General information
Carbohydrate metabolism largely determines the general state of metabolism . Carbohydrates take part in almost all types of metabolism: proteins (glycoproteins), nucleic acids (ribose/deoxyribose), lipids (glycolipids), nucleotides (ATP, AMP, ADP), nucleosides (adenosine), ions. Simple and complex carbohydrates are one of the main sources of energy that ensure the vital functions of the body and are an essential component of the diet. Disorders of carbohydrate metabolism are combined into several typical forms (groups) of pathology: hypo- and hyperglycemia , aglycogenoses , glycogenoses , hexoses and pentosemias .
Hyperglycemia is a clinical symptom characterized by an increase in blood glucose (in plasma) of more than 6.5 mmol/L on an empty stomach and more than 8.9 mmol/L at any time of the day). ICD-10 hyperglycemia code: R73.9 - Hyperglycemia, unspecified. Based on the glucose level (GLU), a mild state of 6.7-11.1 is distinguished. It is characterized by a significant and persistent increase in BPC to a level of 10.5-11.0 mmol/l and is combined with a disorder of the body’s vital functions. This kind of hyperglycemia is defined as hyperglycemic syndrome. The most severe manifestation is a hyperglycemic crisis (GPC > 16.5).
The subject of the article is early disorders of carbohydrate metabolism, which some authors define as “prediabetes”. Early disorders of carbohydrate metabolism usually include the state of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) or a combination of these conditions (IGT+IGN). It is generally accepted that prediabetes is accompanied by a high risk of developing type 2 diabetes, but in some cases prediabetes does not convert into type 2 diabetes and is assessed by a number of authors as an independent risk factor for the development of cardiovascular diseases. Essentially, these are borderline disorders of carbohydrate metabolism that precede the development of diabetes mellitus , i.e. hyperglycemia with glucose values insufficient for the diagnosis of diabetes.
It has been established that with IGN, liver insulin resistance and hyperproduction of glucose by the liver are more pronounced than with isolated IGT, which is confirmed by higher liver glucose production and the insulin resistance index. IGT is characterized by peripheral insulin resistance, confirmed by lower insulin . In cases of a combination of these conditions (IGT+NGN), the first phase of insulin secretion is disrupted.
According to the literature, the global prevalence of IGT in people aged 30 to 70 years is about 6.7% and continues to increase, and in the Russian Federation, about 19% of the active population have prediabetes, that is, these people are at risk of developing diabetes. Prediabetes, like T2DM, is associated with age and weight gain. Gender differences in the prevalence of early carbohydrate metabolism disorders have not been identified.
According to expert data, the risk of developing type 2 diabetes in people with IGT is 6 times higher than in people with normal glucose tolerance, and in cases of a combination of IGT/NGN, the risk is twelve times higher. The relative risk of overall mortality in persons with IGT is 1.48 times higher than normal, while the risk of cardiovascular complications increases by 1.66 times. In the presence of IFN, the risk of developing T2DM is 4.7 times higher than in persons with normal glucose tolerance. IFN is also associated with a relatively high risk of developing cardiovascular complications.
Thus, active intervention must be carried out already at the prediabetic level of glycemia (stage of NGN and IGT), thereby preventing the development of type 2 diabetes, which is accompanied by various complications in the form of visual impairment, atherosclerosis of the vessels of the heart, lower extremities and brain, nephropathy , and damage to the nervous system.
For this purpose, all individuals need regular screening, which makes it possible to identify IGT, IFN, and type 2 diabetes as early as possible and, accordingly, begin timely treatment, thereby preventing the risk of developing severe complications and potential disability of the patient in the future. For this purpose, the Postprandial Glucose test should be performed regularly, especially in persons at high risk of diabetes, which determines the blood sugar level after a meal (after 2 hours). This test allows you to identify prediabetes at an early stage, when fasting blood glucose levels are still normal. The frequency of self-monitoring of glucose levels is adjusted depending on the needs, specific circumstances and goals of the patient. The emergence of individual glucometers of various types for measuring glycemic levels makes self-monitoring relatively simple and accessible to most interested parties.
of diabetes mellitus, postprandial glucose test indicators are also used to assess the risk of complications from the cardiovascular system ( atherosclerosis , coronary artery disease) in T2DM.
Irkutsk City Clinical Hospital No. 9
Memo for the patient:
What to do to prevent the development of hyperglycemia and diabetes.
Facts about hyperglycemia and diabetes:
- There is a new case of diabetes every 20 minutes in the United States, and every forty minutes in Europe.
- Currently, the prevalence of overt diabetes mellitus among the population of economically developed countries reaches 4-7%. However, mass surveys have shown that there are twice as many patients with latent forms of diabetes.
- In individuals whose body weight exceeds the norm by 20%, diabetes mellitus is detected 10 times more often than in the population. Among people with severe obesity, the incidence of diabetes increases 30 times. The combination of several risk factors has been shown to increase the likelihood of developing clinical diabetes mellitus by approximately 29 times.
- The mortality rate among patients with diabetes mellitus who have suffered a myocardial infarction is 1.5 - 2.5 times higher than in persons without carbohydrate metabolism disorders.
Hyperglycemia (high blood sugar) occurs when blood sugar levels rise above normal. This occurs when the pancreas does not produce enough insulin or it does not work as well as it should. Then glucose, the main source of energy, is not absorbed by the cells, the cells begin to “starve”, and weakness develops; blood sugar, on the contrary, rises and draws water from the cells - thirst appears; Due to metabolic disorders, small and large vessels of the brain, heart, kidneys and other organs are quickly affected, and immunity is impaired.
Check if you have any signs of diabetes?
- strong thirst;
- drowsiness;
- blurred vision;
- frequent urination;
- irritability;
- itching (especially in the perineal area);
- dry skin, pustules and boils;
- increased appetite;
- sticky urine.
If blood glucose levels are too high, diabetes develops. In 95% of cases, this is type 2 diabetes, which occurs more often in people over 40 years of age who lead an unhealthy lifestyle. Look, maybe you also have risk factors for this dangerous disease?
- age over 45 years;
- diabetes mellitus in relatives;
- excess body weight;
- low physical activity;
- accidentally detected elevated glucose levels during examination;
- increased blood sugar during pregnancy and the birth of a large fetus;
- high blood pressure, above 140/90 mmHg;
- changes in cholesterol metabolism (low high-density lipoprotein levels ≤ 0.9 mmol/l and/or triglyceride levels ≥ 2.82 mmol/l);
- polycystic ovary syndrome;
- suffered strokes, heart attacks.
If something has alerted you, then the only way to check whether you have diabetes or not is to do a blood test: determine your glucose level on an empty stomach and/or 2 hours after taking 75 grams of glucose. The frequency of examination depends on the risk group you fall into.
