bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nocturnal Enuresis
Authors: Smith Leigh R. 
Published: December 2021

Enuresis has long been a problem for children, parents, and physicians. Much has been written on the subject from various points of view. A brief review of the subject is presented, followed by a description of the author's approach to the problem. The emphasis is on removing enuresis from the category of a disease to be cured and placing it among those conditions which may be considered variations of normal development. The physician's role is to help resolve family problems which result from misconceptions about enuresis and to avoid overinvestigation of a largely self-limiting condition.
Nocturnal enuresis may be defined simply as wetting the bed at night beyond the age at which most children have stopped. Parents often consider enuresis a disease to be cured. The condition is seldom bothersome to the child, however, until parent, sibling, peer, or relative makes him feel that he is different from other children.
The concept of nocturnal enuresis as a disease is often reinforced by textbooks and literature which define a specific age after which bedwetting is unusual and which convey the impression that the etiology is frequently organic. The age most often assigned as an end point to bedwetting is 5 to 6 years, or school age.1-3
Hyponatremia in Children
Authors: Kelsch Robert C. , Oliver William J. 
Published: December 2021

Hyponatremia is usually recognized following an electrolyte screen since it is not symptomatic, except in its severest degrees. The pathophysiologic implications of hyponatremia and its therapy are quite varied. The purpose of this review is to present a diagnostic plan which in most instances will resolve the therapeutic dilemma. This approach is a minor modification of that developed by Schrier and Berl1 for evaluating hyposmolar states.
GENERAL PRINCIPLES
The occurrence of hyponatremia indicates a failure of those receptor and effector mechanisms designed to assure that the quantity of water in the body will closely relate to the amount of solute in the major bodywater spaces. The principal sensors are designed to recognize osmolar changes, not changes in sodium concentration. Nevertheless, measurement of serum sodium concentration is the most readily available tool for estimation of disturbances in osmolality. Fanestil2 has recorded 14 formulae designed to estimate osmolality from serum sodium concentration or sodium, glucose, and urea concentrations. The simplest of these formulae, osmolality = 2 x Na+ + 10, is satisfactory in the vast majority of clinical circumstances occurring in pediatrics. Diabetes mellitus is the only relatively common state that requires the use of alternate formulations to correct for hyperglycemia. The contribution to serum osmolality by glucose can be approximated by adding to the above formula 1 mOsm for each 18 mg/100 ml of blood glucose above the level of 100 mg/100 ml.
Medical Issues in Sports Medicine
Authors: Smith Nathan J. 
Published: December 2021

Today's children live in an environment that prompts an increasing interest in medical issues related to recreational activities and sports participation. The restrictive urban environment, in which most children live, allows for little self-directed play and much of the play of school-aged children is rigidly regulated and organized by adults. The affluence and abundant leisure time of today's adults supports and allows for their involvement in much of children's play. The most readily identified models accepted for the play and games of young people are the varsity and professional sports so prominently displayed through the mass media. Little concern has been given for the appropriateness of these games for the very young; yet they have become the "play" and the games of millions of very young American children. The general secular advance of maturational status allows children of certain highly motivated parents to become highly competent and even elite athletes at younger and younger ages.
Only in the past two decades have organized sports come to make up much of the play opportunity for the elementary school-aged child. More than 17 million young people, many of them preadolescent and as young as 5 or 6 years of age, participate in community-based youth sports programs that are highly organized and generously supported.
The Schoolchild with Encopresis
Authors: Levine Melvin D. 
Published: December 2021

