Diabetic foot ulcer
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Transcript Diabetic foot ulcer
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