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Normal pregnancy

This is a state of relative insulin resistance secondary to the release of placental hormones such as cortisol, estradiol. HCG and human placental lactogen. The pancreas is however able to compensate and insulin production doubles by the end of pregnancy. Fasting glucose levels are reduced however in early pregnancy.

In a pregnancy complicated by diabetes there is therefore a tendency to early morning hypoglycaemia but a global increase in insulin requirements as the pregnancy progresses. This emphasises the need for good home monitoring and regular HbA1c estimations. In the most recent confidential enquiry into maternal deaths there were 2 deaths directly related to hypoglycaemia (1) and a Cochrane review of diabetes control in pregnancy they concluded that tight control was preferable to very tight control as the perinatal outcome was the same but with less episodes of hypoglycaemia (2). This raises the question of the definition of very tight control, which differed in the two articles in the review – one with fasting<4.4 and the other fasting and 2 hour post prandial <5.6. The generally accepted targets are fasting<5mmol/l and 2hour postprandial 7.8mmol/l. One way of achieving that outcome is with the basal-bolus regime – one long or intermediate acting insulin at night to provide basal control and bolus doses before meals (3). The frequency and timing of blood glucose estimation depends upon the woman’s blood glucose control.

Even with the best antenatal care fetuses are at risk of macrosomia. This can potentially be detected by fortnightly growth scans although estimates of fetal weight are much less accurate at extremes of weight (4). Unexplained stillbirth is becoming less common but is thought to relate to chronic hyperglycaemia causing fetal hyperinsulinaemia resulting in hypokalaemia, arrhythmias and death. Hypoxia in the presence of hyperglycaemia can also prompt lactic acidosis and death. Unfortunately no means of monitoring has been shown to predict stillbirth in these situations. In addition surveillance may be complicated by the presence of polyhydramnios and one retrospective study has concluded that the Dawes-Redman criteria may not be valid in the interpretation of computerised cardiotocographs of fetuses of diabetic women (5). However in the absence of good trial data most would agree on fortnightly growth scans with additional monitoring from 36 weeks.

In the presence of maternal microvascular disease there is additional risk of placental insufficiency resulting in growth restriction. This can be monitored in the usual way with regular ultrasound and additional Doppler and liquor volume estimation.

In the absence of complications, a vaginal delivery should be planned for 38-40 weeks. The caesarian section rate is usually 2-3 times the background rate at 40-60%. In a recent series the main reason for elective caesarians was elective repeats and for emergencies was fetal distress (6). This study also demonstrated a higher rate in Caucasian women with both Type 1 and Type 2 diabetes, compared to Asian women. The difference was most marked in Type 2 and may have been related to parity, which was significantly higher in the Asian population. Fetal macrosomia was also significantly greater in the Caucasian population, which may have contributed to their higher caesarian section rate although this was only documented as the reason for caesarian in 9/294 cases.

Labour and delivery

During labour blood glucose should be maintained between 4-6mmol/l to help prevent neonatal hypoglycaemia (7). This should be achieved by means of a dextrose infusion and sliding scale insulin infusion. Hyperglycaemia can precipitate fetal acidaemia and fetal heart rate abnormalities. The fetal heart should be monitored with continuous electronic fetal monitoring and there should be facilities for fetal blood sampling.

1.Why Mothers Die. Report on Confidential enquiries into Maternal Deaths in the United Kingdom 1994-1996.

2. Walkinshaw SA. Very tight versus tight control for diabetes in pregnancy. Cochrane database of Systematic reviews(computer file). (2): CDOOO226, 2000, Abstract

3. Nachum Z Ben-Shlomo I Weiner E Shalev e. Twice daily versus four times daily insulin dose regimens for diabetes in pregnancy: randomised controlled trial. BMJ. 1999; 319:1223-7, Abstract

4. Landon MB. Prenatal diagnosis of macrosomia in pregnancy complicated by diabetes mellitus. Journal of Maternal-Fetal Medicine.2000; 9:52-54, Abstract

5. Tincello DG, el-Sapagh KM, Walkinshaw SA. Computerised analysis of fetal heart rate recordings in patients with diabetes mellitus: the Dawes Redman criteria may not be valid indicators of fetal well-being. Journal of Perinatal medicine. 1998; 26(2):102-6, Abstract

6. Dunne FP, Brydon PA, Proffitt M, Smith T, Gee H, Holder RL. Fetal and maternal outcomes in Indo-Asian women compared to Caucasian women with diabetes in pregnancy. Q J Med 2000; 93:813-8, Abstract

7. Anderson O, Hertel J, Schmolker L et al. Influence of the maternal plasma glucose concentration at delivery on the risk of hypoglycaemia in infants of insulin-dependant diabetic mothers. Acta Paediatr Scand.1985; 74:268-73, Abstract