1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060012001
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060016003
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.—Dr Rinsler's suggestion that pediatricians be trained to assume care of "young adults" in the third decade of life is an appealing one. The skills that pediatricians have developed in the prevention of disease and in the care of chronically ill children would be particularly applicable to the care of young adults. The opportunities to work with young adults in their pursuit of healthy lifestyles and the opportunities to continue to care for chronically ill children surviving into adolescence and young adulthood are multiple. I further agree with Dr Rinsler that no physician group currently focuses on young adults. It is a logical extension of pediatrics, and it would be interesting to hear from our colleagues as to what their thoughts might be concerning Dr Rinsler's interesting suggestion.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060016002pmid: 3578174
Abstract Sir.—Dr McAnarney1 forsees an increasing oversupply of pediatricians. I agree with her. She suggests that some pediatricians shift to geriatric medicine. I disagree with this and instead suggest an alternative closer to her own subspecialty—the medical care of those between their late teens and 30s ("young adults"). I base this recommendation on my experience with this group in private practice from 1978 through 1985 and on demographic and epidemiologic data and projections. Consider the following: (1) Young adults are numerous, but no physician group focuses particularly on them; (2) they are the most logical focus for preventive health measures; (3) the medical problems they have are by and large the same as those of the adolescent or older child; (4) pediatricians have the greatest experience of any group in dealing with these persons, since they more commonly visit a physician as parents than as patients; and (5) the References 1. McAnarney ER: Pediatrics to geriatrics? AJDC 1986;140:866.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060016004pmid: 3578175
Abstract Sir.—I have been following with interest the recent editorials in AJDC1 and other pediatric journals2,3 questioning pediatricians' involvement in pediatric primary care. In his excellent letter in AJDC, Dr Comerci4 made a nice rebuttal with which I happen to be in full agreement. What prompted me to write this letter was the reply of Dr Helfer.5 As a currently full-time academic practicing pediatrician with an extensive academic subspecialty and general pediatric background, I wonder if such an attitude reflects a lack of contact with the reality of pediatrics as a specialty. Dr Helfer divided the practice of pediatrics into three tasks: yellow, green, and red. Unless all pediatricians hire a screening person, I cannot see how they will predetermine which of the patients sitting in the waiting room belong to which category and whether one is going to change category from yellow to red in References 1. Helfer RE: Primary care: Does it belong in pediatrics? AJDC 1985;139:974-975. 2. Garfunkel JM: The pediatrician of the future . J Pediatr 1985;207:910-912. 3. Cleveland WW: Dormant correspondence Cleveland J Pediatr 1985;107:910-911.Crossref 4. Comerci GD: Primary care is an end in itself . AJDC 1986;140:848-849. 5. Helfer RE: Primary care is an end in itself . AJDC 1986;140:849.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060017005pmid: 3578176
Abstract Sir.—Traditionally, most of us have been taught that a female chaperone should be present during pelvic examinations by male physicians. One textbook of adolescent medicine1 stated, "It is advisable to examine adolescent girls only in the presence of a chaperone." Implicit in this recommendation was concern about possible allegations of assault and battery directed toward male physicians by female patients if there were no witnesses to testify to the contrary. Chaperones usually were nurses who helped physicians with procedures and explained those procedures to patients. Most physicians were taught that proper medical practice dictated such protocol. As pediatricians have increasingly provided services for adolescents, the use of chaperones during genital examinations has become a subject of scientific inquiry. Furthermore, as more women physicians are being trained, questions have been raised about whether chaperones should be present while female physicians perform genital examinations on male patients.2 Questions have References 1. Gallagher JR: The care of adolescents , in Gallagher JR, Heald FP, Farrell DC (eds): Medical Care of the Adolescent , ed 3. East Norwalk, Conn, Appleton-Century-Crofts, 1976, p 71. 2. Phillips S, Friedman SB, Seidenberg M, et al: Teenagers' preferences regarding the presence of family members, peers and chaperones during examination of genitalia . Pediatrics 1981; 68:665-669. 3. Phillips S, Bohannon W, Heald FP: Teenagers' choices regarding the presence of family members during the examination of the genitalia . J Adolesc Health Care 1986;7:245-249.Crossref 4. Faigel HC: Attitude of college students toward medical genital examination and self-examination of their own genitals , abstracted. J Adolesc Health Care 1981;2:163. 5. Buchta RM: Use of chaperones during pelvic examinations of female adolescents: Results of a survey . AJDC 1987;141:666-667.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060018007pmid: 3578177
Abstract Sir.—I read with great interest the report by Huseman and colleagues1on a child with prolactinoma. The letter was extremely valuable in pointing the efficacy of bromocriptine therapy even in large tumors. It is reassuring to read that this conservative approach to treatment is as efficacious in children as it is in adults. In their report, the authors referenced 11 other cases of prolactinoma in children 13 years of age or younger. It should be pointed out that other cases the have been reported. I searched the literature following the referral of a 13-year-old boy who exhibited hypopituitarism after the surgical removal of a nonsecretory pituitary adenoma. Richmond and Wilson2 described 25 children and adolescents with pituitary adenomas, 11 of which were prolactinomas. The adenomas reprefound sented 33% of parasellar tumors found in their series of individuals younger than 20 years old. Nine of the 25 young_ References 1. Huseman CA, Rizk G, Hahn F: Long-term bromocriptine treatment for prolactin-secreting macroadenoma . AJDC 1986;140:1216-1217. 2. Richmond IL, Wilson CB: Pituitary adenomas in childhood and adolescence . J Neurosurg 1978;49:163-168.Crossref 3. Lucas C: Adenomes à prolactine de l'enfant, thesis. Faculté de Médecine de Mar seille, France, 1977.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060017006
Abstract In Reply.—I appreciate the comments by Dr McAnarney. One of my main purposes for submitting my article was to elicit such a discussion. What is the role of a chaperone for patients in our present society? Is it the same role as in 1950? Is the role of the chaperone different in regard to minors vs adults? Is a chaperone mainly for the benefit of the physician or for the patient? These questions remained unanswered. At least in my practice (and from my survey, in the practices of up to 30% of physicians who deal with adolescents), the preference for usage of a chaperone during a genital examination has moved from hypothetical into reality.1 I certainly do not advocate this "change in tradition" for everyone until further research to answer the many questions has been completed. However, I have become comfortable with this arrangement, and it has been References 1. Buchta R: Adolescent females' preferences regarding use of a chaperone during a pelvic examination: Observations from a private practice setting . J Adolesc Health Care 1986;7: 409-411.Crossref
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060019008pmid: 3578178
Abstract Sir.—We read with interest the article these "Learning Disabilities and Attentional Problems in Boys with the Fragile X Syndrome" by Hagerman et al 1 in the July 1985 issue of AJDC. The authors described four boys with incontrovertible evidence of fragile X (fra[X]) chromosome but a higher than usual cognitive level of development, who also showed language difficulties and poor arithmetic skills with a relative strength in reading. All children also showed some atypical behavior, such as hand flapping, mouthing of objects, hand bitting, and a general pattern of distractibility and impulsiveness; one child showed fascination with spinning objects. The authors identified these children as showing a clinical picture of learning disabilities, but the behavioral, abormalities and the neurocognitive profile of these children would lead us to classify them instead as having Asperger's syndrome. In 1944, Asperger2d a syndrome that somewhat resembles Kane's8 picture of infantile autism. Curetly, we are investigating whether Asperger's8 syndrome is a variety of autism without mental retardation, or a separate syndrome. Wing4 resurrected the syndrome and slightly modified the diagnostic criteria on the basis of her experience with 34 cases. In this modified version, children with Asperger's syndrome snowed a delay References 1. HagermansR, Kemper s,bilities and attentional problems in boys with the fragile Xsyndrome . AJDC e fragile X syndrome. 2. Asperger H: Die 'PsychopiKinderP Nerv 1944;117:76-136. 3. Kanner L: Autistic disturbances of affective contact . Nervous Child 1943;2:217-250. 4. Wing L: Asperger's syndrome: A clinical account . Psychol Med
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060019009
Abstract In Reply.—Drs Bartolucci and Szatmari present an interesting speculation that I have considered many times in the past. Although approximately 16% of male children with fra(X) chromosome will fulfill Diagnostic and Statistical Manual, ed 3, criteria for infantile autism, the majority of boys with fra(X) syndrome demonstrate only some autistic features, such as hand flapping, hand biting, and poor eye contact without a pervasive lack of relatedness.1 These problems, combined with perseverations in language and behavior, such as fascination with spinning objects, makes one consider the terms autisticlike or a high-functioning autistic child, and yet many children with fra(X) syndrome can relate quite well to their family and peers. The juxtaposition of an ability to relate with some autistic features is perhaps the source of controversy concerning the incidence of autism in fra(X) syndrome and the incidence of fra(X) chromosome in autism. Asperger's syndrome can be simplistically viewed References 1. Hagerman RJ, Jackson AW, Levitas A, et al: An analysis of autism in 50 males with the fragile X syndrome . Am J Med Genet 1986;23:359-374.Crossref
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060020011pmid: 3578179
Abstract Sir.—Several new observations on the natural history of multicystic dysplastic kidneys (MCDKs) may help to deliver Hartman et all from their dilemma. On serial prenatal ultrasonography (US) of six fetal MCDKs, Hashimoto et al2 found that four MCDKs one increased in size, one shrank, and one initially grew larger but subsequently shrank. Only for this last MCDK was a postnatal sonogram reported: the MCDK had become diminutive when the infant was 6 months old. Pedicelli et al3 described nine infants with MCDKs that either diminished in size or completely disappeared over periods of serial US ranging up to three years. Two of these infants, aged 6 and 9 months, underwent operative flank explorations that failed to disclose any vestiges of cysts or renal tissue. The authors postulated that spontaneous involution of MCDKs might account for some cases of apparent, unilateral renal agenesis. nat Both reports2,3 suggest that the natural course of References 1. Hartman GE, Smolik LM, Shochat SJ: The dilemma of the multicystic dysplastic kidney . AJDC 1986140: 2. HashimotoBE, Filly RA, Callen PW: Multicystic dysplastic kidney in utero: Changing 107 109 appearance on ultrasound . Radiology 1986;159: 3. Pedicelli G, Jequier S, Bowen A, et al: Multicystic dysplastic kidneys: Spontaneous regression demonstrated with ultrasound . Radiology 1986;160:23-26. 4. Stanisic TH: Review of'The Dilemma of the Multicystic Dysplastic Kidney .' AJDC 1986;140:865.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060020010pmid: 3495169
Abstract Sir.—Although my dossier of correspondence about the current "diphtheria-pertussis-tetanus vaccine controversy" is almost 1 in thick, I feel compelled to write about it one more time after reading the letters by Hinman1 and Somervill2 in the December 1986 issue of AJDC. It is obvious that the medical and legal professions do not share anything resembling a consensus reality, but I think it is important for both of the professions to be aware of just how skewed their thinking has become by their respective educations and experiences, and not to become too defensive. Although I quite frankly think this issue is a disagreement where no disagreement should exist, this is a real problem for the medical profession. A cornerstone of preventive medicine, vaccination, has been eroded by people who we think do not have the expertise to accurately judge the situation. I think the legal profession does not References 1. litigation AJDC 1. Himan AR: DTP vaccin e 1986;140:1210. 2. Somervill RR: DTP vaccine and liability . AJDC 1986;140:1210-1211.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060021013
Abstract Sir.—I welcome any effort to increase awareness of the problems of nuclear energy, such as Dr Beverly Morgan's1 "Nuclear Energy and Its Effect on Mankind." However, I was disappointed that her opinion piece concluded by asking a question and stating a generality. We know enough now to give answers to most questions about nuclear energy and to make specific recommendations for remedies. We know that the health effects of the atomic bombs dropped over Japan, the weapon tests in the Pacific and the American West, and accidents that have occurred in nuclear power plants in several countries (including our own) are only mild warnings of possible (indeed probable) future nuclear disasters that threaten the health and lives of millions of persons, if not the future of mankind itself. We know that the only way to prevent such possible disasters is for nationsake specific steps, including the following: (1) a complete cessation of development and testing of References 1. Morgan BC: Nuclear energy and itsfect on onind . AJDC 1987;1987;141:33.
