For decades, due to the paucity of evidence, hot debate has raged as to whether gestational diabetes mellitus (GDM) should be diagnosed and treated. However, in recent years a number of large, multicentre studies have provided good-quality evidence to say that GDM is no longer ‘a diagnosis looking for a disease’.1
The current diagnostic criteria for GDM are based on the likelihood of later development of type 2 diabetes, rather than on pregnancy outcome. The diagnosis of GDM varies between countries. For example, when diagnostic criteria were reset in New Zealand, in 1992, they were adjusted to reduce the prevalence of GDM so that obstetric services could cope with the numbers and offer treatment to those who would benefit the most.
We waited with bated breath for the results of the Hyperglycaemia and Adverse Pregnancy Outcome (HAPO) study, involving 25,000 pregnancies, to demonstrate the level of hyperglycaemia that results in excessive adverse pregnancy outcomes. A linear association between maternal hyperglycaemia and increased rates of adverse outcomes was found, starting from a relatively low level of hyperglycaemia, with no clear inflection point at which to trigger screening.2 Even mild GDM can influence pregnancy outcomes.
Following the HAPO study, the International Association of Diabetes and Pregnancy Study Groups (IADPSG) Consensus Panel convened and recently published recommendations for diagnosis (one or more post-75g oral glucose tolerance tests [OGTT] plasma glucose values > 5.1, 10.0, 8.5 mmol/L for fasting, one, and two-hour glucose respectively).3 The ripples are spreading and healthcare providers are assessing how this may impact their provision of diabetes in pregnancy care.
To treat or not to treat
During the 1990s, a large case control study assessing pregnancy outcomes in treated versus untreated GDM showed a composite adverse outcome, including large for gestational age (LGA), neonatal respiratory disease, hypoglycaemia, hyperbilirubinaemia, shoulder dystocia and stillbirth, was present in 59 per cent untreated compared with 18 per cent treated and 11 per cent for the non-diabetic population.4 Those women with mild GDM (fasting glucose less than or equal to 5.2 mmol/L) were analysed separately and treatment reduced the rate of LGA from 20 per cent to ten per cent in this subgroup.
Other adverse outcomes known to be associated with hyperglycaemia include caesarean delivery, spontaneous preterm delivery, preeclampsia and offspring’s long-term relative weight and degree of glucose tolerance, or GDM during female offspring’s pregnancies.5
Fetuses of women with mild GDM lack the ventricular hypertrophy and diastolic dysfunction that is common in fetuses of diabetic mothers, but they have decreased ventricular myocardial performance late in gestation when compared with fetuses of non-diabetic women.6
The Australian Carbohydrate Intolerance Study in Pregnant Women (ACHOIS), a randomised treatment trial for GDM, concluded that treatment of milder carbohydrate intolerance significantly reduced serious perinatal morbidity, especially LGA and birth weight over 4000 g.7 There were also lower rates of depression and higher quality of life scores, consistent with improved health status in the intervention group.
A multicentre randomised trial of treatment for GDM showed that neonatal fat mass, shoulder dystocia, caesarean delivery and hypertensive disorders of pregnancy are reduced by treatment.8 Therefore, strong evidence now exists that the benefit outweighs the risks associated with the diagnosis and treatment of mild GDM.
Diabetes education and oversight by a multidisciplinary diabetes in pregnancy team is important. Mild GDM diagnosed at 26 weeks may advance to significant insulin resistance by late gestation.
Close glucose self-monitoring has been shown to reduce rates of fetal overgrowth and gestational weight gain in women with mild GDM9, being helpful to both the clinician and the woman. If not anaemic, a monthly glycated haemoglobin (HbA1c) gives a good overview of glucose control (target under six per cent).
Since birth weight is influenced by maternal weight gain, women with a high booking BMI should be encouraged to minimise weight gain in pregnancy. Dietary compliance is reflected by weight gain and should be monitored.
