bedah

1. Diabetic Foot Infections
Dr.khomeini SpB

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