Diabetes sugar

Diabetes is a disease caused by absolute or relative insufficiency of insulin and characterized by a gross violation of carbohydrate metabolism with hyperglycemia and glucosuria, as well as other metabolic disorders.

Etiology. Are hereditary predisposition, autoimmune, vascular disorders, obesity, mental and physical trauma, viral infections.

Pathogenesis. With absolute insulin deficiency, the level of insulin in the blood decreases due to a violation of its synthesis or secretions by beta cells of the islets of Langerhans. Relative insulin deficiency may result from a decrease in insulin activity due to its increased binding to protein, increased destruction by liver enzymes, the predominance of hormonal and nonhormonal insulin antagonists (glucagon, adrenal cortex hormones, thyroid, growth hormone, unesterified fatty acids), changes in the sensitivity of insulin-dependent tissues To insulin.

Insulin deficiency leads to a violation of carbohydrate, fat and protein metabolism. The permeability to glucose of cell membranes in fat and muscle tissues decreases, glycogenolysis and gluconeogenesis intensify, hyperglycemia, glucosuria, accompanied by polyuria and polydipsia. The formation decreases and the decomposition of fats increases, which leads to a rise in the blood level of ketone bodies (acetoacetic, beta-oxymethylene and the condensation product of acetoacetic acid-acetone). This causes a shift in the acid-base state towards acidosis, promotes increased excretion of potassium, sodium, magnesium ions in the urine, disrupts the function of the kidneys.

Alkaline blood reserves may decrease to 25 vol. % Of carbon dioxide, the pH of the blood drops to 7.2-7.0. There is a decrease in buffer bases. The increased intake of non-esterified fatty acids into the liver due to lipolysis leads to an increased formation of triglycerides. There is an increased synthesis of cholesterol. The synthesis of protein decreases, including antibodies, which leads to a decrease in resistance to infections. Incomplete protein synthesis is the cause of the development of dysproteinemia (a decrease in the albumin fraction and an increase in alpha globulins). A significant loss of fluid due to polyurine leads to dehydration of the body. The release of potassium, chlorides, nitrogen, phosphorus, calcium from the body is increasing.

Symptoms, course. The accepted classification of diabetes mellitus and related categories of impaired glucose tolerance, proposed by the WHO research group on diabetes mellitus (1985), distinguishes: A. Clinical classes, which include diabetes mellitus (DM); Insulin-dependent diabetes mellitus (IDDM); Insulin-independent diabetes mellitus (NIDDM) in individuals with normal body weight and in obese individuals; Diabetes associated with malnutrition (DOSP); Other types of diabetes associated with certain conditions and syndromes: 1) diseases of the pancreas, 2) diseases of the hormonal nature, 3) states caused by drugs or chemicals, 4) changes in insulin and its receptors, 5) certain genetic syndromes, 6 ) Mixed states; Impaired glucose tolerance (NTG) in individuals with normal body weight and obese streets, impaired glucose tolerance associated with other conditions and syndromes; Diabetes mellitus pregnant.

B. Statistically significant risk classes (individuals with normal glucose tolerance, but with a significantly increased risk of developing diabetes). Preceded violations of glucose tolerance. Potential violations of glucose tolerance.

In clinical practice, the most common are patients with NTG, in which the fasting blood glucose level does not exceed the norm within 24 hours, but when glucose levels are easily assimilated, the level of glycemia exceeds the values ​​typical for healthy individuals and the true diabetes: IDDM type I and NIDDM type II in persons with normal body weight or streets with obesity, characteristic clinical and biochemical symptoms of the disease.

IDDM often develops in young people under the age of 25, has a pronounced clinical symptomatology, often a labile course with a tendency to ketoacidosis and hypoglycemia, in most cases begins acutely, sometimes with the onset of a diabetic coma. The content of insulin and C-peptide in the blood is below normal or not determined.

The main complaints of patients: dry mouth, thirst, polyuria, weight loss, weakness, decreased ability to work, increased appetite, pruritus and itching in the perineum, pyoderma, furunculosis. Often observed headache, sleep disturbance, irritability, pain in the heart, in the calf muscles. In connection with the reduction of resistance in patients with diabetes often develops tuberculosis, inflammatory diseases of the kidneys and urinary tract (pyelitis, pyelonephritis). In the blood there is an increased level of glucose, in the urine - glucosuria.

