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

is a collective concept that combines atherosclerotic lesions of large arteries in DM, which is clinically manifested by coronary heart disease (CHD), 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	The risk of developing coronary heart disease in DM-2 is 6 times higher than in the streets without DM. Arterial hypertension is detected in 20% of patients with DM-1 and in 75% with DM-2. Obliterating atherosclerosis of peripheral vessels develops in 10%, and thromboembolism of cerebral vessels in 8% of patients with DM
Main clinical manifestations	Similar to those in individuals without DM. In DM, myocardial infarction in 30% of cases is painless
Diagnostics	Similar to those in people without DM
Differential Diagnosis	Other cardiovascular diseases, symptomatic arterial hypertension, secondary dyslipidaemias
	Antihypertensive therapy, correction of dyslipidemia, antiplatelet therapy, screening and treatment of coronary artery disease
	75% of patients with type 2 diabetes and 35% of patients with type 1 die from cardiovascular diseases

Etiology and pathogenesis

Probably similar to the etiology and pathogenesis of atherosclerosis in the streets without DM. Atherosclerotic plaques do not differ in the microscopic structure of streets with and without DM. However, in DM, additional risk factors may come to the fore, or DM exacerbates known non-specific factors. Those with SD should 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; it may be associated with glycosylation of the end products of LDL metabolism and vascular wall collagen.

2. Arterial hypertension(AG). In pathogenesis, great importance is attached to the renal component (diabetic nephropathy). Hypertension in DM-2 is no less significant risk factor for heart attack and stroke than hyperglycemia.

3. Dyslipidemia. Hyperinsulinemia, which is an integral component of insulin resistance in T2DM, causes a decrease in HDL levels, an increase in triglycerides and a decrease in density, i.e. increased atherogenicity of LDL.

4. Obesity, which affects the majority of patients with type 2 diabetes, 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. Violation of 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 an increase in the expression of the 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, at which there is an increase in the expression of fibrinogen and C-reactive protein.

The most significant risk factors for the development of coronary artery disease in DM-2 are elevated LDL, low HDL, arterial hypertension, hyperglycemia and smoking. One of the differences between the atherosclerotic process in DM is the more common and distal nature of the occlusal lesion, i.e. relatively smaller arteries are often involved in the process, which complicates surgical treatment and worsens the prognosis.

Epidemiology

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

Clinical manifestations

Basically do not differ from those streets without SD. In the clinical picture of DM-2, macrovascular complications (myocardial infarction, stroke, occlusive lesion of the vessels of the legs) often come to the fore, and it is during their development that hyperglycemia is often first detected in a patient. Perhaps due to concomitant autonomic neuropathy, up to 30% of myocardial infarctions in streets with diabetes occur without a typical anginal attack (painless infarction).

Diagnostics

The principles of diagnosing complications of atherosclerosis (CHD, cerebrovascular accident, occlusive lesions of leg arteries) do not differ from those for persons without DM. Measurement blood pressure(BP) should be carried out at each visit of a patient with diabetes to a doctor, and the determination of indicators lipid spectrum blood (total cholesterol, triglycerides, LDL, HDL) in 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 80 mmHg. Most patients will need multiple antihypertensive drugs to achieve this goal. The drugs of choice for antihypertensive therapy in diabetes are ACE inhibitors and angiotensin receptor blockers, which, if necessary, are supplemented with thiazide diuretics. Beta-blockers are the drugs of choice for patients with DM who have had myocardial infarction.
Correction of dyslipidemia. The drugs of choice for lipid-lowering therapy are inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase (statins).
antiplatelet therapy. Therapy with aspirin (75-100 mg/day) is indicated for patients with diabetes older than 40 years with an increased risk of developing cardiovascular disease (complicated family history, arterial hypertension, smoking, dyslipidemia, microalbuminuria), as well as for all patients with clinical manifestations of atherosclerosis as secondary prevention.
Screening and treatment of coronary artery disease. Stress tests to exclude coronary artery disease are indicated for patients with symptoms of cardiovascular disease, as well as in the detection of pathology in the ECG.

