What is diabetic angiopathy, why it occurs and how it is treated. Diabetic angiopathy of the lower extremities

- a collective concept that unites atherosclerotic lesions of large arteries in diabetes, clinically manifested coronary disease heart disease (IHD), obliterating atherosclerosis of the vessels of the brain, lower extremities, internal organs and arterial hypertension (Table 1).

Table 1

Diabetic macroangiopathy

Etiology and pathogenesis	Hyperglycemia, arterial hypertension, dyslipidemia, obesity, insulin resistance, hypercoagulability, endothelial dysfunction, oxidative stress, systemic inflammation
Epidemiology	Risk development of ischemic heart disease with DM-2 is 6 times higher than in streets without DM. Arterial hypertension is detected in 20% of patients with type 1 diabetes and in 75% of patients with type 2 diabetes. Obliterating atherosclerosis of peripheral vessels develops in 10%, and thromboembolism of cerebral vessels in 8% of patients with diabetes
Main clinical manifestations	Similar to those in persons without diabetes. In diabetes, myocardial infarction is painless in 30% of cases
Diagnostics	Similar to those in persons without diabetes
Differential diagnosis	Other cardiovascular diseases, symptomatic arterial hypertension, secondary dyslipidemias
	Antihypertensive therapy, correction of dyslipidemia, antiplatelet therapy, screening and treatment of coronary artery disease
	75% of patients with T2DM and 35% of patients with T1DM die from cardiovascular diseases

Etiology and pathogenesis

Probably similar to the etiology and pathogenesis of atherosclerosis in streets without diabetes. Atherosclerotic plaques do not differ in microscopic structure streets with and without diabetes. However, in DM, the following may come to the fore: additional factors risk, or diabetes aggravates known nonspecific factors. These for diabetes include:

1. Hyperglycemia. It is a risk factor for the development of atherosclerosis. An increase in HbAlc levels by 1% in patients with type 2 diabetes increases the risk of myocardial infarction by 15%. The mechanism of the atherogenic effect of hyperglycemia is not entirely clear; perhaps it is associated with glycosylation of the end products of LDL metabolism and collagen of the vascular wall.

2. Arterial hypertension(AG). In pathogenesis great value attributed to the renal component (diabetic nephropathy). Hypertension in type 2 diabetes is no less a significant risk factor for heart attack and stroke than hyperglycemia.

3. Dyslipidemia. Hyperinsulinemia, which is an integral component of insulin resistance in type 2 diabetes, causes a decrease in HDL levels, an increase in triglyceride levels and a decrease in density, i.e. increased atherogenicity of LDL.

4. Obesity, which affects the majority of patients with T2DM, is an independent risk factor for atherosclerosis, myocardial infarction and stroke.

5. Insulin resistance. Hyperinsulinemia and high level insulin-proinsulin-like molecules increase the risk of atherosclerosis, which may be associated with endothelial dysfunction.

6. Impaired blood coagulation. In diabetes, an increase in the level of fibrinogen, platelet inhibitor activator and von Willebrand factor is determined, resulting in the formation of a prothrombotic state of the blood coagulation system.

7. Endothelial dysfunction, characterized by increased expression of plasminogen inhibitor activator and cell adhesion molecules.

8. Oxidative stress, leading to an increase in the concentration of oxidized LDL and F2-isoprostanes.

9. Systemic inflammation, in which there is an increase in the expression of fibrinogen and C-reactive protein.

The most significant risk factors for the development of IHD in T2DM are increased level LDL, reduced HDL, arterial hypertension, hyperglycemia and smoking. One of the differences between the atherosclerotic process in diabetes is its more widespread and distal nature of the occlusal lesion, i.e. relatively smaller arteries are more often involved in the process, which makes it difficult surgical treatment and worsens the prognosis.

Epidemiology

The risk of developing coronary heart disease in streets with type 2 diabetes is 6 times higher than in streets without diabetes, while it is the same for men and women. Arterial hypertension is detected in 20% of patients with type 1 diabetes and in 75% of patients with type 2 diabetes. In general, in patients with diabetes it occurs 2 times more often than in those without it. Obliterating atherosclerosis of peripheral vessels develops in 10% of patients with diabetes. Thromboembolism of cerebral vessels develops in 8% of patients with diabetes (2-4 times more often than in persons without diabetes).

Clinical manifestations

Basically they do not differ from those of streets without SD. IN clinical picture T2DM macrovascular complications (myocardial infarction, stroke, occlusive lesions of the vessels of the legs) often come to the fore, and it is with their development that hyperglycemia is often first detected in the patient. Perhaps, due to concomitant autonomic neuropathy, up to 30% of myocardial infarctions in people with diabetes occur without a typical anginal attack (painless infarction).

Diagnostics

Principles for diagnosing complications of atherosclerosis (CHD, violation cerebral circulation, occlusive lesions of the arteries of the legs) do not differ from those for persons without diabetes. Measurement blood pressure(BP) should be carried out at every visit of a patient with diabetes to the doctor, and the determination of indicators lipid spectrum blood ( total cholesterol, triglycerides, LDL, HDL) for diabetes should be carried out at least once a year.