Golden, SamuelE.;Kelly, JamesC.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060021014
Abstract Sir—.In a recent issue of the ARCHIVES, Likitnukul et al1 found arthritis to be a complication of Haemophilus influenzae and Neisseria meningiditisismeningitis in 3% to 4% of cases. Arthritis was not identified, however, in 179 cases of pneumococcal meningitis. We describe herein a patient with pneumococcal meningitis complicated by possible immune complex–mediated Patient Report— A full-term male infant was born by cesarean section because of maternal preeclampsia and cephalopelvic disproportion. Membranes were ruptured for five hours prior to delivery, and there were no signs of maternal or fetal infection. Apgar scores were 8 at both one and five minutes. The infant remained well until the fourth day of life when irritability and a temperaure of 39.5°C Blood and cerebrospinal fluid specimens yielded Streptococcus pneumoniae susceptible to penicillin by oxacillin disk testing. Therapy with ampicillin and gentamicin was begun; the latter drug was discontinued the followingy. Repeated blood cultures obtained after two and five days of therapy were sterile, as were cerebrospinal fluid specimens examined after three days of treatment. His condition stabilized and his course References 1. LikitnukulkS,HMcCrackenJr, Arthritis in children with bacterial meningitis . AJDC 1986;140:424-427. 2. Rush PJ,ore A, Inman R, et al: thritis associated with Haemophilus meningitis:c or reactive? JP 415. 3. Davis JAS, Peters N, Mohammed I, et al: Circulating immune complexes in a patient with meningococcal disease . Br Med J 11446.Crossref 4. Larsen HE, Nicholson KG, Loewi G, et aal: Arthritis after meningococcal meningitis . Br Med J J91977;1:618.Crossref
Hartman, Gary E.;Shochat, Stephen J.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060020012
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.—We appreciate Dr Bowen's letter calling out attention to the recent reports of prenatal US identification of MCDKs, as well as his thoughts regarding the natural history of these lesions. Although the number of prenatally identified lesions is small, it is interesting to note the high rate of decrease in size documented by the two reports.While decrease in size is understandable, it is hard to explain the complete resorption or dissolution of a dysplastic organ. While many of these kidneys may indeed decrease in size, it is not clear that a decrease in size is equivalent to a decrease in risk to the patient, specifically in regard to the development of hypertension or malignant change. It is clear that we have inadequate knowledge of the natural history of MCDK to make an unequivocal recommendation for either routine resection or nonoperative observation. Our dilemma revolves around a lack of such information and a documentation of potentially serious complications, such as hypertension and malignant lesions, in retained MCDKs. Since it is unclear whether the risk of these complications is greater in MCDK patients than in the general population, the only definitive statement that can be rendered is that if such lesions are left in place, careful monitoring on a regular basis for the development of such complications is incumbent on the primary physician.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060022017
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.—Dr Lee's first point cannot be answered directly, since the population served by the Los Angeles County/USC Medical Center pediatric Diabetic Clinic is 90% to 95% Hispanic. There were not enough white or black patients to provide an internal comparison of the prevalence of AMAs, and we were forced to rely on data in the literature for this purpose. The main questions raised by Dr Lee concern the process of laboratory screening for thyroid dysfunction, the clinical evaluation of thyroid function in patients with diabetes, and the indications for treatment in this population. We recommended screening for thyroid autoimmunity with laboratory assessment of thyroid funtion in those patients who are found to have circulating AMAs. This approach first asks a pathogenetic question and reserves laboratory assessment of thyroid function for those patients found to have a marker of thyroid autoimmunity. As Dr Lee indicates, the assessment of autoimmunity must
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060022015
Abstract Sir.— Dr Brouhard's editorial "Surreptitious Insulin Administration" in the January issue of AJDC discussed an important cause of unexplained hypoglycemia in the type I diabetic patient. Surreptitious insulin administration be considered seriously in any diabetic with drastically reduced insulin requirements. However, Dr Brouhard failed to mention the possibility of autoimmune adrenalitis presenting similarly. Any type I diabetic patient is at risk for other autoimmune disease as part of an autoimmune polyglandular syndrome. Although adrenal failure is uncommon in the pediatric patient, the life-threatening nature of this condition makes early diagnosis essential. Autoimmune adrenalitis should be considered in all type I diabetics with unexplained hypoglycemia, especially those with other autoimmune diseases (most commonly autoimmune thyroiditis) or a family history of an autoimmune polyglandular syndrome. References 1. Brouhard reptitious insulin administratioistratio n .1987;141:28-29.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060022016pmid: 3578181
Abstract Sir.—The data of Frasier et al1 regarding an increased prevalence of antithyroid microsomal antibodies (AMAs) among Hispanic children with insulin-dependent diabetes mellitus are certainly intriguing and lend support to previous recommendations for routine thyroid screening in children with diabetes. However, I have the following questions and concerns regarding their data interpretation and conclusions: 1. While the authors point out the many problems with the performance and interpretation of assays for antithyroid antibodies, they also suggest that their data support an increased prevalence of AMA positivity in Hispanic diabetic children relative to non-Hispanic diabetic children. The authors do not, however, present their own data in a non-Hispanic population, and it is not clear that the assays used in previous studies are comparable with those used in their report. 2. The authors recommend careful clinical assessment for thyroid dysfunction, yet do not report whether their hypothyroid diabetics manifested any suggestive signs or References 1. Frasier SD, Penny R, Snyder R, et al: Antithyroid antibodies in Hispanic patients with type I diabetes mellitus AJDC 1986;140:1278-1280.
DembDembert, Mark;Keith, Julian F.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060023019
Abstract In Reply.—The points raised by Brouhard et al regarding our recommendation not allowing a person with IDDM to dive are well taken. We fully agree that the patient with IDDM should be allowed to lead as normal a life-stylele, including most sports. However, we believe that it is not prudent to allow these patients to participate in scuba diving, for the following reasons: In contrast to land-based the undersea environment is unpredictable and unforgiving, with sudden changes in temperature, current, and surface conditions; there is also the potential to encounter marine animals and for equipment to fail. Diving partners should be equally healthy, physically fit and responsible; each should have the physical and mental stamina required to cope with dangerous situations. A diver should not be present to "watch out" for a partner who has a disease or disorder that can be exacerbated underwater. Adiver cannot predict that any dive will be without problems. The above characteristics References 1. Davis JC (ed): Medical Examination of Sport Scuba Divers , ed 2. San Antonio, Tex, Medical Seminars Inc, 6. 2. Hickey DD: Outline of medical Stanstandards divers . Undersea BiomBiomed 11:401984;11:407-432.
BroBrouhard, Ben;MTravis, LutLuthers;SBarbaraMSchreiner, Barbara;Hende, S;McMahon, P
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060023018
Abstract Sir.— The article "Evaluating the Potential Pediatric Scuba Diver" by Dembert and Keith1 stated that a an absolute disqualification to scuba diving is insulin-dependent diabetes mellitus (IDDM). We certainly concur with the auhors that "if a hypoglycemic episode occurs underwater or away from shore, the results could be incapacitating and tragic." However, this same warning applies to almost any activity in which the insulin-dependent diabetic chooses to participate (eg, driving a car). It would be unfair to disallow those responsible adolescents to participate in an activity they choose without some individualization. Although editorial space limitations may not have permitted the authors elaborate on conditions for disqualifications, absolute prohibition of this activity for a person with IDDM is inappropriate. As with any physical activity that may potentiate hypoglycemia, bolicrol should be as good as sible, glucose levels should be monitored before the activity is taken, and an appropriate plan of action should be taken to prevent hypoglycemia during the activity. Furthermore, sufficient training in a more protected environment (eg, swimming pool) should allow the person with diabetes to know what to expect and the degree to which such activity will affect the blood glucose level. As with any strenuous exercise, a "buddy system" References 1. Dembert ML, Keith JF: Evaluating the potential pediatricver . AJDC 1986;140:1986;140: 1136-11411136-1141. 2. Adamkin DH: Medical care of the athlete . AJDC 1978;132:181-187. 3. Travis LB, Speegle D: Diabetes mellitus and athletics . AJDC 1978;132:725.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060024021
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 We made a specific effort in our article to refrain from generalizing the observed adjustment disorders seen in some adolescents to all adolescents. We agree with Dr Buchta's comments that some adults exhibit these same traits; neither of us would want to dive with such a person, whether he or she was an adolescent or an adult. Our article served as a means for us to educate nondiving physicians about scuba diving, particularly as follows: (1) It is an elective hobby for most people, but it is a hobby fraught with the potential for serious medical emergencies and adverse sequelae because it is conducted at sea or in lakes, far from land-based emergency medical services. (2) There is a definite need for all diving partners to be in equally good health and to have equally good skills and knowledge so that they can dive safely and react appropriately to emergencies. (3) It is incumbent on physicians performing examinations on potential
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060024020pmid: 3578183
Abstract Sir.—I recently finished reading an article published in AJDC on the pediatric scuba diver1This article was informative, but I take exception to the unjustified generalization made about adolescents by the authors. Concerning the minimum age requirements scuba divers, the authors stated that during the normal stresses of development, certain children and adolescents develop adjustment disorders with symptoms and signs of impulsivity, lack of responsibility, egocentricity, and emotional lability. These characteristics can impair physical performance and responses to environmental hazards; therefore, such characteristics are not desirable in dive partners. From this, the authors concluded that a higher minimum age requirement is recommended for diving. As a physician with over 16 years of experience dealing with children, adolescents, and their families, the undesirable characteristics listed in the article apply equally to some adults as to the pediatric/adolescent population. Certainly, there may be some valid physiologic and developmental reasons for increasing the minimum age for scuba diving. However, to exclude the pediatric/adolescent age group because a References 1. Dembert ML, Keith JF III: Evaluating the potential pediatric scuba diver . AJDC 1986;140: 1135-1141.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060025022
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060027023
