1. Gestational Diabetes
A transient, self-limiting, hyperglycaemia, which occurs during pregnancy due to
maternal endocrine changes.
Glucose Control
Insulin causes glucose cellular uptake. Cortisol and glucagon increase glucose
production. In pregnancy the placenta produces extra:
 Cortisol increases glucose production
 Insulin antagonists  human placental lactogen, progesterone, and human
chorionic gonadotrophin.
If the pancreas is unable to produce enough insulin to overcome this, or there is
maternal insulin resistance  hyperglycaemia can develop  ‘gestational diabetes’
Glucose in the foetus
Glucose levels are similar to those in the mother due to glucose being transferred by
facilitated diffusion. Maternal insulin does not pass through the placenta. The foetus
produces its own insulin from the 10th
week (has a role in growth). In diabetes the
maternal glucose levels are increased, resulting in higher levels in the fetus, so the
fetus has to produce more insulin. The increased insulin causes:
 Macrosomia (big babies)
 Organolegaly
 Increased erthropoiesis
 Neonatel polycythaemia
 Increase in congenital abnormality
 Unexplained uterine death  ? fetal hyperinsulinaemia leads to chronic
hypoxia and lactic acidaemia.
Risk Factors
 FHx of 1st
degree relative with DM
 Obesity (BMI >30)
 Previous large baby (>4kg)
 Previous unexplained still birth
 Previous gestational DM
 Polycystic Ovaries
 Polyhydramnios in this pregnancy
 Glycosuria on 2+ occasions in this pregnancy

2. Diagnosis
Oral glucose tolerance test – normally 26-28 weeks
OGTT  overnight fasting. 75mg glucose load in 250-300ml of water. Glucose
measured fasting and 2 hours after:
 DM  fasting - >7 or 2 hour >11.1
 Impaired glucose tolerance – fasting <7 and 2 hour > >7.8 <11
An early result in pregnancy doesn’t rule it out for the future.
Management
 Glucose levels 4 x/day
 1st
line – diet.
 2nd
line – insulin