Differential diagnosis

Other cardiovascular diseases, symptomatic arterial hypertension, secondary dyslipidemia.

Treatment

Blood pressure control. The proper level of systolic blood pressure in diabetes is less than 130 mmHg, and diastolic blood pressure is 80 mmHg. For most patients, several treatments are required to achieve this goal. antihypertensive drugs. Drugs of choice antihypertensive therapy for diabetes, ACE inhibitors and angiotensin receptor blockers are used, which, if necessary, are supplemented with thiazide diuretics. The drugs of choice for patients with diabetes who have suffered a myocardial infarction are beta-blockers.
Correction of dyslipidemia. The drugs of choice for lipid-lowering therapy are 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins).
Antiplatelet therapy. Aspirin therapy (75-100 mg/day) is indicated for patients with diabetes over 40 years of age with an increased risk of developing cardiovascular pathology(complicated family history, arterial hypertension, smoking, dyslipidemia, microalbuminuria), as well as in all patients with clinical manifestations of atherosclerosis as secondary prevention.
Screening and treatment of ischemic heart disease . Stress tests to exclude coronary artery disease are indicated for patients with symptoms of cardiovascular diseases, as well as when pathology is detected by ECG.

Forecast

75% of patients with T2DM and 35% of patients with T1DM die from cardiovascular diseases. Approximately 50% of patients with T2DM die from complications of coronary artery disease, 15% from cerebral thromboembolism. Mortality from myocardial infarction in people with diabetes exceeds 50%.

Dedov I.I., Melnichenko G.A., Fadeev V.F.

The main cause of any complications of diabetes mellitus is harmful influence glucose on body tissues are especially affected nerve fibers and vessel walls. Defeat vascular network, diabetic angiopathy, is detected in 90% of diabetics 15 years after the onset of the disease.

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In severe stages, the case ends in disability due to amputations, loss of organs, and blindness. Unfortunately, even best doctors can only slightly slow down the progression of angiopathy. Only the patient himself can prevent complications of diabetes. This will require an iron will and an understanding of the processes occurring in the diabetic body.

What is the essence of angiopathy?

Angiopathy is an ancient Greek name, literally translated as “vascular suffering.” They suffer from the excessively sweet blood that flows through them. Let us consider in more detail the mechanism of development of disorders in diabetic angiopathy.

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The inner wall of the vessels is in direct contact with the blood. It consists of endothelial cells that cover the entire surface in one layer. The endothelium contains inflammatory mediators and proteins that promote or prevent blood clotting. It also works as a barrier - it allows water, molecules smaller than 3 nm, and selectively other substances to pass through. This process ensures the supply of water and nutrition to the tissues, cleansing them of metabolic products.

With angiopathy, it is the endothelium that suffers the most, its functions are impaired. If diabetes is not kept under control, elevated glucose levels begin to destroy blood vessel cells. Special chemical reactions between endothelial proteins and blood sugars - glycation. The products of glucose metabolism gradually accumulate in the walls of blood vessels, they thicken, swell, and cease to function as a barrier. Due to disruption of the coagulation processes, blood clots begin to form, as a result, the diameter of the vessels decreases and the movement of blood through them slows down, the heart has to work with increased load, the blood pressure.

The smallest vessels are most severely damaged; impaired blood circulation in them leads to a cessation of oxygen and nutrition supply to the body tissues. If in areas with severe angiopathy the damaged capillaries are not replaced with new ones in time, these tissues will atrophy. Lack of oxygen prevents the growth of new vessels and accelerates the overgrowth of damaged connective tissue.

These processes are especially dangerous in the kidneys and eyes; their performance is impaired until they completely lose their functions.

Diabetic angiopathy large vessels often accompanied by atherosclerotic processes. Due to metabolic disorders, fats are deposited on the walls cholesterol plaques, the lumen of blood vessels narrows.

Factors in the development of the disease

Angiopathy develops in patients with types 1 and 2 diabetes only if blood sugar is elevated for a long time. The longer the glycemia and the higher the sugar level, the faster the changes in blood vessels begin. Other factors can only aggravate the course of the disease, but not cause it.

Factors in the development of angiopathy	Mechanism of influence on the disease
Duration of diabetes	The likelihood of angiopathy increases with diabetes, as changes in blood vessels accumulate over time.
Age	The older the patient, the higher his risk of developing diseases of large vessels. Young diabetics are more likely to suffer from impaired microcirculation in the organs.
Vascular pathologies	Concomitant diseases vessels increase the severity of angiopathy and contribute to its rapid development.
Availability	Elevated levels of insulin in the blood accelerate the formation of plaques on the walls of blood vessels.
Short clotting time	Increases the likelihood of blood clots and death of the capillary network.
Overweight	The heart wears out, the level of cholesterol and triglycerides in the blood increases, blood vessels narrow faster, and capillaries located far from the heart are less well supplied with blood.
High blood pressure	Increases the destruction of vessel walls.
Smoking	Interferes with the work of antioxidants, reduces oxygen levels in the blood, and increases the risk of atherosclerosis.
Standing work, bed rest.	Both lack of exercise and excessive leg fatigue accelerate the development of angiopathy in the lower extremities.

