How to Save a Leg from Amputation?

Types of Defects and Risk Factors for Their Development

In addition to impaired circulation, neuropathy significantly contributes to the development of defects. Its complex adverse impact on the trophism and anatomy of the diabetic's limb causes defects to form even on limbs that show no clinical signs of ischemia. These are known as neuropathic defects. In the presence of a certain degree of ischemia, we speak of neuro-ischemic defects or purely ischemic defects. Risk factors include male gender, diabetes duration over 10 years, peripheral neuropathy, abnormal anatomical foot structure/deformities, altered biomechanical anatomical foot relationships, peripheral arterial disease, smoking, previous ulcerations or amputations, inadequate footwear or orthotics, poor glycemic control, and obesity.

The development of ulcers typically involves a combination of two or more factors. 50–60% of defects are purely neuropathic and, in the absence of infection, are optimally treatable. 40–50% of defects are neuro-ischemic, requiring some form of limb revascularization, with up to 50% of defects becoming infected. Infection is a very important factor, particularly the degree of colonization of the defect base and the infection around the lesion, which goes hand in hand with the amount of affected tissue mass.

Specific Risks in Diabetics

High plantar pressures, which decrease the effective blood flow in the affected segments and anatomical foot roll-off edges, hinder the immune system's efforts and complicate the availability of antibiotics. All this is exacerbated by the degree of ischemia due to obliterative atherosclerosis (which is 10 times more common in diabetics than in non-diabetics), preferentially affecting the crural arteries. The risk of amputation is about 10–20 times higher in diabetics than in cases of “pure” peripheral arterial disease. The prevalence of peripheral arterial disease in diabetic feet is 20%, and the prevalence of ulcers is 4–10%. Another very important fact is that 60% of all ulcers recur at the original site within 2 years.

In summary, diabetic foot is typically characterized by a certain degree and type of neuropathy, infection, and ischemia, which are key determinants for the fate of the limb. Diabetic neuropathy, affecting both sensory and autonomic nerve fibers, further alters and distorts clinical symptoms. For example, warning signs of tissue damage pain are absent, most often due to inappropriate footwear, which, together with high plantar pressures, initially causes typical hyperkeratosis or callus at the site of the stressed area.

The actual defect, varying in depth, often develops under this hard protective layer and can remain unnoticed for a long time. It is often discovered only during secondary infection, affecting varying depths of tissue structures. The second very common trigger for defect or local gangrene formation is external trauma, such as a small stone in the shoe or other bruises that the patient does not feel. Diabetic limbs are warm and swollen, the skin is dry and often cracked, and the toes move into a hammer position due to motor neuropathy. The fat pad (pulvinar) migrates peripherally, losing its protective effect under the metatarsal heads, facilitating defect formation precisely there. Patients also typically do not have a history of claudication, which would indicate developing limb ischemia.

Therapy Course

Treatment of developed defects follows several levels. The first is to prevent further tissue destruction, decompress structures, drain, and primarily sanitize wet gangrene, especially when there is a risk of retention in the demarcation zone. The procedure must be sufficiently radical in terms of decompression and infection control, but not in terms of hasty amputation. Other levels include aggressive systemic antibiotic treatment, locally considered interventions in the defect in terms of regular dressings with suitable coverings and mechanical wound cleaning. Equally important is quality offloading. All this is aimed at gaining time for vascular evaluation and revascularization, if indicated.

Local coverings can be divided into several groups, each suitable for a certain phase of chronic wound healing:

• Initially, the need to clean the wound from necrosis, i.e., dead tissue residues, and decontaminate the base along with reducing wound secretion dominates. Specially developed preparations supporting moist environment in the wound, gentle dissolving of impurities and dead tissue residues with their gradual removal from the wound along with bacteria or their simple absorption, serve this purpose.
• In the next phase, HydroTherapy supports so-called granulation, i.e., the formation of new tissue, which gradually fills and covers the developed defect up to its edge. It also absorbs the forming excess tissue fluid and maintains constant conditions on the wound base suitable for quick healing. Another advantage is the reduction of local pain and protection against secondary infection. Properly indicated agents significantly speed up and simplify the entire healing process in this way.
• In the final phase – epithelialization – the growth of new skin cells is supported. These grow from the edges of the defect and gradually cover it or support the attachment and integration of surgically placed skin grafts.

The choice of moisture therapy preparation type for the given wound healing phase should always be made by an experienced physician dealing with this issue.

MUDr. Vítězslav Vaverka
Surgical Clinic of LF MU and FN Brno