- MANAGEMENT—ANTENATAL
- Evidence suggests that outcomes are improved if women with pre-existing diabetes mellitus are managed jointly by obstetricians and physicians with expertise in the management of pregnant women with diabetes.1
An early dating and viability scan should be offered, as well as a nuchal translucency scan. Regular fetal ultrasounds for growth and liquor volume assessment are generally recommended. -
PHYSIOLOGY OF GLUCOSE METABOLISM IN PREGNANCY
Glucose is transported across the placenta and fetal glucose values are approximately 80% of maternal values. Amino acids are actively transported across the placenta.Pregnancy is normally associated with pancreatic beta cell hyperplasiaand increased serum insulin levels in the fasting and fed state. This results
in a doubling of the insulin production from the first to the third trimester.Fasting blood glucose levels are 10–15% lower compared to the nonpregnant state and post-prandial blood glucose levels are elevated.
Insulin resistance develops as pregnancy continues due to placental production of hormones (e.g., cortisol, growth hormone, human placental lactogen). This explains the increased insulin requirements in pre-existing diabetes mellitus and the development of gestational diabetes where there is insufficient insulin production to account for the increasing insulin resistance.
Pregnancy is a state of “accelerated starvation”; fasting is associated with a switch from the use of hepatic glycogen for energy production to lipolysis and ketone body formation. Thus, there is an increased risk of diabetic ketoacidosis throughout pregnancy. - FETAL AND NEONATAL EFFECTS OF PRE-EXISTING DIABETES
Poor maternal diabetic control in the first trimester, as evidenced by elevated glycosylated haemoglobin (HbA1C) values, is associated with an increased incidence of congenital abnormalities and spontaneous abortion. Later in pregnancy there is an increased risk of polyhydramnios and pre-eclampsia. The rate of pre-eclampsia is increased in the presence of hypertension with or without nephropathy. The exact molecular mechanisms involved in the development of these complications are uncertain. - Maternal hyperglycaemia is associated with fetal hyperglycaemia. This then results in fetal pancreatic beta cell hyperplasia causing fetal perinsulinaemia. Chronic fetal hyperinsulinaemia leads to increased
activity of hepatic enzymes, glycogen accumulation in the liver and fat accumulation in adipose tissue. The increased metabolic rate leads to increased oxygen consumption and fetal hypoxaemia. Fetal hypoxaemia
stimulates the synthesis of erythropoietin, which can result in olycythaemia and promotes catecholamine production, which can lead to hypertension and cardiac hypertrophy. - Approximately half of all pregnancies will have an uneventful course.
- Early Pregnancy Effects
The overall risk of one or more major congenital malformations is 6–7%,which is double the risk compared to the general obstetric population.Infants of women with diabetes appear to be at significantly higher risk of
renal agenesis/caudal dysgenesis syndrome, congenital heart defects andneural tube defects. The congenital heart defects which increase in diabeticpregnancy include heterotaxia, tetralogy of Fallot, transposition of the greatarteries, septal defects, anomalous pulmonary venous return and variousdefects causing left or right outflow tract obstruction. Central nervoussystem defects include anencephaly, spina bifida, encephalocele,hydrocephaly and anotia/microtia. The risks of limb deficiencies,hypospadias and orofacial clefts are also increased.
Late Pregnancy Fetal and Neonatal Effects
Macrosomia is a frequent complication, particularly if there has been poor maternal control. The most serious potential complication of macrosomiais an obstructed delivery. This may result in any or all of the following:traumatic delivery, fractured clavicles, brachial plexus injury, hypoxic ischaemic encephalopathy (HIE) and death. Macrosomia also increases thelikelihood that a caesarean delivery will be performed (up to 60% in somestudies).
Intrauterine growth restriction (IUGR) can occur in some pregnancies.This carries its own risks and complications Infants of diabetic mothers have a greater risk of developing respiratorydistress syndrome. This is not just related to prematurity. It occurs in termbabies as well. Proposed mechanisms include delayed lung maturation,polycythaemia and surfactant inactivation by insulin.Pregnant women with pre-existing diabetes mellitus have significantly higher rates of both spontaneous preterm delivery (16% for diabetes versus 11% for healthy controls) and preterm delivery for some specific indications(22% for diabetes versus 3% for healthy controls).2Polycythaemia can occur in up to 40% of babies. Hyperviscosity
syndrome secondary to polycythaemia occurs more rarely. Hypocalcaemia,hypomagnesaemia and hyperbilirubinaemia are also more common ininfants of diabetic mothers. - Hpertrophic cardiomyopathy predominantly affects the intraventricularseptum and may cause outflow tract obstruction. Severe cases have beenassociated with neonatal death. However, in most cases it is transient and resolves over the first few months of life.
Dr. Jayaprakash
Superintendent, ICH.
Institute of Child Health.
Gov. Medical College Kottayam.
Kerala, India.