Low blood sugar in children

Introduction to low blood sugar in children Hypoglycemia means that the blood glucose concentration caused by different causes is lower than normal. The blood glucose level drops to the lowest point 1 to 2 hours after birth, and then gradually rises. The normal plasma glucose should be >2.8mmol/L (>50mg/dl) at 72h, and the neonatal blood glucose< 2.2mmol/L (<40mg/dl) is hypoglycemia, and fasting blood glucose <2.8mmol/L (<50mg/dl) in older infants and children is hypoglycemia. When a baby's blood glucose <2.24mmol/L (<40mg/dl) is born, active treatment should begin. Hypoglycemia can cause irreversible damage to the brain and affect brain function. basic knowledge Sickness ratio: 0.05% Susceptible people: children Mode of infection: non-infectious Complications: coma

Causes of hypoglycemia in children

(1) Causes of the disease

1. Plasma glucose and brain development in newborns

Glucose is an important part of human energy metabolism. Glucose is almost all substances in the brain's oxygen metabolism. 60% to 80% of the glucose produced by the adult liver is used by the brain, while 80% to 100% of the newborn is used by the brain. When the weight of the newborn is 3.5kg, the brain weight is about 450g. Each 100g brain tissue uses 4-5mg of glucose per minute, about 20mg/min. Infants and children produce glucose 5-8mg/kg per minute, and the liver produces glucose. 5 to 7 mg/kg per minute, so the glucose produced by the liver is all used by the brain. The production of endogenous glucose is completely positively correlated with the growth of human and brain with weight less than 40 kg, due to the fastest brain development in the first year after birth. The utilization rate of glucose is the largest. The degree of brain damage is also the most serious in the first year after birth. The lower the age of the baby, the greater the harm of hypoglycemia, and the damage to brain development and brain function. Importantly, when the neonatal hypoglycemia is limited due to the storage of hepatic glycogen, in order to maintain the energy of the brain cells, the components of the brain tissue such as structural proteins, myelin and the like are cleaved, and amino acids and ketone bodies are generated as brains. Xie's substance, and thus the brain tissue is damaged. Although the ability of the neonatal brain to use ketone bodies is high, the amount of ketone bodies produced is extremely limited. In particular, high insulin and hypoglycemia inhibit the decomposition of glycogen and fat, and lack gluconeogenesis. The matrix, thus the brain damage is more serious, the brain cell membrane function completely destroys the permanent brain damage, the gray matter is atrophied, the white matter myelin is reduced, and the cerebral cortex is also atrophied.

2. Etiology classification and characteristics

(1) Insufficient glycogen matrix in neonatal period: The main reason for the high incidence of hypoglycemia in premature infants and low birth weight infants is that due to insufficient reserve of hepatic glycogen and muscle glycogen, body fat becomes the main substance for supplying energy due to infants. Small, especially premature infants and immature children or impaired nutritional supply of the placenta and inadequate development of the enzyme system required for gluconeogenesis are the main causes of hypoglycemia.

Most newborns have normal hormone levels, decreased insulin after birth, increased glucagon, more normal hGH and cortisol, immature children and especially twins, severe respiratory distress syndrome, infants with pregnancy toxemia mothers In addition to the reduction of hepatic glycogen storage, the storage of fat is also small, the free fatty acids and ketone bodies produced by fat mobilization are low, so it is prone to hypoglycemia. In recent years, early attention has been paid to the early administration of fatty acids to newborns and low birth weight infants. Fatty foods and other raw sugar precursors such as pyruvic acid, lactic acid, etc. promote neonatal gluconeogenesis, which can cause gluconeogenesis to increase blood sugar and prevent hypoglycemia caused by fasting; and prevent blood sugar from inhibiting gluconeogenesis The reaction of the substance now advocates feeding the newborn as soon as possible, and feeding begins 4 to 6 hours after birth. The intravenous glucose input that cannot be fed is input in the amount of 5 to 10 mg/kg per minute. If necessary, the cortisone can be given 5 mg/kg per day. 3 times or 3 times of prednisone or puppus, 1 time / d, monitor and maintain blood sugar concentration, normal babies 3 to 5 days after birth can naturally maintain normal blood sugar.

