Acute complications include coma, chronic - microangiopathy, macroangiopathy (MiP and MaP), insulin resistance, neuropathy, nephropathy, immunodeficiencies. For NIDDM, hyperosmolar and hyperlactacidemic coma are more characteristic.

MAP are more common and are manifested by chronic coronary heart disease, impaired cerebral circulation And obliterating atherosclerosis arteries lower extremities. In the pathogenesis of MAP, the accelerated development of atherosclerosis plays a leading role, while in MIP it is hyperglycemia. Mechanisms accelerated development atherosclerosis are multiple - hyperlipoproteinemia, hypertension, hyperglycemia, hyperinsulinism, thrombophilic syndrome.

Pathogenesis of acute complications of diabetes mellitus. Ketoacidotic coma. As diabetes develops, all pathways for the use of excess acetyl-CoA are blocked, with the exception of those that lead to ketosis and cholesterol synthesis, metabolic acidosis, loss of water and electrolytes, hemoconcentration, insufficiency peripheral circulation, arrhythmias, shock. Compensatory metabolic acidosis develops with loss of sodium in the urine and compensatory release of proton cells from the cells, which exacerbates the acidosis. Due to deep hypoxia of the central nervous system, the functions of the pneumotaxic center are replaced by a gasping center, Kussmaul breathing, hyperventilation, hypocapnia, hypobicarbonatemia develop, which deepens acidosis. Due to hypoxia, an excess of lactate accumulates in the brain tissue, which leads to an aggravation of acidosis. Vicious circle acidosis diabetic coma causes an increase in insulin resistance, since insulin in an acidic environment loses its affinity for its receptor. In addition, insulin resistance is associated high level FFA and the release of contrainsular hormones - insulin antagonists (adrenaline, glucocorticoids, glucagon, vasopressin). Diabetic (ketonemic, acidotic) coma conditioned toxic influence ketone bodies and tissue hypoxia on CNS cells, dehydration, acidosis. Enhanced protein catabolism leads to an increase in the content of ammonia and urea, production hyperazotemia, which deepens brain intoxication and hypoxia. Hypoxia of neurons leads to respiratory failure, vascular collapse, decreased muscle tone, and impaired IRR.

Lactic acidosis and hyperlactacidemic coma. They occur quite often (toxic dystrophies, cirrhosis of the liver), with heart failure and other diseases, and often in severe form- with decompensation of NIDDM, which was treated with biguanides - blockers of gluconeogenesis.

In the blood, the level of lactate increases more than 5 mmol / l at a rate of up to 1.5 mmol / l, the pH value arterial blood 7.25 units and less. Lactic acidosis is the result of hypoxia and physical overwork. Clinically characteristic Kussmaul respiration, hypotension, hypothermia, dehydration, acidosis, circulatory collapse, no ketonuria.

Hyperglycemic (hyperosmolar) coma occurs less frequently than ketoacidotic, mainly in patients older than 50 years, more often helpless. It is provoked by dehydration of the body (vomiting, diarrhea, treatment with diuretics, restriction of fluid intake). Ketoacidosis is absent, hyperglycemia may increase over time to high numbers (55 mmol/l or more). The following factors are important in pathogenesis:

· Hyperglycemia 55-200 mmol/l (1000-3600 mg/dl).

Hypernatremia, hyperchloremia (due to hyperaldosteronism in response to dehydration hypovolemia),

· Hyperazotemia (due to urea) due to diuresis limitation.

· Lack of Kussmaul's breath, smell of acetone.

The pathogenesis of chronic complications. Diabetic angiopathies are the main complications of diabetes, disability and death of patients (Scheme 3.1). The concept of "angiopathy" includes microangiopathy (damage to capillaries, venules, arterioles, primarily their basement membrane) and macroangiopathy (damage to large arteries).

During diabetes of any type, combined angiopathy is observed with a predominance in young people of IDDM of the microangiopathy type, in people over 40 years of age and NIDDM of the macroangiopathy type with progressive development of atherosclerosis. Common to MIP of all localizations are capillary aneurysms, thickening of the walls of arterioles, capillaries, venules due to the accumulation of homogeneous or layered substances in the basement membrane, proliferation of the endothelium into the lumen of the vessels (up to complete obliteration), mast cell reaction in the perivascular tissue. For example, IDDM is the main cause of blindness and one of the leading systemic causes HPN.

Microangiopathies

Macroangiopathies

pathogenesis of microangiopathies. In the pathogenesis of angiopathy, firstly, non-enzymatic glycosylation of various extracellular proteins (proteins of the basement membrane of the glomerular apparatus of the kidneys, the lens of the eye, the fluid of the vitreous body of the eye, etc.) is important. Secondly, the enzymatic conversion of glucose into sorbitol and further into fructose within certain cells. The end products of irreversible deep glycosylation have pathogenic effects on connective tissue:

cause cross-linking of collagen in the basement membranes of microvessels and plasma proteins,

Insulin deficiency or its insufficient perception by the cells of the body leads to the development of hyperglycemia (increased sugar concentration). The process of diabetes mellitus is characteristic. The disease is divided into 2 types.

