Reactive hypoglycemia in a child. How to protect your child from hypoglycemia. Factors contributing to the development of the disease
– a pathology consisting in a significant decrease in the concentration of glucose in the blood.
If the level of this substance does not reach 2.2 mmol/l, serious diseases can develop, leading to significant functional deterioration and even death.
Hypoglycemia is especially dangerous in children, due to the fact that in childhood there is active growth, development and formation of the body. What are the main causes of hypoglycemia in children, why is it dangerous and how is it treated?
Causes
Forecasts for the course of this disease largely depend on whether the true reasons for the decrease in glucose levels in the child are identified. In accordance with the reasons, the treatment necessary for this disease is developed.
Quite often, hypoglycemia is a symptom of problems in the child’s endocrine system, in particular, due to improper functioning of the adrenal glands.
After all, one of their main functions is the synthesis of special hormones that have a complex effect on the body, protecting it from an excessive drop in glucose levels. These steroid-type enzymes promote the production of glucose in the liver, inhibit the absorption of this substance by cells of peripheral tissues, and also reduce the activity of hormones involved in glycolysis.
The next reason for this phenomenon, especially in infants, may be heredity. Almost all children of diabetic women have. This is due to the peculiarities of the hormonal metabolism of the fetus and the influence of improper metabolism of the mother on the development of the child and the formation of his body.
Hypoglycemia in a child can also occur due to hyperinsulinism - excessive production of insulin. There is primary and secondary hyperinsulinism.
Primary develops due to lesions of the pancreas, for example, insulinoma - a benign formation, or carcinoma - pancreatic cancer. In practice, insulinoma is more common and responds quite well to surgical treatment.
Secondary hyperinsulinism is the result of the body's response to some stimulus. The main reasons for its occurrence are:
Hypoglycemia in a child without diabetes can also begin as a result of malnutrition. If a child's growing body, which actively consumes energy, does not receive sufficient amounts of necessary nutrients, glucose levels constantly drop.
After all, a child’s body does not know how to “save” energy the way an adult does.
Irregular eating and lack of routine can also cause low blood sugar in a child.
Finally, this disease can also be caused by heredity.
Hereditary hypoglycemia most often occurs in children under two years of age, and it mainly affects boys. Usually in this case we are talking about McCurry syndrome - an unpleasant feature of the enzyme that breaks down insulin - insulinase.
In children with this syndrome, insulinase breaks down insulin too slowly, resulting in a lack of glucose in the body. This disease can have very serious consequences, including coma. Often with this disease, the occurrence of various brain lesions is noted.
The most dangerous age for children with McCurry syndrome is between two and five years of age. Further, from the age of six, deep remission usually occurs, characterized by an almost complete absence of symptoms of hypoglycemia.
Pancreas
A decrease in sugar levels may also not be related to the pancreas. Disturbances in the child's gastrointestinal tract can also lead to hypoglycemia. The fact is that in the stomach and intestines, the polysaccharides contained in foods are exposed to enzymes, mainly amylase and maltase. These substances break down polysaccharides into glucose, which is absorbed through the walls of the digestive organs.
If the production of these enzymes is impaired, the body cannot process complex enzymes, and accordingly, glucose does not enter the body from food. This situation is typical for damage to the digestive system by certain poisons, and can also occur due to the development of a tumor.
Quite often, so-called “idiopathic” glycemia occurs, the causes of which doctors cannot determine.
Symptoms of the disease
Since hypoglycemia itself is very dangerous for the health and life of the child, and, in addition, can be caused by serious diseases, its early diagnosis is very important.
Regardless of the causes, hypoglycemia in children has the same symptoms.
Initially, the child appears irritable and restless. The patient's mood changes sharply and often, he becomes uncontrollable. At the same time, apathy, indifference to everything and lethargy appear from time to time.
With low sugar, the skin is whiter than usual. There is no blush, even after active games the blood does not rush to the face. Increased sweating appears, disturbances in sleep and wakefulness are possible - during the day the child wants to sleep, and at night he is prone to active noisy games.
Over time, signs of damage to the nervous system appear - trembling of the limbs, numbness, muscle spasms, as well as digestive disorders, expressed in loose stools and vomiting. With a serious drop in glucose levels, headache begins, body temperature is lower than 36.5 ° C. Next, arterial hypotension develops, and the pressure can drop quite significantly.
Often other symptoms appear, for example temporary, decreased alertness, tachycardia.
Very often there is severe hunger and chills. If your blood sugar levels drop seriously, you may experience dizziness and loss of consciousness.
If there are several similar symptoms, or one recurs over a long period of time, contacting a doctor should never be delayed. Only a qualified specialist, after receiving the results of appropriate tests, is able to determine the disease and prescribe its treatment.
Early contact with a medical facility will help avoid the negative effects of low sugar levels on the child’s brain and nervous system.
Treatment options
In case of severe hypoglycemia, accompanied by life-threatening symptoms for the child, treatment measures begin immediately, without waiting for test results.First of all, they practice taking a ten percent glucose solution orally. If hypoglycemia causes fainting, an intravenous infusion of a sterile glucose solution is performed.
Next, the practice is to prescribe antibiotic drugs, as well as drugs that support the mechanism weakened by the disease. After carrying out these measures, based on the examination, the probable cause of the decrease in blood sugar levels is identified, and subsequent treatment is prescribed depending on the causes of the disease.
In any case, therapy includes special therapy, which requires five to six small meals per day, as well as strict adherence to the prescribed regimen. At the same time, measures to treat the causes of hypoglycemia begin - drug treatment or surgery.
If the child is close to losing consciousness and there are other signs of hypoglycemic coma, you must independently give him a spoonful of sugar dissolved in a glass of boiled water.
Video on the topic
In this cartoon you will find answers to questions about what hypoglycemia is and what to do if it occurs:
If you contact a doctor early and prescribe the right treatment, long-term remission can occur. If the underlying cause of the disease is identified and treated, the child often does not suffer from more dangerous low blood sugar levels, especially if he follows dietary recommendations.