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 The history of medical science is an important part of our education and heritage. Scientific "discoveries" are sometimes the result of serendipity, but most of the time the accomplishments are based on previous observation by many investigators. Thus, those individuals who have been recognized nationally and internationally have made their discoveries by building on observations of previous work by these unsung heroes. Who were these investigators who are now forgotten but whose inquisitiveness and powers of observation allowed for later substantial understanding of disease or disease processes? With this issue of AJDC, we are beginning a new section entitled THE AJDC ARCHIVES. The Editorial Board has been given the challenge of going back and reviewing the very early issues of AJDC and finding key articles they consider interesting and important. Most of these past investigators did not receive the Nobel prize, did not have a National Institutes of Health (Bethesda,
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060028024pmid: 3578184
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 Milt joined our editorial board in 1986 and has been a workhorse for us ever since. This is not surprising to those who know Milt, as his work ethic is well known and respected in American pediatrics. He attended Franklin and Marshall College in Lancaster, Pa, and received his MD degree from the Chicago Medical School in 1952. He interned and completed his pediatric residency at UCLA-Harbor General Hospital, Torrance, Calif. Afterward, he entered private practice and for the next 30 years remained an active practitioner and a participant in multiple activities in pediatrics in California and the nation. He became a clinical professor of pediatrics at UCLA and was clinical cochairman of the Department of Pediatrics at Harbor Hospital. Milt's credits are lengthy. He has been medical director of Project Head Start in Los Angeles County. He has been a member of many committees, including the Committee on Drug Abuse and the
[sic], V. P. Sydenstricked;Mulherin, W. A.;Houseal, R. W.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060030025
Abstract J. B. Herrick,1 in 1910, reported a peculiar dyscrasia characterized by severe anemia, with the occurrence in the blood of elongated and sickle-shaped erythrocytes. Three instances of this condition have since been described, one by R. E. Washburn;2 one by Cook and Myer,3 and one by V. R. Mason.4 Emmel5 further studied the blood of Cook and Myer's case, demonstrating the existence of phagocytosis of the erythrocytes by large mononuclear leukocytes in the peripheral circulation. He also pointed out the fact that when sealed sterile preparations of the fresh blood were allowed to stand at room temperature for varying periods of time, many of the circular erythrocytes underwent transformation into elongated and sickle shapes similar to those seen in the freshly drawn blood. Furthermore, he showed that the blood of the patient's father, though normal to all appearances when drawn, underwent similar changes on standing. Guthrie
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060034026
Abstract The historical aspects of sickle cell anemia are well known and described in two recent texts.1,2 Even though red blood cells were seen and described by Antonj Van Leeuwenhoek in 1674, Paul Ehrlich developed stains for examining tissue and cells microscopically in 1877, and the signs and symptoms of sickle cell anemia were appreciated for years (perhaps hundreds of years) it took J. B. Herrick, in 1910, to put all this together when he described the first case of sickle cell anemia. The cause of the red blood cell abnormality continued to be a mystery until in 1948-1949, when a newly developed electrophoresis method showed that the hemoglobin of sickle cells was different from that of normal cells. (A Nobel prize was awarded for this.) Subsequently, the genetics of the disorder were clarified and the sickle hemoglobin was found to be an abnormality of the β-polypeptide chain (glutamic acid References 1. Conley CL: Sickle-cell anemia: The first molecular disease , in Wintrobe MM (ed): Blood, Pure And Eloquent . New York, McGraw-Hill International Book Co, 1980, pp 319-371. 2. Serjeant GR: Sickle Cell Disease . New York, Oxford University Press 1985. 3. Sydenstricked [sic] VP, Mulherin WA, Houseal RW: Sickle cell ane mia: Report of two cases in children, with necropsy in one case . AJDC 1923;26:132-154. 4. Emmel VE: A study of the erythrocytes in a case of severe anemia with elongated and sickle-shaped red blood corpuscles . Arch Intern Med 1917;20: 586-598.Crossref 5. Sydenstricker VP: Further studies on sickle cell anemia . JAMA 1924;83:12-15.Crossref 6. Johnson CS: Sickle cell anemia . JAMA 1985;254:1958-1963.Crossref 7. Mills ML: Life-threatening complications of sickle cell disease in children . JAMA 1985;254:1487-1491.Crossref
Armstrong, Dawna L.;Sauls, C. Dan;Goddard-Finegold, Jan
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060035027pmid: 3578185
Abstract •Intraventricular hemorrhage (IVH) occurs in 31% to 43% of infants weighing less than 1500g. Intraventricular hemorrhage is rarely an Isolated lesion at autopsy. To document associated cerebral abnormality, 24 brains of infants with a diagnosis of IVH and who survived for at least one week were examined. The diagnosis was verified in 20 infants. Choroid plexus hemorrhage and brain calcification had been misdiagnosed as IVH in two infants and in two other infants, IVH was not evident at autopsy. Eleven Infants (46%) had choroid plexus hemorrhage. Twenty-two infants (92%) had additional cerebral abnormalities: periventricular leukomalacia, brainstem necrosis, hydrocephalus, or cerebellar necrosis. This study demonstrates that IVH is rarely an isolated abnormality in the preterm Infant brain. The associated brain lesions should be considered in attempts to prevent or treat IVH and their presence should be suspected during clinical assessment of survivors. (AJDC 1987;141:617-621) References 1. Volpe JJ: Neurology of the Newborn . Philadelphia, WB Saunders Co, 1981, pp 262-301. 2. Donn SM, Roloff DW, Goldstein GW: Prevention of intraventracular hemorrhage in preterm infants by phenobarbitone: A controlled trial . Lancet 1981;2:215-217.Crossref 3. Morgan MEI, Benson JWT, Cooke RWI: Ethamsylate reduces the incidence of periventricular hemorrhage in very low birth weight babies . Lancet 1980;2:830-831. 4. Morgan MEI, Massey RF, Cooke RWI: Does phenobarbitone prevent periventricular hemorrhages in very low birth weight babies? A controlled trial . Pediatrics 1982;70:186-189. 5. Ment LR, Duncan CC, Ehrenkranz RA, et al: Randomized indomethacin trial for prevention of intraventricular hemorrhage in very low birth weight infants . J Pediatr 1985;107:937-943.Crossref 6. Speer ME, Blifeld C, Rudolph AJ, et al: Intraventricular hemorrhage and vitamin E in the very low-birth-weight infant: Evidence for efficacy of early intramuscular vitamin E administration . Pediatrics 1984;74:1107-1112. 7. Krishnamoorthy KS, Shannon DC, DeLong GR, et al: Neurologic sequelae in the survivors of neonatal intraventricular hemorrhage . Pediatrics 1979;64:233-237. 8. Williamson WD, Desmond MM, Wilson GS, et al: Early developmental outcome of low birth weight infants surviving neonatal intraventricular hemorrhage . J Perinat Med 1982;10:34-40.Crossref 9. Shulz DM, Giordano DA, Schulz DH: Weights of organs of fetuses and infants . Arch Pathol Lab Med 1962;74:244-250. 10. Friede RL: Gross and microscopic development of the central nervous system , in Friede RL (ed): Developmental Neuropathology . New York Springer-Verlag NY Inc, 1975, pp 1-7. 11. Papile L-A, Burstein J, Burstein R, et al: Incidence and evolution of subependymal and intraventricular hemorrhage: A study of infants with birth weights less than 1500 grams . J Pediatr 1978;92:529-534.Crossref 12. Banker BQ, Larroche J-C: Periventricular leukomalacia of infancy: A form of neonatal anoxic encephalopathy . Arch Neurol 1962;7: 32-57.Crossref 13. Leech RW, Alvord EC Jr: Perinatal leukoencephalopathy: An expanded concept . J Neuropathol Exp Neurol 1974;33:468-469. 14. Gilles FH, Leviton A, Dooling EC: The Developing Human Brain: Growth and Epidemiologic Neuropathology . Littleton, Mass, John Wright PSG Inc, 1983, pp 174-183. 15. Chaplin ER, Goldstein GW, Myerburg DZ, et al: Post-hemorrhagic hydrocephalus in the preterm infant . Pediatrics 1980;65:901-909. 16. Papile L-A, Burstein J, Burstein R: Posthemorrhagic hydrocephalus in low birth weight infants: Treatment by serial lumbar punctures . J Pediatr 1980;97:273-277.Crossref 17. Revene MD, Starke D: A longitudinal study of post-hemorrhagic ventricular dilatation in the newborn , in Syllabus of the Perinatal Intracranial Hemorrhage Conference, Dec 11-13, Washington, DC . Columbus, Ohio, Professional Services Department of Ross Laboratories, 1980, pp 391-409. 18. Burstein J, Papile L-A, Burstein R: Intraventricular hemorrhage and hydrocephalus in premature newborns: A prospective study with CT . AJR 1979;131:631-635.Crossref 19. Leech RW, Olson Ml, Alvord EC Jr: Neuropathologic features of idiopathic respiratory distress syndrome . Arch Pathol Lab Med 1979; 103:341-343. 20. Armstrong DL, Goddard J, Schwartz M, et al: Another look at the pathology of intraventricular hemorrhage , in Syllabus of the Perinatal Intracranial Hemorrhage Conference, Dec 11-13, Washington , DC. Columbus, Ohio, Professional Services Department of Ross Laboratories, 1980, pp 1-21. 21. Friede RL: Pontosubicular lesions in perinatal anoxia . Arch Pathol Lab Med 1972;94: 343-354. 22. Ahdab-Barmada M, Moossy J, Painter M: Pontosubicular necrosis and hyperoxemia . Pediatrics 1980;66:840-847. 23. McAdams AJ: Pulmonary hemorrhage in the newborn . AJDC 1967;113:255-262.
Amitai, Yona;Mitchell, Allen;Carrel, Jade C.;Luciw, Helen;Lovejoy, Frederick H.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060040028pmid: 2883880
Abstract • Over a one-month period all telephone calls from the public (n=3828) to a regional poison center were analyzed. The proportion of early calls (within ten minutes of exposure) decreased with age. Late calls (>30 minutes) were significantly associated with higher hospital referral rates when compared with earlier calls in children younger than 5 years (4.6% vs 1.8%) and adults (33% vs 15%). Ipecac was available in 59% of the homes of callers with children younger than 5 years. Hospital referrals were significantly less common among children who had ipecac at home (1%) compared with children who did not (3%). While the availabilty of ipecac was similar among callers and a matched sample of households who previously called the poison center (58%), ipecac was much less frequently available (24%) among households whose members had not previously called the center. These data infer that educating the public to call the poison center promptly may result in reduction of hospital referrals. Poison education efforts should be targeted to populations with low ipecac availability and low utilization of the poison center. (AJDC 1987;141:622-625) References 1. Thompson DT, Trammel HL, Robertson NJ, et al: Evaluation of regional and nonregional poison centers . N Engl J Med 1983;308:191-194.Crossref 2. Litovitz T, Veltri JC: 1984 Annual Report of the American Association of Poison Control Centers' National Data Collection System . Am J Emerg Med 1984;3:423-450.Crossref 3. Report of the Poison Control Center, Japan: September 1, 1983–August 31, 1984 . Vet Hum Toxicol 1985;27:106-110. 4. Mowry JG, Sketris IS, Czajka PA: Ipecac syrup for poisoning at home: Availability, compliance and response monitored by telephone . Am J Hosp Pharm 1981;38:1028-1030. 5. Alpert JJ, Levin MD, Kosa J: Public knowledge of ipecac syrup in the management of accidental poisoning . J Pediatr 1967;71:890-894.Crossref 6. Veltri JC, Temple AR: Telephone management of poisoning using syrup of ipecac . Clin Toxicol 1976;9:407-417.Crossref 7. Lacouture P, Minisci M, Gouveia WA, et al: Evaluation of community based poison education program . Clin Toxicol 1978;13:623-629.Crossref 8. Waldman JM, Mofenson HC, Greensher J: Evaluating the function of a poison control center . Clin Pediatr 1976;15:75-79.Crossref 9. Polakoff JM, Lacouture PG, Lovejoy FH Jr: The environment away from home as a source of potential poisoning . AJDC 1984;138:1014-1017. 10. Chafee-Bahamon C, Lovejoy FH Jr: Effectiveness of a regional poison center in reducing excess emergency room visits for children's poisoning . Pediatrics 1983;72:164-169. 11. Wood G, Chamberlain S, Duffy J: Impact of a poison prevention program on a metropolitan population , abstracted. Clin Toxicol 1979;15:476. 12. Marcus SM, Chafee-Bahamon C, Arnold VW, et al: A regional poison control system: Effect on response to hypothetical poisonings . AJDC 1984;138:1010-1013.
