diabetic foot infection - swedish

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DIABETIC FOOT INFECTION ISABELLE TREPICCIONE, MD

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Page 1: Diabetic foot infection - Swedish

DIABETIC FOOT INFECTIONISABELLE TREPICCIONE, MD

Page 2: Diabetic foot infection - Swedish

OUTLINEScope of problem

Predisposition

PreventionDiagnosis

Treatment

Page 3: Diabetic foot infection - Swedish

SCOPE OF THE PROBLEMLifetime incidence of foot ulcer is 25%

50% are infected

50% of non-traumatic lower extremity amputations are due to DFI

131 million diabetics worldwide in 2000

366 million diabetics by 2030

Page 4: Diabetic foot infection - Swedish

COST OF THE PROBLEMMean annual cost of treatment in 2001:

$9,000 for an uninfected foot ulcer

$25,000 for an infected foot ulcer

$45,000 for a foot ulcer with osteomyelitis

Page 5: Diabetic foot infection - Swedish

PREDISPOSING FACTORS

NEUROPATHY VASCULAR DISEASE

IMMUNE DYSFUNCTION

NEUROPATHY VASCULAR DISEASE IMMUNE DYSFUNCTION

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Page 6: Diabetic foot infection - Swedish

NEUROPATHY Sensory neuropathy: Wounds go undetected and worsen with exposure to repetitive trauma

Autonomic neuropathy: Gland dysfunction makes skin dry and susceptible to tearing

Motor neuropathy: Atrophy of intrinsic foot muscles leads to anatomic deformities

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Page 7: Diabetic foot infection - Swedish

VASCULAR DISEASEHyperglycemia causes endothelial cell dysfunction and smooth muscle cell abnormalities

Hyperglycemia is associated with an increase in thromboxane A2 contributing to hypercoagulability

Co-existing hypertension and hyperlipidemia

Page 8: Diabetic foot infection - Swedish

IMMUNE DYSFUNCTIONFewer inflammatory cytokines

Impaired neutrophil chemotaxis

Impaired neutrophil phagocytosis

http://physrev.physiology.org/content/physrev/83/2/475/F26.large.jpg

Page 9: Diabetic foot infection - Swedish

IDENTIFYING THOSE AT RISKHemoglobin a1c >9% (OR 3.2)

>10 years with diabetes (OR 3.0)

Prior lower extremity amputation (RR 2.8)

Visual acuity less than 20/40 (RR 1.9)

Prior foot ulceration (RR 1.6)

Page 10: Diabetic foot infection - Swedish

PREVENTIONPatient education: Improvement in patient knowledge and behavior. No ulcer or amputation prevention.

Yearly screening foot exam: Decreased ulcer recurrence at 1 year if referred to podiatry. No reduction in amputation.

Diabetic footwear: Custom footwear prevents ulcer recurrence.

Optimize glycemic control: Improves neuropathy. Nonsignificant reduction in amputation.

Smoking cessation: Nonsmoking diabetics have lower rates of foot ulceration and amputation.

Not studied: Callus debridement, treatment of tinea pedis or onychomycosis, and lower extremity revascularization.

Page 11: Diabetic foot infection - Swedish

Infection indicated by presence of 2 or more of: Swelling or induration Erythema Tenderness Warmth Purulent discharge

Lavery LA, Armstrong DG, Murdoch DP, Peters EJ, Lipsky BA. (2007). Validation of the Infectious Diseases Society of America’s diabetic foot classification system. Clin Infect Dis

Page 12: Diabetic foot infection - Swedish

UNINFECTED MILD INFECTION-Local infection confined to skin

and subcutaneous tissue

-Circumference of erythema >0.5cm

and <2cm

MODERATE INFECTION

-Local infection with involvement

of deeper structures

-Circumference of erythema >2cm

SEVERE INFECTION-Local infection plus systemic inflammatory

response syndrome

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Page 13: Diabetic foot infection - Swedish

IDENTIFYING INFECTED ULCERSProbe to bone, RR 6.7

Ulceration present >30 days, RR 4.7

History of recurrent ulcers, RR 2.4

Traumatic foot wound, RR 2.4

Presence of vascular disease in same limb, RR 1.9

http://www.antimicrobe.org/printout/e26printout/e26assessment.htm

Page 14: Diabetic foot infection - Swedish

WOUND CULTURE INDICATIONS

Culture and gram stain moderate to severely infected wounds

Consider culture of mild infection if there are MRSA or pseudomonas risk factors

Don’t culture uninfected wounds

TECHNIQUE

Clean and debride wound

Obtain culture specimen from base

Aspirate purulence if present

Do not send superficial swabs or swabs of wound drainagef wound or wound drainage for culture

http://lermagazine.com/wp-content/uploads/2012/10/10diabetes-CG-debride-30.jpg

Page 15: Diabetic foot infection - Swedish

IMAGINGXrays of all new diabetic foot infections

MRI if there is concern for other deep space infection

MRI when a chronic ulceration becomes infected

http://learningradiology.com/images/boneimages1/osteomyelitisarr.jpg

Page 16: Diabetic foot infection - Swedish

TREATMENT OF THE INFECTED ULCERAntibiotics

Wound care

Sometimes surgery

Does anything else make a difference?