Forecast

75% of patients with DM-2 and 35% of patients with DM-1 die from cardiovascular diseases. Approximately 50% of patients with type 2 diabetes 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 the detrimental effect of glucose on body tissues, especially nerve fibers and vascular walls. Damage to the vascular network, diabetic angiopathy, is determined in 90% of diabetics already 15 years after the onset of the disease.

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

What is the essence of angiopathy

Angiopathy is an ancient Greek name, literally it is translated as “suffering of the vessels”. 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 is 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 to pass through, molecules smaller than 3 nm, selectively other substances. This process ensures the supply of water and nutrition to the tissues, cleansing them from 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 vascular cells. There are 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 stop working as a barrier. Due to a violation 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 an increased load, and blood pressure rises.

The smallest vessels are most severely damaged, the violation of blood circulation in them leads to a cessation of oxygen and nutrition in the tissues of the body. If in areas with severe angiopathy there is no timely replacement of destroyed capillaries with new ones, these tissues will atrophy. The 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 disrupted up to the complete loss of their functions.

Diabetic angiopathy of large vessels is often accompanied by atherosclerotic processes. Due to a violation of the metabolism of fats, cholesterol plaques are deposited on the walls, the lumen of the vessels narrows.

Disease development factors

Angiopathy develops in patients with type 1 and type 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 the vessels begin. Other factors can only aggravate the course of the disease, but not cause it.

Angiopathy development factors	The mechanism of influence on the disease
Duration of diabetes	The likelihood of angiopathy increases with the experience of diabetes, as changes in the vessels accumulate over time.
Age	The older the patient, the higher the risk of developing diseases of the large vessels. Young diabetics are more likely to suffer from impaired microcirculation in organs.
Vascular pathologies	Concomitant vascular diseases 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 the death of the capillary network.
Excess weight	The heart wears out, the level of cholesterol and triglycerides in the blood rises, the vessels narrow faster, the capillaries located far from the heart are worse supplied with blood.
High blood pressure	Enhances the destruction of the walls of blood vessels.
Smoking	It interferes with the work of antioxidants, reduces the level of oxygen in the blood, increases the risk of atherosclerosis.
Standing work, bed rest.	Both the lack of load and excessive fatigue of the legs accelerate the development of angiopathy in the lower extremities.

What organs are affected in diabetes?

Depending on which vessels are most affected by the influence of sugars in uncompensated diabetes, angiopathy is divided into types:

- is 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 pass a huge amount of blood through them. As a result of the development of angiopathy, renal failure occurs: blood filtration from metabolic products worsens, the body does not completely get rid of toxins, urine is excreted in a small volume, edema forms throughout the body, squeezing the organs. The danger of the disease lies in the absence of symptoms in the initial stages and the complete loss of kidney functionality in the final. 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 influence of diabetes mellitus on small vessels. Circulatory disorders leading to trophic ulcers and gangrene can develop even with minor disturbances in the main arteries. It turns out a paradoxical situation: there is blood in the legs, and the tissues are starving, since the network of capillaries is destroyed and does not have time to recover due to constantly high blood sugar. Angiopathy of the upper extremities is diagnosed in isolated cases, since the human hands work with less load and are located closer to the heart, therefore, the vessels in them are less damaged and recover faster. ICD-10 code - 10.5, 11.5.
- leads to damage to the vessels of the retina. Like nephropathy, it has no symptoms until serious stages of the disease require treatment with expensive drugs and laser retinal surgery. 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, followed by blindness due to scarring at the site of damage. Angiopathy at the initial stage, which can be detected only in the office of an ophthalmologist, is cured on its own with long-term diabetes compensation. H0 code.
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 of the coronary arteries causes oxygen starvation of the tissues of the heart, to which it responds with pressing, squeezing pain. The destruction of capillaries and their subsequent overgrowing with connective tissue impairs the function of the heart muscle, and rhythm disturbances occur.
- violation of the blood supply to the brain, at the beginning manifested by headaches and weakness. The longer 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 destruction is not critical, the body has time to grow new vessels to replace the damaged ones. At the first, preclinical stage, metabolic disorders can only be determined by an increase in blood cholesterol 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 is able to reverse the process and fully restore the functions of the vascular network.

