Correction of hyperglycemia in acute disorders of cerebral circulation. Transient hypoglycemia of newborns: etiology, diagnostic criteria, prevention and correction tactics in the early neonatal period What can you do

Encephalopathies of varying severity are common in dogs, but rare in cats. Problems arise from a disruption in the conversion of intestinal ammonia to urea in the liver, so that ammonia remains in the bloodstream and in the central nervous system, resulting in decreased levels of excitatory neurotransmitters and increased levels of inhibitory neurotransmitters. Absorbable mercaptans and volatile fatty acids produced by bacteria in the intestine are also implicated in encephalopathy.

If hepatic coma develops, treatment should be started immediately to reduce the level of ammonia in the blood. It includes a break in feeding, emptying the large intestine with enemas, administering neomycin and lactulose in a therapeutic enema, and administering intravenous fluid therapy to correct hypokalemia, hypoglycemia, and metabolic alkalosis. Intravenous administration of branched-chain amino acids also helps in treatment.

If encephalopathy is not life threatening, then treatment should be aimed at reducing the formation and absorption of ammonia in the intestine. This can be achieved by creating a less favorable environment for urea bacteria, reducing pH within the intestine, and also accelerating the transport of fecal matter through the large intestine without inducing severe diarrhea. At low pH, ammonia is converted to ammonium salt, which is less aborbable. This is accomplished by administering lactulose (Lactulose Solution BP; Duphar Laboratories), a polysynthetic disaccharide, orally 1–2 ml / kg three times daily, although the dosage should be adjusted for each patient and according to the nature of the bowel movement. In cats, the dose of lactulose is 1 ml orally twice daily.

The development of microflora is suppressed by the use of antibacterial drugs. Neomycin at a dose of 20 mg / kg twice a day is suitable for this purpose, but cases of bacterial resistance and toxicosis have been observed, especially in cats. Metronidazole (Flagyl; RMB Animal Health) also has a beneficial effect in the control of encephalopathy at a dose of 7.5 mg / kg twice daily. Some authors recommend probiotics to control encephalopathy, but others find these drugs not effective enough. Oral administration of lactulose together with neomycin at the initial stages of encephalopathy is also proposed, but after a sufficient degree of control is achieved, neomycin can be canceled, leaving lactulose. 10-20 ml of 1% neomycin solution with 5-10 ml of lactulose can be administered rectally. To reduce bacterial growth, it is also proposed to inject into the large intestine a 10% solution of povidone and iodine in a dose of 5-10 ml.

The conversion of ammonia to urea can be enhanced by maintaining blood sugar levels, and an additional reduction in encephalopathy is achieved by correcting hypokalemia, azotemia and alkalosis. In addition, every effort should be made to reduce protein catabolism, which increases the formation of ammonia and the requirements for its conversion by the liver to urea. Arginine is also mandatory in the urea cycle and can be used in acute encephalopathy. The use of any sedatives, tranquilizers and anesthetics should be avoided, as they further depress the central nervous system. You should also not use methionine and lipotropic drugs, as they increase the formation of mercaptan. It is necessary to control bleeding in the gastrointestinal tract due to the formation of ulcers, for which cimetidine is used at a dose of 4 mg / kg twice a day orally, since with bleeding a source of protein appears for bacterial fermentation and the production of ammonia.

In some cases of encephalopathy, it is necessary to correct the vascular pathology, such as portosystemic anastomosis. However, medical treatment should be given prior to surgery to reduce the risk of anesthesia.

Pancreatic hormone medications and synthetic hypoglycemic (blood sugar lowering) medications

DRUGS OF THE INSULIN GROUP

INSULIN

Synonyms: Depo-N-insulin, Isofaninsulin, Iletin I, Insulatard, Insulin B, Insulin-B S.C. Insulin BP, Insulin M, Insulin Aktrapid MS, Insulin Aktrapid ChM, Insulin Aktrapid ChM Penfill, Insulin Velosulin, Insulin tape, Insulin tape GP, Insulin tape MK, Insulin monotard, Insulin monotard MK, Insulin penotard NM, NM, NM Rapitard MK, Insulin Semilente MS, Insulin Superlenta, Insulin Ultralente, Insulin Ultralenthe MS, Insulin Ultraard NM, Insulinlong, Insulinminilente, Insulinsemilong, Insulinultralong, Insulong, Insulrapuman GPP, Insulrapid Baz SP, Insulrapuman rapid for optipen, Comb-N-insulin Hoechst, Lente Iletin I, Lente Iletin II, Monosuinsulin, N-Insulin Hechst, N-Insulin Hoechst 100, NPH Iletin I, NPH Iletin II, Regular Iletin I, Regular Iletin II, Suinsulin, Homorap-100, Homofan 100, Humulin L, Hu-mulin Mi, Humulin Mj, Humulin Mz, Humulin M4, Humulin N, Humulin NPH, Humulin R, Humulin S, Humulin tape, Humulin Regular, Humulin ultralente.

Insulin is a hormone produced by the beta cells of the pancreas.

Pharmachologic effect. Insulin is a specific sugar-lowering agent, has the ability to regulate carbohydrate metabolism; enhances the absorption of glucose by tissues and promotes its conversion into glycogen, also facilitates the penetration of glucose into tissue cells.

In addition to the hypoglycemic effect (lowering blood sugar levels), insulin has a number of other effects: it increases muscle glycogen stores, stimulates peptide synthesis, reduces protein consumption, etc.

Exposure to insulin is accompanied by stimulation or inhibition (suppression) of certain enzymes; glycogen synthetase, pyruvate dehydrogenase, hexokinase are stimulated; inhibited lipase, which activates fatty acids of adipose tissue, lipoprotein lipase, which reduces the "clouding" of the blood serum after ingestion of food rich in fats.

The degree of biosynthesis and secretion (release) of insulin depends on the concentration of glucose in the blood. With an increase in its content, the secretion of insulin by the pancreas increases; conversely, a decrease in blood glucose concentration slows down the secretion of insulin.

In the realization of the effects of insulin, the leading role is played by its interaction with a specific receptor localized on the plasma membrane of the cell, and the formation of an insulin-receptor complex. The insulin receptor in combination with insulin penetrates the cell, where it affects the processes of phospholation of cellular proteins; further intracellular reactions are not fully understood.

Insulin is the main specific treatment for diabetes mellitus, as it reduces hyperglycemia (increased glucose in the blood) and glycosuria (the presence of sugar in the urine), replenishes the glycogen depot in the liver and muscles, reduces the formation of glucose, alleviates diabetic lipemia (the presence of fat in the blood) , improves the general condition of the patient.

Insulin for medical use is obtained from the pancreas of cattle and pigs. There is a method for the chemical synthesis of insulin, but it is not readily available. Recently, biotechnological methods for producing human insulin have been developed. Insulin obtained by genetic engineering methods fully corresponds to the amino acid series of human insulin.

In cases where insulin is obtained from the pancreas of animals, due to insufficient purification, various impurities (proinsulin, glucagon, samotostatin, proteins, polypeptides, etc.) may be present in the preparation. Poorly purified insulin preparations can cause a variety of adverse reactions.

Modern methods make it possible to obtain purified (mono-peak - chromatographically purified with the isolation of the "peak" of insulin), highly purified (mono-component) and crystallized insulin preparations. Currently, crystalline human insulin is increasingly used. Of the insulin preparations of animal origin, preference is given to insulin obtained from the pancreas of pigs.

Insulin activity is determined biologically (by the ability to lower blood glucose in healthy rabbits) and by one of the physicochemical methods (by electrophoresis on paper or by chromatography on paper). For one unit of action (ED), or international unit (IE), the activity of 0.04082 mg of crystalline insulin is taken.

The main indication for the use of insulin is type I diabetes mellitus (insulin-dependent), but under certain conditions it is prescribed for type II diabetes mellitus (non-insulin dependent).

Method of administration and dosage. In the treatment of diabetes mellitus, insulin preparations of various durations of action are used (see below).

Short-acting insulin is also used for some other pathological processes: for causing hypoglycemic conditions (lowering blood sugar levels) in certain forms of schizophrenia, as an anabolic (enhancing protein synthesis) agent for general exhaustion, lack of nutrition, furunculosis (multiple purulent inflammation of the skin) , thyrotoxicosis (thyroid disease), with stomach diseases (atony / loss of tone /, gastroptosis / gastric emptying /), chronic hepatitis (inflammation of the liver tissue), initial forms of liver cirrhosis, as well as a component of "polarizing" solutions used for treatment acute coronary insufficiency (mismatch between the heart's need for oxygen and its delivery).