(2) neonatal hyperinsulinemia: infants with diabetes may have temporary hyperinsulinemia, the incidence of gestational diabetes is about 2%, such infants are large, bloody, glycogen, protein and The fat is sufficient, the mother of the diabetic mother has hyperinsulinemia after birth and the secretion of glucagon is reduced, which is different from normal newborns. At the same time, due to sympathetic excitation, the adrenaline of the adrenal medulla is depleted, so the endogenous glucose is The amount of production is reduced, so that hypoglycemia is apt to occur.

Neonatal erythrocytosis at birth is also hyperinsulinemia, the body is also larger, the mechanism of increased insulin secretion is not fully understood, may be related to hemolysis to produce increased glutathione, because glutathione makes insulin The rupture of the disulfide bond is associated with an excessively high rate of compensatory secretion.

Treatment of diabetic mothers and infants requires intravenous glucose, but hyperglycemia can cause insulin to release, leading to hypoglycemic rebound. Therefore, infusion of glucose needs to be maintained until hyperinsulinemia disappears, insulin falls to normal levels, and blood glucose remains at 6.7-8.3. Mmmol / L, the input glucose rate of 6 ~ 10mg / kg per minute, can prevent hypoglycemia rebound, but the amount of sugar in each child should be adjusted according to individual needs, monitoring blood sugar to avoid hyperglycemia, insulin secretion Increase, in addition to the normal control of blood glucose in pregnant mothers during pregnancy, can reduce the incidence of complications in birth.

(3) Hyperinsulinemia in infants and children: Hyperinsulinemia can occur at any age, and neonatal hyperinsulinemia may not be caused by a diabetic mother. When clinically, infants develop symptoms of hypoglycemia, such as seizures. When the weakness is weak, nervous or convulsive, blood should be taken and blood glucose and insulin should be measured at the same time. When the blood glucose is <2.2mmol/L (40mg/dl), the blood insulin concentration should be <5U/ml instead of >10U/ml. In children with hyperinsulinemia, blood insulin is often >10U/ml in hypoglycemia. If hyperglycemia occurs twice or more and insulin levels are high, it can be diagnosed as hyperinsulinemia. Some infants or children are small and do not eat. That is, hypoglycemia symptoms, in general, hypoglycemia and high blood insulin > 10U / ml can be diagnosed as hyperinsulinemia.

1Beckwith-Weidemann syndrome: About 50% of patients with this syndrome have hyperinsulinemia, characterized by large body and internal organs, large tongue, microcephaly and umbilical hernia, cracks on the lateral or earlobe of the ear, brain development, high insulin Hemorrhage is due to diffuse islet cell proliferation or islet cell proliferation and hypoglycemia, and there is a tendency for hepatoblastoma, teratoma, and the like to occur.

2 leucine-sensitive hypoglycemia: patients diagnosed with leucine-sensitive hypoglycemia in the past due to the advancement of modern diagnostic techniques, most diagnosed as beta cell hyperplasia, adenoma or islet cell proliferation, the diagnosis of this disease Reduced, this patient may be a variant of islet cell dysmature syndrome, such as leucine-sensitive functional hyperinsulinemia when the disease continues to occur after 5 to 7 years of hypoglycemia. It is characterized by the induction of hypoglycemia after consumption of protein foods and leucine, and hypoglycemia may be controlled by administration of low leucine food or diazoxide (chloroxylazine) or corticosteroids.

(4) Lack of endocrine hormones: Cortisol and growth hormone are hormones that mainly antagonize insulin, and are important factors for maintaining blood sugar stability in the body. Simple growth hormone deficiency or total pituitary dysfunction, and/or ACTH-glucocorticoid Insufficient, the zymogenic enzyme activity and matrix production are reduced, gluconeogenesis disorder, hypoglycemia on fasting, Edison disease and adrenal leukoencephalopathy, etc. may also have hypoglycemia, in addition, people with adrenal medullary deficiency When blood sugar is lowered, the secretion of adrenaline does not increase, and the decomposition of glycogen is not promoted, so that blood sugar cannot rise, often stays at a low level, and glucagon deficiency also causes hypoglycemia.