Risk group | Frequency of examination |
Persons over 45 years of age | At least once every 3 years; |
Combination of 3 or more risk factors | At least once every 3 years; |
Persons with prediabetes, especially those who are overweight | Once every 1-2 years |
Capillary blood glucose level
Carrying out analysis | Norm | Prediabetes | Diabetes |
On an empty stomach | 3,3-5,5mmol/l | 5,5-6,1mmol/l | > 6,1mmol/l |
2 hours after taking 75 grams of sugar or any time of the day | < 7,8mmol/l | 7,8-11,1mmol/l | >11,1mmol/l |
You can also check your risk of developing prediabetes or type 2 diabetes in the next 10 years using the following questionnaire:
- Age: up to 45 years (0 points), 45-54 years (2 points), 55-64 years (3 points), over 65 years (4 points).
- Body mass index - height (m) divided by body weight (kg) squared, for example, with a height of 165 cm and a weight of 73 kg, the index is 73: (1.65 m X 1.65) = 26.8 = 27 kg /m2: below 25 kg/m2 (0 points), 25-30 kg/m2 (1 point), more than 30 kg/m2 (3 points).
- Waist circumference - measured under the ribs at the level of the navel. Men: less than 94 cm (0 points), 94-102 cm (3 points), more than 102 cm (4 points). Women: less than 80 cm (0 points), 80-88 cm (3 points), more than 88 cm (4 points).
- How often do you eat vegetables, fruits or berries? Every day (0 points), not every day (1 point);
- Do you exercise regularly? Do you exercise 30 minutes every day or 3 hours during the week? Yes (0 points), no (2 points);
- Have you ever taken medications regularly to lower your blood pressure? No (0 points), yes (2 points).
- Have you ever had your blood sugar level higher than normal (during preventive examinations, during illness or pregnancy)? No (0 points), yes (5 points).
- Did your relatives have type 1 or type 2 diabetes? No (0 points), yes: grandparent, aunt/uncle, cousins (3 points), parents, brother/sister or own child (5 points).
TOTAL POINTS__________________________
Your risk of developing type 2 diabetes over 10 years is:
Total points | DM risk level 2 | Probability of developing type 2 diabetes |
Less than 7 | Low risk | 1 in 100 (1%) |
7-11 | Slightly elevated | 1 in 25 (4%) |
12-14 | Moderate | 1 out of 6 (17%) |
15-20 | High risk | 1 out of 3 (33%) |
more than 20 | Very high risk | 1 out of 2 (50%) |
- If you score less than 12 points, you are in good health and should maintain a healthy lifestyle.
- If you score 12-14 points, you may have prediabetes. You should ask your doctor about lifestyle changes.
- If you score 15-20 points, you may have prediabetes or type 2 diabetes. It is advisable for you to check your blood sugar levels. You may need to change your lifestyle and may need medication to control your blood sugar levels.
- If you score more than 20, you most likely have type 2 diabetes. You should regularly check your blood sugar levels with a glucometer. You need to change your lifestyle and need medications to control your blood sugar levels.
Diabetes prevention should start in the kitchen.
About 80% of patients with type 2 diabetes are overweight, which weakens the effect of insulin. Therefore, the primary task in this situation is to reduce weight (not to the full norm, but 5-10% below the original) and maintain it at this level through continued dieting. This diet should be tasty, varied, not cause a feeling of hunger, but contain fewer calories than the patient consumed before; for this you just need to follow some rules:
These products should be sharply limited:
a) Severely increases blood sugar:
- Sugar, honey, dried fruits, fruit juices, confectionery, sweets, jam, lemonades (“Fanta”, “Pepsi”, etc.), natural kvass.
- Semolina porridge, mashed potatoes, heavily boiled porridge.
b) Contain a lot of calories:
- Butter, vegetable oil (especially in salads, vinaigrettes and when heating food), sour cream, mayonnaise, butter substitutes (Rama, etc.).
- Lard, sausages and sausages, sausages and pates, smoked meats, fatty meat, fatty fish, meat by-products (liver, liver), chicken legs, poultry skin.
- Fatty (“yellow” and processed) cheeses, cream, fatty cottage cheese.
- Nuts and seeds, pies and pies.
The consumption of these products should be halved:
- Bread (black or white), cereals (rice, buckwheat, oatmeal, etc.).
- Potatoes, pasta, corn and soy products, crackers, crackers (unsweetened), etc.
- Fruits: distribute throughout the day.
- Candies, waffles, etc.: as an “infrequent treat” (once a week).
- Acceptable in moderation: lean meat, fish, cottage cheese.
Increase consumption:
- Vegetables (but without added fat) in the form of vegetable side dishes : cabbage, cauliflower, carrots, beets, turnips, radishes, cucumbers, tomatoes, greens.
- Drinks without sugar: mineral water, tea).
Physical activity to prevent diabetes Aerobic exercises are indicated, such as: walking, jogging, swimming, tennis, cycling, rhythmic gymnastics (promote more intense absorption of oxygen by the body and are beneficial for the heart and blood vessels). Aerobic physical activity ensures maximum oxygen delivery to organs and tissues, so they must be performed at a certain heart rate, which is calculated individually for each person.
|
Pathogenesis
The pathogenesis of prediabetes is caused by a qualitative/quantitative deficiency of insulin, which is based on a decrease in insulin activity in adipocytes, muscle tissue and hepatocytes, caused by a deficiency in insulin production by pancreatic β-cells and insulin resistance (decreased sensitivity of receptors to insulin). These disturbances in the post-receptor action of insulin, together with an increasing decrease in insulin production, contribute to an increase in glucose to the corresponding values of NGN (6.1–6.9 mmol/l) and/or IGT (7.8–11.0 mmol/l after OGTT with glucose) . In patients with moderate hyperglycemia, the underlying cause is a decrease in insulin sensitivity of peripheral tissues, mainly muscle tissue. And with hyperglycemia on an empty stomach, an additional negative effect may be an increase in glucose production by the liver.