The first of these is called insulin dependent. It manifests itself due to a deficiency of insulin, which is a hormone that transports glucose into cells.

The second type is called non-insulin dependent and occurs due to poor production or perception of the hormone. Each type of disease has its own clinical picture and consequences for the body, but late complications of diabetes are especially dangerous.

Danger for the body of a diabetic is high concentration blood sugar. If it affects the vessels long time, then they become brittle, capillaries are especially damaged. The nutrition of tissues is disturbed and the patient's skin dries up, visual acuity decreases, the work of internal organs is disrupted and worsens nervous innervation. Complications appear mainly due to non-compliance with a healthy lifestyle and insufficient compensation for diabetes. By following all the doctor's recommendations, such complications can be avoided.

Diabetics face late complications after 15 to 20 years of fighting the disease. They wear mostly chronic. The following systems are most susceptible to long-term effects of high sugar levels:

• cardiovascular;
• nervous.

The degree of damage and the severity of manifestations depends on the compensation of diabetes. With her prolonged absence complications of the disease can lead to disability and death of the patient.

Vascular damage

A complication on the vessels is called angiopathy. With diabetes, there are such types of it:

• microangiopathy:
  • retinopathy;
  • nerophpathy.
• macroangiopathy.

Microangiopathy

Microangiopathy is a damage small vessels. Most often, diabetics suffer from retinopathy and nephropathy. In the first case, the vessels of the eye are damaged, and in the second case, the kidneys. Each complication has its own characteristics.

Retinopathy to some extent manifests itself in every person suffering from diabetes.

On late stages in the absence of full compensation for diabetes, it often leads to blindness. A complication arises as a result of narrowing of the vessels of the retina on elevated level blood sugar. The body tries to compensate for the lack of nutrients, which causes protrusion of the capillary walls. Gradually, more and more salts and lipids are deposited in the retina due to impaired blood circulation. Then, instead of them, scars and tissue indurations appear. The final stage is retinal detachment, hemorrhage or glaucoma. Each of the diseases leads to blindness.

Retinopathy appears with a decrease in visual acuity. The diabetic gradually notices a decrease in the field of vision and clouding before the eyes. To prevent the development of complications, it is recommended to go to the optometrist every six months for examination and examination.

Nephropathy is not detected in every diabetic, but the percentage of development is still high (70%). It is a kidney injury caused by vasoconstriction. Gradually nephropathy leads to kidney failure, which is then the main reason lethal outcome with insulin-dependent diabetes. The disease is diagnosed by urinalysis. Pathological changes appear at about 5-10 years of development of diabetes and go through 3 stages of development:

• Microalbuminuria. The clinical picture is mild. IN rare cases an increase in pressure is observed.
• Proteinuria. Excreted with urine a large number of squirrel. Its deficiency contributes to the development of edema in the patient, especially on the face. The pressure often rises.
• Renal failure. Urine is excreted in a much smaller volume. Skin covering the patient dries up and turns pale. Seizures arterial hypertension become more frequent. Against their background, nausea manifests itself up to vomiting.

Macroangiopathy

With macroangiopathy, large blood vessels are damaged. Atherosclerotic plaques gradually begin to form in them, leading to thrombosis. Damage occurs mainly to the following vessels:

• Damage to the vessels of the heart leads to the development of a heart attack and angina pectoris (pain in the heart).
• Macroangiopathy of cerebral vessels leads to the development of strokes and diabetic encephalopathy. The patient has a decrease mental capacity and headaches occur.
• Damage to the vessels of the lower extremities leads to blanching and thinning of the skin on them. If treatment is not done in a timely manner, then due to any scratch, an ulcer can develop, which tends to develop into gangrene due to the weak regenerative abilities of the diabetic organism.
• Violation of blood supply in the abdomen (in the mesenteric vessels) leads to the development of mesenteric thrombosis.

Damage to central and peripheral neural pathways caused by exposure to high concentrations of sugar is called diabetic neuropathy (neuropathy). There are several theories of its origin:

• Polyolmyoinositol version. With hyperglycemia in nerve fibers the level of sugar increases, which leads to the deposition of sorbitol. It belongs to the visually active group of substances. Due to the effect of sorbitol, the activity of sodium-potassium adenosine triphosphatase decreases and axons (neuronal processes) and other structural parts of nerve cells swell.
• Version of endoneural microangiopathy. The destruction of capillaries by a high level of sugar leads to a lack of nutrition of axons, which disrupts metabolic processes in nervous tissues and microbleeds occur.

