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At least 19 recordsLinked to original sources
PubMed1992

[Sudden, unexplained infant death--sudden infant death syndrome. Forensic pathological aspects].

Delimitation of the sudden unexplained infant death syndrome (SIDS) is difficult as the diagnosis is made by exclusion. The difficulties in the differential diagnosis are concentrated on interpretation of the significance of positive viral and bacterial findings, inflammatory changes in the respiratory organs, heart and central nervous system together with malformations. Classification of SIDS appears, therefore, to vary according to time and place. New techniques, e.g. DNA analysis, have explained the etiology in a few per cent of the cases but have not yet solved the riddle of SIDS. The article reviews hypotheses about apnoea, arrhythmia, overheating and inefficient surveillance of the infant. It is emphasized that assessment of risk factors for SIDS requires valid epidemiological investigations where the basis for the diagnosis is a uniform classification of SIDS infants as compared with other groups of sudden death in infancy. An investigation of this nature has been initiated in the Nordic countries. It is important to examine and treat infants with abnormal sleep apnoea but generalized employment of monitoring has not reduced the number of unexplained infantile deaths.

Autopsy↗
PubMed1977

Sudden infant death syndrome (crib death).

Sudden infant death syndrome (SIDS) is diagnosed by the absence of lethal autopsy findings, or in a resuscitatable, "near miss" form with cyanosis, apnea, and bradycardia. The event is unexpected, although a minor respiratory infection is common, and occurs during sleep, between 1 and 6 months of age. There is growing evidence that the victims have had previous hypoxic episodes. Although suffocation is no longer considered a tenable explanation, other forms of airway obstruction are still postulated by many; the evidence, however, favors hypoxia as the common feature. A lethal arrhythmia had been proposed by several groups, based on inappropriate reflex activity, "pathology" of the conduction system, and the long QT syndrome, but the evidence is against arrhythmia as the primary event in most cases of SIDS. Based on the reversible "near miss," apnea is likely as the primary event in SIDS. Several reflexes have the ability to produce apnea, in addition to the relatively common sleep apnea; the crucial aspect, rather, appears to be thefailure of the immature infant to resume respiration. The possibility exists that the infant, who did not have to breather for 9 months of fetal life, literally is not alarmed and aroused by the persistance of apnea. In human and animal studies, respiratory infections and sleep deprivation have been proved to increase the likelihood and duration of sleep apnea. If primary apnea continues for long (45 seconds or more), a dangerous positive feedback develops into hypoxic apnea. Hhis will persist until circulatory failure occurs, or until gasping occurs. The gasp is a highly effective mechanism at birth, but will occur too late for autoresuscitation after the anerobic capacity of fetal life dimineshes; we believe this capacity lasts for approximately 1 month, accounting for the hiatus of crib death, sparing the first month. The "near-miss" infant, after resuscitation, should be monitored at home, if practical, until 6 months of age. A simple cardiac monitor for bradycardia has definite advantage over an apnea monitor alone.

Airway Obstruction↗
PubMed1978

Sudden infant death syndrome in Cardiff, association with epidemic influenza and with temperature - 1955-1974.

The effects of social class, season, low temperature and sudden falls in temperature are investigated in 286 cases of Sudden Infant Death Syndrome in Cardiff in the years 1955--1974. The association with low temperature was striking: unsuspected hypothermia may be an important feature of these deaths. Sudden infant death incidence was associated with influenza A but not influenza B epidemics.

Cold Temperature↗
PubMed1992

[Psychosocial aspects of sudden infant death].

Following the sudden death of an infant, the parents and the siblings, if any, go through a very severe crisis with repercussions on the psychoaffective and professional domain, as well as on social relations. The parents' mourning after a sudden infant death is very often morbid. The characteristics of this infantile death which predispose to a complicated mourning period are the parents' impossibility to anticipate and the lack of cause of the baby's death. One of the most adverse consequences of such a situation would be the birth of a subsequent child before mourning is completed, for this child might well be regarded as a replacement child, and this would jeopardize his future psychosocial development.

Activities of Daily Living↗
PubMed1979

The epidemiology of sudden infant death in upstate New York.

The epidemiology of sudden infant death among infants born during 1974 to mothers residing in upstate New York was studied. Death-certificate characteristics for 190 infants with sudden infant death syndrome (SIDS) are compared with those for 434 infants dying of other causes in the same age range. The overall incidence of SIDS was 1.43 per 1,000 live births. No relationship was found between SIDS rate and population density. The SIDS deaths peaked in January, with an overall seasonal pattern compatible with that of viral respiratory infections. The SIDS infants were more likely to die during sleeping hours than infants dying suddenly of other causes. Their age at death distribution is significantly different from that of other infant deaths. Progress in understanding sudden death in infancy is still hampered by the lack of positive diagnostic criteria.

Autopsy↗
PubMed1992

Sudden infant death syndrome in New Jersey: 1991.

Sudden infant death syndrome (SIDS) is the leading cause of death in infants one month to one year of age. The New Jersey Sudden Infant Death Syndrome Resource Center gathers epidemiological data on all SIDS deaths in New Jersey, noting differences in population and countries.

Humans↗
PubMed1977

Sudden infant death due to congenital adrenal hypoplasia.

