Diabetic Foot Infections:

Diagnosis & Treatment

11/05/2008

Epidemiologic Considerations
7% US population, 21 M have DM
15-20% will develop LE ulcer (LEU)
lifetime
5-7%/year with neuropathy
15% LEU will require amputation

Epidemiologic Considerations 2
65% LE amputations in the US-DM
Hispanics, AA, NA have 2-fold risk
DM foot wound treatment accounts for
DM based hospital admissions

Pathophysiology: DM LE Ulcers

Motor Neuropathy:intrinsic mm. Wasting

Fat pad displacement
Prominence metatarsal heads
Hammer toe deformity
Repetitive trauma through ADLs

Pathophysiology: 2
Sensory neuropathy: insensate foot
Autonomic neuropathy: fissuring-portal for
bacterial entry
Arthropathy: decreased mobility at ankle,
subtalar joint and MTP
Impaired healing:

Macro/microvascular disease
PMN dysfunction 2ry hyperglycemia

Greatest Risk : LUE

Prior ulcer
1/3 develop new ulcer < one year
2/3 within 5 years

Amputations: 40% probability of contralateral

amputation at 2 years

Clinic Evaluation: The Key To

Prevention
Prior foot problems
Neuropathic Symptoms: Dyesthesias
Claudication
Exam: Deformity, Callus

Monofilament testing
Edema
Pulses, venous refilling time
Footwear

Preventive Foot Care

Examine daily for cracks, callus, skin
breakdown
Warm soapy water bathing
Moisturizing cream
Toenails trimmed straight across, toe level
Clean cotton or wool socks
Well fitting comfortable shoes

Diabetic Foot Infection-1

Criteria for ulcer infection

A) > 2 of erythema, warmth, tenderness,
swelling
B) purulent discharge from ulcer or nearby
sinus tract

*Culture of clinically uninfected ulcers is not

necessary, unless done for surveillance
purposes

Diabetic Foot Infection-2

Culture Technique
CID 2006; 42: 57-62
Percutaneous bone biopsy culture
compared to surface swab cultures

Concordance rate overall 22%

Concordance rate for S. aureus 43%
Isolate from bone culture isolated from only
30% of swab cultures
DONT DO SUPERFICIAL SWAB CULTURES

Collection of Soft Tissue Cultures

From Diabetic Foot Lesions
Cleanse and mechanically debride lesion
Use a sterile dermal curette or scapel
blade to obtain material from debrided
base of lesion
Collect aerobic and anaerobic specimens

Wagner Classification of Diabetic

Foot Infections
Grade 1 superficial dermal ulcer
Grade 2 deep ulcer penetrating to tendon
or joint capsule
Grade 3 deep ulcer to bone or joint
Grade 4 localized gangrene forefoot/heel
Grade 5 gangrene of entire foot

IDSA Diabetic Foot Infection

Classification

Uninfected: lacking purulence or signs of

inflammation

Mild:infection limited to superficial tissue,

cellulitis < 2 cm around ulcer, no systemic signs

Moderate: Systemically well & metabolically

stable, > 1 of- cellulitis > 2 cm from ulcer, deep
tissue involvement, abscess, gangrene,
involvement of muscle, tendon, joint or bone

IDSA Classification

Severe: foot infection and systemic toxicity

and/or metabolic instability
Fever or chills
Leukocytosis
Tachycardia, hypotension
Confusion
Severe hyperglycemia or azotemia

Prognostic Validity of IDSA

Classification
CID 2004; 39: 885-910
N= 1666, 27 months of follow-up
15% developed LE wound, 9% infected
IDSA
Hospitalization
Amputation
Mild
4%
3%
Moderate
52%
46%
Severe
89%
78%

Clinical Diagnosis of Osteomyelitis

Exam
+LR
+ Swab culture
1.0
Ulcer inflammation
1.5
Bone exposed
9.2
Probe to bone
6.4
Wagner grade > 3
5.5
ESR > 70
11
JAMA 2008; 299: 806-813

-LR
1.0
0.84
0.70
0.39
0.40
0.34

Clinical Applications
Case 1: 52 Y.O F. 2.2X1.5 cm ulcer that
probes to bone. ESR = 82, X-ray: cortical
erosions bone contiguous to ulcer. Would
you order an MRI to prove osteo?
Case 2: 62 Y.O.M 1cm ulcer with 1 cm
surrounding erythema and swelling.
Superficial Wagner grade1. ESR 25.
Would you order an MRI to R/O osteo?

