Graves disease is associated with thyroid-stimulating antibodies. The prevalence of clinical hyperthyroidism in pregnancy has been reported to be about 0.1% to 0.4%; it is thesecond most common endocrine disorder during pregnancy(after diabetes). Neonatal hyperthyroidism is due to thetransplacental passage of thyroid-stimulating antibodies;hyperthyroidism can appear rapidly within the first 12 to 48hours. Symptoms may include intrauterine growth restriction, prematurity, goiter (may cause tracheal obstruction),exophthalmos, stare, craniosynostosis (usually coronal),flushing, heart failure, tachycardia, arrhythmias, hypertension, hypoglycemia, thrombocytopenia, and hepatosplenomegaly. Treatment includes propylthiouracil, iodine drops, and propranolol. Autoimmune induced neonatal hyperthyroidism usually resolves in 2 to 4 months.
Diabetes mellitus that develops during pregnancy (gestational diabetes is noted in about 5% of women) or diabetes that is present before pregnancy adversely influences fetal and neonatal well-being. The effect of diabetes on the fetus depends, in part, on the severity of the diabetic state: age of onset of diabetes, duration of treatment with insulin, and presence of vascular disease. Poorly controlled maternal diabetes leads to maternal and fetal hyperglycemia that stimulates the fetal pancreas, resulting in hyperplasia of the islets of Langerhans. Fetal *Trimethoprim, triamterene, phenytoin, primidone, phenobarbital, carbamazepine.
hyperinsulinemia results in increased fat and protein synthesis, producing a fetus that is large for gestational age. After birth, hyperinsulinemia persists, resulting in fasting neonatal hypoglycemia. Strictly controlling maternal diabetes during pregnancy and preventing hyperglycemia during labor and delivery prevent macrosomic fetal growth and neonatal hypoglycemia. Additional problems of the diabetic mother and her fetus and newborn are summarized in Table 59-2.
Other maternal illnesses, such as severe pulmonary disease(cystic fibrosis), cyanotic heart disease, and sickle cell anemia,may reduce oxygen availability to the fetus. Severe hypertensive or diabetic vasculopathy can result in uteroplacentalinsufficiency. The fetus and the newborn may also be adverselyaffected by the medications used to treat maternal illnesses.These effects may appear as teratogenesis (Table 59-3) or as anadverse metabolic, neurologic, or cardiopulmonary adaptationto extrauterine life (Table 59-4). Acquired infectious diseasesof the mother also may affect the fetus or newborn adversely.
Table 59-4 Agents Acting on Pregnant Women That May Adversely Affect the Newborn Infant AGENT POTENTIAL CONDITION(S) Acebutolol IUGR, hypotension, bradycardia Acetazolamide Metabolic acidosis
Amiodarone Bradycardia, hypothyroidism
Aspirin Neonatal bleeding, prolonged gestation
Atenolol IUGR, hypoglycemia
Bromides Rash, CNS depression, IUGR
Captopril, enalapril Transient anuric renal failure, oligohydramnios
Caudal-paracervical anesthesia with mepivacaine (accidental Bradypnea, apnea, bradycardia, convulsions introduction of anesthetic into scalp of infant)
Cholinergic agents (edrophonium, pyridostigmine) Transient muscle weakness
CNS depressants (narcotics, barbiturates, benzodiazepines) during CNS depression, hypotonia labor