(5) Substrate limited:

1 ketosis hypoglycemia: the most common cause of hypoglycemia in children, more than 18 months to 5 years old, until the natural remission of 8 to 9 years old, history of eating less or dinner did not eat, the next morning sleep is difficult Arousal or convulsions, ketonemia and ketonuria in hypoglycemia, blood insulin is a normal lower limit of 5 ~ 10U / ml, the basic state after overnight is a significant reduction in alanine in the blood, input alanine (250mg / After kg), blood glucose can be increased, while blood lactic acid and pyruvic acid are basically normal. Fructose and glycerol are input, and blood sugar is also increased. All of the above indicate that the gluconeogenesis matrix is lacking. After eating, blood sugar is normal, and other metabolisms and hormones are normal.

Alanine is the only raw sugar amino acid. Other amino acids are metabolized to form alanine. The ketosis hypoglycemia is actually hypoalaninemia, which may involve some processes of complex protein metabolism, mainly muscle protein catabolism. Alanine is a matrix of gluconeogenesis. It may have a history of temporary hypoglycemia in the neonatal period. It is prone to ketosis hypoglycemia when muscle tissue is reduced. Natural remission after 8 to 9 years of age may increase due to muscle mass development. Some people think that it is the result of adrenaline secretion disorder, but patients with bilateral adrenal gland replacement with glucocorticoids rarely have hypoglycemia, and the cause of ketotic hypoglycemia is also controversial.

The treatment of ketosis hypoglycemia is to give a high-protein and high-glucose diet. The urine ketone body should be tested frequently during the period of hypoglycemia. If the appearance of urinary ketone body (), hypoglycemia will occur after a few hours, giving sugary drinks, not Tolerate intravenous glucose or take cortisol for a course of treatment.

2 Maple urinary tract: a lack of branched-chain -keto acid oxidative decarboxylase in branched-chain amino acid metabolism, branched-chain amino acids with leucine, isoleucine, and proline increased in blood The urinary ketone acid is increased, the urine has a similar taste of maple syrup, the child has vomiting, apathy, lethargy, high muscle tension and convulsions, and the blood leucine is increased before hypoglycemia occurs.

(6) Glycogen storage disease: Type I, type III, type IV and type O of glycogen storage disease have hypoglycemia, of which type I glucose-6-phosphatase deficiency is more common.

Type 1I: a glucose-6-phosphatase deficiency, an enzyme required for the final step of glycogenolysis and gluconeogenesis to produce glucose. This enzyme deficiency reduces glucose production and has severe hypoglycemia and glucose metabolism from early childhood. Disorder, high lactateemia, increased blood ketone body, hyperuricemia, acidosis and liver enlargement, improvement of treatment improves prognosis, in order to avoid the occurrence of hypoglycemia, continuous feeding of nighttime gastric tube after early diagnosis, or Eat day and night 3 ~ 4h, food ingredients should be 60% ~ 70% sugar and starch, less fructose and galactose, protein 12% ~ 15%, fat 15% ~ 25%, night nose feeding to the total daily food 1/3 of the calories are continuously instilled continuously at 8 to 12 hours (commodity formulas abroad), which can improve metabolic disorders and prevent hypoglycemia. Recently, it has been reported that the treatment with raw corn starch paste 4-6 times/d can improve symptoms. The ultimate treatment is liver transplantation.

Type 2III: Depletion of debranching enzymes causes the glycogen to decompose to produce glucose, but the gluconeogenesis pathway is normal, so the symptoms of hypoglycemia are mild.

Type 3IV: It is a deficiency of liver phosphorylase, which can occur in any step of activating phosphorylase in glycogenolysis. Occasionally, hypoglycemia occurs and liver function is impaired.

Type 4O: Deficient in glycogen synthase, reduced hepatic glycogen synthesis, prone to fasting hypoglycemia and ketosis, and high blood sugar and urine sugar after meals. It is treated with multiple high-protein diets to improve metabolism and growth.

(7) gluconeogenesis: gluconeogenesis disorders can cause hypoglycemia, common are:

1 fructose-1,6-bisphosphate aldolase deficiency: this enzyme deficiency blocks the conversion of gluconeogenesis precursor to fructose-1,6-diphosphate, affecting gluconeogenesis, can cause fasting hypoglycemia, liver glycogen reserve Hypoglycemia may occur in normal times, clinically similar to glycogen storage disease type I, treatment should prohibit the consumption of fructose-containing food, and give low protein (12%), normal fat (30%) and high sugar foods, can be maintained Normal growth and development, if necessary, can also be used to inject food into the stomach at night to prevent hypoglycemia.