What organs are affected by diabetes mellitus

Depending on which vessels suffer most from the influence of sugars in uncompensated diabetes, angiopathy is divided into types:

- represents a lesion of the capillaries in the glomeruli of the kidneys. These vessels are among the first to suffer, as they work under constant load and allow a huge volume of blood to pass through them. As a result of the development of angiopathy, renal failure: filtration of blood from metabolic products worsens, the body does not completely get rid of toxins, urine is excreted in a small volume, swelling forms throughout the body, compressing organs. The danger of the disease lies in the absence of symptoms initial stages and complete loss of end-stage renal function. The disease code according to the ICD-10 classification is 3.
Diabetic angiopathy of the lower extremities- most often develops as a result of the effect of diabetes on small vessels. Circulatory disorders leading to trophic ulcers and gangrene, can develop even with minor disturbances in main arteries. It turns out a paradoxical situation: there is blood in the legs, but the tissues are starving, since the network of capillaries is destroyed and does not have time to recover due to constant high sugar in the blood. Angiopathy upper limbs diagnosed in isolated cases, since a person’s hands work with less load and are located closer to the heart, therefore, the vessels in them are less damaged and are restored faster. ICD-10 code – 10.5, 11.5.
- leads to damage to the vessels of the retina. Like nephropathy, it does not have symptoms until serious stages of the disease, which require treatment with expensive drugs and laser operations on the retina. The result of the destruction of blood vessels in the retina is blurred vision due to edema, gray spots in front of the eyes due to hemorrhages, retinal detachment with subsequent blindness due to the formation of scars at the site of damage. Angiopathy at the initial stage, which can only be detected in an ophthalmologist’s office, is cured on its own with long-term compensation of diabetes. Code H0.
Diabetic angiopathy of the heart vessels- leads to angina pectoris (code I20) and is the main cause of death from complications of diabetes mellitus. Atherosclerosis coronary arteries causes oxygen starvation of the heart tissue, to which it responds with pressing, squeezing pain. The destruction of capillaries and their subsequent overgrowth with connective tissue impairs the functions of the heart muscle, and rhythm disturbances occur.
- a violation of the blood supply to the brain, initially manifested by headaches and weakness. The longer the hyperglycemia, the greater the oxygen starvation of the brain, and the more it is affected by free radicals.

Symptoms and signs of angiopathy

At first, angiopathy is asymptomatic. While the damage is not critical, the body manages to grow new vessels to replace the damaged ones. At the first, preclinical stage, metabolic disorders can only be determined by an increase in cholesterol in the blood and an increase in vascular tone.

The first symptoms of diabetic angiopathy occur at the functional stage, when the damage becomes extensive and does not have time to recover. Treatment started at this time can reverse the process and completely restore the function of the vascular network.

Possible signs:

pain in the legs after a long exercise - ;
numbness and tingling in the limbs;
convulsions;
cold skin on the feet;
protein in urine after exercise or stress;
spots and a feeling of blurred vision;
weak headache, not relieved by analgesics.

Well-defined symptoms occur at the last, organic, stage of angiopathy. At this time, changes in the affected organs are already irreversible, and drug treatment can only slow down the progression of the disease.

Clinical manifestations:

Constant pain in the legs, lameness, damage to the skin and nails due to lack of nutrition, swelling of the feet and calves, the inability to stand for a long time with angiopathy of the lower extremities.
High blood pressure that cannot be treated, swelling on the face and body, around internal organs, intoxication due to nephropathy.
Severe loss of vision due to retinopathy, fog before the eyes as a result of edema due to diabetic angiopathy of the center of the retina.
Dizziness and fainting due to arrhythmia, lethargy and shortness of breath due to heart failure, chest pain.
Insomnia, memory and motor coordination disorders, decreased cognitive abilities in cerebral angiopathy.

Symptoms of vascular damage in the extremities

Symptom	Cause
Pale, cool skin on feet	Damage to capillaries that is still treatable
Leg muscle weakness	Insufficient muscle nutrition, the onset of angiopathy development
Redness on the feet, warm skin	Inflammation due to associated infection
Absence of pulse in the limb	Significant narrowing of the arteries
Prolonged swelling	Severe vascular damage
Reduced calf or thigh muscles, stunted hair growth on legs	Prolonged oxygen starvation
Unhealed wounds	Multiple capillary damage
Black fingertips	Angiopathy of large vessels
Blue cold skin on extremities	Severe damage, lack of blood circulation, beginning gangrene.

Diagnosis of the disease

Early diagnosis angiopathy is a guarantee that treatment will be successful. Waiting for symptoms to appear means starting the disease, completely recovery at stage 3 is impossible, some of the functions of the damaged organs will be irretrievably lost. Previously, screening was recommended 5 years after diabetes was diagnosed. Currently, changes in blood vessels can be detected even earlier, which means they can be treated while the lesions are minimal. Type 2 diabetes is often diagnosed several years after the onset of the disease, and blood vessels begin to be damaged even at the stage of prediabetes, so it is worth checking the blood vessels immediately after hypoglycemia is detected.

