Zheng Chengzhong, Chief Physician and Professor, Pediatrics, No. 306 Hospital of the People's Liberation Army

Approximately 3% to 8% of people have abnormal glucose tolerance during pregnancy, and a considerable number of them have gestational diabetes (GD), which is generally mild hyperglycemia, but fetal and birth abnormalities are not parallel to blood sugar levels. Diabetic mothers Infants of diabetic mothers (IDMs) are twice as likely to have severe birth injuries, twice as likely to have a cesarean section, and three times as likely to be admitted to the neonatal intensive care unit (NICU) as babies of the same weight as mothers without diabetes. , this risk is positively correlated with the degree of maternal hyperglycemia. Therefore, to some extent, fetal and neonatal abnormalities of diabetic mothers are preventable, at least through reasonable prenatal treatment to reduce these risks. Additionally, gestational diabetes can have a range of short- and long-term effects on the newborn.

Gestational diabetes can be divided into two situations: one is diabetes combined with pregnancy: diabetes already exists before pregnancy; the other is gestational diabetes (GD): abnormal glucose tolerance that occurs or is first discovered during pregnancy. Infants of diabetic mothers (IDMs): Infants born to mothers with gestational diabetes are a type of high-risk neonates that pediatricians often encounter in clinical work. The following is an introduction to the problems that may arise in such newborns.

1. Short-term implications of the neonate

Short-term problems generally refer to newborn problems within a few days of birth.

(1) Neonatal hypoglycemia

1. Definition: Currently, blood glucose 44mg/dl (2.6mmol/L) is generally used as the "operational threshold". A value below this value is an indication for medical action (treatment). Although it is not a diagnostic criterion.

2. Incidence: The reported incidence of neonatal hypoglycemia varies greatly (25%-50%), mainly due to different diagnostic standards, methods, and maternal blood sugar control standards.

3．Etiology of neonatal hypoglycemia (Etiology)

① The generally accepted theory is maternal hyperglycemia-fetal hyperinsulinemia.

Elevated blood sugar in gestational diabetes → fetal hyperglycemia → stimulation of fetal pancreatic islet cells to secrete and release insulin → persistent fetal hyperinsulinemia. After birth, hyperinsulinemia persists and insufficient or no sugar intake → neonatal hypoglycemia. Fetal hyperinsulinemia is also related to inhibition of blood free fatty acids and liver glycogen metabolism.

② Further research found that

All nutrients (sugar, amino acids, fats) required by the fetus are transported through the placenta in a concentration-dependent-fashion, and the concentration of these substances in the fetal blood depends on the concentration of these substances in the mother's body. The metabolism of these substances is regulated by maternal insulin. Maternal insulin and metabolic disorders will inevitably affect fetal metabolism, eventually leading to fetal hyperinsulinemia;

4. Clinical manifestations of neonatal hypoglycemia:

① Most patients have no obvious symptoms of hypoglycemia; even when blood sugar is very low, there are still no clinical symptoms.

② May have the following clinical manifestations:

A. Nervous system: tremors, startles, blinks, screams, twitches, etc.

B. Respiratory system: shortness of breath, cyanosis, apnea, etc.

C. Cardiovascular system: tachycardia, heart enlargement, heart failure.

D. Digestive system: milk rejection, etc.

E. Metabolic problems: hypothermia (body temperature does not rise), sweating.

③ There is no effective method to predict severe hypoglycemia in newborns. Therefore, all IDMS should have their blood glucose measured immediately after birth. Test time: 1, 2, 4 hours after birth, before feeding, until blood sugar is stable.

5. Complications of neonatal hypoglycemia (Complications)

Early diagnosis and timely and appropriate treatment are crucial to preventing long-term damage from neonatal hypoglycemia. Research shows that severe and long-lasting hypoglycemia, in addition to causing acute neurological damage, may also cause permanent damage to the nervous system. For example: degeneration of neurons and glial cells in the cerebral cortex, most obvious in the occipital lobe.

6. Treatment of neonatal hypoglycemia (Treatment)

The key to dealing with neonatal hypoglycemia is prevention.

Feeding should be done as early as possible after birth, with priority given to breastfeeding. For those with poor sucking ability, feeding should be done through nasogastric feeding. When the blood sugar is still lower than 44mg/dl after starting feeding, or the child has mild hypoglycemia, start intravenous infusion treatment (10% glucose 6-8mg/Kg/min); in case of severe hypoglycemia, immediately inject 10 % glucose 2ml/Kg, and then maintain intravenous infusion of 10% glucose 6-8mg/Kg/min.

