Diabetic Foot Infections Improving Outcomes (or why I’m not going into vascular!)

1. Diabetic Foot InfectionsImproving 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