Treatment of hyperglycemia in a hospital setting
The relationship between hyperglycemia and acute illness is complex [1,3,4]. Hyperglycemia often occurs in hospitalized patients due to increased levels of stress hormones. Experimental studies have shown that severe hyperglycemia [blood glucose levels above 250 mg/dL (13.9 mmol/L)] has negative effects on the cardiovascular and immune systems (Fig. 1) [1,3,4]. Several retrospective studies have shown that hyperglycemia is associated with mortality in inpatients. Glucose levels after surgery are an important predictor of the likelihood of developing infectious complications in patients who have undergone cardiac surgery [5,6]. In a study of diabetic patients with myocardial infarction, elevated glucose levels during hospitalization were associated with mortality both during hospitalization and during the first year after infarction [7]. Similar results were obtained in patients treated in intensive care units (ICU) [8], patients after surgery [9], as well as people who suffered acute cardiovascular disorders other than a heart attack, including stroke [10–12]. The association between blood glucose levels and the risk of death continued to be significant even after controlling for disease severity [12]. Such observations are not limited to patients with diabetes [10–12]. According to one study, mortality during hospital stay is higher in patients in whom hyperglycemia was diagnosed for the first time, compared with those diagnosed with diabetes mellitus [13]. Such data, although interesting, do not allow us to talk about the presence of a cause-and-effect relationship. The question of whether increased glucose levels are a potentially remediable mechanism for the development of complications or whether it is simply a symptom accompanying serious diseases continues to remain open. If an increase in glucose levels in itself is dangerous, then intensive correction may be simply necessary. Obviously, insulin therapy and monitoring its results require time and money. In addition, such treatment increases the risk of developing hypoglycemia, which can lead to serious complications. What is the evidence that tight glucose control during hospitalization improves treatment outcomes? Strategies and evidence Several studies have examined the effects of close blood glucose control in critical care settings, but these studies included very heterogeneous groups of patients (with and without diabetes). In addition, study designs, treatment goals, and insulin administration techniques varied widely. Accordingly, the results obtained were very different. In a study that included 1,499 patients treated in the ICU of the cardiothoracic surgery department, the use of insulin in the form of an infusion to reduce glucose levels to 150–200 mg/dL (8.3–11.1 mmol/L) over 24 hours after open heart surgery led to a significant reduction in the incidence of infection of postoperative wounds compared to patients who were treated with insulin according to the standard regimen (0.8% vs. 2.0%). The lack of randomization complicates the interpretation of these results due to the fact that the control group was formed retrospectively and during the time that elapsed from the moment these patients were in the hospital, the quality of medical care could have improved. It should be noted, however, that similar results were obtained in smaller randomized and non-randomized studies that also examined the effectiveness of blood glucose control after cardiac surgery. In the Diabetes Insulin–Glucose Infusion in Acute Myocardial Infarction (DIGAMI) trial, 620 diabetic patients with myocardial infarction were randomized to intensive or standard glucose management during hospitalization and for 3 months after discharge [16]. Intensive treatment with insulin infusion within the first 24 hours of hospitalization to reduce glucose levels to 126–196 mg/dL (7.0–10.9 mmol/L), followed by multiple insulin injections to maintain mean glucose concentrations at 173 mg/dL (9.6 mmol/L) was significantly different from the standard, against which the average glucose level was 211 mg/dL (11.7 mmol/L) (p<0.001). In the group of patients receiving intensive treatment, mortality during the first year was 29% lower compared to the group receiving standard treatment (18.6% vs. 26.1%, p = 0.03), a significant difference in mortality rates remained at follow-up for 5 years [17]. However, the study design did not allow definitive conclusions about whether inpatient or outpatient treatment resulted in improved survival. The DIGAMI-2 study aimed to address this issue by randomizing 1253 patients with diabetes to receive three different treatments after acute myocardial infarction: intensive inpatient [insulin infusion, target glucose concentration 126 to 180 mg/dL (7.0 up to 10.0 mmol/l)] and outpatient treatment, intensive treatment only in a hospital setting and standard treatment [18]. There were no significant differences in mortality or complication rates between the groups, but the statistical power of the study was weak and the differences in mean glucose levels between the groups were small. In this regard, it is difficult to draw definite conclusions from the results of this and another study that had the same shortcomings [19]. Studies examining the effectiveness of glucose-insulin-potassium infusion (GIK) also yielded conflicting results [20]. In these studies, the goal was not to achieve a specific blood glucose level, but to evaluate the potential beneficial effects of insulin administration itself during or shortly after myocardial infarction. According to the largest of the studies, which included 20 thousand patients, the introduction of GIK did not lead to improved treatment results, although it should be noted that glucose levels in the study group were higher than in the control group. However, there is fairly good evidence that tight blood glucose control in the ICU setting improves treatment outcomes. Thus, a randomized trial of 1548 intubated patients in the surgical ICU (13% had diabetes mellitus) compared intensive treatment with insulin infusion [target glucose 80 to 110 mg/dL (range 4.4 to 6 .1 mmol/l)] with standard treatment [intravenous insulin administration only to those patients whose glucose levels exceeded 215 mg/dl (11.9 mmol/l)] [22]. Mortality was 42% lower in the intensively treated group (4.6% vs. 8.0%, p<0.04). This decrease occurred primarily in patients who were in the ICU for more than 5 days. In addition, patients receiving intensive treatment had a significantly lower incidence of dialysis and septicemia, as well as the need for blood transfusion or mechanical ventilation. In another study, which included 1200 patients in general ICU, conducted according to the same scheme, the results were less clear [23]. Overall, in-hospital mortality was not significantly reduced in patients receiving intensive versus standard treatment (37.3% vs. 40.0%, p=0.33). At the same time, intensive treatment led to a decrease in the incidence of complications (including a decrease in the duration of mechanical ventilation) and earlier discharge. In addition, in the group of patients who were in the ICU for 3 days or more (767 patients), intensive treatment led to a decrease in in-hospital mortality (43.0% vs. 52.5%, p=0.009). However, it is impossible to predict in advance the duration of stay in the ICU, and intensive treatment increased mortality among patients who were in the ICU for less than 3 days. This increase, although not statistically significant (relative risk 1.09; 95% confidence interval 0.89 to 1.32), may be of great significance. In both studies, hypoglycemia [defined as glucose levels less than 40 mg/dL (2.2 mmol/L)] was significantly more common in patients receiving intensive care compared with standard care (5.2% vs. 0.7% in surgical ICU [22] and 18.7% vs. 3.1% in general ICU [23]). Although hypoglycemia did not lead to hemodynamic disturbances or seizures, its significance in severely ill patients remains unclear. Moreover, in a study conducted in a general ICU, hypoglycemia was an independent predictor of the risk of