(2) Neonatal hypocalcemia

1. Diagnostic criteria for neonatal hypocalcemia: serum calcium <8 mg/dl in term infants, <7 mg/dl in premature infants, or free calcium <3-4 mg/dl.

2. The incidence of neonatal hypocalcemia: Hypocalcemia is very common in babies born to pregnant mothers with diabetes, almost as much as perinatal neonatal respiratory distress, about 20-50%, and its incidence and severity are similar to those of perinatal respiratory distress. Maternal diabetes is positively correlated, and strict control of maternal blood sugar can greatly reduce the incidence of neonatal hypocalcemia.

3. The etiological mechanism of hypocalcemia in diabetic mothers and children

A. Functional hypoparathyroidism is the main cause of IDMS combined with hypocalcemia. When calcium is low, parathyroid hormone (PTH) secretion cannot be increased accordingly. Compared with children of non-diabetic mothers, PTH levels in IDMS are significantly lower within 4 days after birth. It takes 3-4 days for PTH to respond to low calcium stimulation.

B. Hypomagnesemia may be another cause of hypocalcemia. In gestational diabetes, magnesium excretion in the urine increases, causing magnesium deficiency in the pregnant mother and fetus. Low magnesium inhibits the secretion of PTH and causes hypocalcemia.

4. Clinical manifestations of neonatal hypocalcemia

It often occurs within 24-72 hours after birth, and blood calcium reaches its lowest point one day after birth. Hypocalcemia often has no clinical symptoms. Those with hypocalcemia usually have neuromuscular symptoms: such as muscle tremors, startles, agitation, convulsions, etc.

5. Treatment of neonatal hypocalcemia:

①10% calcium gluconate 0.5-1g/Kg/d, orally divided into 4-6 times;

② Dilute 10% calcium gluconate injection 500mg/Kg/d and infuse slowly intravenously;

③ Those with severe hypocalcemia or severe symptoms can receive intramuscular injection of MgSO4;

(3) Neonatal hypomagnesemia:

1. The definition and incidence of neonatal hypomagnesemia: serum magnesium <1.5mg/dl (0.62mmol/L) is considered hypomagnesemia. The incidence rate is closely related to the condition of the pregnant mother. In the past, when gestational diabetes was not strictly controlled, the incidence of hypomagnesemia in IDMS could be as high as 38%, but it has dropped significantly recently.

2. The etiology, pathogenesis and clinical manifestations of neonatal hypomagnesemia:

Hypomagnesemia in IDMS is related to factors such as maternal hypomagnesia (accompanied by urine glucose and magnesium excretion from the body), neonatal hypocalcemia, high phosphorus, and reduced parathyroid function. Research shows that the amniotic fluid magnesium concentration in diabetic pregnancy is significantly lower than that in normal pregnancy (suggesting that the fetus is in a state of magnesium deficiency). Low fetal magnesium affects parathyroid activity. Therefore, hypocalcemia can occur. Clinical manifestations: similar to those of hypocalcemia.

(4) Neonatal polycythemia and hyperviscosity (Polycythemia and Hyperviscosity)

1. Definition and incidence of neonatal polycythemia

If the hematocrit of venous blood is >65%, neonatal polycythemia is diagnosed (>70% at 2 hours after birth, >68% at 6 hours after birth, and >65% at 12-18 hours after birth). The incidence of polycythemia in IDMS is 20% (incidence of normal newborns is 5%).

2. The etiological mechanism of neonatal polycythemia

① The main factor is the increased production of erythropoietin → increased red blood cell production caused by intrauterine ischemia and hypoxia (hypomexia) in the fetus during diabetic pregnancy. Research shows that erythropoietin in the fetal umbilical cord is higher in diabetic pregnancy than in normal pregnancy; it is closely related to unsatisfactory control of gestational diabetes and the increase in sugar and insulin in amniotic fluid and cord blood; erythropoietin in the cord blood of IDMS newborns rise.

② Changes in placental-fetal blood distribution

Due to intrauterine hypoxia, the blood flow between the placenta and the fetus changes. The blood flow in the placenta accounts for only 25% (normally 35%), and the fetal blood flow accounts for 75% → polycythemia.

