Hypoglycemic shock (crisis), an attack of hypoglycemia. What is a hypoglycemic episode Hypoglycemia and β-cell hyperplasia in infants

Hypoglycemia is when blood sugar drops below normal. Mild hypoglycemia causes unpleasant symptoms, which are described below in the article. If severe hypoglycemia occurs, the person loses consciousness, and this can lead to death or disability due to permanent brain damage. The official definition of hypoglycemia is a decrease in blood glucose to a level of less than 2.8 mmol/l, which is accompanied by adverse symptoms and may cause impaired consciousness. Also, hypoglycemia is a decrease in blood sugar to a level of less than 2.2 mmol / l, even if the person does not feel symptoms.

There are two main causes of hypoglycemia in diabetes mellitus:

• insulin injections;
• taking pills that cause the pancreas to produce more of its own insulin.

Insulin injections for the treatment of type 1 and type 2 diabetes are extremely important, and the benefits far outweigh the possible risk of hypoglycemia. Moreover, when you master and can manage with small doses of insulin, the risk of hypoglycemia will be very low.

From pills that cause the pancreas to produce more insulin, we strongly recommend that you avoid. These include all diabetes drugs from the sulfonylurea and meglitinide classes. Not only can these pills cause hypoglycemia, but they are harmful in other ways. Read " ". Doctors who are behind the times still continue to prescribe them to patients with type 2 diabetes. Alternative methods, which are described in, allow you to control blood sugar without the risk of hypoglycemia.

Symptoms of hypoglycemia are more pronounced the faster the decrease in blood glucose levels.

Early symptoms of hypoglycemia (you need to urgently eat “fast” carbohydrates, and specifically glucose tablets):

• pale skin;
• sweating;
• trembling, palpitations;
• severe hunger;
• inability to concentrate;
• nausea;
• anxiety, aggression.

Symptoms of hypoglycemia, when blood sugar is critically low, and hypoglycemic coma is already very close:

• weakness;
• dizziness, headache;
• feeling of fear;
• speech and visual disturbances of behavior;
• confusion;
• impaired coordination of movements;
• loss of orientation in space;
• trembling of limbs, convulsions.

Not all symptoms of glycemia appear at the same time. In the same diabetic, signs of hypoglycemia can change each time. In many patients, the symptoms of hypoglycemia are "blunted". Such diabetics suddenly lose consciousness every time due to the development of hypoglycemic coma. They have a high risk of disability or death due to severe hypoglycemia. Why is this happening:

• persistently very low blood sugar;
• a person has been suffering from diabetes for a long time;
• elderly age;
• if hypoglycemia occurs frequently, then the symptoms are not felt so brightly.

Such people are obliged not to pose a danger to others at the time of sudden severe hypoglycemia. This means that it is contraindicated for them to perform work on which the lives of other people depend. In particular, such diabetics should not drive a car and public transport.

Some patients with diabetes realize in time that they have hypoglycemia. They retain enough clarity of thought to get a glucometer, measure their sugar and stop a hypoglycemia attack. Unfortunately, many diabetics have great problems with the subjective recognition of their own hypoglycemia. When the brain lacks glucose, a person may begin to behave inappropriately. Such patients remain confident that they have normal blood sugar, right up to the moment until they lose consciousness. If a diabetic has experienced several acute episodes of hypoglycemia, then he may have problems with the timely recognition of subsequent episodes. This is due to dysregulation of adrenergic receptors. Also, taking certain medications makes it difficult to recognize hypoglycemia in time. These are beta-blockers that lower blood pressure and heart rate.

Here is another list of typical symptoms of hypoglycemia that develop as its severity increases:

• Slow reaction to surrounding events - for example, in a state of hypoglycemia, a person cannot slow down in time when driving a car.
• Irritable, aggressive behavior. At this time, the diabetic is sure that he has normal sugar, and aggressively resists the attempts of others to force him to measure sugar or eat fast carbohydrates.
• Clouding of consciousness, difficulty speaking, weakness, clumsiness. These symptoms may continue after the sugar has returned to normal, up to 45-60 minutes.
• Drowsiness, lethargy.
• Loss of consciousness (very rare if you are not injecting insulin).
• Convulsions.
• Death.

Nocturnal hypoglycemia during sleep

Signs of nocturnal hypoglycemia during sleep:

• the patient has cold, clammy skin with sweat, especially on the neck;
• erratic breathing;
• restless sleep.

If your child has type 1 diabetes, you should sometimes watch him at night, checking his neck by touch, you can also wake him up and, just in case, measure his blood sugar with a glucometer in the middle of the night. To reduce insulin dosages and with them the risk of hypoglycemia, follow. Start a child with type 1 diabetes on a low-carbohydrate diet as soon as you finish breastfeeding.

If the symptoms of hypoglycemia are blunted

In some patients with diabetes, the early symptoms of hypoglycemia are blunted. With hypoglycemia, hand trembling, skin pallor, rapid pulse and other signs are caused by the hormone epinephrine (adrenaline). In many diabetics, its production is weakened or the sensitivity of receptors to it is reduced. This problem develops over time in patients who have chronically low blood sugar or frequent jumps from high sugar to hypoglycemia. Unfortunately, these are the categories of patients who most often experience hypoglycemia and who, more than others, would need normal sensitivity to adrenaline.

There are 5 causes and circumstances that can lead to blunting the symptoms of hypoglycemia:

• Severe autonomic diabetic neuropathy is a complication of diabetes that causes nerve conduction disorders.
• Fibrosis of the adrenal tissue. This is the death of tissue from the adrenal glands, the glands that produce adrenaline. It develops if the patient has a long history of diabetes, and he was lazy or incorrectly treated.
• Blood sugar is chronically low.
• A diabetic takes medication - beta-blockers - for high blood pressure, after a heart attack, or to prevent it.
• In diabetics who eat a "balanced" diet, overloaded with carbohydrates, and therefore forced to inject themselves with large doses of insulin.

If the glucometer shows that blood sugar is below 3.5 mmol / l, take glucose tablets, even if there are no symptoms of hypoglycemia. You need just a tiny bit of glucose to bring your blood sugar back up to normal. 1-3 grams of carbohydrates will be enough - this is 2-6 glucose tablets. Don't eat extra carbs!

Some diabetics refuse to take glucose tablets even when they have measured their sugar and found it to be below normal. They say that even without pills they feel fine. Such diabetics are the main “clients” for emergency doctors so that they can practice getting a person out of a hypoglycemic coma. They also have a particularly high likelihood of car accidents. When you drive, check your blood sugar every hour with a glucometer, whether you have hypoglycemia or not.

People who have frequent episodes of hypoglycemia or who have chronically low blood sugar levels develop a “addiction” to the condition. Adrenaline in their blood appears often and in large quantities. This leads to the fact that the sensitivity of receptors to adrenaline is weakened. In the same way that excessive doses of insulin in the blood impair the sensitivity of insulin receptors on the surface of cells.

Causes of hypoglycemia in diabetes

Hypoglycemia develops in situations where too much insulin circulates in the blood relative to the intake of glucose from food and from stores in the liver.

Reasons for the development of hypoglycemia

Official medicine claims that if a patient with diabetes is effectively treated with insulin or sugar-lowering pills, then the symptoms of hypoglycemia will have to be experienced 1-2 times a week and, they say, there is nothing wrong with that. We declare: if you perform or, then hypoglycemia will happen much less often. Because with type 2 diabetes, we abandoned the ones that can cause it. As for insulin injections, in type 1 and type 2 diabetes, it allows several times to reduce insulin dosages and thus reduce the risk of hypoglycemia.

Typical causes of hypoglycemia in those treated according to the methods of the site site:

• They didn't wait 5 hours for the previous dose of rapid insulin to wear off and injected the next dose to bring down the elevated blood sugar. This is especially dangerous at night.
• They injected fast insulin before eating, and then started eating too late. The same is true if you take pills before meals that make the pancreas produce more insulin. It is enough to start eating 10-15 minutes later than you should in order to feel the symptoms of hypoglycemia.
• Diabetic gastroparesis is slow emptying of the stomach after eating.
• After the end of an infectious disease - insulin resistance suddenly weakens, and the diabetic forgets to return from increased doses of insulin or sugar-lowering pills to their usual doses.
• A diabetic injects himself with “weakened” insulin for a long time from a vial or cartridge that was incorrectly stored or expired, and then he began to inject “fresh” normal insulin without lowering the dose.
• Switching from an insulin pump to injections with insulin syringes and vice versa if it occurs without careful self-monitoring of blood sugar.
• The diabetic injected himself with high-power ultrashort insulin in the same dose that usually injects short.
• The dose of insulin does not match the amount of food eaten. Ate less carbs and/or protein than planned for breakfast, lunch, or dinner. Or they ate as much as they were going to, but for some reason they injected more insulin.
• The diabetic engages in unplanned physical activity or forgets to monitor blood sugar hourly during physical activity.
• Alcohol abuse, especially before and during meals.
• A diabetic patient who injects himself with the medium NPH-insulin Protafan forgot to shake the vial well before drawing up a dose of insulin into the syringe.
• Accidentally gave intramuscular injection of insulin instead of subcutaneous.
• They made the correct subcutaneous injection of insulin, but in that part of the body that is subjected to intense physical activity.
• Long-term treatment with intravenous gamma globulin. Causes a random and unpredictable recovery of part of the beta cells in patients with type 1 diabetes, thereby reducing the need for insulin.
• Taking the following medications: high doses of aspirin, anticoagulants, barbiturates, antihistamines, and some others. These drugs lower blood sugar or inhibit the liver from making glucose.
• Sharp warming. At this time, in many diabetic patients, the need for insulin drops.

Hunger is the most common early symptom of hypoglycemia. If you are performing or well in control of your disease, then you should never experience severe hunger at all. Before the planned meal, you should be only slightly hungry. On the other hand, hunger is often only a sign of fatigue or emotional stress, not hypoglycemia. Also, when blood sugar is too high, the cells don't have enough glucose, and they send hunger signals intensely. Conclusion: feel hungry - immediately measure your blood sugar with a glucometer.

Risk factors for severe hypoglycemia:

• the patient has had previous cases of severe hypoglycemia;
• a diabetic does not feel the symptoms of hypoglycemia in time, and therefore his coma occurs suddenly;
• secretion of insulin by the pancreas is completely absent;
• low social status of the patient.

How to figure out what caused hypoglycemia

You need to recreate the whole sequence of events that leads to episodes when your blood sugar is too low. You need to do this every time, even if there were no visible symptoms, in order to find where you went wrong. In order to be able to restore events, insulin-dependent diabetic patients need to continuously live in the mode, i.e. measure it often, record the results of measurements and related circumstances.

Severe hypoglycemia can cause events a few hours before it to be completely erased from the memory of a diabetic patient. If he carefully keeps his diary of self-control, then in such a situation the records will be of invaluable help. It is not enough to record only the results of blood sugar measurements, it is also necessary to record the accompanying circumstances. If you have had several episodes of hypoglycemia, but you cannot understand the cause, then show the notes to the doctor. Perhaps he will ask you clarifying questions and figure it out.

Treatment (stopping) of hypoglycemia

If you're experiencing any of the symptoms of hypoglycemia that we've listed above - especially severe hunger - measure your blood sugar right away with a glucometer. If it is 0.6 mmol/L below your target level or even below, then take action to stop the hypoglycemia. Eat enough carbs, specifically glucose tablets, to get your blood sugar up to your target level. If there are no symptoms, but you have measured your blood sugar and noticed that it is low, the same thing, you need to eat glucose tablets in a precisely calculated dosage. If sugar is low, but there are no symptoms, then fast carbohydrates should still be eaten. Because hypoglycemia without symptoms is more dangerous than one that causes obvious symptoms.