death. The potential for more cautious intensive treatment was explored in a study involving a mixed group of surgical and general ICU patients in which insulin was administered subcutaneously to achieve glucose levels below 140 mg/dL (7.8 mmol/L). Insulin infusion was administered only if glucose levels exceeded 200 mg/dL [24]. In-hospital mortality was significantly lower among patients receiving intensive care compared with the control group based on medical records (14.8% vs. 20.9%, p=0.002). To date, there is no data on the effectiveness of intensive treatment of hyperglycemia in inpatients outside the ICU. Factors influencing the choice of treatment Insulin resistance and the ability of patients to secrete this hormone is influenced by a number of factors, including the severity of the disease, medications taken (primarily glucocorticoids and pressor agents). In addition, the nutrition of patients in the hospital is often interfered with by examinations and operations, which can also interfere with the medication regimen, which prevents adequate control of blood glucose levels [3,4,25]. It is important to know whether the patient has diabetes and, if so, its type (since patients with type 1 diabetes are at increased risk of developing ketoacidosis), as well as how glucose levels were corrected before hospitalization. You should also pay attention to: – the patient’s dietary habits, which determine the dosage of insulin; – normal blood glucose level, which is important for deciding on the intensity of treatment and the speed of correction of hyperglycemia; – degree of control over blood glucose levels before hospitalization; – level of glycated hemoglobin (may allow assessing the need for more intensive treatment in patients with diabetes mellitus, and in patients with newly diagnosed hyperglycemia, an increase in the concentration of glycated hemoglobin indicates the presence of diabetes before hospitalization). When determining the advisability of intensive therapy, it is necessary to evaluate the duration of the patient's stay in the hospital. Oral drugs Insulin is the preferred drug for the treatment of inpatients, since its dose can be more carefully and quickly selected and has no restrictions. However, in certain patients (especially those whose condition is not severe and who are able to eat normally), oral medications can be continued if they are effective before hospitalization. Particular attention should be paid to the prescription of metformin, taking into account contraindications to its use (including renal failure, heart failure and the need for X-ray studies with the introduction of a contrast agent). Thiazolidinediones should be discontinued if signs of heart or liver failure are present (even after discontinuation, the antihyperglycemic effects of these drugs may persist for several weeks). For patients who eat irregularly, drugs that cause insulin release (for example, from the sulfonylurea group) are especially dangerous, and alpha-glucosidase inhibitors are ineffective. A moderate reduction in drug dosage can be made in patients undergoing hospital treatment and receiving a calorie-restricted diet, since such a diet may reduce the severity of hyperglycemia. If glucose levels are significantly elevated on admission or if glucose control deteriorates while in hospital, as is often the case, insulin treatment should be started. Insulin In ICU settings, insulin is usually administered by long-term intravenous infusion. There are several generally accepted administration protocols [3,22,26–30]. The most effective are those that use a dynamic scale, allowing dose changes depending on changes in glucose levels [29,31]. Frequent glucose testing (usually every hour) is essential to minimize the risk of hypoglycemia. As the patient's condition improves, you can proceed to subcutaneous insulin administration; in this case, for calculations, the last infusion rate is used, multiplied by the intervals between administrations, the final dose is divided into the main and food-related parts (Fig. 2). It should be noted that long breaks between intravenous and subcutaneous administration should be avoided, especially in patients with type 1 diabetes mellitus. Patients with type 2 diabetes who require less than 2 units of insulin per hour may receive less intensive treatment; For some patients, oral medications may be sufficient. Outside of intensive care units, insulin dosing scales are still widely used to determine the level of hyperglycemia [4]. The use of such tactics is usually not effective enough [32], especially in patients with type 1 diabetes who require a constant supply of insulin to suppress ketogenesis. Better control can be achieved with preventive administration. Administration methods including basal insulin (intermediate-acting or long-acting) and short-acting insulin administered before meals to reduce postprandial hyperglycemia provide results that are closer to physiological levels [3,33–35]. Fast-acting insulin analogues (lispro, aspart and glulisine) should be administered immediately before meals. Standard human insulin should be administered 30 minutes before meals, which is often difficult in hospital settings due to busy staff. In addition, rapid-acting medications provide better control of postprandial hyperglycemia. In patients whose diet is uncertain, conservative management should be followed. An alternative is to administer rapid-acting insulin immediately after a meal, the dose being determined based on the amount of food consumed. Additional adjustment doses may be administered along with prandial insulin to compensate for premeal hyperglycemia. Insulin-sensitive patients (most patients with type 1 diabetes, thin patients receiving relatively small doses of insulin (less than 30-40 units per day), and those prone to hypoglycemia) require small adjustment doses (for example, 1 unit to correct glucose levels 150 mg/dL (8.3 mmol/L), 2 units for 200 mg/dL (11.1 mmol/L), etc.). Most patients with type 2 diabetes (who are overweight or receiving moderate doses of insulin - 40 to 100 units per day) require moderate adjustment doses (for example, 2 units for a glucose level of 150 mg/dL, 4 units for a glucose level of 200 mg). /dl, etc.). Some patients with type 2 diabetes and severe insulin resistance (severely obese, receiving large doses of insulin (more than 100 units per day), or taking corticosteroids) should receive large adjustment doses (eg, 4 units at a blood glucose level of 150 mg/dL , 8 units at 200 mg/dL, etc.). As the patient's general condition improves, insulin sensitivity may increase. As a rule, if the patient's condition is stable, the dose ratio of basal and prandial insulin is 1:1. The dose of basic insulin is selected depending on the overall dynamics of changes in glucose concentration. If glargine or detemir is used, dose determination is based on morning glucose concentrations. When using NPH, its dosage is calculated based on the morning glucose concentration or its values before the evening meal. During the dose selection period, you can also include a corrective dose in the main one, adding 50% of the corrective dose applied on the previous day to the main one. The dose of prandial insulin is determined based on levels of postprandial hyperglycemia. The corrective dosage of insulin can be selected based on the effectiveness of the previously used dose. To ensure the patient's safety, insulin requirements should be reassessed immediately after any dietary changes. Some people with type 2 diabetes may benefit from less aggressive treatment, such as basal insulin alone (eg, glargine once daily, detemir once or twice daily, or NPH twice daily) or a convenient premix that includes insulin. medium and short or very short action (for example, “70/30”). A similar approach can be justified in patients with moderate hyperglycemia, especially if you plan to extract and there is no time for a thorough selection of dose of insulin. If the patient receiving insulin does not eat, only the main dose in the form of standard insulin every 6 hours should be administered. This is absolutely necessary in