Adolescents and older adults with long-term diabetes develop several angiopathies different organs, both large and small vessels are damaged. Once they have been diagnosed with one type of disease, they need full examination cardiovascular system.

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All forms of angiopathy are characterized by the same changes in the metabolism of proteins and fats. With vascular disorders, metabolic abnormalities characteristic of patients are aggravated diabetes mellitus. With the help biochemical tests blood, the so-called lipid status is revealed. On high probability angiopathy indicates an increase in cholesterol, especially an increase in low-density lipoproteins, a decrease in albumin levels, an increase in phospholipids, triglycerides, free fatty acids and alpha globulin.

Patients with diabetes often show signs of diabetic angiopathy when small vessels are affected. Diabetic angiopathy of the lower extremities is diagnosed most often, and this type of complication occurs in diabetics with type 1 or type 2 pathology. If surgical or conservative treatment with diabetic angiopathy, it is possible serious complications with damage to many organs.

What kind of disease?

Diabetic angiopathy is characterized by damage to small and large vessels and arteries. Disease code according to IBC 10 is E10.5 and E11.5. As a rule, diabetic foot disease is noted, but damage to blood vessels in other parts of the body and internal organs is also possible. It is customary to divide angiopathy in diabetes mellitus into 2 types:

Microangiopathy. Characterized by damage to capillaries.
Macroangiopathy. Arterial and venous damage is noted. This form is less common and affects diabetics who have been ill for 10 years or longer.

Often, due to the development of diabetic angiopathy, the patient’s general health and life expectancy is reduced.

Main causes of diabetic angiopathy

The main reason for the development of diabetic angiopathy is regularly elevated levels of sugar in the blood fluid. Highlight following reasons leading to the development of diabetic angiopathy:

prolonged hyperglycemia;
increased concentration of insulin in the blood fluid;
presence of insulin resistance;
diabetic nephropathy, in which kidney dysfunction occurs.

Risk factors

Alcohol and cigarette abuse can trigger the development of angiopathy.

Not all diabetics experience this complication; there are risk factors when the likelihood of vascular damage increases:

long-term diabetes;
age category over 50 years;
wrong way of life;
poor nutrition, with a predominance of fatty and fried foods;
slowing down metabolic processes;
being overweight;
excessive consumption of alcohol and cigarettes;
arterial hypertension;
cardiac arrhythmia;
genetic predisposition.

Target organs

It is difficult to predict the occurrence of diabetic angiopathy. Angiopathy of the lower extremities is more common, since diabetes places a greater burden on them. But vascular, arterial, capillary damage to other parts of the body is possible. There are target organs that most often suffer from angiopathy:

heart;
brain;
eyes;
kidneys;
lungs.

Symptoms of pathology

Early diabetic angiopathy may not manifest itself special features, and the person may not be aware of the disease. As it progresses, different pathological symptoms, which are difficult not to notice. Symptomatic manifestations depend on the type and stage of vascular lesion. The table shows the main stages of the disease and characteristic manifestations.

View	Stage	Manifestations
Microangiopathy	0	There are no obvious symptoms
	1	Change in skin color, minor ulcerative lesions without inflammatory manifestations
	2	Deepening of ulcers with damage muscle tissue and bones, presence of pain
	3	Dying of the area with ulcers, redness and swelling at the site of the affected skin, inflammatory process in bone tissue
	4	Spread of necrosis beyond the ulcerative lesion, often the foot is injured
	5	Complete damage to the foot followed by amputation
Macroangiopathy	1	Stiffness of movement after sleep, heaviness when walking, increased sweating and frequent freezing of the feet
	2a	Feeling of coldness in the legs, regardless of the time of year, numbness of the lower extremities, pale skin
	2b	Signs of stage 2a, but with the addition of lameness, appearing every 50-200 meters
	3a	Painful sensations, especially at night, cramps, burning and peeling of the skin, pale skin when horizontal position legs
	3b	Constant pain, swelling of the lower extremities, ulcerative lesions with tissue death
	4	Spread of necrosis to the entire foot with subsequent death of the limb, infectious lesions of the body with increased body temperature and weakness

Diagnostics

Diabetic angiopathy of the vessels of the lower extremities is detected through laboratory and instrumental studies.

Ultrasound of the vessels of the legs is necessary to monitor their condition.

It is recommended to additionally consult an endocrinologist, nephrologist, neurologist, ophthalmologist, cardiologist, gynecologist, angiologist surgeon, podiatrist or other specialists. The following tests are prescribed for diabetics:

general analysis of urine and blood;
blood biochemistry for sugar, cholesterol and other lipids;
electrocardiography;
Ultrasound of the vessels of the brain and neck, legs, heart and other target organs;
blood pressure measurement;
analysis for glycated hemoglobin;
glucose tolerance test.