Often, a schoolchild with encopresis feels desperate, lacking a most primitive form of control, harboring a painful secret, susceptible to exposure and peer ridicule, wounded by the disdainful remarks of parents and siblings, and perplexed over why he messes. Often children with encopresis receive inconsistent care; management may vacillate from intentional disregard of the problem to active coercion or vindiction. Parents may be baffled by conflicting advice from neighbors, teachers, grandparents, pharmacists, and even pediatricians.
Most "accidents" occur in the late afternoon (commonly 3:00 to 7:00 PM). Unlike enuresis, nocturnal encopresis is rare and more difficult to treat successfully. Many children insist (correctly) that they do not receive a "signal" or feel the call to use a bathroom. They may plan furtively to conceal their shameful out-flow, burying underwear in the garden or sequestering soiled clothing in trash cans and behind dressers!
Encopresis is defined as the deposition of formed or semiformed stools in a child's underwear (or other unorthodox sites), occurring after the age of 4 years on a regular basis. Some authors differentiate between encopresis and fecal soiling, basing the distinction on the extent to which full-bowel movements are passed.1 This classification, however, often does not conform to clinical experience, since longstanding cases commonly fluctuate over time in patterns of incontinence and stool consistency.
Jaundice in the Newborn
Authors: Maisels M. Jeffrey 
Published: December 2021

Pediatricians are confronted daily with the problem of the jaundiced newborn infant. The newborn infant is unique because (a) some elevation of serum bilirubin concentration is found in virtually all babies in the first few days of life, (b) the serum bilirubin concentration frequently rises to levels that are almost never encountered outside of the neonatal period, and (c) the newborn period remains the only time in which an elevated plasma bilirubin concentration per se represents a threat to the well-being of the organism.
FETAL AND NEONATAL BILIRUBIN METABOLISM
Chemical Structure and Properties of Bilirubin
Bilirubin IXα (so called because it is derived from cleavage at the α position of the heme ring of ferropro-toporphyrin IX) is the end product of the catabolism of heme, of which the major source is circulating hemoglobin. Recent observations on the stereochemistry and conformation of the bilirubin molecule are helpful in understanding the potential neurotoxicity of bilirubin as well as the mechanism of phototherapy.1 The isomer, bilirubin IXα(Z,Z), is the major form of bilirubin as it exists in the blood where it is tightly bound to albumin. When this form of bilirubin takes up two hydrogen ions, it forms bilirubin IXα(Z,Z) acid, which is an involuted structure containing intramolecular hydrogen bonds.
Cytogenetics in the Practice of Pediatrics
Authors: Gerald Park S. 
Published: December 2021

The best known chromosomal abnormalities are alterations in the number of chromosomes. This type of chromosomal alteration is found in approximately 5% of all fetuses, most of whom are unable to survive pregnancy. Because of this selection process, only 0.6% of living newborns have a chromosomal abnormality. Approximately half of this group is grossly clinically abnormal. The remainder may not exhibit any clinical disturbance until later in childhood or at the time of reproduction.
The pediatrician must have sufficient knowledge of the overt cytogenetic syndromes to suspect the probable diagnosis. The pediatrician must also be sufficiently informed of the origins of chromosomal abnormalities to participate in the genetic counseling of the parents. Further, many of the recently recognized cytogenetic abnormalities are subtle and difficult to detect. Their demonstration will only be possible if the pediatrician is alert to the clinical situations in which they are likely to occur.
HUMAN CHROMOSOMES
The chromosomes which are seen through the microscope are chromosomes that have replicated. They are bipartite bodies, each half (or sister chromatid) is identical with the other half (Fig 1). The process of preparing the chromosomes for examination involves arresting cell division so that the chromosome does not undergo the normal process of division. The two chromatids touch each other at the constricted region known as the centromere.
Live Measles Vaccine Not a Cause of Atypical Measles Syndrome
Authors: Amler Robert William , Rapkin R. H. ,   colleagues
Published: December 2021