2 pyruvate carboxylase deficiency: This enzyme is an important enzyme that acts on the conversion of pyruvate to acetoacetate. The disease is characterized by subacute encephalomyelopathy. The blood lactic acid and pyruvic acid cannot be used, and the blood is increased. There is mild hypoglycemia on an empty stomach.

Phosphoenol pyruvate carboxkinase (PEPCK) deficiency: This enzyme is a rate-limiting enzyme for gluconeogenesis. In the absence of severe fasting hypoglycemia, it can occur at 24 h after birth, the total enzyme of PEPCK in the liver. The activity is normal, but the enzyme is lacking in the cytosolic part of the mitochondria, and it is believed that this part of the enzyme activity plays an important role in gluconeogenesis. In the liver and kidney and other tissues, the PCPCK deficiency is extensively fat infiltrated. Due to the increase of acetyl CoA, the fat is synthesized. The clinical features are severe hypoglycemia. The blood lactic acid and pyruvic acid are normal. There is mild metabolic acidosis. Only the liver biopsy activity is determined. The clinical diagnosis is rarely made. The treatment is Multiple high-sugar diets, avoiding long-term fasting, help glycogen synthesis, and have a certain compensatory function due to the normal decomposition of glycogen.

(8) Defects in fatty acid oxidation: It is also important to provide a matrix for blood sugar in the oxidation of fatty acids. For example, congenital or drug-induced fatty acid metabolism defects can cause fasting hypoglycemia. Congenital deficiency of various fat metabolism enzymes can cause botulism. Deficiency of alkali or fatty acid metabolism, the fat metabolism is stagnant in the middle, can not produce ketone body, hypoglycemia, liver, muscle tension and convulsions.

Plasma carnitine is also reduced in the absence of acetyl CoA dehydrogenase in long-chain, medium- or short-chain fatty acid metabolism, clinical manifestations similar to Reye's syndrome, severe hypoglycemic coma, cardiac and respiratory depression, metabolic acidosis without Ketoacidosis, low muscle tone, convulsions and corrosive odor can be used as a clue to diagnosis. The survival of children depends on the severity of enzyme deficiency. The incidence of fatty acid metabolism disorder is about 1:15000, which is waiting for the development of molecular diagnostic methods. In order to make newborn screening possible.

(9) Lack of other enzymes and other reasons:

1 galactosemia: galactose-1-phosphate uridine transferase deficiency, children with hypoglycemia after lactation, galactose-1-phosphate can not be used and accumulated in the body, resulting in symptoms of poisoning, such as diarrhea, liver Large, jaundice, acidosis, and can cause kidney and brain damage, and inhibit liver release of glucose.

2 fructose intolerance: a defect of fructose 1-phosphate aldolase or fructose 1,6-bisphosphatase, the baby only eats breast milk, no symptoms, but appears when adding non-staple food.

3 other liver damage: severe and chronic liver disease (damage more than 80% of the liver) can affect glucose metabolism, acute viral hepatitis, cirrhosis, liver poisoning and other liver and gallbladder diseases can cause hypoglycemia, young children suffering from Reye syndrome, with encephalopathy associated with hepatic steatosis, may also have hypoglycemia.

4 drug poisoning:

A. Acute alcoholism, rarely seen in children, mostly due to increased glucose utilization, and interfere with gluconeogenesis, can cause hypoglycemia.

B. Salicylate poisoning, salicylate increases insulin secretion and causes hypoglycemia.

5 small intestinal absorption reduction: such as chronic diarrhea, malabsorption syndrome, edema of kidney disease, etc., can cause intestinal absorption function disorder, fasting no more than 24h can appear hypoglycemic episodes.

6 difficult to control hypoglycemia episodes: 2 cases of infants have difficulty in controlling symptoms of hypoglycemia, hypoglycemia, cerebrospinal fluid glucose reduction, lactate reduction and normal blood glucose, normal cerebrospinal fluid glucose and blood glucose ratio of 0.8, the patient is 0.2 ~0.4, red blood cell examination found that red blood cell glucose transporter is defective, suggesting that cerebrospinal fluid glucose transport may have the same defects, to be further proved.