Ultrasound for fetal growth is recommended at least at diagnosis of GDM and again near delivery, using both serial biometric and customised growth charts to guide management. If the estimated fetal weight on scan is greater than 4000 to 4500 g, a caesarean section should be considered to prevent birth trauma.
Induction of labour may be indicated if the intrauterine environment is suboptimal or when the risk of continuing the pregnancy outweighs the benefit. When planning an early delivery, remember that reduced fetal lung maturity is associated with hyperglycaemia.
The need for augmentation and instrumental delivery in diabetic pregnancies is associated with shoulder dystocia and birth trauma.
With the incidence of GDM on the increase and the obesity epidemic in full swing there is often a feeling of overwhelming helplessness. However, basic measures such as dietary modification, exercise and lifestyle change are very effective in normalising blood glucose and thereby reducing the risk of maternal and perinatal morbidity. There is growing consensus on the safety of moderate exercise in pregnancy and its benefit in the management of GDM.
Oral hypoglycaemic agents, such as glyburide10 and metformin11, have been found to be safe and efficacious in the treatment of GDM. Meta-analysis of two studies involving 90 women showed a significant reduction in caesarean section rates, but no change in other pregnancy outcomes, in women receiving oral hypoglycaemic agents compared to insulin.12
Insulin is indicated when glycaemic goals or ideal fetal growth cannot be achieved with lifestyle change, with or without oral hypoglycaemic agents.
Hypoglycaemic agents can be discontinued immediately after delivery, but glucose self-monitoring should be continued for a few days to ensure a prompt return to normoglycaemia.
Since GDM is a marker of insulin resistance, an oral glucose tolerance test should be done at six to 12 weeks postpartum to exclude diabetes or impaired glucose tolerance (IGT). If negative, regular diabetes screening should continue thereafter.
- Hunter DJS, Milner R. Gestational diabetes and birth trauma [letter]. Am J Obstet Gynecol.1985;152(7):918-19.
- The HAPO study Cooperative Research Group. Hyperglycemia and adverse pregnancy outcomes. N Engl J Med. 2008; 358(19):1991-2002.
- IADPSG consensus panel. Diab Care 2010; 33(3)676-82.
- Langer O, Yogev Y, Most O, Xenakis EMJ. Gestational diabetes: The consequences of not treating. Am J Obstet Gynecol. 2005;192(4):989-97.
- Pettitt DJ, Knowler WC. Long-term effects of the intrauterine environment, birth weight and breast-feeding in Pima Indians. Diab Care 1998; 21(Suppl. 2):B138-41.
- Wong ML, Wong WHS, Cheung WF. Ultrasound Obstet Gynecol. 2007; 29(4):395-400.
- Crowther CA, Hiller JE, Moss JR, McPhee AJ, Jeffries WS, Robinson JS; Australian Carbohydrate Intolerance Study in Pregnant Women (ACHOIS) Trial Group. The effect of treatment of gestational diabetes mellitus on pregnancy outcome. N Engl J Med. 2005; 352(24):2477-86.
- Landon MB, Spong CY, Thom E, et al. A multicenter randomized trial of treatment for mild gestational diabetes. N Engl J Med. 2009; 361(14):1339-48.
- Hawkins JS. Glucose monitoring during pregnancy. Curr Diab Rep. 2010;10(3):229-34.
- Langer O, Conway D, Berkus M, Xenakis EMJ, Gonzales O. A comparison of glyburide and insulin in women with gestational diabetes mellitus. N Engl J Med. 2000; 343(16):1134-8.
- Rowan JA, Hague WM, Gao W, Battin MR, Moore MP, for the MiG Trial Investigators. Metformin versus insulin for the treatment of gestational diabetes. N Engl J Med. 2008; 358(19):2003-15.
- Alwan N, Tuffnell DJ, West J. Treatments for gestational diabetes. Cochrane Database of Systematic Reviews 2009, Issue 3.