③ Increased red blood cells → hyperviscosity.

3. Clinical manifestations of neonatal polycythemia:

Polycythemia, cardiopulmonary abnormalities, and neurological abnormalities may be seen. However, a considerable number of children are asymptomatic.

Nervous system: convulsions, agitation, convulsions.

Cardiopulmonary aspects: tachypnea, cyanosis, respiratory distress, tachycardia, and heart enlargement.

The main pathophysiological problem caused by neonatal polycythemia is hyperviscosity, which results in slowed blood flow, stasis, and promotion of platelet aggregation → thrombosis. It can cause vascular embolism in the brain, heart, lungs, kidneys, adrenal glands, mesentery, retina and limbs.

4. Treatment of neonatal polycythemia

For those with obvious symptoms or venous hematocrit >70%, albumin or normal saline can be infused to partially dilute the blood. Treatment should be implemented within 2-4 hours after birth to reduce hematocrit and blood viscosity.

(5) Neonatal hyperbilirubinemia

1. Definition and incidence: Serum total bilirubin is greater than 12mg/dl (205mmol/L), and the incidence is 20-25%.

2. The etiological mechanism of neonatal hyperbilirubinemia

Although some factors are clearly associated with hyperbilirubinemia in IDMS, overall the mechanisms remain unclear.

① Determinant factors

A: Increased decomposition of hemoglobin → increased production of bilirubin;

B: Increased carbon monoxide production → increased hemoglobin destruction and increased bilirubin production;

C: Changes in maternal metabolism lead to → changes in red blood cell membrane structure (red blood cells are more sensitive to oxidation and physical damage) → increased red blood cell destruction

D: Intrauterine hypoxia → increased erythropoietin → increased red blood cell production

②Contributory factors

A: High incidence of polycythemia → more destruction of red blood cells → hyperbilirubinemia

B: Secondary to injury, hematoma or birth trauma of macrosomia → increased bilirubin reabsorption → hyperbilirubinemia

C: Delayed enteral nutrition → weakened intestinal motility → increased enterohepatic circulation → hyperbilirubinemia

3. Treatment of neonatal hyperbilirubinemia:

Feed early, correct metabolic disorders (low sugar, hypoxia, increased red blood cells) and other unfavorable factors that aggravate jaundice; provide timely phototherapy.

(6) Neonatal respiratory distress syndrome (Respiratory distress syndrome)

1. Definition:

Clinical manifestations of RDS: shortness of breath, moaning, intercostal descent, nasal flaring, cyanosis, etc. Auxiliary examination findings: evidence of metabolic acidosis and hypoxemia. X-ray tips: decreased lung transparency, air bronchus sign, ground glass or reticular changes. The main cause is: surfactant deficiency, other causes include hypertrophic cardiomyopathy, polycythemia and meconium aspiration syndrome.

2. Incidence rate of RDS:

The incidence rate is 50% higher than that in non-diabetic pregnant infants. Since the introduction of strict blood sugar control measures during pregnancy and delivery, the incidence rate of RDS has dropped significantly (from 31% to 3%); however, RDS is still a serious complication of IDMS in premature delivery. One of the symptoms.

3. Causes and mechanisms of RDS

The high incidence of RDS is mainly caused by fetal hyperinsulinemia due to lack of or poor blood glucose control during pregnancy. Fetal hyperinsulinemia can prevent type II pneumocyte cortisone enzyme-inducing activities and hinder the production of pulmonary surfactant. Insulin can be converted into acetone and acetyl-CoA through glycerol-β-phospholipid → leading to a reduction in the raw materials (phospholipids) for the synthesis of surfactants → reduction in surfactants. In addition, insulin appears to interfere with the conversion of phosphatidic acid to phosphatidyl, a process that plays an important role in stabilizing surfactants. Newborns generally do not develop RDS if phosphatidyl is present in the amniotic fluid. Simple fetal hyperglycemia can also affect the formation of pulmonary surfactant: hyperglycemia inhibits the synthesis of lecithin from choline, further inhibiting the process of mRNA transcribing surfactant protein.

4. Treat according to neonatal RDS. However, this type of RDS is more difficult than neonatal simple idiopathic RDS, and pulmonary surfactant is used more aggressively and may need to be used multiple times.