What if you don't have a glucometer with you? This is a grave sin for an insulin-dependent diabetic. If you suspect that you have hypoglycemia, then play it safe and eat some glucose to raise your sugar by 2.4 mmol / l. This will save you from severe hypoglycemia, which has irreversible consequences.

As soon as the glucometer is at your disposal, measure your sugar. It will probably be high or low. Bring it back to normal and do not sin anymore, i.e. always keep the glucometer with you.

The most difficult thing is if your blood sugar has dropped due to the fact that you injected too much insulin or took an excessive dose. In such a situation, sugar may drop again after taking glucose tablets. Therefore, measure your sugar again with a glucometer 45 minutes after taking the remedy for hypoglycemia. Make sure everything is ok. If the sugar is low again, take another dose of tablets, then repeat the measurement after another 45 minutes. And so on, until everything finally returns to normal.

How to cure hypoglycemia without raising sugar above normal

Traditionally, diabetic patients eat starchy foods, fruits and sweets, drink fruit juices or sweet sparkling water to stop hypoglycemia. This method of treatment does not work well for two reasons. On the one hand, it acts more slowly than necessary. Because the carbohydrates found in foods still have to be digested by the body before they begin to raise blood sugar. On the other hand, such a “treatment” raises blood sugar excessively, because it is impossible to accurately calculate the dose of carbohydrates, and the diabetic patient eats too much of them out of fear.

Hypoglycemia can wreak havoc in diabetes. A severe attack can lead to the death of a diabetic patient or disability due to irreversible brain damage, and it is not easy to figure out which of these outcomes is worse. Therefore, we strive to bring blood sugar back to normal as quickly as possible. Complex carbohydrates, fructose, milk sugar lactose - all of them must go through the process of digestion in the body before they begin to raise blood sugar. The same applies even to starch and table sugar, although for them the absorption process is very fast.

Use glucose tablets to prevent and manage hypoglycemia. Buy them at the pharmacy, do not be lazy! Fruits, juices, sweets, starchy foods are undesirable. Eat exactly the amount of glucose you need. Don't let sugar "bounce" up after you've dealt with a bout of hypoglycemia.

The foods we listed above contain a mixture of fast and slow carbohydrates that act with a delay and then raise blood sugar unpredictably. It always ends with the fact that after the relief of an attack of hypoglycemia, the sugar in a diabetic patient “rolls over”. Ignorant doctors are still convinced that after an episode of hypoglycemia, it is impossible to avoid a rebound increase in blood sugar. They consider it normal if after a few hours the blood sugar in a diabetic patient turns out to be 15-16 mmol / l. But this is not true if you act correctly. Which drug raises blood sugar the fastest and works predictably? Answer: pure glucose.

Glucose tablets

Glucose is the same substance that circulates in the blood and is what we call “blood sugar”. Dietary glucose is immediately absorbed into the blood and begins to act. The body does not need to digest it, it does not undergo any transformation processes in the liver. If you chew a glucose tablet in your mouth and drink it with water, then most of it will be absorbed into the blood from the oral mucosa, even swallowing is not necessary. Some more will enter the stomach and intestines and will be instantly absorbed from there.

In addition to speed, the second advantage of glucose tablets is the predictability of action. During hypoglycemia in a type 1 or type 2 diabetic weighing 64 kg, 1 gram of glucose will raise blood sugar by about 0.28 mmol/L. In this condition, in a type 2 diabetic patient, insulin production by the pancreas is automatically turned off, and in a type 1 diabetic patient, it is not produced at all. If blood sugar is not below normal, then glucose will have a weaker effect on a patient with type 2 diabetes, because the pancreas “extinguishes” it with its insulin. For a type 1 diabetic, 1 gram of glucose will still raise blood sugar by 0.28 mmol/l, because he does not produce his own insulin.

The more a person weighs, the weaker the effect of glucose on him, and the lower the body weight, the stronger. To calculate how much 1 gram of glucose will raise blood sugar at your weight, you need to make a proportion. For example, for a person with a body weight of 80 kg, it will be 0.28 mmol / l * 64 kg / 80 kg = 0.22 mmol / l, and for a child weighing 48 kg, it will be 0.28 mmol / l * 64 kg / 48 kg \u003d 0.37 mmol / l.

So, for the relief of hypoglycemia, glucose tablets are the best choice. They are sold in most pharmacies and are very cheap. Also, in grocery stores in the checkout area, ascorbic acid (vitamin C) tablets with glucose are often sold. They can also be used against hypoglycemia. Vitamin C doses are usually very low. If you are too lazy to stock up on glucose tablets, carry refined sugar with you. 2-3 pieces are enough, no more. Sweets, fruits, juices, starchy foods are not suitable for patients who are on a type 1 diabetes treatment program or a type 2 diabetes treatment program.

If you have touched glucose tablets, wash your hands before checking your blood sugar with a glucometer. If there is no water, use a damp cloth. As a last resort, lick the finger you are about to pierce and then dry it with a clean cloth or handkerchief. If traces of glucose remain on the skin of the finger, then the results of measuring blood sugar will turn out to be distorted. Keep glucose tablets away from your meter and test strips.

The most important question is how many glucose tablets should I eat? Eat only enough of them to raise your blood sugar to normal, but no more. Let's take a practical example. Let's say you weigh 80 kg. Above, we calculated that 1 gram of glucose will raise your blood sugar by 0.22 mmol/L. Your blood sugar is currently 3.3 mmol/L and your target is 4.6 mmol/L, i.e. you need to raise your blood sugar by 4.6 mmol/L - 3.3 mmol/L = 1.3 mmol/l. To do this, you need to take 1.3 mmol / l / 0.22 mmol / l \u003d 6 grams of glucose. If you use glucose tablets weighing 1 gram each, then it will be 6 tablets, no more and no less.

What to do if blood sugar is low just before eating

It may happen that you find yourself low in sugar just before you start eating. If you are following to control type 1 or type 2 diabetes, then in this case, eat glucose tablets right away, and then “real” food. Because low-carbohydrate foods are digested slowly. If you do not stop hypoglycemia, then this can result in overeating and a jump in sugar after a few hours, which then will be difficult to bring back to normal.

How to cope with a bout of overeating with hypoglycemia

Mild and "moderate" hypoglycemia can cause severe, unbearable hunger and panic. The urge to gorge on carbohydrate-laden foods can be almost uncontrollable. In such a situation, a diabetic can immediately eat a whole kilogram of ice cream or flour products or drink a liter of fruit juice. As a result, blood sugar in a few hours will be monstrously high. Below you will learn what to do with hypoglycemia to reduce the harm to your health from panic and overeating.

First, experiment ahead of time and make sure glucose pills work very predictably, especially in type 1 diabetes. How many grams of glucose you ate - exactly how much your blood sugar will increase, no more and no less. Check it out for yourself, see for yourself in advance. This is necessary so that in a situation of hypoglycemia you do not panic. After you take glucose tablets, you will be sure that loss of consciousness and death are definitely not in danger.

So, we got the panic under control, because we prepared in advance for a situation of possible hypoglycemia. This allows the diabetic to remain calm and sane, and there is less chance that the urge to overeat will get out of control. But what to do if, after taking glucose tablets, wild hunger still cannot be restrained? This may be due to the fact that the half-life of adrenaline in the blood is very long, as described in the previous section. In this case, chew and eat low-carb foods from.

Moreover, it is desirable to use products that do not contain carbohydrates at all. For example, meat slices. You can’t snack on nuts in such a situation, because you won’t be able to resist and eat too many of them. Nuts contain a certain amount of carbohydrates, and in large quantities they also increase blood sugar, causing. So, if hunger is unbearable, then you drown it out with low-carbohydrate animal products.

Sugar increased to normal, and the symptoms of hypoglycemia do not go away

In a situation of hypoglycemia, a sharp release of the hormone epinephrine (adrenaline) into the blood occurs. It is he who causes most of the unpleasant symptoms. When blood sugar drops excessively, the adrenal glands respond by producing adrenaline and increasing its concentration in the blood. This occurs in all patients with diabetes, except those who have impaired recognition of hypoglycemia. Like glucagon, epinephrine signals the liver to convert glycogen into glucose. It also speeds up the pulse, causes pale skin, trembling hands and other symptoms.

Adrenaline has a half-life of approximately 30 minutes. This means that even an hour after the episode of hypoglycemia has ended, ¼ of the adrenaline is still in the blood and continues to act. For this reason, the symptoms may continue for some time. You need to be patient 1 hour after taking glucose tablets. During this hour, the most important thing is to resist the temptation to overeat. If symptoms of hypoglycemia persist after an hour, measure your sugar with a glucometer again and take additional measures.

Aggressive behavior of a diabetic in a state of hypoglycemia

If a diabetic patient has hypoglycemia, then this greatly complicates the life of his family members, friends and colleagues. This happens for two reasons:

• in a state of hypoglycemia, diabetics often behave rudely and aggressively;
• the patient may suddenly lose consciousness and require emergency medical attention.

What to do if a diabetic patient has really severe hypoglycemia or passes out, we will discuss in the next section. Now let's discuss what causes aggressive behavior and how to live with a diabetic patient without unnecessary conflicts.

In a state of hypoglycemia, a diabetic may behave strangely, rudely and aggressively for two main reasons:

• he lost control of himself;
• attempts by others to feed him sweets can really cause harm.

Let's look at what happens in the brain of a diabetic patient during an attack of hypoglycemia. The brain does not have enough glucose to function properly, and because of this, a person behaves as if he is drunk. Mental activity is impaired. This can be manifested by various symptoms - lethargy or vice versa irritability, excessive kindness or the opposite of aggressiveness. In any case, the symptoms of hypoglycemia resemble alcohol intoxication. A diabetic is sure that he now has normal blood sugar, just like a drunk person is sure that he is completely sober. Alcohol intoxication and hypoglycemia disrupt the activity of the same centers of higher nervous activity in the brain.

A diabetic patient has firmly learned that high blood sugar is dangerous, destroys health, and therefore should be avoided. Even in a state of hypoglycemia, he firmly remembers this. And just now he is sure that his sugar is normal and, in general, the sea is knee-deep. And then someone tries to feed him with harmful carbohydrates ... Obviously, in such a situation, the diabetic will imagine that it is the second participant in the situation who is behaving badly and trying to harm him. This is especially likely if a spouse, parent or colleague has already tried to do the same thing before, and then it turned out that the sugar in a diabetic patient was indeed normal.

The greatest likelihood of provoking aggression in a diabetic patient is if you try to stuff sweets into his mouth. Although, as a rule, verbal persuasion is enough for this. The brain, irritated by the lack of glucose, prompts its owner with paranoid ideas that a spouse, parent or colleague wishes him harm and even tries to kill him by tempting him with harmful sweet food. In such a situation, only a saint could refrain from retaliatory aggression... The surrounding people are usually upset and shocked by the negative situation of a diabetic patient in their attempts to help him.

The spouse or parents of a diabetic may develop a fear of severe episodes of hypoglycemia, especially if the diabetic has previously passed out in such situations. Usually sweets are stored in different places in the house so that they are at hand and the diabetic eats them quickly when needed. The problem is that in half the cases, people around suspect that a diabetic patient has hypoglycemia, when his sugar is actually normal. This often happens during family scandals due to some other reasons. Opponents think that our diabetic patient is making such a big fuss because he is currently suffering from hypoglycemia. In this way, they are trying to avoid the real, more complex causes of the scandal. But in the second half of cases of unusual behavior, hypoglycemia is really present, and if a diabetic patient is sure that he has normal sugar, then he is needlessly putting himself at risk.

So, half the time people try to feed a diabetic with sweets, they are wrong, because he does not actually have hypoglycemia. Eating carbohydrates causes a spike in blood sugar, and this is quite unhealthy for a diabetic. But in the second half of the cases, when hypoglycemia is present, and the person denies it, he creates unnecessary problems for others, exposing himself to significant risk. How to behave correctly for all participants? If a patient with diabetes behaves unusually, then you need to persuade him not to eat sweets, but to measure his blood sugar. After that, in half of the cases it turns out that there is no hypoglycemia. And if it is, then glucose tablets immediately come to the rescue, which we have already stocked up and learned how to correctly calculate their doses. Also make sure that the glucometer is accurate in advance (). If it turns out that your glucometer is lying, then replace it with an accurate one.

