Back to Pregnancy
Control blood sugars. Poorly controlled diabetes
is associated with a higher rate of miscarriage,
which can be reduced to that of the background
population if good glycaemic control is established.
The miscarriage rate relates to HbA1c levels
and first trimester hyperglycaemia. Type 2 diabetics
on oral hypoglycaemic agents should be changed
to diet+/- insulin as oral hypoglycaemic agents
may not allow optimal control and are not licensed
Congenital anomalies are now the leading cause
of perinatal mortality and morbidity in diabetic
pregnancies. The incidence is three to four times
that of non diabetic pregnancies and is related
to hyperglycaemia. However, this can be reduced
with good glycaemic control, which needs to be pre
conceptual as fetal malformations occur before
the seventh gestational week (1,2).
Thus at routine presentation to antenatal clinic
any potential structural damage will have been
In vitro studies have identified three main
||Hyperglycaemia causes a reduction in myo-inositol,
which in turn reduces arachidonic acid and
prostaglandins. This causes glucose-induced
neural-tube closure defects in rodents but
can be prevented by supplementation with
myoinositol, arachidonic acid and prostaglandin
||Evidence for the involvement of free oxygen
radicals in diabetes related malformations
has been provided by the ability of oxygen
radical scavengers to reduce the frequency
of congenital malformations in rats (4).
||Maternal diabetes has been linked to disruptions
of DNA synthesis and structure; for example,
beta-hydroxybuterate has been shown in high
concentration to inhibit the pentose phosphate
pathway that usually provides ribose molecules
for nucleic acid synthesis. This has resulted
in neural tube defects (5).
Early morning hypoglycaemia is more common in
early pregnancy (see Antenatal
Care) as tighter control is established.
Both the woman and her partner must be made aware
of this and be able to deal with such events
by administering glucagon if necessary.
Pregnant women must also be made aware of the
dangers of hyperglycaemia and ketoacidosis.
||All pregnant women should receive folic acid
for at least 3 months preconceptually and until
12 weeks gestation.
||All pregnant women should be screened for retinopathy.
The presence and severity of retinopathy is strongly
predictive of fetal outcome (6).
In addition the severity is related to the degree
of progression during pregnancy. Those with minimal
or no retinopathy at the beginning of pregnancy
have a 10% chance of progression whilst those with
proliferative retinopathy have a 50% chance of
The deterioration is worst for those whose control
undergoes rapid improvement in early pregnancy.
Laser photocoagulation is safe in pregnancy and
should be used for those who develop proliferative
retinopathy. Fortunately post partum regression
||Renal function as assessed by urea and electrolytes,
creatinine clearance and proteinuria estimation
should be checked pre pregnancy. Diabetic nephropathy
is present in 5-10% of diabetic pregnancies (8).
For those with pre existing nephropathy, pregnancy
outcome is partly dependant on the degree of renal
impairment. Those with a creatinine clearance<50ml
or a serum creatinine >150μmol/l have a
much higher chance of poor pregnancy outcome. Renal
impairment is associated with prematurity, growth
restriction and perinatal mortality. Those with
severe renal insufficiency also risk permanent
deterioration of renal function.
||Those with hypertension pre pregnancy have a
higher risk of preeclampsia in pregnancy. Preconceptual
care should aim to optimise hypertension control.
Angiotensin converting enzyme inhibitors may cause
fetal renal impairment, growth restriction and
incomplete skull ossification and should therefore
be stopped and changed to safer alternatives such
as methyldopa or labetalol.
Pre conceptual care does improve outcome (9)
and is cost effective (10).
However, attendance is usually 25-35% in this country
and this was identified as one of the potential reasons
for suboptimal outcome in this country.
1. Steel JM, Johnstone FD, Hepburn DA, Smith AF. Can
pre pregnancy care of diabetic women reduce the risk
of abnormal babies? BMJ 1990; 301:1070-1074, Abstract
2. Miller E, Hare JW, Cloherty JP, Dunn PJ, Gleason
RE, Soeldner JS, Kitzmiller JL. Elevated maternal haemoglobin
A1c in early pregnancy and major congenital anomalies
in infants of diabetic mothers. N Engl J Med 1981;
304: 1331-4, Abstract
3. Baker L, Piddington R, Goldman A, Egler J.Myoinositol
and prostaglandins reverse the glucose inhibition of
neural tube fusion in cultured mouse embryos. Diabetologia
1990; 33:593-596, Abstract
4. Eriksson UJ, Borg LAH. Diabetes and embryonic malformations:
role of substrate-induced free oxygen radical production
for dysmorphogenesis in cultured rat embryos.Diabetes.1993;
5. Hunter ES, Sadler TE, Wynn RE. A potential mechanism
of DL-B-hydroxybuterate-induced malformations in mouse
embryos. Am J. Physiol. 1987; 253:E72-E80, Abstract
6. Klein BE, Klein R, Meuer SM, Moss SE. Does the
severity of diabetic retinopathy predict pregnancy
outcome? J. Diabetes complications. 1988;2:179-184, Abstract
7.Chew E et al. Metabolic control and progression
of retinopathy: the diabetes in early pregnancy study.
Diabetes Care. 1995; 18:950-954, Abstract
8.Landon MB, Gabbe SG. Diabetes mellitus and pregnancy.
Obstet Gyn Clin North Am 1992; 19:633-48, Abstract
9. Fuhrmann K, Reiher H, Semmler K, Fischer F, Fischer
M, Glockner E. Prevention of congenital malformations
in infants of insulin-dependent diabetic mothers. Diabetes
care. 1993; 6:219-23, Abstract
10. Elixhauser A et al. Cost benefit analysis of preconceptual
care for women with established diabetes mellitus.
Diabetes care. 1993; 16(8): 1146-57