Diabetic Foot Infections

Improving Outcomes
(or why Im not going into vascular!)
John C. Lantis II, MD
Assistant Professor of Surgery
College of Physicians and Surgeons
Columbia University
 Epidemiology
Cellulitisoccurs 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
Ketosisimpairs 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 deformities
Hammer 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
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
 Microbiology
Normal skin bacteria
Coag neg Staph, alpha-hemolytic strep, corynebacteriae
Acute wound
Monomicrobial (Gram positive)
Chronic wound
Polymicrobial (GNRs, Anaerobes, enterococcus, GPCs)
 Wound Cultures
Uninfected wound
If concerned about unique pathogen - MRSA
Infected wound
Help tailor and constrain antibiotic therapy
Antibiotic nave wound staph or strep alone
Antibiotic resistant organisms
 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
 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
Sensitivity55 %, specificity 75%
Focal osteopenia, cortical erosions, periosteal reaction
 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
 Osteomyelits
Etiologic organisms
Staph aureus 40% of infections
Streptococci 30%
Staph epidermidis 25%
Enterobacteriaceae 40%
 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 of the longitudinal arch and skin creases
Foot 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
Peptideantibiotic 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
isnt 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