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Craniofacial birth defects can elude early recognition and management
To prognosticate adequately on the crowding potential of a patient, the following steps should be taken : Measure with a pair of calipers the mesiodistal width of each incisor and &en measure the space for these teeth. Subtracting one series of measurements from the othrr produces the incisor discrepancy. Mtasure the size of the deciduous canines and molars on both sides of the mout,h, in bot,h the upper and lower arches. Take two bimolar roentgenograms and calculate the. size of the unernpted permanent successors. The difference between these two sets of measurements is the premolar discrepancy in each quadrant. IMesial molar shifting may be ignored in the maxillary arch, but one should allow 1 to 5 mm. per side in the mandibular arch for this shift. The premolar discrepancy minus incisor discrepancy minus molar shift,ing allowance represents the total arch discrepancy in each arch. Record the arch widths at the incisal tips of the deciduous canines and at the mesiolingual cusps of the upper and mesial pits of the lower deciduous molars. When the patient returns for a further examination in 6 to 12 months, repeat the arch width measurements. Tell the parent how much the child has grown in the previous 6 months. (During the eruption of the incisors the arch widths usually grow approximately 1 to 2 mm.) When it is explained that, although there is an arch discrepancy, the arches are growing, the mother will be content to have the crowding reviewed again in 6 to 12 months, particularly if it is stressed that the incisors will align themselves if extractions are necessary at this later stage. Craniofacial Birth .1. 1. X. A. 208: June
Defects
Can
Elude
Early
Recognition
and
Management
16, 1969
( ‘r;tniof;lcial birth defects may not, be recognized in neonates. In addition, thtx~- ina!- be associated with even more serious undetected anomalies. 1)uring a recent seminar at the University of Illinois Medical Center Campus in Chic,ago, participants learned that a bifid uvula or a submucous defect can signal the prescn~ of congenital palatopharyngeal incompetence (CPI) . If a routine tonsillcrtomy and adenoidectomy is performed, speech may bc permanently impaired. The association between cleft defects and congenital heart disease is also more common than previously suspected. Early recognition could have cliagn~lbtiic and prognostic significance. The prognosis for children with cleft paintt-5s who 1151x-cthe Pierre Robin syndrome can also be greatly improved if ari il
Amer.
J. Orthodoat. November 1910
t,he posterior wall of the pharynx, enabling the child to speak almost normally. In a series of 110 children referred to the center because of CPI, the condition was not.iced in twenty-three only after a tonsillectomy and adenoidectomy resulted in speech impairment. Fifteen of the twenty-three patients had at least one of the three clinical signs often associated with CPI. The signs are a bifid uvula (which can be masked by an upper respiratory infection), hypernasality of speech, and submucous defects of the hard or soft palate. Those with a bifid uvula and submucous defects should be carefully screened before a surgical procedure is considered. Studies demonstrate that the incidence of facial clefts and bifid urulas differs according to race. Negroes have a reported incidence of 0.27 per cent; Caucasians, 1.44 per cent; and Japanese, 9.95 per cent. Burt Shapiro, professor and chairman of the Oral Biology Division at the University of Minnesota Dental School, found that American Indians have an even higher incidence of bifid uvula-from 10 to 15 per cent or higher. However, there appeared to be no increase in nasality associated with the bifid uvula in seventy-six Indian children as compared to seventy-six normal controls. In a prospective survey of 150 consecutive patients (average and median age, 9.5 years) attending the cleft palate clinic at the University, two (1.3 per cent) had congenital heart malformations. This compares to about 0.2 per cent for the general population of school children. Nine other children attending the clinic between 1954 and 1968 were known to have heart disease. In a postmortem study of thirty-two children with a cleft lip and/or palate, twenty-one (62.5 per cent) were found to have severe congenital cardiac malformations. Sixteen of the twenty-one (76 per cent) died before the age of 6 months and two died before the age of 1 year. With one exception, all twenty-one children who died of heart disease had cleft palates. Three had a single cardiac malformation, and sixteen had multiple defects. In two patients the nature of the defect was not determined at autopsy. The investigators discovered that the types of heart defect found in patients with facial clefts (including ten of the eleven children treated at the clinic and the twenty-one who were studied at autopsy) differ from those found in the general population. Although autopsy studies have shown that the incidence of transposition of the great vessels in children with congenital heart disease is about 15 to 20 per cent, none of the children in their series of thirty-one had this defect. Nor did any patient have another defect-single ventricle-often associated with transposition complexes. Apparently, the combination of this defect and cleft palate is lethal to fetuses. A high incidence of heart disease (15 to 20 per cent) has been reported in children dying of the Pierre Robin syndrome. However, the University of Illinois investigators were surprised to find the incidence considerably higher (‘75 per cent) in autopsied children with cleft palate who did not have the syndrome. In children with this disorder, airway obstruction caused by glossoptosis and recurring respiratory infections may lead to pulmonary hypertension. The ventricular hypertrophy which may be induced could lead to car pulmonale and congestive heart failure.