Treatment of pathology

Drugs

For diabetic angiopathy it is required complex treatment which involves taking medications different groups and compliance strict diet and mode. Before treating the pathology, you should stop drinking alcohol and narcotic substances which negatively affect blood vessels. Pharmacotherapy of diabetic angiopathy consists of taking the following drugs:

Sugar-lowering:
- "Siofor";
- "Diabeton";
- "Glucophage."
Cholesterol-lowering agents:
- "Lovastatin";
- "Simvastatin".
Blood thinners:
- "Trombonet";
- "Ticlopidine";
- "Warfarin";
- "Clexane."
Agents that improve blood circulation and microcirculation:
- "Tivortin";
- "Ilomedin";
- "Plestasol."

Ibuprofen is prescribed for pain that bothers the patient.

In addition, the doctor will recommend treatment with vitamin E or nicotinic acid. If the patient is worried severe pain for diabetic angiopathy, the use of painkillers is indicated: “Ibuprofen”, “Ketorolac”. If a secondary infectious lesion, then antibacterial medications are indicated: “Ciprinol”, “Ceftriaxone”.

Diabetic angiopathy- generalized vascular damage, extending to small vessels (the so-called “microangiopathy”), as well as to medium and large vessels (i.e. macroangiopathy). If changes in small vessels (capillaries, arterioles and venules) are specific to diabetes, then damage to large vessels is equivalent to early and widespread atherosclerosis.
A characteristic feature of the lesion small vessels with endothelial proliferation, thickening basement membrane small capillaries, deposition of glycoprotein PA5-positive substances in the vessel wall. The term “diabetic microangiopathy” was proposed to denote a generalized process in small vessels.
Despite the widespread nature of microangiopathies, the vessels of the kidneys, fundus of the eye, lower extremities with typical manifestations in the form of nephropathy, retinopathy and peripheral microangiopathy.

The term “diabetic microangiopathy” is the most successful of all those proposed, since it reflects the two most characteristic features- relationship with the underlying disease and localization of the process in small vessels. Other names such as "universal capillaropathy", "disseminated vascular disease", "peripheral angiopathy" have not been vaccinated in history.
When developing the nomenclature, one should proceed from the established fact of double vascular damage characteristic of diabetes - atherosclerosis of medium and large vessels, which develops earlier and is more common in diabetes, and specific diabetic microangiopathy. In addition, there is a third form of damage - arteriolosclerosis, which is clinically diagnosed only when the process is localized in the kidney.
As for thromboangiitis obliterans (endarteritis), this form of pathogenetic connection has no pathogenetic connection with diabetes, and it would be erroneous to classify it as vascular complications diabetes Thrombangiitis occurs no more often in diabetes than in people without diabetes. The confusion of the concepts of “atherosclerosis obliterans” and “thromboangiitis obliterans” occurred because the latter term often refers to early and favorable developing forms obliterating atherosclerosis. At the same time, thromboangiitis itself is an allergic collagen disease with a clear clinical picture.
We can talk about thromboangiitis obliterans only when the ischemic syndrome is combined with other symptoms of collagenosis: fever, progressive course, allergic manifestations, inflammatory reaction blood, arthritis, damage to the skin and mucous membranes, systemic involvement of blood vessels. True, at the stage of advanced obliteration, when trophic changes the leader may be ischemic syndrome, and the signs allergic inflammation recede into the background. However, their presence is mandatory in the anamnestic history. The expressed consideration about the staged course of thromboangiitis is illustrated by a classification that distinguishes three stages:
Allergic stage;
Ischemic stage;
stage of trophoparalytic disorders.
There are 3 forms of vascular damage to the lower extremities in diabetes mellitus, which are pathogenetically related to the underlying disease:

diabetic microangiopathy;
obliterating atherosclerosis;
combination of atherosclerosis with damage to the vessels of the lower extremities.

Obliterating endarteritis can also occur in patients with diabetes. However, as already indicated, this form has no pathogenetic connection with diabetes, and is no more common than in persons without diabetes.
When developing a classification of diabetic angiopathy, in addition to dividing it into two main forms (macro- and microangiopathy), it is advisable to clarify the localization of the vessel lesion, since differentiated therapy, in particular local therapy, depends on this. This applies not only to specific microangiopathies (retino-, nephropathy, etc.), but also to the predominant localization of atherosclerosis of medium and large vessels (cerebral, coronary, etc.).
It is necessary to take into account one more principle of classification of diabetic angiopathy. It's about the stage of development vascular lesions. This question was not raised while the idea of angiopathy as a “late diabetic syndrome”, which crowns long-term diabetes. Indeed, when long term diseases are more often diagnosed vascular disorders, and usually in an advanced organic stage. As research methods improved, changes in blood vessels began to be detected from the first years of the disease and even during the period of latent diabetes and prediabetes. Especially often are functional changes in vessels in the form of changes in diameter, permeability, venous stasis found from the conjunctiva, glomeruli of the kidneys, and lower extremities.
Quality improvement diagnostic studies made it possible to recognize vascular changes before the appearance of complaints and clinical symptoms. Due to the functional (reversible) nature of the initial changes in blood vessels, the therapeutic approach will be different compared to the treatment of advanced organic vascular lesions.
These considerations served as the basis for distinguishing three stages of diabetic angiopathy:
I - preclinical (metabolic),
II - functional,
III - organic.
Patients with stage I (preclinical) diabetic angiopathy have virtually no complaints. On clinical examination pathological changes not detected. However, compared with uncomplicated diabetes, at this stage, according to data biochemical research, a more pronounced increase in the level of ester-bound cholesterol, (3-lipoproteins, total lipids, agglucoproteins, mucoproteins). Changes in the capillaroscopic picture of the nail bed of the toes are reduced to an increase in the number of capillaries, narrowing of the arterial branches, and the appearance of granular blood flow. Promotion vascular tone according to tachooscillography and sphygmography, it is expressed in an increase in average pressure, an increase in the pulse wave velocity (PWV) to 10.5 m/sec and specific peripheral resistance.