In the August issue of PIR (3:55, 1981)1 there is an abstract regarding atypical measles which we believe is misleading and may deter vaccination of a group of adolescents for whom live measles vaccine is indicated. We have received calls from a number of concerned pediatricians and believe the abstract should be corrected. The author states that the atypical measles syndrome is a possible consequence of administering live measles vaccine to former recipients of killed measles vaccine. Although severe local reactions and occasionally systemic reactions do occur following administration of live measles vaccine to former recipients of killed measles vaccine, there is no evidence that the live vaccine causes classic atypical measles syndrome.
Three patients, referred to as having severe systemic reactions by Krause et al,2 experienced fever to 103 F (39.4 C), malaise, marked local pain, swelling and erythema seven days following vaccination; these reactions lasted an average of eight days. However, the abstract was incorrect because these patients did not develop the atypical measles syndrome. Although the reactions were more severe than reactions that might be observed in persons who had never received killed measles vaccine, they were substantially less severe than the atypical measles syndrome. Atypical measles is characterized by high fever, pneumonitis (often with pulmonary consolidation and pleural effusion), pedal and hand edema, and an unusual rash which may be maculopapular, petechial, vesicular or urticarial. The rash is often most concentrated on the extremities.3 Revaccination with live measles vaccine is indicated for former recipients of killed measles vaccine to induce permanent immunity to measles, so that the atypical measles syndrome does not develop when the vaccinee is exposed to natural measles. Revaccination will not cause the syndrome. Atypical measles has occasionally been reported in individuals exposed to natural measles who had previously received live measles virus vaccine within a few months of receiving inactivated measles vaccine.4-6 This raises the possibility that the temporary immunity conferred by the killed vaccine precluded an adequate immunologic response to the live measles virus vaccine. Therefore, persons who received live measles vaccine within three months of receiving inactivated measles vaccine should also be revaccinated with live measles vaccine. Killed measles vaccine was used in the United States between 1963 and 1967 when an estimated 1,836,000 doses were distributed. Persons vaccinated with an unknown type of measles vaccine during that period should also be revaccinated with live measles vaccine as the unknown vaccine may have been killed measles vaccine.
Fungal Infections in Children
Authors: Esterly Nancy Burton 
Published: December 2021

Fungal disorders are some of the most common cutaneous infections of childhood and adolescence. Despite their frequency and the ease with which an infectious agent can be correctly identified, fungal lesions are readily mistaken for other diseases or misdiagnosed in patients with entirely different skin conditions. One of the chief reasons for inaccurate diagnosis is a preconceived notion on the part of the physician as to how the lesions should look clinically. In fact, cutaneous fungal infections are extremely pleomorphic in appearance and can be macular and scaly, papular, pustular, vesiculobullous, or nodular. Their morphology may also be altered by self-medication, by treatment prescribed by another physician, or by an immunologic deficit in the host.
Even the most experienced physician will be baffled by these lesions some of the time. Studies assessing clinical acumen by verification with culture data demonstrate a significant degree of error in diagnosis, particularly in nondermatologic settings. Fortunately, most of these mistakes are preventable if three simple procedures are carried out. A Wood's lamp examination and a KOH preparation can be performed rapidly in the office and may provide all of the confirmatory evidence necessary for certain diagnosis. A positive culture of a properly obtained specimen is additional unqualified evidence of a fungous infection.
Depression in Children and Adolescents
Authors: Schowalter John E. 
Published: December 2021

CASE HISTORY
Ted is a 10-year-old only child who was brought to his pediatrician with the following history. He was well until about two months before referral at which time he began to lose interest in things. This was manifested by poor concentration, a falling off of school performance, a disinterest in friends, and a decrease in appetite. Ted's teacher was the first to note the personality change and urged the parents to get a medical checkup. Physical examination findings were normal, but Ted seemed sad. History revealed no recent illnesses or incidents likely to be disturbing, but it was learned that Ted's mother and maternal grandfather had suffered multiple depressions, and each had been hospitalized for this on one occasion. Ted said that he felt sad lately, but did not know why. He commented that he never felt this way before and had never thought of hurting himself. When asked, he said he feared he would never feel better, but hoped that he would. The pediatrician diagnosed a major depressive episode. After a discussion with Ted and his mother about depression, the pediatrician made the referral to a child psychiatrist.
Every adult has felt depressed. It is part of the human condition. Sometimes the cause of the depression is clear; sometimes the depression seems to appear for no apparent reason.
Study of the Malformed Fetus and Infant
Authors: Opitz John M. 
Published: December 2021