Possible signs:

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

Well-marked 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 development 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 stay in a standing position for a long time with angiopathy of the lower extremities.
High, not amenable to therapy, blood pressure, swelling on the face and body, around the internal organs, intoxication with nephropathy.
Severe loss of vision in retinopathy, fog before the eyes as a result of edema in 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, impaired memory and coordination of movements, a decrease in cognitive abilities in cerebral angiopathy.

Symptoms of vascular lesions in the extremities

Symptom	Cause
Pale, cool feet	Destruction of capillaries, still treatable
Weakness of leg muscles	Insufficient muscle nutrition, the beginning of the development of angiopathy
Redness on the feet, the skin is warm	Inflammation due to an attached infection
No pulse in limb	Significant narrowing of the arteries
Prolonged swelling	Severe vascular injury
Shrinking calves or thigh muscles, stopping hair growth on the legs	Prolonged oxygen starvation
Non-healing wounds	Multiple capillary damage
Black fingertips	Angiopathy of the great vessels
Blue cold skin on limbs	Severe damage, lack of circulation, incipient gangrene.

Diagnosis of the disease

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

Adolescents and the elderly with long-term diabetes develop several angiopathies of different organs, both large and small vessels are damaged. After identifying one type of disease in them, they require a complete examination of the 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 with diabetes mellitus are aggravated. With the help of biochemical blood tests, the so-called lipid status is revealed. An increase in cholesterol indicates a high probability of angiopathy, especially an increase in low-density lipoprotein, a decrease in albumin, 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, while a complication of this variety occurs in diabetics with type 1 or type 2 pathology. If surgical or conservative treatment for diabetic angiopathy is not carried out in time, then serious complications are possible with damage to many organs.

What is the disease?

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

Microangiopathy. It is characterized by damage to the capillaries.
Macroangiopathy. Arterial and venous lesions are 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 well-being worsens and life expectancy is reduced.

The main causes of diabetic angiopathy

The main reason for the development of diabetic angiopathy is a regularly elevated level of sugar in the blood fluid. There are the following reasons leading to the development of diabetic angiopathy:

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

Risk factors

Abuse of alcohol and cigarettes can provoke the development of angiopathy.

Not all diabetics have such a complication, there are risk factors when the likelihood of vascular damage increases:

prolonged course of diabetes;
age category over 50 years;
wrong way of life;
malnutrition, with a predominance of fatty and fried foods;
slowing down metabolic processes;
the presence of excess weight;
excessive consumption of alcohol and cigarettes;
arterial hypertension;
Heart arythmy;
genetic predisposition.