The traditional approach of coaxing a diabetic into eating sweets does at least as much harm as good. The alternative, which we outlined in the previous paragraph, is to bring peace to families and ensure a normal life for all concerned. Of course, if you do not save on test strips for a glucometer and lancets. Living with a diabetic is almost as many problems as the diabetic has. To measure your sugar immediately at the request of family members or colleagues is the direct responsibility of a diabetic. Then it will be seen whether it is necessary to stop hypoglycemia by taking glucose tablets. If suddenly there is no glucometer at hand or the test strips have run out, then eat enough glucose tablets to raise your blood sugar by 2.2 mmol / l. This is guaranteed to protect against severe hypoglycemia. And you will figure it out with high sugar when you have access to a glucometer.

What to do if a diabetic is already on the verge of losing consciousness

If a diabetic is already on the verge of losing consciousness, then this is moderate hypoglycemia, turning into severe. In this state, the patient with diabetes looks very tired, inhibited. He does not respond to calls, because he is unable to answer questions. The patient is still conscious, but is no longer able to help himself. Now it all depends on others - do they know how to help with hypoglycemia? Especially if the hypoglycemia is no longer mild, but severe.

In such a situation, it is too late to try to measure sugar with a glucometer, you will only lose precious time. If you give a diabetic patient glucose tablets or sweets, he is unlikely to chew them. Most likely, he will spit out solid food or worse, choke. At this stage of hypoglycemia, it is correct to give a diabetic patient a liquid glucose solution to drink. If not, then at least a solution of sugar. American guidelines for the treatment of diabetes recommend using glucose in the form of a gel in such situations, which is lubricated from the inside of the gums or cheeks, because this way there is less risk that a diabetic patient will inhale the liquid and choke. In Russian-speaking countries, we only have a pharmacy glucose solution or homemade instant sugar solution at our disposal.

Glucose solution is sold in pharmacies, and the most prudent diabetic patients have it at home. It is produced in order to conduct a 2-hour oral glucose tolerance test in medical institutions. When you give a diabetic a solution of glucose or sugar to drink, it is very important to ensure that the patient does not choke, but actually swallows the liquid. If you manage to do this, then the formidable symptoms of hypoglycemia will quickly pass. After 5 minutes, the diabetic will be able to answer questions. After that, he needs to measure his sugar with a glucometer and use insulin to lower it to normal.

Emergency help if a person with diabetes has passed out

You should be aware that a diabetic patient can lose consciousness not only because of hypoglycemia. The cause can also be a heart attack, stroke, a sudden drop in blood pressure. Sometimes diabetics pass out if they have very high blood sugar (22 mmol/l or more) for several days in a row, and this is accompanied by dehydration. This is called, it happens to elderly lonely diabetic patients. If you disciplinedly perform or, then it is very unlikely that your sugar will rise so high.

As a rule, if you see that a diabetic has lost consciousness, then there is no time to find out the reasons for this, but treatment must be started immediately. If a patient with diabetes has lost consciousness, then he first needs to inject glucagon, and then understand the reasons. Glucagon is a hormone that quickly raises blood sugar, causing the liver and muscles to convert their glycogen stores into glucose and saturate the blood with that glucose. People who surround a person with diabetes should know:

• Where is the glucagon emergency kit stored?
• how to inject.

An emergency kit for glucagon injection is available from pharmacies. This is a case that contains a syringe with liquid, as well as a vial of white powder. There is also a visual instruction in pictures on how to inject. It is necessary to inject the liquid from the syringe into the vial through the cap, then remove the needle from the cap, shake the vial well to mix the solution, draw it back into the syringe. An adult needs to inject the entire volume of the contents of the syringe, subcutaneously or intramuscularly. The injection can be done in all the same zones where insulin is usually injected. If a diabetic is receiving insulin injections, family members can practice giving them these injections beforehand so that they can easily cope later if they need to inject glucagon.

If you don't have a glucagon emergency kit on hand, call an ambulance or take an unconscious diabetic to the hospital. If a person has lost consciousness, then in no case should you try to inject something through his mouth. Do not put glucose tablets or solid food in his mouth, and do not try to pour in any liquids. All this can get into the respiratory tract, and the person will suffocate. In an unconscious state, a diabetic cannot chew or swallow, so he cannot be helped in this way.

If a diabetic patient has lost consciousness due to hypoglycemia, then convulsions may begin. In this case, saliva is abundantly secreted, as well as teeth chattering and clenching. You can try to insert a wooden stick into the teeth of an unconscious patient so that he cannot bite his tongue. At the same time, it is important to prevent him from biting off your fingers. Lay him on his side so that saliva flows out of his mouth, and he does not choke on it.

It happens that glucagon causes nausea and vomiting in a diabetic. Therefore, the patient should lie on his side so that the vomit does not enter the respiratory tract. After an injection of glucagon, a diabetic patient should come to the establishment within 5 minutes. No later than 20 minutes later, he should already be able to answer questions. If within 10 minutes there are no signs of a clear improvement in the condition, an unconscious diabetic patient needs urgent medical attention. The emergency doctor will give him intravenous glucose.

A single injection of glucagon can raise blood sugar up to 22 mmol/L, depending on how much glycogen is stored in the liver. When consciousness has fully returned, a diabetic patient needs to measure their blood sugar with a glucometer. If it has been 5 hours or more since the last injection of rapid insulin, then you need to give an injection of insulin to bring the sugar back to normal. This is important to do because this is the only way the liver can begin to replenish its glycogen stores. They will recover within 24 hours. If a diabetic patient passes out 2 times in a row within a few hours, then a second injection of glucagon may not help, because the liver has not yet restored its glycogen stores.

After a diabetic patient is brought to his senses with an injection of glucagon, over the next day he needs to measure his sugar with a glucometer every 2.5 hours, including at night. Make sure hypoglycemia does not recur. If blood sugar drops, use glucose tablets immediately to bring it back up to normal. Careful monitoring is very important, because if a diabetic patient loses consciousness again, then a second injection of glucagon may not help him wake up. Why - we explained above. At the same time, elevated blood sugar needs to be corrected less frequently. A second injection of fast insulin can be done no earlier than 5 hours after the previous one.

If hypoglycemia is so severe that you pass out, you need to carefully review your diabetes treatment regimen to understand where you are making a mistake. Re-read the list of typical causes of hypoglycemia, which are given earlier in the article.

Hypoglycemic supplies include glucose tablets, a glucagon emergency kit, and preferably liquid glucose. It is easy, not expensive, and it can save the life of a diabetic patient to buy all this in a pharmacy. At the same time, hypoglycemic supplies will not help if the people around you do not know where they are stored, or do not know how to provide emergency care.

Store hypoglycemic supplies in several convenient places at home and at work at the same time, and let family members and colleagues know what is stored where. Keep your glucose tablets in your car, wallet, briefcase, and purse. When traveling by plane, keep hypoglycemic supplies in your hand luggage, as well as a duplicate supply in the luggage you check in. This is necessary in case some luggage is lost or stolen from you.

Replace the glucagon emergency kit when the expiration date is up. But in a situation of hypoglycemia, you can safely give an injection, even if it is overdue. Glucagon is a powder in a vial. Since it is dry, it retains its effectiveness for several years after the expiration date has ended. Of course, this is only if he was not exposed to very high temperatures, as happens in the summer in a car locked in the sun. The emergency kit with glucagon should preferably be stored in the refrigerator at a temperature of +2-8 degrees Celsius. The prepared glucagon solution can only be used within 24 hours.

If you have used up any of your supplies, then replenish them as quickly as possible. Store excess glucose tablets and meter test strips. At the same time, bacteria are very fond of glucose. If you don't use glucose tablets for 6-12 months, they may develop black spots. This means that bacterial colonies have formed on them. It is better to immediately replace such tablets with new ones.

In English-speaking countries, diabetic identification bracelets, straps and medallions are popular. They are very helpful if a diabetic passes out because they provide valuable information to healthcare professionals. A Russian-speaking diabetic is hardly worth ordering such a thing from abroad. Because it is unlikely that the emergency doctor will understand what is written in English.

You can make yourself an identification bracelet by ordering an individual engraving. A bracelet is better than a locket because it's more likely to be noticed by healthcare professionals.

Hypoglycemia in diabetes mellitus: conclusions

You've probably heard a lot of horror stories about how hypoglycemia is common and very severe in type 1 diabetics. The good news is that this problem only affects people with diabetes who follow a “balanced” diet, eat a lot of carbohydrates and therefore have to inject themselves with a lot of insulin. If you follow ours, then the risk of severe hypoglycemia is extremely low. The multiple reduction in the risk of hypoglycemia is a strong, but not even the most important, reason to switch to our type 1 diabetes control regimen.

If you switch to , your insulin needs will drop significantly. Also, our patients do not take harmful diabetes pills that cause hypoglycemia. After that, hypoglycemia can occur only in one of two cases: you accidentally injected yourself with more insulin than necessary, or you injected a dose of fast insulin without waiting 5 hours for the previous dose to stop. Feel free to ask your family members and work colleagues to study this article. Although the risk is reduced, you can still find yourself in a situation of severe hypoglycemia, when you cannot help yourself, and only the people around you can save you from loss of consciousness, death or disability.

Hypoglycemia is a pathological condition associated with an abnormally low level of glucose in the blood. People suffering from diabetes mellitus, severe diseases of the liver and pancreas, malfunctions of the digestive tract, dysfunctions of the endocrine glands (adrenal cortex, pituitary gland, etc.), some infectious diseases (encephalitis, meningitis) may experience attacks of hypoglycemia. At risk are also people who use too actively low-carbohydrate diets, which are now very popular with losing weight.

Let's get acquainted with those signs of hypoglycemia, which in no case can not be ignored.

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Constant hunger

With a mild form of hypoglycemia, the feeling of hunger, as a rule, occurs suddenly. This is the reaction of the corresponding brain center to a low concentration of glucose in the blood. Sudden hunger often occurs in diabetics on the background of physical exertion, eating disorders or incorrect use of hypoglycemic drugs. Hunger may be accompanied by nausea.

In healthy people on a low-carbohydrate diet, unexpected hunger also appears due to the rejection of foods rich in fiber (vegetables, fruits, cereals). It is they who, getting into the stomach, create a long-lasting feeling of satiety. With a complete rejection of carbohydrates, a person can be hungry all the time, even immediately after eating.

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Headache

A significant drop in blood glucose usually results in a drop in blood pressure. The result is a headache, often accompanied by dizziness. Sometimes there are short-term speech disturbances and visual effects (for example, a split image or color spots before the eyes).

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Disorders of the central nervous system

The human body uses glucose as a universal source of energy. With its deficiency in the blood, nerve cells are especially affected, so signs of a deterioration in the functioning of the brain appear almost immediately.

Hypoglycemia is accompanied by the following manifestations:

• drowsiness, lethargy;
• difficulties with orientation in space;
• disorders of coordination of movements;
• inability to concentrate;
• memory impairment;
• hand tremor;
• fainting;
• epileptic-like seizures.

The lack of help with the appearance and growth of these symptoms leads to a hypoglycemic coma, which is fraught with death.

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Thermoregulation disorders

The lack of "universal fuel" has a bad effect on the state of all organs and systems of the human body. During an attack of hypoglycemia, the patient may experience chills, complain of cold in the fingers and toes. The appearance of cold sweat (sweating the back of the neck and the entire scalp) is possible. If an attack of hypoglycemia occurs at night, the whole body sweats profusely: a person wakes up in completely wet underwear.