The choice of insulin for the treatment of diabetes mellitus depends on the severity and characteristics of the course of the disease, the general condition of the patient, as well as on the rate of onset and duration of the hypoglycemic effect of the drug. It is desirable to carry out the primary administration of insulin and setting the dose in a hospital (hospital) setting.

Short-acting insulin preparations are solutions intended for subcutaneous or intramuscular administration. If necessary, they are also administered intravenously. They have a fast and relatively short-term sugar-lowering effect. Usually they are injected subcutaneously or intramuscularly 15-20 minutes before meals from one to several times during the day. The effect after subcutaneous injection occurs within 15-20 minutes, reaches a maximum after 2 hours; the total duration of action is no more than 6 hours.They are used mainly in the hospital to establish the dose of insulin required for the patient, as well as in cases where it is required to achieve a rapid change in insulin activity in the body - with a diabetic coma and precoma (complete or partial loss of consciousness due to a sudden sharp rise in blood sugar).

In addition to that, short-acting insulin preparations are used as an anabolic agent and are usually prescribed in small doses (4-8 IU 1-2 times a day).

Prolonged (long-acting) insulin preparations are produced in various dosage forms with different duration of the sugar-lowering effect (semilong, long, ultralong). For different drugs, the effect lasts from 10 to 36 hours. Thanks to these drugs, you can reduce the number of daily injections. They are usually produced in the form of suspensions (suspension of solid particles of the drug in a liquid), administered only subcutaneously or intramuscularly; intravenous administration is not allowed. In diabetic coma and precomatous conditions, prolonged-release drugs are not used.

When choosing an insulin preparation, it is necessary to ensure that the period of maximum sugar-lowering effect coincides in time with the intake of food. If necessary, 2 prolonged-release drugs can be administered in one syringe. Some patients need not only long-term, but also rapid normalization of blood glucose levels. They have to prescribe long-acting and short-acting insulin preparations.

Usually, long-acting drugs are administered before breakfast, but if necessary, the injection can be given at other hours.

All insulin preparations are used subject to mandatory adherence to the dietary regimen. The determination of the energy value of food (from 1700 to 3000 khal) should be determined by the patient's body weight during the period of treatment, by the type of activity. So, with reduced nutrition and heavy physical labor, the number of calories required per day for the patient is at least 3000, with excess nutrition and a sedentary lifestyle, it should not exceed 2000.

Introducing too high doses, as well as a lack of carbohydrate intake from food, can cause a hypoglycemic state (low blood sugar), accompanied by hunger, weakness, sweating, body tremors, headache, dizziness, palpitations, euphoria (unreasonable complacent mood) or aggressiveness ... Subsequently, hypoglycemic coma may develop (loss of consciousness, characterized by a complete lack of body reactions to external stimuli, due to a sharp decrease in blood sugar levels) with loss of consciousness, convulsions and a sharp decline in cardiac activity. To prevent a hypoglycemic state, patients need to drink sweet tea or eat a few lumps of sugar.

In hypoglycemic (associated with a decrease in blood sugar) coma, a 40% glucose solution is injected into a vein in an amount of 10-40 ml, sometimes up to 100 ml, but no more.

Correction of hypoglycemia (lowering blood sugar levels) in acute form can be carried out using intramuscular or subcutaneous administration of glucagon.

Side effect. With the subcutaneous administration of insulin preparations, lipodystrophy (a decrease in the volume of adipose tissue in the subcutaneous tissue) may develop at the injection site.

Modern high-purity insulin preparations rarely cause allergy phenomena, but such cases are not excluded. The development of an acute allergic reaction requires immediate desensitizing (preventing or inhibiting allergic reactions) therapy and drug replacement.

Contraindications Contraindications to the use of insulin are diseases occurring with hypoglycemia, acute hepatitis, cirrhosis of the liver, hemolytic jaundice (yellowing of the skin and mucous membranes of the eyeballs caused by the breakdown of red blood cells), pancreatitis (inflammation of the pancreas), nephritis (inflammation of the kidneys), amyloid kidney disease associated with impaired protein metabolism / amyloid /), urolithiasis, stomach and duodenal ulcers, decompensated heart defects (failure of the heart due to disease of its valves).

Great care is required in the treatment of patients with diabetes mellitus, suffering from coronary insufficiency (a discrepancy between the heart's need for oxygen and its delivery) and brain impairment | blood circulation. Caution is required when using insulin! in patients with thyroid diseases, Addison's disease (insufficient adrenal function), renal failure. |

Insulin therapy for pregnant women should be> carefully monitored. During the 1st trimester of pregnancy, the need for insulin usually decreases slightly and increases in the 2nd and 3rd trimesters.

Alpha-adrenergic blockers and beta-adrenostimulants (see page 106), tetracyclines, salicylates increase the secretion of endogenous (secretion formed in the body) insulin. Thiazide diupetics (diuretics - see page 296), beta-blockers (see "page 113), alcohol can lead to hypoglycemia.

Release form. Insulin for injection by syringe is available in | glass vials, hermetically sealed with rubber stoppers with aluminum rolling: 1 ml of solution or suspension usually contains 40 units.

Depending on the source of production, insulin is distinguished, isolated from the pancreas of animals, and synthesized using genetic engineering methods. According to the degree of purification, insulin preparations from animal tissues are divided into mono-peak (MP) and mono-component (MC). Currently obtained from the pancreas of pigs are additionally denoted by the letter C (SMP - pork monopic, SMK - pork mono-component); cattle - with the letter G (beef: GMP - beef monopic, GMC - beef monocomponent). Human insulin preparations are designated by the letter C.

Depending on the duration of action, insulins are divided into:

a) short-acting insulin preparations: onset of action in 15-30 minutes; peak action after U / 2-2 h; the total duration of action is 4-6 hours;

b) prolonged-acting insulin preparations include drugs of medium duration (onset after 1 "/ 2-2 hours, peak after 3-12 hours; total duration 8-12 hours); long-acting drugs (onset after 4-8 hours; peak after 8-18 h; total duration 20-30 h).

Storage conditions. Store at temperatures from +2 to + 10 "C. Freezing of drugs is not allowed.

This information is not a guide to self-treatment.

A doctor's consultation is required.

Product added to cart

Humulin mz suspension d / in. 100 units / ml bottle. 10ml

1 ml of suspension for injection contains:

Active ingredients
• Insulin isophane human biosynthetic suspension 100 IU.

Excipients

Distilled M-cresol (1.6 mg / ml), glycerol, phenol (0.65 mg / ml), protamine sulfate, sodium phosphate dibasic, zinc oxide, water d / i, hydrochloric acid, sodium hydroxide.

In a bottle 10 ml of suspension. In a cardboard box 1 bottle.

Cost: 570,00 rub.

Indications for use:

• Diabetes mellitus in the presence of indications for insulin therapy.
• Newly diagnosed diabetes mellitus.
• Pregnancy with type 2 diabetes mellitus (non-insulin dependent).

Application during pregnancy and lactation:

During pregnancy, it is especially important to maintain good glycemic control in patients with diabetes mellitus. During pregnancy, the need for insulin usually decreases in the first trimester and increases in the second and third trimesters.

In patients with diabetes mellitus during lactation (breastfeeding), it may be necessary to adjust the dose of insulin, diet, or both.

In studies of genetic toxicity in in vitro and in vivo series, human insulin did not have a mutagenic effect.

Contraindications:

• Hypoglycemia.
• Hypersensitivity to insulin or to one of the components of the drug.

Side effect:

Side effect associated with the main action of the drug

Hypoglycemia.

Severe hypoglycemia can lead to unconsciousness and (in exceptional cases) death.

Allergic reactions

Local allergic reactions are possible - hyperemia, swelling or itching at the injection site (usually stop within a period from several days to several weeks); systemic allergic reactions (occur less often, but are more serious) - generalized itching, difficulty breathing, shortness of breath, decreased blood pressure, increased heart rate, increased sweating. Severe cases of systemic allergic reactions can be life threatening.

The likelihood of developing lipodystrophy is minimal.

Overdose:

• Symptoms: hypoglycemia, accompanied by lethargy, increased sweating, tachycardia. pallor of the skin, headache, tremors, vomiting. confusion of consciousness.

Under certain conditions, for example, with a long duration or with intensive control of diabetes mellitus, the precursor symptoms of hypoglycemia may change.