NIDDM type II usually develops maturely often in individuals with overweight, characterized by a calm, slow onset. The level of insulin and C-peptide in the blood is normal or may exceed it. In some cases, DM is diagnosed only with the development of complications or with an accidental examination. Compensation is achieved mainly by diet or oral hypoglycemic drugs, without ketosis.

Depending on the level of glycemia, sensitivity to therapeutic effects and the presence or absence of complications, three degrees of severity of diabetes are distinguished. "Mild cases include cases when the compensation is achieved by diet, ketoacidosis is absent.It is possible to have grade 1 retinopathy.It is usually a patient with type 2. 2. With an average degree, compensation is achieved by combining diet and oral hypoglycemic drugs or by administering insulin at a dose of no more than 60 U / Day, the fasting blood glucose level does not exceed 12 mmol / l, there is a tendency to ketoacidosis, there may be mildly pronounced phenomena of microangiopathy.Heavy degree of DM is characterized by a labile course (pronounced fluctuations in blood sugar level during the day, hypoglycemia, ketoacidosis), sugar level Fasting blood exceeds 12.2 mmol / l, the insulin dose necessary for compensation exceeds 60 units / day, there are severe complications: grade III-IV retinopathy, kidney failure, peripheral neuropathy, disability.

Complications of diabetes mellitus. Vascular complications are typical: specific lesions of small vessels-microangiopathy (angioretinopathy, nephropathy and other visceropathies), neuropathy, angiopathy of the vessels of the skin, muscles and accelerated development of atherosclerotic changes in large vessels (aorta, coronary cerebral arteries, etc.). The leading role in the development of microangiopathies is played by metabolic and autoimmune disorders.

The defeat of the retina vessels (diabetic retinopathy) is characterized by dilatation of retinal veins, the formation of capillary microaneurysms, exudation and point bleeding into the retina (stage I, non-proliferative); Expressed by venous changes, capillary thrombosis, marked exudation and hemorrhages in the retina (stage II, pre-proliferative); At stage III - proliferative - there are the above changes, as well as progressive neovascularization and proliferation, which are the main threat to vision and leading to retinal detachment, optic nerve atrophy. Often other patients with diabetes have other eye injuries: blepharitis, refractive disorders and accommodation, cataracts, glaucoma.

Although kidneys are often infected with diabetes, the main cause of impairment is the microvascular pathway, manifested by glomerulosclerosis and sclerosis of afferent arterioles (diabetic nephropathy).

The first sign of diabetic glomerulosclerosis is transient albuminuria, in the future - microhematuria and cylindruria. Progression of diffuse and nodular glomerulosclerosis is accompanied by an increase in blood pressure, isohypostenuria, leads to the development of uremic state. Three stages are distinguished during glomerulosclerosis: in the prenaphrotic stage there are moderate albuminuria, dysproteinemia; In nephrotic-albuminuria increases, there are microhematuria and cylindruria, edema, increased blood pressure; In the nephrosclerotic stage, the symptoms of chronic renal failure appear and grow. Often there is a discrepancy between the level of glycemia and glucosuria. In the terminal stage of glomerulosclerosis, the blood sugar level may drop sharply.

Diabetic neuropathy is a frequent complication with a long-term current diabetes; Both the central and peripheral nervous system are affected. The most characteristic is peripheral neuropathy: patients are disturbed by numbness, a feeling of crawling, cramps in the limbs, pain in the legs, worse at rest, at night and diminishing when walking. There is a decrease or a complete absence of knee and Achilles reflexes, a decrease in tactile, pain sensitivity. Sometimes muscle atrophy develops in the proximal parts of the legs. There are disorders of the bladder, men are violated potency.

Diabetic ketoacidosis develops as a result of severe insulin deficiency with improper treatment of diabetes, violation of diet, attachment of infection, mental and physical trauma or serves as the initial manifestation of the disease. It is characterized by increased formation of ketone bodies in the liver and an increase in their content in the blood, a decrease in alkaline blood reserves; An increase in glucosuria is accompanied by increased diuresis, which causes dehydration of cells, increased excretion in the urine of electrolytes; Hemodynamic disorders develop.