Humans sustain a reproductive loss of approximately two of every three fertilizations; prenatally, much of this death is associated with malformations that are mainly due to chromosome abnormalities. Up to half of all pre- and postimplantation ova in man may have chromosome defects that are more than 98% lethal. The earlier the stage of development at the time of the spontaneous abortion the greater is the number of malformations and chromosome defects; nearly 80% of embryos that reach a 2-week stage of development have a chromosome defect, as do more than 60% of those developing to 12 weeks, approximately 6% of stillborn infants, and 0.6% of all live-born infants. Even nonchromosomally caused single congenital defects have a high prenatal death rate. Besides chromosome defects, multifactorial traits and single gene (mendelian) mutations are the next most common class of congenital defects. Prior fetal wastage with or without prematurity of previous live-born infants increases the risk of subsequent fetal loss; the greater the number of preceding spontaneous abortions the smaller is the chance of a subsequent live-born child.
One fourth of all stillborn fetuses have one or more than one malformation or a syndrome, in many cases associated with a substantial risk of recurrence. After "certain diseases of early infancy" (mostly prematurity and hyaline membrane disease) congenital malformations remain the most important cause of infant mortality (60% of which occurs by the seventh day of life).
It is important for pediatricians to take much greater cognizance of the amount of genetic disease involved in fetal wastage and infant death, to collaborate more effectively with obstetricians, pathologists, anatomists, and geneticists in determining diagnosis and risk of recurrence, and to counsel more accurately those who have lost a fetus or infant. Such fetuses and infants deserve the same meticulous examination, evaluation, and documentation as an older malformed child being brought in for diagnostic, prognostic, and genetic counseling. A fetal loss may cause as much sorrow as an infant death; this grief must be addressed explicitly but gently and sympathetically before any other considerations are put before the parents as they decide on whether or not to create a new life.
A Workbook Exercise on Necrotizing Enterocolitis
Authors: Burg Fredric D. , Polin Richard A. 
Published: December 2021

Readers will immediately notice that the following article departs from the usual style in medical journals. We all recognize that active learning is far better than passive, but this is difficult to achieve in the usual journal article. Drs Burg and Polin have developed a sequential workbook approach in the following article which will require your active participation. We believe that it will result in better learning, but would appreciate reader comment.
R.J.H.
The following are a series of exercises aimed to help you in: (1) identifying the factors that cause necrotizing enterocolitis (NEC); (2) Explaining the pathophysiology of NEC; (3) developing a proper approach to diagnosing necrotizing enterocolitis in the neonate; and (4) managing a newborn with this disease.
EXERCISE 1
Factors That Contribute to Development of Necrotizing Enterocolitis
Please read through the following case history.
K.W. was a 1,600-gm girl delivered to a 17-year-old primigravida by emergency cesarean section for fetal distress at 31 weeks' gestation. Apgar scores at one and five minutes were 2 and 5. The infant was given 3 mEq of sodium bicarbonate through an umbilical vein (UV) catheter in the delivery room and then intubated. Following admission to the intensive care nursery an umbilical arterial (UA) catheter was inserted and positioned at L-1.
Bonding and Screening: Myth and Reality
Authors: CHAMBERLIN ROBERT W. 
Published: December 2021

McCall's article in this issue raises questions about two recent developments in pediatrics—the effectiveness of bonding and screening for development. These are emotional issues with partisans on both sides. I have been asked to respond to McCall's comments as a "neutral observer."
The thrust of McCall's arguments is that the long-term importance of both early mother-infant contact and detecting and treating early developmental lags has been overrated and this has created some iatrogenic problems. He points out that many children with early developmental lags turn out to be normal and that many mothers who do not undergo early and extended contact with their infant at birth still manage to develop a warm and loving relationship with their child.
Hypertension in Children
Authors: Goldring David , Hernandez Antonio 
Published: December 2021