Treatment:

• Mild conditions of hypoglycemia can usually be controlled by ingestion of glucose (dextrose) or sugar. Adjustments to your insulin dose, diet, or physical activity may be required.
• Correction of moderate hypoglycemia can be carried out with the help of intramuscular or subcutaneous administration of glucagon. followed by ingestion of carbohydrates.
• Severe conditions of hypoglycemia, accompanied by coma. convulsions or neurological disorders, are stopped by i / m or s / c administration of glucagon or i / v administration of a concentrated solution of glucose (dextrose). After the restoration of consciousness, the patient must be given food rich in carbohydrates in order to avoid the re-development of hypoglycemia.

Method of administration and dosage:

The dose is set by the doctor individually, depending on the level of glycemia.

The drug should be administered subcutaneously, possibly intramuscularly.

IV injection of Humulin NPH is contraindicated!

S / c the drug is injected into the shoulder, thigh, buttocks or abdomen. The injection site must be alternated so that the same site is used no more than about 1 time / month.

When administered subcutaneously, care must be taken to avoid entering the blood vessel. After injection, do not massage the injection site. Patients should be trained in the correct use of insulin delivery devices.

Rules for the preparation and administration of the drug

Use Humulin NPH cartridges only with a pen-injector 3 ml (Syringe-pen HumaPen Ergo II 3 ml pack. 1 Eli Lilly).

Before use, Humulin NPH cartridges should be rolled between the palms 10 times and shaken, turning 180 ° also 10 times to resuspend the insulin until it looks like a homogeneous cloudy liquid or milk. Do not shake vigorously. this can lead to foam, which can interfere with the correct dose selection.

The cartridges should be checked carefully. Do not use insulin if it contains flakes after stirring, if hard white particles adhere to the bottom or walls of the bottle, creating a frosty pattern.

The design of the cartridges does not allow mixing their contents with other insulins directly in the cartridge itself. Cartridges are not refillable.

When using cartridges, follow the manufacturer's instructions for cartridge refilling and needle attachment. The drug should be administered in accordance with the instructions of the manufacturer of the syringe pen.

Using the outer needle cap, unscrew the needle immediately after insertion and safely discard. Removing the needle immediately after injection ensures sterility, prevents leakage, air ingress and possible clogging of the needle. Then put the cap on the handle.

The needles should not be reused. Needles and pen pens must not be used by others. Use the cartridges until they are empty and then discard them.

Precautionary measures:

The transfer of a patient to another type of insulin or to an insulin preparation with a different trade name should be carried out under strict medical supervision. Changes in the activity of insulin, its type (for example, Humulin Regular solution for injection 100 IU / ml vial 10 ml vial 1. Humulin M3 suspension for injection 100 IU / ml vial 10 ml unit 1), species (porcine, human insulin, human insulin analog) or production method (DNA recombinant insulin or animal insulin) may require dose adjustments.

The need for dose adjustment may be required as early as the first administration of a human insulin preparation after an animal insulin preparation, or gradually over several weeks or months after transfer.

The need for insulin may decrease with insufficient function of the adrenal glands, pituitary gland or thyroid gland, with renal or hepatic insufficiency.

With some diseases or emotional stress, the need for insulin may increase.

Dose adjustments may also be required if you increase your physical activity or change your usual diet.

Symptoms-precursors of hypoglycemia during the administration of human insulin in some patients may be less pronounced or differ from those observed during the administration of insulin of animal origin. With the normalization of blood glucose levels. for example, as a result of intensive insulin therapy, all or some of the symptoms-precursors of hypoglycemia may disappear, and patients should be informed about this.

Symptoms-precursors of hypoglycemia may change or be less pronounced with a prolonged course of diabetes mellitus, diabetic neuropathy, or with the simultaneous use of beta-blockers.

In some cases, local allergic reactions can be caused by reasons not related to the action of the drug, for example, skin irritation with a cleansing agent or improper injections.

In rare cases of the development of systemic allergic reactions, immediate treatment is required. Sometimes insulin changes or desensitization may be required.

Application for violations of liver function

Insulin requirements may decrease with liver failure.

Application for impaired renal function

Insulin requirements may decrease with kidney failure.

Influence on the ability to drive vehicles and use mechanisms

During hypoglycemia, the patient's ability to concentrate may deteriorate and the speed of psychomotor reactions may decrease. This can be dangerous in situations where these abilities are especially needed (driving a car or using machinery).

Patients should be advised to take precautions to avoid hypoglycemia while driving. This is especially important for patients with mild or absent symptoms, predictors of hypoglycemia, or with frequent development of hypoglycemia. In such cases, the physician should evaluate the appropriateness of the patient's driving.

Storage conditions:

• Store at temperatures from 2 ° to 8 ° C, keep away from freezing, keep away from direct exposure to light and heat.

The drug in use in a 10 ml bottle should be stored at room temperature 15-25 C ° for no more than 28 days.

Expiration date: 2 years.

Keep out of the reach of children.

Do not use after the expiration date.

In most cases, hyperglycemia occurs not as an independent disease, but as a consequence of various changes in the vital activity of the body. The main reason why hyperglycemia in children can be is diabetes mellitus.

In this condition, the child's body does not produce enough insulin. He is not able to transport sugars from food to the cells. Glucose accumulates in the blood, which is the main manifestation of hyperglycemia.

However, diabetes is not the only cause of this symptom. Hyperglycemia can be caused by other malfunctions and disturbances in the work of the child's body:

• unhealthy diet: eating high-calorie foods that contain a large number of carbohydrates;
• frequent overeating, non-compliance with the diet;
• severe stress and emotional distress;
• trauma;
• transferred infectious diseases.

The peculiarities of how hyperglycemia arises and manifests itself in a child's body, determine the presence of several options for classifying a pathological condition.

According to the severity of hyperglycemia, it happens:

• mild (with a blood glucose content of 6-10 mmol / l);
• moderate severity (glucose level is 10-16 mmol / l);
• severe form (blood sugar levels exceed 16 mmol / l).

Hyperglycemia also differs depending on the characteristics of the manifestation:

• an increase in sugar levels after 8 hours of fasting,
• an increase in glucose levels after a meal.

Symptoms

Hyperglycemia in a child is often accompanied by characteristic symptoms. The child can indicate some of the first signs of a pathological condition:

• feeling of intense thirst and dry mouth,
• frequent urge to urinate,
• labored breathing,
• rapid pulse,
• painful sensations in the abdomen,
• nausea followed by vomiting
• blurred vision
• a general state of malaise and fatigue.

It can be quite difficult to independently recognize signs of hyperglycemia among such symptoms. A specialist should determine the cause and nature of the manifestations.

Diagnosis of hyperglycemia in a child

If a child begins to have a strong thirst for no apparent reason, parents should pay attention to such changes. A timely visit to the doctor will help to recognize hyperglycemia in the early stages of manifestation to prevent complications.

You can diagnose the condition using:

• a random blood test at the moment to determine blood sugar levels;
• conducting a blood sugar test after 8 hours of fasting (on an empty stomach);
• complex reusable blood test (glucose tolerance test).

Diagnostics are necessary to track changes in blood glucose levels. This will help determine the primary diagnosis that provoked hyperglycemia and prescribe a course of treatment.

Complications

Complications of hyperglycemia develop with prolonged manifestations of the pathological condition and the absence of timely treatment. The consequences, than hyperglycemia can be dangerous for a child, are:

• development of diseases of the heart and cardiovascular system;
• impaired renal function, which can lead to the development of renal failure;
• diseases of the organs of vision;
• malfunctions of the central nervous system;
• ketoacidosis (with diabetes mellitus).

Attention to the child's condition and a timely visit to the attending physician will help prevent the development of complications.

Treatment

What can you do

It is necessary to treat hyperglycemia depending on what disease caused such changes in the body. So, if an increase in the blood sugar level of a child occurred against the background of diabetes mellitus, you need to:

• consult a specialist to correct prescriptions in accordance with insulin therapy,
• regularly measure the child's blood sugar to track all changes,
• ensure proper nutrition while following a low-carb diet,
• carry out insulin injections to maintain important biological processes in the child's body.

However, not all parents know what to do if hyperglycemia occurs against the background of other, non-diabetic problems. To maintain the state will help:

• adherence to proper nutrition with eating a large amount of fruits and vegetables,
• compliance with the drinking regime,
• accustoming the child to a certain dietary regimen,
• control of the implementation by the little patient of all the instructions of the specialist.

