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PubMed1992

Flexible endoscopic intubation of the neonate.

The development of the ultrathin bronchoscope has provided a means of providing flexible endoscopic intubation for the neonate and small infant. We report our experience of 26 such endoscopic intubations in 23 neonates with birth weights from 1,200 to 4,600 g and post-conceptional ages varying from 31.5 to 60 weeks. The most common indications for the procedure were dysmorphic airways with variable degrees of micrognathia, acquired airway lesions, and severe degrees of hydrocephalus. With the use of the current 2.2 mm and 2.7 mm diameter instruments, it is now possible to utilize this technique with 2.5 mm endotracheal tubes. There were no failed procedures and no evidence of laryngospasm, the most frequent adverse effect being a transient fall in oxygen saturation. The procedure as practiced by experienced individuals is well tolerated and is an important adjunct for intubation of neonates with dysmorphic upper airways or other disorders that prevent adequate visualization of the larynx.

Airway Obstruction↗
PubMed2002

Altered mandibular development precedes the time of palate closure in mice homozygous for disproportionate micromelia: an oral clefting model supporting the Pierre-Robin sequence.

BACKGROUND: Development of the human craniofacial anatomy involves a number of interrelated, genetically controlled components. The complexity of the interactions between these components suggests that interference with the spaciotemporal interaction of the expanding tongue and elongating Meckel's cartilage correlates with the appearance of cleft palate. Mice homozygous for the semi-dominant Col2a1 mutation Disproportionate micromelia (Dmm), presenting at birth with both cleft palate and micrognathia, provide the opportunity to test the hypothesis that mandibular growth retardation coincides with formation of the secondary palate as predicted from our understanding of the Pierre Robin sequence. The present study was conducted in embryonic day 14 (E14) mice, 1 day before palate closure, to describe the relationship between growth of the lower jaw/tongue complex versus genotype of the embryo. METHODS: Whole heads, isolated from E14.25, E14.5 and E14.75 wild-type and homozygous mutant embryos, were fixed in Bouin's solution, embedded in paraffin, and serially sectioned. Mid-sagittal sections, stained with toluidine blue, were used to estimate growth of both tongue and lower jaw (Meckel's cartilage length) during a 12-hr period preceding palate closure. RESULTS: In control embryos, the largest increase in Meckel's cartilage length occurred between E14.5 and E14.75. Compared to control, the mean Meckel's cartilage length in the mutant was similar at E14.25, but was significantly less at E14.5 and E14.75. Absolute tongue size in control embryos increased linearly during this period of E14.25 to E14.75. Relative to the rapidly growing Meckel's cartilage, however, relative tongue size in control embryos actually decreased over time. Absolute tongue size in the mutant was not significantly different from that of control at any of the embryonic stages examined, however, relative tongue size in the mutant was significantly greater at E14.75 compared to control. CONCLUSION: Mandibular growth retardation, coupled with relative macroglossia in E14 Dmm/Dmm mice, suggests that the concerted development of the palate and lower jaw complex in the mutant is aberrant. Detection of micrognathia and pseudomacroglossia in homozygotes, before the time of palate closure, supports the hypothesis that a relationship exists between growth retardation of Meckel's cartilage and malformation of the secondary palate, as predicted by the Pierre-Robin sequence.

Animals↗
PubMed1975

Action of the phenothiazine derivative methophenazine on prenatal development in rats.

Single doses of 100-400 mg/kg or multiple doses of 10 or 50 mg/kg of the phenothiazine derivative methophenzaine were given per osto Wistar rats at various times on the 7th-14th days fo gestation and the fetuses examined near term. Results indicated that methophenazine was mainly embryolethal when administered on the 8th-11th days, and was teratogenic at later times, producing types of malformations that depended on the day of treatment, the most susceptible period being the 13th and 14th days of gestation. Teratogenicity occurred only when the dosages were highly toxic to the pregnant rats. Ribovlavin given ip on the 14th day significantly reduced the embryolethal but not the teratogenic action of methophenazine.

Abnormalities, Drug-Induced↗
PubMed1977

Effect of intraamniotic administration of vitamin A on rat fetuses.