patients with type 1 diabetes and preferably in patients with type 2 diabetes. In such cases, you can also use insulin infusion, especially if the adequacy of absorption from subcutaneous tissues is in doubt. In patients who independently eat and receive insulin, the administration regimen used before hospitalization can be preserved with its effectiveness. As in the case of oral preparations, depending on the clinical situation, it is possible to reduce the dose of insulin with a decrease in the calorie content of the nutrition. This is especially true for patients with type 2 diabetes. If the concentration of glucose during admission is high (more than 200 mg/DL), the dose of insulin should be increased. The possibility of transition to corrective doses should be considered. If severe hyperglycemia [glucose level from 300 to 400 mg/DL (from 16.7 to 22.2 mmol/l)] remains for more than 24 hours and is not amenable to the correction of increased doses of subcutaneous insulin, the possibility of its intravenous infusion should be considered. It should be noted that due to the short period of the half -life of insulin with intravenous administration (5–9 minutes), with the development of hypoglycemia, it can be quickly eliminated. For safety reasons, when using insulin infusion in general chambers (compared to Pete), one should strive for slightly higher concentrations of blood glucose. Monitoring the concentration of glucose in patients receiving constant enterenal nutrition through the probe is best achieved when using the main insulin, with the addition of corrective doses, if necessary, every 6 hours. If the feeding is interrupted, the same amount of carbohydrates (for example, dextrose) should be intravenously introduced, which should be entered endino to prevent hypoglycemia. If the patient is completely on parenteral nutrition, insulin can be added directly to the bottles with the latter. The dose is titrated with a step of 5-10 units per liter to achieve optimal control. For good control, a frequent assessment of the concentration of blood glucose is necessary, on the basis of which the dosage of insulin should be adjusted every 1-2 days. However, before increasing the dosage of the drug, it is necessary to evaluate the possible causes of hyperglycemia (for example, missed doses, excessive nutrition, infection) and eliminate them. Untimely control of glucose concentration, nutrition and the introduction of prandial insulin are also frequent causes of glucose levels in hospital conditions. For high -quality control of glucose levels, coordination of the actions of nurses and employees who ensure the nutrition of patients is necessary. Ideally, blood examination from the finger must be performed every time before meals and before bedtime. Early study of postprandial glycemia (within 2-3 hours after eating) can lead to excessively intense treatment with insulin, which should be avoided with the exception of special situations (for example, the treatment of pregnant women). Before the discharge, the insulin administration scheme should be simplified depending on the possibilities of the patient. In some patients with type 2 diabetes, it can be possible to prescribe prolonged insulin 1 time per day. Other patients who, during the period of stay in the hospital, required small doses of insulin or, with excellent monitoring of the blood glucose level with an introduction of less than 25-30 units per day, there may be sufficient diet correction or oral drugs. In the case of prescribing or cancellation of antihyperglycemic drugs or a change in their dosage during the period in the hospital, a second examination of patients is necessary 1-2 weeks after discharge. Similarly, stationary patients with first detected hyperglycemia should be carried out, although some patients do not need to continue treatment aimed at reducing glucose levels after compensation for the underlying disease. In such patients, the concentration of glucose on an empty stomach (and, if possible, glycated hemoglobin) should be controlled 1-2 months after discharge. Recommendations in two works [2.36] presents recommendations for monitoring the level of blood glucose in stationary patients (Table 1). These data are ambiguous because a small amount of randomized studies have been conducted. It is generally accepted that insulin should be introduced intravenously in the conditions of Pete and that other methods of insulin administration should be as close as possible to physiological conditions, especially in patients with type 1 diabetes [1–4,25]. Due to the lack of studies of the effectiveness of the subcutaneous administration of insulin in a hospital, recommendations are based on clinical experience. Firm areas have accumulated little data on the role of tight control of blood glucose levels in stationary patients. Although most studies show that a decrease in glucose levels in seriously ill patients improves survival rate [37], the exact targeted concentration, the optimal method of introduction and a group of patients, which are most in need of this approach (as well as methods for its determination), continue to be unknown [38 , 39]. Since intensive insulin therapy reduces mortality mainly among patients in Pete for a long time, we can conclude that not all seriously ill patients have the effectiveness of hard control of glucose levels is the same [22,23,40]. Continuing studies of intestatic treatment with insulin in Pete will provide new information on this issue [41]. The optimal approach to the correction of hyperglycemia in patients who have undergone myocardial infarction is unknown [14–17.42]. The data of the two recent studies that demonstrated the relationship between the development of hyperglycemia during hospitalization for myocardial infarction and an increased risk of death [43,44] deserve special attention. Although, in acute coronary syndromes, insulin has not only a hypoglycemic effect (but also anti -lobitic, vasodilating, anti -inflammatory and profibrinolytic) [45], the clinical significance of this phenomenon is unclear and contradictory [21]. It is unclear that the results of research in Pit can be distributed to not so severe patients. It should be carefully assessed the ratio between possible benefits and dangers (primarily the development of hypoglycemia). Conclusion and recommendations in surgical and general PIT concentration of blood glucose should be maintained at a level of less than 140 mg/DL [24,39] and, possibly, even less than 110 mg/DL [22,23]. The optimal indicators of the concentration of glucose in patients in cardioremation departments are more controversial: it is likely to strive for higher values (up to 180 mg/DL) [15]. Intravenous administration of insulin allows you to quickly choose a dose in seriously ill patients than with subcutaneous injections. In surgical and therapeutic patients who are not in serious condition, it is advisable to achieve the concentration of glucose before eating from 90 to 150 mg/DL (from 5.0 to 8.3 mmol/l) [39] not only to reduce the probability of hyperglycemia, But also in order to avoid hypoglycemia. It is important to note that tight control over glucose concentration should be carried out under the guidance of qualified personnel. Although the exact targeted concentrations of glucose in stationary patients remain uncertain [1–3,38,39], it is important to understand that during hospitalization, insulin treatment should be active, with frequent dose correction, in the form of intravenous infusion. When discharge, the patient needs to explain the treatment regimen on an outpatient basis.
Abstract prepared by V.V. Iremashvili based on the article by Inzucchi SE “Management of Hyperglycemia in the Hospital Setting”. New England Journal of Medicine 2006; No.355: pp.1903–1911.