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Weight stabilization while dieting

People trying to get rid of excess weight with the help of low-carb diets often notice that at some point the weight stops falling, despite a severely restricted diet. This may be a sign of hypoglycemia. The fact is that with insufficient intake of carbohydrates, the liver begins to process glycogen stores into glucose, the intensity of the breakdown of accumulated fats decreases.

Both options are dangerous to humans. Therefore, it is necessary to know the causes of seizures and avoid provoking factors.

hyperglycemia

• the smell of acetone from the oral cavity;
• a feeling of constant dryness in the mouth (drinking water does not quench thirst);
• cramping intense pain in the abdomen.

hypoglycemic

Attacks of hypoglycemia often occur in. A complication develops when glucose falls below 3 mmol / l. The more sugar falls, the more pronounced the symptoms of an attack become.

Signs of low glycemia:

• tachycardia;
• irritability;
• tremor of the limbs;
• disorder of consciousness;
• cold sweat;
• convulsions;
• causeless anxiety;
• epilepsy;
• weakness.

Having noticed signs of hypo- or hyperglycemia, it is necessary to check the sugar level with a glucometer and take appropriate measures.

Diabetic coma as a consequence of sugar spikes

Due to a sharp jump in sugar, a diabetic may experience a coma. Under understand a serious condition, which is characterized by an acute violation of the functioning of organs and systems, irreversible changes.

Coma is of different types:

• lactic acidosis. Occurs due to anaerobic glycolysis with the synthesis of lactic acid. The main causes of this condition are sepsis, severe trauma, shock, significant blood loss. This type of coma is rare, but poses the maximum threat to human life;
• . Typical for type 2 diabetics. The reason is increased urination. As a result of dehydration, the blood thickens and the level of glucose in the serum rises. Glycemia reaches 50-60 mmol/l;
• ketoacidotic. The rise in blood glucose is due to an increase in plasma ketone bodies. The glucometer shows the concentration of sugar in the range from 13 to 20 mmol / l. It is found in the urine;
• hypoglycemic. It develops with an overdose of hypoglycemic drugs, excessive physical activity, etc. The sugar level rises to 10-20 mmol / l.

In any case, coma is a serious health hazard and threatens the life of the patient. The consequences may be:

• disorders in the work of the heart muscle;
• damage to brain cells.

To prevent diabetic coma and its complications, you must immediately respond to the symptoms of low or high sugar.

What to do?

If a person suddenly became ill, the first thing to do is to measure the level of glycemia with a glucometer.

If there is no such device at home, then it is better to call an ambulance. If the device shows minor deviations from the norm, you can stabilize the sugar on your own, by injecting insulin, or by eating something.

It is necessary to understand how to competently provide first aid, what drugs are available to improve well-being, and whether traditional methods help in reducing diabetic attacks.

First aid

To provide first aid for a hypoglycemic seizure, you need to perform the following steps:

• give the patient water to drink. Suitable sweet, high in glucose. Carbohydrate food should not be given during an attack: in this state, a person may not be able to chew it;
• anoint the gums with a special glucose paste;
• if the patient is sick, he should be helped to lie on his side. If vomiting has begun, it is necessary to clean the victim's mouth from vomit;
• if convulsions are observed, it is required to ensure that the patient does not bite his tongue. It is recommended to insert a spoon or stick between the teeth.

To stop a hyperglycemic attack, the following actions are recommended:

• if the glucose concentration is above 14 mmol / l, it is worth promptly injecting short-acting insulin (about two units). Large doses should not be used. The next injection should be done no earlier than a couple of hours after the first injection;
• saturate the body with carbohydrates and proteins. These elements restore the acid-base balance. Soda solution and mineral water help.

If, after the measures taken, the person does not feel better, you need to urgently call emergency help.

Medical treatment

It is important that patients with a similar diagnosis always have the necessary medications with them.

This will help to quickly remove the attack. In hyperglycemia, insulin is used, which quickly lowers sugar. For example, Biogulin, Diarapid, Actrapid, or.

Glucagon is administered intravenously to treat a hypoglycemic attack. To prevent seizures of high or low sugar from recurring, it is necessary to adjust the dosage of the hypoglycemic agent used, to review your own. You may need to select another drug.

Folk remedies

For the treatment of non-insulin-dependent diabetes mellitus and the prevention of attacks of the disease, folk methods are used. Good results and fees based on it. The plant lowers sugar, improves intestinal microflora, normalizes digestion, and improves the functioning of the liver and respiratory system.

The following are effective recipes:

• mix in equal parts, nettles, lingonberries and. Take two tablespoons of the composition and pour 0.5 liters of boiling water. Take 2/3 cup three times a day;
• nettle, clover, and yarrow take in a ratio of 4:2:1:3. Pour 200 ml of boiling water over a tablespoon. Drink a third of a glass three times a day.

You cannot treat diabetes on your own. All medicines and folk recipes must be agreed with the doctor.

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Symptoms and consequences of hyperglycemia and hypoglycemia in diabetes mellitus:

Thus, it is important to be able to recognize a diabetic attack at the very beginning. It is manifested by characteristic symptoms, the severity of which increases with a decrease or increase in plasma sugar concentration. In case of a hypo-, hyperglycemic seizure, it is necessary to act promptly in order to prevent the development of coma.

Glucose is an essential component of human metabolism processes. Being a source of energy for the life of cells and, in particular, brain cells, it performs plastic functions in the body.

There is practically no free glucose inside the cells. Glucose is stored in cells as glycogen. During oxidation, it is converted into pyruvate and lactate (anaerobic pathway) or into carbon dioxide (aerobic pathway), into fatty acids in the form of triglycerides. Glucose is an integral part of the molecule of nucleotides and nucleic acids. Glucose is necessary for the synthesis of certain amino acids, the synthesis and oxidation of lipids, polysaccharides.

The concentration of glucose in human blood is maintained within a relatively narrow range - 2.8-7.8 mmol / l, regardless of gender and age, despite large differences in nutrition and physical activity (postprandial hyperglycemia - an increase in blood glucose levels after eating , stress factors and its decrease in 3-4 hours after eating and physical activity). This constancy provides the brain tissues with sufficient amounts of glucose, the only metabolic fuel they can use under normal conditions.

Depending on the method of glucose intake, all organs and tissues of the body are divided into insulin-dependent: glucose enters these organs and tissues only in the presence of insulin (adipose tissue, muscles, bone, connective tissue); insulin-independent organs: glucose enters them along a concentration gradient (brain, eyes, adrenal glands, gonads); relatively insulin-independent organs: the tissues of these organs use free fatty acids as nutrients (heart, liver, kidneys). Maintaining glucose within certain limits is an important task of a complex system of hormonal factors. Each time you eat, your glucose level rises and your insulin level rises in parallel. Insulin promotes the entry of glucose into cells, which not only prevents a significant increase in its concentration in the blood, but also provides glucose for intracellular metabolism.

The concentration of insulin during the fasting period fluctuates around 10 mcU / ml and rises to 100 mcU / ml after a normal meal, reaching maximum values ​​30-45 minutes after a meal. This influence is mediated through ATP-sensitive potassium channels, which are composed of protein subunits SUR-1 and Kir 6.2. The glucose entering the beta cell with the participation of the enzyme glucokinase undergoes transformation with the formation of ATP. An increase in ATP promotes the closure of potassium channels. The concentration of potassium in the cytosol of the cell increases. Glutamate metabolites act on these channels in the same way, through oxidation by the enzyme glutamate decarboxylase. An increase in potassium in the cell causes the opening of calcium channels, and calcium rushes into the cell. Calcium promotes the transfer of secretory granules to the cell periphery and the subsequent release of insulin into the intercellular space, and then into the blood. Food secretogens of insulin are amino acids (leucine, valine, etc.). Their effect is enhanced by small intestinal hormones (gastric inhibitory polypeptide, secretin). Other substances stimulate its release (sulfonylurea drugs, beta-adrenergic agonists).

Glucose enters the blood in different ways. After a meal, within 2-3 hours, exogenous carbohydrates serve as the main source of glycemia. In a person engaged in physical labor, food should contain 400-500 g of glucose. Between meals, most of the glucose in the circulating blood is supplied by glycogenolysis (accumulated glycogen in the liver is broken down to glucose, and glycogen in the muscles to lactate and pyruvate). During starvation and depletion of glycogen stores, gluconeogenesis becomes a source of glucose in the blood (the formation of glucose from non-carbohydrate substrates: lactate, pyruvate, glycerol, alanine).

Most dietary carbohydrates are represented by polysaccharides and consist mainly of starches; a smaller portion contains lactose (milk sugar) and sucrose. Digestion of starches begins in the oral cavity with the help of salivary ptyalin, which continues its hydrolytic action in the stomach until the pH of the medium becomes too low. In the small intestine, pancreatic amylase breaks down starches into maltose and other glucose polymers. The enzymes lactase, sucrase and alpha-dextrinase, which are secreted by the epithelial cells of the brush border of the small intestine, break down all disaccharides into glucose, galactose and fructose. Glucose, which makes up more than 80% of the end product of carbohydrate digestion, is immediately absorbed and enters the portal circulation.

Glucagon, synthesized by A-cells of the islets of Langerhans, changes the availability of substrates in the intervals between meals. By stimulating glycogenolysis, it ensures a sufficient exit of glucose from the liver in the early period of time after a meal. As liver glycogen stores are depleted, glucagon, together with cortisol, stimulates gluconeogenesis and ensures the maintenance of normal fasting glycemia.

During an overnight fast, glucose is synthesized exclusively in the liver and most of it (80%) is consumed by the brain. In a state of physiological rest, the rate of glucose metabolism is approximately 2 mg/kg/min. People with a body weight of 70 kg need 95-105 g of glucose for a 12-hour interval between dinner and breakfast. Glycogenolysis is responsible for approximately 75% of nocturnal glucose production in the liver; the rest is provided by gluconeogenesis. The main substrates for gluconeogenesis are lactate, pyruvate, and amino acids, especially alanine and glycerol. When the fasting period is prolonged and insulin levels fall, gluconeogenesis in the liver becomes the only source of maintenance of euglycemia, since all glycogen stores in the liver have already been used up. At the same time, fatty acids are metabolized from adipose tissue to provide an energy source for muscle activity and available glucose for the central nervous system. Fatty acids are oxidized in the liver to form ketone bodies - acetoacetate and beta-hydroxybutyrate.

If fasting continues for days and weeks, other homeostatic mechanisms are activated that ensure the preservation of the protein structure of the body, slowing down gluconeogenesis and switching the brain to the utilization of ketone molecules, acetoacetate and beta-hydroxybutyrate. The signal for the use of ketones is an increase in their concentration in arterial blood. With prolonged fasting and severe diabetes, extremely low concentrations of insulin in the blood are observed.

Hypoglycemia and hypoglycemic conditions

In healthy people, the inhibition of endogenous insulin secretion after the absorption of glucose into the blood begins at a concentration of 4.2-4 mmol / l, with a further decrease in it, it is accompanied by the release of contra-insular hormones. After 3-5 hours after a meal, the amount of glucose absorbed from the intestine progressively decreases and the body switches to endogenous glucose production (glycogenolysis, gluconeogenesis, lipolysis). During this transition, the development of functional hypoglycemia is possible: early - in the first 1.5-3 hours and late - after 3-5 hours. "Hunger" hypoglycemia is not associated with food intake and develops on an empty stomach or 5 hours after eating. There is no strong correlation between blood glucose levels and clinical symptoms of hypoglycemia.

Manifestations of hypoglycemia

Hypoglycemia is more a clinical concept than a laboratory one, the symptoms of which disappear after the normalization of blood glucose levels. The development of symptoms of hypoglycemia is affected by a rapid decrease in blood glucose. This is evidenced by the factors of a rapid decrease in high glycemia in patients with diabetes mellitus. The appearance of clinical symptoms of hypoglycemia is observed in these patients with high glycemia with active insulin therapy.

