Complications of Diabetes in Pregnancy

Diabetic gastropathy can severely exacerbate nausea and vomiting in early pregnancy. In addition to the standard obstetrical regimens, patients may benefit from drugs such as cisapride and/or reglan, and some will need hyperali- mentation.

Background diabetic retinopathy (BDR) can develop or worsen during pregnancy, but it is not a risk to vision, since it usually regresses postpartum. If BDR is present in early pregnancy, progression to proliferative diabetic retinopathy (PDR) occurs in 6–9%. Therefore sequential ophthalmologic exam- inations are required during pregnancy, and laser photocoagulation treatment of the retina may be necessary. Risk factors for progression to PDR include poor glycemic control, rapid improvement in glycemic control in early preg- Background diabetic retinopathy (BDR) can develop or worsen during pregnancy, but it is not a risk to vision, since it usually regresses postpartum. If BDR is present in early pregnancy, progression to proliferative diabetic retinopathy (PDR) occurs in 6–9%. Therefore sequential ophthalmologic exam- inations are required during pregnancy, and laser photocoagulation treatment of the retina may be necessary. Risk factors for progression to PDR include poor glycemic control, rapid improvement in glycemic control in early preg-

The course of diabetic neuropathy is variable during pregnancy and treatment is often relatively ineffective. Agents commonly used may produce neo-

natal withdrawal symptoms. The risk of worsening of diabetic nephropathy during pregnancy depends on baseline renal function and the degree of hypertension. Total urinary albumin excretion does not increase much in normal pregnancy, but total urinary protein collections, which obstetricians have used to define preeclampsia, may show a twofold increase in uncomplicated gestation. Diabetic women with microalbuminuria (30–299 mg/24 h) may have worsening of the albumin- uria during pregnancy with regression postpartum, and 15–45% will develop the preeclamptic syndrome. Based on pooled data from several studies of pregnant diabetic women with a clinical level of proteinuria (24-hour urinary albumin ?300 mg) at the beginning of pregnancy, if initial renal function is preserved (serum creatinine =1.2 mg/dl or =106 lM; creatinine clearance ? 80 ml/min with complete collection), then 15–20% are expected to show moderate decline during gestation, and 6% will have renal failure at follow- up several years after pregnancy. If initial renal function in pregnancy is impaired (Cr ?1.2 mg/dl or ?106 lM; CrCl =80 ml/min with complete collection), then 35–40% are expected to show further decline during pregnancy, and 45–50% will have renal failure at follow-up. Thus, careful preconcep- tion counseling is important for these patients and their family members.

Obstetrical Management (table 5) Decades ago the incidence of apparently sudden intrauterine fetal demise

in the third trimester of diabetic pregnancies was at least 5%. Since the risk increased as pregnancies approached term, preterm delivery was instituted but the incidence of neonatal deaths from respiratory distress syndrome (RDS) increased. The risk of fetal demise was associated with poor glycemic control, and the incidence of fetal death exceeded 50% with ketoacidosis. Some in- stances of fetal demise were associated with preeclampsia, which is a common complication of diabetic pregnancy which can produce fetal hypoxia via de- creased uteroplacental perfusion.

Advances in perinatal medicine have led to techniques for detecting fetal hypoxia and preventing stillbirth. The infrequency of fetal movement as noted in fetal activity determinations (=4/h) may indicate fetal jeopardy, and semi- quantitative ultrasonographic studies of fetal activity patterns such as the biophysical profile have proved useful. The primary mode of fetal assessment

Table 5. Obstetrical management procedures Procedure

Risk based on glycemic control, vascular disease low risk

high risk Dating ultrasound

8–12 weeks Prenatal genetic diagnosis

8–12 weeks

As needed Targeted perinatal ultrasound; fetal

As needed

18–22 weeks Fetal kick counts

echocardiography

18–22 weeks

28 weeks Ultrasound for fetal growth

28 weeks

28 and 37 weeks 1 Monthly Antepartum FHR monitoring, backup

27 weeks, 1–3/week Amniocentesis for lung maturity

c biophysical profile

36 weeks, weekly

35–38 weeks Induction of labor

41 weeks 2 35–38 weeks 1 Not needed in normoglycemic, diet-treated women with GDM.

2 Earlier for obstetrical reasons or for impending fetal macrosomia.

is antepartum fetal heart rate (FHR) monitoring. The presence of FHR accel- erations and variability on the nonstress test (NST) and the absence of late decelerations persisting after a uterine contraction almost always suggests that the fetus is well oxygenated and has a low risk of demise within several days, unless episodes of severe hyperglycemia or hypertension occur.

In the past, insulin-treated patients were usually admitted to the hospital at 36 weeks’ gestation or earlier for fetal monitoring and careful control of diabetes. However, with reliable SMBG, normotensive women without hyperglycemia have no excess risk of fetal hypoxia and do not require antepartum admission to the hospital except for the usual obstetrical complications.

Unless maternal or fetal complications arise, the goal for timing of delivery should be 39–41 weeks, in order to reduce neonatal morbidity from preterm deliveries. On the other hand, the obstetrician may wish to induce labor by 37–38 weeks if there is concern about increasing fetal weight. Before a decision to de- liver before 39 weeks is made in a patient who has been hyperglycemic in spite of treatment, fetal pulmonary maturity should be determined by amniocentesis. Standard tests of amniotic fluid for pulmonary maturity indicating a low risk for RDS include the lecithin/sphingomyelin (L/S) ratio ?3.0, presence of phos- phatidylglycerol (PG), and reflectance polarization tests. Amniocentesis is not necessary in gravidas who have been normoglycemic in the last months of pregnancy, unless delivery is contemplated before 37 weeks’ gestation.

Table 6. Protocol for intrapartum insulin Infusion 1

Intravenous fluids 1. If BG ?7.2 mmol/l (130 mg/dl), infuse mainline LR at 125 ml/h 2. If BG =7.2 mmol/l (130 mg d/L), infuse mainline LR at TKO and begin D5-LR at

125 ml/hr controlled by infusion pump Insulin infusion

1. Mix 25 U regular human insulin (U 100) in 250 cm 3 NaCl 0.9% and piggyback to mainline. Concentration is 1 unit/10 cm 3 . Adjust intravenous insulin hourly according to algorithm when BG is ?3.9 mmol/l (70 mg/dl) 2. Algorithm

BG mmol/l (mg/dl)

Infusion, ml/h =

Insulin, units/h

10.6 (190) call MD and check urine ketones 1 Protocol also useful for diabetic pregnant women who are npo or treated with b-adrenergic

tocolytics or corticosteroids; scale may need to be doubled for latter. Boluses of short-acting insulin will be needed to cover meals.

Once fetal lung maturity is likely, the route of delivery is selected based on the usual obstetric indications. If the fetus seems large (?4,200 g) on clinical and ultrasonographic examination, cesarean section probably should

be performed because of the possibility of shoulder dystocia and damage from birth trauma. Otherwise, induction of labor is reasonable, because maternal and peripartum risks are fewer following vaginal delivery. Once labor is under way, continuous FHR monitoring should be performed and maternal BG levels should be kept =7.2 mmol/l (110 mg/dl) with an intravenous insulin infusion (table 6) in order to prevent fetal hypoxia and neonatal hypoglycemia.

Complications of Diabetes in Pregnancy