neonatal hypoglycemia
Introduction
Introduction to neonatal hypoglycemia Neonatal glucose metabolism is prone to hypoglycemia, neonatal hypoglycemia (neonatalhypoglycemia) refers to lower blood glucose levels than normal infants of the same age, hypoglycemia is easy to cause brain damage, leading to hypoglycemia encephalopathy, causing irreversible central Nervous system damage, so active prevention. basic knowledge Sickness ratio: 5% Susceptible people: children Mode of infection: non-infectious Complications: shock
Cause
Causes of neonatal hypoglycemia
Insufficient storage of glycogen and fat (20%):
The storage of fetal liver glycogen mainly occurs in the last 4 to 8 weeks of gestational age. The differentiation of fetal brown fat begins from 26 to 30 weeks of gestational age and continues until 2 to 3 weeks after birth. On the one hand, low birth weight infants include Premature infants and small for gestational age (SGA) children have less glycogen and fat storage. On the other hand, the energy required for postnatal metabolism is relatively high, which is prone to hypoglycemia. Data confirm the glycogen synthesis of SGA children. The enzyme activity is low, so the glycogen synthesis is less, and the amount of sugar required for metabolism of some important organs and tissues is relatively large. The brain requirement and utilization rate of SGA children are significantly increased, and the ratio of brain weight to liver weight is The normal 3:1 increase to 7:1, the brain uses twice as much sugar as the liver.
Too much sugar (15%):
Newborns with serious diseases such as asphyxia, RDS, scleredema, etc. are prone to hypoglycemia, these stress states are often accompanied by increased metabolic rate, hypoxia, decreased body temperature and intake, hypoxia can promote hypoglycemia, lack Oxygen has different effects on glucose metabolism in term infants and premature infants. Hypoglycemia occurs in neonates with Apgar scores of 1 to 3, which are term infants because of the rapid use of glucose in full-term children under stress. The ability of children to use glucose is poor. Domestic scholars have confirmed that the incidence of hypoglycemia in neonates with cold or hypothermia is high, which is related to the ability of hypothermia to meet the need of thermoregulation. The rate of glucose metabolism increases during neonatal infection. The average glucose consumption rate is about 3 times higher than that of normal children. The neonatal gluconeogenesis enzyme activity is low, while the infection aggravates the deficiency of gluconeogenesis. The amino acid is not easily converted into glucose. The neonatal gluconeogenesis depends mainly on Brown fat releases glycerin. When the infection is severe, the brown fat is depleted, the source of gluconeogenesis is interrupted, and the blood sugar is lowered. In addition, the patient's intake is reduced during infection. Weakened digestion and absorption, can easily lead to hypoglycemia.
Hyperinsulinemia (10%):
Temporary hyperinsulinemia is common in infants with diabetes in their mothers. Because of high blood sugar in pregnant women, fetal blood sugar is also increased. Hypoglycemia occurs after the birth of glucose from the mother. The fetus of severe hemolytic disease is destroyed by red blood cells. The release of glutathione in plasma can counteract the action of insulin, and can also cause hyperinsulinemia in the islet hyperplasia of fetal islet B cells. The blood transfusion of children with polycythemia after treatment with citrate glucose as maintenance fluid Hypoglycemia may occur, due to higher glucose concentration in the maintenance solution, stimulate insulin secretion, insulin levels are still high in a short time after transfusion, and persistent hyperinsulinemia includes islet cell adenoma, islet cell proliferation and Beckwith syndrome (Characteristics are large, large tongue, umbilical hernia and some malformations with hyperinsulinemia).
Endocrine and metabolic diseases (10%):
In neonates with galactosemia, the amount of galactose in the blood increases, the glucose decreases accordingly, the glycogen decomposition of children with glycogen storage disease decreases, the amount of glucose in the blood is low, and the newborn with leucine allergy, breast milk The leucine in the body can increase insulin secretion, and other congenital dysfunction such as the pituitary gland, thyroid or adrenal gland can also affect blood sugar levels.
Genetic metabolic disease (2%):
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Pathogenesis
1. Characteristics of glucose metabolism
Glucose is the most important nutrient in fetal energy metabolism. It can be easily dispersed from the mother through the placenta like other monosaccharides (if sugar, galactose), while disaccharides such as sucrose and lactose cannot be used by the fetus through the placental barrier. In recent years, a large number of studies on the transfer process of nutrients between maternal and fetal have confirmed that the other nutrients other than the supply of monosaccharides by the mother's placenta are extremely limited, including only the right amount of amino acids, certain peptides and unsaturated fatty acids, so glucose is It has important significance.