(two) pathogenesis

1. The mechanism of matrix, energy and hormones for blood sugar stabilization The fetal blood glucose concentration is similar to that of mother's blood glucose (equivalent to 80% of maternal blood), but the mechanism of blood glucose regulation is not exactly the same. Fetal blood glucose is not dependent on hormone regulation. The mother's blood sugar is drastically reduced or increased, and no changes in fetal hormone secretion occur. However, when the fetus is in the long-term hyperglycemic environment, the insulin secretion is increased to lower the blood sugar. On the contrary, when the mother is chronically starved and the blood sugar is low, the fetal insulin is Decreased secretion and increased glucagon, the slow response of the fetus to blood glucose changes is related to the maturation of cAMP and enzyme system produced by hormone receptors in the fetus, and some of the delayed response can be extended to the neonatal period.

After the birth of the fetus leaves the mother, the glucose in the maternal blood is stopped. After birth, the newborn's own internal glucose needs to be mobilized. This change requires changes in hormones, hormone receptors and key enzyme activities, and a matrix with appropriate synthetic glucose. The glucagon secretion increased sharply by up to 5 times within a few hours after birth, and insulin decreased to the normal basal value range. At this time, catecholamine stimulated glucagon and GH secretion, inhibiting insulin secretion, and the three were related to each other. The blood hormones in normal newborns are high adrenaline, high glucagon and high growth hormone and low insulin, and cortisol is increased. These hormones decompose glycogen, produce glucose, and fat decomposes to produce fatty acids and ketone bodies. And glycerol, muscle protein breakdown produces alanine, provides a gluconeogenesis matrix to produce glucose, hormone changes can make the blood sugar temporarily rise after the temporary decline in blood sugar, but the blood sugar is stable, but the newborn liver glycogen reserves are limited, accounting for newborns 10% of the glucose produced within a few hours after birth, is quickly depleted, due to alanine glucose production by gluconeogenesis Ketones lipolysis brain may also be utilized.

Hormonal changes after birth are caused by changes in postnatal hormone receptors, which decrease insulin receptors and increase the amount of glucagon receptors, while producing key enzymes such as phosphorylase and phosphoenolpyruvate. The activity of phosphoenol pyruvate carboxykinase (PEPCK) is greatly increased after birth, and the latter is the rate-limiting enzyme of gluconeogenesis. These changes are the key to the rapid return of neonatal blood glucose to normal.

The regulation of blood glucose in infants over 1 year old is the same as that in adults. The liver glycogen storage capacity of infants weighing 10kg is 20-25g, which can supply 4-6mg/kg glucose per minute for 6~12h. Hepatic gluconeogenesis is also active, but the sugar is different. The raw matrix is mainly derived from the alanine produced by muscle protein. The muscle tissue of infants and children is relatively less than that of adults. Therefore, the ability to produce glucose by gluconeogenesis is limited. Especially when there is amino acid metabolism disorder, only fat metabolism is produced. Ketone body, so it is very prone to ketosis.

(1) Regulation of hormones on blood glucose stability:

1 Insulin: Insulin is the only hormone in the body that lowers blood sugar. Its role is to stimulate the utilization of glucose and inhibit the production of glucose. Inhibition of hepatic glycogen decomposition and stimulation of hepatic glycogen production is the main mechanism for lowering blood glucose, while increasing peripheral tissue. Mainly muscle intake of glucose to synthesize muscle glycogen; promote fat tissue synthesis of fat, increased utilization of glucose, lower blood sugar; insulin also promotes protein synthesis, insulin has strong gluconeogenesis, lipolysis and ketone body production Inhibition.

2 hormones that raise blood sugar: There are several hormones that promote the rise of blood sugar, prevent hypoglycemia in the fasting state and maintain the stability of blood sugar. These hormones are glucagon, adrenaline, growth hormone and cortisol, collectively known as Regulate hormones.

A. Glucagon is most sensitive to hypoglycemia, inhibits liver and tissue uptake of glucose and promotes glycogen decomposition, increases gluconeogenesis and inhibits glucose glycolysis to increase blood sugar.