(7) Ventricular septal hypertrophy (VSHT)

1. Definition of ventricular septal hypertrophy:

VSHT refers to the ventricular septal thickness exceeding the average ventricular septal thickness of normal children of the same sex and age by two standard deviations (2SD). Usually occurs in the third trimester of pregnancy (30-40 weeks).

2. Incidence of ventricular septal hypertrophy:

In diabetic pregnancies without effective blood sugar control, the incidence of ventricular septal hypertrophy at birth can be as high as 75%, while in those with strict blood sugar control, the incidence of VSHT can be reduced to 7.5%. When IDMS is macrosomic, the incidence of VSHT is much higher than that of normal-weight infants (8.3% and 1.8%, respectively). Children with VSHT have smaller left ventricular volumes in both systolic and diastolic phases than healthy infants. When VSHT (sometimes hypertrophy is not obvious), it affects ventricular filling during diastole, indicating poor myocardial diastolic function or reduced myocardial compliance.

1. The etiological mechanism of VSHT

Myocardial hypertrophy is the result of fetal hyperinsulinemia. The target of hyperinsulinemia is insulin receptors or insulin-like growth factor II (IGF) receptors. Myocardium, especially the ventricular septum, is rich in these two receptors. Stimulates the proliferation, increase, and enlargement of myocardial cells → leading to ventricular septal hypertrophy. This VSHT is often accompanied by obstruction of left ventricular function and left ventricular blood flow. ECG and non-invasive ultrasound examination indicate that the thickness of the ventricular septum is significantly negatively correlated with cardiac output. .

2. Clinical manifestations of VSHT

(1) Most children with VSHT do not have any clinical manifestations. Ventricular septal hypertrophy is only found in ECG examination, which does not necessarily cause cardiac function decline or disorder.

(2) A small number of patients have left ventricular blood flow obstruction leading to left ventricular dysfunction or failure, and may experience respiratory distress symptoms, such as tachypnea, tachycardia, increased oxygen consumption, etc.

3. Treatment of VSHT

VSHT usually recovers spontaneously within 3-6 months after birth and generally does not require treatment. When accompanied by obstructive heart failure, propranolol should be used for treatment, and inotropic drugs such as digoxin are prohibited.

(8) Ovarian cyst (OC)

1. Incidence rate and type

OC is common in the general neonatal population. Using three-dimensional ultrasound to continuously track and examine babies from 1 day to 2 years old, the incidence of OC can be as high as 80%. There are many histological types of OC, but the most common are follicular cysts.

2 Etiological mechanisms of OC

The exact mechanism is unclear. It may be related to endocrine disorders of the ovarian-pituitary axis. Studies have found that blood estradiol levels are higher in newborns with OC, and the incidence of OC in IDMS is higher. It is speculated that this is due to excessive increase in placental HCG secretion or increased placental permeability to HCG.

3. Clinical manifestations of OC

Ovarian cysts are smooth, mobile lower abdominal masses, often unilateral, ranging from several mm to 20cm in diameter. Increased amniotic fluid is found in about 10% of cases, which may be the result of the mass compressing the small intestine.

4. Complications of OC

Uncomplicated OC often shrinks and resolves spontaneously, and three types of complications may occur: primary, secondary, and maternal.

(1) Primary: OC torsion, bleeding or rupture.

(2) Secondary: Larger OC can cause secondary complications. Such as: closed inguinal hernia, intestinal or ureteral compression obstruction.

(3) Maternal: Polyhydramnios and cyst rupture lead to dystocia during vaginal delivery.

5. Treatment of OC

Treatment depends largely on the size, type and risk of complications of the cyst. Single cysts less than 4cm in diameter can be followed up, and most of them disappear on their own.

Those with a diameter greater than 5cm should be treated: cyst removal, laparoscopic aspiration, etc. can be used.

Large cysts should be aspirated before birth to reduce the risk of secondary pulmonary hypoplasia. It is very important to preserve as much gonadal tissue as possible during surgery.

(9) Neonatal Small left colon (NSLC)

1. Definition of NSLC: Neonatal NSLC is a transient functional disease, typically manifesting as low intestinal obstruction. In 1974, Davis proposed and described NSLC for the first time. He performed barium enema examination on 20 newborns with low intestinal obstruction and found signs of uniform stenosis in the colon from the anus to the splenic flexure (the diameter was less than 1 cm), and found that there was a sudden transformation into the colon at the splenic flexure. Dilated right colon. NSLC is usually smooth and straight and smaller than normal. Eight of the 20 cases (40%) had IDMS, and 12 cases of asymptomatic IDMS were further studied, of which 6 (50%) had similar narrow colons.