The pathogenesis of primary hypertension remains unknown despite extensive investigative contributions. Evidence is mounting that the disease may have its inception in childhood or possibly in infancy. What is needed are long-term longitudinal studies to determine whether the child with primary hypertension eventually becomes the adult hypertensive. A method for the identification of the hypertensive either by specific chemical or physiologic characteristics is very much needed.
Nonpharmacologic therapeutic intervention needs careful evaluation, especially in the pediatric patient, to determine whether the disease can be arrested. A thorough study of pediatric patients with primary hypertension should be strongly encouraged. It may be that the solution to the complex puzzle of primary hypertension may have a higher probability of being solved at the inception of the disease in infancy or childhood rather than in the later irreversible stage in adulthood.
What the General Pediatrician Should Know About Developmental Anomalies
Authors: Opitz John M. 
Published: December 2021

It would be a "fallacy of misplaced emphasis" to devote this review only to facts, data, and specific syndromes. A necessary minimum of developmental biology will be presented; however, the main focus will be on method, ie, on effective use of eyes and intellect to learn "phenotype analysis," which is the analysis of normal and abnormal developmental variability.
In spite of the valiant efforts of the late David W. Smith,1 pediatric education on this subject remains handicapped in several major ways:
1. Overemphasis on the metabolic and biochemical aspects of disease and lack of expertise in methods of morphologic analysis by staff and faculty lead to lack of confidence in ability to do a complete physical examination and to interpret structural changes correctly;
2. Excessive preoccupation with the abnormal without encouraging study of the normal frequently results in over-interpretation and misinterpretation of normal variants as minor anomalies and the persistence of that offensive nonentity—"the funny looking kid (FLK)";
3. Lack of instruction in anthropometric methods results in frequent failure to quantitate and to interpret physical traits accurately and leads to such erroneous statements as "height at birth..." (length is meant); "this microcephalic child had large ears" (head is small, ears are normal); "this Down syndrome child had a highly arched palate" (palate height is normal in the Down syndrome, it is length that is mostly severely reduced);
Viral Hepatitis in School-Aged Children
Authors: Chilton Lance 
Published: December 2021

Hepatitis A is a common disease in children, usually passed by the fecal-oral route. Because of its route of transmission, day care centers, especially those caring for infants and toddlers in diapers, are a likely site of passage of the disease, unlike schools, where transfer of HAV occurs uncommonly. The pediatrician encountering a case of HA must ascertain (1) that other possible aiagnoses have been eliminated, (2) whether the patient or a sibling attends a day care center, and (3) the likelihood of a common source outbreak associated with contaminated food or drink. Public health help should be sought to determine that all wider implications of the patient's disease have been taken into account. In some instances, immunoglobulin use may be indicated beyond the usual group of family and sexual contacts. In many cases, the pediatrician will be asked to stretch the indications for immunoglobulin prophylaxis; the forces may be so strong as to force mass immunoglobulin administration even if inschool transmission is unlikely. There is no specific treatment for hepatitis; previously prescribed diets and restrictions of activity are unnecessary. Recovery without complications occurs in the vast majority of patients, especially children, with HA.
Hepatitis B and non-A, non-B hepatitis are less common than HA in children, except those in certain groups. Those infected have a 10% likelihood of contracting chronic active hepatitis; with HB, a chronic carrier state contributes substantially to the epidemiology of the disease. The same is likely to hold true for non-A, non-B hepatitis. In patients with needle-stick, blood product, or sexual xposure to HB, standard immunoglobulin or HBIG is recommended as prophylaxis; for those exposed to NANB, immunoglobulin may be given. A vaccine to give active protection against HB exists; one is being developed for HA as well.