The diabetic (ketoacidotic) coma develops gradually. Diabetic precoma is characterized by the symptoms of rapidly progressing decompensation of diabetes: severe thirst, polyuria, weakness, lethargy, drowsiness, headache, lack of appetite, nausea, acetone odor in the exhaled air, dry skin, hypotension, tachycardia. Hyperglycemia exceeds 16.5 mmol / L, the reaction

Urine per acetone positive, high glucosuria. If timely assistance is not provided, a diabetic coma develops: confusion and then loss of consciousness, multiple vomiting, deep noisy breathing such as Kussmaupia, severe vascular hypotension, hypotension of eyeballs, dehydration symptoms, oliguria, anuria, hyperglycemia exceeding 16.55-19, 42 mmol / l and sometimes reaching 33.3 - 55.5 mmol / l, ketonemia, hypokalemia, hyponatremia, lipemia, increased residual nitrogen, neutrophilic leukocytosis.

With hyperosmolar non-ketone diabetic coma, there is no acetone odor in the exhaled air, there is pronounced hyperglycemia - more than 33.3 mmol / L at normal ketone levels in the blood, hyperchloremia, hypernatremia, azotemia, increased blood osmolarity (effective plasma osmolarity above 325 mosm / L) , High hematocrit.

Lactacidotic (lactic) coma occurs usually against a background of renal insufficiency and hypoxia, most often occurs in patients receiving biguanides, in particular, phenformin. In the blood there is a high content of lactic acid, an increase in the lactate / pyruvate ratio, acidosis.

Diagnosis of diabetes mellitus. The diagnosis is based on: 1) the presence of classical symptoms of diabetes: polyuria, polydipsia, ketonuria, weight loss, hyperglycemia; 2) an increase in the fasting glucose level (with repeated determinations) of not less than 6.7 mmol / l or 3) fasting glycemia less than 6.7 mmol / L, but with high glycemia during the day or against glucose tolerance test (more than 11, 1 mmol / L).

In unclear cases, as well as for detecting a violation of glucose tolerance, a glucose load test is performed, the fasting glucose in the blood is examined after ingestion of 75 g of glucose dissolved in 250-300 ml of water. Blood from the finger to determine the glucose content is taken every 30 minutes for 2 hours.

In healthy people with a normal glucose tolerance, fasting glycemia is less than 5.6 mmol / L, between 30th in the 90th minute of the test - less than 11.1 mmol / l, and 120 minutes after taking glucose, glycemia is less than 7.8 mmol / L.

Impaired glucose tolerance is fixed if fasting glycemia is less than 6.7 mmol / L, between 30 and 90 minutes corresponds to or less than 11.1 mmol / L and after 2 hours fluctuates between 7.8 and 11.1 mmol / L.

Treatment. They use dietotherapy, oral hypoglycemic drugs and insulin, and exercise therapy. The purpose of therapeutic measures is the normalization of disturbed metabolic processes and body weight, the preservation or restoration of the working capacity of patients, the prevention or treatment of vascular complications.

Diet is mandatory in all clinical forms of diabetes. Its main principles: individual selection of daily calories; The content of physiological quantities of proteins, fats, carbohydrates and vitamins; Elimination of easily assimilated carbohydrates; Fractional food with a uniform distribution of calories and carbohydrates.

The calculation of the daily caloric value is made taking into account the body weight and physical load. With moderate physical activity, the diet is built at the rate of 30-35 kcal per 1 kg of ideal body weight (growth in centimeters minus 100). With obesity, calorie content is reduced to 20-25 kcal per 1 kg of ideal body weight.

The ratio of proteins, fats and carbohydrates in food should be close to physiological: 15-20% of the total number of calories account for proteins, 25-30% for fats and 50-60% for carbohydrates. The diet should contain not less than 1-1.5 g of protein per 1 kg of body weight, 4.5-5 g of carbohydrates and 0.75-1.5 g of fat per day. One should adhere to the tactics of limiting or completely eliminating refined carbohydrates from food. However, the total amount of carbohydrates should be at least 125 g per day in order to prevent ketoacidosis. The diet should contain a small amount of cholesterol and saturated fats: of the total amount of fats about 2/3 should be accounted for mono- and polyunsaturated fatty acids (sunflower, olive, corn, cottonseed oil). Food is taken fractionally 4-5 times a day, which contributes to its better absorption with minimal hyperglycemia and glucosuria. The total amount of food consumed during the day is usually distributed as follows; The first breakfast is 25%, the second breakfast is 10-15%, lunch is 25%, lunch is 5-10%, dinner is 25%, the second dinner is 5-10%. A set of products is made according to the corresponding tables. It is advisable to include in the diet foods rich in dietary fiber. The content of table salt in food should not exceed 10 g / day due to the tendency of patients to hypertension, vascular and renal lesions.