target organs

It is difficult to predict the appearance of diabetic angiopathy. Angiopathy of the lower extremities is more often noted, since they are under heavy load in diabetes. But damage to the 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 show any special signs, and the person may not be aware of the disease. As it progresses, various pathological symptoms appear, which are difficult not to notice. Symptomatic manifestations depend on the type and stage of the 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	Discoloration of the skin, minor ulcerative lesions without inflammatory manifestations
	2	Deepening of ulcers with damage to muscle tissue and bone, the presence of pain
	3	Death of the area with ulcers, redness and swelling at the site of the affected skin, inflammation in bone tissues
	4	Spread of necrosis beyond the ulcerative lesion, the foot is often injured
	5	Complete foot injury followed by amputation
Macroangiopathy	1	Stiffness after sleep, heaviness when walking, increased sweating and frequent freezing of the legs
	2a	Feeling cold in the legs, regardless of the season, numbness of the lower extremities, blanching of the skin
	2b	Signs of stage 2a, but with the addition of lameness, which manifests itself every 50-200 meters
	3a	Painful sensations, especially at night, cramps, burning and peeling of the skin, pallor of the skin with the horizontal position of the legs
	3b	Constant pain, swelling of the lower extremities, ulcerative lesions with tissue death
	4	Spread of necrosis to the entire foot, followed by death of the limb, infectious lesions of the body with fever 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 seek a consultation with an endocrinologist, nephrologist, neurologist, ophthalmologist, cardiologist, gynecologist, angiologist surgeon, podiatrist or other specialists. Diabetics are assigned the following studies:

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;
measurement of blood pressure;
analysis for glycated hemoglobin;
glucose tolerance test.

Treatment of pathology

Preparations

In diabetic angiopathy, complex treatment is required, which involves taking drugs from different groups and following a strict diet and regimen. Before treating the pathology, you should abandon the consumption of alcohol and drugs that negatively affect the blood vessels. Pharmacotherapy of diabetic angiopathy consists in taking the following drugs:

Sugar-reducing:
- "Siofor";
- "Diabeton";
- "Glucophage".
Cholesterol lowering agents:
- "Lovastatin";
- "Simvastatin".
Blood thinners:
- "Trombonet";
- "Ticlopidine";
- "Warfarin";
- "Clexane".
Means 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 about severe pain in diabetic angiopathy, then painkillers are indicated: Ibuprofen, Ketorolac. If a secondary infectious lesion has joined, then antibacterial medicines are indicated: "Ciprinol", "Ceftriaxone".

Diabetic angiopathy- a generalized vascular lesion that spreads 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 for diabetes, then damage to large vessels is equated to early and widespread atherosclerosis.
A characteristic feature of the defeat of small vessels with is the proliferation of the endothelium, thickening of the basement membrane of small capillaries, deposition of glycoprotein PA5-positive substances in the vessel wall. The term "diabetic microangiopathy" has been proposed to refer to a generalized process in small vessels.
Despite the widespread nature of microangiopathies, the vessels of the kidneys, the fundus of the eye, and the lower extremities are affected much more intensively, with typical manifestations in the form of nephropathy, retinopathy, and peripheral microangiopathy.

The term "diabetic microangiopathy" is more successful than all those proposed, as it reflects the two most characteristic features - the relationship with the underlying disease and the localization of the process in small vessels. Other names such as "universal capillaropathy", "disseminated vascular disease", "peripheral angiopathy" have not taken root in history.
When developing the nomenclature, one should proceed from the established fact about the dual vascular damage characteristic of diabetes - about atherosclerosis of medium and large vessels, which develops earlier and is more common in diabetes, and about specific diabetic microangiopathy. In addition, another third form of the lesion is distinguished - arteriolosclerosis, which is clinically diagnosed only with renal localization of the process.
As for thromboangiitis obliterans (endarteritis), this form of pathogenetic connection with diabetes does not have, and it would be erroneous to classify it as a vascular complication of diabetes. Thromboangiitis is no more common in people with diabetes than in people without diabetes. The confusion of the concepts of "obliterating atherosclerosis" and "obliterating thromboangiitis" occurred because the latter term often refers to early and favorably developing forms of obliterating atherosclerosis. At the same time, thromboangiitis itself is an allergic collagen disease with a clear clinical picture.
One can talk about thromboangiitis obliterans only when the ischemic syndrome is combined with other symptoms of collagenosis: fever, progressive course, allergic manifestations, inflammatory reaction of the blood, arthritis, skin and mucous membranes, systemic vascular involvement. True, at the stage of advanced obliteration, with the appearance of trophic changes, ischemic syndrome may be leading, and signs of allergic inflammation recede into the background. However, their anamnestic presence is mandatory. The above 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 damage to the vessels of the lower extremities in diabetes mellitus, which are pathogenetically associated with the underlying disease:

