Diabetes in pregnancy

Published on 09/03/2015 by admin

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Chapter 46 Diabetes in pregnancy

Nikki Whelan

Diabetes in pregnancy is either preexisting/pregestational diabetes or acquired gestational diabetes.

Physiology and pathophysiology

Maternal glucose homeostasis

• Normally, blood sugar levels are stable in all trimesters. This is achieved by doubling the insulin secretion from the end of the first trimester to the end of the third trimester.
• In early pregnancy, raised oestrogen and progesterone levels cause cell hyperplasia in the pancreas, which results in a rise in insulin secretion and an increase in fat stores.
• In the second and third trimesters, increases in the diabetogenic hormones human placental lactogen, prolactin and free cortisol cause insulin resistance and lipolysis. Therefore, the increased insulin concentration is counterbalanced by increasing insulin resistance, the mechanism of which is not clearly understood.
• Fasting blood glucose level (BGL) decreases, while postprandial BGL increases in pregnancy. The pregestational diabetic is at risk of hypoglycaemia in early pregnancy and ketoacidosis in later pregnancy, as the demand for insulin is increased.
• Fetal glucose homeostasis: maternal glucose crosses the placenta freely by facilitated diffusion. Therefore, the mother is responsible for regulating fetal blood sugar levels. Fetal insulin appears in the circulation at the end of the first trimester, but the exact role of fetal insulin is uncertain and it may act by promoting growth. It normally plays no role in blood glucose homeostasis. In response to fetal hyperglycaemia due to elevated maternal blood sugar, fetal pancreatic cells hypertrophy, leading to inappropriate release of insulin.

Pregestational diabetes

Effects on pregnancy

Maternal effects

Increased risks of:

• polyhydramnios
• pre-eclampsia
• placental abruption
• infection, including urinary tract and candidiasis
• diabetic ketoacidosis
• trauma during delivery
• caesarean section

Fetal effects

• Congenital malformation: pregestational diabetics (both type 1 and type 2) have an increased risk of fetal malformation with increasing levels of hyperglycaemia (see Table 46.1). Literature suggests only small increases in HbA1c are associated with increased risk.
• Type 1 diabetics with an HbA1c of 7.2% (normal range 6%) have double the risk of fetal malformation and type 2 diabetics may have twice the risk of fetal malformation of the non-pregnant population with a normal HbA1c. If their HbA1c rises to 7.3%, their risk of fetal malformation may be as high as 11%.
• Malformations include neural tube defects, cardiovascular and vertebral defects. The risk of malformation is proportional to imperfect metabolic control during organogenesis; improved blood sugar control decreases anomalies. Many malformations can be diagnosed by mid-trimester ultrasound.
• Abortion and perinatal mortality: diabetic women have higher abortion rates. An HbA1c of 6.5% increases the risk of spontaneous abortion by 3%. Perinatal mortality rates also rise in proportion to the rise in mean BGL. The exact mechanisms for the increased risk demise are uncertain.
• Abnormal fetal growth: there is an increase in the incidence of large-for-dates and small-for-dates fetuses, and consequently fetal morbidity. Macrosomia in all organs (except the brain) is due to an increase in cytoplasmic mass. Macrosomic babies are at risk of trauma during delivery, with definite risk of shoulder dystocia in the diabetic mother with a fetus >4000 g. Intrauterine growth restriction (IUGR) may be a complication of placental vasculopathy and may be related to underlying renal disease or the development of pre-eclampsia.
• Preterm delivery is common.

Table 46.1 Maternal diabetes and risk of congenital malformation

Congenital malformation Increased risk over non-diabetics
Cardiac 4 times
Neural tube defects 2–10 times
Gastrointestinal atresia 3–10 times
Caudal regression 200 times (though still rare)
Urinary tract 10 times

Neonatal effects

• Respiratory distress syndrome: carries six times the risk of non-diabetics. Fetal hyperinsulinaemia results in reduced pulmonary phospholipid production and a decrease in surfactant.
• Hypoglycaemia: 50% of babies of insulin-dependent diabetic mothers have blood sugar levels below 2 mmol/L due to fetal hyperinsulinaemia and discontinuation of the maternal glucose supply.
• Hypocalcaemia is present in 25%–50% of infants.
• Polycythaemia and jaundice: polycythaemia is due to an increase in erythropoietin caused by raised fetal insulin. Jaundice, which occurs in up to 50% of babies, is mainly due to elevated red cell destruction and immaturity of the liver.
• Macrosomia is common.
• Hypertrophic cardiomyopathy is usually reversible.
• Risk of diabetes: when one parent is diabetic, this is associated with a 3% risk of the offspring developing diabetes in 20 years. If both parents are diabetic, the risk is 20%.