At the II (functional) stage of diabetic angiopathy, there are minor and transient clinical manifestations in the form of pain in the legs during long walking, paresthesia, convulsions, a decrease in skin temperature by 2-3°C, a decrease in the oscillatory index and more distinct changes in the capillaries in the form of deformation branches, background turbidity, intermittency of blood flow. In all patients (mainly under 40 years of age), an increase in the tone of arterioles and precapillaries is determined according to the above indicators, including an increase in all types of pressure, elastic modulus, PWV up to 11.5 m/sec. The same applies to biochemical changes.
Stage III is characterized by clinically pronounced lesions of the blood vessels of the legs in the form of intermittent claudication, pain in the feet, trophic disorders of the skin and nails, sharp decline or lack of pulse in the dorsal artery of the foot, a drop in the oscillatory index up to the absence of oscillations. In addition to deformation of the capillaries, their obliteration occurs with the appearance of “bald patches”. According to mechanocardiography, the patency of the precapillary bed is significantly reduced. The speed of propagation of the pulse wave increases above 11.5 m/sec. Basic distinctive feature patients in Stage III Diabetic angiopathy compared to I and II is the irreversible nature of vascular changes, lack of response to functional tests and small dynamics under the influence of treatment. Most patients at this stage are over 40 years old.
Further progression of the vascular process leads to deeper trophic disorders, non-healing trophic ulcers with transition to gangrene.
The initial stages of vascular changes (stages I and II of diabetic angiopathy) are characterized by reversible changes that can appear not only from the first years of diabetes development, but even during the period of latent diabetes and prediabetes. It should also be noted that the thickening of the basement membrane of the capillaries due to impaired metabolism of the vascular wall is initially reversible and can appear in the initial stages of vascular changes.
The detection of vascular lesions from the first years of diabetes and even in persons with prediabetes gives the right to consider angiopathy not as the end of the disease, but as component pathological process, apparently caused by a violation hormonal regulation vascular tone and deep metabolic shifts.
Taking into account all that has been said, it is most figurative to accept the following clinical classification diabetic angiopathy.
Clinical classification of diabetic angiopathy.
According to the location of vascular damage:
1. Microangiopathies:
a) retinopathy,
b) nephropathy,
c) generalized microangiopathy, including microangiopathy of internal organs, muscles and skin,
c) microangiopathy of the lower extremities.

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Diabetic angiopathy- generalized damage to large (macroangiopathy) and small (primarily capillaries - microangiopathy) blood vessels for diabetes mellitus; manifested by damage to the walls of blood vessels in combination with impaired hemostasis

Pathogenesis of diabetic angiopathy. The following pathogenic factors are important in the pathogenesis of diabetic angiopathy: ( 1 ) decreased secretion of endothelial relaxing factor and other factors regulating vascular tone; ( 2 ) increased synthesis of glycosaminoglycans and non-enzymatic glycosylation of proteins, lipids and other components of the vascular wall and, as a result, a violation of the permeability and strength of the vessel wall, the development of immunopathological reactions in it, narrowing of the lumen of blood vessels, reduction in area inner surface vessels; ( 3 ) activation of the polyol pathway of glucose conversion causes the accumulation of sorbitol and fructose in the walls of blood vessels with a change in the osmotic balance in them with the subsequent development of edema, narrowing of the lumen of microvessels and deepening in them dystrophic processes; (4 ) violation fat metabolism promotes activation of lipid peroxidation, which is accompanied by vasospasm; a damaging effect on the vascular endothelium is caused by an increase in the concentration of low and very low density lipoproteins in the blood; ( 5 ) disturbance of nitrogen metabolism with the development of diabetic dysproteinemia (increase in the blood serum relative content of a2-globulins, haptoglobins, C-reactive protein and fibrinogen) against the background of impaired vascular permeability, creates conditions for infiltration of the subendothelial space with coarse proteins; ( 6 ) absolute excess growth hormone, cortisol and catecholamines have a direct vasodilating effect, activate the polyol pathway for glucose utilization, cause persistent vascular spasm, etc.