Wasserman, Abby L.;Thompson, Elizabeth I.;Wilimas, Judith A.;Fairclough, Diane L.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060044029pmid: 3578186
Abstract • To assess psychosocial late effects of childhood/adolescent cancer, semistructured interviews were conducted with 40 subjects who had achieved complete remission from Hodgkin's disease and completed therapy at least five years previously. Mean ages were 12.8 years at diagnosis and 24.7 years at interview. Side effects of treatment were most often mentioned as the "worst thing" about having had Hodgkin's disease. Although subjects had missed a mean of six months of school, and 40% had reported unpleasant school experiences, their educational levels exceeded those expected in sex-, age-, and state-matched populations. Almost all subjects said that they had benefited in some way from the experience of having cancer. In contrast to the female subjects, male subjects expressed little interest in having their reproductive status assessed. Current concerns included discrimination in employment or in obtaining life or health insurance. (AJDC 1987;141:626-631) References 1. Meadows AT, Krejmas NL, Belasco JB: The medical cost of cure: Sequelae in survivors of childhood cancer , in Van Eys J, Sullivan MP (eds): Status of the Curability of Childhood Cancers . New York, Raven Press, 1980, pp 263-276. 2. Meadows AT, Hobbie W: The medical consequences of cure. Read before the American Canthe Care National Conference on Advances in ofthe Child with Cancer, Los Angeles, June 1985. 3. Zittoun R, Audebert A, Hoerni B, et al: Extended vs involved fields irradiation combined with MOPP chemotherapy in early clinical stages of Hodgkin's disease . J Clin Oncol 1985;3;207- 214. 4. Hollingshead AB: Two Factor Index of Social Position . New Haven, Conn, Yale University Press, 1957. 5. American Psychiatric Association, Committee on Nomenclature and Statistics: Diagnostic and Statistical Manual of Mental Disorders , ed 3. New York, Biometrics Research Division, New York State Psychiatric Institute, 6. Mor V, Laliberte L, Morris JN, et al: The Karnofsky performance status scale . Cancer 1984;53:2002-2007.Crossref 7. Bureau of the Census: Marital Status and Living Arrangements: March 1984 , US Dept of Commerce publication series P-20, No. 399, 1985. 8. Myers JK, Weissman MM, Tischler GL, et al Six-month prevalence of psychiatric disorders in three communities . Arch Gen Psychiatry 1984;41:959-967.Crossref 9. Zwartjes WJ: The psychological costs of curing the child with cancer , in Van Eys J, Sullivan MP (eds): Status of the Curability of Childhood Cancers . New York, Raven Press, 1980, pp 277-284. 10. Pfefferbaum B: Criteria for functional cure of cancer , in Van Eys J, Sullivan MP (eds): Status of the Curability of Childhood Cancers . New York, Raven Press, 1980, pp 27-32. 11. Fergusson JH: Late psychologic effects of a serious illness in childhood . Nurs Clin North Am 1976;11:83-93. 12. Holmes HA, Holmes FF: After ten years, what are the handicaps and life styles of children treated for cancer? Clin Pediatr 1975;14:819-823.Crossref 13. Pfefferbaum B: Pediatric oncology: A review of the changing psychological aspects . Int J Psychiatry Med 1979;9:289-296.Crossref 14. Malmquist CP: Development from 13 to 16 years , in Noshpitz JD (ed): Basic Handbook of Child Psychiatry . New York, Basic Books Inc, 1979, vol 1, pp 209-210. 15. Brunstetter RW, Silver LB: Normal adolescent development , in Kaplan HI, Sanock BJ (eds): Comprehensive Textbook of Psychiatry/IV . Baltimore, Williams & Wilkins, 1986, pp 1608-1613. 16. Sullivan MP, Fuller LM, Butler JJ: Hodgkin's disease , in Suton WW, Fernbach DJ, Vietti TJ (eds): Clinical Pediatric Oncology , ed 3. St Louis, CV Mosby Co, 1984, pp 437-442. 17. Kaplan HS: Hodgkin's Disease . Cambridge, Mass, Harvard University Press, 1980, pp 421-441, 469-477. 18. Belfer ML, Lukens PF: Body image: Impacts and distortions , in Levine MD, Carey WB, Crocker AC, et al (eds): Developmental-Behavioral Pediatrics . Philadelphia, WB Saunders Co, 1983, pp 623-632. 19. Petersen AC, Offer D: Adolescent development: Sixteen to 19 years , in Noshpitz JD (ed): Basic Handbook of Child Psychiatry . New York, Basic Books Inc, 1979, vol 1, p 219. 20. Fobair P, Hoppe RT, Bloom J, et al: Psychosocial problems among survivors of Hodgkin's disease . J Clin Oncol 1986;4:806-814. 21. Feldman FL: Work and Cancer Health Histories: Work Expectations and Experiences of Youth With Cancer Histories (Ages 13-23) . Oakland, Calif, American Cancer Society, 1980. 22. Koocher GP, O'Malley JE: The Damocles Syndrome and Psychosocial Consequences of Surviving Childhood Cancer . New York, McGraw-Hill International Book Co, 1981. 23. Brunnquell D, Hall M: Issues in the psychological care of pediatric oncology patients . Am J Orthopsychiatry 1982;52:32-44.Crossref 24. Anderson JL: Insurability of cancer patients: A rehabilitation barrier . Oncol Nurs Forum 1984;2:42-45. 25. Chapman RM, Sutcliffe SB, Malpas JS: Cytotoxic-induced ovarian failure in Hodgkin's disease . JAMA 1979;242:1882-1884.Crossref 26. Sherins RT, DeVita VT: Effect of drug treatment for lymphoma on male reproduction capacity . Ann Intern Med 1973;79:216-220.Crossref 27. Chapman RM, Sutcliffe SB, Malpas JS: Male gonadal dysfunction in Hodgkin's disease . JAMA 1981;245:1323-1328.Crossref 28. Zanini M, Zucali R, Banfi A: Bone and softtissue sarcomas in the follow-up of Hodgkin's disease. Tumori 1983;69:473-476. 29. Pederson-Bjergaard J, Larsen SO: Incidence of acute non-lymphocytic leukemia preleukemia, and acute myeloproliferative syndrome up to ten years after treatment of Hodgkin's disease . N Engl J Med 1982;307:965-971.Crossref 30. Door FA, Coltman CA: Second cancers following antineoplastic therapy . Curr Probl Cancer 1985;9:1-43.Crossref 31. Reed HI), Janis IL: Effects of a new type of psychological treatment on smoker's resistance . J Consult Clin Psychol 1974;42:748-750.Crossref 32. Mattsson A: Long-term physical illness in childhood: A challenge to psychosocial adaptation . Pediatrics 1972;50:801-811. 33. Koocher GP, O'Malley JE, Gogan JL, et al: Psychological adjustment among pediatric cancer survivors . J Child Psychol Psychiatry 1980; 21:163-173.Crossref
Tran, Anthony T. B.;Arensman, Robert M.;Falterman, Kenneth W.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060050030pmid: 3578187
Abstract • Hydrohematometrocolpos anomalies denote the different types of accumulation of fluid and menstrual products in the vagina and the uterus. They are rare conditions due to an intact hymen, vaginal membrane, or vaginal atresla. They may present at different times during development. The method of presentation is variable, and the presence of other genitourinary abnormalities and anorectal anomalies makes prompt diagnosis and treatment necessary. Review of our experiences with these conditions for the last ten years reveals a total of ten cases. This study reports three cases in detail and describes the others in tabular form. (AJDC 1987;141:632-634) References 1. Godefroy M: Imperforation de la membrane hymen: Loucette Franc . Gaz d Hosp 1856;29:567. 2. Mahoney PJ, Chamberlin JW: Hydrometrocolpos in infancy: Congenital atresia of the vagina with abnormal abundant cervical secretions . J Pediatr 1940;17:772-780.Crossref 3. Cook GT, Marshall VP: Hydrocolpos causing urinary obstruction . J Urol 1964;92:127-132. 4. Spencer R, Levy DM: Hydrometrocolpos: Report of three cases and review of the literature . Ann Surg 1962;155:558-571.Crossref 5. Reed MH, Griscom NT: Hydrometrocolpos in infancy . Am J Roentgenol Radium Ther Nucl Med 1973;118:1-13.Crossref 6. Gravier L: Hydrocolpos . J Pediatr Surg 1969;4:563-568.Crossref 7. Ceballos R, Hicks GM: Plastic peritonitis due to neonatal hydrometrocolpos: Radiologic and pathologic observation . J Pediatr Surg 1970; 5:63-70.Crossref 8. Robinow MR, Shaw A: The McKusick-Kaufman syndrome: Recessively inherited vaginal atresia, hydrometrocolpos, uterovaginal duplications, anorectal anomalies, postaxial polydactyly and congenital heart disease . J Pediatr 1979;94: 776-778.Crossref 9. Lide TN, Coker WG: Congenital hydrometrocolpos: Review of the literature and report of a case with uterus duplex and incompletely septate vagina . Am J Obstet Gynecol 1952;64: 1275-1281. 10. Mallet R, Ribierre M, Labrune B, et al: Les hydrocolpos du nouveaune avec duplicite vaginale et agenesis renale homolaterale . Ann Pediatr 1966;13:540-547. 11. Wilson, Stacy TM, Smith EI: Ultrasound diagnosis of hydrocolpos and hydrometrocolpos . Ultrasound 1978;128:451-454. 12. Ramenofsky ML, Raffensperger JG: An abdomino-perineal-vaginal pull-through for definitive treatment of hydrometrocolpos . J Pediatr Surg 1971;6:381-387.Crossref
Dutton, Robert V.;Singleton, Edward B.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060053031pmid: 3578188
Abstract • Metrizamide is a safe, water-soluble contrast medium suitable for bedside gastrointestinal studies in low-birth-weight infants. We describe our experience with 26 patients and 34 examinations. We present Illustrative cases and indicate the clinical applications. Similar results are anticipated when less expensive nonionic contrast agents are approved by the Food and Drug Administration for pediatric use. (AJDC 1987;141:635-638) References 1. Berner A, Johansen JG: Histologic effects of Amipaque (metrizamide) and various contrast media on mouse peritoneum . Invest Radiol 1978;13:161-162.Crossref 2. Johansen JG, Kolmannskog S: Osmotic effect and solubility of Amipaque (metrizamide) in the gastrointestinal tract . Invest Radiol 1978;13: 93-97.Crossref 3. Cohen M: Prolonged visualization of the gastrointestinal tract with metrizamide . Radiology 1982;143:327-328.Crossref 4. Cohen M, Jansen R, Lemons J, et al: Evaluation of the gasless abdomen in the newborn and young infant with metrizamide . AJR 1984;142: 393-396.Crossref 5. Cohen M, Smith JA, Slabaugh RD, et al: Neonatal necrotizing enterocolitis shown by oral metrizamide (Amipaque) . AJR 1982;138:1019-1023.Crossref 6. Cohen M, Smith WL, Smith JA, et al: The use of metrizamide (Amipaque) to visualize the gastrointestinal tract in children: A preliminary report . Clin Radiol 1980;31:635-641.Crossref 7. Cohen M, Weber T: Metrizamide in neonatal and childhood small-bowel obstruction . AJR 1982;139:689-692.Crossref 8. Cohen M, Weber TR, Grosfeld JL: Bowel perforation in the newborn: Diagnosis with metrizamide . Radiology 1984;150:65-69.Crossref 9. Singleton EB, Wagner ML, Dutton RV: Radiology of the Alimentary Tract in Infants and Children , ed 2. Philadelphia, WB Saunders Co, 1977. 10. Harris PD, Neuhauser EBD, Gerth R: The osmotic effect of water-soluble contrast media on circulating plasma volume . AJR 1964;91:694. 11. McAlister WH, Askin FB: The effect some contrast agents in the lung: An experimental study in the rat and dog . AJR 1983;140:245-251.Crossref 12. Beltaxe HA, Mooring P, Kugler J, et al: Comparative hemodynamic effect of metrizamide and renografin 76 in infants with congenital heart disease . AJR 1983;140:1097-1101.Crossref 13. Robey G, Reilly BJ, Carusi PA, et al: Pediatric urography: Comparison of metrizamide and methylglucamine diatrizoate . Radiology 1984;150:61-63.Crossref 14. Siegle RL, Davies P, Fullerton GD: Urography with metrizamide in children . AJR 1982;139:927-930.Crossref
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060056032
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 Incorrect Phrasing.—In the Ambulatory Pediatric Association abstract entitled "Hepatitis B Virus Markers and Antigenemia in Adolescents," published in the April 1987 AJDC (1987;141:368-369), an error in phrasing appeared in the second sentence in the third paragraph. That sentence should have read as follows: "The difference in the HBV marker rate for Puerto Ricans, five (3.7%) of 136, vs Dominican Republicans, six (12.8%) of 47, was significant P<.05)." We regret this error.
Heydarian, Mahmood;Kelly, Patricia J.;Young, Lionel W.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060059033
Abstract A 9-year-old girl with Down's syndrome had a one-week history of cough, fever, and dyspnea. Three days prior to hospital admission, she had been started on a regimen of penicillin by her local physician for a presumed pneumonia. However, her respiratory distress increased, and a chest roentgenogram was obtained on admission (Fig 1). Although she had had a known heart murmur since infancy, she had remained asymptomatic until this illness. On physical examination she was an agitated dyspneic child with the stigmata of Down's syndrome. Her temperature was 38°C; respirations, 30/min; pulse rate, 120 beats per minute; blood pressure, 90/72 mm Hg, with a paradoxical pulse of 20 mm Hg. There were a few bilateral basilar rhonchi. The heart sounds were soft and distant, and the second heart sound was widely split and fixed. There was a grade 2/6 systolic ejection murmur maximal at the high left sternal border. No References 1. Feigenbaum H: Echocardiographic diagnosis of pericardial effusion . Am J Cardiol 1970;26: 475-479.Crossref 2. Martin RP, Rakowski H, French J, et al: Localization of pericardial effusion with wide angle phased array echocardiography . Am J Cardiol 1978;42:904-912.Crossref 3. Tierney RC: Pericardial disease in children . Paediatrician 1978;7:52-64. 4. Hayford JT, Schieken RM, Thompson G: Cardiac function in primary hypothyroidism . AJDC 1980;134:556-559. 5. Rasmussen N, Vazquez AM, Trip ME, et al: Pericardial effusion: A complication of hypothyroidism . AJDC 1979;133:329. 6. Farooki ZQ, Hoffman WH, Perry BL, et al: Myocardial dysfunction in hypothyroid children . AJDC 1983;137:65-68.