Symptoms of hypoglycemia are characterized by polymorphism and non-specificity. For hypoglycemic disease, the Whipple triad is pathognomonic:

• the occurrence of attacks of hypoglycemia after prolonged fasting or exercise;
• a decrease in blood sugar during an attack below 1.7 mmol / l in children under two years old, below 2.2 mmol / l - over two years old;
• relief of a hypoglycemic attack by intravenous administration of glucose or oral administration of glucose solutions.

Symptoms of hypoglycemia are due to two factors:

• stimulation of the sympathetic-adrenal system, resulting in increased secretion of catecholamines;
• a deficiency in the supply of glucose to the brain (neuroglycemia), which is tantamount to a decrease in oxygen consumption by nerve cells.

Symptoms such as profuse sweating, constant feeling of hunger, tingling of the lips and fingers, pallor, palpitations, fine trembling, muscle weakness and fatigue are due to the excitation of the sympathetic-adrenal system. These symptoms are early warning signs of hypoglycemia.

Neuroglycemic symptoms are manifested by headache, yawning, inability to concentrate, fatigue, inappropriate behavior, hallucinations. Sometimes there are mental symptoms in the form of depression and irritability, drowsiness during the day and insomnia at night. Due to the variety of symptoms of hypoglycemia, among which the anxiety reaction often dominates, many patients are erroneously diagnosed with neurosis or depression.

Prolonged and deep hypoglycemic coma can cause edema and swelling of the brain, followed by irreversible damage to the CNS. Frequent attacks of hypoglycemia lead to a change in personality in adults, a decrease in intelligence in children. The difference between the symptoms of hypoglycemia and real neurological conditions is the positive effect of food intake, the abundance of symptoms that do not fit into the clinic of a neurological disease.

The presence of pronounced neuropsychiatric disorders and insufficient awareness of doctors about hypoglycemic conditions often lead to the fact that, due to diagnostic errors, patients with organic hyperinsulinism are treated for a long time and unsuccessfully under a variety of diagnoses. Erroneous diagnoses are made in 3/4 of patients with insulinoma (epilepsy is diagnosed in 34% of cases, a brain tumor in 15%, vegetovascular dystonia in 11%, diencephalic syndrome in 9%, psychosis, neurasthenia in 3%).

Most of the symptoms of hypoglycemia are due to insufficient supply of glucose to the central nervous system. This leads to a rapid increase in the content of adrenaline, norepinephrine, cortisol, growth hormone, glucagon.

Episodic hypoglycemic states can be compensated by the activation of contra-insular mechanisms or food intake. In the event that this is not enough, a fainting state or even a coma develops.

Hypoglycemic coma

Hypoglycemic coma is a condition that develops when blood glucose levels drop to 2.2 mmol/L or less. With a rapid drop in blood sugar, it can develop rapidly, without warning, and sometimes even suddenly.

With a short coma, the skin is usually pale, moist, its turgor is preserved. The tone of the eyeballs is normal, the pupils are wide. The tongue is wet. characteristic tachycardia. Blood pressure (BP) is normal or slightly elevated. Breathing is normal. The temperature is normal. Muscle tone, tendon and periosteal reflexes are increased. There may be muscle tremors, convulsive twitches of facial muscles.

As the coma deepens and duration increases, sweating stops, breathing becomes more frequent and shallow, blood pressure decreases, and bradycardia sometimes appears. Changes in the neurological status are distinctly increasing: pathological symptoms appear - nystagmus, anisocoria, meningism, pyramidal signs, muscle tone decreases, tendon and abdominal reflexes are inhibited. In prolonged cases, death is possible.

Of particular danger are hypoglycemic attacks in elderly people suffering from coronary heart disease and the brain. Hypoglycemia can be complicated by myocardial infarction or stroke, so ECG monitoring is mandatory after stopping the hypoglycemic state. Frequent, severe, prolonged hypoglycemic episodes gradually lead to encephalopathy, and then to personality degradation.

Causes of hypoglycemia

Hypoglycemia is a syndrome that can develop both in healthy people and in various diseases (table).

Hypoglycemia due to insufficient glucose production

Hormone deficiency

Hypoglycemia always occurs in panhypopituitarism - a disease characterized by a decrease and loss of the function of the anterior pituitary gland (secretion of adrenocorticotropin, prolactin, somatotropin, follitropin, lutropin, thyrotropin). As a result, the function of peripheral endocrine glands is sharply reduced. However, hypoglycemia also occurs in the primary lesion of the endocrine organs (congenital dysfunction of the adrenal cortex, Addison's disease, hypothyroidism, hypofunction of the adrenal medulla, glucagon deficiency). With a deficiency of contra-insular hormones, the rate of gluconeogenesis in the liver decreases (influence on the synthesis of key enzymes), glucose utilization in the periphery increases, and the formation of amino acids in the muscles, a substrate for gluconeogenesis, decreases.

Glucocorticoid deficiency

Primary adrenal insufficiency is a consequence of a decrease in the secretion of hormones of the adrenal cortex. This term refers to various variants of hypocorticism in terms of etiology and pathogenesis. Symptoms of adrenal insufficiency develop only after the destruction of 90% of the volume of adrenal tissue.

The causes of hypoglycemia in adrenal insufficiency are similar to the causes of hypoglycemia in hypopituitarism. The difference is the level of occurrence of the block - with hypopituitarism, cortisol secretion decreases due to ACTH deficiency, and with adrenal insufficiency, due to the destruction of the tissue of the adrenal glands themselves.

Hypoglycemic conditions in patients with chronic adrenal insufficiency can occur both on an empty stomach and 2-3 hours after a meal rich in carbohydrates. Attacks are accompanied by weakness, hunger, sweating. Hypoglycemia develops as a result of a decrease in cortisol secretion, a decrease in gluconeogenesis, and glycogen stores in the liver.

Deficiency of catecholamines

This condition can occur with adrenal insufficiency with damage to the adrenal medulla. Catecholamines, getting into the blood, regulate the release and metabolism of insulin, reducing it, and also increase the release of glucagon. With a decrease in the secretion of catecholamines, hypoglycemic conditions are observed, caused by excessive production of insulin and reduced activity of glycogenolysis.

Glucagon deficiency

Glucagon is a hormone that is a physiological antagonist of insulin. It is involved in the regulation of carbohydrate metabolism, affects fat metabolism by activating enzymes that break down fats. The main amount of glucagon is synthesized by the alpha cells of the pancreatic islets. However, it has been established that special cells of the duodenal mucosa and gastric mucosa also synthesize glucagon. When it enters the bloodstream, glucagon causes an increase in the concentration of glucose in the blood, up to the development of hyperglycemia. Normally, glucagon prevents an excessive decrease in glucose concentration. Due to the existence of glucagon, which prevents the hypoglycemic action of insulin, a fine regulation of glucose metabolism in the body is achieved.

Some hypothalamic-pituitary syndromes may be accompanied by hypoglycemia: Laurence-Moon-Biedl-Bordet syndrome, Debre-Marie syndrome, Pehkranz-Babinski syndrome (adiposogenetal dystrophy).

• Laurence-Moon-Biedl-Bordet syndrome is characterized by obesity, hypogonadism, mental retardation, retinal degeneration, polydactyly, and profound degenerative changes in the hypothalamic-pituitary system.
• Debre-Marie syndrome is a disease caused by hyperfunction of the posterior lobe of the pituitary gland and hypofunction of the adenohypophysis. It appears in early childhood. Patients are infantile, undersized, overweight. In the clinical picture, a violation of water metabolism with oliguria and oligodipsia is typical, the urine density is high. Mental development is not disturbed.
• Pehkranz-Babinski syndrome - the cause of the disease is considered to be organic and inflammatory changes in the hypothalamus, which lead to obesity, anomalies in the development of the skeleton and hypoplasia of the genital organs.

In these syndromes, the insulin content is reduced, and the excretion of ketone bodies in the urine is increased.

Hypoglycemia due to enzyme deficiency

Defect in the enzyme glucose-6-phosphatase (Girke's disease)

Deficiency of glucose-6-phosphatase is the basis of Gierke's disease, or type 1 glycogenosis. Deficiency of this enzyme leads to the inability to convert glucose-6-phosphate to glucose, which is accompanied by the accumulation of glycogen in the liver and kidneys. The disease is inherited in an autosomal recessive manner.

The intake of glucose into the body with food, in principle, makes it possible to maintain a normal level of glucose in the blood, however, for this, the intake of food containing glucose must be practically continuous. In real conditions of existence, i.e., in the absence of a continuous supply of glucose, in a healthy body the latter is deposited in the form of glycogen, which, if necessary, is used in its polymerization.

The primary disorder in Gierke's disease occurs at the genetic level. It consists in the complete or almost complete inability of cells to produce glucose-6-phosphatase, which ensures the cleavage of free glucose from glucose-6-phosphate. As a result, glycogenolysis is interrupted at the level of glucose-6-phosphate and does not proceed further. Dephosphorylation with the participation of glucose-6-phosphatase is a key reaction not only of glycogenolysis, but also of gluconeogenesis, which, therefore, is also interrupted at the level of glucose-6-phosphate in Gierke's disease. The occurrence of stable hypoglycemia, which in real conditions is inevitable due to the lack of glucose in the blood as the end product of glycogenolysis and gluconeogenesis, in turn leads to a constant increased secretion of glucagon as a stimulator of glycogenolysis. Glucagon, however, under conditions of interruption of this process, is only capable of continuously stimulating its initial stages without benefit to the organism.

If the deficiency of the enzyme is moderate, patients reach adolescence, and often older. However, mental and somatic development, as well as biochemical status (increased levels of triglycerides, cholesterol, hyperuricemia, hypophosphatemia) in these patients are severely impaired. Characteristic features are oligophrenia, growth retardation, obesity, osteoporosis, large abdomen (a consequence of an enlarged liver and kidneys), xanthomatosis, retinal lipemia, hemorrhagic diathesis. The fasting plasma glucose content is constantly reduced, and therefore, even with short-term fasting, hypoglycemic convulsions, ketonuria and metabolic acidosis develop. The latter is caused not only by hyperketonemia, but also by increased accumulation and formation of pyruvate and lactate in the blood, which is the result of impaired gluconeogenesis. Violation of lipid metabolism is accompanied by pancreatitis.

Diagnosis is based on clinical findings, low blood glucose, and elevated blood lipids and lactate. Plasma glucose levels remain virtually unchanged after administration of glucagon. However, the content of lactate in the blood after its introduction increases. Liver biopsy, special histochemical methods confirm the deficiency of the corresponding enzymes.

Amylo-1,6-glucosidase deficiency

Amyl-1,6-glucosidase deficiency, referred to as type 3 glycogenosis or Cori's disease, is one of the most common glycogenoses and has a relatively mild clinical course. The function of this enzyme is to degrade the protein branches of glycogen and cleave free glucose from them. However, the decrease in blood glucose in this disease is not as significant as in type 1 glycogenosis, since a certain amount of glucose is formed by the activation of phosphorylase in the liver. The clinical picture of the disease is characterized by hepatomegaly, muscle weakness, growth retardation and periodic "hungry" hypoglycemia. In a laboratory study, an increase in the level of hepatic transaminases is detected. The content of lactate and uric acid in the blood plasma is usually normal. In response to the administration of glucagon, there is no increase in plasma glucose if the test with glucagon is performed on an empty stomach, while when glucagon is administered 2 hours after a meal, the response is already normal. To confirm the diagnosis, a biopsy of the liver and muscles is necessary, in which altered glycogen and insufficiency of the corresponding enzyme are detected.

Hepatic phosphorylase defect - Hers disease

Glycogenosis caused by deficiency of liver phosphorylase (glycogen disease type 6). Liver phosphorylase catalyzes the phosphorylation (breakdown) of glycogen to form glucose-1-phosphate. Violation of this mechanism leads to excessive deposition of glycogen in the liver. Inherited presumably in an autosomal recessive manner.