Pathogenesis of hemostasis disorders with diabetes mellitus. The concentration of vasoactive and thrombogenic derivatives increases in the blood arachidonic acid(prostaglandins and thromboxanes), at the same time the content of substances with antiaggregation and antithrombogenic effects decreases. Hypercatecholaminemia developing in diabetes mellitus is accompanied by stimulation of platelet aggregation, synthesis of thrombin, fibrinogen and other coagulogenic metabolites. Hyperglycemia and dysproteinemia increase the aggregation ability of platelets and erythrocytes. As a result of polyol edema, red blood cells lose the ability to pass through capillaries, the lumen of which is smaller than the diameter of the red blood cells. Inhibition of the secretion of endothelial relaxing factor leads to a decrease in disaggregant activity and an increase in thrombogenic activity of platelets.

Diabetic microangiopathy. Microangiopathy is characterized by a triad of Senaco-Virchow factors: changes in the vascular wall, disorders of the blood coagulation system and slowing of blood flow, which create conditions for microthrombi. These changes, as the disease progresses, are found throughout the entire vascular bed, having a major effect on the kidneys, retina, peripheral nerves, myocardium and skin, leading to the development diabetic nephropathy, retinopathy, neuropathy, cardiopathy, dermatopathy. Most early manifestations diabetic angiopathy are vascular changes in the lower extremities, the frequency of which ranges from 30 to 90%.

A number of authors believe that microangiopathy is not a complication, but is included in the clinical syndrome of diabetes mellitus. In this case, the main or initial form Some authors consider neuropathy to be the manifestation of the disease, which in turn leads to the development of angiopathy. At the same time, W. Kane (1990) believes that neuropathy in diabetes is a consequence of nerve ischemia, that is, the result of damage to the vasa nervorum. In his opinion, damage to small vessels (capillaries, vasa vasorum, vasa nervorum) is characteristic and pathognomic of diabetes. Damage to the autonomic nerves in turn leads to impaired vascular function. Developing in parallel degenerative changes V peripheral nerves, as a result of which complete loss may occur pain sensitivity on the foot and lower leg.

Classification of diabetic microangiopathy(W. Wagner, 1979): Degree (ischemic damage to the lower extremities) 0 – without visual changes in the skin; grade 1 – superficial ulcerations that do not extend to the entire dermis, without signs of inflammation; grade 2 - deeper ulcerations involving adjacent tendons or bone tissue; degree 3 – ulcerative-necrotic process, accompanied by the addition of infection with the development of edema, hyperemia, the occurrence of abscesses, phlegmon, contact osteomyelitis; grade 4 – gangrene of one or more toes or gangrene of the distal foot; grade 5 – gangrene of most or all of the foot.

Diabetic macroangiopathy. Macroangiopathy is the main cause of death in patients with diabetes mellitus. The risk of developing these complications in such patients is 2-3 times higher than that in the general population. Morphologically, diabetic macroangiopathy is a consequence of accelerated atherosclerosis, which in diabetes mellitus has a number of features: multisegmental arterial damage, a more rapid (progressive) course, occurrence in at a young age(both in men and women), poor response to treatment with antithrombotic drugs, etc. Coronary and cerebral arteries, arteries of the lower extremities. Clinical manifestations of such atherosclerosis (ischemic heart disease, cerebrovascular disease, etc.), on the one hand, are not specific complications diabetes mellitus, but on the other hand are often considered as manifestations of diabetic macroangiopathy due to the specificity of the atherosclerotic process in diabetes mellitus. In addition to atherosclerosis, calcification of the tunica media (Mönckeberg sclerosis) and diffuse arteriofibrosis are found in large arteries. These changes are not specific to diabetes, except for ossification of the femoral and tibial arteries, which occurs exclusively in patients with diabetes.

Classification of diabetic macroangiopathy. Stage 1 compensation peripheral circulation: stiffness of movement in the morning, fatigue, feeling of numbness and “chilliness” in the fingers and feet, sweating of the feet; intermittent claudication after 500-1000 m. Stage 2a subcompensations: acute sensitivity to cold, “chilliness” and numbness of the feet, changes in the nail plates (hyperkeratosis), pallor of the skin, hair loss on the legs; sweating, intermittent claudication after 200-500 m. Stage2b subcompensation: intermittent claudication after 50–200 m; regional systolic pressure(RSD) – 75 mm Hg. Art.; ankle-brachial index (ABI) 0.65; regional systolic perfusion pressure deficit (RSPD) 60–65%. Stage 3a decompensation without trophic disorders: RSD – 41 mm Hg. Art., ABI 0.32; DRSPD – 80–90%; pain at rest, especially at night, cramps in the calf muscles; parasthesia in the form of a burning sensation, distinct acrocyanosis when lowering the limb and waxy pallor in a horizontal position; the skin is worn out, dry, peeling, the furrow symptom is pronounced; plantar ischemia was noted; lameness – up to 50 m. Stage 3b decompensation with trophic disorders: constant pain in a limb; hypostatic swelling of the feet and legs, stiffness of the foot joints, signs chronic intoxication, individual necrotic ulcers appear on the fingers and toes, cracks in the heel area and sole. Stage4 gangrene: irreversible large necrotic areas of tissue on the foot and lower leg, gangrene of the fingers and toes, severe intoxication, RSD 29–31 mm Hg. Art.; ABI<0,30; ДРСПД 84–95%.

