Diabetic foot ulceration

Background

• Diabetes mellitus has reached epidemic proportions worldwide and its epicenter is in South Asia.
• One of its main complications is lower extremity ulceration and infection leading to amputation. And this is the main contributor to lower limb amputations outside trauma. The good news is foot ulceration is preventable.
• Furthermore aggressive appropriate management of early lesions prevents amputation.
• This is achieved only with good knowledge and understanding of the pathophysiological processes involved.
• This would be best achieved by teaching the subject as a stand-alone module.
• It is important to remember that diabetics do not lose their limb overnight and 70-90% of amputations are preceded by ulceration.
• It is a major contributor to amputation, ironically 30-50% of amputees lose the other limb within 5 yrs moreover approximately 100% die within 5 years of the second amputation.

Economic cost

 

Pathophysiology of diabetic foot ulceration

• Hyperglycemia ultimately leads to microangiopathy
• The molecular mechanics that link hyperglyceamia with microangiopathy are still unknown.Advanced Glycosylation End products,AGE, Sorbitol, PCK enzyme mediated pathways have been postulated.
• Microangiopathy is unique to DM it affects skin, nerves, retina & kidney - Arteriolar & capillary VSMC’s, endothelium, structurally & functionally without occlusion.
• Microangoipathy impairs diffusion & the inflammatory response of the affected area.

Neuropathy is another complication of microangiopathy and hyperglycaemia

• Sensory neuropathy is loss of protective sensation to pain, temperature and loss of sensation of joint movements. This will render the patient unaware of minor cuts and bruises.
• Motor neuropathy leads to foot deformity causing distorted weight distribution leading to pressure ulcers.
• Autonomic neuropathy leads to poor blood flow regulation causing dry, stiff skin with cracks which allows easy entry of bacteria.
• All the above mentioned factors lead to EASY WOUNDING.

 

• Loss of protective sensation permits skin injury, which is most commonly at a site of high plantar pressure.
• Dorsal injury results from shoes that do not fit the foot or foot deformities.
• These include dorsal deformities like hammer or clawed toes or prominent metatarsals causing high plantar pressures.
• Dry skin, particularly on the heel, can cause cracks that can be a portal for infection.
• Most amputations result from infection, ischemia, or both complicating a neuropathic ulcer.

Identifying High Risk Foot

Alert signs

•       Previous ulceration/ toe amputation

•       Callosity

•       Deformities

•       Neuropathy (Pins and needles, Burning sensation, Pain)i

•       Absent pedal pulses

If the pedal pulses are absent:

Check for,

• Ankle Pressure <70mm Hg
• ABPI <0.5,
• Toe Pressure (<30mm Hg) more predictable,

In consultation with the vascular surgeon

Colour Duplex arterial mapping

Angiography (Conventional, MR) – (? Contrast injury to diabetic kidneys)

Management of High Risk Foot – Preventing Ulceration

Blood sugar control

•       Strict control of blood sugar at all times is mandatory.

•       Current reference values

•       FBS – 80-110 mg/dl / 3.9 to 6.0 mmol/l

•       PPBS - 70–145 mg/dL (less than 7.9 mmol/L)

•       Hb A1c - < 7 %    (Ref: WHO)

·         Education, behavioral modification and appropriate footwear:

1. Good glyceamic control and compliance with diet and treatment
2. Regular inspection of feet for injuries
3. Always use foot ware when out of bed
4. Correct size shoes
5. Cotton padding between toe webs
6. Avoid activities risking damage to feet

                * Most problems start with minor injuries at home.        

Behavioral Modification is the key to successful management

•       After identification of a high risk foot patient should be guided through the cycle of behavioral change and empowered with knowledge to manage and monitor.