Management

Prepregnancy counselling

General measures

• Stop smoking.
• Reduce alcohol intake.
• Review all medications, including complementary medications, for safety in pregnancy.
• Screen and vaccinate for infectious diseases, including rubella, varicella, bordetella pertussis and cervical human papillomavirus (HPV).
• Provide weight management, nutrition and exercise advice.
• Provide contraceptive advice until conception is desired.

Diabetes-specific measures

• The multidisciplinary team should include an obstetrician, physician, diabetes educator and dietician (wherever possible).
• Achieve optimal glycaemic control: HbA1c should be maintained in the normal range wherever possible. This should be possible in most women with type 2 diabetes, but may not be possible in all women with type 1 diabetes.
• The woman should take folic acid (5 mg daily).
• Medications include the use of the newer rapid-acting insulin analogues and insulin pump therapy. Oral agents should be ceased and switched over to insulin (e.g. basal bolus regimen). Although they are probably not teratogenic, the oral agents are not used routinely.
• Antihypertensive agents should be suitable for continued use in pregnancy.
• Statins should be ceased.
• Review diabetic complications, including retinopathy, nephropathy, macrovascular disease and autonomic neuropathy.
• Assess thyroid function and screen for other autoimmune diseases where appropriate.

Antenatal management

Management should be by a multidisciplinary team wherever possible.

Medical

• Assess BGL control with HbA1c and reinforce the necessity for regular self-monitoring of BGLs.
• Aims: fasting BGL of 4.0–5.5 mmol/L, 1 hour postprandial <8.0 mmol/L, and 2 hours postprandial <7.0 mmol/L.
• Monitor with HbA1c every 4–8 weeks.
• Advise that hypoglycaemia is common, especially overnight from 6–18 weeks, and that insulin requirements may increase substantially in late second trimester with increasing insulin resistance.
• Insulin requirements may reduce from 32 weeks gestation and should prompt assessment of fetal wellbeing if this is >5%–10%.
• Assess diabetic complications if no prepregnancy counselling has been performed, especially retinopathy (regular formal eye examinations) and nephropathy (24-hour urine analysis, spot albumin:creatinine ratio, dip stick urine analysis and serum electrolytes, creatinine and urea).

Obstetric management

• Offer nuchal translucency scan and serum screen at 12–13 weeks gestation for aneuploidy. If not performed, a dating scan should be performed.
• Perform a fetal morphology scan at 18–20 weeks and in selected cases repeat a morphology scan at 24 weeks, especially targeting the heart.
• Assess fetal growth and wellbeing at 28–30 weeks and at 34–36 weeks, or more frequently in the presence of medical or obstetric complications.
• Aim for delivery at term unless obstetric or medical complications arise (e.g. fetal macrosomia, polyhydramnios, poor metabolic control, pre-eclampsia or IUGR).
• Vaginal delivery is preferable, unless obstetric or medical contraindications exist (e.g. risk of shoulder dystocia increases with birthweight >4000 g).
• Anticipate the need for neonatal nursery admission if delivery is earlier than 36 weeks or poor metabolic control is present.

Labour

Monitor BGL 1–2 hourly, aiming for 4–7 mmol/L, which can be achieved with various regimens, including:

• insulin/dextrose infusion
• insulin/dextrose infusion if BGL is <4 mmol/L or >7mmol/L
• subcutaneous insulin injections
• insulin pump therapy

Postpartum

• Type 1 diabetes: insulin requirements fall rapidly postdelivery, and hence the primary goal is to avoid hypoglycaemia.

• Close monitoring is needed.
• Breastfeeding mothers need to be encouraged to test prefeeds and postfeeds to check for hypoglycaemia.

• Type 2 diabetes: many women can be managed with diet alone; some will need ongoing insulin therapy.

Contraception

There is no evidence that any present contraceptive methods are contraindicated in diabetes.

Gestational diabetes

Definition. This is the development of abnormal glucose tolerance during pregnancy in a woman who did not have diabetes before pregnancy.

Incidence. International criteria differ as to diagnosis, and so incidence ranges from 1%–10% at 26 weeks gestation. Most Australian centres report a 5%–9% incidence. These may include previously undiagnosed non-insulin-dependent diabetics. The Hyperglycaemia Adverse Pregnancy Outcome (HAPO) Study suggests there is a continuous, linear association between BGLs and major adverse pregnancy outcomes.

Diagnosis

The International Association of Diabetes in Pregnancy Group (IADPG) is developing a position statement on screening and diagnosis of hyperglycaemic disorders in pregnancy, based largely on the HAPO data. It is hoped this will standardise criteria for these definitions worldwide.

Gestational diabetes has increased perinatal morbidity, with characteristics for babies similar to preexisting diabetes. These include fetal macrosomia, neonatal hypoglycaemia, hyperbilirubinaemia and respiratory distress syndrome, with a probable long-term risk of obesity and diabetes.

Between 4% and 9% of women have plasma glucose >8 mmol/L at 2 hours after a non-fasting 75 g oral glucose load. The 95th percentile for true fasting BGL in pregnancy is >5.5 mmol/L.