References 1. Clement S, Braithwaite SS, Magee MF, et al. Management of diabetes and hyperglycemia in hospitals. Diabetes Care 2004; 27:553–91. [Errata, Diabetes Care 2004;27: 856, 1255.] 2. Garber AJ, Moghissi ES, Bransome ED Jr, et al. American College of Endocrinology position statement on inpatient diabetes and metabolic control. Endocr Pract 2004;10:77–82. 3. Trence DL, Kelly JL, Hirsch IB. The rationale and management of hyperglycemia for in–patients with cardiovascular disease: time for change. J Clin Endocrinol Metab 2003;88:2430–7. 4. Metchick LN, Petit WA Jr, Inzucchi SE. Inpatient management of diabetes mellitus. Am J Med 2002;113:317–23. 5. Zerr KJ, Furnary AP, Grunkemeier GL, Bookin S, Kanhere V, Starr A. Glucose control lowers the risk of wound infection in diabetics after open heart operations. Ann Thorac Surg 1997;63:356–61. 6. Golden SH, Peart–Vigilance C, Kao WHL, Brancati FL. Perioperative glycemic control and the risk of infectious complications in a cohort of adults with diabetes. Diabetes Care 1999;22:1408–14. 7. Malmberg K, Norhammar A, Wedel H, Ryden L. Glycometabolic state at admission: important risk marker of mortality in conventionally treated patients with diabetes mellitus and acute myocardial infarction: long–term results from the Diabetes and Insulin–Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study. Circulation 1999;99:2626–32. 8. Krinsley JS. Association between hyperglycemia and increased hospital mortality in a heterogeneous population of critically ill patients. Mayo Clin Proc 2003; 78:1471–8. 9. Pomposelli JJ, Baxter JK III, Babineau TJ, et al. Early postoperative glucose control predicts nosocomial infection rate in diabetic patients. JPEN J Parenter Enteral Nutr 1998;22:77–81. 10. Capes SE, Hunt D, Malmberg K, Gerstein HC. Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview. Lancet 2000;355:773–8. 11. Capes SE, Hunt D, Malmberg K, Pathak P, Gerstein HC. Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview. Stroke 2001;32:2426–32. 12. Kosiborod M, Rathore SS, Inzucchi SE, et al. Admission glucose and mortality in elderly patients hospitalized with acute myocardial infarction: implications for patients with and without recognized diabetes. Circulation 2005;111:3078–86. 13. Umpierrez GE, Isaacs SD, Bazargan N, You X, Thaler LM, Kitabchi AE. Hyperglycemia: an independent marker of inhospital mortality in patients with undiagnosed diabetes. J Clin Endocrinol Metab 2002;87:978–82. 14. Lazar HL, Chipkin SR, Fitzgerald CA, Bao Y, Cabral H, Apstein CS. Tight glycemic control in diabetic coronary artery bypass graft patients improves perioperative outcomes and decreases recurrent ischemic events. Circulation 2004;109:1497–502. 15. Hruska LA, Smith JM, Hendy MP, Fritz VL, McAdams S. Continuous insulin infusion reduces infectious complications in diabetics following coronary surgery. J Card Surg 2005;20:403–7. 16. Malmberg K, Ryden L, Efendic S, et al. Randomized trial of insulin–glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction (DIGAMI study): effects on mortality at 1 year. J Am Coll Cardiol 1995;26:57–65. 17. Malmberg K. Prospective randomized study of intensive insulin treatment on long-term survival after acute myocardial infarction in patients with diabetes mellitus. BMJ 1997;314:1512–5. 18. Malmberg K, Ryden L, Wedel H, et al. Intense metabolic control by means of in– sulin in patients with diabetes mellitus and acute myocardial infarction (DIGAMI 2): effects on mortality and morbidity. Eur Heart J 2005;26:650–61. 19. Cheung NW, Wong VW, McLean M. The Hyperglycemia: Intensive Insulin Infusion in Infarction (HI–5) study: a randomized controlled trial of insulin infusion therapy for myocardial infarction. Diabetes Care 2006;29:765–70. 20. Fath–Ordoubadi F, Beatt KJ. Glucoseinsulin–potassium therapy for the treatment of acute myocardial infarction: an overview of randomized placebo–controlled trials. Circulation 1997;96:1152–6. 21. Mehta SR, Yusuf S, Diaz R, et al. Effect of glucose–insulin–potassium infusion on mortality in patients with acute ST–segment elevation myocardial infarction: the CREATE–ECLA randomized controlled trial. JAMA 2005;293:437–46. 22. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med 2001; 345:1359–67. 23. Van den Berghe G, Wilmer A, Hermans G, et al. Intensive insulin therapy in the medical ICU. N Engl J Med 2006;354:449–61. 24. Krinsley JS. Effect of an intensive glucose management protocol on the mortality of critically ill adult patients. Mayo Clin Proc 2004;79:992–1000. [Erratum, Mayo Clin Proc 2005;80:1101.] 25. Moghissi ES, Hirsch IB. Hospital management of diabetes. Endocrinol Metab Clin North Am 2005;34:99–116. 26. Furnary AP, Gao G, Grunkemeier GL, et al. Continuous insulin infusion reduces mortality in patients with diabetes undergoing coronary artery bypass grafting. J Thorac Cardiovasc Surg 2003;125:1007–21. 27. Markovitz LJ, Wiechmann RJ, Harris N, et al. Description and evaluation of a glycemic management protocol for patients with diabetes undergoing heart surgery. Endocr Pract 2002;8:10–8. 28. Goldberg PA, Siegel MD, Sherwin RS, et al. Implementation of a safe and effective insulin infusion protocol in a medical intensive care unit. Diabetes Care 2004; 27:461–7. 29. Goldberg PA, Roussel MG, Inzucchi SE. Clinical results of an updated insulin infusion protocol in critically ill patients. Diabetes Spectrum 2005;18:188–91. 30. Ku SY, Sayre CA, Hirsch IB, Kelly JL. New insulin infusion protocol improves blood glucose control in hospitalized patients without increasing hypoglycemia. Jt Comm J Qual Patient Saf 2005;31:141–7. 31. Meijering S, Corstjens A, Tulleken JE, Meertens JHJM, Zijlstra JG, Ligtenberg JM. Towards a feasible algorithm for tight glycemic control in critically ill patients: a systematic review of the literature. Crit Care 2006;10:R19. 32. Queale WS, Seidler AJ, Brancati FL. Glycemic control and sliding scale insulin use in medical inpatients with diabetes mellitus. Arch Intern Med 1997;157:545–52. 33. Hirsch IB. Insulin analogues. N Engl J Med 2005;352:174–83. 34. Riddle MC. Glycemic management of type 2 diabetes: an emerging strategy with oral agents, insulins, and combinations. Endocrinol Metab Clin North Am 2005;34:77–98. 35. Edelman SV, Morello CM. Strategies for insulin therapy in type 2 diabetes. South Med J 2005;98:363–71. 36. American Diabetes Association. Standards of medical care in diabetes. Diabetes Care 2005;28:Suppl 1:S4–S36. [Erratum, Diabetes Care 2005;28:990.] 37. Pittas AG, Siegel RD, Lau J. Insulin therapy for critically ill hospitalized patients: a meta-analysis of randomized controlled trials. Arch Intern Med 2004; 164:2005–11. 38. Bryer–Ash M, Garber AJ. Point: inpatient glucose management: the emperor finally has clothes. Diabetes Care 2005; 28:973–5. 39. Inzucchi SE, Rosenstock J. Counterpoint: inpatient glucose management: a premature call to arms? Diabetes Care 2005;28:976–9. 40. Falciglia M, D'Alessio DA, Almenoff PLMD, Freyberg RW, Diab D, Render ML. Hyperglycemia and mortality in 252,000 critically ill patients. Presented at the 66th Scientific Sessions of the American Diabetes Association, Washington, DC, June 9–13, 2006. abstract. 41. ClinicalTrials.gov. Normoglycaemia in intensive care evaluation and survival using glucose algorithm regulation (NICESUGAR study). (Accessed October 6, 2006, at https://www.clinicaltrials.gov/ct/show/NCT00220987.) 42. Furnary AP, Zerr KJ, Grunkemeier GL, Starr A. Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures. Ann Thorac Surg 1999;67:352–62. 43. Pinto DS, Skolnick AH, Kirtane AJ, et al. U–shaped relationship of blood glucose with adverse outcomes among patients with ST–segment elevation myocardial infarction. J Am Coll Cardiol 2005; 46:178–80. 44. Svensson AM, McGuire DK, Abrahamsson P, Dellborg M. Association between hyper– and hypoglycaemia and 2 year allcause mortality risk in diabetic patients with acute coronary events. Eur Heart J 2005;26:1255–61. 45. Chaudhuri A, Janicke D, Wilson MF, et al. Anti–inflammatory and profibrinolytic effect of insulin in acute ST–segmentelevation myocardial infarction. Circulation 2004;109:849–54. 46. Cryer PE. Hypoglycaemia: the limiting factor in the glycemic management of the critically ill? Diabetologia 2006;49:1722–5. 47. Inpatient diabetes and glycemic control: management: a call to action conference, January 2006. AACE–ADA Consensus Development Conference position statement. (Accessed October 6, 2006, at https://www.aace.com/meetings/consensus/IIDC/.)
