Effects of Maternal Medication

During pregnancy, the average fetus is exposed to four physician-prescribed and five self-prescribed drugs. Every drug administered or taken by a pregnant woman presents the mother with both risks and benefits. The risks include the drug's potential as a teratogen or as a cause of toxicity in the fetus. Most human teratogens affect the embryo during a very narrow period of early development as illustrated by the time (24 to 33 days gestation) during which the fetus is susceptible to limb reduction defects caused by thalidomide. Several human teratogens, such as alcohol, androgens, cocaine, diphenylhydantoin, radiation, tetracycline, valproic acid, and warfarin have serious side effects beyond the period of organogenesis. These effects may include cell deletion, vascular disruption, necrosis, physiologic decompensation, organ pathology, and intrauterine growth retardation. Drugs taken in the third trimester may not have teratogenic effects, but may be toxic to the fetus. Some examples include indomethacin (causing oligohydramnios), propylthiouracil (causing fetal goiter), and erythromycin (causing cholestatic hepatitis). A detailed history of maternal drug use and abuse is essential in evaluating most malformations and diseases in the neonatal period.

Philtrum Reduction

Figure 3.1. This illustration contrasts the craniofacial features of a healthy child on the right to those of a child with fetal alcohol syndrome on the left. Note the microcephaly, short palpebral fissure, flat maxillary area, poorly developed philtrum and thin upper lip (Peter Shvartsman, Canadian Medical Association Journal, July 15, 1981 cover).

Microcephaly

Figure 3.2. This infant, age 6 weeks, was born to a mother with severe, chronic alcoholism. There was failure to thrive and hypotonia. Note the microcephaly (head circumference less than the third percentile), short nose, absence of philtrum and thin vermilion border of the upper lip.

Findings in fetal alcohol syndrome include intrauterine growth retardation, microcephaly, dysplastic facial features, hypoplasia of the midface, and a hypoplastic philtrum with a thin vermilion border of the upper lip. Later there may be continued failure to thrive and developmental and behavioral disorders.

Figure 3.2. This infant, age 6 weeks, was born to a mother with severe, chronic alcoholism. There was failure to thrive and hypotonia. Note the microcephaly (head circumference less than the third percentile), short nose, absence of philtrum and thin vermilion border of the upper lip.

Findings in fetal alcohol syndrome include intrauterine growth retardation, microcephaly, dysplastic facial features, hypoplasia of the midface, and a hypoplastic philtrum with a thin vermilion border of the upper lip. Later there may be continued failure to thrive and developmental and behavioral disorders.

Newborn Short Upturned Nose

Figure 3.3. Close-up of the face of the same infant shows the short nose, absence of the philtrum, and thin vermilion border of the upper lip. Many other findings in fetal alcohol syndrome have been reported, including epican-thic folds, ptosis, hypoplastic maxilla, deep or accentuated palmar creases, and clinodactyly.

Figure 3.3. Close-up of the face of the same infant shows the short nose, absence of the philtrum, and thin vermilion border of the upper lip. Many other findings in fetal alcohol syndrome have been reported, including epican-thic folds, ptosis, hypoplastic maxilla, deep or accentuated palmar creases, and clinodactyly.

Clinodactyly Toes

Figure 3.4. Soon after birth, this infant of a narcotic addict shows hypotonia. Note die concavity of the inner aspect of the thighs and the position of the lower extremities. This has resulted from a postural deformation in which the fetus has had its thighs flexed over its abdomen in utero. Because of the mother's narcotic habit there was minimal fetal movement in utero.

Figure 3.4. Soon after birth, this infant of a narcotic addict shows hypotonia. Note die concavity of the inner aspect of the thighs and the position of the lower extremities. This has resulted from a postural deformation in which the fetus has had its thighs flexed over its abdomen in utero. Because of the mother's narcotic habit there was minimal fetal movement in utero.

Figure 3.5. Drug withdrawal is a major problem in neonates delivered of narcotic addicted mothers. This figure stresses the fact that one should always check for signs of drug addiction in the mother. This figure shows needle tracks at both elbows of a mother.

Figure 3.5. Drug withdrawal is a major problem in neonates delivered of narcotic addicted mothers. This figure stresses the fact that one should always check for signs of drug addiction in the mother. This figure shows needle tracks at both elbows of a mother.

