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
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

Arterial

skin

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
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 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
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
Staph

organisms

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
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

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