of a topical gel formulation of recombinant human platelet-derived growth factor-BB (becaplermin) in patients with chronic neuropathic diabetic ulcers. A phase III randomized placebo-controlled double-blind study. | journal=Diabetes Care | year= 1998 | volume= 21 | issue= 5 | pages= 822-7 | pmid=9589248 | doi=10.2337/diacare.21.5.822 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9589248  }} </ref>
*Some new types of [[biology|biologically active]] [[Implant (medicine)|implants]] such as [[Bioengineering|bioengineered]] [[skin]] (Apligraf) and [[human]] [[dermis]] (Dermagraft) (which are derived from [[Infant|neonatal]] [[foreskin]]) are recommended for faster [[wound healing]]. These [[Implant (medicine)|implants]] function as a source of [[growth factors]] and [[extracellular matrix]] which are critical for [[wound healing]].<ref name="ArmstrongHarkless2000">{{cite journal|last1=Armstrong|first1=DG|last2=Harkless|first2=LB|last3=Nguyen|first3=H|last4=Krasner|first4=D|last5=Hogge|first5=J|title=The potential benefits of advanced therapeutic modalities in the treatment of diabetic foot wounds|journal=Journal of the American Podiatric Medical Association|volume=90|issue=2|year=2000|pages=57–65|issn=8750-7315|doi=10.7547/87507315-90-2-57}}</ref><ref name="pmid11213881">{{cite journal| author=Veves A, Falanga V, Armstrong DG, Sabolinski ML, Apligraf Diabetic Foot Ulcer Study| title=Graftskin, a human skin equivalent, is effective in the management of noninfected neuropathic diabetic foot ulcers: a prospective randomized multicenter clinical trial. | journal=Diabetes Care | year= 2001 | volume= 24 | issue= 2 | pages= 290-5 | pmid=11213881 | doi=10.2337/diacare.24.2.290 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11213881  }} </ref>
===Selection of Antibiotic Regimen===
===Selection of Antibiotic Regimen===
* Clinically [[infection|uninfected]] [[wounds]] should ''not'' be [[treatment|treated]] with [[antibiotic]] [[therapy]]. For all [[infection|infected]] [[wounds]], [[antibiotic]] [[therapy]] combined with appropriate [[wound]] care is recommended.
* Clinically [[infection|uninfected]] [[wounds]] should ''not'' be [[treatment|treated]] with [[antibiotic]] [[therapy]]. For all [[infection|infected]] [[wounds]], [[antibiotic]] [[therapy]] combined with appropriate [[wound]] care is recommended.

Revision as of 10:31, 7 July 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alonso Alvarado, M.D. [2] Anahita Deylamsalehi, M.D.[3]

Overview

Appropriate wound care is essential for the management of all diabetic foot ulcers. Uninfected diabetic ulcers do not require antibiotic therapy. For acutely infected wounds, empiric antibiotic with efficacy against Gram-positive cocci should be initiated after obtaining a post-debridement specimen for aerobic and anaerobic culture. Infections with antibiotic-resistant organisms and those that are chronic, previously treated, or severe usually require broader spectrum regimens.

Diabetic Foot Infection

Principles of Therapy Adapted from Diabetes Care. 2013;36(9):2862-71.[1] and Clin Infect Dis. 2012;54(12):e132-73.[2]


Diagnosis of Diabetic Foot Infection
  • Diabetic foot infection (DFI) is diagnosed clinically by the presence of at least two signs or symptoms of inflammation:
Indications for Hospitalization
  • Severe (grade 4) infections
  • Moderate (grade 3) infections with complicating features
  • Patients unable to comply with the required outpatient treatment regimen for psychological or social reasons
  • Patients not responding to outpatient treatment
Obtaining Specimens
  • Properly obtained specimens for culture prior to initiating empiric therapy provide useful information for guiding antibiotic selection, particularly in those with chronic or previously treated infections which are commonly caused by Gram-negative bacilli or obligate anaerobic organisms.
  • Infected wounds should be cultured by obtaining tissue samples during any surgical procedure or by tissue biopsy or wound base curettage.
  • Bone cultures are optimal for detecting the pathogen in osteomyelitis, but blood cultures are only necessary for those with a severe (grade 4) infection.
  • Cultures may be unnecessary for mild infections in patients who have not recently received antibiotic therapy and who are at low risk for methicillin-resistant Staphylococcus aureus (MRSA) infection; these infections are predictably caused solely by staphylococci and streptococci.
  • Cultures may yield organisms that are commonly considered to be contaminants (eg, coagulase-negative staphylococci, corynebacteria), but these may be true pathogens in DFIs and are often resistant to the empiric antibiotics.
Consultation
  • Conditions to request consultation from specialists:
  • Urgent surgical intervention should be sought for DFIs accompanied by gas in the deeper tissues, an abscess, or necrotizing fasciitis, and less urgent surgery for DFIs with substantial nonviable tissue or extensive bone or joint involvement.
  • Consult a vascular surgeon to consider revascularization if ischemia complicates a DFI.
  • Infectious diseases specialists should be consulted when cultures yield multiple or antibiotic-resistant organisms, the patient has substantial renal impairment, or the infection does not respond to appropriate medical or surgical therapy in a timely manner.
Adjunctive Therapy