Information that a child has been diagnosed with diabetes is often discouraging and instills fear, especially when, in addition to the awareness of the seriousness of the disease, worries about possible attacks of hypoglycemia are added. As a rule, the diagnosis of diabetes has a greater psychological impact on the parents than on the child, because in addition to the difficult task of raising their child, they now need to bear the responsibility for treating their diabetes - a responsibility that, at first glance, seems completely overwhelming. First of all, you need to understand that you are far from the only parent facing the problem of childhood diabetes. Moreover, diabetes does not have to control or ruin your child's life. With proper care, monitoring, following recommendations and treatment of diabetes, the child has every chance to live a long and happy life.
The possibility of hypoglycemia developing in a child is not a reason for additional worries. Infrequent episodes of mild hypoglycemia are part of living with diabetes; they do not increase the risk of developing long-term complications. Even with the most careful control of diabetes, you are unlikely to be able to avoid hypoglycemia, because many factors lead to its development. However, armed with the necessary knowledge, you can minimize the risk of developing hypoglycemia and prepare for any eventuality.
Symptoms of hypoglycemia in children
Hypoglycemia (often simply "hypo") is a term used to describe a condition in which blood sugar levels are too low. This condition can occur for a number of reasons. Although episodes of hypoglycemia are easy to treat, the symptoms of hypoglycemia are often quite unpleasant, especially for a child. Moreover, hypoglycemia can be very dangerous, so it is important to be able to correctly recognize the symptoms and act as quickly as possible.
The first step to reducing your child's risk of hypoglycemia is knowing the most common symptoms. Unlike adults, young children are unable to recognize the symptoms of impending hypoglycemia, so it is important that you regularly check your child's blood sugar (glucose) levels to prevent levels from falling outside the target range. If a child has hypoglycemia, he or she may experience the following symptoms:
- Weakness
- Dizziness
- Excessive sweating
- Hunger
- Headache
- Disorientation in space
- Blurred vision
Because the severity of hypoglycemia can vary, you should check your blood sugar regularly after consuming sugar or taking glucose tablets.
Relieving hypoglycemia
When hypoglycemia occurs, it is very important to act quickly, but without panic. Don't make things worse—your child may already be frightened and unable to talk about their symptoms.
Depending on the severity of hypoglycemia, after its relief, the child may experience a feeling of mental apathy - be prepared to help and calm down. Unfortunately, episodes of hypoglycemia are an inevitable part of living with diabetes (and sometimes even occur in completely healthy people). That is why children should be able to provide themselves with the necessary help from a very young age. Your task is to teach your child to cope with hypoglycemia and remain calm.
It is important to remember that the main task when relieving hypoglycemia is to return the sugar level to the target range, that is, to raise it to a normal value. To do this you can:
- eat glucose tablets
- eat candy (such as lollipops)
- drink fruit juice
- drink a glass of sweet drink
- use a glucagon kit if available (only for the treatment of severe episodes of hypoglycemia)
- If the child loses consciousness, call an ambulance
15-20 minutes after completing the above steps, you should measure your blood sugar levels to ensure that the levels are back within the target range. Hypoglycemia can make you feel anxious and may take some time to recover from. Give your child the opportunity to sit down, take a few deep breaths and relax.
Methods for treating hypoglycemia in a child should be discussed with your doctor - each organism is unique, so you need to determine which method will be most effective in your case.
Nocturnal hypoglycemia
Controlling blood sugar levels is a 24/7 task. Even when a child is asleep, his body is working, and blood sugar levels can decrease due to many factors, including:
- evening meal (amount of carbohydrates eaten)
- intensity of physical activity
- insulin dose before bed
- type of insulin
Many parents are motivated by the above factors to choose to purchase a continuous glucose monitoring system for use in combination with an insulin pump, such as the MiniMed Paradigm Veo, to continuously monitor their child's diabetes. The CGM system eliminates the need to regularly measure blood sugar levels at night - as soon as the child's blood glucose level drops, the system will automatically notify about this.
Since the CGM system's sensor monitors indicators around the clock, you will have the opportunity to get complete information about how your child's blood sugar levels change during sleep. Such data can be very useful in assessing the effectiveness of diabetes treatment in a child.
The LMWH system can be used at any age, starting from 2 years. If you have any additional questions, please contact the Medtronic MiniMed team.
Full readiness
Watching a child experience hypoglycemia is not a pretty picture. However, we should not forget that it is impossible to completely avoid hypoglycemia, and its occurrence is not a reason to blame yourself. All people with diabetes experience episodes of hypoglycemia at one time or another. Armed with information on how to recognize the symptoms of hypoglycemia and how to stop it, now you just need to stock up on everything you need: glucose tablets, sugary drinks and foods with fast-acting carbohydrates in your home. Also make sure that the adults caring for your child and the child's caregivers/teachers know when and how to treat hypoglycemia and are equipped to do so.
Diabetes in children requires the development of a special support system for the child, regardless of his age. For example, it would be completely useful to notify the adults around the child about the existing disease. Educating your child's caregivers or teachers about diabetes will allow them to better understand how to recognize the symptoms of an impending episode of hypoglycemia/hyperglycemia and how to treat it.
Glucose plays a central role in energy metabolism. It not only participates in the formation of energy reserves in the form of glycogen, fat and protein, but also serves as a direct source of energy: the oxidation of 1 mole of glucose produces 38 moles of ATP. The brain uses primarily glucose, and almost all the oxygen it consumes is spent on its oxidation. The brain absorbs glucose using non-insulin-dependent transporters. Thus, the transport of glucose into brain cells is a carrier-mediated process of facilitated diffusion that depends only on the concentration of glucose in the blood. Deficiency of glucose transporters in the brain leads to seizures even when blood glucose levels are normal. The body has a complex system of glycemic regulation that prevents a decrease in blood glucose concentration that is dangerous for the brain.
Protection against hypoglycemia is organized by the autonomic nervous system and hormones, the combined action of which increases glucose production (by changing the activity of glycogenolysis and gluconeogenesis enzymes) and at the same time reduces its absorption by peripheral tissues. Therefore, hypoglycemia reflects a violation of complex interactions that ensure the maintenance of normoglycemia under conditions of satiety and fasting. Maintaining normoglycemia is especially important during the abrupt transition from intrauterine life (when glucose enters the fetus through the placenta) to independent existence.
