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Maternal Diabetes And Neonatal outcomes

Jan 23, 2024

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WHITE’S CLASSIFICATION FOR MATERNAL DIABETES

MONITORING DURING PREGNANCY

CUT-OFFS IN MOTHER

MANAGEMENT

TREATMENT

FETAL EFFECTS

INFANT OF DIABETIC MOTHER

NEONATAL EFFECTS

MANAGEMENT

LONG-TERM EFFECTS

Maternal Diabetes And Neonatal outcomes

  • Gestational diabetes is very common and affects 6-8% of pregnancies. It is a serious disease with potential fetal complications, with better antenatal diagnosis and management, the outcomes are better. Women with advanced microvascular diseases like hypertension, nephropathy, and retinopathy have a 25% risk of preterm delivery due to gestational diabetes. The most important complication is fetal embryopathy leading to malformations.
  • The most common anomaly is cardiac and neural tube defects. - Approximately 3-5% of patients with GDM actually have underlying type 1 or 2 DM, which was undiagnosed. Women diagnosed with GDM have a 60% lifetime risk of developing overt type 2 DM. Throughout pregnancy, insulin requirements increase because of increasing production of placental hormones, which antagonize insulin action. This is most prominent in the mid-third trimester.

PATHOPHYSIOLOGY

  • It is based on Pederson’s theory. It states that maternal hyperglycemia will lead to fetal hyperglycemia and further fetal hyperinsulinemia. This is followed by increased hepatic glucose intake, glycogen synthesis, lipogenesis, and augmented protein synthesis. As a result, the size of all organs except the brain is increased.

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WHITE’S CLASSIFICATION FOR MATERNAL DIABETES

Gestational Diabetes

Diabetes not known before pregnancy

Class A

Chemical diabetes

Pre diabetes: h/o large babies>4kg or unexplained stillbirth after 28 wk

Class B

Insulin-dependent with an onset later than twenty years and duration <10yr 

Class C

Onset during 10-19 years

Duration >20 yr

Class D

Onset less than 10 years of age

Duration > 20 yr 

Class F

Nephropathy

Class R

Proliferative retinopathy or vitreous hemorrhage

Class RF

Both R and F features

Class G

Reproductive (gonadal failure)

Class H

Heart disease 

Class T

Prior renal transport

  • Risk factors for GDM include advanced maternal age, obesity, high parity, previous macrosomic baby, family history of type 2 DM, short stature, PCOD, GDM in a previous pregnancy, previous neonatal death, previous stillbirth or CMF, multiple pregnancy, and high BP during pregnancy. Maternal complications include miscarriage, preeclampsia, gestational hypertension, polyhydramnios, preterm delivery, and chances of LSCS.
  • Maternal ketoacidosis is rare and uncommon, but it has a 50% risk of fetal death. Polyhydramnios can occur due to diuresis secondary to hyperglycemia or osmotic diuresis. Stillbirth is uncommon these days due to better healthcare facilities.

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MONITORING DURING PREGNANCY

  • During the first trimester, do the dating scan and look at the nuchal lucency. In the second trimester, scans are very important to look for malformations as the incidence of neural tube defects is ten times higher in GDM pregnancies than in normal ones. In the third trimester, observe the child's growth and look for macrosomia (the baby's weight is greater than 4kg).

CUT-OFFS IN MOTHER

  • The cut-off of fasting blood sugar in mothers is 95mg/dL. The post-prandial cut-off after one hour is 140mg/dL, and after two hours is 120mg/dL. The glucose challenge test is done between 24-48 weeks.

MANAGEMENT

  • Tight glucose control during pregnancy is of utmost importance. Targeting the post-meal glucose is more effective than controlling the fasting level alone to reduce fetal overgrowth. Preconception glucose for women with pregestational DM can reduce the risk of malformations. Women with pregestational DM may have reduced glycemic profiles and insulin requirements postpartum, especially in women who are breastfeeding (honeymoon period).