Page 17: Diabetic foot infection - Swedish

ANTIBIOTICSMILD infection: target gram positive cocci, maybe MRSA (ORAL)

MODERATE infection: target gram positive cocci, maybe MRSA (ORAL)

SEVERE infection: target gram positive cocci, gram negative and obligate anaerobes, MRSA and pseudomonas (PARENTERAL)

Page 18: Diabetic foot infection - Swedish

WHEN DO I NEED TO COVER FOR MRSA?When the patient has a history of MRSA or MRSA colonization within the

past yearWhen the infection is severeWhen local MRSA prevalence is 50% (for mild) or 30% (for moderate)

Page 19: Diabetic foot infection - Swedish

WHEN DO I NEED TO COVER FOR MRSA?

25% MRSA

40% MRSA

DO NOT ROUTINELY NEED TO COVER (UNLESS SEVERE)

COVER IN MODERATE AND SEVERE INFECTION

Page 20: Diabetic foot infection - Swedish

WHEN DO I NEED TO COVER FOR PSEUDOMONAS?Not as common a pathogen in DFI as previously thoughtIncreasing evidence that it may be a wound colonizerThe IDSA recommends coverage in:Severe infectionsTropical climatesFrequent exposure of the foot to water

Page 21: Diabetic foot infection - Swedish

WOUND CARE

Debridement Off-loadingMoist wound environment

No topical antimicrobials

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Page 22: Diabetic foot infection - Swedish

WHEN SHOULD I CONSULT A SURGEON?Evidence of life or limb threatening infection

Evidence of critical ischemia

Evidence of deep-space infection or abscess

Failure to improve with otherwise appropriate treatment

Page 23: Diabetic foot infection - Swedish

OTHER TREATMENTSNegative-pressure wound therapy AKA wound vac

Hyperbaric oxygen

Granulocyte colony stimulating factors (G-CSF)

Stem cell

Not studied: intensive glycemic control limb revascularization

http://m3.i.pbase.com/o6/12/421212/1/101374523.kIMZ12if.wrecked_foot_vacuum_dressin.jpg

Page 24: Diabetic foot infection - Swedish

LEARNING POINTSWhen it comes to prevention; focus on appropriate footwear, a1c control, and smoking cessation

Send a tissue culture in all but mild diabetic foot infections

Most mild and moderate infections do not require MRSA or pseudomonas coverage

Wound care is critical to complete healing

Call a podiatrist or orthopedic surgeon when the infection is deep or severe

Page 25: Diabetic foot infection - Swedish

QUESTIONS?

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Page 26: Diabetic foot infection - Swedish

REFERENCESClayton W, Elasy TA. (2009). A review of pathophysiology, classification and treatment of foot ulcers in diabetic patients. Clinical Diabetes.

Conte, MS. (2012) Diabetic revascularization: endovascular versus open bypass—do we have the answer? Seminars in Vascular Surgery.

Dorresteijn, J., & Kriegsman, D. (2014). Educating people with diabetes about foot care to help reduce foot ulcers and amputations. The Cochrane Library.

Dumville, J., & Hinchliffe, R. (2013). Negative pressure wound therapy for treating foot wounds in people with diabetes mellitus. The Cochrane Library.

Edmonds M, Foster A. (2004) The use of antibiotics in the diabetic foot. Am J Sur.

Geerlings SE, Hoepelman AI. (1999) Immune dysfunction in patients with diabetes mellitus (DM). FEMS Immunol Med Microbiol.

Gordois A, Scuffham P, Shearer A, Oglesby A, Tobian JA. (2003) The health care costs of diabetic peripheral neuropathy in the US. Diabetes Care.

Gravely SS, Hensley BK, Hagood-Thompson C. (2011). Comparison of three types of diabetic foot ulcer education plans to determine patient recall of education. J Vasc Nurs.

Hill HR, Augustine NH, Rallison ML, Santos JI. (1983). Defective monocyte chemotactic responses in diabetes mellitus. J Clin Immunol.

