Gestational diabetes and the newborn (diabetic mothers’ children)
I. Definition.
(a) Diabetes mellitus in pregnancy can be divided into two conditions.
1. Diabetes mellitus combined with pregnancy: diabetes mellitus existed before pregnancy.
2. Gestational Diabetes Mellitus (GDM): abnormal glucose tolerance that occurs or is first detected during pregnancy.
(2) Infans of Dibetes Mothers (IDMs): Infants born to mothers with gestational diabetes are a type of high-risk infants that pediatricians often encounter in their clinical work.
(iii) Indications for insulin therapy.
Fasting >5.8 mmol/L, 1 h after meal >7.8 mmol/L, 2 h after meal >6.7 mmol/L Ideal control criteria: fasting 3.5-5.0, preprandial 3.5-5.8, 2 h after meal <6.7.
Mothers with fasting glucose ≥5.8 h or postprandial hyperglycemia have a high risk of intrauterine or neonatal death of their children. Antenatal fetal monitoring is mandatory for these mothers, and with satisfactory antenatal monitoring and normalization of blood glucose levels, perinatal mortality in the offspring of GDM who maintain normal blood glucose levels is not higher than in the general population.
(iv) Causes of diabetogenic tendency of pregnancy.
1, increased glucose consumption metabolism: among the nutrients delivered by the mother to the fetus through the placenta during pregnancy, amino acids and free fatty acids are transported more slowly, only glucose can pass freely through the placental tissue, and glucose is an important source of energy for the fetus. The maternal glucose consumption metabolism increases and is in a state of accelerated starvation.
2, placental hormones antagonize the role of insulin: the placental syncytiotropic cells produced by lactogen, estrogen and progesterone in the peripheral blood of pregnant women have antagonistic effects of insulin. As the placenta grows, the production of these hormones increases, and the syncytiotropic cells also produce enzymes that break down insulin and reduce the insulin receptor function of target cells. Therefore, the pancreatic beta cells during pregnancy must double the amount of insulin than during non-pregnancy in order to maintain the blood glucose balance in the body, and those with insufficient pancreatic compensatory function are prone to diabetes.
3, accelerated fat decomposition, lactogen also has a hypolipidemic effect, so that the transformation of fat into carbohydrates and fatty acids. In the absence of insulin, carbohydrates are not used, so that the relative free fatty acids increase, so non-pregnant women are prone to ketoacidosis.
4. The increase of corticosteroids in maternal blood during pregnancy can increase blood glucose, thus increasing insulin secretion, and if the pancreas is not functional enough, abnormal glucose tolerance can occur.
(E) The effects of gestational diabetes on the mother.
(①High incidence of gestational hypertension, which is 4 times higher than that of non-diabetic pregnant women. Diabetic vascular disease changes are prone to eclampsia, pre-eclampsia, placental abruption, cerebrovascular accidents, etc.
②High incidence of amniotic fluid overload.
③Ketoacidosis.
④High incidence of surgical delivery.
(⑤ Decreased resistance to infection.
(vi) The effects of gestational diabetes on the fetus (newborn).
Immediate effects include: giant baby, birth injury, hypoglycemia, respiratory distress, hypocalcemia, erythrocytosis; long term effects include: obesity, type 2 diabetes, abnormal intellectual neuropsychiatric development, etc.
Second, the treatment during pregnancy
1, strict control of blood sugar up to the ideal standard, insulin therapy, without oral hypoglycemic drugs.
2, choice of delivery time: varies from person to person, weighing intrauterine risks and various problems after preterm delivery.
3, emergency delivery: decreased maternal weight growth rate, decreased insulin requirement, decreased fetal movement, decreased estriol level, abnormal OCT, etc.
① Strict control of maternal fluid intake and blood sugar.
② Develop a delivery treatment plan, cooperation between obstetricians and pediatricians, and infant evaluation treatment.
Infant evaluation
1.At the moment of delivery: take sterile amniotic fluid specimens and send them for bacterial culture, Gram stain, L/S ratio or foam test, etc. respectively.
2. Scoring at the moment of delivery of the infant: Apgar score is used as the basic evaluation. Warmth, removal of respiratory mucus, screening for congenital malformations, placental examination, and determination of blood glucose from cord blood specimens (to predict infant-responsive hypoglycemia associated with hyperglycemia of delivery).
3. Infant room: Complete physical examination of the infant, with particular attention to the heart, kidneys, and extremities.
Reported in the literature: 47% hypoglycemia, 22% hypocalcemia, 19% hyperbilirubinemia, 34% erythrocytosis Therefore.