The absence of symptoms does not yet guarantee normal glucose concentrations and their maintenance at a level that is safe for the brain. Hypoxemia and cerebral ischemia enhance the effect of hypoglycemia, contributing to the development of chronic central nervous system disorders. The lower limit of acceptable blood glucose levels for newborns with any diseases that impair brain metabolism remains unknown. Even without regard to the possible neurological, intellectual and mental consequences, many authors currently consider blood glucose levels in newborns below 50 mg% dangerous, insisting on the need for its correction. This is especially important in the first 2-3 hours of life, when the glucose level is normally minimal. Then it began to grow and after 12-24 hours reaches 50 mg% or more. After this period, glucose concentrations below 50 mg% in whole blood (in serum or plasma - 10-15% less) are considered hypoglycemia.
Meaning and consequences
The turnover of glucose is determined mainly by its participation in brain metabolism. In newborns and young children, the brain consumes almost all of the glucose produced by the liver. In addition, at any age, there is a correlation between the production of brain elements that break down into lactate, pyruvate, rhino- and keto acids, which support brain metabolism at the cost of its growth. The ability of the newborn brain to absorb and oxidize ketone bodies is almost 5 times higher than the corresponding ability of the mature brain. However, the production of ketone bodies by the liver during this period does not always satisfy the needs of the brain, especially under conditions of hyperinsulinemia, when not only the flow of glucose from the liver into the blood is suppressed, but also lipolysis and ketogenesis, so the brain is deprived of alternative energy sources. As a result, with hyperinsulinemia, oxygen consumption by the brain decreases, the breakdown of brain structures increases and the integrity of cell membranes is disrupted, which can lead to irreversible impairment of brain growth and function. Hypoxia enhances the damaging effects of hypoglycemia, and in conditions of even a slight decrease in blood glucose levels it itself causes brain damage.
The main consequences of severe and prolonged hypoglycemia are mental retardation and/or recurrent seizures. Some character changes are also possible. Frequent attacks of hypoglycemia in children under 6 months of age (the period of most rapid brain growth) in more than 50% of cases lead to irreversible changes in the central nervous system - smoothing of the gyri and atrophy of the cerebral cortex, impaired myelination of the white matter of the brain. If the only damaging factor is hypoglycemia (without hypoxia/ischemia), then there are no cerebral infarctions, and cerebellar functions are preserved. Severe consequences of hypoglycemia are most likely when the brain is deprived of alternative sources of nutrition (as is the case with hyperinsulinemia), with repeated or prolonged attacks of hypoglycemia, and with simultaneous brain hypoxia. It is impossible to accurately determine the degree or duration of hypoglycemia in children, which leads to permanent brain damage. Although less common, hypoglycemia can also cause irreversible damage to the nervous system in older children, inducing the release of neurotoxic mediators and neuronal death.
Regulation of glucose homeostasis
Newborns.
Normally, the fetus receives glucose from the mother (through the placenta). Therefore, the fetal glucose concentration usually matches (albeit slightly lower) its level in the mother's blood. Under stress conditions (for example, hypoxia), catecholamines are released, which, interacting with β-adrenergic receptors in the liver and adipose tissue of the fetus, mobilize glucose and free fatty acids. At the same time, catecholamines inhibit insulin secretion and stimulate glucagon secretion.
Acute cessation of maternal glucose supply at birth requires immediate mobilization of endogenous glucose. This is facilitated by the change:
secretion of hormones;
hormonal receptors;
activity of key enzymes.
Already in the first minutes and hours after birth, the concentration of glucagon increases 3-5 times. Insulin levels usually decrease and remain low for several days, during which time their normal response to glucose is absent. A sharp increase in the secretion of catecholamines is also characteristic. Adrenaline stimulates the secretion of growth hormone through a-receptors. These hormonal changes increase glycogenolysis and gluconeogenesis, activate lipolysis and promote ketogenesis. As a result, the plasma glucose concentration stabilizes after a short-term decrease, liver glycogen stores are rapidly depleted, and in the first few hours after birth, approximately 10% of the glucose produced is derived from alanine (the main amino acid precursor of gluconeogenesis). The release of glucagon and adrenaline also leads to an increase in the concentration of free fatty acids in the blood, which enhances the formation of ketone bodies. Thus, glucose is stored for the brain, and free fatty acids and ketones provide energy for the muscles. Oxidation of fatty acids in the liver, in addition, leads to the formation of acetyl-CoA and NADP necessary for gluconeogenesis.
Increased secretion of glucagon by the pancreas in the early postnatal period maintains normal blood glucose concentrations. At the same time, sharp adaptive changes occur in hormonal receptors and key enzymes involved in the formation of glucose. After birth, the activity of glycogen synthase quickly decreases, and phosphorylase increases sharply. The activity of phosphoenolpyruvate carboxykinase (which limits the rate of glucogenesis) also increases significantly, which is partly facilitated by the release of glucagon and a decrease in insulin secretion.
Therefore, hypoglycemia in newborns may be associated with impaired hormonal secretion, deficiency of substrates (liver glycogen, muscle amino acids and fatty acids) or deficiency of key enzymes of glucose metabolism.
Children older than 1-3 months.
At this age, as in adults, blood glucose levels immediately after meals are maintained by glycogenolysis, and in the interval between meals by gluconeogenesis. In a child weighing 10 kg, the liver contains 20-25 g of glycogen and this is enough to compensate for normal glucose consumption (4-6 mg/kg/min) for only 6-12 hours. Then activation of gluconeogenesis is necessary. Glycogenolysis and glucineogenesis require the preservation of metabolic pathways. Disorders of gluconeogenesis in a child may remain hidden while he is fed every 3-4 hours, and appear only when he stops feeding at night (usually at 3-6 months of age). The source of gluconeogenesis substrates is mainly muscle proteins. In young children, the relative muscle mass is significantly lower than in adults, and the glucose requirements per unit of body weight are much higher. Therefore, they are not able to withstand prolonged fasting. In addition, less alanine is produced in their muscles. As a result, the blood glucose level in a healthy child of this age drops after 24 hours of fasting, the insulin concentration is correspondingly less than 5-10 µU/ml, lipolysis and ketogenesis are activated, and ketone bodies appear in the urine.