Pascucci, Stephen E.;Margo, Curtis E.;Feingold, Murray
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060061034
Abstract The statements listed below are best associated with which of the above figures: If other congenital anomalies are present, a chromosomal analysis is indicated. The diagnosis of retinoblastoma should be considered. Infants with this condition may have excessive tearing and photophobia, and they require immediate surgery. Denouement and Discussion Fig 1.—Abnormal appearance of white pupil due to mass behind crystalline lens. Normal light reflex in pupil is lost because retinoblastoma has caused retinal detachment.Fig 2.—Enlarged hazy cornea in infant with congenital glaucoma.Fig 3.—Iris coloboma.(a) An iris coloboma (Fig 3) in the presence of other congenital anomalies may also be associated with various chromosomal abnormalities, such as deletion of the short (p) arm of chromosome 4. It usually results from failure of fusion of the embryonic fissure of the optic cup. A child with an iris coloboma should have a thorough ocular examination because of References 1. Shields JA, Augsberger JJ: Current approaches to the diagnosis and management of retinoblastoma . Surv Ophthalmol 1982;23: 347-372. 2. DeLuise VP, Anderson DR: Primary infantile glaucoma (congenital glaucoma) . Surv Ophthalmol 1983;28:1-19.Crossref 3. Pagon RA: Ocular coloboma . Surv Ophthalmol 1981;25:233-236.Crossref
Giuffre, Randal M.;Rubin, Steven;Mitchell, Ian
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060064035pmid: 3578189
Abstract • We reviewed the medical records of nine Infants with severe bronchopulmonary dysplasia and gastroesophageal reflux who underwent fundoplication-gastrostomy surgery. All the Infants were born prematurely, required preoperative mechanical ventilation, and were falling to thrive. The operative procedure was well tolerated by all the infants. Seven patients were extubated by day 11, and two patients required long-term ventilation. There were two post operative deaths, both attributed to acute respiratory deterioration followed by cardiorespiratory failure. The post-surgical respiratory response was observed to be a rapid decrease in oxygen requirements and an absence of further aspiration episodes. A mean decrease of 0.14 in fractional inspired oxygen concentration was noted by 30 days postoperatively, and by 180 days the decrease in fractional inspired oxygen concentration was 0.22. All infants were fed by gastrostomy by postoperative day 4, with no evidence of clinical reflux. The nutritional response was noted to be an Increase in growth velocity with increasing age (ie, catch-up growth) and ease of feeding. At both 30 and 180 days postoperatively, the mean growth velocity was more than double the preoperative growth velocity. In addition, ease of postoperative feeding reduced the nursing care requirements and allowed earlier discharge from hospital. Fundoplication and gastrostomy is effective in facllitating growth and feeding in addition to decreasing oxygen requirements in infants with severe bronchopulmonary dysplasia and gastroesophageal reflux. (AJDC 1987;141:648-651) References 1. Northway WH, Rosan RC, Porter DY: Pulmonary disease following respiratory therapy of hyaline membrane disease . N Engl J Med 1967; 276:357-368.Crossref 2. Brown JK, Cockburn F, Forfar J, et al: Problems in the management of assisted ventilation in the newborn and followup of treated cases . Br J Anaesth 1973;45:802-822. 3. Lew C, O'Neal M, Keens T, et al: Gastroesophageal reflux prevents recovery from BPD , abstracted. Clin Res 1981;29:149A. 4. Nissen R, Rosetti M: Die Behendlung von Hiatushernien und Reflux-Oesophagitis mit Gastropexic und Fundoplication . Stuttgart, West Germany, Georg Thieme Verlag, 1959. 5. Johnson JD, Malachowski NC, Grubsten R, et al: Prognosis of children surviving with the aid of mechanical ventilation in the newborn period . J Pediatr 1974;84:272-276.Crossref 6. Northway WH: Observations on bronchopulmonary dysplasia . J Pediatr 1979;95:815-818.Crossref 7. Markestad T, Fitzharding PM: Growth and development in children recovering from bronchopulmonary dysplasia . J Pediatr 1981;98:597-602.Crossref 8. Vohr BR, Bell EF, Oh W: Infants with bronchopulmonary dysplasia. Growth pattern and neurologic and developmental outcome . AJDC 1982;136:443-447. 9. Yu VY, Orgill AA, Lim SB, et al: Growth and development of very low birthweight infants recovering from bronchopulmonary dysplasia . Arch Dis Child 1983;58:791-794.Crossref 10. Mayes L, Perkett E, Stahlmon M: Severe bronchopulmonary dysplasia: A retrospective review . Acta Paediatr Scand 1983;72:225-229.Crossref 11. Nickerson BG: Bronchopulmonary dysplasia . Chest 1985;87:528-535.Crossref 12. Weinstein MR, Oh W: Oxygen consumption in infants with bronchopulmonary dysplasia . J Pediatr 1981;99:958-961.Crossref 13. Herbst JJ: Gastroesophageal reflux in infants . J Pediatr Gastroenterol Nutr 1985;4:163-164.Crossref 14. Sondheimer JM, Morris BA: Gastroesophageal reflux among severely retarded children . J Pediatr 1979;94:710-714.Crossref 15. Byrne WJ, Euler AR, Ashcraft E, et al: Gastroesophageal reflux in the severely retarded who vomit: Criteria for and results of surgical intervention in 22 patients . Surgery 1982;92:95-98. 16. Hoyoux CL, Forget P, Lambrechts L, et al: Chronic pulmonary disease and gastroesophageal reflux in children . Pediatr Pulmonol 1985;1: 149-153.Crossref 17. Ramenofsky ML, Leope LL: Continuous upper esophageal pH monitoring in infants and children with gastroesophageal reflux . J Pediatr Surg 1981;16:74-78. 18. Gregory GA: Respiratory Failure in the Child . New York, Churchill Livingstone Inc, 1981, pp 146-161. 19. Dionigi R, Gves F, Bonera A, et al: Nutrition and infection . JPEN 1979;3:62-68.Crossref 20. Katz M, Stiehm ER: Host defense in malnutrition . Pediatrics 1977;59:490-495.
Brenbridge, A. Norman;Chevalier, Robert L.;El-Dahr, Samir;Kaiser, Donald L.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060068036pmid: 3554984
Abstract • Ultrasonic renal volume and length measurements are easily performed in pediatric patients. Increases in volume over the normal level provide a potentially attractive method of assessing the severity and progression or regression of renal diseases. However, an analysis of data on 59 children with clinical renal disease and nephromegaly did not demonstrate any correlation with severity of the disease. We conclude that increases in renal length and volume in pediatric patients may indicate the presence of disease but not its severity. (AJDC 1987;141:652-654) References 1. Rasmussen SN, Haase L, Kjeldsen H, et al: Determination of renal volume by ultrasound scanning . JCU 1978;26:160-164. 2. Moskowitz PS, Carroll BA, McCoy JM: Ultrasonic renal volumetry in children: Accuracy and simplicity of the method . Radiology 1980;134: 61-64. 3. Jones TB, Riddick LR, Harpen MD, et al: Ultrasonographic determination of renal mass and renal volume . Ultrasound Med Biol 1983;2: 151-154. 4. Halloway H, Jones TB, Robinson AE, et al: Sonographic determination of renal volumes in normal neonates . Pediatr Radiol 1983;13:212-214.Crossref 5. Hricak H, Lieto RP: Sonographic determination of renal volume . Radiology 1983;148: 311-312. 6. Haugstvedt S, Lundberg J: Kidney size in normal children measured by sonography . Scand J Urol Nephrol 1980;14:251-255.Crossref 7. Currarino G, Williams B, Dana G: Kidney length correlated with age: Normal values in children . Radiology 1984;150:703-704. 8. Rosenbaum DM, Korngold E, Teele RL: Sonographic assessment of renal length in normal children . AJR 1984;142:467-469.Crossref 9. Han BK, Babcock DS: Sonographic measurements and appearance of normal kidneys in children . AJR 1985;145:611-616.Crossref 10. Schwartz GJ, Feld LG, Langford DJ: A simple estimate of glomerular filtration rate in full-term infants during the first year of life . J Pediatr 1984;104:849-854.Crossref 11. Schwartz GJ, Haycock GB, Edelmann CM Jr, et al: A simple estimate of glomerular filtration rate in children derived from body length plasma creatinine . Pediatrics 1976;58:259-263. 12. Asperia A, Broberger O, Thodenius K, et al: Development of renal control of salt and fluid homeostasis during the first year of life . Acta Paediatr Scand 1975;64:393-398.Crossref 13. Nelson WE, Vaughan VC, McKay RJ: Textbook of Pediatrics . Philadelphia, WB Saunders Co, 1969, p 1137. 14. McEnery PT, Strife CF: Nephrotic syndrome in childhood . Pediatr Clin North Am 1982;29:875-894.
Rossi, Livia N.;Candini, Gianna;Scarlatti, Gabriella;Rossi, Giuliana;Prina, Emilia;Alberti, Silvana
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060071037pmid: 3578190
Abstract • We describe six Italian families afby microcephaly with an apparently autosomal mode of inheritance (total number of microcephalic children and adults, 21). All microcephalic subjects were of normal height, with the exception of one. The head volume was measured directly in at least one adult microcephalic member from five of the six families, and lower values were obtained in these subjects than in control subjects. Psychometric tests were performed on seven children and five adults among the microcephalic subjects. Normal values were found for all but one of the subjects. In the selected families microcephaly seems to be inherited in an autosomal dominant manner. Because some families showing autosomal dominant microcephaly have normal intelligence, psychometric evaluation of microcephalic children and their microcephalic relatives is important for genetic counseling. (AJDC 1987;141:655-659) References 1. Pryor HB, Thelander H: Abnormally small head size and intellect in children . J Pediatr 2. Sells CJ: Microcephaly in a normal school Pediatrics 1977;59:262-265. 3. Menkes H: Textbook of Child Neurology . Philadelphia, Lea & Febiger, 1985, pp 224-228. 4. Haslam RHA, Smith DW: Autosomal nant microcephaly . J Pediatr 1979;95:701-705.Crossref 5. Ramirez ML, Rivas F, Cantu JM: Silent A distinct autosomal dominant Clin Genet 1983;23:281-286.Crossref 6. Burton BK: Dominant inheritance of cephaly with short stature . Clin Genet 1981;20: 25-27.Crossref 7. Feingold M: Case report 30 . Syndrome Identification 1975;3:1-16. 8. Feingold M: An unusual microcephaly . Hosp Pract 1978;13:44-49. 9. Halal F: Dominantly inherited syndrome of microcephaly and cleft palate . Am J Med Genet 1983;15:135-140.Crossref 10. Say B, Barber DH, Hobbs J, et al: A new dominantly inherited syndrome of cleft palate . Hum Genet 1975;26:267-269. 11. Leung AKC: Dominantly inherited syndrome of microcephaly and congenital lymphedema . Clin Genet 1985;27:611-612.Crossref 12. Alzial C, DufierJL, Brasnu C, 'vraie' avec dysplasie dominante . Ann Genet 1980;23:91-94. 13. Rossi LN, Battilana MP: Autosomal dominant microcephaly . J Pediatr 1982;101:481-482.Crossref 14. Nellhaus G: Head circumference from birth to 18 years . Pediatrics 1968;41:106-114. 15. Moesch D, Moesch HP, Kaiser G: Clinical determination of the volume of the neurocranium in infancy . Helv Paediatr Acta 1983;38:133-139. 16. Milani F, Cortinovis J, Rainisio M, et al: Structural analysis of a set of socio-economic indexes as an aid to define the socio-economic level of family: Results of an Italian multicentric survey . Soc Sci Med 1983;17:803-818.Crossref 17. JB, Paridon E, Quaade F: The external cranial volume of normal children . Acta Paediatr Scand 1959;48:371-378.Crossref
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060075038
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 It is always a pleasure to review good books written by one's former residents. Dr Evans' new "red book" is the "Harriet Lane" handbook of child neurology. It is written as a manual for pediatricians and others involved in the Primary health care of children. The eight sections cover neurologic evaluation, neurodiagnostic procedures, neonatal neurologic disorders, developmental disorders, neurodegenerative and metabolic diseases, neuromuscular diseases, acquired disorders of the central nervous system, and paroxysmal disorders. The text is succinct, pertinent, and useful. Tables, drawings, and illustrations are used liberally. Some statements are made with which not all child neurologists would agree, eg, "Asphyxia continues to be one of the major causes of cerebral palsy in term infants" (page 159). The standard topics are covered succinctly. A few magnetic resonance imaging scans are included. It would have been nice to have arrows precisely depicting the pertinent findings for those readers unfamiliar with