What the doctor does

If hyperglycemia was provoked by non-diabetic reasons, it is quite possible to cure it. The doctor prescribes therapeutic therapy aimed at achieving three main goals:

• normalization of sugar levels in the child's body;
• treatment of the underlying disease causing changes in glucose readings;
• preventing similar changes in the future.

Treatment includes both drug therapy and changes in the child's lifestyle and nutrition.

Prevention

If a child has diabetes mellitus, adherence to a certain lifestyle will help prevent hyperglycemia. To do this, parents need:

• monitor and keep track of changes in blood glucose levels,
• monitor the child's diet,
• teach to perform simple physical exercises,
• make insulin injections in a timely manner.

If there is a risk of developing hyperglycemia with a nondiabetic condition, the following will help to avoid the consequences:

• compliance with the regime and quality of food,
• moderate physical activity,
• timely treatment of acute infectious and chronic diseases,
• avoidance of stressful situations and emotional changes.

A timely visit to a doctor will help protect the younger family member from possible health problems.

You will also learn what the danger of untimely treatment of the disease of hyperglycemia in children can be, and why it is so important to avoid the consequences. Everything about how to prevent hyperglycemia in children and prevent complications.

And caring parents will find on the pages of the service complete information about the symptoms of hyperglycemia in children. What is the difference between the signs of the disease in children at 1, 2 and 3 years old from the manifestations of the disease in children at 4, 5, 6 and 7 years old? What is the best treatment for hyperglycemia in children?

Take care of the health of loved ones and be in good shape!

According to world statistics, at present, diabetes mellitus (DM) suffers from 2 to 4% of the population. This disease can seriously complicate the course and the possibilities of rehabilitation of patients who have suffered a stroke. Inadequate diabetes therapy, especially in the acute period of stroke, significantly increases the risk of recurrent stroke or increases the area of ​​the ischemic focus.

IN AND. Pankiv, Ukrainian Scientific and Practical Center for Endocrine Surgery, Transplantation of Endocrine Organs and Tissues of the Ministry of Health of Ukraine, Kiev

Patients with diabetes mellitus are 25 times more likely to develop strokes, renal failure, heart attacks and blindness, and life expectancy is, on average, 15 years less than in the general population.

Stroke is the second leading cause of death in the world. Almost 6 million people die from acute cerebrovascular accidents (ACVI) every year, with more than 70% of deaths occurring in developing countries, including Ukraine. Unless urgent action is taken, the death rate from stroke will increase by 12% globally over the next 10 years and more than 20% in countries with low living standards. Already today, the mortality rate from CVA in our country is much higher not only the indicators of the Western countries, but also of Russia.

Since acute ischemic strokes (AII) account for up to 80% of all strokes, the development of optimal management of this particular type of stroke has become a priority in angioneurology. OIS is a dynamic process that begins with focal ischemia and ends with the formation of a cerebral infarction (MI). Due to the narrow therapeutic window and other barriers, the rate of use of thrombolytic therapy remains low, even in advanced centers.

Epidemiology of stroke in diabetes mellitus

The presence of type 2 diabetes significantly increases the risk of stroke by 2-6 times, while the mortality rate from cardiovascular diseases in general and from stroke in particular is more than 2-4 times higher in patients with type 2 diabetes. The course of cerebral circulation disorders in such patients is severe, since more severe disorders of carbohydrate metabolism are associated with a higher mortality rate and disability. According to the large-scale study UKPDS, it was found that the level of HbA 1c is closely related to the likelihood of death due to acute heart attack and stroke: an increase in its concentration by 1% was accompanied by a 17% increase in the incidence of stroke. It is important that not only severe forms of type 2 diabetes, but also insulin resistance are also associated with an increased risk of stroke.

The role of diabetes mellitus as a risk factor for the first stroke was demonstrated in a 55-84-year-old population based on a ten-year follow-up conducted in Framingham (USA).

Thus, it was found that in people over 40 years of age, acute cerebrovascular accident occurs against the background of diabetes one and a half to two times more often than in people who do not suffer from this disease, and at the age of 40 years - three to four times more often, and among patients with significant the preponderance is dominated by women. At the age of up to 40 years, in the case of a short course of diabetes with hypoglycemic coma, cerebral hemorrhage develops, and with prolonged (more than 15-20 years) - MI. Often, especially in elderly patients with stroke, diabetes is not diagnosed, although it can occur in 50% of patients. Stroke mortality rates are significantly higher among people with diabetes.

Until now, the ratio of the incidence of ischemic and hemorrhagic stroke in patients with diabetes has not been fully established. So, according to the data of pathological studies, this indicator practically does not differ from the average population - MI with diabetes is observed 3-4 times more often than hemorrhage. At the same time, according to clinical data, MI in diabetic patients develops 5-6 times more often than hemorrhage.

Pathophysiological mechanisms of stroke in diabetes mellitus

The overwhelming majority of patients with diabetes mellitus with MI (72-75%) have a non-thrombotic nature of stroke, while among the general population this figure reaches only 60%. Chronic cerebral vascular insufficiency plays a leading role in the development of the more common nonthrombotic MI in patients with diabetes, among the reasons for which should be noted damage to sympathetic vasomotor nerves, a decrease in oxidative processes, and hypocapnia. Non-thrombotic stroke often occurs in patients with vigorous activity, when the need to increase the blood supply to the brain increases significantly, as a result of which conditions are created for the appearance of cerebrovascular insufficiency. The reasons for the development of myocardial infarction of a thrombotic nature in persons with diabetes are significant atherosclerotic changes in cerebral vessels, an increase in blood viscosity and a violation of its coagulation properties (inhibition of the anticoagulant and activation of the coagulation system). A direct dependence of the depression of the protective anticoagulant reactions of the body on the duration of diabetes mellitus, the severity and prevalence of damage to the vascular system was revealed.

An important role in the development of cerebrovascular disorders is played by the pathology of the main arteries of the head (carotid and vertebral arteries), which are often affected by atherosclerosis in diabetes. The importance of studying the effect of glucose and insulin on the thickness of the muscular layer of the arteries (intima-media thickness index [TIM]) has been confirmed by the works carried out within the framework of the international IRAS program. Thus, an increase in this indicator compared with the control group, revealed during prospective observations using ultrasound sonography, not only indicates the presence of atherosclerosis, but also allows one to judge the influence of various risk factors in patients with diabetes. Moreover, a significant correlation was found with both low and high insulin concentrations of factors such as gender, body mass index, glucose tolerance, triglyceride (TG) levels, A1 and B1 apolipoproteins, fibrinogen, and blood pressure (BP). Hyper- and hypoinsulinemia are assessed as independent risk factors for carotid atherosclerosis. The lower the insulin level, the more pronounced atherosclerosis of the internal carotid artery (ICA). The relationship between RF and carotid atherosclerosis is less pronounced in elderly patients. Maximum stenosis and wall thickness of the common carotid artery (CCA) and ICA increase with age more in men than in women, and correlate better with data on stroke and coronary heart disease. The relationship of these parameters with systolic blood pressure, left ventricular hypertrophy, the concentration of low-density lipoprotein cholesterol, TG, glucose and insulin, and the level of high-density lipoprotein cholesterol and the value of diastolic blood pressure had an inverse relationship with the maximum indicators of ICA TIM and the degree of arterial stenosis.

In elderly patients with type 2 diabetes, TIM in the bifurcation area of ​​the CCA was higher than in the control group and correlated with plasma insulin levels (1 hour after glucose loading), serum concentration of low-density lipoproteins, triglycerides and apolipoprotein. B. The main factor influencing TIM in diabetes mellitus is insulin level after glucose loading together with impaired lipoprotein profile and insulin resistance syndrome.