Dosage is shown to be adequate daily exercise, which increases the utilization of glucose by tissues.

In the form of an independent method of treatment, dietotherapy is used in violation of tolerance to carbohydrates and mild form of NIDDM. Indication of compensation for diabetes is the glycemia during the day 3,85-8,9 mmol / l and the absence of glucosuria.

Tableted hypoglycemic drugs are referred to the two main groups: sulfonamides and biguanides.

Sulfanilamide preparations are derivatives of sulfanylurea. Their hypoglycemic effect is caused by the stimulating effect on the beta cells of the pancreas, by increasing insulin sensitivity of insulin-dependent tissues by affecting the receptors for insulin, by increasing the synthesis and accumulation of glycogen, and by reducing gluconeogenesis. The drugs also have anti-lipolytic effects.

There are sulfanilamide preparations I and II generation.

Preparations of I generation are dosed in decigrams. This group includes chlorpropamide (diabinez, mellanez), bucarban (nadizan, oranyl), oradian, butadamide (tolbutamide, orabet, diabetol), etc. The preparations dosed in hundredths and thousandths of a gram (II generation) include glibenclamide (manilil , Daonil, euglucan), glenororm (glycidone), gliclazide (diamicron, predian, diabeton), glipizide (minidiab).

When using drugs I generation, treatment starts with small doses (0.5-1 g), increasing to 1.5-2 g / day. Further increase in dose is not appropriate. Gipoglikemiziruyuschee effect is manifested on the 3-5th day from the start of treatment, the optimal - after 10-14 days. The dose of preparations of II generation usually should not exceed 10-15 mg. It should be borne in mind that almost all sulfanilamide preparations are excreted by the kidneys, with the exception of the gljurenorm, which is excreted from the body mainly by the intestine, so the latter is well tolerated by patients with kidney damage. Some drugs, such as predian (diamicron), have a normalizing effect on the rheological properties of blood - reduce the aggregation of platelets.

Indications for the prescription of sulfanylurea are NIDDM of moderate severity, as well as the transition of a mild form of diabetes to a moderate one, when one diet is not enough to compensate. With type II diabetes of moderate severity, sulfanylurea preparations can be used in combination with biguanides; In severe and insulin resistant forms of type 1 diabetes, they can be used with insulin.

Combined treatment with insulin and sulfonamides is performed in a number of cases with small surgeries, with infection, with kidney and liver damage without pronounced impairment of their function.

Side effects with the use of sulfonamide drugs are rare and are expressed by leukopenia and thrombocytopenia, skin, allergic reactions, impaired liver function and gastrointestinal disorders. Overdose may cause hypoglycemia.

The criterion of compensation for prescribing sulfanilamide preparations is normal blood sugar level on an empty stomach and its fluctuations during the day, not exceeding 8.9 mmol / l, absence of glucosuria. In patients with severe concomitant lesions of the cardiovascular system that do not sense the initial signs of hypoglycemia, in order to avoid possible hypoglycemia, an increase in the blood sugar level during the day up to 10 mmol / l, glucosuria no more than 5-10 g.

In outpatient settings, compensation is assessed on the basis of determining the fasting blood sugar level and 1-2 hours after breakfast. At the same time, 3-4 servings of 24-hour urine are collected.

Biguanides are derivatives of guanidine. These include phenylethylbiguanides (phenformin, dibotin), butylbiguanides (adebit, buformin, silubin) and dimethyl biguanides (glucophag, diformin, metformin). Distinguish the drugs, the effect of which lasts 6-8 hours, and preparations prolonged (10-12 h) action. Hypoglycemizing effect is caused by potentiating the influence of insulin, increasing the permeability of cell membranes for glucose in muscles, inhibiting neoglucogenesis, reducing the absorption of glucose in the intestine. An important property of biguanides is the inhibition of lipogenesis and the enhancement of lipolysis.

