Cause and pathogenesis of diabetic foot

Classification of diabetic foot

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

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

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

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

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

According to the classification of chronic obliterating diseases of the arteries of the lower extremities (COA) by Fontaine-Pokrovsky, the following stages are distinguished:

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

It is obvious that this classification of HOZANK is not applicable to patients with diabetes mellitus with distal polyneuropathy. The presence of severe neuropathy may be the reason for the absence of pain when walking and even pain at rest at the stage of critical reduction of blood flow. On the other hand, ulcerative defects of the feet may appear on the foot not because of critical reduction of blood flow, but because of damage that was caused by trauma and remained unnoticed due to impaired sensitivity.

In this regard, additional information is provided by objective studies of the state of the main blood flow (Dopplerography). The diagnosis of critical ischemia in patients with diabetes mellitus is justified if one of the following indicators is present:

• ankle-brachial index (ABI) < 30 mmHg
• systolic blood pressure:
  • in the arteries of the leg < 50 mm Hg
  • in the digital artery < 30 mmHg
• foot oxygen tension by transcutaneous oximetry < 20 mmHg.

Causes and pathogenesis of diabetic foot syndrome

The main reasons for the development of diabetic foot syndrome:

• peripheral neuropathy;
• lower limb ischemia;
• "minor" foot injury;
• foot deformation;
• infection.

Risk factors for developing diabetic foot syndrome:

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

Factors that determine a high risk of amputation in diabetic foot syndrome:

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

Diabetic peripheral polyneuropathy leads to loss of pain sensitivity and disruption of autonomic innervation. Significant reduction in pain sensitivity poses a risk of developing 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, HOSANK is detected.

Diabetic neuroosteoarthropathy of Charcot is a relatively painless progressive and destructive arthropathy of one or more joints, accompanied by a pronounced neurological deficit. For diabetes mellitus, the localization of the arthropathic process in the small joints of the feet, ankle, and less often 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 lesion, bilateral and multiple localization of stenosis, development of the process at a young age, comparable incidence in men and women) allow us to speak of a specific form of atherosclerotic lesion in diabetes mellitus.

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

As a result, necrosis of the skin and soft tissues may occur without any additional mechanical damaging effect - only due to a sharp disruption in the supply of oxygen and nutrients to the distal parts of the limb. Nevertheless, in some patients, the immediate cause of the ulcerative defect is some damaging factor that disrupts the integrity of the skin. Such factors may be damage to the skin and soft tissues when treating nails, wearing tight shoes, the formation of cracks against the background of dry skin, mycotic damage in the 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 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.