It usually appears in the first year of life. Growth retardation, a doll face, a significant increase in the liver as a result of glycogen infiltration of hepatocytes, hypoglycemia, hyperlipemia, and an increased content of glycogen in erythrocytes are characteristic. The diagnosis is based on a decrease in phosphorylase activity in leukocytes.

Deficiency of glycogen synthetase

A very rare hereditary disease. In patients with a defect in the synthesis of this enzyme, glycogen is not synthesized at all. Fasting causes severe hypoglycemia.

Phosphoenolpyruvate carboxykinase deficiency

Phosphoenolpyruvate carboxykinase is the key enzyme of gluconeogenesis. A defect in this enzyme is a very rare cause of hypoglycemia. Phosphoenolpyruvate carboxykinase is involved in the synthesis of glucose from lactate, metabolites of the Krebs cycle, amino acids and fatty acids. Therefore, in the absence of this enzyme, infusion of lactate or alanine does not achieve normoglycemia. On the contrary, the introduction of glycerol normalizes the concentration of glucose, since phosphoenolpyruvate carboxykinase is not required for the synthesis of glucose from glycerol. In severe hypoglycemia, infusion of glucose is carried out.

Hunger hypoglycemia

severe malnutrition

Starvation is the most common cause of hypoglycemia in healthy people. During starvation, glucose does not enter the body, but continues to be consumed by muscles and other organs. During short-term fasting, glucose deficiency is covered by glycogenolysis and gluconeogenesis in the liver. With prolonged starvation, glycogen stores in the liver are depleted and hypoglycemia occurs.

Hypoglycemia often occurs in people who observe religious canons in nutrition (for example, Orthodox Christians during Lent and Muslims during Ramadan). It is clear that in such cases, hypoglycemia is due to a complete or almost complete long-term lack of food.

The same form of hypoglycemia develops against the background of exhausting physical activity, for example, when running, swimming and cycling for long distances, among all-rounders, climbers, skiers, and bodybuilders. In such situations, the main cause of hypoglycemia is increased glucose uptake by the muscles.

Hypoglycemia during pregnancy

All types of metabolism during pregnancy undergo significant changes, enzymatic reactions are rebuilt. Glucose is the main material for providing the energy needs of the fetus and mother. With the progression of pregnancy, glucose consumption continuously increases, which requires constant restructuring of regulatory mechanisms. The secretion of both hyperglycemic hormones (glucagon, estrogens, cortisol, pituitary prolactin, placental lactogen, somatotropin) and the hypoglycemic hormone insulin increase. Thus, a dynamic balance of mechanisms regulating carbohydrate metabolism is established. The blood glucose level in pregnant women remains within the normal range, while the need for glucose in the mother's and fetus's organisms is fully met.

In late pregnancy, against the background of depletion of compensatory mechanisms, a hypoglycemic state may occur. The clinical picture of hypoglycemia in pregnancy includes hunger, headache, sweating, weakness, tremor, nausea, paresthesia, blurred and narrowed visual fields, confusion, stupor, loss of consciousness, coma and convulsions.

Acquired liver disease

Diffuse and severe liver damage, in which 80-85% of its mass fails, can lead to hypoglycemia due to impaired glycogenolysis and gluconeogenesis. It has been associated with lesions such as acute liver necrosis, acute viral hepatitis, Reye's syndrome, and severe passive congestive heart failure. A metastatic or primary liver tumor (if most of the liver tissue is involved) can cause hypoglycemia, but liver metastases are usually not accompanied by hypoglycemia. Hypoglycemia has been described as part of the fatty liver syndrome of pregnancy. A combination of hypoglycemia with HELLP syndrome (hemolysis, elevated liver enzymes and a decrease in the number of platelets in peripheral blood) has also been reported. During pregnancy, a variety of liver damage can occur - from preeclampsia and HELLP syndrome to acute fatty degeneration. Therefore, all unhealthy women in the third trimester of pregnancy should determine the level of glucose. Chronic liver disease is very rarely accompanied by hypoglycemia. Patients with severe liver failure capable of causing hypoglycemia are often in a coma. Hypoglycemia as a cause of coma may be overlooked if coma is regarded as a consequence of hepatic encephalopathy.

Hypoglycemia may be accompanied by chronic renal failure. This is due to the fact that a healthy kidney is capable of gluconeogenesis. In some cases, this process accounts for up to 50% of endogenous glucose produced. In uremia, gluconeogenesis may be suppressed. In addition, the kidney produces insulinases that destroy insulin, which accumulates in patients with chronic renal failure. For the same reason, the risk of hypoglycemia increases in patients with diabetes mellitus complicated by chronic renal failure.

Alcohol and medicines

Drinking alcohol is a common cause of hypoglycemia in both adults and children. The breakdown of ethanol to form acetaldehyde in the liver is catalyzed by the enzyme alcohol dehydrogenase. This enzyme works only in the presence of a special cofactor, nicotinamide dinucleotide (NAD). But the same substance is also necessary for hepatic gluconeogenesis. Alcohol intake leads to a rapid consumption of NAD and a sharp inhibition of gluconeogenesis. Therefore, alcoholic hypoglycemia occurs when glycogen stores are depleted, when gluconeogenesis is especially necessary to maintain normal blood glucose levels. When drinking large amounts of alcohol in the evening, symptoms of hypoglycemia usually occur the next morning.

Most often, alcoholic hypoglycemia occurs in malnourished patients with alcoholism, but it also happens in healthy people after taking large amounts of alcohol or when drinking alcohol "on an empty stomach."

Alcoholic hypoglycemia often occurs in children who mistakenly or intentionally drink beer, wine, or spirits. Children under 6 years of age are especially sensitive to alcohol - alcoholic hypoglycemia occurs after alcohol compresses. Mortality due to alcoholic hypoglycemia in children reaches 30%, while in adults it is approximately 10%. . The diagnosis of alcoholic hypoglycemia is based on the history and finding of hypoglycemia in combination with elevated levels of alcohol and lactic acid in the blood.

Cases of hypoglycemia have been described when taking non-selective beta-blockers. They are used to treat coronary heart disease, cardiac arrhythmias, and some forms of hypertension. This effect is due to increased utilization of glucose by the muscles, a decrease in the formation of glucose from glycogen, inhibition of lipolysis and a decrease in the content of non-esterified fatty acids in the blood. Beta-blockers are not recommended for insulin-dependent diabetes mellitus because they mask most of the symptoms of hypoglycemia and may be toxic to pancreatic islet cells. It is also worth remembering that with the simultaneous use of propranolol and hypoglycemic drugs, there is a risk of developing hypoglycemia, due to the enhancement of their action.

Hypoglycemia can cause anti-inflammatory and analgesic drugs from the class of salicylates (Paracetamol, Aspirin). Salicylates have an effect on metabolism: when administered in large doses, a decrease in synthesis and an increase in the breakdown of amino acids, proteins and fatty acids are observed. In diabetes mellitus, salicylates help lower blood glucose levels. Also, salicylates, like beta-blockers, enhance the effect of drugs used to lower blood sugar levels.

Hypoglycemia associated with increased glucose intake

insulinoma

Insulinoma is an insulin-producing tumor originating from the beta cells of the islets of Langerhans, causing the development of hypoglycemic syndrome on an empty stomach. In tumor cells, insulin secretion is impaired: secretion is not suppressed when blood glucose levels decrease. In 85-90% of cases, the tumor is solitary and benign, only in 10-15% of cases the tumors are multiple, and extremely rarely the tumors are located outside the pancreas (hilum of the spleen, liver, duodenal wall). The frequency of new cases of the tumor is 12 per 1 million people per year, most often the tumor is diagnosed between the ages of 25 and 55 years.

In the clinic, insulinoma is characterized by attacks of hypoglycemia associated with a constant, independent of the level of glucose in the blood, the release of insulin. Frequent bouts of hypoglycemia cause changes in the central nervous system. In some patients, they resemble an epileptic seizure, with which they are hospitalized in the neurological department. Attacks of hypoglycemia are interrupted by food intake, and therefore patients constantly consume a large amount of food, mainly carbohydrates, which contributes to the development of obesity.

Diagnosis of insulinoma is based on the identification of the classic and pathogomonic Whipple triad for it, as well as the clinical picture typical of hypoglycemia. The “gold standard” at the first stage of diagnosing hypoglycemic syndrome and confirming endogenous hyperinsulinism is a fasting test. The test is carried out within 72 hours and is considered positive with the development of the Whipple triad. The beginning of fasting is noted as the time of the last meal. The blood glucose level on the sample is assessed initially 3 hours after the last meal, then every 6 hours, and when the blood glucose level drops below 3.4 mmol/l, the interval between its studies is reduced to 30-60 minutes.

The rate of insulin secretion in insulinoma is not inhibited by a decrease in blood glucose levels. In fasting patients with insulinoma, hypoglycemia develops due to the fact that the amount of glucose in the blood on an empty stomach depends on the intensity of glycogenolysis and gluconeogenesis in the liver, and excessive insulin secretion blocks glucose production. It is recommended to calculate the insulin/glycemic index. Normally, it is no more than 0.3, and with insulinoma it exceeds 1.0. The concentration of C-peptide is also sharply increased.

The second stage in the diagnosis of insulinoma is the topical diagnosis of the tumor. Ultrasound, computed tomography, magnetic resonance imaging, endoscopic ultrasound, scintigraphy, angiography, intraoperative ultrasound are used. The most informative in the diagnosis of insulin endoscopic ultrasound (endo-ultrasound) and blood sampling from the hepatic veins after intra-arterial stimulation of the pancreas with calcium. Many patients, with the help of modern research methods, manage to establish the localization of the tumor, its size, stage and rate of progression of the tumor process, and identify metastases at the preoperative stage.

Certain difficulties in diagnosing insulinoma may occur in patients using insulin or sulfonylurea drugs. To prove exogenous insulin administration, it is necessary to look at a blood test: with exogenous insulin administration, antibodies to insulin will be detected in the blood, a low level of C-peptide with a high level of total immunoreactive insulin (IRI). In order to exclude hypoglycemia caused by taking sulfonylurea drugs, it would be advisable to determine the content of sulfonylurea in the urine.

Treatment of insulinoma in most cases is surgical: enucleation of the tumor, distal resection of the pancreas. Conservative therapy is carried out in the case of an unresectable tumor and its metastases, as well as when the patient refuses surgical treatment and includes:

1. chemotherapy (streptozotocin, 5-fluorouracil Ebeve, Epirubicin-Ebeve);
2. biotherapy (analogs of somatostatin (Octreotide-depot, Sandostatin Lar);
3. immunotherapy (interferon alfa);
4. elimination or reduction of symptoms of hypoglycemia (diazoxide, glucocorticoids, phenytoin).

Five-year survival among radically operated patients is 90%, with the detection of metastases - 20%.

Hyperplasia of beta cells in newborns and infants

Insulinoma should be differentiated from hyperplasia or an increase in the number of pancreatic islets. Normally, the volume of the endocrine part is 1-2% in adults and 10% in newborns. In young children, islet hyperplasia occurs with nesidioblastosis, fetal erythroblastosis, Beckwith-Wiedemann syndrome, and also in children born to mothers with diabetes mellitus.