Selection of Antibiotic Regimen

1. Is there high risk of MRSA?
  • Prior history of MRSA infection or colonization within the past year
  • High local prevalence of MRSA infection or colonization (50% for a mild and 30% for a moderate soft tissue infection)
  • Clinically severe diabetic foot infection
2. Is the infected wound chronic or treated with antibiotics in the past month?
3. Are there risk factors for infection with Pseudomonas aeruginosa or extended-spectrum β-lactamase (ESBL)–producing organisms?
  • Anti-pseudomonal agent is usually unnecessary except for patients with risk factors:
  • Coverage of ESBL-producing gram-negative organisms should be considered in countries in which they are relatively common.
4. What is the severity status?
  • DFI is classified based on its severity according to the Infectious Diseases Society of America (IDSA) guideline or the PEDIS grade developed by International Working Group on the Diabetic Foot (IWGDF). (see Table below)
  • Selection of empiric antimicrobial regimen should be determined by the severity of DFI and the likely etiologic agents.
  • Mild (grade 2) to moderate (grade 3) DFI without recent antibiotic treatment:
  • Severe (grade 4) DFI:
  • Broad-spectrum antibiotics are recommended while culture results and susceptibility data are pending.
Clinical Manifestation PEDIS Grade IDSA Severity
Wound lacking purulence or any manifestations of inflammation 1 Uninfected
2 Mild
Infection in a patient who is metabolically stable and systemically well, but with ≥1 of the following characterisitics: 3 Moderate
Infection in a patient with metabolic instability (eg, acidosis, severe hyperglycemia, or azotemia) or systemic toxicity as manifested by ≥2 of the following: 4 Severe
5. What is the appropriate route, setting, and duration of antibiotic therapy?
  • The table below describes the recommended route, setting, and duration of antibiotic therapy based on the extent and severity of DFI.
Site of Infection, by Severity or Extent Route of Administration Setting Duration of Therapy
Soft-tissue only Mild (Grade 2) Oral (or topical for superficial infections) Outpatient 1–2 wk
Moderate (Grade 3) Oral (or initial parenteral) Outpatient (or inpatient) 1–3 wk
Severe (Grade 4) Initial parenteral, switch to oral when possible Inpatient, then outpatient 2–4 wk
Bone or joint No residual infected tissue Parenteral or oral Inpatient, then outpatient 2–5 d
Residual infected soft tissue Parenteral or oral Inpatient, then outpatient 1–3 wk
Residual infected, viable bone Initial parenteral, switch to oral when possible Inpatient, then outpatient 4–6 wk
Residual dead bone or no surgery Initial parenteral, switch to oral when possible Inpatient, then outpatient ≥3 mo

Empiric Therapy

Click on the following categories to expand treatment regimens.

    Uninfected (Grade 1)

  ▸  No Evidence of Infection

    Mild (Grade 2)

  ▸  Acute Infection Without Recent Antibiotic Use

  ▸  High Risk for MRSA

    Moderate to Severe (Grade 3–4)

