American Journal of Diseases of Children

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320010001

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

VET, THŸS W.;OTTENKAMP, JAAP

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320011004

Abstract In Reply.—We thank Dr Sissman for his comments. We aimed to compare This department of AJDC is reserved for comment, criticism, observation, and discussion of "issues of current concern and importance for children's health." The Editor encourages our readers to express themselves on a variety of topics and issues. Further, we encourage the submission of unique and brief clinical and scientific observations that do not fulfill the criteria for original articles. patients with atrioventricular septal defect (AVSD) and Down syndrome with those with AVSD without Down syndrome. We did not mean to claim that the results of surgical correction of a complete AVSD were sufficient to warrant surgical treatment of these patients. The surgical mortality is indeed high in our study, but is comparable with that observed by others. The grim prognosis attendant on conservative treatment often leaves one no choice but to undertake attempts at surgical correction, even References 1. Kirklin JW, Blackstone EH, Bargeron LM Jr, Pacifico AD, Kirklin JK. The repair of atrioventricular septal defects in infancy . Int J Cardiol . 1986;13:333-351.Crossref 2. Marino B, Guccinone P, Corno A, Papa M, Marceletti C, Dallapiccola B. Facial anomalies in patients with atrioventricular canal and normal chromosomes: the non-Down atrioventricular canal syndrome . Eur Heart J . 1989;10:295. Abstract.

FULGINITI, VINCENT A.

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320011002

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract Sir.—While aware that most of my young patients are being exposed to computer concepts and applications, both at school and in their homes, I was not quite prepared for a recent office encounter. I entered an examining room and questioned Judy, a 9-year-old, why she had come to see me. She responded by handing me the enclosed "print-out." Will office practice soon become obsolete and will care be provided via modems? Russell S. Asnes, MD Tenafly Pediatrics, PA 32 Franklin St Tenafly, NJ 07670 Comment.—Advances have often occurred because our youth have shown us the way. This interesting encounter points out that youngsters in our society are rapidly becoming computer literate at an increasingly younger age. They will drive us into the modern era even if we attempt to dig in our heels. I have observed the same phenomenon in medical education. Medical students have

SISSMAN, NORMAN J.

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320011003pmid: 2378325

Abstract Sir.—It is reassuring to learn from Vet and Ottenkamp1 that their surgical results in repairing complete atrioventricular septal defects in patients with Down syndrome are good enough to warrant doing this surgery on infants with these diagnoses, although other studies2 indicate an expected surgical mortality of 0.3% to 8%. However, in trying to explain why the authors' surgical mortality was so high in infants with complete atrioventricular septal defect who did not have Down syndrome, much more data are required before the statistics can be used in formulating management strategies. The following comments in particular are noted: No information is available about the pulmonary pressures and pulmonary vascular resistances in any of the patients despite the great influence these factors exert on operative morbidity and mortality. The causes of death listed in Vet and Ottenkamp's Table 4 are not specific enough to guide one in References 1. Vet TW, Ottenkamp J. Correction of atrioventricular septal defect . AJDC . 1989;143:1361-1365. 2. Kirklin JW, Blackstones EH, Bargeron LM Jr, Pacifico AD, Kirklin JK. The repair of AV canal defects in infancy . Int J Cardiol. 1986;13: 333-351.Crossref 3. Feldt RH, Edwards WD, Hagler DJ, Puga FJ. Endocardial cushion defect . In: Moller JH, Neal WA, eds. Fetal, Neonatal and Infant Cardiac Disease . East Norwalk, Conn: Appleton & Lange; 1989:411-432.

SLATER, PAUL E.

