Gestational diabetes mellitus (GDM)

Aetiopathogenesis

Physiological basis and development

• During pregnancy, insulin resistance physiologically increases, driven by hPL, progesterone, oestrogens, cortisol, prolactin.
• This resistance begins to increase from around 20 weeks and reaches its peak at around 32 weeks of gestation.
• Gestational diabetes develops when maternal insulin secretion can no longer compensate for this resistance, which first manifests postprandial hyperglycaemia.

Pedersen hypothesis and foetal consequences

• According to the Pedersen hypothesis, glucose crosses the placenta but maternal insulin does not, leading to foetal hyperglycaemia and, reactively, to hyperinsulinism.
• In the foetus, insulin acts as a growth factor, causing a typically disproportionate macrosomia with truncal adiposity.
• Characteristically, the trunk, abdomen and shoulder girdle grow more than the head, which increases the risk of shoulder dystocia.

Obesity risk complex

• Even before pregnancy, obesity increases the risk of infertility and miscarriages.
• During pregnancy, obesity increases the risk of pre-eclampsia, intrauterine foetal death and foetal macrosomia.

Clinical features

Further foetopathic complications

• Polyhydramnios can be caused by osmotically induced foetal polyuria.
• Other consequences of hyperinsulinism include myocardial hypertrophy, delayed surfactant production and polycythaemia with hyperbilirubinaemia.
• The risk of intrauterine foetal death increases due to heightened foetal oxygen consumption with relative hypoxia, acidosis and electrolyte shifts with arrhythmias.

Clinical signs during the course of pregnancy

• A clinical sign of undiagnosed gestational diabetes can be polyhydramnios.
• During the external examination, an important measurement is the symphysis-fundal height (SFH), especially if it increases rapidly.
• On ultrasound, a foetal abdominal circumference > 90th percentile is a clear warning sign.

More facts from the study questions

• Insulin resistance physiologically increases during pregnancy.
• It begins to rise from around 20 weeks' gestation and peaks around 32 weeks' gestation.
• Foetal hyperinsulinism acts as a growth factor and leads to disproportionate macrosomia.
• Growth of the trunk, abdomen and shoulder girdle is characteristically greater than that of the head.
• Foetal hyperglycaemia leads to osmotic diuresis.
• The resulting foetal polyuria is a typical cause of polyhydramnios.
• The increase in insulin resistance is driven by various placental and maternal hormones.
• These include human placental lactogen (hPL), progesterone, oestrogens, cortisol and prolactin.
• Severe malformations (embryopathy) are caused by hyperglycaemia during early organogenesis.
• This is typical of poorly controlled diabetes existing before conception.

Diagnosis

Preparation and procedure

• The test is performed in the morning on a fasting patient, after at least an eight-hour fast and after three days of a normal high-carbohydrate diet.
• The blood glucose measurement is taken from fluoride-inhibited venous plasma.

Cut-offs and diagnosis

• For a diagnosis of gestational diabetes, it is sufficient if a single value is met or exceeded.
• Pre-analytics play a crucial role: without glycolysis inhibition or immediate centrifugation, the values will be falsely low.

Keep learning in the app

Further reading (selection)

1. StatPearls: Gestational Diabetes (NCBI Bookshelf)
2. DocCheck Flexikon, Gestationsdiabetes
3. DocCheck Flexikon, Oraler Glukosetoleranztest

Cross-references