A CASE OF SUDDEN INFANT DEATH SYNDROME (SIDS) AS REPORTED IN 1863

PEDIATRICS ◽  
1982 ◽  
Vol 70 (3) ◽  
pp. 369-369
Author(s):  
T. E. C.

On March 9, 1863, Dr David Cheever, Adjunct Professor of Clinical Surgery at the Harvard Medical School, presented the following case report of the sudden infant death syndrome at a meeting of the Boston Society for Medical Improvement.1 His report is one of the earliest descriptions of this syndrome in the American medical literature. An infant, 10 weeks old, apparently in perfect health, suddenly died while sleeping, and after having been asleep one and a half hours. There had been no struggle, and the face was not livid. On post-mortem examination, Dr C. found no morbid appearances, except some serous effusion in the ventricles and at the base of the brain; the latter organ was also somewhat congested. The thoracic organs were all healthy, and the larynx free of obstruction. An infant cousin of the child had died in a precisely similar manner. Dr C. was unable to account for the death, unless the effusion might possibly have been accumulating insidiously for some time until it became sufficient to destroy life.

Author(s):  
Siri Hauge Opdal ◽  
Linda Ferrante ◽  
Torleiv Ole Rognum ◽  
Arne Stray-Pedersen

AbstractSeveral studies have indicated that a vulnerability in the development and regulation of brain function is involved in sudden infant death syndrome (SIDS). The aim of this study was to investigate the genes encoding the brain aquaporins (AQPs) AQP1 and AQP9 in SIDS. The hypothesis was that specific variants of these genes are part of the genetic vulnerability predisposing infants to sudden unexpected death. The study included 168 SIDS cases with a median age of 15.5 (range 2–52) weeks and 372 adolescent/adult deceased controls with a median age of 44 (range 11–91) years. In the AQP1 gene, the rs17159702 CC/CT genotypes were found to be associated with SIDS (p = 0.02). In the AQP9 gene, the combination of a TT genotype of rs8042354, rs2292711 and rs13329178 was more frequent in SIDS cases than in controls (p = 0.03). In the SIDS group, an association was found between genetic variations in the AQP1 gene and maternal smoking and between the 3xTT combination in the AQP9 gene and being found lifeless in a prone position. In conclusion, this study adds further evidence to the involvement of brain aquaporins in SIDS, suggesting that specific variants of AQP genes constitute a genetic predisposition, making the infant vulnerable to sudden death together with external risk factors and probably other genetic factors.


PEDIATRICS ◽  
1982 ◽  
Vol 69 (3) ◽  
pp. 301-304 ◽  
Author(s):  
Joseph Werthammer ◽  
Elizabeth R. Brown ◽  
Raymond K. Neff ◽  
H. William Taeusch

The association between bronchopulmonary dysplasia and sudden infant death syndrome was studied retrospectively in low-birth-weight infants discharged from the neonatal program at Harvard Medical School. The incidence of sudden infant death syndrome was seven times greater in infants with bronchopulmonary dysplasia when compared with a group of control infants without bronchopulrnonary dysplasia. Confounding factors, including birth weight, sex, multiple birth, socioeconomic status, and apnea were evaluated. The results indicate that there is an association between bronchopulmonary dysplasia and sudden infant death syndrome.


2018 ◽  
Vol 36 (05) ◽  
pp. 460-471 ◽  
Author(s):  
Anna Lavezzi ◽  
Stefano Ferrero ◽  
Beatrice Paradiso ◽  
Liliya Chamitava ◽  
Francesco Piscioli ◽  
...  