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320012005pmid: 2378326

Abstract Sir.—In the unending debate between the proponents of oral polio virus vaccine (OPV) and those favoring the addition or substitution of the now enhanced-potency inactivated polio vaccine (E-IPV), the 1988 Israel poliomyelitis outbreak1 was cited by Katz2 in support of continuing, for the time being, the routine use of OPV in the United States. The 15 cases in the Israel outbreak occurred mainly in young adults immunized in the distant past with OPV, in a subdistrict where E-IPV had been used exclusively for several years. We agree with Dr Katz that the spread of wild poliovirus to susceptible people via the under-protected gastrointestinal tracts of E-IPV–vaccinated children was a major factor in the development of the epidemic. Nevertheless, despite wide circulation of wild virus, only a single case of paralytic disease was observed among some 27 000 children who had received E-IPV demonstrating the excellent individual protection References 1. Poliomyelitis-Israel . MMWR . 1988;37:624-625. 2. Katz SL. Poliovirus vaccine policy: another perspective . AJDC . 1989;143:1007-1009. 3. Institute of Medicine. An Evaluation of Poliomyelitis Vaccine Policy Options . Washington, DC: National Academy of Sciences; 1988. IOM publication 88-04. 4. Marcuse EK. Why wait for DTP-E-IPV? AJDC. 1989;143:1006-1007. 5. Melnick JL. Poliomyelitis vaccines: an appraisal after 25 years . Compr Ther. 1980;5:6-14.

KATZ, SAMUEL L.

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320012006

Abstract In Reply.—Dr Slater writes of the unending debate between the proponents of OPV and those favoring the addition or substitution of the new E-IPV. The exchange of commentaries by Drs Marcuse and me was not such a debate but a presentation of positions both favoring the addition of E-IPV. The question was a matter of timing; whether to make the addition now for the private sector only or to introduce it later when all infants and children would benefit, and when E-IPV could be integrated into our immunization schedule to include DTP and conjugate Haemophilus influenza B for infants. We agree with his conclusion that the need exists for "harnessing the special virtues of both of these excellent products." The combined schedule that eventually will be used in the United States will probably differ from that initiated in Israel (E-IPV at 2, 4, and 12 months; trivalent OPV at References 1. Tulchinsky T, Abed Y, Shaheen S, et al. A ten-year experience in control of poliomyelitis through a combination of live and killed vaccines in two developing areas . Am J Pub Health . 1989;79:1648-1652.Crossref

STRONG, W. B.

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320013008

Abstract In Reply.—The letter by Drs Newman, Browner, and Hulley is much appreciated. They raised several important issues and provided an opportunity to expand on the rationale for screening children's total serum cholesterol levels in an office setting (eg, pediatrician, family practitioner, clinic). The data of Lauer et al1 cited in their letter are among the strongest to support the importance of tracking. Adults whose total cholesterol (TC) level exceeds the 95th percentile account for only a small percentage of coronary artery mortality. The vast majority of deaths occur at values that are between the 50th and 95th percentiles. Eighty-three percent of the youngsters described by Lauer et al who were initially above the 90th percentile were above the 50th percentile when measured as young adults. Those youngsters, therefore, become adults at increased risk of coronary artery disease (CAD). Additionally, the distribution of TC in the United States is References 1. Lauer RM, Lee J, Clarke WR. Factors affecting the relationship between childhood and adult cholesterol levels: the Muscatine study . Pediatrics . 1988;82:309-318. 2. Golubjatnikov R, Passkey TR, Inhorn SL. Serum cholesterol levels of Mexican and Wisconsin school children . Am J Epidemiol . 1972;96:36-39. 3. Grundy SM. Cholesterol and coronary artery disease: a new era . JAMA . 1986;256:2849-2858.Crossref 4. Lifshitz F, Moses N. Growth failure: a complication of dietary treatment of hypercholesterolemia . AJDC . 1989;143:537-542.

GRETHER, JUDITH K.

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320014009pmid: 2248653

Abstract Sir.—Your publication of the article by Naeye and Peters1 in the October 1989 issue of AJDC is puzzling. Although presumably written to add clarity to the debate on the role of birth asphyxia as a cause of cerebral palsy (CP), this article offers us a fair measure of further confusion. The article by Naeye and Peters presents analysis of a data set that has already undergone very sophisticated analysis by Nelson and Ellenberg2,3 and Freeman and Nelson.4 Assuming that Drs Naeye and Peters feel the Nelson and Ellenberg analyses to be deficient on some accounts (why else bother to reanalyze the same data?), they fail to enlighten the reader with specific criticisms of their analyses, with information on how their classification of cases and exposure factors and their results differ from those of Nelson and Ellenberg.2,3 Further, Naeye and Peters do not adequately distinguish between References 1. Naeye RL, Peters EC. Origins of cerebral palsy . AJDC . 1989;143:1154-1161. 2. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy, I: univariate analysis of risks . AJDC . 1985;139:1031-1038. 3. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy, II: multivariate analysis of risk . N Engl J Med . 1986;315:81-86.Crossref 4. Freeman JM, Nelson KB. Intrapartum asphyxia and cerebral palsy . Pediatrics . 1988;82: 240-249.