Causes
The causes of increased blood glucose vary widely, the main ones being:
- Hormonally caused hyperglycemia ( hyperthyroidism , diabetes mellitus , familial polyendocrine adenomatosis , acromegaly , pheochromocytoma , Itsenko-Cushing's disease ).
- Hyperglycemia of central origin (poisoning, brain injury with hemorrhages in the fourth ventricle of the brain, encephalitis , tumors ).
- Psychogenic disorders (stress).
- Diseases of the pancreas ( pancreatitis ), liver failure .
- Extreme prematurity of the child.
- Hyperglycemia against the background of the development of various critical conditions.
- Nutritionally-induced hyperglycemia (eating disorders - bulimia / long-term excess consumption of easily digestible carbohydrates; Prader-Willi syndrome - a predisposition against the background of obesity to the development of insulin-resistant diabetes in childhood; Sipe-Lawrence lipodystrophy - a predisposition to the development of T2DM; Urbach-Wiethe syndrome - a tendency to fasting hyperglycemia).
- Drug-induced hyperglycemia ( glucocorticosteroids , second-generation antipsychotics , stanines , thiazide diuretics , calcineurin inhibitors , etc.).
Risk factors for the development of carbohydrate metabolism disorders include:
- Presence of relationship with patients with T2DM.
- Age 40 years and older with a BMI ≥25 kg/m.
- Low (insufficient) physical activity.
- Persons with arterial hypertension , coronary artery disease.
- Polycystic ovary syndrome.
Symptoms
A feature of prediabetes is the absence of clear specific clinical symptoms characteristic of diabetes mellitus, which is primarily due to preserved energy supply to tissues and organs and slight glucosuria . In rare cases, symptoms of hyperglycemia at the stage of NGN and IGT manifest in the form of nonspecific patient complaints of increased fatigue, decreased ability to work, and worsening healing of wound defects.
Indirect signs of hyperglycemia at an early stage include:
- obesity or overweight;
- arterial hypertension;
- disorders of the cardiovascular system;
- atherogenic dyslipidemia (increased triglyceride levels and decreased cholesterol levels due to HDL (high-density lipoprotein);
- increased levels of uric acid in the blood ( hyperuricemia );
- fibrinolysis disorder .
On examination, most patients with prediabetes experience an increase in waist circumference to >94 cm in males and >80 cm in females. At the same time, fat mass is distributed predominantly on the torso with its relative decrease in the hips/buttocks area.
Hyperglycemia in children
Carbohydrates play a big role in the development and growth of a child and are an essential and significant component of food. They are involved in almost all types of metabolism: nucleic acids, proteins, lipids, nucleosides. Carbohydrates are essential for optimal functioning, especially brain function. Given the high metabolic rate in children, even minor deviations in carbohydrate metabolism cause disruption of other types of metabolism.
The causes of hyperglycemia in childhood are:
- neurogenic disorders;
- various endocrinopathies;
- liver pathology;
- psychogenic factors;
- binge eating.
In the neonatal period, hyperglycemia is more common and is found in 20-80% of premature babies weighing less than 1500 g. This condition is a prognostically unfavorable sign in this period, which can lead to death. The main cause of hyperglycemia is excessive infusion of glucose solutions during intensive care. An infectious process cannot be ruled out as the cause. Hyperglycemia often occurs in children who have suffered asphyxia and had respiratory disorders. An increase in sugar levels may be a manifestation of transient neonatal diabetes (decreased pancreatic function).
Endocrinopathies are associated with increased activity of hyperglycemic hormones: with an excess of glucagon , the formation of glucose from amino acids and intensive breakdown of glycogen , which is accompanied by an increase in blood sugar. Excess glucocorticosteroids stimulate the formation of glucose, and excess catecholamines stimulate the breakdown of glycogen. With hyperthyroidism, glycogenolysis (the breakdown of glycogen) is enhanced, glycogenesis (the formation of glycogen from glucose, the formation of glucose and its absorption in the intestine are stimulated.
Increased secretion of growth hormone enhances the breakdown of glycogen and inhibits glucose consumption. Neuro- and psychogenic disorders cause activation of the sympathoadrenal system, adrenal glands and the release of thyroid hormones. The hormones of these systems activate the breakdown of glycogen in the liver and the formation of excess glucose.
Overeating (consuming excessive amounts of simple carbohydrates over a long period of time) is considered a cause of hyperglycemia. In this case, glucose is quickly absorbed in the intestines, its level in the blood increases, and the liver is not able to convert it into glycogen in such quantities. When liver function is impaired, transient hyperglycemia always occurs after eating, which is associated with the inability of liver cells to quickly utilize glucose.
Hyperglycemia manifests itself in children as hyperglycemic syndrome and hyperglycemic coma.
Hyperglycemic syndrome includes:
- A persistent increase in sugar levels to 10.5–11.5 mmol/l.
- Detection of sugar in the urine ( glucosuria , which should not be normal).
- Severe, unquenchable thirst ( polydipsia ).
- Polyuria is excessive urination (urine output more than 3 L/day) due to increased glomerular filtration, increased urine osmolality and decreased reabsorption (reabsorption) of water in the tubules.
- Dry skin and signs of dehydration due to polyuria.
- Decreased blood pressure as a result of fluid loss and decreased cardiac output.
- Hyperglycemic (hyperosmolar) coma in children develops with diabetes mellitus due to a lack of insulin. There is an increase in sugar of 22–28 mmol/l or more. Hyperglycemia causes an increase in plasma osmolarity. An increase in osmolarity causes an increase in the permeability of the blood-brain barrier , which causes neurological symptoms. In newborns, increased osmolarity not only depresses the central nervous system and causes cerebral edema , but also causes hemorrhages inside the ventricles of the brain. In newborns with elevated levels of indirect bilirubin, its neurotoxicity increases.
Dysfunction of the central nervous system depends entirely on the level of increase in sugar:
- depression of consciousness;
- tonic-clonic seizures;
- dehydration;
- respiratory failure;
- apnea;
- disorders of the cardiovascular system;
- development of coma .
What to do if you have hyperglycemia (or suspect it)
The first step is to see a therapist. You will be asked to take a blood sugar test to determine your sugar levels. If hyperglycemia is confirmed, the doctor will begin to understand its causes. And, as mentioned above, it is highly likely to suspect diabetes or a condition preceding it.
Depending on your diagnosis, you may be prescribed medications. Most often insulin or other medications to lower glucose levels. In addition, you will need to regularly measure your blood sugar levels to monitor your condition and prevent prolonged episodes of hyperglycemia. The doctor will give detailed instructions on how to do this.