Objective To find a possible pathogenetic mechanism of the early sudden infant death occurring in newborns during the skin-to-skin care (SSC), through the examination of neuronal centers regulating the vital activities. Study Design This is an in-depth examination of the brain stem in 22 healthy term newborns, suddenly died in the first hour of life without the identification of a cause at autopsy (early sudden infant death syndrome [eSIDS]), 12 of them concomitantly with SSC, and 10 with age-matched controls died of known pathology. Results Developmental alterations of neuronal structures of the brain stem were highlighted in 19 of the 22 eSIDS, but not in control. The hypoplasia of the pontine Kölliker-Fuse nucleus (KFN), an important respiratory center, was diagnosed at the histological examination, validated by morphometric quantifications, in 11 of the 12 eSIDS while they were placed on the mother's chest and in 2 of the 10 SSC unrelated neonatal deaths. Conclusion The delayed development of the KFN could represent a specific finding of eSIDS occurring during SSC. Therefore, it is necessary to point out that the SSC represents a further risk factor that must be added to others already known for sudden infant death syndrome. Then this practice needs appropriate monitoring strategies of the infant's conditions.


PEDIATRICS ◽  
1980 ◽  
Vol 66 (4) ◽  
pp. 597-614
Author(s):  
Marie A. Valdeś-Dapena

In the last five years there have been literally hundreds of articles in the world's medical literature regarding sudden infant death syndrome. This work has shed some light on various epidemiologic aspects of the problem, on pathologic anatomy, and on clinical issues such as the relative importance of spontaneous, protracted, idiopathic apnea and prolongation of the Q-T interval. This relatively comprehensive review treats only a limited number of these subjects and publications in an attempt to bring the reader more or less up-to-date on the major aspects of developments over the last five years.


Author(s):  
Anatoly V. Kopylov

Sudden infant death syndrome (SIDS) is an unexpected non-violent death of apparently healthy child aged 7 days to 1 year, in which the anamnesis and autopsy data do not allow to find out the cause of the fatal outcome. Researchers have not come to a consensus on the thanatological role of morphological changes in the brain. Aim. To determine pathomorphological changes in the brain in the case of sudden death syndrome in children. Material and methods. Forensic medical studies of 118 deaths of healthy children who died suddenly for the period 2008-2017 were carried out and analyzed on the territory of the Stavropol region. Autopsy material was divided into groups: the main group (1) consisted of 74 observations (62.8%), where SIDS was the main final sectional diagnosis. The comparison group (2) consisted of 44 (37.2%) observations; the children died suddenly at home as a result of viral-bacterial pneumonia. For control, the third group was formed (3), which included 45 observations, where the death of children occurred as a result of drowning and carbon monoxide poisoning. Results and its discussion. A histological examination of pieces of the brain in the case of sudden death syndrome revealed the foci of angiomatosis of the vessels of the pia mater and brain matter with the normal structure of the elastic membrane of the arteries, the effects of glial proliferation in the subependymal region of the lateral ventricles and subcortical formations. In the medulla oblongata, in a detailed study of the posterior (vegetative) nucleus of the vagus nerve, degenerative changes in neurons were detected in the form of chromatolysis and karyolysis, a glial reaction of the type of neuronophagy. Conclusion. Pathomorphological changes in the brain stem may be due to combined intrauterine hypoxic and intrapartum traumatic factors, which, potentiating each other, lead to dysregulation of the respiratory rhythm with the development of a fatal outcome during sleep.


PEDIATRICS ◽  
1981 ◽  
Vol 68 (1) ◽  
pp. 143-144
Author(s):  
Paul C. Young

Dr Valdeś-Dapena's well-organized review article, "Sudden Infant Death Syndrome: A Review of the Medical Literature 1974-1979" in the October issue (Pediatrics 66:597, 1980) was an excellent analysis of the current literature of this confusing and complex entity. The extensive bibliography will be most helpful to any individual interested in the subject. The clinician providing primary care for children is likely to be confronted with the sudden infant death syndrome (SIDS) phenomenon in one of three ways: First, there is the necessity of dealing with a family who has just lost a baby.


Physiology ◽  
1999 ◽  
Vol 14 (4) ◽  
pp. 155-161 ◽  
Author(s):  
David Mendelowitz

It is well known that the neuronal projections from the brain to the heart strongly influence cardiac function, and an abnormal activity has been implicated in diseases such as cardiac arrhythmia and sudden infant death syndrome. This short review describes recent advances focused on the neurobiology of cardiac vagal neurons, utilizing cellular techniques.


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