The transition from glycogen synthesis during and immediately after meals to its breakdown, and later to gluconeogenesis, is regulated by hormones, among which insulin plays a central role. After a meal, the plasma insulin concentration reaches a maximum (50-100 µU/ml), which stimulates glycogen synthesis, enhances the absorption of glucose by peripheral tissues and inhibits the formation of glucose, preventing a sharp increase in its level in the blood. At the same time, genesis is enhanced and lipolysis and ketogenesis are inhibited. In this case, the insulin level drops to 5-10 µU/m71 and below, which, along with other hormonal changes, leads to the activation of gluconeogenesis. It should be emphasized that the insulin level in such conditions above 5 μU/mL against the background of glycemia below 40 mg% (2.2 mIU) indicates hyperinsulinism and a violation of the normal mechanisms of suppression of its secretion during fasting. The effects of insulin are counteracted by a number of hormones, the concentration of which in plasma increases as glucose levels fall. These so-called counter-regulatory hormones - glucagon, growth hormone, cortisol and adrenaline - increase blood glucose levels by activating glycogenolysis enzymes (glucagon, adrenaline), inducing gluconeogenesis enzymes (glucagon, cortisol) and inhibiting muscle glucose uptake (adrenaline, growth hormone, cortisol). ). In addition, cortisol enhances the mobilization of muscle amino acids used for gluconeogenesis, and adrenaline, cortisol, growth hormone and glucagon activate lipolysis, providing gluconeogenesis with glycerol and ketogenesis with free fatty acids. Adrenaline also inhibits insulin secretion and stimulates glucagon secretion.
Congenital or acquired deficiency of these hormones can cause hypoglycemia, leading to insufficient glucose production between meals or during fasting. With a simultaneous deficiency of several hormones (hypopituitarism), hypoglycemia is more severe or occurs more often during fasting than with a deficiency of any one of them. Hypoglycemia in children most often reflects a violation of the mechanisms of adaptation to starvation.
Clinical manifestations
Clinical manifestations of hypoglycemia can be divided into two groups.
One of them includes symptoms associated with activation of the autonomic nervous system and the secretion of adrenaline. They usually occur when blood glucose levels drop quickly.
The second group consists of symptoms caused by a deficiency of glucose in the brain, which usually appear with a slow decrease in glucose levels or with prolonged hypoglycemia.
In infants, the symptoms of hypoglycemia may be different and include cyanosis, apnea, hypothermia, decreased muscle tone, sluggish sucking, drowsiness and convulsions. Sometimes these symptoms are so minor that they do not attract attention. In the immediate postnatal period, hypoglycemia may be asymptomatic. With hyperinsulinemia, macrosomia in newborns is often observed; at older ages, due to chronic hypoglycemia, children eat a lot and become obese. Hypoglycemia in children may be accompanied by behavioral changes, impaired attention, gluttony or convulsions, which are sometimes mistaken for manifestations of epilepsy, intoxication, psychosis, hysteria or mental retardation. The glucose level in the blood of newborns must be determined for any deviations from the norm, and if it is below 50 mg%, it should be corrected immediately. Hypoglycemia can be the cause of the first seizures or sudden changes in mental status at any age.
Classification of hypoglycemia in neonatal and childhood
Hypoglycemia is classified according to known information about the regulation of glucose metabolism in children.
Neonatal transient hypoglycemia, small for gestational age and preterm infants. The overall incidence of hypoglycemia accompanied by clinical symptoms is 1-3:1000 newborns. Among newborns of certain risk groups, it increases many times. Preterm infants and small-for-gestational-age neonates are predisposed to hypoglycemia. The high incidence of hypoglycemia among them, as among other groups, is explained by insufficient reserves of hepatic glycogen, muscle protein and fat. In such children, transplacental transfer of nutrients either stopped early or was impaired. They may have an underdeveloped enzymatic system for gluconeogenesis.
In contrast to substrate or enzyme deficiencies, the hormonal system in most low-risk infants is normal at birth. Plasma concentrations of alanine, lactate, and pyruvate are elevated despite hypoglycemia, indicating a decrease in the rate of gluconeogenesis from these substrates. The introduction of alanine increases the secretion of glucagon, but has virtually no effect on blood glucose levels. On the first day, the concentration of acetoacetate and P-hydroxybutyrate in plasma in children with small body weight for gestational age is below normal. This suggests low lipid stores, insufficient mobilization of fatty acids or impaired ketogenesis, or possibly a combination of all these factors. The most likely role is insufficient lipid reserves, since feeding triglycerides to newborns increases the content of glucose, free fatty acids and ketone bodies in plasma. In addition, hypoxic neonates and some small-for-gestational-age infants may experience transient hyperinsulinemia, which reduces plasma glucose and free fatty acid levels.
Free fatty acids play a critical role in stimulating gluconeogenesis in newborns. Feeding with high-fat formula or breast milk prevents hypoglycemia, which usually develops in the first hours after birth. Therefore, children should begin to be fed no later than 4-6 hours after birth. In case of respiratory distress syndrome or in cases where the blood glucose level during feeding does not exceed 50 mg%, it is necessary to administer intravenous glucose at a rate of 4-8 mg/kg/min. Neonatal transient hypoglycemia usually persists for no more than 2-3 days.
Children whose mothers suffer from diabetes.
In such children, transit hyperinsulinemia is observed especially often. Transient diabetes mellitus during pregnancy (gestational diabetes) develops in 2% of women, and the incidence of insulin-dependent diabetes mellitus among pregnant women is approximately 1:1000. Children are born large with a full-blooded face and large reserves of glycogen, protein and fat.
Hypoglycemia in such cases is caused mainly by hyperinsulinemia and partly by reduced glucagon secretion. The pancreatic islets are hypertrophied and hyperplastic. The insulin response to glucose (unlike newborns from healthy mothers) is rapid and biphasic, as in adults. The release of glucagon immediately after birth is lower than normal, and glucagon secretion is less responsive to stimulation. Increased activity of the adrenergic system can lead to depletion of the adrenal medulla, which is manifested by decreased urinary excretion of adrenaline. Instead of the normally observed low levels of insulin and high levels of glucagon and catecholamines in plasma, these newborns have high levels of insulin and low concentrations of glucagon and epinephrine. This inhibits endogenous glucose production and contributes to the development of hypoglycemia.