TREATMENT

  • Diet control is the most preferred type of treatment. Human insulin analogs that do not cross the placenta can be given to these patients. Oral agent’s glyburide and metformin are as effective as insulin in managing GDM. Glyburide is a sulfonylurea that acts as beta cell ATP-calcium channel receptors, increasing insulin secretion and sensitivity to peripheral tissues.
  • Metformin is a biguanide that inhibits hepatic gluconeogenesis and glucose uptake and stimulates glucose uptake in peripheral tissues. The ideal time for delivery is 39-40 weeks, as uncontrolled GDM can lead to surfactant deficiency. During postpartum, for women with type 2 DM, metformin and glyburide are compatible with breastfeeding.

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FETAL EFFECTS

  • Chronic fetal hyperinsulinemia can cause increased fetal metabolism. The fetal metabolic demands increase metabolically, and this can cause acidosis and fetal death. Macrosomia is due to the increased size of insulin-sensitive tissues. Truncal asymmetry with a disproportionate ratio of “shoulder to head” and “abdomen to head” are seen, which can cause difficult extraction and birth trauma.

INFANT OF DIABETIC MOTHER

  • There is increased weight of the placenta and organs except for the brain. At birth, the separation of the placenta suddenly interrupts the glucose supply chain of the neonate without the proportional effect of hyperinsulinemia. The main cause of hypoglycemia is hyperinsulinemia. Other contributing factors include decreased epinephrine and decreased glucagon responses. At birth, the baby is large and plump with enlarged viscera and a plethoric face.
  • Hypoglycemia can occur in 25-50% of infants of diabetic mothers. Nadir in glucose is seen in 1-3 hours. The target pre-feed RBS is >=45mg/dL. There is a higher risk of jaundice, polycythemia, and renal vein thrombosis. There is three times the risk of congenital malformations. The most common malformations are cardiac and lumbosacral agenesis. Caudal agenesis is highly specifically associated with GDM.
  • Cardiac lesions include VSD, TGA, TA, DORV, tricuspid atresia, and CoA. Other diseases include double ureter, holoprosencephaly, situs inversus, hydronephrosis, renal agenesis, anal atresia, and small left colon syndrome. There is a higher incidence of tachypnea and respiratory disorders. 30% chance of cardiomegaly and heart failure in 5-10% of the infants seen. Asymmetrical septal hypertrophy is specific to GDM and may manifest as transient idiopathic hypertrophic sub-aortic stenosis. Ionotropic agents are contraindicated here, and they may worsen the situation.

NEONATAL EFFECTS

  • Neonatal effects include mortality and prematurity. Large GA is the 90th percentile. Respiratory distress like RDS, TTNB, and Pneumothorax is seen. There are chances of air leaks as the lungs are less compliant. Hypoglycemia will typically be seen 1-3 hours after birth and lasts 2-4 days.
  • Hypocalcemia is seen when there is less than 7mg/dL of calcium in the blood and within 24-72 hours after birth. It is seen in 5-30% of patients. Hypomagnesemia is seen within the first 72 hours of birth. There is a 25% risk of neonatal jaundice, and contributing factors include prematurity and polycythemia.
  • The small left colon syndrome’s treatment is conservative and supportive. HOCM is seen in the late 2nd to early 3rd trimester and is treated with IV fluids, and propranolol improves within 2-3 weeks and resolves on echo in 4-6 months.

MANAGEMENT

  • Target RBS should be greater than 45. If below 25 or persistently below 40 despite feeds, then IV fluids are given.

LONG-TERM EFFECTS

  • It includes obesity, diabetes, obesity, hypertension, dyslipidemia, and glucose intolerance. Impaired neurodevelopmental outcomes are seen. High HbA1C levels are associated with long-term decreased intellect and low head circumference.

Hope you found this blog helpful for your NEET SS Pediatric Endocrinology preparation. For more informative and interesting posts like these, keep reading PrepLadder’s blogs.

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