Indication for the use of biguanides is NIDDM (type II) of medium severity without ketoacidosis and in the absence of liver and kidney diseases. The drugs are prescribed mainly by patients with excessive body weight, with resistance to sulfonamides, used in combination with insulin, especially in patients with excessive body weight. Combination therapy with biguanides and sulfonamides is also used, which allows obtaining the maximum sugar reduction effect with minimal doses of preparations.

Adverse events: violations of the function of the gastrointestinal tract (sensation of metallic taste in the mouth, nausea, vomiting, diarrhea) and liver, allergic reactions in the form of skin rashes. When using large doses, with a tendency to ptpoksii, the presence of heart failure, a violation of the liver and kidneys can develop a toxic reaction in the form of an increase in the content of lactic acid (lactate-tacidosis). The least toxic are metformin, diformin and gliobmenin.

General contraindications to the appointment of oral hypoglycemic agents: ketoacidosis, ketoacidotic, hyperosmolar, lactacidotic coma, pregnancy, lactation, extensive operations, severe injuries, infections, marked renal and hepatic impairment, blood diseases with leukopenia or thrombocytopenia. Insulin therapy is prescribed for the following indications: type 1 diabetes, ketoacidosis of varying severity, ketoacidotic, hyperosmolar, lactic acid coma, depleted patient, severe forms of diabetes with complications, infections, surgical interventions; Pregnancy, childbirth, lactation (for any form and severity of diabetes), the presence of contraindications to the use of oral hypoglycemic drugs.

The main criterion determining the dose of insulin is the blood glucose level. Apply drugs, different in the duration of the action. Short-acting insulin preparations (simple insulin) are necessary for the rapid elimination of acute metabolic disorders (especially in the state of precoma and coma), as well as in acute complications caused by infection and trauma. Simple insulin is applicable for any form of diabetes, but the short-term action (5-6 hours) makes it necessary to introduce it up to 3-5 times a day.

With decompensation of diabetes, simple insulin is administered 4-5 times a day. The use of the drug can also determine the true need for insulin. With constant treatment, simple insulin is used together with long-acting drugs. In addition to insulin obtained from the pancreas of cattle, pig insulin (suinsulin), actrapid (Denmark) is also used.

Among prolonged drugs of insulin are distinguished medium duration and long-term action.

Medium-duration drugs include a suspension of zinc-insulin amorphous (ICS-A); The effect is manifested in 1-1.5 hours, maximum after 4-6 hours, the duration of the action is 12-16 hours. By the action of ICS-A it is close to the foreign preparation Insulinum semilente, insulin B (GDR). The onset of action 1-2 hours after the introduction, a maximum - after A-6 hours, the duration of the action is 10-18 hours.

Long-acting insulin preparations: protamine zinc-insulin (PDH); The onset of action after 6-8 hours, maximum after 14-18 hours, duration of action 20-24 hours (with the appointment of PDP, additional introduction of simple insulin in the morning to reduce hyperglycemia in the afternoon hours); Insulin-protamine suspension (SIP), the onset of action after 60-90 min, maximum after 8-12 h, duration of action 20-24 h; Suspension of zinc-insulin crystalline (ICS-C. Insulinum ultralente) - the onset of action in 6-8 hours, maximum after 12-18 hours, duration of action 30 hours; Insulin-zinc suspension (ICS, Insulinum 1e-te) - a mixture of 30% ICS-A and 70% ICS-K; The onset of action after 60-90 minutes, maximum after 5-7 and 10-14 hours, duration of action - 18-24 hours.

In recent years, the production of purified, deprived high-molecular-weight protein impurities of monopic or monocompetent insulins of short, medium duration and long-term action has been started. This: M-insulin, which has the same beginning, maximum and duration of action, as well as su-insulin. Suspensions of insulin semilong, long and ultralong according to the parameters of hypoglycemizing action correspond to the insulin of the ICS group (respectively, ICS-A, ICS and ICS-K). These insulin preparations have less allergenic properties, so it is much less likely to cause allergic reactions, as well as lipoatrophy. The corresponding foreign preparations are actrapid-MS, monotard-MS, rerpard-MS, protafan-MS, tape-MS, semilente-MS, ultralente-MS. Production of human insulin preparations (actrapid-CM, protopan-NM, monotard-NM) has been set up abroad. These drugs are preferable to prescribe only if type I diabetes is diagnosed, especially in childhood and adolescence, with allergy to insulin, lipodystrophy, pregnancy.