WHO criteria

• impaired glucose tolerance: a fasting serum glucose of <7.8 mmol/L and/or a 2-hour blood sugar level >7.8 and <11.1 mmol/L after a fasting 75 g oral glucose load
• diabetes: a fasting BGL of ≥7.8 mmol/L and a 2-hour BGL of ≥11.1 mmol/L after a 75 g glucose load

Australasian Diabetes in Pregnancy Society criteria

• gestational diabetes: a fasting BGL of >5.5 mmol/L and a 2-hour BGL of >8.0 mmol/L after a 75 g glucose load (Australia) and >9.0 mmol/L (New Zealand)

Screening

Risk factors

• family history of type 2 diabetes, personal or family history of gestational diabetes or glucose intolerance
• past history of macrosomic baby >4000 g
• poor obstetric history (e.g. intrauterine fetal death)
• belonging to a high-risk ethnic group, such as Polynesian, Southern Asian (Indian), Middle Eastern or other Asian origin
• Australian Aboriginal or Torres Strait Islander background
• being overweight (body mass index >25) or obese (body mass index >30)
• maternal age >30 years
• previous abnormal glucose tolerance test (recurrence in 60%)
• multiple pregnancy
• glycosuria

Screening methods

• Risk factors only: with this method 30% of the population will have a glucose tolerance test and the false-negative rate is 40%.
• Random BGL sampling has poor sensitivity.
• Non-fasting glucose challenge: the screening test is performed at 24–28 weeks gestation with a non-fasting sugar load of 75 g. If >8.0 mmol/L is used as the cutoff level, 16% of the population will screen positive and 16% of these will have gestational diabetes. The false-positive rate is 10%.
• It is likely the IADPG will recommend abandoning the challenge test and move to a 75g oral glucose tolerance test (OGTT) with a fasting and a 1-hour level for diagnosis of gestational diabetes.
• International studies show the incidence of gestational diabetes is increasing over time, reflecting the increase in incidence of being overweight and obese in the world.
• Between 2000–01 and 2005–06, the incidence of confinements with gestational diabetes in Australia increased by 22%.

Management

Medical management

• a team approach with an obstetrician, endocrinologist, diabetic nurse educator and dietitian
• patient education mandatory
• modifying dietary habits and increasing physical activity levels (including resistance work)
• limit weight gain, especially in obese women (body mass index >30) to 5 kg
• monitoring by self-testing with:

• fasting BGL of <5.5 mmol/L
• 1-hour postprandial BGL of <8 mmol/L
• 2-hour postprandial BGL of <7 mmol/L

• insulin treatment: shown to reduce the rate of large-for-gestational-age infants in pregnancies with levels consistently higher than above treated only by diet
• metformin: being used with caution in New Zealand and Australia following the MiG Study (a randomised control trial of metformin versus insulin for women who met the usual criteria for commencing insulin with no differences in major outcomes in the two arms); may be suitable for 50% of women with gestational diabetes who are currently being treated with insulin
• HbA1c levels (may be used as ancillary testing)
• in labour: regular BGL tests, especially in women treated with insulin and or oral agents (insulin or dextrose infusion are rarely necessary)
• immediately postpartum, cease insulin and monitor BGL
• postpartum glucose tolerance test: performed at 6 weeks
• 1–2 yearly fasting or OGTT for early detection of type 2 diabetes

Obstetric management

• Fetal growth and surveillance of fetal wellbeing: at 28–30 and 34–36 weeks gestation to monitor growth; more frequently if complications develop.
• Timing of delivery: if uncomplicated, await spontaneous labour, but avoid postdates.

Postpartum follow-up

• At discharge, counsel regarding contraception and recurrence risk. The woman with gestational diabetes has a long-term risk of developing non-insulin-dependent diabetes of up to 50%, compared with 7% of controls. Risk of progression to type 2 diabetes can be reduced by diet and exercise (up to 50%), metformin (up to 30%) and acrabose (up to 25%).

Further reading

Australasian Diabetes in Pregnancy Society. Consensus guidelines for management of patients with type 1 and type 2 diabetes in relation to pregnancy. Medical Journal of Australia. 2005;183(7):373-377.

Australian Institute of Health and Welfare (AIHW):. Templeton M, Pieris-Caldwell I. In Gestational diabetes mellitus in Australia, 2005–06. Diabetes Series No. 10. Cat. No. CVD44. Canberra:: AIHW; 2008.

HAPO Study Cooperative Research Group. Hyperglycemia and adverse pregnancy outcomes. New England Journal of Medicine. 2008;358(19):1991-2002.

Rowan J.A., Hague W.M., Wanzhen G., et al. for the MiG Trial Investigators 2008 Metformin versus insulin for the treatment of gestational diabetes. New England Journal of Medicine. 2008;358(19):2003-2015.

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