Clinical features of stroke in patients with diabetes

In type 2 diabetes, both large and small caliber arteries are affected. Damage to the vascular bed is initiated already at the stage of insulin resistance in the absence of disturbances in carbohydrate metabolism, which is clinically manifested by early vascular complications of type 2 diabetes. Stenosing lesions of the main arteries of the head, primarily the ICA, are characteristic. Subsequently, the formation of hemodynamically significant stenoses of large arteries with an increased risk of parietal thrombus formation and the threat of complete vessel occlusion is possible. In the case of fragmentation of a thrombus, there is a threat of embolization of the distal vascular bed. The risk of developing myocardial infarction increases with insufficient functioning of the anastomoses, in particular, the inferiority of the vessels of the Willis circle. Widespread damage to the arterial system of the brain is accompanied by a decrease in vascular reactivity, which also adversely affects the state of cerebral circulation. Fluctuations in systemic blood pressure under these conditions can be a decisive factor in the occurrence of both acute and chronic cerebral ischemia. For persons with type 2 diabetes, lesions of small-caliber arteries with the development of microangiopathy are characteristic. The risk of developing disorders of cerebral circulation in such patients in the presence of microvascular complications increases, especially with a long duration of the disease. Due to the defeat of small-caliber arteries in patients with type 2 diabetes, there is an increased risk of developing "silent" strokes - small-sized heart attacks located in the deep sections of the white matter of the cerebral hemispheres. In addition to the vascular process, brain damage in patients with type 2 diabetes can be directly caused by disorders of carbohydrate metabolism. Excess glucose can have a toxic effect on neurons due to an increase in glycolysis products, activation of lipid peroxidation, and apoptosis processes. The combination of these factors often determines not only the occurrence and progression of vascular brain damage, but also an earlier and more severe course of neurodegenerative processes. Hyperglycemia due to the accumulation of glycated metabolic products can contribute to the deposition of amyloid in the brain tissue. With increasing age in the population, the number of patients with "pure" vascular, degenerative variants of dementia decreases and the incidence of mixed dementia increases. The risk of developing cerebrovascular pathology in patients with type 2 diabetes is determined by the severity of the disease, the effectiveness of blood glucose control, and the presence of concomitant diseases. The combination of type 2 diabetes and arterial hypertension (AH) is extremely unfavorable, and the severity of cognitive disorders increases with age. For example, in people who have not previously suffered a stroke under 60 years of age, type 2 diabetes and hypertension are accompanied by moderate disorders of higher cerebral functions, while the combination of these two factors is a more significant disorder of cognitive functions. In such patients, the likelihood of developing "silent" strokes significantly increases, and multiple postischemic foci in various parts of the brain are often observed.

Along with focal lesions of the medulla, individuals with type 2 diabetes have leukoaraiosis - an extensive lesion of the periventricular white matter associated with a decrease in cognitive functions. At the same time, an atrophic lesion of the medulla can be detected (the hippocampus and tonsils of the brain are most affected). The severity of these changes corresponds to the severity of insulin resistance. To date, there is no doubt about the existence of a causal relationship between disorders of carbohydrate metabolism and a high risk of developing disorders of cerebral circulation, including discirculatory encephalopathy and vascular dementia. The problem of the relationship between type 2 diabetes and the risk of developing other types of dementia, in particular Alzheimer's disease, is being actively discussed.

In patients with diabetes, in comparison with those who do not suffer from this disease, there are a number of features in the ACVA clinic:

• occurs more often during the day, during a period of activity;
• often develops against the background of increased blood pressure;
• accompanied by a higher mortality rate;
• in some patients it has a pseudotumorous course.

Patients with diabetes have a more severe course of stroke, more pronounced cerebral edema, and a higher mortality rate. With cerebral hemorrhages, a very high mortality rate, pronounced decompensation of diabetic disorders are noted, in half of the patients, prolonged coma is observed. Parenchymal hemorrhages often develop gradually; with subarachnoid hemorrhage, the onset is not acute, accompanied by mild meningeal symptoms and moderate psychomotor agitation.

Of particular interest is the differential diagnosis of stroke with metabolic disorders, which can often mimic the clinical picture of stroke in diabetic patients.

Encephalopathies due to metabolic or toxic disorders usually cause subacute development of impairment of consciousness with or without systemic disorders and minimal focal disorders. Most often, generalized hyperreflexia and Babinsky's symptom are found as focal neurological symptoms. Sometimes metabolic disorders are manifested by focal neurological symptoms, which can begin acutely and mimic a stroke. This applies to both hypo- and hyperglycemia. Hyper-osmolarity in hyperglycemia can cause a decrease in cerebral blood flow, focal neurological deficits, that is, symptoms that mimic a stroke.

Usually hypoglycemia causes adrenergic activity (sweating and tachycardia), but sometimes patients have only focal neurological manifestations. In this case, when making a final diagnosis, it is necessary to carry out a differential diagnosis with a stroke. Patients almost always receive hypoglycemic drugs for diabetes, so they may develop hypoglycemia. Complaints are usually stereotyped and occur before meals (in the morning before breakfast, at night) or after exercise. Symptoms decrease after glucose intake. Blood sugar levels drop to 2-2.5 mmol / L at the onset of an attack, but may return to normal spontaneously or after taking glucose. However, it should be remembered that with a prolonged course of diabetes, a hypoglycemic state can occur in a patient even with seemingly normal blood glucose values. If a patient with diabetes is suspected of having a stroke, the symptoms of which appeared early in the morning, it is imperative to bear in mind the possibility that the patient has hypoglycemia, which requires adequate correction.

Hyperglycemia (blood sugar levels above 8 mmol / L in a single study or above 6.7 mmol / L in monitoring) is observed in 43% of patients with acute stroke. Of these, 25% of patients were diagnosed with diabetes earlier, and another 25% had an increased level of HbA 1c, which indicates the latent course of diabetes. However, 50% of patients had HbA 1c levels within normal limits; this suggests that increased glucose levels are associated with stroke. The theory that hyperglycemia is a consequence of the stress release of corticosteroids and catecholamines is controversial.

Features of stroke therapy in diabetes

When treating patients with diabetes who have suffered a stroke, the practitioner faces a number of problems.

First, this is due to the need for more careful monitoring of blood glucose levels. In addition, in patients with long-term diabetes, there are, as a rule, other lesions of internal organs caused by diabetes, which should also be taken into account in the course of complex therapy.

Basic stroke therapy

Basic stroke therapy is aimed at correcting vital functions and maintaining homeostasis, and also includes monitoring of basic physiological parameters (blood pressure, heart rate, electrocardiogram, respiratory rate, SaO2, body temperature, glycemia) in the first at least 48 hours from the onset of development stroke, regardless of the severity of the patient's condition, as well as correction and maintenance of hemodynamic parameters, respiration, water-electrolyte metabolism and glucose metabolism, correction of cerebral edema and increased intracranial pressure, adequate nutritional support, prevention and control of complications. Basic therapy is the foundation that ensures the effectiveness and correctness of other high-tech and specific measures for the treatment of stroke.

At the heart of ischemic stroke is a local disturbance of cerebral circulation, in connection with which all therapeutic measures of basic therapy should be aimed at maintaining adequate cerebral perfusion.

It is necessary to strive to maintain normovolemia with a balanced electrolyte composition of blood plasma. In the presence of cerebral edema, it is possible to maintain a negative water-electrolyte balance, but only if this does not lead to a decrease in blood pressure.

When assessing the water-electrolyte balance, it should be borne in mind that the body is constantly losing fluid and electrolytes, and therefore, the water-electrolyte balance must not only be controlled, but also constantly replenished. The volume and composition of the injected fluids should be sufficiently physiological, and with an adequate condition of the patient (in a clear mind, without aphatic disorders and swallowing disorders, able to control his water-electrolyte balance) can only be taken orally. Carrying out intravenous infusions in such patients is dictated exclusively by the peculiarities of the administration of certain drugs.

The main infusion solution in the treatment of patients with stroke is 0.9% sodium chloride solution. Hypoosmolar solutions (0.45% sodium chloride solution, 5% glucose solution) are contraindicated due to the risk of increased cerebral edema. Due to the risk of developing hyperglycemia, the routine use of glucose-containing solutions is also inappropriate.

Hyperglycemia after stroke is a poor prognostic sign. This can be explained by the fact that a more severe course of strokes entails a more pronounced stress response and, therefore, causes hyperglycemia, which in the acute period of stroke plays an important role in the choice of patient management tactics. There is evidence that hyperglycemia can increase the area of ​​the lesion. T.A. Baird, M.W. Parsons et al. found a direct negative effect of an increase in blood glucose levels on the process of ischemization of a region of the brain.

At the same time, diabetic micro- and macroangiopathies significantly complicate the pathophysiological picture of stroke. When managing patients after acute stroke, it is important to monitor blood glucose levels, determine the concentration of HbA 1c, and it is also possible to perform a glucose tolerance test.

Hypoglycemia, as mentioned earlier, can mimic the clinical picture of stroke or transient ischemic attacks. At the same time, in the acute period of stroke, due to a decrease in food intake, it often occurs in patients receiving sugar-reducing drugs. Since hypoglycemia can significantly complicate the course of a stroke and cause an increase in neurological deficits, the blood sugar level in patients receiving antihyperglycemic drugs should be monitored especially carefully.