Imaging
Test

+LR

-LR

Plain films

2.3

0.6

WBC scan

3.0

0.2

MRI

4.0

0.14

Management Considerations

Define extent & severity of injury clinically

Plain x-rays: bone, gas, foreign bodies
Use IDSA classification with additional
description of size, depth of lesion, undermining,
involvement of tendon, joint, bone, gas,
gangrene
Vascular status: pulses, venous filling time,
Doppler ABI
Culture if infected, use appropriate technique

Management-2
Offload
Debridement of non-viable soft tissue and
bone by experienced surgeon/podiatrist
Moist dressing approach +/- enzymatic
debriding agent or antibacterial absorbing
agent
Additional vascular evaluation and imaging
if necessary
Control sugar < 150 mg%

Management-3
Antibiotic Therapy: Myth vs. Data
Arch Intern Med 1990; 150: 790-7
Curette cultures, initial infection
90% Staph, Strep A, B, C, G, 42% sole pathogen
36% Aerobic GNB*
13% anaerobic*
* Always polymicrobial, and role of GNB unclear,
increasing GNB with chronicity

Pathogens Asssociated With

Clinical foot-infection Syndromes
Syndrome

Pathogens

Cellulitis, no ulcer

Staph, hemolytic Strep.

Infected ulcer, no
prior antibiotic therapy

Staph & Strep,

Infected ulcer, chronic,

prior antibiotics

Staph & Strep, nonPseudomonal GNB, unless

macerated from soaking

Pathogens and Foot Syndromes-2

Syndrome
Long duration, non
healing, prior broad
spectrum antibiotics,
or the fetid necrotic foot

Pathogens
Staph, strep,
anarobes, nonfermentative GNB

Surgical Intervention
Most data support resection of infected
bone, including ray and transmetatarsal
amputations to accelerate recovery
Curr Clin Top Infecti Dis 194; 14: 1-22
N=110, ray resection, transmet.
88% cure with 2 weeks post op antibiotics
* Revascularization if indicated

Newer Approaches

Becaplermin (Regranex) Gel

Recombinant platelet derived growth factor
Increases granulation tissue ingrowth rate
Expensive
Statistical association with increased rate of
malignancy in those with > 3 prescriptions

Newer Approaches
Dermal Matrix
Integra, Graftjacket
acellular dermal scaffolfd
encourage epithelization and ulcer
closure
Infection adequately treated and wound
completely debrided to viable tissue

Hyperbaric Oxygen
Indication: Wagner grade > 3, not
responding to conventional therapy. Better
response compared to controls if ABI low
Mechanism: increased bone marrow
mobilization of endothelial precursor cells
Local deposition of stromal derived growth
factor-1 alpha into wound recruits EPC

Case

55 YO man with DM-2. Acute foot pain

and swelling after minor trauma. No skin
breakdown or sinus tracts. Foot is
edematous, red, warm with pounding
pulses and dilated pedal veins. Patient is
afebrile with normal WBC and ESR=19

Case 1
What is your diagnosis, what additional
tests would you order, why is he having
acute pain, what is appropriate therapy?
Plain x-ray: deformity of midfoot without
evidence of osteo.

Case 2

55 YO man with foot ulcer. Present for two

months. No prior antibiotic therapy. Some
purulent discharge. Probe down to tendon.
No cellulitis or systemic toxicity. Plain film
with small cortical erosions adjacent to
ulcer.

Case 2
Is the patient infected?
What is the Wagner and IDSA
classification? What is his chance of
requiring an amputation within 2 years?
Are other diagnostic tests indicated for
osteomyelitis?
Describe your therapeutic approach.