Defects
Can
Elude
Early
Recognition
and
Management
16, 1969
( ‘r;tniof;lcial birth defects may not, be recognized in neonates. In addition, thtx~- ina!- be associated with even more serious undetected anomalies. 1)uring a recent seminar at the University of Illinois Medical Center Campus in Chic,ago, participants learned that a bifid uvula or a submucous defect can signal the prescn~ of congenital palatopharyngeal incompetence (CPI) . If a routine tonsillcrtomy and adenoidectomy is performed, speech may bc permanently impaired. The association between cleft defects and congenital heart disease is also more common than previously suspected. Early recognition could have cliagn~lbtiic and prognostic significance. The prognosis for children with cleft paintt-5s who 1151x-cthe Pierre Robin syndrome can also be greatly improved if ari il
Amer.
J. Orthodoat. November 1910
t,he posterior wall of the pharynx, enabling the child to speak almost normally. In a series of 110 children referred to the center because of CPI, the condition was not.iced in twenty-three only after a tonsillectomy and adenoidectomy resulted in speech impairment. Fifteen of the twenty-three patients had at least one of the three clinical signs often associated with CPI. The signs are a bifid uvula (which can be masked by an upper respiratory infection), hypernasality of speech, and submucous defects of the hard or soft palate. Those with a bifid uvula and submucous defects should be carefully screened before a surgical procedure is considered. Studies demonstrate that the incidence of facial clefts and bifid urulas differs according to race. Negroes have a reported incidence of 0.27 per cent; Caucasians, 1.44 per cent; and Japanese, 9.95 per cent. Burt Shapiro, professor and chairman of the Oral Biology Division at the University of Minnesota Dental School, found that American Indians have an even higher incidence of bifid uvula-from 10 to 15 per cent or higher. However, there appeared to be no increase in nasality associated with the bifid uvula in seventy-six Indian children as compared to seventy-six normal controls. In a prospective survey of 150 consecutive patients (average and median age, 9.5 years) attending the cleft palate clinic at the University, two (1.3 per cent) had congenital heart malformations. This compares to about 0.2 per cent for the general population of school children. Nine other children attending the clinic between 1954 and 1968 were known to have heart disease. In a postmortem study of thirty-two children with a cleft lip and/or palate, twenty-one (62.5 per cent) were found to have severe congenital cardiac malformations. Sixteen of the twenty-one (76 per cent) died before the age of 6 months and two died before the age of 1 year. With one exception, all twenty-one children who died of heart disease had cleft palates. Three had a single cardiac malformation, and sixteen had multiple defects. In two patients the nature of the defect was not determined at autopsy. The investigators discovered that the types of heart defect found in patients with facial clefts (including ten of the eleven children treated at the clinic and the twenty-one who were studied at autopsy) differ from those found in the general population. Although autopsy studies have shown that the incidence of transposition of the great vessels in children with congenital heart disease is about 15 to 20 per cent, none of the children in their series of thirty-one had this defect. Nor did any patient have another defect-single ventricle-often associated with transposition complexes. Apparently, the combination of this defect and cleft palate is lethal to fetuses. A high incidence of heart disease (15 to 20 per cent) has been reported in children dying of the Pierre Robin syndrome. However, the University of Illinois investigators were surprised to find the incidence considerably higher (‘75 per cent) in autopsied children with cleft palate who did not have the syndrome. In children with this disorder, airway obstruction caused by glossoptosis and recurring respiratory infections may lead to pulmonary hypertension. The ventricular hypertrophy which may be induced could lead to car pulmonale and congestive heart failure.