doi: 10.1001/archpedi.1985.02140110003001pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archpedi.1985.02140110011002pmid: 4036905
Abstract Sir.—Interestingly, the effectiveness of pediatric cardiopulmonary resuscitation (CPR) as described by Torphy et al1 parallels the results specific to the effectiveness of adult CPR in our community's paramedic system (data unpublished). In fact, recent analysis of more than 400 adult prehospital cardiac arrests occurring over a three-year period provides a similar mortality rate of greater than 90%. In some of the prior reports on this subject specific to adults, the methodology utilized, such as what connotates the definition of long-term survivor and the exclusion of certain patient groups such as asystole patients, has probably contributed to an inaccurate representation of the actual adult mortality rate secondary to cardiac arrest in the majority of paramedic systems in this country. There is no doubt that the findings of Torphy et al probably represent a more accurate mortality rate secondary to cardiac arrest in the community for both pediatric and adult patients References 1. Torphy DE, Minter MG, Thompson BM: Cardiorespiratory arrest and resuscitation of children . AJDC 1984;138:1099-1102. 2. Eisenberg MS, Copass MK, Hallstrom AP, et al: Treatment of out-of-hospital cardiac arrests with rapid defibrillation by emergency medical technicians . N Engl J Med 1980;302:1379-1383.Crossref 3. Stults KR, Brown DD, Schug VL, et al: Prehospital fibrillation performed by emergency medical technicians in rural communities . N Engl J Med 1984;310:219-223.Crossref
WILKINS, JEANETTE;WEHRLE, PAUL F.
doi: 10.1001/archpedi.1985.02140110011003pmid: 4036906
Abstract Sir.—We read with interest the article by Lampe et al1 concerning measles reimmunization in children immunized before 1 year of age. The data were compared with our earlier publication.2 It is important to recognize that Lampe et al have included 13 of the 18 infants who responded to the first dose of measles vaccine. Our study included 37 infants who were selected because each had failed to develop detectable hemagglutination inhibition (HI) antibody at a dilution ≥1:8 by four or more weeks after inoculation and had undetectable titer at the time of inoculation. For a true comparison, only five of the infants in their study qualify. Because each of these five infants developed detectable HI antibody, the authors did not identify any nonresponders to the second dose. However, it should be appreciated that, as in the present report, 24 of our 37 infants had HI antibody detectable References 1. Lampe RM, Weir MR, Scott R: Measles reimmunization in children immunized before 1 year of age . AJDC 1985;139:33-35. 2. Wilkins J, Wehrle PF: Additional evidence against measles vaccine administration to infants less than 12 months of age: Altered immune response following active/passive immunization . J Pediatr 1979;94:865-869.Crossref
KOÇAK, NURTEN;ÖZSOYLU, ŞINASI;SARIALIOGLU, FAIK;GOKSU, NESRIN
doi: 10.1001/archpedi.1985.02140110012005pmid: 2994464
Abstract Sir.—Association between hepatitis B surface antigen (HBsAg) and hepatocellular carcinoma (HCC) has been strongly suggested by Szmuness,1 and integrated hepatitis B virus DNA (HBV-DNA) has been demonstrated in human HCC cell lines.2 It has also been strongly suggested that HCC patients acquire hepatitis B virus from their mothers during the perinatal period in populations with a high HBsAg prevalence. To our knowledge, this association has been reported only in adults, more in men than in women. Patient Report.—A 10-year-old Turkish boy had HCC in whom HBsAg was present but in whom anti–HBs remained negative. He was seen in this hospital on Sept 21, 1984, because of a protuberant abdomen, lassitude for 1½ months' duration, and recent jaundice. He was underdeveloped, cachectic (weight, 24 kg; height, 125 cm; both values less than third percentile), and jaundiced. The liver was markedly enlarged with several very hard masses. The spleen References 1. Szmuness W: Hepatocellular carcinoma and the hepatitis B virus: Evidence for a cause association . Prog Med Virol 1978;24:40-69. 2. Chakraborty PR, Ruíz Opazo N, Shouval D, et al: Identification of integrated hepatitis B virus DNA and expression of viral RNA in an HBsAg-producing human hepatocellular carcinoma cell line . Nature 1980;286:531-533.Crossref 3. Hino O, Kitagawa T, Hirama T, et al: Hepatitis B virus DNA integration in hepatoblastoma . Lancet 1984;1:462-463.Crossref
LAMPE, RICHARD M.;WEIR, MICHAEL R.
