The body controls glucose metabolism through excretion of insulin from the pancreas. Those unable to produce, release, or make use of the necessary amounts of insulin are said to have diabetes mellitus.
Pregnancy affects glucose metabolism. The placenta produces hPL (Human Placental Lactogen) in large quantities that decreases glucose uptake an promotes lipolysis, leading to increases in circulating free fatty acids. The placenta also produces large amounts of estrogen, progesterone and insulinase, all of which have the effect of increasing the insulin requirements of the mother.
Women with pre-existing diabetes (Type 1 or Type 2) are said to have pre-gestational diabetes. We find it useful to further categorize these women according to White’s Criteria:
- Class B – onset over age 20, for less than 10 yr
- Class C – onset age 10-19, for less 19 yrs
- Class D – onset < age 10, for more than 20 yr
- Class F -nephropathy
- Class R – proliferative retinopathy
During the course of their pregnancy, insulin requirements usually change, typically with increased insulin needs early, then less, then more insulin as the pregnancy advances, sometimes with a drop in insulin requirements towards the end of pregnancy.
In managing these pregnant women, we aim for very tight control of their blood sugars, tighter than they normally would expect. The reason for this tight control is to minimize the additional risks of pregnancy complicated by diabetes, namely:
- Increased risk of miscarriage
- 3-fold increase in major malformations
- 5-fold increase in stillbirth
- 3-fold increase in neonatal death
- 5-fold increase in respiratory distress syndrome
- 4-fold increase in preterm deliveries <37 weeks
- 8-fold increase in Large for Gestational Age infants
- 4-fold increase in cesarean sections, approaching 50%
- More than 50-fold increase in shoulder dystocia at delivery, leading to about a 2% Erb’s palsey risk
- Increased risk of polyhydramnios, pre-eclampsia, heart disease, thyroid disease, retinopathy, and
- Increased risk of maternal diabetic ketoacidosis
With good control, these risks can be substantially reduced. Good control means:
- FBS ≤ 95
- 1-hour PP ≤ 140
- 2-hour PP ≤ 120
- HgbA1C < 6%
To accomplish this tight control patients usually respond best to multiple insulin injections each day, with a varying mixture of longer and shorter acting insulin.
Some insulins are better for use during pregnancy than others, reflecting their varying abilities to cross the placenta and be immunogenic. Usually, Lantus insulin is avoided and NPH and Regular insulin are used.
Ideally, patients with pregestational diabetes will enter the perinatal care system prior to their pregnancy, so that gycemic control is already achieved and preconceptual counseling completed. Because hyperglycemia is teratogenic, with heart defects being the most commen, it is best to initiate tight control prior to attempting to conceive. Frequently, this ideal is not met.
The best outcomes occur when a team approach is taken, including obstetricians, endocrinologists, dieticians, and supporting laboratory specialists, all skilled in managing these high risk patients.
Initial obstetrical care of these patients includes all of the normal prenatal evaluation, plus:
- Hemoglobin A1c every 4 weeks as a long term measure of glycemic control
- Glucose fingersticks taken and recorded at least 4 times daily
- Baseline TSH and FT4 as thyroid disease is a common association with diabetes
- Baseline eye evaluation with a retinologist, as retinopathy can worsen during pregnancy
- Baseline ECG since cardiovascular disease is more common among these patients
- Serum creatinine (repeated in 2nd and 3rd trimester) since nephropathy may not be picked up otherwise.
- Urine protein/glucose dipsticks at each visit, watching for the development of pre-eclampsia or renal disease
- Urine protein/creatinine ratio (repeated in each trimester) as a useful surrogate to the annoying and often inaccurate 24 hour urine protein
- 1st trimester ultrasound scanning for accurate gestational age and nuchal translucency, to screen for anomaly
- Usually an increase in calories of 250 to 300 per
The patients are seen every 2-4 weeks. By the 20th week of pregnancy, we prefer that all of these patients undergo a detailed fetal anatomic ultrasound survey, looking for abnormalities.
By the 32nd week of pregnancy, we usually initiate sequential fetal monitoring:
- Weekly non-stress testing with EFM to screen for problems with fetal well-being. We’ll increase this to twice weekly NSTs at the 34th
- Periodic assessments of amniotic fluid volume to assure the absence of oligohydramnios and deal effectively with polyhydramnios
- Periodic fetal weight estimates to assure a normal growth pattern and allow earlier intervention in the event of abnormal growth.