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

Obliterating endarteritis can also occur in patients with diabetes. However, as already mentioned, this form has no pathogenetic connection with diabetes, and is no more common than in people without diabetes.
When developing a classification of diabetic angiopathy, in addition to dividing into two main forms (macro- and microangiopathy), it is advisable to clarify the localization of the vascular 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 diabetic angiopathy classification. We are talking about the stage of development of vascular lesions. This question was not raised while the idea of angiopathy dominated as a "late diabetic syndrome", which is crowned by long-term diabetes. Indeed, with a long course of the disease, vascular disorders are more often diagnosed, and usually in a far advanced organic stage. With the improvement of research methods, changes in the vessels began to be detected from the first years of the disease and even during the period of latent diabetes and prediabetes. Especially often, functional changes in the vessels in the form of a change in diameter, permeability, venous stasis were found on the part of the conjunctiva, glomeruli of the kidneys, and lower extremities.
Improving the quality of diagnostic studies has made it possible to recognize vascular changes before the onset of complaints and clinical symptoms. Due to the functional (reversible) nature of the initial vascular changes, the treatment approach will be different compared to the treatment of advanced organic vascular lesions.
These considerations served as the basis for the allocation of three stages of diabetic angiopathy:
I - preclinical (metabolic),
II - functional,
III - organic.
Patients with I (preclinical) stage of diabetic angiopathy have practically no complaints. Clinical examination revealed no pathological changes. However, compared with uncomplicated diabetes, at this stage, according to biochemical studies, a more pronounced increase in the level of ester-bound cholesterol (3-lipoproteins, total lipids, agglucoproteins, mucoproteins) is found. Changes in the capillaroscopic picture of the nail bed of the toes are reduced to an increase in the number of capillaries, narrowing of arterial branches, and the appearance of granular blood flow. An increase in vascular tone according to tachooscillography and sphygmography is expressed in an increase in mean pressure, an increase in the velocity of propagation of a pulse wave (PWV) up to 10.5 m/s 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 shifts from the side of the capillaries in the form of deformation branches, background turbidity, blood flow discontinuity. In all patients (mainly up to 40 years old), an increase in the tone of arterioles and precapillaries is determined according to the above indicators, including an increase in all types of pressure, elasticity modulus, PWV up to 11.5 m/sec. The same applies to biochemical changes.
Stage III is characterized by clinically pronounced lesions of the vessels of the legs in the form of intermittent claudication, pain in the feet, trophic disorders of the skin and nails, a sharp decrease or absence of a pulse on the dorsal artery of the foot, a drop in the oscillatory index up to the absence of oscillations. In addition to the deformation of the capillaries, their obliteration occurs with the appearance of "bald spots". According to mechanocardiography, the permeability of the precapillary bed is significantly reduced. The speed of propagation of the pulse wave increases above 11.5 m/s. The main distinguishing feature of patients in stage III diabetic angiopathy compared to stage I and II is the irreversible nature of vascular changes, lack of response to functional tests and low dynamics under the influence of treatment. Most patients at this stage are over 40 years of age.
Further progression of the vascular process leads to deeper trophic disorders, non-healing trophic ulcers with the transition to gangrene.
The initial stages of vascular changes (stages I and II of diabetic angiopathy) are characterized by reversible shifts that can appear not only from the first years of diabetes development, but even during latent diabetes and prediabetes. It should also be noted that the thickening of the basement membrane of capillaries due to impaired metabolism of the vascular wall at first is reversible and may 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 an integral part of the pathological process, apparently due to a violation of the hormonal regulation of vascular tone and profound metabolic changes.
In view of the foregoing, it is most figurative to accept the following clinical classification of diabetic angiopathy.
Clinical classification of diabetic angiopathy.
According to the localization of vascular lesions:
1. Microangiopathy:
a) retinopathy
b) nephropathy,
c) generalized microangiopathy, including microangiopathy of internal organs, muscles and skin,
c) microangiopathy of the lower extremities.