Hyperinsulinemia with corresponding external manifestations (macrosomia) is also observed in hemolytic disease of the fetus. The cause of hyperinsulinemia in such cases remains unclear.
Women whose diabetes mellitus is well compensated during pregnancy and childbirth usually give birth to children of almost normal height and body weight; neonatal hypoglycemia and other complications (previously considered inevitable) are less likely in such cases. When administering glucose to children with hypoglycemia in these cases, it is important not to overdo it, since hyperglycemia, causing a sharp release of insulin, can provoke a new attack of hypoglycemia. If necessary, glucose is administered for a long time at a rate of 4-8 mg/kg/min, carefully selecting the dose for each child. It is extremely important to eliminate hyperglycemia in the mother during childbirth, since this, leading to hyperglycemia in the fetus, contributes to the development of hypoglycemia in the child when the supply of glucose from the mother suddenly stops. If hypoglycemia persists or occurs after 1 week of age, it is necessary to find out its causes.
Hypoglycemia in children is an acute condition in which the concentration of glucose in the blood falls below 4 mmol/l. It is formed in response to stress or other changes in the external environment. Hypoglycemia can occur in children suffering from type 1 diabetes, but in rare cases it is diagnosed in the second.
Most often it develops while taking sulfonylureas. Incorrect and unbalanced nutrition, physical and mental stress, and incorrect insulin dosage can also lead to this consequence. In the absence of medical care for a long time, hypoglycemia leads to loss of consciousness and coma.
Causes
Hypoglycemia is a fairly serious lesion that has serious reasons for its development.
Experts believe that its appearance can be influenced by:
- Genetic predisposition;
- Pathologies of pregnancy;
- Poor nutrition;
- Excessive physical activity;
- Diseases of the endocrine system;
- Emotional stress;
- Metabolic disorders;
- Incorrect doses of inulin;
- Nervous system lesions;
- Complications during childbirth.
Hypoglycemia can also develop in children who were born prematurely.
For this reason, such children require special monitoring in order to provide the correct medical assistance if necessary.
Symptoms
It is usually extremely difficult to diagnose hypoglycemia in a child. Most often, this condition can be diagnosed based on the results of a blood test. It is very important to monitor any changes in your child's behavior and eating habits. You need to be especially careful if you have impaired glucose tolerance. Hypoglycemia can be recognized by the following signs:
- Increased sweating;
- Feelings of anxiety and fear;
- Constant feeling of hunger;
- Nervousness and irritability;
- Unsteady gait, poor coordination;
- Drowsiness and dizziness;
- Fatigue and apathy;
- Confusion of speech.
Varieties
Hypoglycemia in children can be of two types: acidosis and leucine. They differ in the mechanism of development, symptoms and method of treatment. During hypoglycemia and acidosis, the child’s body produces acetone, or ketone bodies. Such a disorder in the body can be recognized by the appearance of a characteristic chemical odor from the mouth. Hypoglycemia during acidosis requires immediate attention, since ketone bodies are extremely dangerous for the functioning of the nervous system: they destroy it, causing serious complications.
Hypoglycemia during acidosis can be recognized by nausea and vomiting, dizziness, nervousness and lightheadedness.
To stop an attack, it is recommended to rinse the child’s stomach with mineral water, give him a spoonful of honey and plenty of sweet tea. After he gets better, it is necessary to monitor the condition of the body for some time.
Leucine coma develops against the background of intolerance to the leucine amino acid, which forms the basis of proteins. It usually develops after eating a large amount of protein foods. To prevent similar attacks in the future, fatty meats, dairy products, eggs, pasta, fish and nuts are excluded from the diet. It is very important to choose the right diet that will eliminate the risk of hypoglycemia in a sick child.
Treatment methods
If you notice the first signs of developing hypoglycemia in your child, you should immediately contact your doctor.
He will send you for an extensive diagnostic study, with the help of which he will make an accurate diagnosis.
This will allow you to choose a comprehensive and competent drug treatment. If an attack of hypoglycemia takes you by surprise, you need to do everything possible to raise your blood glucose levels. To do this, you can give the child sweet candy, tea, honey, or a piece of bread. It is very important that the child always has some kind of sweet in his pocket in case of such an attack.
If your child has hypoglycemia, blood glucose levels should be monitored regularly. They need to be carried out 2 times a day: in the morning on an empty stomach and after lunch. Also check the sugar concentration if the child complains of feeling unwell. If it is not possible to relieve the malaise at home, you must call an ambulance. Any delay can lead to the development of hypoglycemic coma, which always brings negative consequences for the body. A child with such a disease must regularly take immunomodulators and antibiotics.
Precautionary measures
In order to experience attacks of hypoglycemia as rarely as possible, the child should eat a healthy and balanced diet. It is best to contact a specialist who can create the most optimal diet. Also try to teach your child to adhere to the following recommendations:
- Eat regularly, do not skip a single meal;
- Inject insulin carefully and in a strictly prescribed dose;
- Always eat after taking insulin;
- Correlate the amount of food consumed and insulin administered;
- Consume as much fruit, chocolate and bread as possible, which will help understand your blood sugar levels;
- Increase the dose of insulin before physical activity;
- Always carry something sweet with you.
It is necessary to train all family members in first aid for hypoglycemia.
When this condition develops, it is very important to act quickly. This is the only way to prevent the development of serious complications in the future. It is recommended to give the child a special patch on his clothes so that if something happens, people can provide him with proper assistance. Despite the abundance of medications, it is impossible to completely cure hypoglycemia.
However, you can prevent its development if you follow all your doctor's recommendations. Be regularly examined by an endocrinologist, who will make the necessary changes in the treatment of hypoglycemia in a child.
The fasting blood glucose level in a practically healthy person ranges from 3.3 to 5.5 mmol/l when determined by the glucose oxidase method. During the day, glucose in the blood plasma can normally fluctuate from 2.8 to 8.8 mmol/l. Blood glucose levels below 2.7 mmol/l are commonly called hypoglycemia.
The main cause of the hypoglycemic symptom complex is hyperinsulinism.
Hyperinsulinism is a pathological condition of the body caused by an absolute or relative excess of insulin, causing a significant decrease in blood sugar; as a consequence, glucose deficiency and oxygen starvation of the brain occur, which leads primarily to disruption of higher nervous activity.
