The treatment of late hypocalcemia includes immediatemanagement, as in early hypocalcemia, plus the initiation offeedings with low-phosphate formula. Subcutaneous infiltration of IV calcium salts can cause tissue necrosis; oral supplements are hypertonic and may irritate the intestinal mucosa.
Infants may become passively and physiologically addicted to medications or to drugs of abuse (heroin, methadone, barbiturates, tranquilizers, amphetamines) taken chronically by the mother during pregnancy; these infants subsequently may have signs and symptoms of drug withdrawal. Many of these pregnancies are at high risk for other complications related to IV drug abuse, such as hepatitis, acquired immunodeficiency syndrome (AIDS), and syphilis. In addition, the LBW rate and the long-term risk for sudden infant death syndrome are higher in the infants of these high-risk women.
Neonatal withdrawal signs and symptoms usually begin at 1to 5 days of life with maternal heroin use and at 1 to 4 weekswith maternal methadone addiction. Clinical manifestations of withdrawal include sneezing, yawning, ravenous appetite,emesis, diarrhea, fever, diaphoresis, tachypnea, high-pitchedcry, tremors, jitteriness, poor sleep, poor feeding, and seizures. The illness tends to be more severe during methadonewithdrawal. The initial treatment includes swaddling in blankets in a quiet, dark room. When hyperactivity is constant,and irritability interferes with sleeping and feeding, or whendiarrhea or seizures are present, pharmacologic treatmentis indicated. Seizures usually are treated with phenobarbital. The other symptoms may be managed with replacementdoses of a narcotic (usually tincture of opium) to calm theinfant; weaning from narcotics may be prolonged over 1 to2 months.
Cocaine use during pregnancy is associated with pretermlabor, abruptio placentae, neonatal irritability, and decreasedattentiveness. Infants may be small for gestational age and havesmall head circumferences. Usually no treatment is needed.
Maternal diseases during pregnancy can affect the fetus directly or indirectly (Table 59-1). Autoantibody-mediated diseases can have direct consequences on the fetus and neonate because the antibodies are usually of the IgG type and can cross the placenta to the fetal circulation.
Mild Large for gestational age, hypoglycemia Fetal hyperglycemia—produces hyperinsulinemia promoting growth
Severe Growth retardation Vascular disease, placental insufficiency
Drug addiction Intrauterine growth restriction, neonatal Direct drug effect, plus poor diet withdrawal
Graves disease Transient thyrotoxicosis Placental immunoglobulin passage of thyrotropin receptor antibody
Hyperparathyroidism Hypocalcemia Maternal calcium crosses to fetus and suppresses fetal parathyroid gland
Hypertension Intrauterine growth restriction, intrauterine Placental insufficiency, fetal hypoxia fetal demise placenta after sensitization of mother
Myasthenia gravis Transient neonatal myasthenia Immunoglobulin to acetylcholine receptor crosses the placenta
Myotonic dystrophy Neonatal myotonic dystrophy Autosomal dominant with genetic anticipation
Phenylketonuria Microcephaly, retardation, ventricular septal Elevated fetal phenylalanine levels defect
Rh or other blood group Fetal anemia, hypoalbuminemia, hydrops, Antibody crosses placenta directed at fetal cells with sensitization neonatal jaundice antigen
From Stoll BJ, Kliegman RM: The fetus and neonatal infant. In Behrman RE, Kliegman RM, Jenson HB, editors: Nelson textbook of pediatrics, ed 16, Philadelphia,