Pregnancy Complications · 3 min read
Diabetes and Endocrine Disorders
Glucose Metabolism in Pregnancy
Early pregnancy increases insulin sensitivity, so patients with pregestational diabetes are prone to hypoglycemia in the first trimester. From mid-pregnancy onward, human placental lactogen, progesterone, cortisol, and prolactin create progressive insulin resistance that preserves glucose for the fetus. Glucose crosses the placenta freely by facilitated diffusion; insulin does not. Maternal hyperglycemia therefore produces fetal hyperglycemia and fetal hyperinsulinemia, which drives excess growth and delays lung maturation.
Pregestational and Gestational Diabetes
| Type | Features | Main concerns |
|---|---|---|
| Pregestational type 1 | Autoimmune beta-cell destruction; absolute insulin deficiency | Congenital anomalies with poor periconception control, DKA, hypoglycemia, vasculopathy |
| Pregestational type 2 | Insulin resistance with relative deficiency; often obesity | Anomalies, preeclampsia, macrosomia, stillbirth |
| Gestational diabetes (GDM) | Glucose intolerance first recognized in pregnancy | Macrosomia, shoulder dystocia, neonatal hypoglycemia, later type 2 diabetes in the mother |
Screening for GDM is performed at 24–28 weeks (earlier for patients with obesity and other risk factors). The two-step approach uses a nonfasting 1-hour 50 g glucose challenge; a positive screen is followed by a fasting 3-hour 100 g oral glucose tolerance test, with GDM diagnosed by two or more abnormal values. The one-step approach uses a fasting 2-hour 75 g OGTT, with one abnormal value diagnostic.
| Measurement | Target |
|---|---|
| Fasting | Below 95 mg/dL |
| 1 hour after the start of a meal | Below 140 mg/dL |
| 2 hours after the start of a meal | Below 120 mg/dL |
| Intrapartum (insulin-treated diabetes) | About 70–110 mg/dL, checked hourly during active labor |
- First-line GDM treatment is medical nutrition therapy and exercise. Insulin is the preferred medication because it does not cross the placenta; metformin and glyburide cross the placenta and are second-line.
- Antenatal testing usually begins at 32 weeks for pregestational diabetes and poorly controlled or medication-treated GDM.
- Delivery timing: diet-controlled GDM at 39 0/7–40 6/7 weeks; well-controlled medication-treated GDM at 39 0/7–39 6/7 weeks; earlier for poor control or vasculopathy.
- Insulin requirements fall sharply after placental delivery; many patients with GDM need no insulin postpartum. Screen with a 75 g OGTT at 4–12 weeks postpartum.
Diabetic Ketoacidosis
DKA develops faster and at lower glucose levels in pregnancy (sometimes below 200 mg/dL) because of relative respiratory alkalosis and reduced buffering. Triggers include infection, missed insulin, and betamethasone or beta-agonist administration. Fetal loss rates are high. Treatment is aggressive IV fluids, IV insulin, potassium replacement, and correction of the cause; the fetal heart rate often shows minimal variability and late decelerations that improve as maternal acidosis is corrected, so stabilize the mother before considering delivery.
Thyroid Disorders
| Condition | Findings | Treatment and nursing points |
|---|---|---|
| Hyperthyroidism (usually Graves disease) | Low TSH, high free T4; tachycardia, tremor, weight loss, heat intolerance | Propylthiouracil in the first trimester (methimazole is teratogenic early); methimazole after the first trimester; watch for fetal tachycardia and goiter from maternal antibodies |
| Thyroid storm | Fever, marked tachycardia, agitation or confusion, heart failure | Emergency: thionamide, then iodide, beta-blocker, corticosteroids, cooling, supportive care |
| Hypothyroidism (often Hashimoto) | High TSH; fatigue, cold intolerance, constipation | Levothyroxine; dose usually increases 25–30% in pregnancy; take on an empty stomach, separate from iron and calcium by 4 hours |
| Postpartum thyroiditis | Transient hyperthyroid phase, then hypothyroid phase in the first year | Often resolves; some patients develop permanent hypothyroidism |
- Human placental lactogen causes insulin resistance in the second half of pregnancy.
- Fetal hyperinsulinemia causes macrosomia and neonatal hypoglycemia after the cord is cut.
- DKA can occur at glucose levels below 200 mg/dL in pregnancy; betamethasone can precipitate it.
- Insulin needs drop immediately after delivery of the placenta.
- PTU in the first trimester; methimazole later.
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