Nesidioblastosis

Nesidioblastosis is a congenital dysplasia of endocrine cells (microadenomatosis). From nesidioblasts, which are formed in utero from the epithelium of the pancreatic ducts, the islets of Langerhans are formed. This process begins at 10-19 weeks of fetal development and ends at 1-2 years of a child's life. In some cases, the formation of endocrine cells may be accelerated or additional cells are formed in the acinar tissue of the pancreas. These disorders, which are transient in nature, often occur in normally developing pancreatic tissue. It is believed that up to two years, nesidioblastosis is a variant of the norm; in children older than two years, it is a pathology. Cells that form the focus of nesidioblastosis give a positive reaction to insulin, glucagon, somatostatin and pancreatic polypeptide. However, the proportion of beta cells is significantly higher than normal. Dysplasia of the endocrine part of the pancreas is associated with multiple endocrine neoplasia type 1 (MEN 1). Nesidioblastosis is accompanied by unregulated insulin secretion and severe hypoglycemia.

Some authors propose to introduce the term "congenital hyperinsulinism", which means all varieties of nesidioblastosis, and a specific form should be put after histological diagnosis. Hyperinsulinemic hypoglycemia occurs in children born to mothers with diabetes mellitus. The pathogenesis of hypoglycemia in such newborns is due to the fact that in utero an excess amount of glucose diffuses from the pregnant woman to the fetus and causes hypertrophy of the islet apparatus in the latter. After the baby is born, beta cells continue to overproduce insulin, causing symptoms of hypoglycemia in some babies. It should be borne in mind that with prolonged administration of concentrated glucose solutions to pregnant women, the development of transient hypoglycemia in newborns is possible.

Hyperplasia of the islet apparatus in newborns can occur with hemolytic disease. The destruction of erythrocytes in utero is accompanied by the degradation of insulin, which causes hypertrophy of beta cells. Treatment of such patients with exchange transfusion stops hemolysis and, consequently, the destruction of insulin. But transient hypoglycemia persists for some time. In the neonatal period, hypoglycemia may be a manifestation of the Wiedemann-Beckwith syndrome in children. The cause of severe neonatal hypoglycemia is hypertrophy and hyperplasia of the pancreatic islets. Children are born large. Characterized by an increase in organs: liver, kidneys, pancreas. The presence of a cyst of the umbilical cord, macroglossia, and various organ anomalies are typical. If patients do not die in the neonatal period, then mental retardation is associated with hypoglycemic conditions.

Autosomal recessive hyperinsulinemic hypoglycemia

A family disease that is a consequence of a mutation in the genes responsible for the synthesis of the SUR-1 and Kir 6.2 proteins, which are located on chromosome 11 p151. The protein isoform SUR-1, referred to as SUR-2, is involved in the function of potassium channels localized extrapancreatically, i.e. in the tissues of other organs. Any disruption resulting in loss of SUR-1 or Kir 6.2 function contributes to irregular closure of ATP-sensitive potassium channels, depolarization of beta-cell membranes, increased calcium output and high levels of basal cytosolic concentration, and finally, unregulated insulin secretion.

Hypoglycemia in diabetes mellitus

In patients with diabetes mellitus, hypoglycemia is a serious problem in the treatment of hypoglycemic drugs. This is due to the fact that glycogen stores in the liver are reduced, which in emergency cases must replenish blood glucose.

The main causes of hypoglycemia in the treatment of diabetes mellitus are insulin overdose, i.e., a mismatch between the dose of insulin and the amount of carbohydrates in food, food intake delay, excessive exercise, injection of insulin into the muscle, leading to faster absorption of it, or injection of insulin into areas of lipodystrophy from where it is absorbed at different rates. The risk of developing hypoglycemia in patients with diabetes mellitus increases due to the introduction of intensified insulin therapy, which involves maintaining glycemia during the day close to normal blood glucose values. This provokes the risk of developing hypoglycemia. The lower limit of glucose concentration is recommended to be limited within 4-4.2 mmol / l.

Unrecognized hypoglycemia in patients with long-term diabetes mellitus may occur during sleep (Somogyi phenomenon). The body reacts to this condition by excessive secretion of counter-insular hormones. In the morning hours, blood glucose levels rise significantly and are misdiagnosed as a consequence of an insufficient dose of insulin. In this regard, the dose of the drug increases, thereby worsening the course of diabetes mellitus. In this case, the disease proceeds with sharp fluctuations in glycemia during the day. Given the large number of insulin preparations used in different clinics, it is worth remembering the differences between animal and synthetic insulin in the manifestation of symptoms of hypoglycemia with an overdose of these drugs.

In the treatment of synthetic human insulins, as well as in patients with neuropathy, the symptoms of impending severe hypoglycemia are neuroglycopenic in nature. It develops unexpectedly and very quickly. Impaired coordination and concentration. The patient loses consciousness, or an epileptiform convulsive seizure occurs. For this reason, the patient realizes the threat of hypoglycemia too late. It is difficult to get out of it on your own. Edema and swelling of the brain and the development of postglycemic encephalopathy are associated with this form of hypoglycemic coma.

With an overdose of animal insulin, the onset of a hypoglycemic attack is preceded by the so-called "adrenaline symptoms": early - acute hunger, palpitations, cold sweat, trembling, headache. The patient can take the necessary measures in a timely manner and avoid the transition to a hypoglycemic coma.

Artificially induced hypoglycemia

Euphoria caused by the administration of insulin occurs in healthy girls (Munchausen's syndrome). Some patients with diabetes also actively cause symptoms of hypoglycemia. The motive for such behavior is related to the characteristics of the character and the social environment. Such patients are very inventive and actively hide drugs. Suspected artificial hypoglycemia is diagnosed by the presence of its symptoms, high levels of insulin and low C-peptide in the blood.

Autoimmune hypoglycemic syndrome

Autoantibodies directed against insulin or its receptors can provoke hypoglycemia. In healthy people, antibodies to insulin are constantly formed in the blood, but they are detected only in 1-8%. Autoantibodies to insulin are found in 40% of patients with newly diagnosed diabetes mellitus who are not treated with insulin, and in 30% when it is combined with autoimmune diseases. Autoantibodies that bind insulin can undergo untimely dissociation, usually within a short period immediately after a meal, and dramatically increase free insulin concentration in serum, thus causing hypoglycemia in the late postprandial period. This may be preceded by hyperglycemia in response to food intake. The diagnosis of autoimmune hypoglycemia is made on the basis of a combination with autoimmune diseases, the presence of a high titer of antibodies to insulin, high concentrations of insulin and the absence of a decrease in the level of C-peptide against the background of hypoglycemia.

Antibodies to insulin receptors can provoke hypoglycemia. These antibodies bind to receptors and mimic the action of insulin by increasing the utilization of glucose from the blood. Insulin receptor antibodies are more common in women and are associated with many autoimmune diseases. Attacks of hypoglycemia, as a rule, develop on an empty stomach.

Hypoglycemia with normal insulin levels

Extrapancreatic tumors

Various mesenchymal tumors (mesothelioma, fibrosarcoma, rhabdomyosarcoma, leiomyosarcoma, liposarcoma, and hemangiopericytoma) and organ-specific carcinomas (hepatic, adrenocortical, genitourinary system, and breast) can be associated with hypoglycemia. Hypoglycemia may accompany pheochromocytoma, carcinoid, and malignant blood diseases (leukemia, lymphoma, and myeloma). Its mechanism varies according to the type of tumor, but in many cases hypoglycemia is associated with malnutrition due to the tumor and weight loss due to fat, muscle and tissue wasting, which impairs gluconeogenesis in the liver. In some cases, glucose utilization by exceptionally large tumors can lead to hypoglycemia. Tumors may also secrete hypoglycemic factors such as unsuppressed insulin-like activity and insulin-like growth factors. By binding to hepatic insulin receptors, insulin-like factor-2 inhibits hepatic glucose production and promotes hypoglycemia. Tumor cytokines are also under suspicion, especially tumor necrosis factor (cachectin). Very rarely, the tumor secretes extrahepatic insulin.

Systemic carnitine deficiency

Severe hypoglycemia may occur in patients with systemic carnitine deficiency. Carnitine is a biologically active vitamin-like substance. Its main functions are participation in energy metabolism, binding and excretion of toxic derivatives of organic acids from the body. With a systemic deficiency of carnitine in plasma, muscles, liver and other tissues, the content of carnitine is reduced, which is necessary for the transport of fatty acids to the mitochondria, where they are oxidized. As a result, peripheral tissues are unable to utilize fatty acids for energy, and the liver cannot produce an alternative substrate - ketone bodies. All this leads to the fact that all tissues become dependent on glucose and the liver is unable to meet their needs. Systemic carnitine deficiency is manifested by nausea, vomiting, hyperammonemia, and hepatic encephalopathy. This pathology is one of the forms of Reye's syndrome.

Less often, hypoglycemia occurs when carnitine palmitoyltransferase is insufficient, an enzyme that transfers fatty acids from fatty acyl-CoA to carnitine for oxidation. In most patients, there appears to be a partial defect so that some degree of fatty acid oxidation is preserved and the tendency to hypoglycemia is minimized. Clinically, this is manifested by myopathy during exercise with myoglobinuria. Nonketotic (or hypoketotic) hypoglycemia can also occur with a decrease in the activity of other enzymes of fatty acid oxidation, for example, with a deficiency of dehydrogenase of medium or long chain acyl coenzyme A (acyl-CoA).

Young children are especially sensitive to carnitine deficiency. Their endogenous reserves are quickly depleted in various stressful situations (infectious diseases, gastrointestinal disorders, feeding disorders). The biosynthesis of carnitine is sharply limited due to small muscle mass, and intake with ordinary foods is not able to maintain sufficient levels in the blood and tissues.

Diagnosis and differential diagnosis of hypoglycemia

If hypoglycemia is suspected, the concentration of glucose in the blood or plasma should be urgently determined and treatment initiated. When collecting an anamnesis of the disease, first of all, you need to find out in what conditions it occurs. In some patients, hypoglycemia attacks occur if they do not eat on time (fasting hypoglycemia). Others have seizures after eating, especially after eating a carbohydrate-rich meal (reactive hypoglycemia). This information is important because the etiology and mechanisms of fasting hypoglycemia and reactive hypoglycemia are different. Fasting hypoglycemia is often a manifestation of a serious illness (for example, insulinoma) and is more dangerous for the brain.

To establish the diagnosis, it is necessary to find an association between the onset of symptoms and an abnormally low plasma glucose level, and also to show that symptoms disappear when this level rises. The plasma glucose level at which symptoms occur varies among patients and under different physiological conditions. Abnormally low plasma glucose concentration is usually called when it does not reach 2.7 mmol / l in men or 2.5 mmol / l in women (i.e., it is below the lower limit in healthy men and women after fasting for 72 h) and 2.2 mmol/l in children.

In any patient with impaired consciousness (or seizures of unknown etiology), it is necessary to determine the content of glucose in the blood using test strips using a drop of blood for this. If an abnormally low glucose level is detected, glucose is started immediately. Rapid mitigation of CNS symptoms (observed in most patients) with an increase in blood glucose confirms the diagnosis of fasting hypoglycemia or drug-induced hypoglycemia. A portion of the original blood sample should be retained as frozen plasma to determine baseline insulin, proinsulin, and C-peptide concentrations or, if necessary, to detect any compounds in the blood that have caused hypoglycemia. It is also necessary to determine the pH of the blood and the content of lactate in it, and with the help of test strips to check the content of ketone bodies in the plasma.

Often, the probable cause of hypoglycemia can be identified from the very beginning (alcohol breath, history of the use of sugar-lowering drugs in anamnesis, signs of extensive damage to the liver or kidneys, the presence of a large tumor in the retroperitoneal space or in the chest cavity, and the existence of congenital causes of fasting hypoglycemia).

In patients with insulin-secreting pancreatic tumors (insulinomas, islet cell carcinomas), elevated insulin levels are usually accompanied by elevated levels of proinsulin and C-peptide. In patients receiving sulfonylurea drugs, an increase in the level of C-peptide should also be expected, but in this case, significant amounts of the drug should also be present in the blood.