The present study examines the effect of intraamniotic (i/a) administration of vitamin A to rat fetuses. Vitamin A aquasol in concentrations of 50 I.U., 100 I.U., and 300 I.U., was mixed in 5 microliter of saline. On day 13 of gestation, each of the tree experimental subgroups were injected i/a with varying doses of vitamin A. The four control subgroups consisted of: (1) i/a injection of 5 microliter of saline only, (2) amniotic puncture only, (3) laparotomy or (4) i/a injection of sorethytan oleate. The fetuses were recovered on day 18 of gestation, and were weighed and examined for gross malformations. The viable fetuses from the experimental groups showed various malformations such as cleft palate, micrognathia and limb defects. The percentage of resorbed fetuses was significantly high. The control fetuses showed a moderate number of resorptions; however the percentage of malformations was small. The results show that the i/a method can be used effectively to study the direct teratogenic effect of vitamin A on the fetuses.

Abnormalities, Drug-Induced↗
PubMed1984

Teratogenic effects of avidin-induced biotin deficiency in mice.

Teratogenic effects of maternal biotin deficiency were examined at different levels of severity by adding three levels of avidin (10, 20, or 40 mg/kg) in the basal diet. There was a considerable increase of fetuses with multiple congenital malformations (micrognathia, cleft palate, and micromelia) with increasing amounts of avidin. The dose-response relationship was observable in the incidence of each malformation as well. The body weight of live fetuses was also significantly reduced. However, the dams did not exhibit any typical signs of biotin deficiency, such as loss of hair, dermatitis, or nervous irritability. These results suggest that biotin is important for early embryonic development in the mouse.

Abnormalities, Multiple↗
PubMed1986

Morphogenesis of isotretinoin-induced microcephaly and micrognathia studied by scanning electron microscopy.

Isotretinoin ingestion during the first trimester of human pregnancy can induce malformations of the skull, ears, face, central nervous system, eyes, palate, lungs, circulatory system, limbs, and digits. A single oral dose of isotretinoin on day 8 of gestation in hamsters induces a similar syndrome of congenital malformation. The present study concerned scanning electron microscopic (SEM) observation of embryonic and fetal hamster craniofacial structures at 4, 8, 12, 24, 48, and 72 hr after administration of an oral dose of 50 mg/kg isotretinoin or an equivalent volume of the vehicle. The variability in development among control embryos recovered 4 hr after treatment precluded objective assessment of pathologic change by SEM at very early time points. Craniofacial damage was obvious within 8-12 hr of isotretinoin treatment, and it included hypoplasia of the maxillary and mandibular processes of the first branchial arch, a rudimentary second arch, and apparent collapse of the forebrain. Equivalent fusion between the lateral nasal process and the maxillary process and between the medial nasal process and the maxillary process in treated and control embryos accounts for the very low incidence of cleft lip observed in fetuses. The terminal microstomia was not associated with excessive merging or overgrowth of the first arch components. Hypoplasia of the first arch can account for retinoid-induced macrostomia and microstomia.

Animals↗
PubMed1990

Extrinsic fetal akinesia and skeletal development: a study in oligohydramnios sequence.

Long-bone morphometry and cephalometry were performed in 13 newborns with oligohydramnios sequence (OS) in order to establish whether or not skeletal changes existed in extrinsic fetal akinesia similar to those observed in the fetal akinesia deformative sequence (FADS) (i.e., hypoplastic long bones and micrognathia). Oligohydramnios sequence was caused by bilateral renal agenesis in five cases and obstructive uropathy in eight cases. Twenty-one stillborns and newborns who had died from conditions other than renal anomalies or congenital malformations were used as controls. Normal longitudinal and periosteal long-bone growth and absence of micrognathia were found in OS patients. Skeletal differences between FADS and OS may be explained not only by timing, duration, and degree of reduced motility but also, and more importantly, by the normal muscular stress in OS patients.

Amniotic Fluid↗
PubMed1990

Study of the mechanisms of BUdR-induced cleft palate in the mouse.