The clinical picture and treatment of diabetic neuropathy depend on its form:

• Sensory neuropathy is manifested by impaired perception of vibrations. The disease is checked with a tuning fork. The disease is characterized by numbness, pain and weakness of the lower extremities. Sometimes patients feel unsteadiness and strengthening of a clinical picture at night. Gradually, symptoms appear on the upper limbs, as well as in the chest and abdomen. As complications develop, the smallest ones begin to die off. nerve endings which are responsible for the sensation of pain. This manifests itself in the form of a partial cessation of perception pain on the legs or arms. Violation of sensitivity in the development of sensory neuropathy gradually leads to impaired coordination of movements and difficulty walking. Due to poor perception of pain, a diabetic is often injured and does not notice it. Any scratch that gets infected can become a serious problem for him due to poor tissue regeneration.
• Cardiovascular nephropathy is called autonomous. It is characterized by damage vagus nerve, which increases the impact sympathetic department nervous system to the heart muscle. The disease falls through in the form of rapid heartbeat (tachycardia) even at rest. Gradually, the severity of tachycardia decreases due to progressive damage to the sympathetic nervous system.
• Gastrointestinal neuropathy results from a deficiency in cholinergic regulation of gastric function and intestinal tract. A pathological process is manifested various violations associated with the work of the gastrointestinal tract (constipation, diarrhea, reflux esophagitis, atony (decreased tone) of the esophagus, etc.). The patient, against the background of the development of problems with the stomach, increases salivation, and there are problems with the release of bile.
• The urogenital type of neuropathy occurs when the nerves of the sacral plexus are affected. There is a complication of stagnation of urine, a decrease in the tone of the ureters and reflux. Males often have problems with potency, and women with vaginal hydration.

Sometimes there are failures in hormonal regulation. Normal with a decrease in sugar concentration parasympathetic department nervous system sends a signal to release glucagon. Next, the process is controlled humoral regulation. Due to the development of diabetic neuropathy, the first element of the mechanism falls out. The patient's body loses the ability to defend itself against hypoglycemia.

Most forms of neuropathy are characterized by Argyle-Robertson syndrome and Ahidrosis. In the first case we are talking on impaired adaptation of vision in the dark. The patient does not see anything poor lighting. Ahidrosis is the result of malfunctions sweat glands.

diabetic foot syndrome

Damage to nerve fibers and blood vessels leads to the development of diabetic foot syndrome. There is a complication in every 2-3 cases with varying degrees manifestations. The clinical picture depends on the form of the lesion:

• The neuropathic form occurs in 2/3 of all cases of diabetic foot syndrome. The cause of the complication is damage to the nerve pathways. In the area for which they are responsible, the skin thickens and innervation is disturbed. The foot gradually swells and causes discomfort (fever, burning, pain). Any scratch can develop into an ulcer, which has a chance of becoming gangrene. Over time, bones and joints are damaged, leading to accidental fractures.
• The ischemic form is a consequence of malnutrition due to damaged vessels. The temperature of the skin drops and its color becomes pale blue. There are small painful sores on the fingers.

Update: October 2018

Diabetes mellitus is a disease, the essence of which is the violation of all types of metabolic processes, but especially - carbohydrate metabolism. It proceeds chronically, it has not yet been fully cured, but it is quite possible to control it. The disease affects the whole life of a person: he needs to monitor not only his own diet, but also physical activity and hygiene. Any cold, diarrhea or stress often require an urgent consultation with an endocrinologist and correction of treatment. At the same time, it is necessary to constantly monitor that blood glucose is in the range of 4-6.6 mmol / l, and glycosylated hemoglobin is below 8%.

Such a picky attitude to the disease is not given immediately, and many diabetics believe that it is more important to “feel good”. complete person”, allowing only minimal lifestyle restrictions, than “making concessions” to the disease. I would like to note here: a change in life habits (sometimes their radical revision), constant “jokes” of insulin and a “tasteless” diet are better than non-healing ulcers, vision loss or kidney failure, which will still dictate the same conditions for nutrition and drugs, but the person will feel much worse.

Supporting glucose and glycated hemoglobin at normal levels means that you are moving diabetes from the category of a “disease” to the category of a “special lifestyle”. And, having existed even for more than 15 years, such diabetes will not be complicated by a “bouquet” of damage to the skin, nervous system, kidneys and internal organs, and a person will retain the ability to think sensibly, see well, walk briskly and not count every milliliter of excreted urine.

The mechanism of development of complications

In diabetes, glucose, which must penetrate into cells (especially muscle and fat cells, which together make up almost 2/3 of all cells) and provide them with energy, remains in the blood. If it is constantly elevated, without sharp “jumps”, then, being a substance that creates hyperosmolarity (because of this, the fluid leaves the tissues and overflows the vessels), it leads to damage to both the walls of the vessels and the blood-supplying organs. This is how “gradual”, late consequences develop. When insulin begins to be lacking sharply, acute complications develop that require emergency medical care, without which they can end fatally.

In type 1 diabetes, there is little insulin. If this deficiency is not replenished with an analogue of one's own hormone, administered in injections, complications develop quite quickly and shorten a person's life.

In the case of type 2 diabetes, there is own insulin, but the cells that should work with it do not “feel” it well. Here, treatment is carried out with the help of tableted drugs, which should “indicate” the necessary tissues to insulin, as a result of which the metabolism will be normalized for the duration of the action of these drugs. Acute complications are less likely to develop here. It often happens that a person does not know about the presence of diabetes mellitus by known symptoms when you are thirsty or because of the volume of water consumed you have to go to the toilet at night, and when late complications develop.