Under normal circumstances, the supply of glucose through the placenta is extremely constant, enough to meet all of its energy needs. The fetal blood glucose level is about 60% to 75% of the blood glucose of pregnant women. The mechanism by which the fetus is taken from the mother and reaches this ratio is still unclear. The difference in blood glucose concentration measured from the umbilical artery and umbilical vein was about 3 to 10 mg/dl (the average difference was 5 to 6 mg/dl).
Both the placenta and the fetus can store a certain amount of glycogen to regulate the blood sugar of the fetus. At 20 to 24 weeks of gestation, the liver has less glycogen synthase, and the glycogen storage is not enough to regulate the blood sugar concentration, while the glycogen in the placenta More synthetase, at this time mainly relies on the placenta to release glycogen to regulate blood sugar, and then the placental glycogen gradually decreases until the last few weeks of full-term pregnancy, due to the rapid increase of glycogen synthase in various organs, hepatic glycogen storage The amount is significantly increased, reaching 80-100mg/gm (wet tissue) at full term, which is twice the normal adult value; likewise, the amount of myocardial glycogen can be up to 10 times the adult value; the amount of glycogen in skeletal muscle can be as high as adults The value of the lung is 3 to 5 times; the amount of glycogen in the lung reaches the highest peak in the second trimester, and has decreased to the adult value in the full term, and the glycogen storage is often exhausted in the fetus with malnutrition and intrauterine growth retardation. This shortage can also be seen in diabetic mothers with pregnancy-induced hypertension syndrome and in fetuses with inadequate placental vascular function.
In addition, the stored glycogen is obviously consumed after birth. Under normal circumstances, the fetus has ample supply of glycogen until full-term delivery; it is under stress for a few hours before delivery and the oxygen supply is low. Glycogen provides enough energy for childbirth; and because of the low energy intake of the baby during the period after birth, it is more necessary to supply energy from glycogen, because the use of glycogen is rapidly increasing during this period. The amount of hepatic glycogen decreased to 10% of the initial value, and reached the adult value 2 to 3 weeks after birth; while the decline of glycogen in skeletal muscle and myocardium was slower, but the amount of myocardial glycogen could be rapid if there was asphyxia. reduce.
At the same time that the amount of glycogen decreased rapidly after birth, the respiratory quotient (CO2 production/oxygen consumption) of unmarried infants can be reduced from 1.0 at birth to 0.75 at 2nd to 3rd days, and only rises after establishing sufficient feeding. To 0.8 to 0.85; indicating that energy metabolism at this time depends first on fat rather than glucose, and the glycogen reserve has been quickly depleted, so it is necessary to maintain the necessary reserves as an indispensable glucose in brain and red blood cell metabolism. source.
The blood glucose concentration is determined by the balance between the amount of glucose entering the blood and the tissue utilization rate. The former depends on the amount of glycogen stored, the amount of glucose that enters the blood after feeding, the decomposition of glycogen, and the adrenaline, 17-hydroxyl The gluconeogenesis induced by steroids; the latter depends on the degree of muscle activity, the total amount of metabolically active tissue, oxygen utilization and consumption, pH and insulin secretion, as mentioned above, the first day of birth Insulin secretion is extremely dull, so any abnormality in the above balance can lead to hypoglycemia and hyperglycemia.
There is a large amount of research data indicating the effect of hormones on glucose metabolism. The fetus begins to secrete insulin at the 14th to 20th week, which does not affect the blood sugar stability in the body; but it can affect the concentration of arginine in the blood, suggesting that it is in the fetal period. Insulin secretion can act on protein metabolism; insulin in pregnant women has no effect on the fetus because it cannot pass through the placenta; the function of insulin secretion from pancreatic islet B cells is not sufficient until the delivery of the fetus, and the effect of regulating blood glucose concentration is extremely slow, in the low gestational age It is more pronounced; it often needs to regulate glucose metabolism after feeding after birth. In addition to insulin, hormones that regulate fetal glucose metabolism are pituitary hormones and adrenocortical hormones. These hormones are glycogen accumulation. It is necessary that when the above two hormones are deficient, the activity of diphosphate uridine glucose transferase (which eventually forms glucose as glycogen) and the liver glycogen content are significantly reduced; and when glycogen is cleaved into glucose, glucagon may be required. The involvement of adrenaline.