B. Adrenaline, catecholamine stimulates glycogen decomposition, lipolysis and increases gluconeogenesis. Adrenalin also stimulates the secretion of glucagon and GH, and enhances the glycogenic effect.

C. The effect of growth hormone on glucose metabolism is more complicated. When hGH is secreted, it has insulin-like effect, lowering blood sugar, and prolonged secretion increases hyperglycemia and promotes gluconeogenesis.

D. Cortisol increases gluconeogenesis, lipolysis produces ketone bodies and protein breakdown, provides a substrate for gluconeogenesis, cortisol can reduce the sensitivity of insulin, and directly antagonize insulin.

(2) The mechanism of action of comprehensive anti-regulatory hormones to raise blood sugar:

1 Activate glycogen and gluconeogenesis enzymes are glucagon and epinephrine.

2 increase the gluconeogenesis enzyme activity is glucagon and cortisol.

3 inhibit the peripheral glucose uptake of epinephrine, growth hormone and cortisol.

4 The amino acid that decomposes the muscle protein to provide gluconeogenesis is cortisol.

5 All counter-regulating hormones activate activated fat to produce glycerol for gluconeogenesis and fatty acid production of ketone bodies.

The interaction between the effects of anti-regulatory hormones is different. Adrenalin and glucagon act quickly. The metabolism of glucose between adrenalin and glucagon has a compensatory effect. Growth hormone and cortex. There is also a partial compensatory effect between alcohols. A variety of counter-regulatory hormones such as hypoglycemia occur when the whole pituitary function is reduced, and the time of occurrence is also early. Metabolic steps and key enzymes for glycogenolysis and gluconeogenesis .

2. Regulation of glucose metabolism by the liver The liver affects the activity of the sugar-metabolizing enzyme under the action of hormones. The hepatic glucose-metabolizing enzyme affects the blood sugar level by the activation or inhibition of the above hormones, but the defects of the primary liver metabolic enzymes such as sugar Some enzyme deficiency in the original storage disease is also responsible for hypoglycemia.

Pediatric hypoglycemia prevention

As a child's parents, not only should you be careful during the day, you can't relax your vigilance at night. Because the child's blood sugar is likely to drop significantly at night, even to a level that has never been seen before.

When you have a hypoglycemia episode, first lie quietly, don't mess, and quickly prepare a cup of warm sugar (about 250 ml) to drink. It is better to have glucose in your home. After drinking the sugar water, and then lying still for about 10 minutes, the symptoms are alleviated.

How to deal with hypoglycemia coma

1 If possible, blood sugar should be measured;

2 patients are still conscious, can drink sugar water;

3 The patient has been comatose, and relatives and friends can apply honey on the patient's oral mucosa and gums;

4 Get in touch with your doctor at the same time.

Pediatric hypoglycemia complications Complications

Often complicated by tachycardia, visual impairment, language and thinking disorders, confusion, reduced intelligence, even loss of consciousness and coma, convulsions and permanent nerve damage; small babies can show apnea, difficulty breathing.

Symptoms of hypoglycemia in children Common symptoms: fatigue, nausea, irritability, tremor, tachycardia, lethargy, stunned expression, indifferent coma, thermoregulatory disorder

There are two main clinical manifestations of hypoglycemia. One is the consequences of autonomic nervous system excitability and release of adrenaline, which often occurs with a sharp drop in blood glucose. The other is due to the decrease in brain glucose utilization, often accompanied by slow blood sugar. Decreased or prolonged hypoglycemia occurs, mainly in older children, due to autonomic nervous excitatory release of adrenaline caused by excessive sweating, tremors, tachycardia, irritability, nervousness, irritability, hunger , nausea and vomiting, symptoms caused by decreased brain glucose utilization have headache, visual impairment, fatigue, apathy or depression, restlessness, irritability, language and thinking disorder, mental inability to concentrate, confusion, intelligent reduction, personality behavior change, stiffness Wood is dull, lethargic, and even loss of consciousness and coma and permanent nerve damage.

The symptoms of hypoglycemia in newborns and small infants are not obvious, often ignored, and non-specific. Hypoglycemia in small infants can be manifested as cyanosis, apnea, difficulty breathing, refusal to eat milk, sudden transient myoclonus, Debilitation, lethargy and convulsions, body temperature is often abnormal.

