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
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
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.
Timing of Delivery
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
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