Diabetic Foot Management

Yunita Puspa Sari

Surgery Division
RSUD Cileungsi

Epidemiology
Cellulitis occurs 9 times more
frequently in diabetics than nondiabetics
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 deformities
Hammer or claw toe
High plantar arch
Subluxation 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

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

Evaluation
Describe lesion and signs of inflammation
Measure wound (? Photograph ?)
Define whether infection is present and cause
Examine soft tissue for crepitus, sinus tract,
abscess

Determine inflow
Neurologic status? Sensation, motor,
autonomic
Plain radiographs osteomyelitis (cortical
erosions, periosteal reaction)

Surgical Intervention
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

Debridement
Remove all necrotic tissue and pus including eschar
Remove all callus
Debride bone

Treatment
Plantar abscess
Foot edema
Central plantar infections worse
outcomes
Wide incision and drainage necessary

Treatment
Empiric antibiotic therapy
Staph
Strep
GNR
Enterococcus
Anaerobes
*Tailor to clinical progress

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 Flouroquinolones and clindamycin

Prevention

THANK YOU