2. Causes and mechanisms of NSLC

The etiology and mechanism of NSLC are unclear, but may be related to the neurohumoral disorder between autonomic nerves and glucagon. The increase in glucagon that causes hypoglycemia can inhibit the activity or functional activity of the left colon of fetuses and newborns, leading to intestinal obstruction.

In addition, fetal (newborn) hypermagnesemia caused by maternal magnesium sulfate treatment, immaturity of the left colon wall nerve plexus, and maternal antipsychotic drugs may also be the causes of NSLC.

3. Clinical manifestations of NSLC

NSLC usually appears within 24-48 hours after birth, with abdominal distension and delayed excretion of meconium as precursors. The diagnosis is mainly based on water-soluble contrast agent enema X-ray examination. The contrast agent can stay in the intestine for 24-48 hours. NSLC is a benign process and the prognosis is good when there are no complications. Intestinal size usually returns to normal after 5-7 days. It can be self-healing or can be cured by repeated daily saline enemas. It should be distinguished from Hirschsprung disease because its prognosis and treatment are completely different.

4. Complications of NSLC

Complications often occur in severe cases (eg, hypoglycemic cardiac dysfunction, cyanosis, persistent fetal circulation). Complications include: cecal or ileal perforation and intussusception.

5. Treatment of NSLC

Unless complications arise, NSLC should be treated conservatively. The use of water-soluble contrast agent enema for children with clinical manifestations is not only a diagnosis but also a treatment measure in itself. Daily repeated saline enemas have satisfactory therapeutic effects and can achieve long-term healing effects.

(10) Strict glycemic control and short-term neonatal complications during pregnancy (Strict glycemic control and short-term neonatal complications)

It is theoretically speculated that strict control of blood sugar within the normal range before and during pregnancy can prevent the vast majority of neonatal complications including congenital malformations. A large number of studies have shown that it can indeed significantly reduce the incidence of severe RDS, congenital malformations and other short-term neonatal abnormalities. However, despite this, the occurrence of these abnormalities is still more than double that of the normal population. In order to achieve the goal of equal abnormality rates in infants born to mothers with gestational diabetes and those without diabetes, it is necessary to find other new methods and treatments.

2. Long-term impact of IDMs (long-term implication: child and adult)

(I. Overview

In recent years, the long-term impact of the intrauterine environment of diabetic pregnancy on children and adolescents has been gradually recognized and valued. Its impact is mainly divided into three categories:

1. Anthropometrics

Fetal weight and length grow too fast in late pregnancy, and the growth rate is still faster in children and adolescents. The results are: macrosomia (fetal and neonatal periods), overweight and obesity (in children and adolescents).

2. Metabolic problems (metabolic)

The imbalance of glucose metabolism makes it easier to develop abnormal glucose tolerance and develop into impaired glucose tolerance (IGT) and diabetes.

3 Neurological and psychological problems

Children of high-risk pregnancies often have some minor neurological disorders and may also have psychological and intellectual effects.

4 The key to preventing the above complications is blood sugar control measures before conception and during pregnancy. If the maternal blood sugar is controlled within the normal range, most complications can be prevented.

(2) Obesity

Children of diabetic mothers not only have a tendency to be born with macrosomia, but also have a tendency to become obese in children and adolescents.

Long-term follow-up found that regardless of whether the birth weight was normal or overweight, IDMS had a significantly higher incidence of obesity between the ages of 5 and 20 than children of non-diabetic mothers (the standard for severe obesity: weight ≥140% of the standard weight-for-height value).

The basic cause of childhood obesity is relatively high insulin levels. Increased insulin in amniotic fluid is closely related to childhood obesity, suggesting that the diabetic intrauterine environment plays an important role in childhood obesity. Some people studied the fasting blood insulin levels of IDMS between 5 and 9 years old. Higher than that of children born to non-diabetic mothers, suggesting that increased insulin levels are significantly related to childhood weight gain.

The height and weight of macrosomic infants with IDMS tend to be normal in the first year of life, but the trend of rapid growth resumes in early school-age children and continues into adolescence. In contrast, SGA's weight and height growth does not seem to accelerate significantly, at least in the first few years of life.