Winter, Susan C.;Szabo-Aczel, Steven;Curry, Cynthia J. R.;Hutchinson, H. Terry;Hogue, Rebecca;Shug, Austin
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060076039pmid: 3578191
Abstract • We studied the clinical spectrum associated with secondary plasma carnitine deficiency in 51 pediatric patients. Forty-three patients had total plasma carnitine values below 20 μmol/L and an additional eight patients had total values above 20 μmol/L but had low free plasma carnitine levels. The clinical presentation in the patients with total plasma carnitine deficiency included hypotonia (34 of 43), failure to thrive (27 of 43), recurrent infections (27 of 43), encephalopathy (six of 43), nonketotic hypoglycemia (seven of 43), and cardiomyopathy (nine of 43). Of the eight patients with low free and elevated esterified carnitine levels, the signs and symptoms at presentation included hypotonia (six of eight), recurrent infections (six of eight), failure to thrive (six of eight), encephalopathy (three of eight), nonketotic hypoglycemia (one of eight), and cardiomyopathy (one of eight). All patients were treated with L-carnitine. Treatment time varied from one month to 24 months (average, four months). A subjective improvement in muscle tone was seen in 24 of 38 patients, 22 of 33 patients showed acceleration of incremental growth, and infection frequency appeared to decrease in 18 of 33 patients. After therapy, the echocardiograms of all patients with cardiomyopathy normalized. There were no further hypoglycemic episodes. Of the nine patients with encephalopathy, eight showed improvement in their mental status. Three patients died of complications of their primary disorder. In our experience, secondary plasma carnitine deficiency is a common pediatric finding. The presence of failure to thrive, recurrent infections, hypotonia, encephalopathy, cardiomyopathy, or nonketotic hypoglycemia requires investigation of carnitine status. (AJDC 1987;141:660-665) References 1. Bremer J: Carnitine metabolism and function . Physiol Rev 1983;63:1420-1480. 2. Engel AG, Rebouche CJ: Carnitine metabolism and inborn errors . J Inherited Metab Dis 1984;7( (suppl 1) ):38-43.Crossref 3. Hoppel CL, Genuth S, Brass E, et al: Carnitine and carnitine palmitoyltransferase in metabolic studies , in Frenkel RA, McGarry JD (ed): Carnitine Biosynthesis, Metabolism, and Functions . Orlando, Fla, Academic Press Inc, 1980, pp 287-305. 4. Karpati G, Carpenter S, Engel AG, et al: The syndrome of systemic carnitine deficiency: Clinical, morphologic, biochemical and pathologic features . Neurology 1975;25:15-24.Crossref 5. Glasgow AM, Eng G, Engel AG: Systemic carnitine deficiency simulating recurrent Reye syndrome . J Pediatr 1980;96:889-891.Crossref 6. Cornelio F, DiDonato S, Peluchetti D, et al: Heterogeneity of carnitine deficiency: Clinicopathological aspects of eight cases . Perspect Inherit Metab Dis 1979;3:128-150. 7. Tripp ME, Katcher ML, Peters HA, et al: Systemic carnitine deficiency presenting as familial endocardial fibroelastosis: A treatable cardiomyopathy . N Engl J Med 1981;305:385-390.Crossref 8. Scholte HR, Meijer AEFH, Van Wijngaarden GK, et al: Familial carnitine deficiency: A fatal case and subclinical case in a sister . J Neurol Sci 1979;42:87-101.Crossref 9. Waber LJ, Valle D, Neill C, et al: Carnitine deficiency presenting as familial cardiomyopathy: A treatable defect in carnitine transport . J Pediatr 1982;101:700-705.Crossref 10. Chapoy PR, Angelini C, Brown WJ, et al: Systemic carnitine deficiency: A treatable inherited lipid-storage disease presenting as Reye's syndrome . N Engl J Med 1980;303:1389-1394.Crossref 11. Cannon RA: Reye's syndrome or its metabolic mimics? Hosp Pract 1984;19:134F. 12. Roe CR, Millington DS, Maltby DA, et al: L-Carnitine enhances excretion of propionyl coenzyme A as propionylcarnitine in propionic acidemia . J Clin Invest 1984;73:1785-1788.Crossref 13. Slonim AE, Borum PR, Mrak RE, et al: Nonketotic hypoglycemia: An early indicator of systemic carnitine deficiency . Neurology 1983; 33:29-33.Crossref 14. DiDonato S, Rimoldi M, Garavaglia B, et. al: Propionyl-carnitine excretion in propionic and methylmalonic acidemias: A cause of carnitine deficiency . Clin Chim Acta 1984;139:13-19.Crossref 15. DiDonato S, Peluchetti D, Rimoldi M, et al: Systemic carnitine deficiency: Clinical, biochemical and morphological cure with L-carnitine . Neurology 1984;34:157-162.Crossref 16. Rebouche CJ, Engel AG: Carnitine metabolism and deficiency syndromes . Mayo Clin Proc 1983;58:533-540. 17. Parvin R, Pande SV: Microdetermination of (–)carnitine and carnitine acetyl transferase activity . Ann Biochem 1977;79:190-201.Crossref 18. Shenal JP, Borum PR, Mohan P, et al: Carnitine status at birth of newborn infants of varying gestation . Pediatr Res 1983;17:579-582.Crossref 19. Penn D, Schmidt-Sommerfeld E, Pascu F: Decreased tissue carnitine concentrations in newborn infants receiving total parenteral nutrition . J Pediatr 1981;98:976-978.Crossref 20. Coulter DL: Carnitine deficiency: A possible mechanism for valproate hepatotoxicity . Lancet 1984;2:689.Crossref 21. Ohtani Y, Endo F, Matsuda I: Carnitine deficiency and hyperammonemia associated with valproic acid therapy . J Pediatr 1982;101:782-785.Crossref 22. DiDonato S, Rimoldi M, Cornelio F, et al: Evidence for autosomal recessive inheritance in systemic carnitine deficiency . Ann Neurol 1982; 11:190-192.Crossref 23. Roe CR, Millington DS, Maltby DA, et al: L-Carnitine therapy in isovaleric acidemia . J Clin Invest 1984;74:2290-2295.Crossref 24. Coates PM, Hale DE, Stanley CA, et al: Genetic deficiency of medium-chain acyl CoA dehydrogenase studies in cultured skin fibroblasts and peripheral mononuclear leukocytes . Pediatr Res 1985;19:671-676.Crossref
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060082040pmid: 3578192
Abstract • The male membership of the Society for Adolescent Medicine was surveyed regarding the use of a chaperone during pelvic examination of female adolescents. Five hundred seven questionnaires were mailed, and 292 physicians (58%) responded. One hundred eight (37%) reported performing pelvic examinations without a chaperone present. This was usually done because of patient preference. There was no difference between academic and private practice physicians. There were many categories listed as necessitating the presence of a chaperone. Here again, patient preference was the most frequent. Other reasons for using a chaperone Included a patient with emotional problems, a history of rape or sexual abuse, a seductive patient, an uncomfortable patient or physician, a first pelvic examination, and medicolegal issues. Although it has been traditionally recommended that a chaperone be present during a pelvic examination, our data suggest that this is not sometimes the case for about one third of the male physicians in the Society for Adolescent Medicine. (ADJC 1987;141:666-667) References 1. Phillips S: Teenagers' preferences regarding the presence of family members, peers and chaperones during examination of genitalia . Pediatrics 1981;68:665-669. 2. Buchta R: Adolescent females' preferences of usage of a chaperone during a pelvic examination . J Adolesc Health Care 1986;7:407-411. 3. Feigel HC: Attitude of college students toward medical genital examination and selfexamination of their own genitals , abstracted. J Adolesc Health Care 1981;2:163. 4. Society for Adolescent Medicine member roster . J Adolesc Health Care 1982;3:183-225.Crossref
Light, Michael J.;Sheridan, Mary S.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060084041pmid: 3578193
Abstract • The pathophyslology of "near miss" or "aborted" sudden infant death syndrome (better termed "emergency apnea") is unclear. Emotionally, however, such episodes are significantly stressful for parents. We administered a questionnaire to 50 families who had experienced emergency apnea at home. Sixty percent ranked the experience as one of the most difficult in their lives; 56% believed that the infant's death was averted only because they intervened. The psychodynamics are similar to those seen in families who have lost an infant to sudden infant death syndrome, and they are consistent with posttraumatic stress disorder. The affected Infants may be regarded as "vulnerable children." Many parents believed that their lives were permanently changed. Home apnea monitoring equipment and support from the family physician and monitoring program are important in reducing the stress associated with apneic emergencies. (AJDC 1987;141:668-671) References 1. DeFrain J, Taylor J, Ernst L: Coping With Sudden Infant Death . Lexington, Mass, Lexington Books, 1982. 2. Statement of Terminology . Landover, Md, National SID Foundation Research Board, 1981. 3. Seto DSY, Burch TA: The Epidemiology of Sudden Infant Death Syndrome in Hawaii , (Research and Statistics Report 50.) Honolulu, Hawaii State Department of Health, 1984. 4. Light MJ, Sheridan MS: The home apnea monitoring program for newborns: The first 300 patients . Hawaii Med J 1985;44:419-424. 5. American Psychiatric Association Committee on Nomenclature and Statistics: Diagnostic and Statistical Manual of Mental Disorders , ed 3. Washington, DC, American Psychiatric Association, 1980, pp 236-238. 6. Green M, Solnit AJ: Reactions to the threatened loss of a child: A vulnerable child syndrome . Pediatrics 1964;34:58-66. 7. Green M: Vulnerable child syndrome and its variants . Pediatr Rev 1986;8:75-80.Crossref 8. Costanza M, Lipsitch I, Charney E: The vulnerable child revisited . Clin Pediatr 1968; 7:680-683.Crossref 9. National Institutes of Health, Consensus Development Committee on Apnea and Home Monitoring: Draft Report . Bethesda, Md, National Institutes of Health, 1986, chap 5.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060090042pmid: 3578194
Abstract Throughout one's medical education, beginning in medical school and continuing into residency, the accumulation of clinical experience is always referred to in venerable terms. The message is, the more clinical experience one has, the better a physician one will be. The resident is always reminded that regardless of how bright or how well read he or she may be, his or her skill as a physician is limited due to lack of clinical experience. Yet few of the pediatric practitioners who have accumulated many years of this valuable experience seem to command the resident's respect. The explanation for this paradox lies in the fact that in the area of therapeutics, the lack of clinical experience is better than clinical experience that has not been evaluated critically. Unfortunately, the importance of critical evaluation as a component of clinical experience is not stressed enough in either residency or postresidency education. This often References 1. Millchap JG: Febrile Convulsions . New York, Macmillan Publishing Co Inc, 1968. 2. Mackintosh MB: Studies on prophylactic treatment of febrile convulsions in children: Is it feasible to inhibit attacks by giving drugs at the first sign of fever or infection? Clin Pediatr 1970; 9:283-286.Crossref 3. Faero O, Kastrup KW, Lykkegaard Nielsen I, et al: Successful prophylaxis of febrile convulsions with phenobarbital . Epilepsia 1972;13: 279-285.Crossref 4. Pearce JL, Sharman JR, Farster MB: Phenobarbital in the acute management of febrile convulsions . Pediatrics 1977;60:569-572. 5. Ginsburg CM, Clahsen J: Evaluation of trimethobenzamide hydrochloride (Tigan) suppositories for the treatment of nausea and vomiting in children . J Pediatr 1980;96:267-269.