It is important to start preventing recurrent stroke from the first days after a stroke. In patients with type 2 diabetes, adequate antihypertensive therapy and routine anticoagulant therapy can significantly reduce the risk of stroke.

In patients with diabetes, even if it is long-term, a motor rehabilitation program should be drawn up taking into account possible lesions of the peripheral nervous system, blood vessels, and other organs and systems. For example, the presence of sensitive ataxia due to diabetic polyneuropathy to a certain extent limits the possibilities of motor rehabilitation, and skin lesions may be a contraindication for massage. In some cases, it is necessary to use special orthopedic shoes. Adequate control of carbohydrate metabolism and blood plasma osmolarity is required.

The mortality rate for stroke in diabetic patients is 40.3-59.3%, which is higher than the average in the general population, and for hemorrhages reaches 70-100%. Among the causes of frequent lethal outcomes, one can name difficulties in diagnosis (with a stroke, a diabetic or hypoglycemic coma is mistakenly diagnosed, etc.), decompensation of diabetic metabolic disorders, diabetic vascular changes, concomitant diseases and complications of diabetes (myocardial infarction, nephropathy, increased vulnerability of the skin, etc.) etc.), the vastness of the foci of myocardial infarction, the difficulties of conducting rational therapy in connection with the simultaneous treatment of stroke and diabetes mellitus.

The development of both hypo- and hyperglycemic states in patients with stroke is extremely unfavorable. However, if the correction of hypoglycemia, as a rule, is always timely, then the attitude to hyperglycemia as an emergency in patients with stroke, unfortunately, has not yet developed.

An absolute indication for short-acting insulins is a blood glucose level of 10 mmol / L and above. However, a blood glucose level of 6.1 mmol / L and above is already an unfavorable prognostic factor, regardless of the presence or absence of diabetes in the anamnesis.

Patients with diabetes should be switched to short-acting subcutaneous insulin injections. Subject to adequate glycemic control, an exception can be made by patients in a clear consciousness, without aphatic disorders and swallowing disorders, who are able to continue taking hypoglycemic drugs and / or insulins according to their usual regimens.

Prevention of cerebrovascular complications of diabetes

The main way to prevent cerebrovascular pathology in patients with type 2 diabetes is timely and adequate correction of carbohydrate metabolism disorders. At the same time, it is necessary to eliminate other modifiable risk factors for cardiovascular diseases: achievement of target blood pressure levels, cholesterol and TG levels, correction of disorders of the hemostasis system and microcirculation. Also, the possibility of non-drug correction of risk factors should not be underestimated. Unfortunately, the possibilities of adequate correction of metabolic disorders in people with type 2 diabetes are far from being fully utilized. The results of comparing the effectiveness of controlling risk factors for cardiovascular diseases in persons with type 2 diabetes in different periods of time spent in the United States suggest that in 1988-1994. (NHANES III) and in 1999-2000. (NHANES), only about a third of patients adhered to medical recommendations to control the main risk factors: blood pressure, lipids and HbA 1c in the blood. An extremely important area of ​​prevention of cardiovascular diseases, in particular cerebral stroke in patients with type 2 diabetes, is the implementation of large-scale preventive measures among the population. It is also difficult to overestimate the role of the doctor's explanatory work aimed at ensuring that the patient understands the essence of his disease, the need to control blood glucose levels, blood pressure, the advisability of choosing the optimal level of physical activity, a rational diet, etc. type) to treatment is often due to an insufficient degree of contact between the patient and the attending physician, the patient's lack of understanding of the purpose of the therapeutic and prophylactic measures. Increased adherence of patients to preventive and therapeutic recommendations is a significant reserve for increasing the effectiveness of medical care, reducing the level of disability and mortality.

The efficacy of a combination of medicinal and non-medicinal therapies has been confirmed in a clinical setting. Thus, in elderly patients with type 2 diabetes who do not have manifestations of dementia, adequate correction of carbohydrate metabolism (appropriate diet and systematic intake of antihyperglycemic drugs) made it possible to reduce the risk of developing cognitive impairment by more than 2 times. As a result of effective glycemic control, a 1% decrease in HbA 1c concentration is accompanied by a 25% decrease in the risk of microvascular complications. At the same time, the correction of carbohydrate metabolism by itself is not always able to completely eliminate the changes in the body caused by type 2 diabetes, and reliably prevent the development of cerebrovascular diseases, especially in patients with additional risk factors for cardiovascular diseases. A high probability of the development of repeated episodes of acute cerebral ischemia persists in patients with stroke caused by damage to the carotid arteries. Even lowering blood glucose levels does not eliminate the risk of recurrent ischemic stroke. In this regard, the use of antiplatelet agents is an effective direction for the prevention of cerebrovascular complications in patients with type 2 diabetes. The most widely used for this purpose is acetylsalicylic acid, which has high efficiency and good pharmacoeconomic indicators. In the case of a patient's low sensitivity to the drug, individual intolerance or the development of gastrointestinal complications, it is advisable to use simultaneously other antiplatelet agents (dipyridamole, clopidogrel) in combination with acetylsalicylic acid or as monotherapy. Despite the convincingly proven efficacy of the systematic use of antiplatelet agents for the secondary prevention of cerebral vascular complications in patients with type 2 diabetes, a significant proportion of patients do not receive antiplatelet therapy (less often adequate treatment is carried out in women under the age of 60).

Stress hyperglycemia

The term "stress hyperglycemia" appeared in clinical practice at the end of the 19th century, when they began to record an increase in blood glucose levels in severe wounds and infections in persons who had not previously suffered from diabetes. By some estimates, about half of ICU patients have elevated blood glucose levels. The established relationship between the severity of the condition and an increase in blood glucose has been considered for a long time as an adaptive response to injury that does not require urgent correction. The need for increased energy supply of cells participating in the inflammatory reaction and an increase in blood plasma volume due to hyperosmolarity in the presence of hypovolemia were noted as potentially positive effects of hyperglycemia. Recently, information has begun to accumulate justifying the need to revise the established position. In this regard, the feasibility and ways of eliminating stress hyperglycemia (SG) in ICU patients are discussed.

The diagnostic criteria for FH vary widely. According to most experts, stress-induced hyperglycemia is understood as an increase in the blood glucose content of patients or victims (without indications of a history of diabetes mellitus) of more than 6.1-11.0 mmol / L.

The deepening of the understanding of the essence of metabolic disorders in critical conditions gave reason to consider hyperglycemia as one of the manifestations of the hypermetabolic syndrome characteristic of critical conditions of various nature, caused by an increase in the level of counterinsular hormones, activation of lipolysis, proteolysis and the measles cycle. Decreased activity of pyruvate dehydrogenase leads to incomplete oxidation of glucose, accumulation of pyruvate and stimulation of gluconeogenesis.

An important role in the stabilization of hyperglycemia under conditions of a stress response to injury is played by insulin resistance of skeletal muscle cells, hepatocytes, and adipose tissue in combination with relative insulin deficiency associated with a limited compensatory ability of pancreatic β-cells. At different critical states, different mechanisms that implement SG are dominant. So, in case of mechanical injury, the main reason is an increase in the production of glucose in the liver, and not damage to its utilization by tissues. In the initial stages after severe burns, glucagon is the leading factor contributing to the maintenance of hyperglycemia. In the future, despite the increase in the level of insulin in the blood, persistent hypertension for a long time (more than 3 weeks) is more associated with insulin resistance.

A number of drugs widely used in intensive care practice can enhance and maintain hyperglycemia initiated by endogenous mediators. This primarily applies to epinephrine / norepinephrine and other sympathomimetics, glucocorticosteroids, and some cytostatics (cyclosporine, tacrolimus). The joint administration of catecholamines and glucocorticosteroids is 3 times more likely to be accompanied by the development of hyperglycemia. Hyperglycemia can also be the result of improperly administered parenteral or enteral nutrition; it developed in 50% of patients receiving dextrose at a rate of more than 4 mg / kg / min with total parenteral nutrition.

Hyperglycemia in combination with insulin resistance can have a significant additional damaging effect, contributing to the aggravation of organ dysfunction through 3 mechanisms:

• a decrease in oxygen transport and a violation of water-electrolyte homeostasis due to stimulation of diuresis and additional fluid losses;
• stimulation of the catabolism of structural proteins due to a lack of glucose supply to the cell;
• glycosylation of protein molecules and a decrease in their functional activity.

