Diabetic Foot Infections Improving Outcomes (or why I’m not going into vascular!) John C. Lantis...

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