In type 2 diabetes, human tissues are insensitive only to own insulin. The introduction of the hormone in injections normalizes metabolism. Therefore, if a special diet and hypoglycemic drugs cannot keep blood sugar below 7 mmol / l, remember: it is better to choose the dosage of exogenous (supplying from outside) insulin and constantly inject the drug than to shorten life expectancy and reduce its quality from unnecessary stubbornness. Of course, such treatment should be prescribed by a competent endocrinologist, who needs to first make sure that the diet really does not help, and not just is not followed.

Acute complications

This term refers to conditions that develop as a result of sharp increase or decrease in blood glucose, which must be eliminated in a short time to avoid death. They are conditionally divided into:

1. hypoglycemic (when the sugar level is lowered) to whom;
2. hyperglycemic conditions.

hypoglycemia

This is the most dangerous condition that needs to be identified and eliminated as early as possible, since in the absence enough glucose leads to the death of brain tissue.

Causes of hypoglycemia

Most often, this acute complication develops as a result of:

• overdose of insulin (for example, if insulin units were calculated on a 100-point scale, and injected with a syringe labeled 40 units, that is, the dose turned out to be 2.5 times more) or hypoglycemic tablets;
• if a person forgot or did not want to eat after the introduction of insulin, or there was vomiting after eating;
• there was a pronounced physical activity in a diabetic, including childbirth;
• a diabetic person has taken an alcohol-containing drink;
• the dose of insulin was not adjusted while taking drugs that further reduce blood glucose levels: beta-blockers (Anaprilin, Metoprolol, Corvitol), calcium, lithium, salicylic acid, vitamin B2, fluoroquinolone antibiotics (Levofloxacin) , "Ofloxacin") and tetracycline series.

Hypoglycemia most often occurs in the first trimester of pregnancy, after childbirth, with the development of renal failure as a result of kidney disease, with a combination of diabetes mellitus with adrenal insufficiency or with a hypothyroid state, as a result of an exacerbation chronic hepatitis or hepatosis on the background of diabetes.

People with diabetes, especially type 1, need to clearly know the symptoms of hypoglycemia in order to immediately help themselves by taking a dose of simple and quickly digestible carbohydrates (sweets, sugar, honey). Otherwise, if this is not done while the person is conscious, a violation of consciousness will develop very quickly up to a coma, which needs to be removed in just 20 minutes, until the cerebral cortex dies (it is extremely sensitive to the absence of glucose as an energy substance).

Symptoms of hypoglycemia

Hypoglycemia is very dangerous, so all health workers are taught that in the absence of a glucometer and a person is found in an unconscious state and without witnesses who could tell what the person was sick with, what he could take, the first thing to do is to inject concentrated glucose solution from ampoules into his vein.

Hypoglycemia begins with the appearance of:

• severe weakness;
• dizziness;
• trembling in the hands;
• feelings of hunger;
• cold sweat;
• numbness of the lips;
• skin pallor.

If a decrease in blood glucose occurs at night, a person begins to have nightmares, he cries out, mutters something incomprehensible, shudders. If you do not wake him up and do not let him drink a sweet solution, he will “fall asleep” deeper and deeper, plunging into a coma.

Measuring blood glucose with a glucometer will show that its level is below 3 mmol / l (diabetics with experience begin to feel symptoms even at normal numbers, 4.5-3.8 mmol / l). One stage replaces another quite quickly, so to understand (optimally - with the help of phone call your therapist, endocrinologist or even an ambulance dispatcher) needs 5-10 minutes.

If at this stage you do not drink sweet water, tea, do not eat carbohydrates (sweet fruits do not count, since they contain not glucose, but fructose) in the form of sugar, honey, sweets or glucose, which is sold in a pharmacy in the form of powder or tablets , develops next stage, where it is already more difficult to provide assistance:

• aggression or excessive lethargy;
• crazy statements;
• lack of coordination;
• complaints of double vision, the appearance of "fog" or "flies" before the eyes;
• complaints of a "pounding" heart, when a high frequency is also detected when the pulse is probed.

This stage is very short. Here, relatives can still help by forcing a person to drink a small amount of sweet water. But this can be done only if there is contact with him and the probability that he will swallow the solution is higher than the probability of choking on it. It is precisely because of the possibility of food getting into the "windpipe", with such symptoms that sweets or sugar should not be given, you can only dissolve carbohydrates in a small amount of liquid.

Late symptoms are:

• loss of consciousness;
• convulsions;
• skin pale, cold, covered with sticky sweat.

In this state, only an ambulance team or any health worker who has a first aid kit with 4-5 ampoules of a 40% glucose solution can provide assistance. You need to make injections into a vein, and a maximum of 30 minutes is given to provide such assistance. If you do not have time to perform injections in this interval, or introduce an amount of glucose of 40% insufficient to raise it to the lower norm, there is a chance that in the future the person's personality will be significantly changed: from constant inadequacy and disorientation to a vegetative ("like a plant") state. With complete failure to provide assistance within 2 hours from the development of a coma, the chance of a person dying is very high. The reason for this is energy hunger, which leads to swelling of the brain cells and the appearance of hemorrhages in them.

