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

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