(3) Impaired glucose tolerance and diabetes

Children born to mothers with type II diabetes are more likely to develop diabetes after the age of 5. After the age of 25, the risk is 5-8 times higher than that of the normal population. At the age of 15-24, the abnormality in blood sugar levels 2 hours after a meal increases significantly. Diabetes susceptibility gene inheritance and poor intrauterine environment are the main causative factors.

(4) Effects of diabetes on postnatal development

A variety of psychological tests were used to evaluate children of diabetic mothers, and it was found that children's developmental abnormalities are closely related to the maternal blood sugar control and whether they had diabetes before pregnancy.

1. Intellectual development

Initial research believed that IDMS can cause intellectual development problems or developmental delays, and even believed that IQ values ​​were negatively correlated with maternal β-hydroxybutyric acid and HbA1c levels. Further rigorous controlled studies have found that the real reasons for IDMS’s delayed intellectual development are: maternal diabetes before conception without effective treatment or combined with diabetic nephropathy → leading to intrauterine growth retardation (low weight) of the baby and high rate of premature birth → low rate of premature birth Overweight children are prone to mental retardation, which is not caused by diabetes itself. Therefore, it is very important to avoid LBW and premature birth in diabetic pregnancy.

2. Fine neural dysfunction

Although the intelligence of children of diabetic mothers is not affected, the incidence of slight neurological damage is significantly increased.

These minor neurological damages mainly occur in the second and third trimesters of pregnancy, when accompanied by metabolic abnormalities (diabetic control is not ideal), because the development of the cerebral cortex occurs in the second and third trimesters of pregnancy, and metabolic problems during this period can easily cause damage to the development of the cerebral cortex.

Children with high-risk pregnancies are prone to developmental delays, learning difficulties, and attention deficit disorder (ADD). The American Psychiatric Association diagnostic criteria (DSM-IV) indicate that although the intelligence level of such children is within the normal range, ADD It can be accompanied by a variety of behavioral problems.

It is generally accepted that various unfavorable factors from the mother (such as severe environmental deprivation, glucose metabolism disorders) can delay the brain maturity of the fetus. If the acquired environment is better, the brain maturity of normal children can catch up with age.

Some scholars use a series of cognitive, sensory, motor, behavioral and neurological test methods (scales) to evaluate IDMS at school age, such as comprehensive systematic neurological examination, minor neurological examination, WISC-R and Bender Visual Gestalt intelligence test, etc. .

turn out:

①Cognitive and neurological function: The Bender score of children with IDMS was slightly lower than that of the control group, while the Bruininks-Oseretsky score that evaluates fine and gross motor movements was significantly lower than that of the control group. Sensory-motor comprehensive functions are not affected. Children born to mothers with diabetes before conception (PGDM) have significantly higher incidence rates of soft neuroogical signs than children with gestational diabetes and controls.

②Attention functioning

There was a significant difference between IDMS and the control group in the Pollack Taper test scores that reflect children's attention ability. The IDMS score was significantly lower than that of the control group (control group score 28.9, IDMS group score 24.3). The Conner Brief Parent-Teacher Questionnaire prompts: IDMS are more prone to hyperactivity and attention deficit disorder.

③The relationship between PGDM severity and neurodevelopment

The more severe PGDM is, the more obvious the neurodevelopmental impairment of IDMS is or the easier it is to occur.

Elevated HbA1C, hyperglycemia, and ketosis are closely related to attention deficit, poor sensorimotor integration, hyperactivity disorder, and fine motor impairment in IDMS.

Summary: Mild brain damage in IDMS can correct itself with age, and daily functions can be normal. However, it can be a bit difficult when dealing with complex movements or highly intellectual tasks.

Metabolic abnormalities during pregnancy delay fetal brain maturation. Therefore, impairment of fine neurological functions in children with IDMS during adolescence may exist. As they age, their brain functions can return to normal if a good education and training environment is provided.

The occurrence of brain damage in IDMS is mainly related to metabolic factors (hyperglycemia, ketoacidosis, etc.) in the second and third trimester of pregnancy. In PGDM, metabolic disorders are more obvious, and the brain damage to fetuses and even children in adolescence is also more serious.

These findings remind us that effective control of diabetes throughout pregnancy (to avoid severe metabolic disorders) is very important to prevent and treat short-term and long-term complications of IDMS.