Huijberts MS, Schaper NC, Schalkwijk CG. (2008). Advanced glycation end products and diabetic foot disease. Diabetes Metab Res Rev.

Jiang, X., & Zhang, H. (2016). Effectiveness of Autologous Stem Cell Therapy for the Treatment of Lower Extremity Ulcers.Medicine.

Kranke, P., & Bennett, M. (2015). Hyperbaric oxygen therapy for chronic wounds. The Cochrane Library.

Page 27: Diabetic foot infection - Swedish

REFERENCESLavery, L., & Armstrong, D. (2006). Risk Factors for Foot Infections in Individuals With Diabetes. Diabetes Care, 29(6).

Lavery LA, Armstrong DG, Murdoch DP, Peters EJ, Lipsky BA. (2007). Validation of the Infectious Diseases Society of America’s diabetic foot classification system.Clin Infect Dis.

Lavery LA, Armstrong DG, Vela SA, Quebedeaux TL, Fleischli JG. (1998). Practical criteria for screening patients at high risk for diabetic foot ulceration. Arch Intern Med.

Lewis J, Lipp A. (2013). Pressure-relieving interventions for treating diabetic foot ulcers. Cochrane Database Syst Rev.

Lipsky, B., MD, & Armstrong, D. (2005). Ertapenem versus piperacillin/tazobactam for diabetic foot infections (SIDESTEP): prospective, randomised, controlled, double-blinded, multicentre trial . The Lancet, 366.

Lipsky, B., Berendt, A., & Cornia, P. (2012). 2012 Infectious Diseases Society of America Clinical Practice Guideline for the Diagnosis and Treatment of DiabeticFoot Infections. Clinical Infectious Disease.

Lipsky BA, Berebdt AR, Deery HG, Embil JM, Joseph WS, Karchmer AW, et al. (2004). Diagnosis and treatment of diabetic foot infections. Clinical Infectious Diseases

Malacarne S, Paoli C, Philippe J. (2011). Importance of off loading in the treatment of foot diabetic ulcers. Rev Med Suisse.

Newman L.G., Waller J., Palestro J., et al. (1991). Unsuspected osteomyelitis in diabetic foot ulcers: diagnosis and monitoring by leukocyte scanning with indium In 111 oxyquinoline. J Am Med Assoc 1991.

Noor, S., Zubair, M., & Ahmad, J. (2015). Diabetic foot ulcer—A review on pathophysiology, classification and microbial etiology. Diabetes & Metabolic Syndrome: Clinical Research & Reviews.

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REFERENCESParaskevas KI, Baker DM, Pompella A, Mikhailidis DP. (2008). Does diabetes mellitus play a role in restenosis and patency rates following lower extremity peripheral arterial revascularization? A critical overview. Ann Vasc Surg.

Peleg AY, Weerarathna T, McCarthy JS, Davis TM. (2007). Common infections in diabetes: Pathogenesis, management and relationship to glycaemic control. Diabetes Metab Res Rev.

Prompers , L., & Huijberts, M. (2007). High prevalence of ischaemia, infection and serious comorbidity in patients with diabetic foot disease in Europe. Baseline results from the Eurodiale study. Diabetologia.

Reiber GE. (2001) Epidemiology of foot ulcers and amputations in the diabetic foot. In: Bowker JH, Pfeifer MA, eds. The Diabetic Foot.

Rizzo, L., & Tedeschi, A. (2012). Custom-Made Orthesis and Shoes in a Structured Follow-Up Program Reduces the Incidence of Neuropathic Ulcers in High-Risk Diabetic Foot Patients. The International Journal of Lower Extremity Wounds.

Singh N, Armstrong DG, Lipsky BA. (2005). Preventing foot ulcers in patients with diabetes. JAMA.

Uçkay, I., Aragón-Sánchez, J., Lew, D., & Lipsky, B. A. (2015). Diabetic foot infections: what have we learned in the last 30 years? International Journal of Infectious Diseases.

UK Prospective Diabetes Study (UKPDS) Grou. (1999). Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes . The Lancet.

Young, H., MD, & Knepper, B., MS, MPH. (2015). Pseudomonas aeruginosa; An Uncommon Cause of Diabetic Foot Infection.Journal of the American Podiatric Medical Association , 105(2).

Zingg M, Nicode`me JD, Uc¸kay I, Ray A, Suva` D. (2014). Lower limb amputation: indication, preoperative workup and complications. Rev Med Suisse.

Zochodone DW. (2008). Diabetic polyneuropathy: an update. Curr Opin Neuro.