Issenman, Robert M.;Hewson, Sheila;Pirhonen, Diane;Taylor, Wayne;Tirosh, Ali
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060095043pmid: 3578195
Abstract • We studied 149 healthy children at 22 months of age and 74 at 40 months of age, employing a 24-hour dietary record based on premailed food measurement guide and telephone questionnaire. Parents cooperated in 94% of contacts. Chronic digestive complaints decreased from 27% to 5% of the sample over the study period: constipation from 16% to 3%, chronic diarrhea from 8% to 1%, and abdominal pain from 5% to 1%. Excessive fluid intake (1470±600 vs mL/d) correlated most strongly for seven children at 22 months experiencing alternating symptoms of chronic diarrhea and constipation or abdominal pain. Many other children tolerated dietary extremes without complaint. All macronutrient categories except dietary fiber intake increased over the study period. Thus, excessive fluid intake may provoke symptoms suggesting the irritable bowel syndrome in a susceptible group of younger children. Failure to increase fiber intake from 22 to 40 months of age leaves children on an immature diet whose effects require further study. (AJDC 1987;141:679-682) References 1. Apley J: The Child With Abdominal Pains , ed 2. Boston, Blackwell Scientific Publications Inc, 1975. 2. Almy TP: Dietary fiber: Current role in therapy and preventative medicine . Drug Ther 1984;14:51-59. 3. Feldman WW, McGrath P, Hodgson MA, et al: The use of dietary fiber in the management of simple, idiopathic recurrent, abdominal pain: Results of a prospective, double-blind, randomized, controlled trial . AJDC 1985;139: 1212-1216. 4. Cohen SA, Kristy M, Hendricks RD, et al: Chronic non-specific diarrhea: Dietary relationships . Pediatrics 1979;64:402-406. 5. Green HL, Ghishan FK: Excessive fluid intake as a cause of chronic diarrhea in young children . J Pediatr 1983;102:836-839.Crossref 6. Psoner BM, Borman CL, Morgan JL, et al: The validity of a telephone-administered 24-hour dietary recall methodology . Am J Clin Nutr 1982;36:546-553. 7. Sharp MM, Ahmed K: A computer application for dietary analysis in clinical nutrition . J Can Diet Assoc 1983;44:228-234. 8. Paul AA, Southgate DA, McCance RA, et al (eds): The Composition of Foods . New York, Elsevier Science Publishing Co Inc, 1978. 9. Blishen BR, McRoberts HA: A revised socioeconomic index for occupations in Canada . Can Rev Sociol Anthropol 1976;13:71-73.Crossref 10. Thompson WG, Heaton KW: Functional disorders in apparently healthy people . Gastroenterology 1980;79:283-288. 11. Drossman GA, Sandler RS, McKee DC, et al: Bowel patterns among subjects not seeking health care: Use of a questionnaire to identify a population with bowel dysfunction . Gastroenterology 1982;83:529-534. 12. Weaver LT, Steiner H: The bowel habits young children . Arch Dis Child 13. Lemoh JN, Brooke OG: Frequency and weight of normal stools in infancy . Arch Dis Child 1979;54:719-720.Crossref 14. Davidson M, Wasserman R: The irritable colon of childhood (chronic non-specific diarrhea syndrome) . J Pediatr 1966;69:1027-1038.Crossref 15. Lloyd-Still JD: Chronic diarrhea of childhood and the misuse of elimination diets . J Pediatr 1979;95:10-13.Crossref 16. Hyams JS, Leichtner AM: Apple juice: An unappreciated cause of chronic diarrhea . AJDC 1985;139:503-505. 17. American Academy of Pediatrics Committee on Nutrition: Toward a prudent diet for children . Pediatrics 1983;71:78-80.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060099044pmid: 3578196
Abstract • A one-year prospective study of 454 patients in a pediatric intensive care unit was performed to determine whether the rate of breaks in handwashing technique was different between medical professionals and to determine whether these rates were altered by the use of the gown. A handwashing break in technique was defined as not washing your hands after direct contact with either patients or support equipment before contact with another patient or departure from the unit. Ninety-four two-hour sessions were monitored by a research nurse during four cross-over periods of gown and no-gown use. Physicians did not wash their hands in 834 (79%) of 1056 contacts, nurses in 1073 (63%) of 1714 cases, occupational therapists in 21 (62%) of 34 cases, respiratory therapists in 269 (78%) of 346 cases, and radiology technicians in 59 (78%) of 76 cases. Nurses used significantly better technique when compared with physicians, respiratory therapists, and radiology technicians. Gown usage overall did not affect these breaks in handwashing technique rates. Physicians did not wash their hands 75% of the time when gowns were not used and 82% of the time when gowns were used. Handwashing rates were unaffected by gown use in all other professionals. Handwashing an important but neglected method of interrupting the transmission of hospital pathogens. (AJDC 1987;141:683-685) References 1. Albert RK, Condie F: Handwashing patterns in medical intensive care units . N Engl J Med 1981;304:1465-1469.Crossref 2. Mortimer EA, Lipsitz PJ, Wolinsky E, et al: Transmission of staphylococci between new-borns: Importance of the hands of personnel . AJDC 1962;104:289-295. 3. Steere AC, Mallison GF: Handwashing practices for the prevention of nosocomial infections . Ann Intern Med 1975;83:683-690.Crossref 4. Knittle MA, Eitzman DV, Baer H: Role of hand contamination of personnel in the epidemiology of gram-negative nosocomial infections . J Pediatr 1975;86:433-437.Crossref 5. Interview with Philip A. Pizzo: Isolation techniques in hospitals . Pediatr Infect Dis 6. Salzman TC, Clark JJ, Klemm L: Hand of personnel as a mechanism of cross-infection in nosocomial infections with antibiotic-resistant Escherichia coli and Klebsiella-Aerobacter . Antimicrob Agents Chemother 1967;7:97-100. 7. Rammelkamp CH Jr, Mortimer EA Jr, Wolinsky E: Transmission of streptococcal and staphylococcal infections . Ann Intern Med 1964; 60:753-758.Crossref 8. Frappier-Davignon L, Frappier A, St Pierre J: Staphylococcal infection in hospital nurseries: Influence of three different nursing techniques . Can Med Assoc J 1959;81:531-536. 9. Fleck AC Jr, Klein JO: The epidemiology and investigation of hospital-acquired staphylococcal disease in newborn infants . Pediatrics 1959;24:1102-1107. 10. Wolinsky E, Lipsitz PJ, Mortimer EA Jr, et al: Acquisition of staphylococci by newborns: Direct versus indirect transmission . Lancet 1960;2:620-622.Crossref 11. Eisenach KD, Reber RM, Eitzman DV, et al: Nosocomial infections due to kanamycin-resistant (R)-factor carrying enteric organisms in an intensive care nursery . Pediatrics 1972;50: 395-402. 12. Lowbury EJL, Lilly HA, Bull JP: Disinfection of hands, removal of transient organisms . Br Med J 1964;2:230-233.Crossref 13. Sprunt K, Redman W, Leidy G: Antibacterial effectiveness of routine handwashing . Pediatrics 1973;52:264-271. 14. Larson E: Handwashing and skin physiologic and bacteriologic aspects . Infect Control 1985;6:14-23. 15. Larson E, Leyden JJ, McGinley KJ, et al: Physiologic and microbiologic changes in skin related to frequent handwashing . Infect Control 1986;7:59-63. 16. Morrison AJ, Gratz J, Cabezudo I, et al: The efficacy of several new handwashing agents for removing non-transient bacterial flora from hands . Infect Control 1986;7:268-272.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060101045
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 A wealth of information is contained in this 400-page book. The basic organization is that of a systems-oriented atlas dealing with virtually all commonly seen pediatric abnormalities. Chapters deal with the brain and spine; thorax; gastrointestinal tract; liver, gallbladder, and bile ducts; spleen, pancreas, and retroperitoneal structures; urinary tract; reproductive system; and soft tissues, joints, and miscellaneous structures. The chapters are generally organized with a short section on the normal state followed by a variety of well-illustrated abnormal situations. Throughout, imaging of the pathologic findings is of good quality, and ultrasound images are supplemented by roentgenograms, computed tomograms, scintigrams, and occasional magnetic resonance images. The ultrasound images are labeled on the figures, considerably enhancing their value to the reader. In rare instances, line drawings supplement the studies. I wish there were more, as these are Wonderfully illustrative of the imaging planes being used and the structure visualized. Liberal use of
Hyman, Paul E.;Abrams, Candy E.;Zipser, Robert D.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060102046pmid: 2953236
Abstract • Urinary thromboxane B2 levels increased threefold to 20-fold in infants with neonatal necrotizing enterocolitis compared with healthy infants and infants with benign causes of hemepositive stools. Increased urinary thromboxane B2 levels were detected coincidently with the initial signs of necrotizing enterocolitis, and values paralleled the course of the illness. Infants with serious illnesses other than necrotizing enterocolitis had increased urinary thromboxane B2 levels but with lower values than those of infants with necrotizing enterocolitis. Indomethacin therapy appeared to reduce urinary thromboxane B2 levels and reduce their usefulness as a marker of illness. Another product of platelet activation, β-thromboglobulin, was increased in the urine of infants with necrotizing enterocolitis. Decreased platelet counts in infants with necrotizing enterocolitis correlated inversely with urinary thromboxane. Results of β-thromboglobulin and platelet studies are consistent with the concept that platelet consumption due to ischemic thrombosis was the source of enhanced thromboxane excretion. (AJDC 1987;141:686-689) References 1. Egan EA: Necrotizing enterocolitis , in Lebenthal E (ed): Textbook of Gastroenterology and Nutrition in Infancy . New York, Raven Press, 1981, pp 979-986. 2. Book LS, Herbst JJ, Atherton SO, et al: Neonatal necrotizing enterocolitis in low-birthweight infants fed an elemental formula . J Pediatr 1975;87:603-605.Crossref 3. Stevenson JK, Oliver TK, Graham GB, et al: Aggressive treatment of neonatal necrotizing enterocolitis: Thirty-eight patients with 28 survivors . J Pediatr Surg 1971;6:28-35.Crossref 4. Touloukian RJ, Posh J, Spencer R: The pathogenesis of ischemic gastroenterocolitis of the neonate: Selective gut mucosal ischemia of asphyxiated neonatal piglets . J Pediatr Surg 1972;7:194-205.Crossref 5. Berdon WE, Grossman H, Baker OH, et al: Necrotizing enterocolitis in the premature infant . Radiology 1964;83:879-887.Crossref 6. Reines HD, Halushka PV, Cook JA, et al: Plasma thromboxane concentrations are raised in patients dying with septic shock . Lancet 1982;2: 174-175.Crossref 7. Robertson RM, Robertson D, Roberts LJ, et al: Thromboxane A2 in vasotonic angina pectoris: Evidence from direct measurements and inhibitor trials . N Engl J Med 1981;304:998-1003.Crossref 8. Roberts LJ II, Sweetman BJ, Payne NA, et al: Metabolism of thomboxane B2 in man: Identification of the major urinary metabolite . J Biol Chem 1977;252:7415-7417. 9. Zipser RD, Martin K: Urinary excretion of arterial blood prostaglandins and thromboxanes in man . Am J Physiol 1982;242:E171-E177. 10. Klotz TA, Cohn LS, Zipser RD: Urinary excretion of thromboxane B2 in patients with venous thromboembolic disease . Chest 1984;85: 329-335.Crossref 11. Foegh ML, Winchester JF, Zmubka M, et al: Urine i-TxB2 in renal allograft rejection . Lancet 1981;2:431-434.Crossref 12. Zipser RD, Smorlesi C: Regulation of urinary thromboxane B2 in man: Influence of urinary flow rate and tubular transport . Prostaglandins 1984;27:257-272.Crossref 13. Kuehl PG, Cotton RB, Fitzgerald GA: Systemic production of prostacyclin and thromboxane A2 does not correlate with patency of the ductus arteriosus in very low birth weight infants . J Pediatr 1986;108:977-982.Crossref 14. VanOost BA, Veldhuyzen B, Timmermans APM, et al: Increased urinary β-thromboglobulin excretion in diabetes assayed with a modified RIA kit-technique . Thromb Haemost 1983;49: 18-20. 15. Ludlam CA, Moore S, Bolton AE, et al: The release of a human platelet specific protein measured by a radioimmunoassay . Thromb Res 1975;6:543-548.Crossref 16. Patrignani P, Filabozzi P, Patrono C: Selective cumulative inhibition of platelet thromboxane production by low-dose aspirin in healthy subjects . J Clin Invest 1982;69:1366-1372.Crossref 17. Zipser RD, Radvan GH, Kronborg IJ, et al: Urinary thromboxane B2 and prostaglandin E2 in the hepatorenal syndrome: Evidence for increased vasoconstrictor and decreased vasodilator factors . Gastroenterology 1983;84: 697-703. 18. Patrono C, Ciabattoni G, Remuzzi G, et al: Functional significance of renal prostacyclin and thromboxane A2 production in patients with systemic lupus erythematosus . J Clin Invest 1985;76:1011-1018.Crossref 19. Utsunomiya T, Krausz MM, Levine L, et al: Thromboxane mediation of cardiopulmonary effects of embolism . J Clin Invest 1982;70: 361-368.Crossref 20. Heffner JE, Shoemaker SA, Canham EM, et al: Acetylglycerol ether phosphoryl-choline–stimulated human platelets cause pulmonary hypertension and edema in isolated rabbit lungs: Role of thromboxane A2 . J Clin Invest 1983;71: 351-357.Crossref 21. Saldeen T: Clotting, microembolism, and inhibition of fibrinolysis in adult respiratory distress . Surg Clin North Am 1983;63:285-304. 22. Fisher M, Zipser RD: Increased excretion of immunoreactive thromboxane B2 in cerebral ischemia . Stroke 1985;16:10-14.Crossref 23. Cook JA, Wise WC, Halushka PV: Elevated thromboxane levels in the rat during endotoxic shock: Protective effects of imidazole, 13azaprostanoic acid, or essential fatty acid deficiency . J Clin Invest 1980;65:227-230.Crossref