doi: 10.1001/archpedi.1985.02140110011004pmid: N/A
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 In Reply.—Drs Wilkins and Wehrle have identified important differences between their study and ours. Their study, published in 1979, served as the impetus for us to obtain sera on children who had received rubeola vaccine before 1 year of age and were about to receive the MMR vaccine at 15 months of age. We did not obtain sera later than 52 days after MMR vaccination; therefore, we agree that our results should not be directly compared with their results indicating that 51% of 37 infants identified as vaccine failures had no detectable HI antibody by eight months after revaccination. We would also like to address three points raised by Wilkins and Wehrle. First, some children in the vaccinated group could have experienced wild measles virus infection, although we had no history of this at the time of MMR vaccination. Second, we sought to obtain acute and convalescent sera from
doi: 10.1001/archpedi.1985.02140110012006pmid: 4036907
Abstract Sir.—Sell et al1 recently reported on the neurodevelopmental outcome of infants suspected of having persistent fetal circulation (PFC) in the newborn period. The significant number of infants noted to have a hearing loss is an important finding. The authors' findings, however, may not be applicable to all infants with persistent pulmonary hypertension of the newborn (PPHN) because of a number of apparent flaws in the study. First, the authors give the impression that all infants with PPHN born during the study period were included in their population. If this is true, how do the authors account for a mortality rate of 0% over seven years? The reported mortality rate for PPHN during the same period was 50% to 78%.2,3 Next, less than half of the study population had PPHN as defined by Fox and Duara.4 The authors define PFC or PPHN in the introduction as hypoxemia References 1. Sell EJ, Gaines JA, Gluckman C, et al: Persistent fetal circulation: Neurodevelopmental outcome . AJDC 1985;139:25-28. 2. Peckham GJ: Risk-benefit relationships of current therapeutic approaches , in Peckham GJ, Heyman MA (eds): Cardiovascular Sequelae of Asphyxia in the Newborn . Columbus, Ohio, Ross Laboratories, 1982, pp 110-116. 3. Murphy JD, Vawter GF, Reid LM: Pulmonary vascular disease in fatal meconium aspiration . J Pediatr 1984;104:758.Crossref 4. Fox WW, Duara S: Persistent pulmonary hypertension of the neonate (PPHN): Diagnosis and management . J Pediatr 1983;103:505-514.Crossref 5. Ballard RA, Leonard CH: Developmental follow-up of infants with persistent pulmonary hypertension of the newborn . Clin Perinatol 1984;11:737-744.
doi: 10.1001/archpedi.1985.02140110013008pmid: 4036908
Abstract Sir.—In a recent article, Erenberg and Nowak1 proposed a hypothesis for groove formation secondary to oral endotracheal intubation: "... continuous pressure of the endotracheal tube against the median palatine suture." An alternative explanation would be the absence (or presence) of tongue pressure against the palatal shelves, which allows the shelves to grow toward each other. This would explain grooving in the midline when the endotracheal tube is secured away from the midline, ie, at either corner of the mouth. In our unit, oral endotracheal tubes are secured at the mouth corners and, hence, the endotracheal tubes do not traverse the midline. Still, we invariably see midline grooving in patients treated with prolonged oral endotracheal intubation. In our experience, these grooves eventually resolve after extubation, although this may take some time. The tongue is known to play an important role in palate-shape development.2,3 Absence from its proper position leads to References 1. Erenberg A, Nowak AJ: Palatal groove formation in neonates and infants with orotracheal tubes . AJDC 1984;138:974-975. 2. Smith DW: Recognizable Patterns of Human Deformation . Philadelphia, WB Saunders Co, 1981, pp 139-140. 3. Hanson JW: Prominent lateral palatine ridges: Developmental and clinical relevance . J Pediatr 1976;89:54.Crossref
doi: 10.1001/archpedi.1985.02140110012007pmid: N/A