NAEYE, RICHARD L.;LANDIS, J. RICHARD

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320014010

Abstract In Reply.—Our study used different analytical methods from those employed by Nelson and Ellenberg1 and thereby produced different findings. Nelson and Ellenberg used fetal bradycardia, low Apgar scores, and a delay in a newborn's first cry to identify birth asphyxia. They may have been uncertain about the specificity of these criteria because they did not draw any final conclusions about the number of children in the study who had cerebral palsy (CP) as the result of birth asphyxia. We used specific birth asphyxial disorders that were followed by neonatal seizures to identify asphyxiated neonates. Using these criteria, 9 of the 150 cases of CP in the study could be attributed to birth asphyxia. We found strong indirect evidence that no cases of cerebral palsy due to birth asphyxia were missed in our analyses. We also found that low Apgar scores and several other common clinical consequences of birth References 1. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy, II: multivariate analysis of risk . N Engl J Med . 1986;315:81-86.Crossref 2. Bruzzi P, Green SB, Byar DP, Brinton LA, Schairer C. Estimating the population attributable risk for multiple risk factors using case-control data . Am J Epidemiol . 1985;122:904-914. 3. Benichou J, Gail MH. Variance calculations and confidence intervals for estimates of the attributable risk based on logistic models. Biometrics. In press.

WEDIN, GREGORY P.;RICHARDSON, SHARON L.;WALLACE, GREGORY H.

1990 American Journal of Diseases of Children

doi: 10.1001/archpedi.1990.02150320015011pmid: 2378328

Abstract Sir.—Clonidine hydrochloride is one of several medications that can produce serious toxicity in children with ingestion of only a small amount. We describe a 3-year-old child who ingested a single 0.2-mg clonidine hydrochloride tablet and developed coma, respiratory depression, and hypotension. This is the lowest dose reported to cause such profound toxicity in a young child. Patient Report.—A 3-year-old boy ingested one of his grandmother's 0.2-mg clonidine hydrochloride (Catapres) tablets. Actual ingestion was not observed, but a single tablet placed on a table was missing. The child indicated he had eaten it. He was transported by ambulance to the local emergency department. Approximately 1 hour after ingestion, the child was very lethargic and pale. His vital signs were as follows: heart rate, 76 beats per minute; respiratory rate, 8 to 10 per minute; and blood pressure, 100/80mm Hg. An intravenous line was placed and 5% dextrose in lactated References 1. Olsson JM, Pruitt AW. Management of clonidine ingestion in children . J Pediatr . 1983;103:646-650.Crossref 2. Neuvonen PJ, Vilska J, Keranen A. Severe poisoning in a child caused by a small dose of clonidine . Clin Toxicol . 1979;14:369-375.Crossref 3. Conner CS, Watanabe AS. Clonidine overdose: a review . Am J Hosp Pharm . 1979;36:906-911. 4. MacFaul R, Miller G. Clonidine poisoning in children . Lancet . 1977;1:1266-1267.Crossref 5. Rumack BH, Temple AR. Lomotil poisoning . Pediatrics . 1974;53:495-500. 6. Klein-Schwartz W, Gorman R, Oderda GM, Baig A. Central nervous system depression from ingestion of nonprescription eyedrops . Am J Emerg Med . 1984;2:217-218.Crossref 7. Howrie DL, Moriarty R, Breit R. Candy flavoring as a source of salicylate poisoning . Pediatrics . 1985;75:869-871. 8. Caravati EM, Litovitz TL. Pediatric cyanide intoxication and death from an acetonitrile-containing cosmetic . JAMA . 1988;260:3470-3473.Crossref