... the fate and prognosis, work capacity and quality of life of a patient with diabetes mellitus are determined by cardiovascular disorders.

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

The pathogenesis of diabetic angiopathy. In the pathogenesis of diabetic angiopathy, the following pathogenic factors are important: ( 1 ) decreased secretion of endothelial relaxing factor and other factors that regulate vascular tone; ( 2 ) enhanced 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 the vessels, a decrease in the area of the inner surface of the 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 osmotic balance in them with the subsequent development of edema, narrowing of the lumen of microvessels and deepening of dystrophic processes in them; ( 4 ) violation of fat metabolism contributes to the activation of lipid peroxidation, which is accompanied by vasospasm; a damaging effect on the vascular endothelium has an increase in the blood concentration of low and very low density lipoproteins; ( 5 ) violation of nitrogen metabolism with the development of diabetic dysproteinemia (increase in the blood serum of the 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 ) an absolute excess of somatotropic hormone, cortisol and catecholamines has a direct vasoconstriction effect, activates the polyol pathway for glucose utilization, causes persistent vascular spasm, etc.

The pathogenesis of hemostasis disorders with diabetes. In the blood, the concentration of vasoactive and thrombogenic derivatives of arachidonic acid (prostaglandins and thromboxanes) increases, while the content of substances with antiaggregatory 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, erythrocytes lose their ability to pass through capillaries, the lumen of which is smaller than the diameter of erythrocytes. Inhibition of the secretion of endothelial relaxing factor leads to a decrease in antiplatelet 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 microthrombosis. 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 of diabetic nephropathy, retinopathy, neuropathy, cardiopathy, and dermatopathy. The earliest manifestations of 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. At the same time, some authors consider neuropathy to be the main or initial form of 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. The defeat of the autonomic nerves, in turn, leads to impaired vascular function. In parallel, degenerative changes in the peripheral nerves develop, as a result of which a complete loss of pain sensitivity in the foot and lower leg may occur.

Classification of diabetic microangiopathy(W.Wagner, 1979): Degree (ischemic damage to the lower extremities) 0 - no visual changes in the skin; grade 1 - superficial ulceration, not spreading to the entire dermis, without signs of inflammation; grade 2 - deeper ulceration 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 fingers or gangrene of the distal foot; grade 5 - gangrene of most of the foot or the entire foot.

Diabetic macroangiopathy. Macroangiopathy is the main cause of death in diabetic patients. The risk of developing these complications in such patients is 2-3 times higher than in the general population. Morphologically, diabetic macroangiopathy is a consequence of accelerated atherosclerosis, which in diabetes mellitus has a number of features: multisegmentation of arterial lesions, more rapid (progressive) course, onset at a young age (both in men and women), poor response to treatment with antithrombotic drugs, and others. First of all, the coronary and cerebral arteries, arteries of the lower extremities are affected. Clinical manifestations of such atherosclerosis (IHD, cerebrovascular disease, etc.), on the one hand, are not specific complications of diabetes mellitus, but on the other hand, they are often considered as manifestations of diabetic macroangiopathy due to the specifics of the atherosclerotic process in diabetes mellitus. In addition to atherosclerosis, calcification of the middle lining of the arteries (Menckeberg 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 mellitus.

