GDM (Gestational Diabetes Mellitus) is a carbohydrate intolerance with onset OR first recognition during the present pregnancy. It does not matter if insulin is used as treatment, it does not matter if the intolerance continues post-pregnancy, and it does not preclude that the intolerance may have existed prior to the pregnancy. However, it would not be appropriate to label women with KNOWN pre-existing diabetes as having GDM. They would be said to have pre-gestational DM.
GDM is diabetes mellitus discovered during pregnancy.
Diabetes could generally be chalked up to either a deficiency in insulin secretion from pancreatic ß cells, or a decrease in insulin sensitivity in glucose requiring cells (or both). Under normal conditions, ß cells increase insulin secretion when blood glucose levels rise in order to maintain normoglycemia. As pregnancy progresses, insulin sensitivity decreases (around 50%+ by the end) while hepatic glucose production increases. These changes are likely mediated, at least in part, by placental factors and hormones (human placental lactogen, prolactin, estrogen and progesterone) given that these changes mostly revert once delivery occurs. GDM results from the inability of pancreatic ß cells to increase insulin production enough to deal with the decreased maternal insulin sensitivity and the increased maternal blood glucose. Data suggest that this inability is not caused by pregnancy, but is rather unmasked by pregnancy. GDM indicates an increased risk of developing type 2 diabetes mellitus later in life: 9% in Caucasians to 25% in Mediterraneans and East Indians. It is potentially much higher if the women are followed long enough (40-70%).
There is much debate around the screening and treatment for GDM, but the SOGC (The Society of Obstetricians and Gynaecologists of Canada) has published some guidelines. The recommendations include routine screening during 24-28 weeks of pregnancy with a GCT (glucose challenge test) which is a non-fasting 50g oral load of sugar taken over no more than 5 minutes with a blood glucose measurement after 60 minutes. There are some doctors who choose not to screen anyone based on the lack of evidence of benefit from screening. There are also some criteria for identifying low risk women who may not need to be screened i.e. age<25, pregnant BMI≤27, Caucasian or other low risk population, no history of GDM, or no family history of DM.
If a woman is sent for GCT, a reading higher than 10.3 mmol/L (206 mg/dL) yields an automatic diagnosis of GDM. Something in the range of 7.2-7.8 mmol/L (130-140 mg/dL) up to 10.3 mmol/dL triggers further investigation. Whether the lower limit is 7.2, 7.3 or 7.8 is up to the clinician as they try to optimize the false-positive to false-negative ratio. Further investigation involves an OGTT (oral glucose tolerance test) which is a fasting test with a 100g oral sugar load with blood samples taken at baseline and 1, 2, and/or 3 hours later. Some doctors may also use a 75g version of the OGTT for the second stage (especially in the USA). Abnormal values for the OGTT are a baseline value greater than 5.25 mmol/L (95 mg/dL), a 1 hour greater than 10 mmol/L (180 mg/dL), a 2 hour greater than 8.6 mmol/L (155 mg/dL), or a 3 hour greater than 7.8 mmol/L (140 mg/dL). More than 1 abnormal value is diagnostic for GDM.
Once a woman has been diagnosed with GDM there is a recommendation that she be tested with the 75g OGTT 6-12 weeks post-partum to see if the glucose intolerance persists. It also opens the door to a multitude of considerations during the current pregnancy. GDM potentially increases the risk of perinatal mortality, although that is controversial. GDM is potentially linked to hypertensive disorders of pregnancy (pre-gestational diabetes is definitely linked, but the link with GDM is more tenuous). GDM has been linked with fetal macrosomia (>4kg) which has implications for dystocia (obstruction of labour) and shoulder dystocia (obstruction of labour after delivery of the head due to shoulders being stuck). GDM increases the risk of dystocias even if the fetus is of normal size. Shoulder dystocia has implications for brachial plexus injury. GDM pregnancies have an increased rate of C-section due to these concerns. There is currently no formal indication for delivery prior to 40 weeks with GDM, but many clinicians suggest this due to the known risk of fetal demise in pregnancies where glycemic control has not been tight.
Management of GDM is usually dietary. The goal is to stabilize blood sugar levels by eating smaller more frequent meals, substituting simple carbohydrates for complex ones, and limiting daily caloric intake. The most common approach seems to be to attempt to match the blood glucose profiles of pregnancy matched non-GDM women. Caloric restriction could be problematic if is leads to increased maternal ketone levels which could have negative impacts on baby’s IQ. Pharmacologic therapy usually involves insulin. Both long and short acting forms have been shown to be safe. For women who would rather not inject themselves daily, both metformin and glibenclamide (glyburide) have been used safely in pregnancy. Metformin decreases hepatic production of glucose and increases insulin sensitivity. Glibenclamide increases pancreatic insulin secretion.
Here are the SOGC guidelines
Medscape has a great section on treatment for GDM
Here is a great review paper on GDM in general. Gestational diabetes mellitus: definition, aetiological and clinical aspects