Absolute hyperinsulinism is a condition associated with pathology of the insular apparatus (primary organic hyperinsulinism). The most common causes of organic hyperinsulinism are insulinoma - a tumor of b-cells of the islets of Langerhans, secreting excess amounts of insulin (in adults and older children) and nesidioblastosis - hyperplasia of the pancreatic islets (in children of the first year of life). Another common cause of hyperinsulinism in young children is functional hyperinsulinism in newborns from mothers with diabetes.
Benign adenoma of the islets of Langerhans was first discovered in 1902 during an autopsy by Nicholls. In 1904, L.V. Sobolev described the “struma of the islets of Langerhans.” In 1924, Harris and the domestic surgeon V.A. Oppel independently described the symptom complex of hyperinsulinism. In the same year, G. F. Lang observed multiple adenomatosis of pancreatic islets. In Russia, a successful operation to remove insulinoma was performed in 1949 by A. D. Ochkin, and in 1950 by O. V. Nikolaev. An insulin-secreting tumor has been described in all age groups, from newborns to the elderly, but more often it affects people of working age - from 30 to 55 years. Among the total number of patients, children make up only about 5%. 90% of insulinomas are benign. About 80% of them are solitary. In 10% of cases, hypoglycemia is caused by multiple tumors, 5% of them are malignant, and 5% are nesidioblastosis (Antonov A.V. Clinical endocrinology, 1991).
The term nesidioblastosis was introduced by G. Laidlaw in 1938. Nesidioblastosis is a total transformation of the ductal epithelium of the pancreas into β-cells that produce insulin. In children of the first year of life, this is the most common cause of organic hyperinsulinism (only 30% of hyperinsulinism in children is caused by insulinoma, 70% by nesidioblastosis). This is a genetically determined disease.
The diagnosis is established only morphologically after excluding insulinoma. Clinically, it manifests itself as severe hypoglycemia that is difficult to correct, as a result of which, in the absence of a positive effect from conservative treatment, it will be necessary to resort to reducing the mass of pancreatic tissue. The generally accepted volume of surgery is 80 - 95% resection of the gland.
Insulinomas in children are extremely rare and are located either in the tail or in the body of the pancreas. Their diameter ranges from 0.5 to 3 cm. The small size of insulinomas creates difficulties for diagnosis (the information content of the ultrasound method is no more than 30%). To determine the location of insulinoma, selective angiography, CT and MRI, or scanning with an octreotide isotope (an analogue of somatostatin) are used. The most informative is angiography with selective blood sampling from the pancreatic veins (60 - 90%).
Insulinoma is manifested by a more or less sharp drop in blood sugar levels, which is caused by increased secretion of insulin into the blood. The radical method of treating insulinoma is surgery (insulinomectomy); the prognosis in most cases is favorable (88 - 90%) with timely surgical intervention.
Organic hyperinsulinism (insulinoma, nesidioblastosis) is the cause of severe pancreatic hypoglycemia with a drop in blood sugar to 1.67 mmol/l and lower (during an attack). These hypoglycemias are always non-ketotic (acetone in the urine is negative due to the suppression of lipolysis processes).
The most common in clinical practice is ketotic hypoglycemia (with acetonuria). Ketotic hypoglycemia is extrapancreatic and can be endocrine- and non-endocrine-dependent. They are accompanied by relative hyperinsulinism, that is, not associated with the pathology of the insular apparatus of the pancreas (secondary, functional, symptomatic hyperinsulinism). Relative hyperinsulinism is caused by an increase in the body's sensitivity to insulin normally secreted by b-cells of the pancreatic islets or a violation of the compensatory mechanisms involved in the regulation of carbohydrate metabolism and in the inactivation of insulin.
Endocrine-dependent ketotic hypoglycemia (without increasing the level of insulin in the blood) is detected with a deficiency of counter-insulin hormones in patients with hypofunction of the anterior pituitary gland (cerebral-pituitary nanism, isolated GH deficiency, hypopituitarism), the thyroid gland (hypothyroidism), and the adrenal cortex (Addison's disease).
Without an increase in insulin levels, extrapancreatic hypoglycemia can occur, which occurs with extrapancreatic tumors (chest, abdominal cavity, retroperitoneal, etc.), hypoglycemia accompanying diffuse liver diseases, chronic renal failure. In children of the first year of life, the cause of ketotic non-endocrine-dependent hypoglycemia (without hyperinsulinism) is congenital enzymopathies (glycogenosis).
In clinical practice, reactive hypoglycemia is often encountered - functional hyperinsulinism with vegetative-vascular dystonia. They are observed in obese individuals, in neurotic children of preschool age against the background of acetonemic vomiting due to disruption of the processes of gluconeogenesis, etc.
Hypoglycemia of an exogenous nature (caused by the administration of insulin, hypoglycemic agents, salicylates, sulfonamides and other drugs) is also common.
With functional hyperinsulinism, hypoglycemia is clinically less pronounced, blood sugar does not fall below 2.2 mmol/l.
Hypoglycemia can be detected by clinical signs; more often, low blood sugar levels are a laboratory finding. Detection of hypoglycemia in the early morning hours or on an empty stomach before breakfast in capillary blood at least 2-3 times is considered reliable (in the absence of clear clinical data). The indication for examination in a hospital is a classic clinical picture of hyperinsulinism or three times confirmed morning hypoglycemia (without clinical manifestations) below age indicators (decrease in fasting glycemia for newborns - less than 1.67 mmol/l, 2 months - 18 years - less than 2.2 mmol/l , over 18 years old - less than 2.7 mmol/l).
Whipple's triad is pathognomonic for hypoglycemic disease:
- the occurrence of attacks of hypoglycemia after prolonged fasting or physical activity;
- a decrease in blood sugar during an attack below 1.7 mmol/l in children under 2 years of age, below 2.2 mmol/l - over 2 years of age;
- relief of a hypoglycemic attack by intravenous administration of glucose or oral administration of glucose solutions.
