Diabetic Foot

Diabetic Foot

By Dr. KM Liau

Foot disorders are a major source of morbidity and a leading cause of hospitalization for persons with diabetes mellitus.

Diabetic Foot

The foot of a diabetic patient that has the potential risk of pathologic consequences, including infection, ulceration, and/or destruction of deep tissues associated with neurologic abnormalities, various degrees of peripheral vascular disease, and/or metabolic complications of diabetes in the lower limb.

Primary Goals of Treatment

1. Prevent limb loss
2. Prevention of ulceration and recurrence
3. Early recognition and treatment of diabetic foot complications
4. Maintain quality of life

Risk Factors For Ulceration

1. Peripheral sensory neuropathy
2. Structural foot deformity
3. Trauma and improperly fitted shoes
4. History prior ulcers/amputations
5. Prolonged pressures
6. Limited joint mobility
7. Uncontrolled hyperglycemia
8. Blindness/partial sight
9. Chronic renal disease

Peripheral sensory neuropathy

Peripheral sensory neuropathy in the absence of perceived trauma is the primary factor leading to diabetic foot ulcerations.

Neuropathic Ulcer

Motor neuropathy

Motor neuropathy resulting in anterior crural muscle atrophy or intrinsic muscle wasting can lead to foot deformities such as foot drop, equinus, hammertoes, and prominent plantar metatarsal heads.

Motor Neuropathy With Claw Toes

Autonomic neuropathy

Autosympathectomy with attendant sympathetic failure, arteriovenous shunting, and microvascular thermoregulatory dysfunction impairs normal tissue perfusion and microvascular responses to injury.

Commonly result in dry skin with cracking and fissuring, thus creating a portal of entry for bacteria.

Autonomic Neuropathy

Wagner Grade 1 Ulcer

Superficial ulcer. Disruption of skin without penetration of the subcutaneous fat layer. Superficial infection with or without cellulitis may
be present.This lesion heals quickly with rest and local foot care.

Wagner Grade 1 Ulcer

Wagner Grade 2 Ulcer

Full-thickness ulcer. Penetrates through fat to tendon, or joint capsule without deep abscess or osteomyelitis.

Wagner Grade 2 Ulcer

Wagner Grade 3 Ulcer

Deep ulcer which may or may not probe to bone, with abscess, osteomyelitis, or joint sepsis.

Includes deep plantar space infections or abscesses, necrotizing fasciitis, and tendon sheath infections.

Wagner Grade 3 Ulcer

Wagner Grade 4 - Geographical Gangrene

Denotes gangrene of a geographical portion of the foot such as toes, forefoot or heel. The remainder of the foot is salvageable though it may
be infected.

Wagner Grade 4 - Geographical Gangrene

Wagner Grade 5 - Unsalvagable Gangrene

Gangrene or necrosis to the extent that the foot is beyond salvage and will require a major limb- or life-sparing amputation.

Wagner Grade 5 - Unsalvagable Gangrene

Chronic Wound

Chronic wounds remain in a chronic inflammatory state and therefore FAIL to follow normal patterns of the healing process.

The primary goal in treating the chronic ulcer is to convert it to an acute wound which will then possess the active matrix and cells needed for healing.

Chronic Diabetic Ulcer

Wound Debridement

Debridement describes the removal of necrotic or foreign material from and around a wound to optimise wound healing.

Sharp debridement produces rapid results. It requires a high level of skill and experience and practitioners must have the necessary knowledge and training to complete the task safely and effectively and be able to deal with any complications as they arise.

Why Debride?

Dead tissue acts as a medium for bacterial growth, particularly anaerobes such as Bacteroides species and gas gangrene caused by Clostridium perfringens in military surgical practice

Necrotic tissues retard wound contraction, the principle contribution to wound closure when wounds are left to heal by secondary intention.

When Not To Debride?

When there is underlying vascular disease with associated gangrene it is conventional to wait for a line of demarcation.

It is also possible that necrotic material may auto-amputate itself (see image below).

Early intervention can precipitate wet infected gangrene which spreads proximally and may need an urgent higher amputation.

Do Not Amputate A Mummified Toe!

Pressure Sore With Necrotic 'Cap"

Full thickness dry pressure sore with necrotic 'cap' should NOT be excised if they are not causing discomfort and there is no wound malodour or exudate.

Although the wound will not heal with the necrotic tissue in situ, any potential benefits should be balanced against the need for increased intervention and possible disruption to the patient if the 'caps' are removed.

Care should be taken if a wound is showing clinical signs of infection - surgical debridement may be required.

Pressure sore on the heel with black, full thickness 'cap'.

Charcot Foot

The acute Charcot foot is usually painless and may mimic cellulitis or deep venous thrombosis.

Although the initial radiograph may be normal, making diagnosis difficult, immediate detection and immobilization of the foot are essential in the management of the Charcot foot.

A lifelong program of patient education, protective footwear and routine foot care is required to prevent complications such as foot ulceration.

Pathogenesis of Charcot Foot

The exact pathogenesis is unknown, but underlying sensory neuropathy is nearly universal.

Arteriovenous shunting due to autonomic neuropathy is also thought to play a role.

Repeated unrecognized microtrauma or an identifiable injury may be the inciting factors of Charcot foot.

Acute Charcot Foot

Charcot Foot with Chronic Non-Healing Ulcer

Severely Destructed Ankle Joint

Off-Loading Treatment

Reducing pressure to the diabetic foot ulcer is an essential component of treatment.

Without proper off-loading and pressure reduction, ulcers will continually be traumatized to the point that they cannot heal.

Off-Loading Techniques

1. Total nonweightbearing: crutches, bed, wheel chair

2. Total contact casting

3. Removable walking braces with rocker bottom soles

4. Patellar tendon-bearing braces

Total Contact Cast

The standard of care has become strict immobilization of the foot and ankle in an attempt to stabilize and protect the foot.

Total contact cast allows some measure of ambulation for the patient and appears to prevent the progression of deformity.

Total Contact Cast

Patellar Tendon Bearing Brace

Once the acute Charcot process has subsided and the cast is removed, lifelong protection of the at-risk foot begins.

Patellar tendon bearing brace in addition to custom-molded footwear is a good option for further protection.

The brace can sometimes be eliminated from the regimen after six to 24 months.

Thereafter, continued use of custom footwear to protect and support the foot is essential.

Patellar-tendon brace with custom-molded footwear

Progression of Disease

Charcot fractures that are not treated progress, typically leading to marked deformity and skin ulceration over the new bony prominence (see image below)

Neuropathic ulcer in a patient with Charcot-related foot deformity.

Reconstructive Surgery For Charcot Foot

Reconstructive surgery is reserved for patients who have recurrent ulceration despite compliance with the previously mentioned regimen.

Foot with recurrent ulceration despite compliance with carefully designed footwear. Surgery was required.

The foot remains free of ulcers three years after surgery.