It is very difficult to calculate the need for exogenous insulin because of different individual responses and insulin sensitivity in different periods of the disease. To determine the need for insulin and receive compensation, insulin is administered short-term 4-5 times a day, upon reaching compensation, patients are transferred to a 2-time injection of insulin of medium duration or long-acting in combination with short-acting insulin. For example, the introduction of insulin of average duration of action and simple insulin before breakfast and dinner or before breakfast - medium duration and short action, before dinner - short and long-term sleep; There may be other options. Applying such modes of insulin administration, it is possible to correlate the "secretion peaks" of insulin with periods of post-glucocortic hyperglycemia and, thus, to simulate to a certain degree the secretion of insulin in the norm. Criteria for compensation of type I diabetes mellitus: glycemia should not exceed 11 mmol / l during the day. It is also necessary to take into account the absence of hypoglycemia, signs of decompensation, the patient's ability to work, the duration of the disease, the presence of cardiovascular disorders. Therefore, in each specific case, an individual approach is required for compensation criteria.

The overestimation of insulin doses, the desire to achieve normoglycemia and aglucosuria, especially with the use of a single injection of insulin daily activity, may lead to the development of a chronic overdose of insulin syndrome in the patient (Somoji syndrome). Evening and night hypoglycemia (the maximum effect of insulin daily activity) causes reactive hyperglycemia, which is recorded in the determination of fasting glycemia. This may prompt the doctor to increase the dose of insulin and lead to even more pronounced fluctuations in blood glucose (t. C., To increase lability in the course of the disease).

Diagnosis of the syndrome of chronic overdose of insulin is based on an analysis of the patient's well-being and fluctuations in glycemia and glucosuria during the day. In these cases, it is necessary to gradually reduce the dose of insulin: the patient is transferred to a 4-5-dose short-acting insulin injection, and then to a 2-time insulin administration of short and medium duration of action.

When treating insulin preparations, hypoglycemia-a condition caused by a sharp decrease in blood glucose levels may develop. Provocative moments are: violation of diet and diet, insulin overdose, severe physical stress. Symptoms: severe weakness, sweating, hunger, excitement, trembling of hands, dizziness, unmotivated actions. If you do not give the patient easy digestible carbohydrates, then convulsions arise, consciousness is lost - hypoglycemic coma develops.

Especially dangerous are hypoglycemia in elderly and senile patients due to the possibility of developing myocardial ischemia and cerebral circulation disorders.

Frequent hypoglycemia contributes to the progression of vascular complications. Severe and prolonged hypoglycemia can lead to irreversible degenerative changes in vCTS.

Another complication of insulin therapy is, - allergic reactions: local (redness, condensation and itching of the skin at the site of insulin administration) or general, which is manifested by weakness, skin rash (urticaria), generalized itching, fever, anaphylactic shock can rarely develop.

Insulin resistance is a great need for insulin to achieve compensation. It is believed that the dose of insulin in patients with diabetes should be about 0.6-0.8 U / kg. Insulin resistance in most cases develops as a result of the action of nonhormonal and hormonal insulin antagonists. There are 3 degrees of insulin resistance: light (the daily need for insulin is not more than 80-120 units), medium gravity (daily requirement 120-200 ED) and heavy (daily requirement of more than 200 units of insulin).

Insulin injection sites can develop lipodystrophy (hypertrophic or atrophic). The basis is the immune processes, leading to the destruction of subcutaneous tissue. Their development does not depend on the dose of insulin administered, compensation or decompensation of diabetes. Insulin swelling is a rare complication and is observed in the decompensation of diabetes mellitus.

