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
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
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
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
Pathophysiology
 Metabolic
derangement
 Faulty wound healing
 Neuropathy
 Angiopathy
 Mechanical stress
 Patient and provider neglect
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)
Poor Immune Function
 Poor
PMN functions
 Migration,
phagocytosis, intracellular killing,
chemotaxis
 Ketosis
impairs leukocyte function
 Monocyte mediated immune function diminished
 Hyperglycemia impairs complement fixation
Sensory Neuropathy
 Unaware
of a foreign body
 Pressure
in shoes
 Abrasions in shoes
 Tears or brakes in the skin
Motor Neuropathy
 Architectural
 Hammer
deformities
or claw toe
 High plantar arch
 Subluxation of metatarsals
Autonomic Neuropathy
 Anhidrosis
 Dry,
cracked skin
 Arterial
to venous shunting
 Temperature regulation disorders
Angiopathy
 Can
play a primary role
 Microangiopathy
 Certainly
+/-
plays a primary role in healing
 Pulsatile
flow will augment healing
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
Microbiology
– 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
 Infection
Microbiology
 Normal
 Coag
 Acute
skin bacteria
neg Staph, alpha-hemolytic strep, corynebacteriae
wound
 Monomicrobial
 Chronic
(Gram positive)
wound
 Polymicrobial
(GNRs, Anaerobes, enterococcus, GPCs)
Wound Cultures
 Uninfected
 If
wound
concerned about unique pathogen - MRSA
 Infected
 Help
wound
tailor and constrain antibiotic therapy
 Antibiotic naïve wound – staph or strep alone
 Antibiotic resistant organisms
Wound Cultures
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
 Deep
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
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

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
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
Evaluation
 Measure
wound (? Photograph ?)
 Determine inflow
 Neurologic status? Sensation, motor, autonomic
 Cleanse and debride wound
 Culture the cleansed wound (curettage)
 Plain radiographs
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
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
Osteomyelitis
 Bone
(technitium Tc 99)
 85%
sensitive, 45% specific
 Leukocyte
 85%
scans
sensitive, 75% specific
 MRI
 Sensitivity
> 90%, specificity > 80 %
 Can miss early changes, mis-read evolving neuropathic
osteoarthropathy
Osteomyelits
 Etiologic
organisms
aureus – 40% of infections
 Streptococci – 30%
 Staph epidermidis – 25%
 Enterobacteriaceae – 40%
 Staph
Treatment
 Debridement
 Minor Remove
all necrotic tissue including eschar
 Remove all callus
 Sharply saucerize the wound
 Debride bone
 Repeat visits are normal
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
Treatment
 Plantar
abscess
 Disappearance
 Foot
of the longitudinal arch and skin creases
edema
 Central plantar infections – worse outcomes
 Wide incision and drainage necessary
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
Treatment
 Empiric
antibiotic therapy
 Staph
 Strep
 GNR
 Enterococcus
 Anaerobes
 *Tailor
to clinical progress
Treatment
 Prospective
studies they all work and there really
isn’t a difference
 Cost is an issue
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

Antibiotic thoughts
 Duration
of therapy
 No
good studies
 Once active infection resolved plus 2 days
 Osteomyelitis
6
weeks
 Can use Flouoquinolones and clindamycin