Figure 3.6. Infants with retinoic acid embryopathy (Accutane™ embryopathy) may have craniofacial, cardiovascular, and central nervous system abnormalities. In this infant note the narrow sloping forehead, flat depressed nasal bridge, mild micrognathia, and microtia with absence of the external auditory canal. In addition there was congenital heart disease. Affected infants may have hydrocephalus, microcephaly, or thymic abnormalities. This mother was treated with retinoic acid during the first month of pregnancy.

Retinoic Acid Embryopathy Fetal Hydantoin Syndrome
Micrognathia Newborns
Figure 3.7. Close-up of the ears of the same infant as shown in Figure 3.6 shows the bilateral microtia with absence of the external auditory meatus.
Fetal FontanelsFetal Hydantoin

Figure 3.8. In infants with the fetal hydantoin (Dilantin™) syndrome there is moderate growth retardation, usually prenatal, a wide anterior fontanelle and metopic ridging. In this infant, note the growth retardation, profuse scalp hair, and short neck. Other findings included hypopla-sia of the distal phalanges with small nails and a digital thumb.

Figure 3.8. In infants with the fetal hydantoin (Dilantin™) syndrome there is moderate growth retardation, usually prenatal, a wide anterior fontanelle and metopic ridging. In this infant, note the growth retardation, profuse scalp hair, and short neck. Other findings included hypopla-sia of the distal phalanges with small nails and a digital thumb.

Infant Hirsutism

Figure 3.9. Close-up of the face of the same infant. Note the marked hirsutism, low hairline, low nasal bridge with a short upturned nose ("pug" nose), and long philtrum.

Figure 3.10. Hypertrichosis in another infant with the fetal hydantoin syndrome. Mother was treated throughout pregnancy with hydantoin. The risk of fetal hydantoin syndrome in infants of treated mothers is about 10%.

Fetal Hydantoin Syndrome

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Figure 3.11. Gum hypertrophy in an infant with die fetal hydantoin syndrome. Many other findings have been reported in infants widi fetal hydantoin syndrome, including widely spaced nipples, rib anomalies, abnormal palmar creases, pilonidal sinus, and congenital heart disease.

Figure 3.12. This infant of an epileptic mother on hydantoin developed seizures at the age of 36 hours. He had hypocalcemia with a calcium level of 6.4 mg/dL and a phosphorus level of 11.2 mg/dL. In fetal hydantoin syndrome the digital hypoplasia may be associated with narrow distal phalanges and hypoplastic nails.

Figure 3.11. Gum hypertrophy in an infant with die fetal hydantoin syndrome. Many other findings have been reported in infants widi fetal hydantoin syndrome, including widely spaced nipples, rib anomalies, abnormal palmar creases, pilonidal sinus, and congenital heart disease.

Rib Anomalies

3.11

3.12

3.14

3.15

Fetal Hydantoin Syndrome
Figure 3.13. This infant with the fetal hydantoin syndrome presented with many of the findings already described. There was growth retardation, hypertelorism, small pug nose, anteverted nostrils, long philtrum, and thin vermilion border of the upper lip, and short neck.

Figure 3.14. The same infant shows the characteristic changes in the fingers. Note the hypoplasia of the distal phalanges with hypoplastic or absent nails and the digital thumbs. There is mild webbing.

Figure 3.15. The same infant with fetal hydantoin syndrome shows the marked hypoplasia of the distal phalanges of the toes and absent or hypoplastic nails.

Figure 3.16. Postnatal growth deficiency and microcephaly are present in two-thirds of children exposed to valproic acid in combination with other anticon-vulsants. It does not occur with monotherapy with valproic acid. This infant with the fetal vaproate syndrome shows the typical craniofacial abnormalities. Note the trigonocephaly with a prominent metopic ridge, bifrontal narrowing, outer orbital ridge deficiency, midface hypoplasia, epicanthic folds, small short upturned nose, and long flat philtrum.

Figure 3.17. A cranial view of the same infant shows the trigonocephaly due to premature closure of the metopic suture, bifrontal narrowing, and outer orbital ridge deficiency.

Figure 3.18. Lateral view of the head and face of the same infant shows the marked metopic ridge, small flat short nose, micrognathia and "square" ears.