①Glucose monitoring: measured at 1, 2, 3, 6, 12, 24 and 48 hours of birth.
②Blood calcium monitoring: measured at 6, 12, 24 and 48 hours after birth.
③Erythrocyte specific volume measurement: measured 1, 24 hours after birth.
④Bilirubin measurement: measured 24 or 48 hours after birth or as indicated.
(iv) Special problems often seen in infants of diabetic mothers.
(a) Respiratory distress (Respiratury distress).
The incidence was 6 times higher than that of non-IDM more than 10 years ago. The incidence of RDS decreases with gestational diabetes as gestational age increases with interventional treatment during pregnancy, and the odds of vaginal delivery increase.
Etiology: hyperinsulinemia suppresses corticosteroid secretion and delays lung maturation.
It also needs to be differentiated from diaphragmatic hernia, pneumothorax, congenital heart disease, hypertrophic cardiomyopathy, and temporary respiratory distress.
The following tests should be done regarding RDS: chest X-ray: evaluation of pulmonary ventilation; blood gas analysis, ECG and blood pressure, cardiac ultrasound (suspected cardiomyopathy); blood culture, cerebrospinal fluid examination and culture.
(ii) Hypoglycemia (hypoglycemia)
Regardless of gestational age or presence of symptoms, blood glucose <30mg/dl. incidence 30-40%, common in 1-2h postnatal, giant babies.
Etiology: maternal hyperglycemia – fetal hyperinsulinemia doctrine. SGA hypoglycemia: The mother has vascular lesions and insufficient liver glycogen reserves, so hypoglycemia can persist 12-24 h after birth.
Symptoms: quiet, drowsy-like, apnea, shortness of breath, respiratory distress, shock, cyanosis, convulsions, etc.
Symptomatic infants may be more likely to develop sequelae than asymptomatic infants.
1. Asymptomatic hypoglycemia.
(1) For IDM in good general condition, feed 10% glucose 5 ml/kg by bottle or nasal (oral) feeding at birth or 1 hour after birth. weight below 2 kg without oral feeding. Glucose was administered intravenously during the first hour after birth.
Weight greater than 2 kg was fed sugar water once every hour for 3-4 times until blood glucose was stable, then every 2-3 hours. When the feeding interval is extended, the amount of glucose solution needs to be increased.
(2) If treatment goes well, formula (containing 20cal/) can be fed gradually with additional glucose as needed. This rapid feeding method prevents and corrects hypoglycemia in most well behaved IDM.
(3) Despite giving feedings, glucose is still very low 2 hours after birth or intravenous glucose can be administered for treatment if feeding is not tolerated.
A. Terminal intravenous injection
B. In critically ill children (convulsion, respiratory depression, etc.) 0.5-1g/kg glucose = 25% glucose 2-4ml/kg at 1ml/min, followed by 4-8mg/kg.min of glucose to make blood glucose greater than 30mg/dl. but in order to maintain blood glucose also Glucose concentration and rate can be increased.
C. Treatment of asymptomatic infants: Instead of pushing 25% glucose, just push 5-10ml of 10% glucose at 1ml/min and continue the drip at a rate equivalent to 4-8mg/kg.min. After starting the static drip of glucose, blood glucose must be monitored to adjust the treatment at any time, and to avoid hyperglycemia The glucose should be monitored after starting intravenous glucose in order to adjust the treatment at any time and to avoid hyperglycemia, causing osmotic diuresis and dehydration etc.
D. Intravenous route glucose therapy should not be interrupted suddenly to avoid reactive hypoglycemia. The rate of intravenous glucose drip after breastfeeding can be gradually slowed down, and its rate can be reduced to 5%, and blood glucose should still be monitored during the adjustment process.
E. Most hypoglycemia in IDM is effective for the above treatment. If there is no response or no response for 48h, we should look for other etiologies (infection, insulinoma, etc.).
Hydrocortisone 5mg/kg.d, divided into two intramuscular injections, is sometimes effective. In my clinical experience, other drugs (epinephrine, dexamethasone, growth hormone) are generally not needed for the treatment of hypoglycemia in IDM.
F. Hyperglycemia treatment: infants with adequate glycogen stores, 300ug/kgG. for more than 7 days to look for other causes.
(C) Hypocalcemia
Total calcium less than 7mg/dl, 20-50% IDM occurs, 22% not associated with hypoglycemia occurrence, 24-72h after delivery.
Etiology: delayed PTH response, antagonism of small intestinal Vitamin D absorption by cortisone, hypophosphatemia due to tissue catabolism, preterm asphyxia hypocalcemia in IDM.
Hypocalcemia in asymptomatic IDM often does not require treatment and resolves spontaneously.