2. Hypoglycemia causes brain damage
The only source of energy for the central nervous system is sugar. Energy needs to be extremely large, but glycogen storage is minimal. For example, hypoglycemia will inevitably affect the metabolic activity of brain cells. Because the central nervous system is sensitive to hypoglycemia. The order of injury and the corresponding symptoms appear differently, firstly the cerebral cortex and cerebellum, followed by the cortex, hypoglycemia leading to central nervous system damage, neonatal hypoglycemia encephalopathy, hypoglycemia affecting the brain's energy supply system, Na - K-ATPase function is firstly affected, causing potassium outflow in cells, extracellular sodium enters cells, causing swelling, degeneration and necrosis of cells. It is also reported that hypoglycemia can reduce brain blood flow perfusion and cause brain tissue damage. It is a wide range of neuronal degeneration and necrosis in the cerebral cortex; glial cell hyperplasia, the most severe occipital and basal ganglia, sometimes can damage the lower central part of the hypothalamus, movement, sensory center and autonomic nerve, such as the hypothalamus, basal ganglia, etc. In severe cases, symptoms of cerebral dysfunction in the brain can occur.
Recent studies have shown that newborn animals and human newborns are immature in transporting glucose from the blood to the brain; animal experiments have also shown that the rate of glucose infiltration into the brain from newborn blood is only one-fifth that of adult rats; Compared with adult animals, the immature brain has a low utilization rate of glucose. Under normal oxygen supply, the energy consumption of the brain is about 1/10 of that of the adult brain 7 days after birth. In addition, under hypoxia, The increase in anaerobic glycolysis may not be significant.
The damage of hypoglycemia to brain tissue depends on the severity and duration of hypoglycemia, which is similar to hypoxic brain damage.
Prevention
Neonatal hypoglycemia prevention
Prevention is more important than treatment. Regular monitoring of blood sugar in neonates prone to hypoglycemia, early supplementation of syrup or intravenous rehydration, to ensure adequate calories, and to keep warm.
1. Open the milk early: start feeding within half an hour after birth, feed once every 2 hours within 24 hours, and feed at night.
2. Supplemental glucose: For those who may have hypoglycemia, add glucose at 1 hour after birth. Feed (or nasal feeding) glucose solution 10% glucose solution, 5 ~ 10ml / kg each time, once a hour, for 3 to 4 times.
3. Infusion of glucose: weight less than 2kg, suffocation, difficulty in recovery or long time, should be given as soon as 5% to 10% glucose solution 2 ~ 6ml / kg. At this point, the infusion glucose concentration should not be too high to prevent hyperosmolarity and hyperglycemia.
4. Blood glucose monitoring method
(1) Paper method: Clinically, the paper method and the micro blood glucose meter are used to measure the blood sugar and venous blood of the heel capillary blood. Early scheduled monitoring at 1, 3, 6, 9, 12, and 24 hours after birth or admission to the hospital at the time and regular monitoring.
(2) Scoring method: Tianjin Children's Hospital proposed the application of electronic computer to discriminate the risk factors (day age, body weight, gestational age, infection and hypoxia) of internal hypoglycemia, and establish the discriminant formula Y=-0.18295×1-0.90382 ×2-0.0519×3 5.6895×4 5.10437×5, the newborns were scored by this formula, and those with Y-33.80474 were judged to be high-risk children with hypoglycemia. Precautions should be taken to reduce the incidence of blood glucose. From 310 newborns, the accuracy is high, and the false positive rate is 2.42%, which can be used.
5. For neonates prone to hypoglycemia, blood glucose should be monitored at 3, 6, 9, 12, and 24 hours after birth, and hypoglycemia or hyperglycemia should be discovered sooner or later.
6. For low birth weight infants and high-risk children who can eat after birth, they should be fed sooner or later, and start feeding syrup or milk 2 to 4 hours after birth. Those who cannot be fed by oral or nasal feeding should be infused with glucose to maintain nutrition.
7. Parenteral nutrition, pay attention to supplement amino acids and fat milk when supplementing calories, glucose should not be too high.
8. For high-risk children and premature infants, the glucose infusion rate should be controlled, not 8mg/(kg·min), and blood glucose monitoring should be done. If the increase is high, the input concentration and speed should be reduced immediately, and the infusion should not be stopped to prevent reactive hypoglycemia. .
9. The concentration of glucose used in neonatal asphyxia resuscitation is 5%.
Complication
Neonatal hypoglycemia complications Complications
Hypoglycemic shock; low blood glucose duration or low blood sugar levels can cause neonatal hypoglycemia encephalopathy, causing irreversible damage to the nervous system.