But not with drugs alone. You can return your sugar levels to normal by making simple lifestyle changes.
Drink more water
The liquid allows you to remove excess sugar from the blood through increased urination.
Change your eating habits
You should reduce the amount of fast carbohydrates (especially cakes, pastries, store-bought pastries, sugary drinks), as well as reduce portion sizes and switch to regular meals without snacking. This step may require the help of a qualified nutritionist who will work with you to prescribe a healthy diet.
Move more
When you are active, your organs and tissues consume more glucose. This means that blood sugar levels decrease. But there is an important nuance: in some cases, with diabetes, physical activity is undesirable.
Therefore, before signing up for a gym or going for a morning jog, be sure to consult with your doctor. He will tell you how often and how much you can exercise, as well as which exercises are preferable.
Don't forget to take your medications
It is important. Accidentally missing an insulin injection will lead to a spike in glucose and worsen your condition. If, on the contrary, you forget that you have already used the drug and use it again, there is a risk of developing hypoglycemia - a condition that can be no less dangerous than its hypervariant.
Diet
Diet 9th table
- Efficacy: therapeutic effect after 14 days
- Timing: constantly
- Cost of products: 1400 - 1500 rubles per week
Diet for insulin resistance
- Efficacy: therapeutic effect after a month
- Timing: constantly
- Cost of products: 1500-1600 rubles. in Week
Basic principles of nutrition for patients with hyperglycemia include:
- Reducing total calories to 1500 kcal per day.
- Exclusion of simple carbohydrates (sugar, sweets, baked goods, sweet desserts, confectionery, ice cream, jam, condensed milk, sweet drinks).
- Limiting fat intake due to its high calorie content.
- Increasing the amount of protein, as well as fiber up to 30 g/day due to vegetables with a low glycemic index.
The glycemic index reflects the rate at which carbohydrates are broken down into sugar and released into the bloodstream. Products with a high index sharply increase blood sugar levels, and their predominance in the diet will be accompanied by constant hyperglycemia. Patients' diets should be dominated by foods containing fiber, which is digested slowly and does not cause sudden spikes in blood sugar. These can be green vegetables, lettuce, all types of cabbage, unsweetened fruits, legumes, and whole grains.
Vegetables with a high index are excluded or sharply limited: potatoes, carrots, beets, tomatoes. More detailed recommendations can be found in the articles Diet for high blood sugar , Diet 9th table and Diet for insulin resistance .
Where does hyperglycemia come from?
Here are a few causes of Hyperglycemia in diabetes that can cause hyperglycemia. Spoiler: the most common one is at the end of the list.
You eat too much
And you especially put pressure on carbohydrate foods. Organs and tissues take from the blood exactly as much glucose as they need. And if after they have received their dose, there is still a lot of sugar in the blood, it develops - hyperglycemia.
Your lifestyle is too passive
Due to low mobility, glucose in the blood remains unclaimed for a long time.
You got nervous and continue to do so
When your brain believes you are in danger, it activates the fight or flight response. Escape or fight requires energy, so the body sharply increases Blood sugar levels can fluctuate for many reasons the level of glucose in the blood in order to ensure that organs and tissues are supplied with nutrition.
If you actually rush into battle or flight, this sugar will quickly be used up. But if you are nervous, but do not move, glucose has nowhere to go, because the body’s cells are not hungry and do not need additional energy. Thus, due to stress, blood sugar levels remain elevated for a long time.
Your body is fighting an internal infection or has suffered an injury
This is a type of stress to which the body reacts in the same way as a physical threat.
You have liver disease
The liver knows how to accumulate glucose in order to release it into the blood at the right time, upon command from the brain. However, if the liver is damaged, it can act without command, maintaining constantly high blood sugar levels.
Do you have diabetes?
This is a disease in which organs and tissues simply cannot accept glucose, and it remains in the blood. The point here is insulin: this hormone is a kind of key that “opens” the cells of the body and lets glucose into them.
Sometimes there is a catastrophic lack of insulin in the body, which means there is nothing to “open” the cells - in this case they talk about type 1 diabetes. Sometimes it is there, but the cells are insensitive to it (insulin resistant) - this is the essence of type 2 diabetes.
Most often, hyperglycemia is a consequence of one of the types of diabetes.
Prevention
- Healthy eating.
- Weight loss and constant weight control.
- Increasing physical activity.
- Identification of high-risk groups (presence of abdominal obesity, heredity of diabetes mellitus, lipid metabolism disorders, high blood pressure, presence of fatty liver, polycystic ovary syndrome) and control of sugar levels in this group.
- Identification of patients with impaired glucose tolerance, fasting glycemia or HbA1C from 5.7-6.4%.
- It is especially important for these patients to follow a diet and increase physical activity.
- Periodic examination by a doctor (once every six months) and decision on the issue of taking metformin if non-drug treatment is ineffective.
Diagnostics
Diagnosis is carried out in several stages: the history of the disease, symptoms (the main stage) are determined, and laboratory tests are carried out. Attention is drawn to increased thirst and dry mouth, unreasonable increase in appetite, polyuria. With pathology, difficulty breathing occurs and muscle pain appears, wounds and cuts heal slowly, the skin quickly becomes dry and itching is often noted, the person gets tired very quickly, and shortness of breath occurs. Another symptom is blurred or impaired vision. Sometimes there is a risk of developing infections that are almost impossible to cure with standard methods (otitis media or candidiasis). The essence of the tests is to collect morning blood. Before this, the patient should not eat (the analysis is carried out at least 8 hours after eating). In some cases, repeat tests are prescribed, with a gap of 5-7 days between them, this is done in order to exclude or confirm possible stress factors. In addition, inflammatory processes or taking certain medications may be factors. In this case, you need to take biochemical tests.
List of sources
- Demidova T.Yu., Galieva OP Prevention and management of prediabetic disorders of carbohydrate metabolism in patients with metabolic syndrome. “Obesity and Metabolism”, No. 4 (13), 2007; P.19-P.24.
- Nedogoda S.V., Barykina I.N., Salasyuk A.S., Smirnova V.O., Popova E.A. Prediabetes: main causes, symptoms, prevention and treatment//Medicine Bulletin No. 2 (70). 2021. Volume 12.
- Current issues of endocrinology in therapeutic practice: hands. for doctors / Ed. M. N. Kalinkina, L. V. Shpak. - Tver: Factor and K, 2014. - 698 p.
- Pasyeshvili T.M., Koryak V.V. A patient with hyperglycemia at a family doctor’s appointment / Eastern European Journal of Internal and Family Medicine. — 2021.— No. 2.— p. 35-39.
- P.F. Litvitsky, L.D. Maltseva Disorders of carbohydrate metabolism in children: hypoglycemia, hyperglycemia, glycogenosis, aglycogenosis, hexosemia / Issues of modern pediatrics. — 2021.- VOLUME 16/ No. 5 p. 362-368.