  ▸  Chronic Infection or Recent Antibiotic Use

  ▸  High Risk for MRSA

  ▸  High Risk for Pseudomonas aureuginosa

  ▸  Polymicrobial Infection

Uninfected Wound, No Evidence of Infection
Uninfected wounds should be managed with appropriate wound care.
Antibiotic therapy is not recommended.
Mild DFI, Acute Infection Without Recent Antibiotic Use
Preferred Regimen
Dicloxacillin 125–250 mg PO qid
OR
Clindamycin 150–300 mg PO qid
OR
Cephalexin 500 mg PO qid
OR
Levofloxacin 750 mg PO qd
OR
Amoxicillin-Clavulanate 500 mg PO bid (or 250 mg PO tid)
Usually active against community-associated MRSA, but check macrolide sensitivity and consider ordering a D-test before using for MRSA.
Relatively broad-spectrum oral agent that includes anaerobic coverage.
Mild DFI, High Risk for MRSA
Preferred Regimen
Doxycycline 100 mg PO q12h
OR
TMP–SMX 80-160 mg/400-800 mg PO q12h
Active against many MRSA & some gram-negatives; uncertain against streptococci.
Moderate to Severe DFI, Chronic Infection or Recent Antibiotic Use
Preferred Regimen
Levofloxacin 750 mg IV/PO q24h
OR
Cefoxitin 1 g IV q4h (or 2 g IV q6–8h)
OR
Ceftriaxone 1–2 g/day IV/IM q12–24h
OR
Ampicillin–Sulbactam 1.5–3 g IV/IM q6h
OR
Moxifloxacin 400 mg IV/PO q24h
OR
Ertapenem 1 g IV/IM q24h
OR
Tigecycline 100 mg IV, then 50 mg IV q12h
OR
Imipenem–Cilastatin 0.5–1 g IV q6–8h
Alternative Regimen
Levofloxacin 750 mg IV/PO q24h
OR
Ciprofloxacin 600–1200 mg/day IV q6–12h
OR
Ciprofloxacin 1200–2700 mg IV q6–12h (for more severe cases)
PLUS
Clindamycin 150–300 mg PO qid
Active against MRSA.
Not active against MRSA; consider when ESBL-producing pathogens suspected.
Moderate to Severe DFI, High Risk for MRSA
Preferred Regimen
Linezolid 600 mg IV/PO q12h
OR
Daptomycin 4 mg/kg IV q24h
OR
Vancomycin 15–20 mg/kg IV q8–12h (trough: 10–20 mg/L)
Moderate to Severe DFI, High Risk for Pseudomonas aeruginosa
Preferred Regimen
Piperacillin–Tazobactam 3.375 g IV q6–8h
Moderate to Severe DFI, Polymicrobial Infection
Preferred Regimen
Vancomycin 15–20 mg/kg IV q8–12h (trough: 10–20 mg/L)
OR
Linezolid 600 mg IV/PO q12h
OR
Daptomycin 4 mg/kg IV q24h
PLUS
Piperacillin–Tazobactam 3.375 g IV q6–8h
OR
Imipenem–Cilastatin 0.5–1 g IV q6–8h
OR
Ertapenem 1 g IV/IM q24h
OR
Meropenem 1 g IV q8h
Alternative Regimen
Vancomycin 15–20 mg/kg IV q8–12h (trough: 10–20 mg/L)
OR
Linezolid 600 mg IV/PO q12h
OR
Daptomycin 4 mg/kg IV q24h
PLUS
Ceftazidime 2 g IV q8h
OR
Cefepime 2 g IV q8h
OR
Aztreonam 2 g IV q6–8h
PLUS
Metronidazole 15 mg/kg IV, then 7.5 mg/kg IV q6h


References

  1. Wukich DK, Armstrong DG, Attinger CE, Boulton AJ, Burns PR, Frykberg RG; et al. (2013). "Inpatient management of diabetic foot disorders: a clinical guide". Diabetes Care. 36 (9): 2862–71. doi:10.2337/dc12-2712. PMC 3747877. PMID 23970716.
  2. Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJ, Armstrong DG; et al. (2012). "2012 Infectious Diseases Society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections". Clin Infect Dis. 54 (12): e132–73. doi:10.1093/cid/cis346. PMID 22619242.
  3. 3.0 3.1 Frykberg, Robert G. (1998). "Diabetic foot ulcers: Current concepts". The Journal of Foot and Ankle Surgery. 37 (5): 440–446. doi:10.1016/S1067-2516(98)80055-0. ISSN 1067-2516.
  4. Holstein PE, Sørensen S (1999). "Limb salvage experience in a multidisciplinary diabetic foot unit". Diabetes Care. 22 Suppl 2: B97–103. PMID 10097908.
  5. Frykberg RG, Armstrong DG, Giurini J, Edwards A, Kravette M, Kravitz S; et al. (2000). "Diabetic foot disorders: a clinical practice guideline. American College of Foot and Ankle Surgeons". J Foot Ankle Surg. 39 (5 Suppl): S1–60. PMID 11280471.
  6. American Diabetes Association (1999). "Consensus Development Conference on Diabetic Foot Wound Care: 7-8 April 1999, Boston, Massachusetts. American Diabetes Association". Diabetes Care. 22 (8): 1354–60. doi:10.2337/diacare.22.8.1354. PMID 10480782.
  7. 7.0 7.1 7.2 Armstrong, DG; Harkless, LB; Nguyen, H; Krasner, D; Hogge, J (2000). "The potential benefits of advanced therapeutic modalities in the treatment of diabetic foot wounds". Journal of the American Podiatric Medical Association. 90 (2): 57–65. doi:10.7547/87507315-90-2-57. ISSN 8750-7315.
  8. Wieman TJ, Smiell JM, Su Y (1998). "Efficacy and safety of a topical gel formulation of recombinant human platelet-derived growth factor-BB (becaplermin) in patients with chronic neuropathic diabetic ulcers. A phase III randomized placebo-controlled double-blind study". Diabetes Care. 21 (5): 822–7. doi:10.2337/diacare.21.5.822. PMID 9589248.
  9. Veves A, Falanga V, Armstrong DG, Sabolinski ML, Apligraf Diabetic Foot Ulcer Study (2001). "Graftskin, a human skin equivalent, is effective in the management of noninfected neuropathic diabetic foot ulcers: a prospective randomized multicenter clinical trial". Diabetes Care. 24 (2): 290–5. doi:10.2337/diacare.24.2.290. PMID 11213881.


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