There is evidence of the undeniable clinical significance of hyperglycemia in stroke. In the course of experimental and clinical studies, data were obtained indicating the effect of FH on an increase in the zone of ischemic brain damage and a worsening prognosis. The negative consequences of FH are associated with an increase in the permeability of the blood-brain barrier and the development of acidosis, which could contribute to the expansion of the infarction area. Similar conclusions about the effect of FH were made for the population of patients with stroke. Along with a decrease in survival (after 30 days, 1 year and 6 years), a negative effect on the functional outcome in surviving patients, an increase in hospitalization time and material costs was shown.

The accumulation of evidence of the unfavorable effect of FH on the course of various diseases, along with experimental evidence of the possibility of introducing functional disorders of individual organs and systems, served as the basis for conducting controlled clinical trials. One of them is the Leuven study, a randomized prospective controlled trial, which included 1,548 patients who underwent cardiac surgery (59% - coronary artery bypass grafting; 27% - valve replacement; 14% - combined intervention).

Immediately upon admission to the ICU, patients were randomized into 2 groups: conventional and intensive insulin therapy (IIT). In the conventional insulin therapy group, intravenous insulin was started at a glucose level above 215 mg / dL, which was kept in the “corridor” of 10.0-11.1 mmol / L. In the IIT group, its administration was started with a glucose level exceeding 6.1 mmol / L, trying to reach normal values ​​of 4.4-6.1 mmol / L.

The patients of the 2nd group adhered to the following IIT protocol. Insulin at a dose of 50 units (actrapid) was diluted in 50 ml of physiological saline, which remained stable at 25 ° C for 24 hours. Insulin was injected using a dosing syringe, the dosage regimen of which was determined by the initial glycemic level:

• 6.1-12.2 mmol / l - 2 units / h;
• more than 12.2 mmol / l - 4 units / h.

Further dosage adjustment was carried out depending on the results of dynamic assessment of glucose content: if it exceeded 7.8 mmol / l, the rate of administration was increased by 1-2 units / h; if it remained in the range of 6.7-7.8 mmol / l - by 0.5-1 unit / h; at values ​​of 6.1-6.7 mmol / l - by 0.1-0.5 units / h until values ​​of 4.4-6.1 mmol / l are reached. In the case of reaching the preset glucose level after the starting rate of insulin delivery was established, it remained at the same values.

When the glucose level decreased to 3.3-4.4 mmol / L, the insulin dosage was reduced to 0.5 U / h and stopped at lower values. The introduction of glucose in the form of 10-gram boluses was resorted to when its content was below 2.2 mmol / L, trying to return to the specified range.

Overall, to date, a meta-analysis of the results of studies of acceptable quality (n = 38) has led to the following conclusion: control of glycemic levels with intravenous insulin infusion reduces the risk of death by 15% in the general population of hospitalized patients (relative risk [RR] 0.75 -0.97); in surgical patients - to a greater extent (RR 0.22-0.62).

It is important to emphasize that the tactics of maintaining normal glucose levels of 4.4-6.1 mmol / L used in the studies had advantages over the concept of maintaining moderate glycemia (RR 0.54-0.93).

Most researchers noted the occurrence of hypoglycemic conditions (blood glucose level less than 2.2 mmol / L) against the background of IIT, the frequency of which was, on average, 3 times higher than in the control group (RR 1.9-6.3). The development of hypoglycemia, as a rule, was not accompanied by any severe clinical manifestations and consequences. However, its frequency was different, ranging from 3-10%, which prompted some of the authors to abandon IIT.

Thus, on the basis of the above data, it can be argued that SG is not just a criterion for the severity of a condition, but also a factor that has a direct impact on the course of the pathological process. It should be recognized that it is advisable to strictly control blood glucose levels and maintain normoglycemia.

The established optimistic clinical results required a pathophysiological justification. This could be due to either the control of glycemic levels, or the action of insulin, which has the ability to limit the synthesis and secretion of proinflammatory cytokines. The results of the secondary analysis indicate that the positive effect is primarily associated with the elimination of hyperglycemia, and not with the anti-cytokine effect of insulin: the need for high doses of insulin was combined with an unfavorable outcome. Nevertheless, doubts remained, since other effects of insulin potentially significant for critical conditions are known: a decrease in oxygen demand, inhibition of apoptosis, activation of fibrinolysis, restoration of macrophage function. To a large extent, they were removed after a correct experimental study was carried out, which proved the priority of maintaining normoglycemia in preventing the development or progression of endothelial, hepatic, renal dysfunction and reducing the mortality rate. Insulin had an effect independent of the effect on glucose level, which consisted in an increase in myocardial contractility and partial restoration of the ability of monocytes and neutrophils to phagocytosis.

Glycemic control and real clinical practice

The preservation of normoglycemia fits well into the modern strategy of intensive care for critical conditions - full support of function along with artificial ventilation of the lungs, compensation of hypovolemia, normalization of vascular tone and contractile ability of the myocardium, and artificial nutrition. The evidence obtained served as the basis for the inclusion of glycemic control in the International Interdisciplinary Recommended Protocols. Meanwhile, as in the case of the introduction of any innovation into practice, a number of questions and real problems arise.

The vast majority of the works included in the meta-analysis concern cardiac surgery and cardiac patients. The conclusion about the effectiveness in sepsis was made on the basis of a subpopulation analysis of patients with predominantly angiogenic sepsis. Is it possible to extend its results to other categories of patients - with acute cerebrovascular accidents, major abdominal surgeries, thermal and mechanical trauma?

This is a common problem in newborns, but much less common in children after this period. It is usually determined when plasma glucose concentration is less than 2.6 mmol / L, although the development of clinical signs will depend on how much other energy sources can be used. Clinical signs include:
increased sweating;
pallor;
signs of CNS irritation, including headache, seizures, and coma. Neurological consequences can be permanent if hypoglycemia persists and include epilepsy, severe learning disabilities, and microcephaly. The risk is highest in early childhood, during the period of the most intense brain development.

Children have high energy requirements and relatively low glucose reserves due to gluconeogenesis and glucogenesis... They are at risk of fasting hypoglycemia. Infants should never fast for more than 4 hours, for example, in the preoperative period. It is necessary to check the blood glucose level in those children who:
have signs of septicemia or look seriously ill;
who have prolonged seizures;
who develop impaired consciousness. This is often done at the patient's bedside using glucose sensing strips, which are more accurate when using a meter. However, the bars only indicate that the glucose level is within the low range and any indication of a low value should always be checked with a laboratory measurement.

If the reason hypoglycemia not established, it is vital to draw blood during hypoglycemia. In addition, the first urine sample received is sent for analysis, so as not to miss a valuable opportunity for diagnosis.

Research to be carried out in the presence of hypoglycemia:
Blood:
- Confirmation of hypoglycemia by laboratory tests of blood glucose.
- Determination of the content of GH, cortisol, insulin, C-peptide, fatty acids, acetoacetate, 3-hydroxybutyrate, glycerol, branched-chain amino acids, acetylcarnitine profile, lactate, pyruvate.

First urine after hypoglycemia:
- Determination of the content of organic acids.
- Consider saving blood and urine for toxicological analysis, eg salicylates, sulfonyluria.

Causes of hypoglycemia after the neonatal period:
Starvation

Excess insulin:
- Excessive exogenous insulin intake, for example, in diabetes mellitus (latent insulin intake).
- Tumors / increased b-cell function - PHGM (formerly called pancreatic islet hyperplasia), insulinoma.
- Induced by taking medications.
- Autoimmune (antibodies to insulin receptors).
- Beckwith's syndrome (visceromegaly syndrome and ophthalmocele).

Without hyperinsulinemia:
- Diseases of the liver.
- Ketotic hypoglycemia of childhood.
- Congenital metabolic disorders, for example, disorders of glycogen accumulation.
- Hormonal deficiency: GH, ACTH, Addison's disease, congenital adrenal hyperplasia.

Reactive (not as a result of starvation):
- Galactosemia.
- Sensitivity to leucine.
- Fructose intolerance.
- Maternal diabetes.
- Hormonal deficiency.
- Poisoning with aspirin / alcohol.

P.S. ACTH is an adrenocorticotropic hormone. GH is a growth hormone. PHGM - persistent hypoglycemic hyperinsulinism of infants.

