The cause and pathogenesis of the diabetic foot

Classification of the diabetic foot

According to the etiopathogenetic classification of the diabetic foot syndrome, the following farms are distinguished:

• neuropathic (70% of cases)
  • without osteoarthropathy,
  • diabetic osteoarthropathy (joint of Charcot);
• ischemic (10% of cases);
• neuro-ischemic (mixed) (20% of cases).

This classification reflects the etiopathogenesis of lesions and determines the tactics of conducting a particular category of patients, but it does not take into account the severity of the lesion.

In the combined classification of the diabetic foot syndrome (proposed by the University Group of Tuhas), the depth of ulcerative lesion, the presence of an infectious lesion and the state of the main blood flow are taken into account:

• 0 stage: there is no violation of the integrity of the skin, but there are signs of a high risk of developing a diabetic foot syndrome (areas of hyperkeratosis, cracks, dry skin in the feet, pronounced deformities, decreased sensitivity, decreased / no pulsation on the foot);
• I stage:
  • A - superficial ulcer against the background of normal blood flow, without signs of infection;
  • B - superficial ulcer with signs of decreased blood flow;
• II stage:
  • A - ulcer with involvement of soft tissues, without signs of ischemia;
  • B - ulcerative defect with involvement of soft tissues, with signs of limb ischemia,
• III stage:
  • A - an ulcer involving tendons and bone tissue, with signs of deep infection;
  • B - ulcer with an entrainment of tendons and bone tissue, with signs of deep infection and ischemia;
• IV stage: gangrene of the foot, most often combined with a decrease in the main blood flow or thrombosis of the arteries;
• V stage: gangrene of the entire foot.

According to the classification of chronic obliterating diseases of lower limb arteries (HOZANK) in Fontaineau-Pokrovsky, the following stages are distinguished:

• Stage I - stage of clinically significant stesoses, revealed by non-invasive diagnostic methods (no pains);
• II stage - the stage of overlapping lameness.
  • A - distance of painless walking more than 200 m;
  • B - distance of painless walking less than 200 m;
• Stage III - stage of pain in rest;
• IV stage - the stage of critical ischemia: the presence of chronic pain in rest and trophic disorders (ulcers, gangrene).

Obviously, this classification of HOZANK is not applicable to patients with diabetes mellitus with distal polyneuropathy. The presence of severe neuropathy can be the reason for the absence of pain during walking and even rest pain at the critical flow reduction stage. On the other hand, ulcerative foot defects can appear on the foot not due to a critical decrease in blood flow, but damage that was caused by trauma and left unnoticed due to impaired sensitivity.

In this regard, additional information is provided by objective research data on the state of the main blood flow (Doppler study). The diagnosis of critical ischemia in patients with diabetes is valid in the presence of one of the following indicators:

• ankle-brachial index (LPI) <30 mm Hg.
• systolic blood pressure:
  • in the arteries of the lower leg <50 mm Hg.
  • in the digital artery <30 mm Hg.
• Oxygen tension on the foot with percutaneous oximetry <20 mm Hg.

Causes and pathogenesis of diabetic foot syndrome

The main causes of the development of diabetic foot syndrome:

• peripheral neuropathy;
• ischemia of the lower extremities;
• "Minor" trauma to the foot;
• deformation of the foot;
• infection.

Risk Factors for Diabetic Foot Syndrome:

• diabetic polyneuropathy at the stage of clinical manifestations;
• diseases of peripheral arteries of any origin (including diabetic microangiopathy);
• deformation of feet of any origin;
• marked decrease in visual acuity, blindness;
• diabetic nephropathy;
• lonely living of elderly patients;
• alcohol abuse;
• smoking.

Factors determining a high risk of amputation in diabetic foot syndrome:

• severe infection;
• the depth of the ulcerative-necrotic process;
• critical decrease in the main circulation.

Diabetic peripheral polyneuropathy leads to loss of pain sensitivity and disruption of autonomic innervation. A significant reduction in pain sensitivity poses a threat of developing a ulcerative defect or diabetic gangrene and occurs in approximately 25% of patients with diabetes mellitus. In 20% of cases of diabetic foot syndrome, along with polyneuropathy, the HOZANK is detected.

Charcot's diabetic neuro-osteoarthropathy is a relatively painless progressive and destructive arthropathy of one or more joints, accompanied by a pronounced neurologic deficit. For diabetes mellitus, the localization of the arthropathic process in the small joints of the feet, ankle, and less often the knee joints is specific.

Morphologically, diabetic macroangiopathy is a classic atherosclerotic process. Most often there is a simultaneous lesion of the coronary, cerebral and peripheral arteries. However, a number of features (more distal lesions, bilateral and multiple localization of stenoses, development of the process at a young age, comparable incidence in men and women) allow us to speak about the specific form of atherosclerotic lesion in diabetes mellitus.

Atherosclerosis  and type 2 diabetes mellitus are components of the metabolic syndrome (synonyms: syndrome X, insulin resistance syndrome). As the atherosclerotic plaque grows, the risk of rupture increases with the release of lipid contents into the bloodstream and the formation of a parietal thrombus that covers the rupture of the intima of the artery. Such a process, called atherothrombosis, leads to a sharp increase in the degree of arterial stenosis up to complete occlusion of the lumen of the vessel. Thus, diabetic macroangiopathy leads to the development of critical limb ischemia.

As a result, necrosis of the skin and soft tissues can occur without any additional mechanical damaging effect - only due to a sharp disruption of the supply of oxygen and nutrients to the distal parts of the limb. Nevertheless, in some patients, the direct cause of the formation of a ulcerative defect is any damaging factor that disrupts the integrity of the skin. Such factors can be damage to the skin and soft tissues in the treatment of nails, the wearing of tight shoes, the formation of cracks against the background of dry skin, mycotic lesions in interdigital spaces, etc. A significant decrease in blood flow blocks the reparative capacity of tissues and leads to further expansion of the necrosis zone. The result is the formation of a typical ischemic dry necrosis of the skin in the form of a scab located in the "acral" zones of the foot with a relatively poor vascular network.