diabetic foot infections improving outcomes (or why i’m not going into vascular!) john c. lantis...
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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
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 functionsMigration, phagocytosis, intracellular killing,
chemotaxis Ketosis impairs leukocyte function Monocyte mediated immune function diminished Hyperglycemia impairs complement fixation
Sensory Neuropathy
Unaware of a foreign bodyPressure in shoesAbrasions in shoesTears or brakes in the skin
Motor Neuropathy
Architectural deformitiesHammer or claw toeHigh plantar archSubluxation of metatarsals
Autonomic Neuropathy
Anhidrosis Dry, cracked skin
Arterial to venous shunting Temperature regulation disorders
Angiopathy
Can play a primary roleMicroangiopathy +/-
Certainly plays a primary role in healingPulsatile 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 bacteriaCoag neg Staph, alpha-hemolytic strep, corynebacteriae
Acute woundMonomicrobial (Gram positive)
Chronic woundPolymicrobial (GNRs, Anaerobes, enterococcus, GPCs)
Wound Cultures
Uninfected wound If concerned about unique pathogen - MRSA
Infected woundHelp tailor and constrain antibiotic therapyAntibiotic naïve wound – staph or strep aloneAntibiotic 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
WaldvogelCleary 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 scans
85% sensitive, 75% specific MRI
Sensitivity > 90%, specificity > 80 %Can miss early changes, mis-read evolving neuropathic
osteoarthropathy
Osteomyelits
Etiologic organismsStaph aureus – 40% of infectionsStreptococci – 30%Staph epidermidis – 25%Enterobacteriaceae – 40%
Treatment
DebridementMinor-
Remove all necrotic tissue including escharRemove all callusSharply saucerize the woundDebride boneRepeat 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 mortalityAll necrotic tissue and pus
Treatment
Plantar abscessDisappearance of the longitudinal arch and skin creasesFoot edemaCentral plantar infections – worse outcomesWide incision and drainage necessary
Treatment
AntibioticsDo not improve outcomes of non-infected lesions In PVD – therapeutic antibiotic levels are not achieved
in infected tissuesMild infection –Topical therapy
Peptide antibiotic Pexiganin acetate 1% cream nearly as effective as oral ofloxacin
Treatment
Empiric antibiotic therapyStaphStrepGNREnterococcusAnaerobes*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 therapyNo good studiesOnce active infection resolved plus 2 daysOsteomyelitis
6 weeksCan use Flouoquinolones and clindamycin