Diabetic Foot Management

Yunita Puspa SariSurgery DivisionRSUD Cileungsi

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 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

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