Treatment of hypoglycemia begins at home or in the place where the person was "caught" by a decrease in glucose. Therapy continues in the ambulance and ends in the intensive care unit of the nearest multidisciplinary (which has an endocrinology department) hospital. It is dangerous to refuse hospitalization, because after suffering hypoglycemia, a person needs both medical supervision and a revision of the dosages of insulin taken.

Prevention of hypoglycemia

If you have diabetes, this does not mean that physical activity is contraindicated for you. Before them, you just need to increase the amount of carbohydrates consumed by 1-2 bread units, the same should be done after training. If you plan to go camping or move furniture, which will take more than 2 hours, you need to reduce the dose of "short" insulin administered by a quarter or even half. In such a situation, you also need to monitor your own blood glucose levels with a glucometer.

A diabetic's dinner should include proteins. These substances are able to transform into glucose, and do it for a long time, providing a night without hypoglycemia.

Alcohol is the enemy of a diabetic. The maximum possible amount to be taken during the day is 50-75 grams.

Hyperglycemic conditions

This includes three types of coma (and previous, precomatous conditions):

1. ketoacidotic;
2. lactic acidotic;
3. hyperosmolar.

All these acute complications occur against the background of an increase in blood glucose levels. They are treated in a hospital, in the intensive care unit and intensive care unit.

Ketoacidosis

This is one of frequent complications type 1 diabetes. Usually develops:

• after a long missed intake of insulin or hypoglycemic pills, which usually happens in the absence of appetite, fever, nausea or vomiting;
• after self-cancellation of the above drugs, which mainly occurs for the same reasons;
• development of acute inflammatory diseases, especially those caused by an infectious agent;
• insufficient dosage of insulin;
• exacerbation of any chronic disease;
• administering insulin or taking hypoglycemic agent expired;
• heart attack;
• stroke;
• injury;
• a state of shock (as a result of fluid loss, blood loss, allergies - anaphylaxis, mass decay of microbes when taking the first doses of an antibiotic);
• sepsis;
• any, especially emergency, operation.

Against the background of a sharp deficiency of insulin, glucose (the main energy substrate) ceases to enter the cells, accumulating in the blood. Cells from this experience "energy hunger", which is stressful for the body. In response to stress, "stress hormones" are massively released into the blood: adrenaline, cortisol, glucagon. They further increase blood glucose levels. The volume of the liquid part of the blood increases. This is due to the fact that osmotically active substance, which is glucose, "pulls" water from cells into the blood.

A significant concentration of glucose still cannot be greatly reduced by the increased blood volume, so the kidneys take on the task of removing this carbohydrate. But they are designed in such a way that electrolytes (sodium, chlorides, potassium, fluorine, calcium) enter the urine along with glucose. They hatch by pulling water towards them. As a result, dehydration occurs in the body, the kidneys and brain begin to suffer from their insufficient blood supply. "Oxygen starvation" gives a signal for the formation of lactic acid, as a result of which the pH of the blood shifts to the acid side.

In parallel, the body needs to provide itself with energy, since, although there is a lot of glucose, it does not reach the cells. Then it activates the breakdown of fat in adipose tissue. " side effect"Supplying cells with energy from fat is the appearance of ketone (acetone) structures in the blood. They further oxidize the pH of the blood, and also have a toxic effect on internal organs:

• on the brain - causing oppression of consciousness;
• on the heart - breaking the rhythm;
• on the gastrointestinal tract, causing indomitable vomiting and abdominal pain resembling appendicitis;
• on breathing, causing

Symptoms of ketoacidosis

Ketoacidosis proceeds in the form of 4 successive stages:

1. Ketosis. There is dryness of the skin and mucous membranes, a strong desire to drink, weakness and drowsiness increase, appetite decreases, and a headache appears. There is a lot of urine.
2. Ketoacidosis. A person “falls asleep on the go”, answers questions inappropriately, the smell of acetone is heard from him in the air. Blood pressure drops, heart rate increases, vomiting appears. The amount of urine decreases.
3. Prekom. A person is quite difficult to wake up, and he often vomits in brown-red masses. In between vomiting, you can notice that the rhythm of breathing has changed: it has become frequent, noisy. A blush appears on the cheeks. Touching the abdomen causes a painful reaction.
4. Coma. Loss of consciousness. The man is pale, his cheeks are rosy, his breathing is noisy, he smells of acetone.

Diagnostics given state is based on the determination of an increased level of glucose in the blood, while sugar is determined in the urine and ketone bodies. The latter can be detected at home with special test strips dipped in urine.

Treatment

The therapy is carried out in the intensive care unit of the hospital and consists in replenishing the deficiency of insulin with a short-acting drug, which is administered continuously, in microdoses, into the vein. The second "whale" of treatment is the return to the person of the liquid that he has lost, in the form of solutions rich in ions, intravenously.

