1
Forth stage
Surgery
Lec-1
د.زياد شنشل
17/3/2016
DIABETIC FOOT INFECTIONS
Introduction
Diabetic foot infections (infected foot ulcers, gangrene and osteomyelitis) are a major cause
for admission for patients with diabetes mellitus. It's expensive to treat, may lead to
amputation and need for chronic institutionalized care and if not promptly treated, severe
foot infections can lead to septicaemia and death.
A multidisciplinary team approach (by podiatrists, physicians, vascular and orthopaedic
surgeons and nursing staff) is required to reduce morbidity and mortality for affected
patients.
Pathophysiology
The etiology of diabetic foot ulcers usually has many components. This include the critical
triad of peripheral sensory neuropathy, trauma and ischemia. Although infection is rarely
implicated in the etiology of diabetic foot ulcers, the ulcers are susceptible to infection once
the wound is present.
DM is the largest cause of neuropathy .
1-Vascular disease
Peripheral arterial occlusive disease is four times more prevalent in diabetics than in
nondiabetics.
The arterial occlusion typically involves the tibial and peroneal arteries but
spares the dorsalis pedis artery. Diabetics get arthrosclerosis obliterans or “lead pipe
arteries”. Smoking, hypertension and hyperlipidemia commonly contribute to the increased
prevalence of peripheral arterial occlusive disease in diabetics.
2-Neuropathy
-Sensory
-Motor
-autonomic
Autonomic nerves regulates sweating and perfusion to the limb. Loss of autonomic control
inhibits thermoregulatory function and sweating resulting in dry, scaly and stiff skin that is
prone to cracking and allows a portal of entry for bacteria
For sensory nerves there are two mechanisms of Ulceration
1-Unacceptable stress few times
rock in shoe, glass, burn
2
2-Acceptable or moderate stress repeatedly
-Improper shoe ware
- Deformity
Risk Factors for Lower Extremity Ulcerations /Amputation in the Diabetic Foot
Absence of protective sensation due to peripheral neuropathy.
Arterial insufficiency.
Foot deformity and callus formation resulting in focal areas of high pressure.
Autonomic neuropathy causing decreased sweating and dry, fissured skin.
Limited joint mobility.
Obesity.
Impaired vision.
Poor glucose control leading to impaired wound healing.
Poor footwear that causes skin breakdown or inadequately protects the skin from high
pressure and shear forces.
History of foot ulcer or lower extremity amputation.
Patient Evaluation
Medical
Optimized glucose control will decreases 50% chance of foot problems.
Vascular
Assessment of peripheral pulses of paramount importance.
If any concern, detailed vascular assessment: ABI Less than 0.80: abnormal, Less than 0.45:
severe, limb-threatening.
Orthopedic
Evaluate and treat ulceration, deformity , prominences and contractures.
Identification of “Foot at Risk”
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Wagner Ulcer Classification System
Grade Lesion
0
No open lesions; may have deformity or cellulitis
1
Superficial diabetic ulcer (partial or full thickness)
2
Ulcer extension to ligament, tendon, joint capsule, or deep fascia without abscess or
osteomyelitis
3
Deep ulcer with abscess, osteomyelitis, or joint sepsis
4
Gangrene localized to portion of forefoot or heel
5
Extensive gangrenous involvement of the entire foot
Treatment
The primary goal in the treatment of diabetic foot ulcers is to obtain wound closure.
Management of the foot ulcer is largely determined by its severity (grade) and vascularity,
and the presence of infection.
Rest, elevation of the affected foot, and relief of pressure are essential components of
treatment and should be initiated at first presentation. Ill-fitting footwear should be replaced
with a postoperative shoe or another type of pressure-relieving footwear. Crutches or a
wheelchair might also be recommended to totally off-load pressure from the foot.
A mainstay of ulcer therapy is debridement of all necrotic, callus, and fibrous tissue.
Unhealthy tissue must be sharply debrided back to bleeding tissue to allow full visualization
of the extent of the ulcer and detect underlying abscesses or sinuses. Topical antiseptics, such
as povidone-iodine, are usually considered to be toxic to healing wounds.
Generally, a warm,
moist environment that is protected from external contamination is most conducive to
wound healing.
Wagner 0-2
Distributes pressure and allows patients to continue ambulation
Antibiotics if infected, Surgical if deformity present that will re-ulcerate . Correct deformity
(exostectomy).
Wagner 3
Excision of infected bone. Wound allowed to granulate.
Grafting (skin or bone) not generally effective.
Wagner 4-5
Amputation , what level ?