In IDM infants with symptoms of lethargy or irritability or convulsions without abnormal blood glucose should consider blood calcium measurement and calcium supplementation in case of low calcium. Hypocalcemia should be considered along with the presence of hypomagnesemia. Hypomagnesemia treatment after hypocalcemia to completely recover.
(D) Erythrocythemia Polycythemia: 34% common cause in IDM: placental insufficiency, chronic hypoxia, increased erythropoietin, stimulation of fetal bone marrow hematopoiesis.
(E) Jaundice: 19% hyperbilirubinemia
Etiology.
(1) Insulin-induced increase in erythropoietin.
(2) Erythrocyte glycation, membrane malfunction, shortened erythrocyte life span, mild anemia.
(3) Premature birth, reduced conjugated bilirubin formation; poor feeding, increased hepatic and intestinal rings.
(F) Congenital anomalies: incidence: 4.0-12.9% (normal 1-2%).
Etiology: unclear. Hyperglycemia causes impaired embryonic yolk sac development and affects nutrient delivery; inositol affects metabolism and causes abnormal embryonic morphogenesis; increased growth transmitter inhibitory factor. Increased glycosylated hemoglobin is positively associated with congenital abnormalities.
Major anomalies include: 1. Central nervous system: anencephaly, cerebrospinal bulge, and caudate agenesis syndrome 2. Cardiac malformations. These two account for 2/3, and other spinal, skeletal, and renal malformations.
(G) feeding difficulties (Poor feeding)
37% are related to prematurity, RD, and not related to excessive amniotic fluid. LGA is the same as AGA.
Symptoms include: poor appetite, nausea, poor sucking, need for nasal feeding, gastric retention, etc.
(H) Macrosomia 28%
Causes: Pregnant women are hyperglycemic, glucose passes through the placenta to the fetal circulation, insulin has a large molecular weight and cannot pass through the placenta, excessive glucose increases the fetal pancreatic beta cells and secretes too much insulin, high insulin promotes fetal cell uptake of amino acids, accelerates tissue protein synthesis, decreases lipolysis, increases the deposition of mass fat and glycogen in fetal tissues, and becomes a giant baby. And it is related to the control of glycemia in stage III. Huge babies increase cesarean delivery and increase birth injuries.
In severe diabetes mellitus with vascular or renal lesions, the intrauterine fetal growth is poor due to reduced blood flow to the uteroplacenta, and the fetus becomes a low weight baby.
(ix) Myocardial dysfunction (Myocardial dysfunction) etiology is unclear. It can lead to heart failure, etc.
The diagnosis is confirmed by ultrasound: hypertrophy of the septum, anterior right ventricular wall, posterior right ventricular wall, decreased atrial diastolic function, and decreased cardiac output.
Symptoms usually disappear after 2 weeks, and septal hypertrophy disappears in 4 months.
Digoxin and other cardiac stimulants are contraindicated. Cardiotonic is effective.
Differentiation: post-asphyxial cardiomyopathy, myocarditis, glycogen accumulation, abnormal origin of the left coronary artery.
(x) Renal vein thrombosis and other thrombosis can occur intrauterine or postpartum, with postnatal symptoms: hematuria, bilateral renal masses, increased blood pressure, etc.
(xi) Small left colon syndrom abdominal distension, poor fetal stool expulsion, etc.
(xii) Perinatal survival rate Perinatal survival fetal perinatal death increases: stillbirth often occurs after 36 weeks and is more likely to occur at 38 weeks.
It is mainly due to: ① placental blood sugar abundance, cell increase is obvious, the number of villi increases, the villi septum is reduced accordingly. The increase in cell hypertrophy, cytoplasm, and interstitial cells within the villi widen the blood circulation barrier between mother and child. ③The small metaplastic artery vascular noses are enlarged and the lumen is narrowed. ④There is embolization of the small fetal side artery in the trunk of the chorion. ⑤ Affect the placental oxygen transport function, high blood sugar, high insulin itself makes the fetal metabolism increase, oxygen consumption increase, resulting in fetal chronic hypoxia, acidosis, fetal death in utero. Due to placental hypoxic reserve, once in labor, easy to die or neonatal death.
(xiii) Genetics: Genetics (Risk of insult-dependent diabetes in offspring of dibetic parents): susceptible to the development of type 1 diabetes or type 2 diabetes.
References.
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Neonataology.5th ed.Philadelpin:Lippincott Williams & Wilkins,1999:78-7123.King H.Epidemiology of glucose intolerance and GDM in women of child- Diabetes,1998;21(suppl 2):9-13.
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