Figure 3.17. A cranial view of the same infant shows the trigonocephaly due to premature closure of the metopic suture, bifrontal narrowing, and outer orbital ridge deficiency.

Trigonocephaly

3.17

3.18

3.20

3.21

Micrognathia Newborns

Figure 3.20. Yellow staining of the teeth in a child exposed to maternal tetracycline in utero.

Figure 3.19. The same infant with fetal valpro-ate syndrome as shown in Figures 3.16 to 3.18, had distal phalangeal hypoplasia and tapering of the fingers. Note the abnormal creases on the fingers and palm due to lack of fetal movement in utero. Other changes reported in infants with this syndrome include tracheo-malacia, congenital heart defects, and urogenital anomalies.

Figure 3.20. Yellow staining of the teeth in a child exposed to maternal tetracycline in utero.

Figure 3.21. A Wood's filter shows the fluorescence of the nails in an infant exposed to maternal tetracy-cline. If young infants are given tetracycline after birth the staining of the teeth and nails also occurs.

Figure 3.22. Drug-induced pseudohermaphroditism in a female infant who was virilized by progestational agents during the first trimester of pregnancy. The incidence of this condition has decreased because, with recognition of this iatrogenic cause of virilization of the fetus, there has been a decreased use of incriminating drugs such as progestational agents or androgens during the first trimester. There may be fusion of labioscrotal folds with formation of a urogenital sinus and clitoromegaly. (See Volume V, chapter 5).

Figure 3.22. Drug-induced pseudohermaphroditism in a female infant who was virilized by progestational agents during the first trimester of pregnancy. The incidence of this condition has decreased because, with recognition of this iatrogenic cause of virilization of the fetus, there has been a decreased use of incriminating drugs such as progestational agents or androgens during the first trimester. There may be fusion of labioscrotal folds with formation of a urogenital sinus and clitoromegaly. (See Volume V, chapter 5).

Clitoromegaly

Figure 3.23. The thalidomide syndrome in twin infants born to a mother who took thalidomide early in gestation. Maternal ingestion of thalidomide between the 25th to 44th day after conception may cause malformations. In the thalidomide syndrome the limbs are usually asymmetrically involved and the malformations of the extremities are of all grades of severity (digits are usually present). There may be microph-thalmia, ear deformities, and cardiac, renal and intestinal malformations.

Figure 3.23. The thalidomide syndrome in twin infants born to a mother who took thalidomide early in gestation. Maternal ingestion of thalidomide between the 25th to 44th day after conception may cause malformations. In the thalidomide syndrome the limbs are usually asymmetrically involved and the malformations of the extremities are of all grades of severity (digits are usually present). There may be microph-thalmia, ear deformities, and cardiac, renal and intestinal malformations.

Thalidomide Artificial Limbs

3.23

Figure 3.24. Phocomelia in another infant born to another mother who took thalidomide in early gestation. Note the asymmetric phocomelia.

Fetal Warfarin Syndrome

3.24

Warfarin Syndrome

Figure 3.25. This infant with the fetal warfarin syndrome (Coumadin™ embryopathy) was born to a mother who was being treated with warfarin during the first trimester of pregnancy. These infants typically are low birth-weight and have facial and skeletal abnormalities. Less commonly they may have central nervous system and eye abnormalities. In this baby note the typical facial features of a broad flat face and nasal hypoplasia with a low nasal bridge, a prominent philtrum, and micrognathia.

3.26

3.27

Nasal Deformity Due Cocaine Use
Figure 3.26. The lateral view of the face strikingly demonstrates the marked nasal hypoplasia resulting in a very flat face. Because of the marked nasal hypoplasia these infants often present with upper airway obstruction.

Figure 3.27. Radiograph of die lower extremities of the same infant shows the stippling of die epiphyses at the proximal femora. Stippling of the epiphyses may occur along the vertebral column and the tarsal bones. The stippling disappears in die first few years of life. Coumadin™ embryopadiy is phenotypically similar to hereditary chondrodystrophia punctata and it must thus be distinguished from the different hereditary forms of Coiiradi-Huiiermanii syndrome.

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Responses

  • giovanni lettiere
    Is metopic ridge common with fetal alcohol syndrome?
    6 years ago
  • BINIAM NEBAY
    What causes deep or wide philtrum in babies?
    6 years ago

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