Ketotic hypoglycemia- a poorly defined concept in which young children become prone to hypoglycemia after a short period of fasting, possibly due to limited reserves for gluconeogenesis. The child is often short and thin, and has low insulin levels. Regular snacks and drinks with added glucose when sick can usually prevent hypoglycemia. This state goes away by itself in later life.

Some rare endocrine and metabolic disorders can manifest as hypoglycemia at almost any age in children. Hepatomegaly raises the suspicion of the possibility of a congenital disorder of glycogen accumulation, in which there may be severe hypoglycemia.

Persistent hypoglycemic hyperinsulinism In infants (PHGM), formerly called islet cell hyperplasia of the pancreas) is a rare disease in infancy in which there is a mutation in ion channels that leads to dysregulation of insulin release by the islet cells of the pancreas, resulting in severe non-ketotic hypoglycemia.

Treatment of hypoglycemia in children

Hypoglycemia usually can be corrected by intravenous glucose infusion (2-4 ml / kg 10% dextrose). It is necessary to take measures to avoid the introduction of excess volume, since the solution is hypertonic. If there is a delay in the start of the infusion or there is no response, glucagon (0.5-1 mg) is injected intramuscularly.

Glucocorticoids may also be used if hypopituitarism or hypoadrenalism is likely. Correction of hypoglycemia should always be documented with satisfactory laboratory glucose results.

Hypoglycemia:
Should be ruled out in any child with septicemia, severe condition, prolonged epileptic seizure, or impaired level of consciousness.
Low blood glucose levels when tested near the patient's bed (with test strips) must be confirmed by laboratory findings.
If the cause is unknown, a blood and urine specimen should be collected, if possible, at the same time.

In a condition such as hypoglycemia, treatment is required at any stage.

Emergency relief of hypoglycemia should be carried out if a severe symptomatic picture is observed.

Without quick and proper assistance, a person can fall into a state of hypoglycemic coma and get serious organic brain damage.

It is important for the treatment.

In medicine, there are two types of hypoglycemia:

• fasting, that is, occurring on an empty stomach;
• hypoglycemia after eating.

Fasting hypoglycemia is considered less treatable. When an attack of hypoglycemia occurs, rapid first aid and medical assistance is required.

When conducting differential diagnosis and establishing the causes of hypoglycemic syndrome, complex treatment is prescribed.

Lean hypoglycemia is determined by sugar tests after an eight-hour fast, as well as after 3 days of a special diet. Since it depends on, it is also called insulin hypoglycemia.

Another type of hypoglycemia is more often determined in women with asthenic physique, 2-3 hours after eating. After a short drop, the amount of sugar rises again rather quickly. The violation is confirmed by taking blood sugar during an attack.

Each type of hypoglycemia can be mild or severe.

Relief of mild hypoglycemia

For the treatment of a mild form of the disease, as a rule, easily digestible carbohydrates are used:

• foods containing fructose or sucrose;
• chocolate bars;
• honey, beekeeping products;
• White bread.

With the progressive course of the disease, diagnostics, tracking the dynamics and the use of prescribed drugs are urgently required.

Relief of severe hypoglycemia

Symptoms of a severe form of the disease manifest themselves violently and vividly with the following signs:

• confusion of consciousness, speech and coordination;
• convulsive conditions, muscle contractions;
• fainting, up to coma.

The first medical aid is the application of 50 ml of a 40% glucose solution, which should be administered as soon as possible.

The second option for providing assistance is the injection of the drug Glucagon, the action of which is opposite to insulin.

When the patient returns to consciousness, it is necessary to feed him with food high in carbohydrates, in small portions with short breaks between meals.

The blood sugar level is checked every 5-7 hours until the hypoglycemic state is completely eliminated.

What to do in extreme cases?

How to treat hypoglycemia if a person still does not regain consciousness?

In this case, the attending physician begins intensive therapy for hypoglycemia with the following rehabilitation measures:

1. For several days, continue to inject a 5% glucose solution with the addition of prednisolone solution to it.
2. A cocarboxylase preparation is administered.
3. Introduced 5% solution of ascorbic acid increases glucose levels.
4. Subcutaneous injection of epinephrine before each glucose infusion.

With an increase in blood sugar levels above 12 mmol / l, small doses of insulin are added.

If a person does not come to his senses for a long time, it is necessary to prevent cerebral edema.

For this, the following drugs are used:

• Mannitol solution;
• drug Lasix;
• magnesium sulfate solution;
• Prednisolone solution;
• inhalation of humidified oxygen.

After discontinuation, use means to improve metabolism in the cells of the central nervous system:

• glutamic acid;
• Stugeron;
• Aminalon;
• Cerebrolysin;
• Cavinton.

Rehabilitation therapy is carried out within a month.

Medicines: tablets and gels

For fast and effective relief of hypoglycemia at home, the following tablets and gels are used:

1. Blisters with Girofri tablets, each of which contains 4 grams. dextrose (glucose).
2. Bystroza in the form of tablets, 4 g each. Easy to chew, soft and tasty.
3. Dextro 4 tablets and gel, consisting of pure D-glucose, has a fast absorption process directly in the mouth.

Gel cups are widely used to help faint people.

This form of drug can be easily rubbed into the gums or squeezed out between the teeth. The gel dissolves well in the mouth.

Gel Dextro 4 is approved for use in newborns. Thus, possible brain damage in newly born children is prevented.

Pathologies and low glucose

Differential diagnosis of hypoglycemia consists in separating this pathological condition from many other pathologies of the endocrine system.

The probability of complications and the prognosis for recovery directly depend on the correct formulation of the main diagnosis.

There are the following prerequisites that lead to a hypoglycemic state:

• tumors of the islets of Langerhans;
• liver pathologies, congenital and acquired;
• in pregnant women;
• renal failure;
• early stages of diabetes mellitus;
• alcohol or food intoxication;
• surgical intervention in the area of ​​the digestive tract.

By collecting information about the patient, you can also determine the following reasons affecting the hypoglycemic index:

• stress;
• neuroses;
• mental disorders.

In addition to the medical history, the doctor for differential diagnosis will need ultrasound data of internal organs, as well as an extended biochemical analysis of the patient's blood.

Based on the test results, you can prescribe adequate treatment for the underlying disease, which leads to a drop in blood sugar.

Features of therapy for hypoglycemia after eating

Correction of the hypoglycemic state, which begins after eating, should be carried out using a diet, fractional nutrition. The main condition for this tactic is to reduce the amount of carbohydrates in the diet.

Treatment of fasting hypoglycemia

This type of ailment is corrected by an increase in carbohydrates in the diet. such as Dilatin and Anaprilin do this task well.

But they only remove some of the lowered amount of glucose in the blood, while it is necessary to deal with the elimination of the cause.

Low Sugar Treatment in Newborns

Initial care for newborns with established hypoglycemia is intravenous glucose solution.

If low blood sugar syndrome recurs, hydrocortisone may be used, the dose of which is calculated by weight. It is used every four hours.

With proper medical manipulations, the not serious condition of newborns is completely cured within 1 week after birth, since by this time the insular apparatus is normalized.

What tests are needed?

For an accurate diagnosis, the results of several types of analyzes are required:

• test with insulin hypoglycemia;
• blood chemistry;
• Analysis of urine.

The main thing for determining the severity of the disease is the analysis of a sample with insulin hypoglycemia. This is a special test that involves the introduction of a certain amount of insulin to the patient and when the hypoglycemic threshold of 2.2 mmol / L is reached, a blood test for cortisol is taken.

If the amount of cortisol is less than 540 nmol / L, then true hypoglycemia is confirmed.

Carrying out the test requires special care from a medical professional; all day after the test, the patient is in the hospital under the supervision of doctors.

A comprehensive approach to hypoglycemia

A patient diagnosed with hypoglycemia should undergo the following treatments:

• fortifying therapy with medications;
• physiotherapy;
• a diet rich in protein foods and carbohydrates;
• phytotherapy.

Good tincture of leuzea, lemongrass leaves. Rosehip infusion will not only raise sugar, but also add vitamins C and K necessary for the body.

In hypoglycemic conditions, black currant and lemon are especially suitable. A large amount of sugar is found in these products, as well as special substances that normalize the metabolic process.

Can hypoglycemia be permanently cured? The state of high blood sugar in milder forms can be corrected and controlled with glucose and dextrose preparations.

Severe forms require constant monitoring. Their elimination is facilitated by the successful treatment of the underlying disease, which is the cause of the hypoglycemic state.