This study was designed to examine the pathogenesis of bromodeoxyuridine (BUdR)-induced clefts of the secondary palate in the LACA mouse. Intraperitoneal injections of BUdR (500 mg/kg body weight) were given at various days and combinations of days between E11 and E15 (plug day = E1). Treatment on E11 alone resulted in approximately 22% of fetuses with cleft palate when the latter were examined either on E16 or E19. Treatment on E11 and E12 approximately doubled the above incidence, and treatment on E11, 12 and 13 raised it to 100%. However, no treatment, either single or multiple, caused cleft palate when given later than E11. This suggests that the cellular changes caused by BUdR that lead to cleft palate must be inflicted during E11 and that such damage can be repaired in about 80% of embryos. All fetuses with cleft palate had severe micrognathia on E16 and E19, which skeletal staining showed to be the result of a bilateral sigmoid buckling of Meckel's cartilage. Studies with the scanning electron microscope (SEM) on E15, 16, and 19 suggested strongly that the micrognathia caused a relative macroglossia and hence mechanical interference with palatal shelf reorientation. Histological studies with the light microscope showed that BUdR caused cellular necrosis in many embryonic tissues during the 24 hours after its administration. This necrosis was strikingly more severe in the mandibular rudiment of the first branchial arch than in the maxillary. The latter observation accords well with findings by other workers that cell proliferation is more rapid in the mandibular blastema than in the maxillary. Transmission electron microscope (TEM) studies of the buckled region of Meckel's cartilage failed to reveal any ultrastructural differences from control Meckel's cartilage. Hence BUdR had only interfered with the shape of the cartilage but not with its histiogenesis. We conclude that BUdR, by its cytotoxicity or antidifferentiative effects, interfered with the formation of the anterior end of Meckel's cartilage, initiating a chain of events leading through micrognathia and relative macroglossia to failure of palatal shelf reorientation and cleft palate.

Animals↗
PubMed2003

First-trimester diagnosis of micrognathia as a presentation of Pierre Robin syndrome.

We describe a case of first-trimester diagnosis of micrognathia. A transvaginal ultrasound scan performed at 13 weeks' gestation revealed an abnormal fetal facial profile consisting of a small mandible and a receding chin. A subsequent amniocentesis at 15 weeks' gestation revealed a normal karyotype. A morphology scan and subsequent postmortem examination at 19 weeks confirmed the first-trimester findings and revealed, in addition to the facial pathology, a complex cardiac abnormality and unilateral talipes equinovarus. These findings are consistent with the diagnosis of Pierre Robin syndrome.

Abortion, Induced↗
PubMedDate not supplied

Linkage study in a large pedigree with Stickler syndrome: exclusion of COL2A1 as the mutant gene.

A three generation family with Stickler syndrome is reported. Affected patients exhibited myopia with frequent retinal detachment or glaucoma. Most of them had characteristic facial dysmorphism, the Pierre-Robin sequence being observed in four individuals. Neonatal radiological signs of the Weissenbacher-Zweymüller syndrome were also noticed but early arthopathy was not reported in adults. Restriction fragment length polymorphism studies with the type II collagen gene (COL2A1) showed a recombination event between the disease locus and COL2A1, thus excluding collagen type II as the candidate gene. Although the calculation of the likelihood of genetic heterogeneity versus homogeneity based on 10 families was not statistically significant, we suggest that a second locus is probably involved in this highly variable syndrome.

Abnormalities, Multiple↗
PubMed1984

Reproductive outcomes of paracentric inversion carriers: report of a liveborn dicentric recombinant and literature review.

An abnormal infant had a dicentric chromosome 14 with an inverted tandem duplication [46,XY,inv dup(14) (pter----q32.3::q24.2----pter)], thus making him trisomic for the proximal two-thirds of chromosome 14. This abnormality was derived from a maternal paracentric inversion in chromosome 14 [46,XX,inv(14)(q24.2q32.3)]. To our knowledge, this is the first report of a liveborn infant carrying a stable, dicentric product of crossing over within a paracentric inversion loop. A review of the reproductive outcomes of paracentric inversion carriers in the literature suggests that they are at some risk for pregnancy wastage. The risk for liveborn recombinants is small but such births have occurred, at least to female carriers.

Abnormalities, Multiple↗