40 years ago, a common protocol was to perform elective cesarean section on diabetic patients at 36 weeks, because to wait longer risked an unacceptable number of stillbirths. We don’t practice that way anymore because the combination of our much tighter glycemic control and antepartum monitoring have made unexpected stillbirths a rare event, and also because elective delivery at 36 weeks carries an unacceptably high risk of neonatal complications from immaturity.
Instead, we will generally induce labor at term, between the 39th and 40th week of gestational age, if the cervix is favorable, although some physicians will continue to monitor past the 40th week.
For estimated fetal weights > 4500 grams, we recommend a scheduled cesarean section, and consider the cesarean with the patient for those > 4000 grams.
This is done to try to reduce the risk of shoulder dystocia and Erb’s Palsy.
Pregnancy has a tendency to push people toward diabetes. The placental hormones create some degree of insulin resistance; there are increased adipose stores, increased caloric intake and decreased maternal activity, accompanying markedly increased glucose needs, mostly for the fetus.
For most women, this nudge toward diabetes is not a problem, but for a few more vulnerable women, they can become diabetic, in degrees ranging from mild to severe.
Depending on the severity, there are risks associated with this diabetic state that include all of the risks associated with pregestational diabetes. The more severe the metabolic abnormality, the greater the risk.
Many physicians favor screening all pregnant patients between 24 and 28 weeks for gestational diabetes. In the U.S., the most common method involves giving a 50 gram glucose liquid meal, and drawing a blood glucose level 1 hour later. If the glucose level exceeds 140 (some say 135, some say 130), then the patient undergoes a full 3-hour glucose tolerance test following a 100 g glucose load. If any two of the four values from the GTT are elevated, then gestational diabetes is diagnoses.
- Other physicians favor a one-step, 75 gram load, followed by a one and two-hour glucose
- Some physicians favor screening only those at increased risk for gestational diabetes
Regardless of how the issue is approached, it’s important to remember that the change in risk with increasing glucose intolerance is gradual, not abrupt. Consequently, the distinction between those determined not to have GDM, and those designated as having it, is not as great as you might think.
While we also check the urine of each pregnant woman for glucose at each prenatal visit, this is not as useful a screening test since pregnant woman normally lose up to 300 mg/day of glucose in their urine.
Once diagnosed, it is best to engage the services of obstetricians, endocrinologists and dieticians skilled in managing this clinical problem. Some of these patients will be able to control their GDM with diet alone (A1GDM) while others will require insulin (A2GDM). Oral hypoglycemic agents have not been studied extensively in this setting. While some centers report good experience with such hypoglycemic agents as glyburide and metformin, others are much more comfortable in the well-studied application of insulin for those needing medication.
The obstetrical management of those women with insulin-dependent gestational diabetes is quite similar to the management of Type 1 or Type 2 pregestational diabetes, including close monitoring of blood sugars, fetal growth and well-being, and evidence of maternal complications.
But for gestational diabetics well-controlled with diet alone, the primary increased risk is for fetal macrosomia. For that reason, the A1 GDM patients may not be induced early, and may not undergo serial electronic fetal monitoring, depending on the training and opinions of their own physicians, combined with their past history. The other guidelines for cesarean section with EFW > 4500 grams are generally followed.
While it is true that as soon as delivery occurs, gestational diabetes goes away, it is also true that some of the women diagnosed with GDM actually have recently-diagnosed pregestational diabetes, so followup is necessary.
Even when GDM completely resolves, the patient has already demonstrated a vulnerability to a collection of diabetogenic factors, and this vulnerability may persist throughout her life. Some have found a 10% per year risk of the patient developing overt diabetes in the years following delivery.
During labor, insulin-dependent diabetics have their blood glucose checked every 2 hours and remain NPO. The target range for their glucose is 70-120. If they fall below 70, we initiate a D10W drip sufficient to return their glucose back to normal. If their glucose exceeds 120, then insulin is initiated sufficient to lower their glucose back into the normal range.
After delivery, insulin requirements usually drop substantially and these patients are watched closely for hypoglycemia. For gestational diabetics, their problem is resolved once the placenta is delivered, but they are counseled for followup testing at 6 weeks, because a few of them actually have Type 2 diabetes that has been unmasked by the pregnancy.
Following delivery, it’s important to make sure the pediatricians understand that the mother has diabetes, as they will need to follow the newborn closely for a reactive hypoglycemia.