Hyperosmolar coma

It is a consequence of diabetes mellitus in men and women, usually older, suffering from type 2 diabetes. It occurs as a result of the accumulation of glucose and sodium in the blood - substances that cause dehydration of cells and overflow of the vascular bed with fluid "taken" from the tissues.

Hyperosmolar coma occurs due to a combination of dehydration due to vomiting and diarrhea due to intestinal infection, poisoning, acute cholecystitis, pancreatitis, blood loss, taking diuretics. In this case, there should be an insulin deficiency, aggravated by injuries, interventions, hormone intake.

Symptoms

This condition develops gradually - a few days or a couple of tens of days. Initially, the symptoms of diabetes mellitus increase: thirst, increased amount urine, weight loss. Small muscle twitches appear, which gradually increase and turn into convulsions. The stool is broken, nausea and vomiting appear, which is why

In the first day or later, consciousness is disturbed. At first, this is disorientation in space, then hallucinations and delusional ideas. Later, signs develop that are identical to those of a stroke or encephalitis: paralysis, speech disorders, involuntary movements eyes. Gradually, a person becomes more and more “unwaking”, his breathing is frequent and superficial, and he does not smell of acetone.

Treatment

Therapy consists in replenishing the deficiency of insulin, fluid and electrolytes, as well as treating the condition that caused the hyperosmolar complication of diabetes mellitus. It is carried out in the intensive care unit of the hospital.

lactic acidotic coma

This complication most often develops in people with type 2 diabetes, especially in old age (50 years and older). Its cause is an increase in the content of lactic acid (lactate) in the blood. Provoke this state of the disease of cardio-vascular system and lungs, in which chronic oxygen starvation fabrics.

Symptoms

Pathology manifests itself as decompensation of diabetes mellitus:

• increased thirst;
• weakness, fatigue;
• a large amount of excreted urine.

You can suspect lactic acidosis by muscle pain that occurs due to the accumulation of lactic acid in them.

• change of consciousness;
• change in the rhythm of breathing;
• violation of the heart rhythm;
• lowering blood pressure.

In this condition, death can occur due to respiratory arrest or heart failure, so hospitalization should be immediate.

Diagnosis and treatment

Distinguish this species hyperglycemic coma can only be done in a hospital, while simultaneously assisting a person with the introduction of insulin, solutions containing liquid and electrolytes, as well as a verified amount of an alkalizing soda solution and drugs that support cardiac activity.

Late Complications

These consequences also significantly worsen the quality of life, but they do it gradually, developing gradually.

TO chronic complications two large groups pathologies:

1. Vascular lesions various bodies.
2. Damage to the structures of the nervous system.

These complications usually develop 20 or more years after the onset of the disease. They come the earlier, the longer the constantly elevated level of glucose in the blood lasts.

Angiopathy

This is the name of vascular complications, and they are divided into micro- and macroangiopathies. The main role in their development belongs to a high concentration of glucose in the blood.

Microangiopathies

This is the name of the defeat of small vessels (capillaries, arterioles and venules), through which oxygen is exchanged and nutrients. Microangiopathies include retinopathy (damage to the retinal vessels) and nephropathy (damage to the renal vascular network).

retinopathy

This is a complication that is more or less mild degree occurs in all patients with diabetes and leads to visual impairment. Diabetic retinopathy is the most common late effects leads to disability, depriving a person of vision. For every 1 blind person due to other causes, there are 25 blind people due to diabetic vascular disease.

Long-term high concentration of glucose in the vessels of the retina leads to their narrowing. Capillaries try to compensate for this condition, therefore, in some places, saccular protrusions appear, through which the blood tries to exchange the necessary substances with the retina. It turns out this is bad, and the retina suffers from a lack of oxygen. As a result, calcium salts and lipids are deposited in it, and then scars and seals form in their place. If the process has gone far, retinal detachment may occur, ending in blindness. Bleeding in the blood can also lead to blindness. vitreous body or glaucoma.

The disease is manifested by gradually deteriorating vision, a decrease in visual fields (it becomes poorly visible on the sides). Better to reveal it early stages, therefore, it is important to undergo an examination by an ophthalmologist every 6-12 months, an ultrasound of the eyes, and a study of retinal vessels.

Nephropathy

This complication occurs in ¾ of diabetic patients and implies specific kidney damage, which ultimately leads to the development of chronic renal failure. It most often kills people with type 1 diabetes.

The first signs of diabetic kidney damage can be detected in the urine test already 5-10 years after the onset of the disease.

In its development, nephropathy goes through 3 stages:

1. Microalbuminuria. There are almost no subjective sensations, it can only slightly increase arterial pressure. In urine collected within 24 hours by enzyme immunoassay, radioimmunoassay and immunoturbidimetric methods.
2. Proteinuria. At this stage, a large amount of protein is lost in the urine. Deficiency of a protein that previously held fluid in the vessels leads to the release of water into the tissues. This is how edema develops, especially on the face. Also, in 60-80% of people, both “upper” and “lower” pressure increase.
3. Chronic renal failure. The amount of urine decreases, the skin becomes dry and pale, high blood pressure is noted. Often there are episodes of nausea and vomiting, consciousness also suffers, because of which the person becomes less and less oriented and critical.