Most symptoms of hypoglycemia are caused by insufficient glucose supply to the central nervous system. When glucose levels decrease to hypoglycemia, mechanisms aimed at glycogenolysis, gluconeogenesis, mobilization of free fatty acids, and ketogenesis are activated. These processes involve mainly 4 hormones: norepinephrine, glucagon, cortisol, growth hormone. The first group of symptoms is associated with an increase in the content of catecholamines in the blood, which causes weakness, tremors, tachycardia, sweating, anxiety, hunger, and pale skin. Symptoms from the central nervous system (symptoms of neuroglycopenia) include headache, double vision, behavioral disturbances (mental agitation, aggressiveness, negativism), followed by loss of consciousness, convulsions, and coma with hyporeflexia, shallow breathing, and muscle atony. Deep coma leads to death or irreversible damage to the central nervous system. Frequent attacks of hypoglycemia lead to personality changes in adults and decreased 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.
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, brain tumor - in 15%, vegetative-vascular dystonia - in 11%, diencephalic syndrome - in 9%, psychosis, neurasthenia - 3% (Dizon A. M., 1999).
The period of acute hypoglycemia is the result of a breakdown of counterinsular factors and the adaptive properties of the central nervous system.
Most often, an attack develops in the early morning hours, which is associated with a long night break in eating. Typically, patients cannot “wake up” due to various kinds of disorders of consciousness. There may be lethargy and apathy in the morning. The epileptiform seizures observed in these patients differ from the true ones by their longer duration, chorioform convulsive twitching, hyperkinesis, and abundant neurovegetative symptoms. Recognition of the disease requires a thorough examination of the anamnesis and careful observation of patients. This is especially important for diagnosing organic hyperinsulinism as a cause of hypoglycemia in children.
In children of the first year of life, it is difficult to clinically detect hypoglycemia, since the symptoms are vague and atypical. This may be cyanosis, pallor of the skin, decreased muscle tone, respiratory arrest (apnea), tremors, convulsions, “rolling” of the eyeballs (nystagmus), anxiety. In the congenital form (nesidioblastosis), there is a large body weight (large fetus), swelling, and a round face.
In children of preschool and school age with organic hyperinsulinism, benign insulinoma is more often registered. These children are characterized by morning incapacity, difficulty waking up in the morning, impaired concentration, pronounced feelings of hunger, cravings for sweets, negativism, and palpitations. Hyperinsulinism leads to increased appetite and obesity. The younger the child, the greater the tendency for low blood sugar in response to longer intervals between meals.
Among the laboratory parameters for suspected organic hyperinsulinism (insulinoma or nesidioblastosis), a special place is occupied by the study of immunoreactive insulin (IRI). But, as practice has shown, proven insulinoma does not always have elevated values. IRI is usually assessed simultaneously with the glycemic level. An important index is the ratio of insulin to glucose - IRI mked/ml/venous glucose mmol/l. In healthy people and against the background of hypoglycemia without hyperinsulinism, this index is less than 5.4.
Among the functional tests used to diagnose organic hyperinsulinism, the most common is the fasting test.
The test is based on the development of hypoglycemia in people with hyperfunction of the pancreatic insular apparatus when the intake of carbohydrates from food is stopped. During the test, the patient is allowed to drink only water or tea without sugar. The younger the child and the more frequent the attacks of hypoglycemia, the shorter the test.
Test duration:
children under 3 years old - 8 hours;
2 - 10 years - 12-16 hours;
10 - 18 years - 20 hours;
over 18 years old - 72 hours.
(recommendations from the Department of Pediatric Endocrinology, RMAPO, Moscow).
For children 2 years of age and older, the last meal should be the night before; For children under 2 years of age, the test begins in the early morning hours.
In a healthy person, overnight or longer fasting moderately reduces the level of glycemia and, characteristically, reduces the level of insulin in the blood. In the presence of a tumor that constantly produces excess amounts of insulin, under starvation conditions, the prerequisites are created for the development of hypoglycemia, since there is no glucose supply from the intestine, and hepatic glycogenolysis is blocked by tumor insulin.
Before starting the test, the glucose content in the blood plasma is determined. Next, glycemia in capillary blood (with a glucometer) is examined in children under 2 years of age once an hour, in children aged 2 years and older - once every 2 hours. When blood sugar decreases to 3.3 mmol/l or less, the test intervals are reduced by 2-3 times. The threshold of acceptable glycemia, at which fasting is stopped and research is carried out, is 1.7 mmol/l in a child under 2 years old, 2.2 mmol/l in children over 2 years old. After threshold hypoglycemia is registered with a glucometer, the blood serum is examined for the content of IRI and counter-insulin hormones, blood glucose is examined using a biochemical method (since after the glucose level is reduced to 3.3 mmol/l and below, the glucometer gives an inaccurate result), and the level of blood lipids is examined.
An attack of hypoglycemia is stopped by administering 40% glucose intravenously; immediately after the administration of glucose and 3 hours after the end of the test, urine is examined for the content of ketone bodies.
Interpretation of sample results
- If acetone is not detected in the urine, then hypoglycemia is caused by hyperinsulinism (increased insulin suppresses the breakdown of fatty acids - lipolysis). The presence of acetonuria indicates the intensive formation of ketone bodies from fatty acids coming from fat depots. With hypoglycemia not associated with hyperproduction of insulin, lipolysis is turned on as an energy source, which leads to the formation of ketone bodies and the formation of positive acetone in the urine.
- With hyperinsulinism, the content of lipids in the blood is not changed or reduced; with ketotic hypoglycemia, the lipid level is increased.
- A decrease in the level of counter-insulin hormones is observed in endocrine-dependent ketotic hypoglycemia; with organic hyperinsulinism the indicators are not changed.
- The IRI/venous glycemia index in healthy children and against the background of hypoglycemia without hyperinsulinism was less than 5.4, whereas with organic hyperinsulinism this figure increases significantly.
If hyperinsulinism is confirmed as the cause of hypoglycemia, further examination and treatment in a specialized endocrinology department is necessary.
In all cases, surgical treatment is indicated with insulin. For nesidioblastosis, therapy can be conservative or radical. The drug diazoxide (proglycem, zaroxolin) has currently received the greatest recognition. The hyperglycemic effect of this non-diuretic benzothiazide is based on inhibition of insulin secretion from tumor cells. The recommended dose for children is 10 - 12 mg per kg of body weight per day in 2 - 3 doses. In the absence of pronounced positive dynamics, surgical treatment is indicated - subtotal or total resection of the pancreas (with possible transition to diabetes mellitus).
