1. Diabetic Foot Infections Improving Outcomes (or why I’m not going into vascular!) John C. Lantis II, MD Assistant Professor of Surgery College of Physicians and Surgeons Columbia University

2. Epidemiology  Cellulitis occurs 9 times more frequently in diabetics than non-diabetics  Osteomyelitis of the foot 12 times more frequently in diabetics than non-diabetics  Foot ulcerations and infections are the most common reason for a diabetic to be admitted to the hospital

3. Epidemiology  25 % of diabetics will develop a foot ulcer  40-80% of these ulcers will become infected  25 % of these will become deep  50 % of patients with cellulitis will have another episode within 2 years

4. Epidemiology (of amputation)  25-50 % of diabetic foot infections lead to minor amputations  10-40 % require major amputations  10-30 % of patients with a diabetic foot ulcer will go on to amputation

5. Pathophysiology  Metabolic derangement  Faulty wound healing  Neuropathy  Angiopathy  Mechanical stress  Patient and provider neglect

6. Poor Wound Healing  Poor granuloma formation  Prolonged persistence of abscess  Higher rate of carriage of Staph Aureus in the nares  Bullae, necrobiosis  Nail fungi (Tenia)

7. Poor Immune Function  Poor PMN functions  Migration, phagocytosis, intracellular killing, chemotaxis  Ketosis impairs leukocyte function  Monocyte mediated immune function diminished  Hyperglycemia impairs complement fixation

8. Sensory Neuropathy  Unaware of a foreign body  Pressure in shoes  Abrasions in shoes  Tears or brakes in the skin

9. Motor Neuropathy  Architectural deformities  Hammer or claw toe  High plantar arch  Subluxation of metatarsals

10. Autonomic Neuropathy  Anhidrosis  Dry, cracked skin  Arterial to venous shunting  Temperature regulation disorders

11. Angiopathy  Can play a primary role  Microangiopathy +/-  Certainly plays a primary role in healing  Pulsatile flow will augment healing

12. Foot Anatomy  Compartments, low amount of soft tissue, tendon sheaths  Deep plantar space  Medial, central and lateral  Rigid fascial structures  Edema – rapidly elevates compartment pressures  Ischemic necrosis  Infections spread between compartments  Calcaneal convergence, direct perforation of the septae

13. Microbiology  Infection – invasion of host tissue by pathogens, which elicits a host inflammatory response (erythema, induration, pain or tenderness, warmth, loss of function)  Superficial-confined to skin supeficial to fascia  Deep-invasion of fascia, muscle, tendon, joint or bone

14. Microbiology  Normal skin bacteria  Coag neg Staph, alpha-hemolytic strep, corynebacteriae  Acute wound  Monomicrobial (Gram positive)  Chronic wound  Polymicrobial (GNRs, Anaerobes, enterococcus, GPCs)

15. Wound Cultures  Uninfected wound  If concerned about unique pathogen - MRSA  Infected wound  Help tailor and constrain antibiotic therapy  Antibiotic naïve wound – staph or strep alone  Antibiotic resistant organisms

16. Wound Cultures  Deep space pus – most accurate  Curretage or tissue scraping from the base of a debrided ulcer gives the best information - next most accurate  Cotton swab across the surface is of little utility

17. Wound Cultures  Staph Aureus – most important pathogen in diabetic foot  Serious infections are usually caused by 3 to 5 bacterial species  GNR – Enterobacteriaciae – chronic or previously treated wounds  Pseudomonas – often in wounds treated with hydrotherapy or wet dressings

18. Diagnosis  Clinical presentation  Presence of purulence  Pain, swelling, ulceration, sinus tract formation, crepitation  Systemic infection (fever, rigors, vomitting, tachycardia, change in mental status, malaise)  Surprisingly uncommon  Metabolic disorder (hyperglycemia, ketosis, azotemia)  Should be considered even when local signs are less severe

19. Clinical Presentation  60 years old  66 % male  DM 15-20 years  66 % PVD  80 % loss of protective sensation  33 % have lesion for > 1 month  50% lack – fever, leukocytosis or elevated ESR

20. Evaluation  Describe lesion and drainage  Enumerate signs of infalmmation  Define whether infection is present and cause  Examine soft tissue for crepitus, sinus tract, abscess  Probe skin breaks with sterile metal probe and see if skin can be reached

21. Evaluation  Measure wound (? Photograph ?)  Determine inflow  Neurologic status? Sensation, motor, autonomic  Cleanse and debride wound  Culture the cleansed wound (curettage)  Plain radiographs

22. Osteomyelitis  50-60 % complication in severe foot infections  Where in the foot is the lesion?  Vascular supply to the area  Degree of systemic illness  Two classifications systems  Waldvogel  Cleary and Mader

23. Osteomyelitis  Larger (>2cm)  Deeper (>3mm)  ESR > 70 mm/hr  If you can touch bone 90% correlation with osteo  Xray – changes take 2 weeks to occur  Sensitivity 55 %, specificity 75%  Focal osteopenia, cortical erosions, periosteal reaction

24. Osteomyelitis  Bone (technitium Tc 99)  85% sensitive, 45% specific  Leukocyte scans  85% sensitive, 75% specific  MRI  Sensitivity > 90%, specificity > 80 %  Can miss early changes, mis-read evolving neuropathic osteoarthropathy

25. Osteomyelits  Etiologic organisms  Staph aureus – 40% of infections  Streptococci – 30%  Staph epidermidis – 25%  Enterobacteriaceae – 40%

26. Treatment  Debridement  Minor-  Remove all necrotic tissue including eschar  Remove all callus  Sharply saucerize the wound  Debride bone  Repeat visits are normal

27. Treatment  Surgical  “Salvage the foot but not at the expense of the leg or the patient”  Early surgical debridement decreases LOS, improves foot salvage and decreases morbidity and mortality  All necrotic tissue and pus

28. Treatment  Plantar abscess  Disappearance of the longitudinal arch and skin creases  Foot edema  Central plantar infections – worse outcomes  Wide incision and drainage necessary

29. Treatment  Antibiotics  Do not improve outcomes of non-infected lesions  In PVD – therapeutic antibiotic levels are not achieved in infected tissues  Mild infection –Topical therapy  Peptide antibiotic Pexiganin acetate 1% cream nearly as effective as oral ofloxacin

30. Treatment  Empiric antibiotic therapy  Staph  Strep  GNR  Enterococcus  Anaerobes  *Tailor to clinical progress

31. Treatment  Prospective studies they all work and there really isn’t a difference  Cost is an issue

32. Antibiotic thoughts  Mild (po) – Augmentin/Levofloxacin (+Clinda)  Bactrim/Flagyl  Moderate (IV until stable then po)  Unasyn or other Gorilla-cillin  Clinda & Levofloxacin  Severe (IV only)  Imipenem  Amp/Tobra/Clinda  Vanco/Aztreonam/Flagyl

33. Antibiotic thoughts  Duration of therapy  No good studies  Once active infection resolved plus 2 days  Osteomyelitis  6 weeks  Can use Flouoquinolones and clindamycin