Macroangiopathies

This is the name of the condition when diabetes mellitus creates conditions in large vessels for the development of atherosclerotic plaques. This affects the vessels that supply blood to the heart (then angina pectoris and myocardial infarction occur), the lower limbs (this leads to gangrene), the brain (this causes the development of encephalopathy and stroke), the abdomen (mesenteric thrombosis develops).

So, diabetic encephalopathy is manifested by progressive weakness and decreased ability to work, mood swings, impaired attention, thinking and memory, squeezing headaches.

Macroangiopathy of the lower extremities is manifested by difficulty in moving the legs in the morning, which then disappears, increased fatigue of the leg muscles, a feeling of cold and excessive sweating. Further, the legs become very cold, numb, the surface of the nails becomes dull, whitish. After this stage, the next one develops, when a person begins to limp because it becomes painful for him to walk. These pains can also occur in calm state. On the legs, the skin turns pale and thinner. Last stage This complication is gangrene of the foot, fingers, lower leg.

With less pronounced disorders of the blood supply to the legs, chronic trophic ulcers appear on them.

Damage to the nervous system

Such a pathology, when areas of the central and peripheral nervous system are affected, is called diabetic neuropathy. This is one of the factors leading to the development of a dangerous complication - diabetic foot, which often leads to amputation of the leg (s).

The occurrence of diabetic neuropathy has no clear explanation. Some scientists believe that elevated glucose levels lead to swelling and damage to nerve fibers, while others believe that nerve terminals suffer from malnutrition due to vascular damage.

Neuropathy can manifest itself in different ways, depending on its type:

• Sensory neuropathy leads to sensory disturbance, a feeling of "goosebumps" or chilliness, mainly in the lower extremities. As it progresses, such symptoms move to the hands (in the area of ​​\u200b\u200bthe “gloves”), chest and abdomen. Due to breach and pain sensitivity a person may not notice injury to the skin, which in diabetes tends to heal poorly and suppurate.
• The cardiovascular form is manifested by a rapid heartbeat at rest, which disrupts the adaptability of the heart to physical activity.
• Gastrointestinal form. The passage of food through the esophagus is disturbed, gastric motility is accelerated or slowed down, which impairs food processing. There is an alternation of diarrhea and constipation.
• The urogenital form occurs when the nerves of the sacral plexus are affected. It is manifested by a violation of the coherence of the ureters and Bladder, deterioration of erection and ejaculation in men, in women - vaginal dryness.
• The skin form is manifested by damage to the sweat glands, as a result of which the integument becomes dry.

Neuropathy is a dangerous complication, because due to a violation of the recognition of signals from your body, a person stops feeling hypoglycemia.

Diabetic foot and hand syndrome

It's a combination of defeat peripheral nerves and vessels of the skin, soft tissues, bones and joints. It develops in 30-80% of diabetics, manifests itself in different ways, depending on the form.

neuropathic form

It develops in 60-70% of cases of diabetic foot, occurs due to damage to peripheral nerves, which cease to normally transmit impulses to the tissues of the foot or hand.

It is manifested by thickening of the skin in areas with increased stress (most often on the sole and between the fingers), the appearance of inflammation there, and then ulcerative defects. The foot becomes swollen and hotter to the touch; the bones and joints of the foot are also affected, causing spontaneous fractures to develop. Not only ulcers, but also fractures are not always accompanied by the appearance of pain due to a violation of pain sensitivity.

Ischemic form

Its cause is a violation of blood flow through large vessels that feed the foot. In this case, the skin of the foot becomes pale or cyanotic, cold to the touch. Ulcers appear on the tips of the fingers and the marginal surface of the heel, which are accompanied by pain.

Late complications specific to different forms of diabetes

How to treat late diabetic sequelae

Treatment of complications of diabetes mellitus is based on the "three pillars":

1. Decrease in glucose levels, bringing and maintaining it at the level physiological norm- not lower than 4.4, but not higher than 7 mmol / l. For this purpose, insulin is used - a short and prolonged action(in case of type 1 diabetes) or hypoglycemic tablets (in case of type 2 disease).
2. Compensation of metabolic processes that have "lost" as a result of a lack of insulin. For this, alpha-lipoic acid preparations are prescribed ("Berlition", "Dialipon"), "vascular" preparations: "Pentoxifylline", "", " A nicotinic acid". In the presence of a high atherogenic index (it is determined by lipid profile analysis), cholesterol-lowering drugs are prescribed: statins, fibrates, or a combination thereof.
3. Treatment of a specific developed complication:
   • With retinopathy, especially in the early stages, laser photocoagulation of the retina is used to prevent vision loss. Vitrectomy can also be performed - removal of the vitreous body.
   • With nephropathy, drugs are prescribed that reduce blood pressure (Lizinopril, Enalapril), a low-salt diet is prescribed, an increase in the amount of carbohydrates is prescribed in the diet to cover energy costs. With the development of chronic renal failure, according to indications, peritoneal or hemodialysis is performed. A kidney transplant may even be performed.
   • Neuropathy requires treatment with B vitamins, which improve nerve-to-muscle conduction. Plus central action muscle relaxants: Gabopentin, Pregabalin, Carbamazepine.
   • At diabetic foot need to treat wounds, take systemic antibiotics, wear special shoes for less trauma to the skin, resort to metered physical activity.