Symptom
Symptoms of neonatal hypoglycemia Common symptoms Hypoglycemia, tremor, tremor, sclerosis, stun, drowsiness, asphyxia, erythrocytosis, hypoglycemia
Neonatal hypoglycemia often lacks symptoms. At the same blood glucose level, the symptoms of children are mild and the difference is very large. The cause is still unknown. Asymptomatic hypoglycemia is 10 to 20 times more than symptomatic hypoglycemia.
1. Symptoms and signs: Symptoms and signs are often non-specific, often appear within hours to 1 week after birth, or are concealed due to other diseases, mainly due to poor response, paroxysmal cyanosis, tremor, Eyeballs do not rotate properly, convulsions, apnea, lethargy, do not eat, etc., some appear sweaty, pale and low response.
2. Hypoglycemia encephalopathy: Hypoglycemia can cause damage to the central nervous system, and in severe cases, symptoms of cerebral dysfunction can occur.
Neonatal hypoglycemia often lacks symptoms. Therefore, the clinical should be vigilant against this disease, mainly based on medical history, clinical manifestations, blood glucose diagnosis, corresponding medical history and clinical non-specific symptoms and signs of performance, that is, timely laboratory testing, Early diagnosis, such as the newborn's blood glucose level is lower than the normal blood sugar level of the same age, can be diagnosed.
Examine
Neonatal hypoglycemia check
1. Blood glucose measurement: Blood glucose measurement is the main method for the diagnosis and early detection of this disease. Blood glucose should be monitored within 1 hour after birth. For those who may have hypoglycemia (such as SGA), it should be 3, 6, 12, 24h after birth. Monitor blood sugar.
The whole blood sample was tested. The blood glucose in the first 3 days of full-term infants was lower than 1.7mmol/L (30mg/dl), and the blood glucose was lower than 2.2mmol/L (40mg/dl) after 3 days. The smaller than the gestational age and premature infants were born. The blood glucose was lower than 1.1mmol/L (20mg/dl) within 3 days, and the blood glucose was lower than 2.2mmol/L after 3 days, which is called neonatal hypoglycemia. However, it is considered that the diagnostic threshold of hypoglycemia is low, in fact, blood sugar. Hypoglycemia symptoms often occur at 1.7-2.2 mmol/L, and the symptoms disappear after glucose administration. The low-glycemic standard for low birth weight infants is derived from the mean value of blood glucose minus 2 standard deviations, but it does not represent normal values because of this value. It is derived from an abnormal group. Some data suggest that the average blood glucose level within 3 days after birth is 2.8-3.4 mmol/L (50-60 mg/dl). It is also reported that premature infants who are breast-fed after birth are within 36 hours. The average blood glucose level was 3 mmol/L (54 mg/: dl).
2. Other examinations: If the diagnosis is not clear, check the blood type, hemoglobin, blood calcium, blood magnesium, urine routine and ketone body as needed, and do cerebrospinal fluid examination if necessary. And X-ray chest X-ray, electrocardiogram, echocardiography, EEG, brain CT and other examinations.
Diagnosis
Diagnosis and diagnosis of neonatal hypoglycemia
Diagnostic criteria
1. History: There is often a history of maternal diabetes, a history of pregnancy-induced hypertension syndrome, infants with polycythemia, ABO or Rh blood group incompatibility, perinatal asphyxia, infection, scleredema, RDS, etc., especially premature infants, SGA children and early milking, insufficient intake and so on.
2. Clinical manifestations: The above clinical manifestations, especially those who have improved the symptoms of glucose infusion, or those with neurological symptoms without explanation, should be considered in this case.
3. Blood glucose measurement and other tests: Blood glucose measurement is the main means of diagnosis and early detection of this disease. Blood glucose should be monitored within 1 hour after birth. For those who may have hypoglycemia (such as SGA), after the birth, 3, 6, 12 24h monitoring blood glucose, the diagnosis is not clear, according to the need to check blood type, hemoglobin, blood calcium, blood magnesium, urine routine and ketone body, if necessary, check cerebrospinal fluid, chest X-ray, ECG or echocardiography.
Differential diagnosis
1. Hypocalcemia: Hypocalcemia is one of the important causes of neonatal seizures. Hypoglycemia and hypocalcemia can occur in the early neonatal period, but hypocalcemia occurs in any type of newborn, total blood calcium. The amount is less than 1.75-2mmol/L (7.0-8.0mg/dl) or free calcium is less than 0.9mmol/L (3.5mg/dl), and hypoglycemia is more common in low birth weight infants, with corresponding medical history and clinical manifestations. Laboratory tests for hypoglycemia can aid in diagnosis.
2. Hypoxic-ischemic encephalopathy: occurs mostly in premature infants and asphyxia, and intracranial ultrasound is helpful for diagnosis.
