Introduction

Diabetes in Pregnancy

Diabetes (DM), whether pre-existing (type 1 or type 2) or diagnosed during pregnancy (gestational diabetes), is the most common endocrine problem in pregnancy. At least 1 in 250 pregnancies is complicated by pre-existing diabetes. In the last decade, type 2 diabetes in pregnancy has become more common. This is in part due to earlier age of onset of diabetes, the increasing age of the maternal population, and the obesity epidemic a, b, c.

Adverse outcomes such as congenital anomalies and perinatal mortality is increased 2-4 fold in women with pre-exsisting diabetes over women without diabetes. Over the past 10 years adverse outcomes have risen in women with type 2 diabetes. Hyperglycemia, during organogenesis, in the first 3 to 8 weeks after conception, is a major causal factor in the development of anomalies. Studies have shown that women who achieve recommended glucose targets prior to and during pregnancy reduce the risk for malformations to that of the population without diabetes.

Sadly, only twenty-five per cent of pregnancies among women with pre-exsisting diabetes are planned. Of these pregnancies only 1 in 3 pregnant women with preexisting diabetes attended available preconception clinics which have been shown to help improve pregnancy outcomes.

Quite apart from those women known to have diabetes, there are an increasing number of pregnant women who have undiagnosed type 2 diabetes or impaired glucose tolerance. Thus, those women at risk for diabetes need to be identified prior to pregnancy or early as possible in the pregnancy to correct disturbances in glycemia to minimize consequences to mother and baby.

Gestational diabetes Mellitus (GDM) on the other hand, is glucose intolerance with onset or first recognition during pregnancy. Its prevalence is population-specific and reflects the underlying rise of T2DM in the general population. In Canada, its prevalence varies from 3.7% in the multiethnic, non-Aboriginal population to 8-18% in Aboriginal populations.

There are implications of GDM not only on the mother but also to the baby. Although it usually is resolved postpartum, it carries a high risk of subsequent Type 2 diabetes (T2DM) for the mother. Women who develop GDM have a 20 % increased risk of developing Type 2 diabetes within ten years of the affected pregnancy f.

For the babies of mothers with GDM and also those with preexisting diabetes, there are both neonatal & long-term risks to be avoided. High maternal glucose in second and third trimesters increase the risk of macrosomia (fatness), increasing the risk of birth trauma and complicated delivery as well as neonatal hypoglycaemia. In the long term, there are also increased risks of obesity and the development of diabetes due to epigenetic influences. Studies have also shown that an increased abdominal girth at about 28 weeks gestation can predict increased weight & fatness at birth g, h.

For all of these reasons, achieving glucose targets in pregnancy is paramount. Women with gestational diabetes may manage with nutrition therapy alone and or may require insulin. Pregnant women with type 2 diabetes will need to stop oral antihyperglycemic agents and initiate insulin. For those women already on insulin there will be dramatic increases up to two to three times the doses prior to pregnancy. All women with GDM or pre-exsisting diabetes should receive nutrition counseling and be taught to monitor blood glucose frequently for a healthy pregnancy and to prevent adverse outcomes.


References

a Nice Guidance Summary BMJ 2008
b Feig DS, Lancet 2002
c Lipscombe L. Lancet 2007
d Macintosh et al, The Confidential Enquiry into Maternal and Child Health(CEMACH) study 2006
e Hillman et al, Diabetes Care 2006
f Feig D CMAJ 2008
g Ogata et al: JAMA, 1980
h Dabelea D Diabetes Care. 2007


Objectives

This website should improve your knowledge and understanding of diabetes management in pregnancy

Acknowledgements

Much of the information on this site is taken from the Canadian Diabetes Association Clinical Practice Guidelines 2008, more specifically pages S168-S180.