In patients with diabetes, micro- and macroangiopathies are often combined with changes in the somatic and autonomic nervous systems, and then already in the early functional stages, which are caused by disturbances in the neurohormonal regulation of vascular tone, complaints of vasomotor changes of varying severity (vasoconstriction or vasodilation) appear. The addition of mediocalcinosis or atherosclerosis to vasomotor disorders contributes to impaired elasticity of the vascular wall, reduces the ability of blood vessels to vasodilate during physical activity, which gradually leads to circulatory failure. Vasoconstriction of arteries, arterioles, disturbances in the structure and function of capillaries lead to an increase in total peripheral resistance and, along with neurohormonal factors, lead to the formation of hypertension. In addition, the pressure load on the hypertrophied left ventricle sooner or later causes circulatory failure. Changes in the function of the autonomic nervous system as a result of neuropathy cause serious clinical symptoms and syndromes in patients with diabetes; these are orthostatic hypotension, resting tachycardia, silent myocardial infarction, asymptomatic hypoglycemia, dysregulation of body temperature and others.

Diagnostics. Diagnostics of diabetic angiopathy is carried out in two directions: ( 1 ) research methods aimed at assessing the general condition of the patient; ( 2 ) research methods that assess the degree of damage to the vascular bed of the limb and determine the possibility of performing reconstructive vascular surgery to save the limb (instead of amputation).

(1) Research methods aimed at assessing the general condition of the patient: assessment of the severity of diabetes mellitus, as well as the nature of pathological changes in the heart and kidneys. Outpatient studies: biochemical blood test (blood glucose level; daily glucose profile; urea, creatinine level); electrocardiography (ECG); X-ray of the affected foot in 2 projections; culture from a purulent wound of the foot to determine the microflora and its sensitivity to antibacterial drugs; measurement of blood pressure (BP) in the tibial arteries with determination of the ankle-brachial pressure index (ABI), which is equal to the ratio of systolic pressure in the tibial arteries to that in the brachial artery. In a specialized hospital they perform: biochemical blood test (in addition to the indicators listed above, prothrombin time, fibrinogen level, blood platelets, electrolytes are determined); ECG with stress tests; transesophageal electrical stimulation of the heart (TEC), aimed at identifying hidden coronary insufficiency and determining the reserve of coronary blood supply; duplex scanning of bifurcations of the common carotid arteries (often combined lesions in the absence of clinical manifestations); chest x-ray; X-ray of the affected foot in 2 projections; culture from a foot wound to determine the microflora and its sensitivity to antibacterial drugs.

(2) Research methods assessing the degree of damage to the vascular bed of the limb and determining the possibility of performing reconstructive vascular surgery to save the limb(instead of amputation). Macrohemodynamics are studied by measuring digital blood pressure on the foot; measurement of segmental blood pressure at standard levels of the lower extremities with determination of ABI (in the absence of vascular pathology, the index is equal to one, with obliteration - below 0.7, with critical ischemia its value is 0.5 and below, which requires angiography to determine the area of occlusion and deciding whether angioplasty or luminal angioplasty is necessary); spectral analysis of the Doppler signal from the main arteries throughout the affected limb, including the foot; X-ray contrast angiography with mandatory contrasting of the distal arterial bed of the lower extremities (performed when planning reconstructive vascular intervention, more often in ischemic diabetic foot syndrome).

To assess changes in the microhemodynamics of the lower limb, the following methods are used: determination of transcutaneous oxygen tension on the foot in the first interdigital space with the patient sitting and lying down; laser Doppler flowmetry; computer video capillaroscopy. ( ! ) All studies must be carried out against the background of conservative therapy.

Principles of treatment of diabetic angiopathy: (1 ) normalization of metabolic disorders (primarily carbohydrate metabolism, since hyperglycemia can play a major role in atherogenesis); ( 2 ) monitoring lipid metabolism indicators, especially the levels of triglycerides and LDL (low-density lipoproteins), and if they increase, prescribing lipid-lowering drugs (statins, fibrates, antioxidants); ( 3 ) administration of a metabolic drug (trimetazidine), which activates the oxidation of glucose in the myocardium by inhibiting the oxidation of free fatty acids; ( 4 ) use of antiplatelet agents (acetylsalicylic acid, dipyridamole, Tiklid, heparin, Vazaprostan); ( 5 ) control blood pressure and achieve target blood pressure levels (130/85 mm Hg) to prevent the progression of nephro- and retinopathy, reduce mortality from stroke and myocardial infarction (angiotensin-converting enzyme inhibitors, calcium channel antagonists); ( 6 ) normalization of vegetative homeostasis, which is achieved by inhibiting aldose reductase, increasing the activity of sorbitol dehydrogenase, enhancing antioxidant protection (the use of a-lipoic acid preparations is promising in this regard).