Classification of diabetic macroangiopathy. Stage 1 compensation of peripheral circulation: stiffness of movements in the morning, fatigue, numbness and “chilliness” in the fingers and feet, sweating of the feet; intermittent claudication after 500-1000 m. Stage 2a subcompensations: acute susceptibility to cold, “chilliness” and numbness of the feet, changes in the nail plates (hyperkeratosis), pallor of the skin, hair loss on the shins; sweating, intermittent lameness 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; deficit of regional systolic perfusion pressure (DRSPD) 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, a distinct acrocyanosis when lowering the limb and waxy pallor in a horizontal position; the skin is emaciated, dryness, peeling, a furrow symptom is expressed; marked plantar ischemia; lameness - up to 50 m. Stage 3b decompensation with trophic disorders: persistent pain in the limbs; hypostatic swelling of the feet and lower legs, stiffness of the joints of the foot, signs of chronic intoxication, individual necrotic ulcers appear on the fingers and feet, cracks in the heel and soles. Stage4 gangrene: irreversible large necrotic areas of tissue on the foot and lower leg, gangrene of the fingers and foot, severe intoxication, RSD 29–31 mm Hg. Art.; PoI<0,30; ДРСПД 84–95%.

In diabetic patients, micro- and macroangiopathies are often combined with changes in the somatic and autonomic nervous systems, and then already at the early functional stages, which are caused by violations of the neurohormonal regulation of vascular tone, there are complaints of vasomotor changes of varying severity (vasoconstriction or vasodilation). Accession to vasomotor disorders of mediocalcinosis or atherosclerosis contributes to the violation of the elasticity of the vascular wall, reduces the ability of blood vessels to vasodilate during exercise, 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. A change in the function of the autonomic nervous system as a result of neuropathy in patients with diabetes mellitus causes the appearance of serious clinical symptoms and syndromes; these are orthostatic hypotension, resting tachycardia, painless myocardial infarction, asymptomatic hypoglycemia, dysregulation of body temperature, and others.

Diagnostics. Diagnosis 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 research: biochemical blood test (blood glucose level; daily profile of glucoseemia; level of urea, creatinine); electrocardiography (ECG); x-ray of the affected foot in 2 projections; sowing from a purulent wound of the foot to determine the microflora and its sensitivity to antibacterial drugs; measurement of blood pressure (BP) on the tibial arteries with the determination of the ankle-brachial pressure index (ABI), which is equal to the ratio of systolic pressure on the tibial arteries to that on the brachial artery. Performed in a specialized hospital: biochemical blood test (in addition to the indicators listed above, determine the prothrombin time, the level of fibrinogen, blood platelets, electrolytes); ECG with stress tests; transesophageal electrical stimulation of the heart (TSES), aimed at detecting latent coronary insufficiency and determining the reserve of coronary blood supply; duplex scanning of bifurcations of the common carotid arteries (often a combined lesion in the absence of clinical manifestations); chest x-ray; x-ray of the affected foot in 2 projections; sowing from a foot wound to determine the microflora and its sensitivity to antibacterial drugs.

(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). Macrohemodynamics is studied by measuring digital blood pressure on the foot; measurement of segmental blood pressure at standard levels of the lower extremities with the 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 site of occlusion and deciding on the need for angioplasty or luminal angioplasty); spectral analysis of the Doppler signal from the main arteries throughout the affected limb, including the foot; radiopaque angiography with obligatory contrasting of the distal arterial bed of the lower extremities (performed when planning a reconstructive vascular intervention, more often with 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 in the patient's sitting and lying position; laser Doppler flowmetry; computer videocapillaroscopy. ( ! ) All studies should 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 one of the main roles in atherogenesis); ( 2 - control of lipid metabolism, especially the levels of triglycerides and LDL (low density lipoprotein), and with their increase, the appointment of lipid-lowering drugs (statins, fibrates, antioxidants); ( 3 - the appointment of a metabolic drug (trimetazidine), which activates the oxidation of glucose in the myocardium by inhibiting the oxidation of free fatty acids; ( 4 ) the use of antiplatelet agents (acetylsalicylic acid, dipyridamole, Ticlid, heparin, Vazaprostan); ( 5 ) control of blood pressure and achievement of target levels of blood pressure (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 autonomic 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).