Adrenocortical hypoplasia was found to be the cause of sudden death in a 9-month-old infant. Most sudden infant deaths in the first year of life are related to the sudden infant death syndrome, in which no specific pathologic changes are found at autopsy. Although specific causes for sudden death in infancy are well documented, adrenocortical hypoplasia is not a well-recognized cause of sudden infant death.

Adrenal Glands↗
PubMed1992

Clostridium botulinum and sudden infant death syndrome: a 10 year prospective study.

It has been proposed that sudden and unexpected death in infants due to intestinal infection with Clostridium botulinum may mimic the clinicopathological features of sudden infant death syndrome. Between 3.3 and 3.8% of infants in some series have had this neurotoxin-producing bacterium isolated on faecal culture. Prospective screening of 248 infants presenting with the sudden infant death syndrome to the Adelaide Children's Hospital over a 10 year period from 1981 to 1990 was conducted. Faecal samples were obtained from both small and large intestines and cultured specifically for C. botulinum. No samples were positive. The results of this study suggest that routine post-mortem culture of faeces for C. botulinum has been of limited use within the South Australian infant population over the last decade, and that occult botulism has not been a significant factor in the causation of sudden death.

Botulism↗
PubMed1978

Why should we study the infant 'near miss for Sudden Infant Death'?

The use of 'near miss for Sudden Infant Death syndrome' infants as a model toward understanding the Sudden Infant Death syndrome has been questioned. Although there are numerous problems in delineating this patient population and defining events occurring during sleep, continuous polygraphic monitoring demonstrates potentially life-threatening events.

Bradycardia↗
PubMed1992

Sudden infant death syndrome: the vitamin E/selenium iron hypothesis (dietary anti/pro-oxidant imbalance).

Cot death or Sudden Infant Death Syndrome (SIDS) remains a largely unexplained and unpreventable factor in infant mortality. The existence of a dietary link between SIDS and vitamin E/selenium deficiency, documented through veterinary evidence, is posited as an etiological factor. Further substantiation of this hypothesis is derived from infant nutrition practices and cases of SIDS in New Zealand.

Animals↗
PubMed1979

Neurologic abnormalities in near miss for sudden infant death syndrome infants.

As part of the Sudden Death Research Project at Stanford University School of Medicine, we have performed systematic neurologic examination of 41 near miss infants, 7 normal siblings of babies who died a sudden infant death, and 21 normal control infants. Many infants were examined longitudinally until 2 years of age. We found that near miss infants under 3 months of age had consistent abnormalities of muscle tone, particularly shoulder hypotonia. These abnormalities disappeared with maturation, but only 60% of older infants who had suffered near miss episodes of neurologically and developmentally normal. In addition, only one of the seven apparently normal siblings had an entirely normal neurologic examination when first seen. Thus, infants who present with near miss episodes may have an underlying central nervous system abnormality or may acquire some abnormality as a result of the episode.

California↗
PubMed1977

Toxicology and sudden infant death.

One hundred thirty cases of sudden infant death occurring in Wayne County, Michigan, (population 2.7 million) were analyzed for possible drugs. The toxicological protocol has been outlined. Six cases were found to be positive, and in five of these the drugs found had been prescribed for a variety of illnesses. In one case methadone was found in the blood of an infant whose mother was undergoing methadone treatment for drug addiction, the drug being transmitted through breast milk. In none of the 102 cases of sudden infant death syndrome (SIDS) included in the study did the toxicological results affect the diagnosis. In our study, toxicological analyses never contradicted an initial diagnosis of SIDS, and, therefore, we feel that this diagnosis should be made promptly based on investigative and autopsy findings.

Barbiturates↗
PubMed1992

Hypercapnic and hypoxic ventilatory and cardiac responses in school-aged siblings of sudden infant death syndrome victims.

Siblings of sudden infant death syndrome (SIDS) victims have been shown to have abnormal ventilatory patterns and altered responses to respiratory stimuli during infancy. To evaluate whether these abnormalities persist, we studied ventilatory responses in 20 older SIDS siblings (9.8 +/- 0.9 (mean +/- SEM) years of age) and 20 control subjects (10.2 +/- 0.9 years of age). To evaluate hypercapnic ventilatory responses, we had subjects rebreathe 5% carbon dioxide and 95% oxygen until end-tidal carbon dioxide tension reached 65 mm Hg. Instantaneous minute ventilation, mean inspiratory flow, and respiratory rate were calculated breath by breath. Hypercapnic responses did not differ between SIDS siblings (2.08 +/- 0.14 L/min per mm Hg) and control subjects (1.90 +/- 0.10 L/min per mm Hg; not significant). To assess hypoxic ventilatory responses, we asked subjects to rebreathe 13% oxygen and 7% carbon dioxide, with the balance nitrogen, at mixed-venous end-tidal carbon dioxide tension, until arterial oxygen saturation by pulse oximetry fell to 75%. No differences in hypoxic ventilatory responses were found between the SIDS siblings (-1.39 +/- 0.15 L/min/% saturation) and the control subjects (-1.22 +/- 0.17 L/min/% saturation; not significant). The mean inspiratory flow, tidal volume, respiratory rate, and heart rate responses to hypercapnia and hypoxia were also similar in the two groups. We conclude that there is no difference in hypercapnic and hypoxic ventilatory and cardiac responses, as assessed by rebreathing techniques, between school-aged SIDS siblings and control subjects. We speculate that in SIDS siblings the control of breathing is immature during infancy and that they achieve maturity of control and resolution of breathing abnormalities with time.

Child↗