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060105047
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 Remember the scarf sign, the square window, the lateral propping reaction, and the Recamier position? These terms Were coined by the Claudine Amiel-Tison, the mother of the neonatal neurologic examination. This small monograph is the English translation of Drs Amiel-Tison and Grenier's 1984 French publication. Sections are devoted to the clinical neurologic evaluation of the neonate, the use of Amiel-Tison's grid, evaluation of neuromotor sequelae, the significance of transient neuromotor anomalies, and the use of developmental scales and sensory evaluation. As Harvey Sarnat notes in the introduction, "This concise monograph summarizes and integrates meticulous observations of these two dedicated physicians, formulating their data into thoughtful generalizations, at times evoking imaginative interpretations." While not a standard part of the conventional neurologic assessment of young infants, Amiel-Tison's approach clearly reflects her wealth of experience with both healthy and neurologically impaired infants. The translation is excellent and captures the flavor of the original
Berman, Stephen;Grose, Kathy;Zerbe, Gary O.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060106048pmid: 3554985
Abstract • Prednisone for seven days plus the combination drug sulfamethoxazole and trimethoprim for 30 days was assessed in treating chronic middle-ear effusion present for at least eight weeks. Pneumatic otoscopy, tympanometry, and audiology at entry into the study, and one week and one month after therapy, documented the status of the middle-ear effusion. Clearing in both ears or in one when only one was involved was called complete resolution; clearing in one of two affected ears was called partial resolution. In the initial open trial, 13 of 24 patients experienced partial or complete resolution one month after therapy. Subsequently, 28 patients were enrolled in a randomized, double-blind, placebo-controlled clinical trial in which patients whose effusion failed to clear were crossed over to the alternative regimen. In this trial, ten treated children (71%) experienced partial or complete resolution one month after therapy compared with three (21%) in the control group. Patients enrolled in both trials whose effusion cleared were followed up monthly for six months. Seven of 29 patients required referral for ventilation tubes. (AJDC 1987;141:690-694) References 1. Klein JO: Persistent middle ear effusions: Natural history and morbidity . Pediatr Infect Dis 1982;1( (suppl 5) ):4-13.Crossref 2. Paradise JL, Rogers KD: On otitis media, child development, and tympanostomy tubes: New answers or old questions . Pediatrics 1986; 77:88-91. 3. Riding KH, Bluestone CD, Michaels RH, et al: Microbiology of recurrent and chronic otitis media with effusion . J Pediatr 1978;93:739-745.Crossref 4. Lim DJ: Pathogenesis of otitis media with effusion . Pediatr Infect Dis 1982;1( (suppl 5) ): 515-525. 5. Teele DW, Klein JO, Rosner BA, et al: Otitis media with effusion during the first three years of life and development of speech and language . Pediatrics 1984;74:282-287. 6. Jung TTK, Giebink GS, Juhn SK: Effects of ibuprofen, corticosteroid, and penicillin on the pathogenesis of experimental pneumococcal otitis media , in Lim DJ (ed): Recent Advances in Otitis Media With Effusion . Philadelphia, BC Decker Inc, 1984, pp 269-272. 7. Persico M, Podoshen L, Fradis M: Otitis media with effusion: A steroid and antibiotic therapeutic trial before surgery . Ann Otol Rhinol Laryngol 1978;87:191-196. 8. Schwartz RH, Puglese J, Schwartz DM: Use of a short course of prednisone for treating middle ear effusion: A double-blind crossover study . Ann Otol Rhinol Laryngol 1980;89( (suppl 68) ): 296-300. 9. Macknin ML, Jones PK: Oral dexamethasone for treatment of persistent middle ear effusion . Pediatrics 1985;75:329-335. 10. Niedeman LG, Waller-Buchholtz V, Jakalay T: A comparative trial of steroids versus placebos for treatment of chronic otitis media with effusion , in Lim DJ (ed): Recent Advances in Otitis Media With Effusion . Philadelphia, BC Decker Inc, 1984, pp 273-276. 11. Healy GB: Antimicrobial therapy for chronic otitis media with effusion , in Lim DG (ed): Recent Advances in Otitis Media With Effusion . Philadelphia, BC Decker Inc, 1984, pp 285-287. 12. Marks MJ, Mills RP, Shakien OH: A controlled trial of cotrimoxazole therapy in serous otitis media . J Laryngol Otol 1981;95:1003-1009.Crossref 13. Jerger J: Clinical experience with impedance audiometry . Arch Otolaryngol Head Neck Surg 1970;92:311-324.Crossref 14. Heisse JW: Secretory otitis media: Treatment with depomethylprednisolone . Laryngoscope 1963;73:54-59.Crossref 15. Shea JJ: Autoinflation treatment of serous otitis media in children . J Laryngol Otol 1971;85:1254-1258.Crossref 16. Woodhead JC, Milavetz G, Dusdieker LB, et al: Prednisone treatment of otitis media with effusion . AJDC 1986;140:318. 17. Giebink GS, Le CT, Batalden PB, et al: Antimicrobial and anti-inflammatory treatment of chronic otitis media with effusion , abstracted. Pediatr Res 1986;20:310.
Agah, Ravin;Cherry, James D.;Garakian, Alice J.;Chapin, Martha
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060111049pmid: 3578197
Abstract • Respiratory syncytial virus (RSV) infections in hospitalized children were identified by indirect fluorescent antibody technique. Patients with RSV infections were assigned to one of two isolation categories. In one category, the health care workers entering the child's room did not wear masks and goggles; in the other category, the workers did wear masks and goggles. The RSV Illness rate in health care workers using masks and goggles was 5%, but the rate for those not using masks and goggles was 61%. In the no mask/goggles group, the RSV illness rates in the health care workers correlated directly with the number of exposures. In this modest study, the use of masks and goggles was associated with a significant reduction of RSV illnesses in pediatric health care workers. (AJDC 1987;141:695-697) References 1. Ditchburn RK, McQuillin J, Gardner PS, et al: Respiratory syncytial virus in hospital cross-infection . Br Med J 1971;3:671-673.Crossref 2. Meissner HC, Murray SA, Kiernan MA, et al: A simultaneous outbreak of respiratory syncytial virus and parainfluenza virus type 3 in a newborn nursery . J Pediatr 1984;104:680-684.Crossref 3. Krasinski K: Severe respiratory syncytial virus infection: Clinical features, nosocomial acquisition and outcome . Pediatr Infect Dis 1985;4: 250-257.Crossref 4. Hall CB, Geiman JM, Douglas RG Jr, et al: Control of nosocomial respiratory syncytial viral infections . Pediatrics 1978;62:728-732. 5. Goldson EJ, McCarthy JT, Welling MA, et al: A respiratory syncytial virus outbreak in a transitional care nursery . AJDC 1979;133:12801282. 6. Mintz L, Ballard RA, Sniderman SH, et al: Nosocomial respiratory syncytial virus infections in an intensive care nursery: Rapid diagnosis by direct immunofluorescence . Pediatrics 1979;64:149-153. 7. Hall CB, Douglas RG Jr, Geiman JM, et al: Nosocomial respiratory syncytial virus infections . N Engl J Med 1975;293:1343-1346.Crossref 8. Sims DG, Downham MA, Webb JK, et al: Hospital cross-infection on children's wards with respiratory syncytial virus and the role of adult carriage . Acta Paediatr Scand 1975;64:541-545.Crossref 9. Valenti WM, Clarke TA, Hall CB, et al: Concurrent outbreaks of rhinovirus and respiratory syncytial virus in an intensive care nursery: Epidemiology and associated risk factors . J Pediatr 1982;100:722-726.Crossref 10. Hall CB, Douglas RG Jr: Nosocomial respiratory syncytial viral infections: Should gowns and masks be used? AJDC 1981;135:512-515. 11. Gala CL, Hall CB, Schnabel KC, et al: The use of eye-nose goggles to control nosocomial respiratory syncytial virus infection . JAMA 1986;256:2706-2708.Crossref 12. Garner JS, Simmons BP: CDC guidelines for isolation precautions in hospitals . Infect Control 1983;4:245-325. 13. Murphy D, Todd JK, Chao RK, et al: The use of gowns and masks to control respiratory illness in pediatric hospital personnel . J Pediatr 1981;99:746-750.Crossref 14. Hall CB, Douglas RG Jr, Schnabel KC, et al: Infectivity of respiratory syncytial virus by various routes of inoculation . Infect Immun 1981;33:779-783. 15. Hall CB, Douglas RG Jr: Modes of transmission of respiratory syncytial virus . J Pediatr 1981;99:100-103.Crossref 16. McQuillin J, Gardner PS: Rapid diagnosis of respiratory syncytial virus infection by immunofluorescent antibody techniques . Br Med J 1968;1:602-605.Crossref
Kaufman, Stuart S.;Wood, R. Patrick;Shaw, Byers W.;Markin, Rodney S.;Gridelli, Bruno;Vanderhoof, Jon A.
1987 American Journal of Diseases of Children
doi: 10.1001/archpedi.1987.04460060114050pmid: 3034054
Abstract • A child with the Alagille syndrome of intrahepatic bile duct paucity developed hepatocarcinoma. Disabling cirrhosis had rendered this child a suitable candidate for transplantation before the discovery of carcinoma. However, the extension of the tumor outside the liver precluded the performance of this potentially life-saving operation. Serial monitoring of the serum μ-fetoprotein concentration may be of value in the early identification of tumors in pediatric candidates for transplantation. (AJDC 1987;141:698-700) References 1. Danks DM, Campbell PE, Jack I, et al: Studies of the aetiology of neonatal hepatitis and biliary atresia . Arch Dis Child 1977;52:360-367.Crossref 2. Perrault J: Paucity of interlobular bile ducts: Getting to know it better . Dig Dis Sci 1981;26:481-484.Crossref 3. Shulman SA, Hyams JS, Gunta R, et al: Arteriohepatic dysplasia (Alagille syndrome): Extreme variability among affected family members . Am J Med Genet 1984;19:325-332.Crossref 4. Kahn EI, Daum F, Markowitz J, et al: Arteriohepatic dysplasia: II. Hepatobiliary morphology . Hepatology 1983;3:77-84.Crossref 5. Starzl TE, Zitelli BJ, Shaw BW Jr, et al: Changing concepts: Liver replacement for hereditary tyrosinemia and hepatoma . J Pediatr 1985;106:604-606.Crossref 6. Starzl TE, Koep U, Schroter GPJ, et al: Liver replacement for pediatric patients . Pediatrics 1979;63:825-829. 7. Calne RY: Liver transplantation for liver cancer . World J Surg 1982;6:76-80.Crossref 8. Markowitz J, Daum F, Kahn EI, et al: Arteriohepatic dysplasia: I. Pitfalls in diagnosis and management . Hepatology 1983;3:74-76.Crossref 9. Ishak KG, Glunz PR: Hepatoblastoma and hepatocarcinoma in infancy and childhood: Report of 47 cases . Cancer 1967;20:396-422.Crossref 10. Weinberg AG, Finegold MJ: Primary hepatic tumors of childhood . Hum Pathol 1983;14: 512-537.Crossref 11. Dahms BB: Hepatoma in familial cholestatic cirrhosis of childhood . Arch Pathol Lab Med 1979;103:30-33. 12. Adams PC: Hepatocellular carcinoma associated with arteriohepatic dysplasia . Dig Dis Sci 1986;31:438-442.Crossref 13. Liver transplantation: Consensus conference . JAMA 1983;250:2961-2964.Crossref 14. Iwatsuki S, Klintmalm GBG, Starzl TE: Total hepatectomy and liver replacement (orthotopic liver transplantation) for primary hepatic malignancy . World J Surg 1982;6:81-85.Crossref 15. Heyward WL, Lanier AP, McMahon BJ, et al: Early detection of primary hepatocellular carcinoma . JAMA 1985;254:3052-3054.Crossref 16. Kobayashi K, Sugimoto T, Makino H, et al: Screening methods for early detection of hepatocellular carcinoma . Hepatology 1985;5: 1100-1105.Crossref 17. Liaw Y-F, Tai D-I, Chu C-M, et al: Early detection of hepatocellular carcinoma in patients with chronic type B hepatitis: A prospective study . Gastroenterology 1986;90:263-267. 18. Ebara M, Ohto M, Shinagawa T, et al: Natural history of minute hepatocellular carcinoma smaller than 3 cm complicating cirrhosis: A study in 22 patients . Gastroenterology 1986;90: 289-298. 19. Yandza T, Valayer J: Benign tumors of the liver in children: Analysis of a series of 20 cases . J Pediatr Surg 1986;21:419-423.Crossref