Abstract In Reply.—Dr Horgan has made several important observations regarding our report. We did not address mortality rate in our study nor did we intend to suggest that it was 0%; that information was neither available nor retrievable retrospectively. It is now possible to define PFC (PPHN) with greater accuracy than was available to us, particularly during the early study period. As Dr Horgan notes, Fox and Duara1 suggested one or more of the following as diagnostic tests for PPHN, although it is not clear which one(s) is(are) considered diagnostic: (1) hyperoxia test (term infants only); (2) preductal and postductal arterial oxygen levels; (3) hyperoxia-hyperventilation test; and (4) echocardiographic evaluation of systolic time interval ratios and/or myocardial function. In our study the diagnosis was made by the attending neonatologist from a combination of clinical factors as well as echocardiographic findings in some patients. The four patients who received oxygen References 1. Fox WW, Duara S: Persistent pulmonary hypertension of the neonate (PPHN): Diagnosis and management . J Pediatr 1983;103:505-514.Crossref
doi: 10.1001/archpedi.1985.02140110014011pmid: 4036910
Abstract Sir.—In their report Yarom et al1 comment on the association of secondary gout in childhood with inborn errors of purine metabolism, glycogen storage disease type I, familial syndromes of hyperuricemia and renal disease, severe uremia, and myeloproliferative disorders (leukemia and lymphoma), but they make no mention of secondary juvenile metabolic gout caused by well-compensated intracorpuscular hemolysis.2 Although Vora3 has eloquently described juvenile gout associated with well-compensated hemolysis without anemia due to deficiency of isozymes of phosphofructokinase, and though we have emphasized the importance of measuring red blood cell phosphofructokinase and its isozymes in children with unexplained gout,4 we find no mention of this subject or these studies by Yarom et al.1 We also find no mention of reticulocyte count or red blood cell survival time. We note the hemoglobin value of 16.9 mg/dL in their 14-year-old female patient (case 2) and wonder whether her References 1. Yarom A, Rennebohm RM, Strife CF, et al: Juvenile gouty arthritis: Two cases associated with mild renal insufficiency . AJDC 1984;138: 955-957. 2. Liberman UA, Samuel R, Halabe A, et al: Juvenile metabolic gout caused by chronic compensated hemolytic syndrome . Arthritis Rheum 1982;25:1264-1266.Crossref 3. Vora S: Isoenzymes of phosphofructokinase . Isozymes Curr Top Biol Med Res Isozymes 1982;6:119-167. 4. Jacobs JC: Comment on report by Liberman et al . Arthritis Rheum 1984;27:116.
LEWIS, DONALD W.;BERMAN, PETER H.
doi: 10.1001/archpedi.1985.02140110014010pmid: 4036909
Abstract Sir.—The recent report by Schwarz et al1 regarding prolonged elevation of presumed hepatic enzyme levels in children with unsuspected myopathy cannot be overemphasized. We recently had a similar experience. Patient Report.—A 4-year-old, right-handed boy was referred to the Division of Neurology, Children's Hospital of Philadelphia, for evaluation of progressive muscle weakness. Neurologic examination disclosed mild proximal muscle weakness with preserved deep tendon reflexes. Gowers' sign was present. Pseudohypertrophy of calf muscles was noted. His creatinine phosphokinase (CPK) level was 15,000 IU/L. Muscle biopsy results demonstrated myopathic features consistent with Duchenne type muscular dystrophy (DMD). On admission an extensive family history was taken. He had two 3-year-old siblings—monozygotic twin brothers who had "mild chronic hepatitis." Further history disclosed that they were born eight weeks premature. They did well until about 6 months of life when they were hospitalized with enteritis and dehydration. Screening chemistry tests had revealed elevations of References 1. Schwarz KB, Burris GC, deMello DE, et al: Prolonged elevation of transaminase concentration in children with unsuspected myopathy . AJDC 1984;138:1121-1124. 2. Hudgson P, Pearce GW, Walton JN: Preclinical muscular dystrophy: Histopathologic changes observed on muscle biopsy . Brain 1967;90:565-576.Crossref 3. Pennington RJT: Clinical biochemistry of muscular dystrophy . Br Med Bull 1980;36:123-126.
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