Complications of diabetes mellitus in children

Because in childhood most often it is type 1 disease that develops, in which there is a deficiency of insulin, then the main complications of diabetes mellitus in children are ketoacidosis and hypoglycemia. They appear in the same way as in adults. With hypoglycemia, trembling appears, the body is covered with cold sticky sweat, the child may ask for food.

Sometimes the first symptom by which diabetes is detected is abdominal pain and vomiting, due to which the baby is hospitalized either in an infectious or surgical hospital (the pain is very similar to that of appendicitis). Further, after determining the level of sugar, as well as carrying out some additional tests, the diagnosis of "Diabetes mellitus" is established.

Lactic acidotic and hyperosmolar acute complications are not typical for children, developing extremely rarely.

But there are consequences specific to children:

• chronic insulin deficiency. It develops with an incorrectly selected dose or its unauthorized decrease. It is manifested by a delay in growth, puberty, development, early appearance vascular problems. Treatment: dose revision;
• chronic overdose of insulin. Manifested increased appetite, obesity, early puberty and rapid growth. In the morning, the child feels the symptoms of hypoglycemia (hunger, weakness, sweating, trembling, mood deterioration). Treatment: dose revision.

Late complications, especially macroangiopathy, are more typical for adult type 2 diabetics "with an experience" of 10 years or more, and rarely develop in children.

The development of diabetes mellitus in a child - the risk that at an older age he will develop microangiopathy, damage to the kidneys, heart, early atherosclerotic vascular damage, angina pectoris and chronic renal failure /

How to prevent the development of diabetic consequences

The main prevention of complications of diabetes mellitus is to maintain normal level glucose and glycated hemoglobin in the blood. To do this, you need to take hypoglycemic therapy, selected by a doctor, follow a low-carbohydrate diet, control your own weight, refuse bad habits in the name of quality of life. You also need to remember that blood pressure should not exceed 130/80 mm Hg.

It is important to undergo planned studies: blood tests, urine tests, dopplerography of blood vessels, examination of the fundus, consultations of vascular surgeons, cardiologists and neuropathologists for timely detection complications. Don't give up daily intake aspirin to thin the blood: this is how you can prevent heart attack, thrombosis large vessels or a stroke.

It is also important to give Special attention examining one's own body, especially limbs for early detection and treatment of wounds, cracks and ulcers. To prevent diabetic foot:

• warm your feet not with electrical appliances or hot baths, but with woolen socks;
• wear comfortable shoes;
• do gymnastics for the legs every day;
• process nails with a file;
• after washing, wipe your feet gently with a soft material, moisturize the skin with a fortified cream.

Late complications of diabetes are nonspecific (occur when different types SD), these include:

1. micro- and macroangiopathy (atherosclerosis of large arteries);

2. nephropathy;

3. retinopathy;

4. neuropathy;

The main cause of late complications of diabetes mellitus is hyperglycemia, hyperlipidemia and hypercholesterolemia. They cause damage blood vessels and disruption of the functions of various organs and tissues by glycosylation of proteins, the formation of sorbitol and the activation of atherosclerosis.

During glycosylation of proteins (proteoglycans, collagens, glycoproteins) of basement membranes, their metabolism, ratio and structural organization, there is a thickening of the basal membranes and the development of angiopathy.

Macroangiopathies are manifested in lesions of large and medium-sized vessels of the heart, brain, and lower extremities. Glycosylated proteins of basement membranes and extracellular matrix (collagen and elastin) reduce the elasticity of arteries. Glycosylation in combination with hyperlipidemia of glycosylated drugs and hypercholesterolemia is the cause of atherosclerosis activation.

Microangiopathies are the result of damage to capillaries and small vessels. Manifested in the form of nephro-, neuro- and retinopathy.

Nephropathy develops in about a third of diabetic patients. A sign of the early stages of nephropathy is microalbuminuria (within 30-300 mg/day), which later develops to the classic nephrotic syndrome, characterized by high proteinuria, hypoalbuminemia, and edema.

Retinopathy, the most serious complication of diabetes mellitus and the most common cause blindness, develops in 60-80% of patients with diabetes. In the early stages, basal retinopathy develops, which manifests itself in retinal hemorrhages, retinal vasodilation, and edema. If the changes do not affect yellow spot, loss of vision usually does not occur. In the future, proliferative retinopathy may develop, manifested in the neoplasm of retinal and vitreous vessels. Fragility and high permeability of newly formed vessels determine frequent hemorrhages in the retina or vitreous body. Fibrosis develops at the site of the thrombus, leading to retinal detachment and loss of vision.