Treatment of complications of diabetes mellitus. In case of ketoacidosis, a simple insulin (individual dosage) is prescribed, in the diet they limit fats (up to 20-30 g), increase the amount of easily assimilated carbohydrates (300-400 g / day or more), prescribe vitamins C, group B, cocarboxypase, alkaline Drink, xylitol. With the precomatous state, urgent hospitalization is needed, the insulin preparations of prolonged action are abolished, fractions of simple insulin are injected (in 4-5 injections). The initial dose usually does not exceed 20 units, subsequent injections are dosed taking into account the dynamics of the clinical picture and the level of glycemia. Recommended alkaline drink, xylitol.

Simultaneously with the introduction of the first dose of insulin, a dropping of an isotonic solution of sodium chloride (1.5-2 L for 2-3 hours) begins.

Treatment of ketoacidotic coma is carried out in a hospital. The measures are aimed at compensating carbohydrate, fat, protein, water-electrolyte metabolism and preventing secondary complications. At present, the method of treatment with small doses of insulin administered intravenously, a regime of small doses of insulin, has been recognized. This provides a high stable level of insulin in the blood, reduces its amount necessary for arresting the coma, promotes a smooth decrease in glycemia, a faster elimination of ketosis, reduces the possibility of developing hypoglycemia. The initial dose depends on the severity of the condition, the level of glycemia, the severity of ketoacidosis.

Intravenously injected pig or regular insulin in a dose of 8-12 units at a time. With glycemia exceeding 33.3 mmol / l, the dose of insulin can be increased to 12-16 units. The dose of subsequent administration depends on the level of glucose in the blood, which is determined every 1-2 hours.

If the blood glucose in the first 2-4 hours did not decrease by 30%, then the initial dose is doubled. With a decrease in the sugar level, up to half the initial dose of insulin administered is also reduced by half.

With clinical improvement, lowering of hyperglycemia and ketonemia, restoration of hemodynamics, kidney function, CNS, insulin is injected SC every 3-6 hours.

Introduce intravenously an isotonic solution of sodium chloride (up to 3-5 liters / day). With a rapid decrease in glycemia approximately 5 to 4 hours after the onset of insulin therapy, a 5% solution of glucose is administered. To improve the oxidative processes, 5% solution of ascorbic acid, cocarboxylase, is added to the infusion composition. Conduct oxygen therapy.

To correct electrolyte shifts, a 10% solution of potassium chloride (3-6 g / day) is added to the dropper, administered 4-6 hours after the patient begins to leave the coma, under the control of serum potassium, excretory function of the kidneys and Monitor ECG surveillance. In hyperlactacidemic coma, sodium bicarbonate is administered to eliminate acidosis. According to the testimony-strobathine (korglikon), kordiamin, mezaton, antibiotics. After restoration of consciousness for 3-4 days continue the fractional introduction of insulin and gradually expand the diet. Subsequently they are transferred to treatment with insulin preparations with prolonged action (better than the average duration of action and 2 injections).

The main principle of treatment of microangiopathy is complete compensation of metabolic disorders, achieved by adequate diet and insulin therapy (or oral hypoglycemic agents). Use angioprotectors (dicinone, doxium, trental, divascan, parmidin), anabolic hormones (methandrostenopon, retabolil, silabolin), drugs that lower the cholesterol and lipoprotein content in the blood (clofibrate, miscilon), nicotinic acid preparations (nicospan, nigexin, komplin), Vitamins (ascorutin, vitamins of group B, retinol).

For the treatment of retinopathy, coagulation is used with the help of a laser, for the treatment of uncomplicated neuropathy - physiotherapy methods (inductothermy, electrophoresis, etc.). For elimination of hypoglycemia, inwardly assimilated carbohydrates or IV / 40% glucose solution (20-100 ml), adrenaline, glucagon (IM) are administered orally. To eliminate allergic reactions using the method of rapid desensitization, inject drugs of another type of insulin or more purified insulin preparations (monocomponent, monopic).

With insulin resistance apply purified insulin preparations, corticosteroids (20-40 mg) with a gradual dose reduction, combined treatment - insulin and oral hypoglycemic agents. In the presence of lipodystrophy, pork insulin is recommended, electrophoresis with lidase is recommended.

Of great importance in the treatment of diabetes is the training of patients with self-monitoring methods, peculiarities of hygiene procedures, as this is the basis for maintaining compensation for diabetes, preventing complications and retaining work capacity.