S. A. Stolyarova, T. N. Dubovaya, R. G. Garipov
S. A. Malmberg, Doctor of Medical Sciences
V. I. Shirokova, Candidate of Medical Sciences
Children's Clinical Hospital No. 38, FU "Medbioextrem" under the Ministry of Health of the Russian Federation, Moscow
Patient Zakhar Z., 3 months., was admitted to the Department of Psychoneurology of Children's Clinical Hospital No. 38 of the FU Medbioextrem in Moscow on November 1, 2002 with a referral diagnosis of epilepsy.
A child with a moderately burdened perinatal history. This was the mother’s first pregnancy and proceeded with toxicosis in the first half and anemia. Delivery at 40 weeks, large fetus (birth weight 4050 g, length 54 cm). Apgar score: 8/9 points. From the neonatal period to 2 months. tremor of the chin was periodically noted; from the age of 2 months, paroxysmal states appeared in the form of stopping gaze, decreased motor activity, twitching of the right half of the face, right hand (attacks of focal convulsions) - for several seconds 3-4 times a day. He was treated as an outpatient by a neurologist and received anticonvulsant therapy without a significant positive effect. On the eve of hospitalization, choreiform twitching appeared in the morning against the background of impaired consciousness. Hospitalized in the department of psychoneurology with a referral diagnosis of epilepsy.
Upon admission, the child's condition was moderate. In the somatic status - the skin has manifestations of atopic dermatitis, the pharynx is clean, there are no wheezes in the lungs, heart sounds are sonorous, tachycardia up to 140 - 160 beats. per minute The abdomen is soft, liver +2 cm, spleen +1 cm. Urination is not impaired. In neurological status - lethargic, fixed gaze, poor head support. CN - intact, muscle tone is reduced, more in the arms, symmetrical. Tendon reflexes are low, D = C, unconditioned reflexes are low - according to age. Weight - 7 kg, height - 61 cm (excess weight is noted against the background of the average age growth rate).
In the hospital, a biochemical fasting blood test revealed for the first time a decrease in blood sugar to 1.6 mmol/l in the absence of ketone bodies in the urine.
Results of laboratory and instrumental examination:
- Oculist - no pathology was detected in the fundus.
- ECG - heart rate 140, sinus rhythm, vertical position of the EOS.
- Allergist - atopic dermatitis, common form, mild course.
- Ultrasound of the abdominal organs - the pancreas is not clearly visualized in its typical location. Ultrasound of the adrenal glands - no changes. Ultrasound of the kidneys - reactive changes in the walls of the jaw, Fraley syndrome on the left, pyelectasis on the left cannot be excluded. Spleen - moderate splenomegaly.
- General blood test - Hb 129 g/l, er - 5.08 million, l - 8.7 thousand, ESR - 3 mm/hour.
- General urine analysis - protein, sugar, acetone - neg., L - 2 - 3 in the field of vision, er - 0 - 1 in the field of view.
- Blood biochemistry (upon admission) - total protein. - 60.5 g/l, ALT - 20.2 g/l, AST - 66.9 g/l, bilirubin total. - 3.61 µmol/l, glucose - 1.6 mmol/l, creatinine - 36.8 µmol/l, urea - 1.88 mmol/l, total cholesterol. - 4.44 mmol/l, iron total. - 31.92 µmol/l, potassium - 4.9 mmol/l, sodium - 140.0 mmol/l.
Dynamic monitoring of glucose levels revealed persistent hypoglycemia in capillary and venous blood. On an empty stomach and 2 hours after feeding with breast milk during the day, glycemia ranged from 0.96 to 3.2 mmol/l. Clinically, hypoglycemia was manifested by increased appetite, lethargy, tachycardia, episodes of “rolling” of the right eyeball, and generalized epileptiform convulsions. During the interictal period, the state of health is satisfactory. Hypoglycemic conditions were relieved by oral glucose intake, as well as intravenous administration of 10% glucose.
For diagnostic purposes, to confirm hyperinsulinism, the child underwent a fasting test: the last night feeding at 6 a.m., before feeding, glycemia was 2.8 mmol/l, 3.5 hours after feeding, the glucometer showed a decrease in glycemia to 1.5 mmol/l (below the acceptable threshold). Against the background of hypoglycemia, blood serum was taken for hormonal studies (IRI, c-peptide, cortisol, STH). Venous blood was collected for biochemical testing of glucose and lipid levels. After relief of hypoglycemia with intravenous injection of glucose, a three-hour portion of urine was collected for the content of ketone bodies.
Sample results: no acetonuria. The level of counter-insulin hormones is not reduced (cortisol - 363.6 when the norm is 171 - 536 nmol/l, STH - 2.2 when the norm is 2.6 - 24.9 µU/ml). C-peptide - 0.53 at a normal level of 0.36 - 1.7 pmol/l. IRI - 19.64 with normal - 2.6 - 24.9 mmkE/ml. Venous glucose - 0.96 mmol/l. Blood lipid levels are at the lower limit of normal (triglycerides - 0.4 mmol/l, total cholesterol - 2.91 mmol/l, high-density lipoprotein cholesterol - 1.06 mmol/l, low-density lipoprotein cholesterol - 1.06 mmol/l - 1.67 mmol/l. IRI/glucose index (19.64 /0.96) was 20.45, with the norm being less than 5.4.
Data from the anamnesis, dynamic observation, and clinical and laboratory examination allowed us to make a diagnosis: non-ketotic hypoglycemia. Hyperinsulinism. Nesidioblastosis?
To clarify the genesis of the disease and treatment tactics, the child was transferred to the endocrinology department of the Russian Children's Clinical Hospital in Moscow, where insulinoma was ruled out in the boy. The diagnosis of nesidioblastosis was confirmed. A trial of conservative treatment with proglycem at a dose of 10 mg per kg of body weight was prescribed. There was a tendency towards normalization of carbohydrate metabolism indicators. Further follow-up is planned to adjust treatment tactics.
The considered clinical case dictates the need to study the parameters of carbohydrate metabolism in all young children with convulsive syndrome, due to the erasure of the clinical symptoms of hypoglycemia in infants and young children, in order to exclude diagnostic errors.