Pediatric hypoglycemia check

1. Urine sugar hypoglycemia children, urine sugar positive after meals, may be due to non-glucose reduction substances, should further determine its nature.

2. Urine ketone body often provides some clues for diagnosis, but conventional methods can only detect acetoacetic acid and acetone. 70% of -hydroxybutyric acid is not detected. It should be noted that when -hydroxybutyric acid rises significantly, The increase in acetoacetate may not be obvious, and it is not erroneously judged to be mild ketosis.

3. Plasma glucose, ketone bodies, lactic acid and pyruvic acid in the fasting state, systematic determination of these substances, help to understand the relationship between hormones and sugar balance related substrates, if necessary, simultaneously determine cortisol and growth hormone.

Electrocardiogram examination can have tachycardia, low voltage; chest X-ray examination is generally no abnormal findings.

Diagnosis and diagnosis of hypoglycemia in children

diagnosis

The cause of hypoglycemia in children is extremely complicated. In addition to detailed medical history, the age, time, and condition of hypoglycemia are very important. Birth newborns, especially premature infants, immature or less than gestational age Hypoglycemia in the last week is mostly neonatal transient hypoglycemia, neonatal neonatal diabetic patients, polycythemia or small head, large viscera and large tongue hypoglycemia should consider hyperinsulinemia, when there is liver Considering the lack of various enzymes, the cause of hypoglycemia is found from clinical detailed medical history and detailed physical examination, and necessary examinations are performed. Table 2 lists the abnormal characteristics of major hypoglycemia, which is helpful for diagnosis and differential diagnosis. Blood samples should be taken in time to measure blood sugar, insulin, ketone body, alanine, lactic acid, blood lipids and uric acid. As a differential diagnosis, if necessary, observe the glucagon stimulation test and observe blood glucose after input of alanine and glycerol. The response, clinical acute hypoglycemia episodes can prolong the fasting time to 24-32h induced hypoglycemia, with endocrine gland dysfunction Examination of endocrine gland function can be diagnosed in time, and finally the accurate diagnosis of enzyme deficiency must be carried out to determine the enzyme activity.

Differential diagnosis

This disease is caused by a variety of reasons, it should be promptly in-depth examination, especially to identify islet -cell tumor or hyperplasia of functional and unexplained hypoglycemia, generally the latter are mostly light, only obvious sympathetic The nerve or adrenaline is a syndrome; while the former has a brain nerve and obvious mental symptoms, which can be combined with laboratory and other special examinations to confirm the diagnosis.

1. For episodes (especially on an empty stomach) with psycho-neural abnormalities, convulsions, behavioral abnormalities, disturbances of consciousness or coma, especially for diabetic patients treated with insulin or oral hypoglycemic agents, the possibility of hypoglycemia should be considered. Timely check blood sugar, it is worth noting that some patients with hypoglycemia have normal blood sugar at the time of treatment, and there is no symptoms of hypoglycemia, often only manifested as sequelae of chronic hypoglycemia, such as hemiplegia, dementia, epilepsy, mental disorders, children's IQ is significantly lower, etc. As a result, clinical diagnosis is often misdiagnosed as mental illness, epilepsy or other organic encephalopathy (such as encephalitis). Therefore, it should be differentiated from other diseases of the central nervous system organic disease, such as encephalitis, multiple sclerosis, cerebrovascular accident. , epilepsy, diabetic ketoacidosis coma, diabetes non-ketotic hyperosmolar coma, psychosis, drug poisoning, etc.

2. Fasting, hypoglycemia with sympathetic excitation as the main manifestation after hours of physical activity or after physical activity, should be associated with sympathetic excitation, such as hyperthyroidism, pheochromocytoma, autonomic dysfunction, Diagnostic differentiation of diabetic autonomic neuropathy, menopausal syndrome, etc.

3. Hypoglycemia after alcoholism should be differentiated from alcoholism. Ethanol can not only cause hypoglycemia, but also cause ketosis. Sometimes hypoglycemia and ketosis caused by ethanol can be mistaken for diabetic ketoacidosis. This is a diagnosis. Need to pay attention to.

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