Diabetic Foot InfectionsImproving Outcomes

(or why I’m not going into vascular!)John C. Lantis II, MD

Assistant Professor of SurgeryCollege 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 shoesAbrasions in shoesTears or brakes in the skin

Motor Neuropathy Architectural deformities

Hammer 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 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 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 organisms

Staph aureus – 40% of infectionsStreptococci – 30%Staph epidermidis – 25%Enterobacteriaceae – 40%

Treatment Debridement

Minor- 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 mortality

All necrotic tissue and pus

Treatment Plantar abscess

Disappearance of the longitudinal arch and skin creasesFoot edemaCentral plantar infections – worse outcomesWide incision and drainage necessary

Treatment Antibiotics

Do 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 therapy

StaphStrepGNREnterococcusAnaerobes*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 studiesOnce active infection resolved plus 2 daysOsteomyelitis

6 weeksCan use Flouoquinolones and clindamycin