If hypoglycemia is associated with an overdose of insulin preparations, then the level of proinsulin is normal, and the content of C-peptide is reduced. In autoimmune insulin syndrome, the content of free insulin in plasma during an attack of hypoglycemia is usually sharply increased, the level of C-peptide is reduced, but antibodies to insulin are easily detected in plasma. The differential diagnosis between autoimmune hypoglycemia and a condition caused by excessive insulin administration requires special studies.

Patients with insulinoma often have no symptoms of hypoglycemia when they see a doctor. They are forced to go to medical institutions by attacks of sudden clouding or loss of consciousness, which they have suffered for a number of years and which have become more frequent recently. A characteristic feature of such attacks is that they occur between meals or after an overnight fast; sometimes they are provoked by physical activity. Attacks may go away spontaneously, but more often they disappear quickly after ingestion of sugary foods or drinks. This feature is the most important diagnostic feature.

When examining such patients, it is possible to detect inappropriately high initial plasma insulin levels (> 6 mcU / ml and even more so > 10 mc U / ml) against the background of hypoglycemia. This finding is a strong argument in favor of an insulin-secreting tumor if surreptitious use of insulin or sulfonylurea drugs can be ruled out. Usually, when glycemia falls to an abnormally low level, plasma insulin levels drop to a normal basal level, which is still too high for these conditions. Conditions other than the presence of an insulin-secreting tumor that predispose to fasting hypoglycemia can usually be ruled out on outpatient evaluation.

If the patient does not have objective causes from other organs and systems, which are characterized by episodic symptoms from the central nervous system, the patient is hospitalized in a hospital and a fasting test is performed. The purpose of this test is to reproduce the symptoms in terms of recording the levels of glucose, insulin, proinsulin and C-peptide in plasma. In 79% of patients with insulinoma, symptoms occur already within 48 hours of fasting, and in 98% within 72 hours. Fasting is stopped after 72 hours or at the time of the onset of symptoms. If fasting provokes the onset of characteristic symptoms of the patient, which are quickly relieved by the introduction of glucose, or if the symptoms appear against the background of abnormally low glucose levels and inappropriately high plasma insulin levels, then the presumptive diagnosis of an insulin-secreting tumor can be considered confirmed. The use of x-rays and CT scans is not useful for diagnosing insulinomas because these tumors are usually too small to be detected by these tests.

Treatment of hypoglycemic conditions

Treatment of hypoglycemic conditions in their initial stages includes the oral administration of easily absorbed carbohydrates: sugar, jam, honey, sweet biscuits, sweets, hard candies, white bread or fruit juice.

At the slightest suspicion of a hypoglycemic coma, even if it is difficult to differentiate it from a keto-acidemic coma, the doctor is obliged, after taking blood for analysis, to immediately inject the patient intravenously with 40-60 ml of a 40% glucose solution. If the hypoglycemic coma is shallow and short-lived, then the patient regains consciousness immediately after the end of the injection. If this does not happen, one can think that the coma is not associated with hypoglycemia or the coma is hypoglycemic, but the functions of the central nervous system will be restored later. Having completed this most important treatment, necessary for hypoglycemia, the doctor gets time for further diagnostic studies. The introduction of the indicated amount of glucose will not harm the patient if the coma turns out to be ketoacidemic.

If consciousness returns to the patient after the first intravenous glucose injection, further glucose infusion can be stopped. The patient is given sweet tea, fed at short intervals. In the absence of consciousness after the introduction of 60 ml of glucose, an intravenous drip of a 5% glucose solution is established, which lasts for hours and days. 30-60 mg of prednisolone are added to the dropper, 100 mg of cocarboxylase, 5 ml of a 5% solution of ascorbic acid are injected intravenously.

The level of glycemia should be maintained within 8-12 mmol / l. With its further increase, fractional insulin is administered in small doses (4-8 IU). Before the drip of a glucose solution, 1 ml of a 0.1% solution of adrenaline is injected subcutaneously, 1-2 ml of glucagon intravenously or intramuscularly (the latter can be re-introduced every 3 hours).

With prolonged absence of consciousness, measures are taken to prevent cerebral edema: 15-20% mannitol solution is injected intravenously, 60-80 mg of Lasix, 10 ml of 25% magnesium sulfate solution, 30-60 mg of prednisolone are injected intravenously. Humidified oxygen inhalation is indicated. In case of respiratory depression, the patient is transferred to artificial lung ventilation.

After removing the patient from a coma, agents that improve the metabolism of CNS cells (glutamic acid, Stugeron, Aminalon, Cerebrolysin, Cavinton) are used for 3-5 weeks.

Literature

1. Balabolkin M. I., Klebanova E. M., Kreminskaya V. M. Differential diagnosis and treatment of endocrine diseases (manual). M.: "Medicine", 2002, p. 751.
2. Dizon A. M. et al. Neuroglycopenic and other symptoms in patients with insulinoma // Am. J. Med. 1999, p. 307.
3. Genes S. G. Hypoglycemia. Hypoglycemic symptom complex. M.: "Medicine", 1970, p. 236.
4. Endocrinology and metabolism. In 2 volumes. Ed. Felinga F. et al. Translation from English: Kandrora V. I., Starkovo N. T. M .: "Medicine", 1985, v. 2, p. 416.
5. Kalinin A. P. et al. insulinoma. Medical newspaper, 2007, No. 45, p. 8-9.
6. Kravets E. B. et al. Emergency endocrinology. Tomsk, 2005, p. 195.
7. Dedov I. I. et al. Diabetes mellitus in children and adolescents. M.: Universum Publishing, 2002, p. 391.

V. V. Smirnov, doctor of medical sciences, professor
A. E. Gavrilova

RSMU, Moscow

Almost every woman has experienced increased appetite during the premenstrual period. Increased appetite causes, as a rule, a physiological nature. Especially on such days you want sweets. This craving is called hypoglycemia.

During such a period, the female body needs an additional 500 calories, which are spent on hormonal changes. According to scientists, during the premenstrual period there is not enough chromium, vitamin B, zinc and magnesium.

However, this term has another more serious meaning, in simple words - a sharp decrease in blood sugar. This condition can be very dangerous for people who are sick, so it is very important to know about the concept of hypoglycemia, its main symptoms and first aid.

What is commonly referred to as hypoglycemia?

The cells of the human central nervous system are in great need of such an important source of energy as glucose (simple sugar). Insulin is used to stimulate the uptake of glucose by other cells in the body, regulate its blood levels, and slow down the production of glucose by the liver.

Hypoglycemia is the state of the body of a patient with diabetes mellitus, when an injection of insulin was made, and the blood sugar level turned out to be abnormally low, that is, carbohydrates quickly “burned out”. This is the result of the fact that the rate at which glucose is produced in the liver and used by other tissues of the body is unbalanced and you need to eat as soon as possible so that blood sugar does not decrease so sharply.

The main symptoms and signs of hypoglycemia

• appearance of dizziness
• anxiety
• shiver,
• hunger and excessive sweating.

These attacks do not pose a danger, since people are forced to immediately consume sugar-containing foods or drinks, and adrenaline or others that are produced along the way suggest that blood sugar levels are normal.

However, it must be remembered that if symptoms of severe hypoglycemia are present for a long period, this will be dangerous, as the brain gradually receives less and less glucose. This suggests disorientation, confusion, in the future even to the appearance of convulsions, partial paralysis, and even to loss of consciousness. As a result, if hypoglycemia is not treated, the brain will be damaged, which in the end can lead to death.

How to stop a sudden attack and provide first aid for hypoglycemia?

Patients with this disease are familiar with the possibility of a sharp drop in blood sugar levels, so they are very often concerned about the main question: how, by consuming minimal doses of glucose, it is possible to stop an attack of hypoglycemia?

Let's look at an example: if one of the symptoms of hypoglycemia occurs, that is, you experience a feeling of severe hunger, you must immediately determine the presence of sugar in the blood with a glucometer. If you have determined that your sugar level is below your target level by 0.6 mmol / l or even lower, you need to stop an attack of hypoglycemia as soon as possible.

If, after measuring blood sugar, it was found that it had decreased, and at the same time you did not experience symptoms of hypoglycemia, it is still recommended to accurately calculate the dosage of glucose and take pills. Since, under the condition of low sugar, even without symptoms, it is simply necessary to eat, since asymptomatic hypoglycemia is much more dangerous than one that has obvious symptoms.

What to do if there is no glucometer “at hand”

The fact of the absence of a glucometer is unacceptable for an insulin-dependent diabetic. If you have suspicions that you have been overtaken by hypoglycemia, then it is better not to risk it and eat a small amount of glucose so that your blood sugar level rises by at least 2.4 mmol / l. Thus, you can protect yourself from severe hypoglycemia, the consequences of which are irreversible.

Measure your sugar as soon as possible. The likelihood that it will be increased or decreased is quite high. Try to bring sugar back to normal and no longer allow the absence of a glucometer, always keep it with you. If the dose of diabetes pills or an insulin shot (), with which you tried to stop the attack, is more than the required level, then you will have the hardest time.

Then, after taking glucose tablets, the blood sugar level may drop again. Therefore, 45 minutes after you have taken the means for hypoglycemia, you need to re-measure your blood sugar readings. Make sure everything is good. If the sugar content is low, you need to use another dose of tablets, then repeat the measurement again after 45 minutes. And so on until the sugar content in your blood returns to normal.

Attacks of hypoglycemia can be conditionally divided into two types:

• alimentary
• and fasting hypoglycemia.

Symptoms of the first may appear two to five hours after eating, but when prolonged fasting, for example, at night, this is more related to the second type.

The danger of alimentary hypoglycemia is not high enough, its attacks can be easily removed with food or drink and exposure to the hormones produced. Quite often in diabetics, due to the intake of excessively large amounts of insulin, fasting hypoglycemia occurs. Here its danger is very great due to the fact that there is a risk of brain damage. Among other things, if people suffer from diabetes for a long time, then typical signs of hypoglycemia may not be present. Its attacks can be prevented if you carefully follow a certain diet and your lifestyle is appropriate.

Symptoms of hypoglycemia

• Symptoms that are caused by the appearance of adrenaline in the blood: tingling in the hands, increased heart rate, increased sweating, anxiety, trembling, hunger or weakness. These signs are not inherent in people who constantly take beta-blockers, or those who have had diabetes for a long time.
• Symptoms of the so-called nocturnal hypoglycemia: increased sweating, signs of restlessness, the appearance of nightmares.
• Symptoms that appear when glucose is not supplied to your brain in adequate amounts, slowly onset hypoglycemia: consciousness is confused, amnesia and excitement appear, you are not oriented in space, coordination is impaired, you feel a change in personality, numbness, excitement, vision is impaired, headache, constant feeling of coldness .
• Symptoms that appear when the disease is sufficiently pronounced: frequent loss of consciousness, convulsions, paralysis of one side of the body is possible.

IMPORTANT! What can you do on your own:

• The patient will need to be constantly injected with a sugar-raising hormone - glucagon. Therefore, your relatives and friends should know how to do this if you suddenly become unconscious with hypoglycemia. Then an ambulance must be called. Also explain to them that food or liquid and insulin are contraindicated in this state.
• Get if you feel that the dose of insulin or one of the other medicines you are taking that causes hypoglycemia in susceptible people is too high. Your doctor can help you change your medication or adjust your dose to the correct level.
• During the operation, which is needed in the fight against a pancreatic tumor that causes hypoglycemia, in many cases it becomes necessary to remove the maximum part of the pancreas. Therefore, if it is possible to avoid surgery to destroy malignant cells, use chemotherapy.

Careful adherence to the diet and treatment is very important for people who have diabetes, they must do physical exercises, produce with a glucometer or other devices in their blood, they must always have some carbohydrate that is quickly absorbed (for example, sweets). in the form of lozenges, glucose tablets or fruit juice) in order to use them at the first appearance of a symptom.

If you have one of the signs of hypoglycemia, you just need to consult an endocrinologist, self-medication in these cases is not recommended. Only following all the above recommendations will make your life much better.

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