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PubMed1987

Diphtheria-tetanus-pertussis immunization and sudden infant death: results of the National Institute of Child Health and Human Development Cooperative Epidemiological Study of Sudden Infant Death Syndrome risk factors.

The possible association between diphtheria-pertussis-tetanus (DTP) immunization and the subsequent occurrence of sudden infant death has been examined using data from the National Institute of Child Health and Human Development (NICHD) Sudden Infant Death Syndrome (SIDS) Cooperative Epidemiological Study, a large multicenter, population-based, case-control study. In a preliminary report based on the first 400 eligible singleton SIDS victims and 800 matched living control infants, no temporal association between SIDS and DTP immunization was found. From the final sample of 800 eligible singleton SIDS victims, 95% (n = 757) were defined as definitely or probably having died of SIDS on the basis of pathology data. Data from these 757 case infants and their corresponding control infants (n = 1,514) are presented in this report. Two control infants, both living, were randomly selected for each case infant: an age-matched control A and an age-, race-, and low birth weight-matched control B. Overall, case infants were less likely to have received any DTP immunization. Only 39.8% of case infants had received at least one DTP immunization compared to 55.0% of control A infants and 53.2% of control B infants. Based on maternal interviews and postnatal medical records, 1.8% of case infants (five infants) immunized with DTP died within the first 24 hours following immunization. Similarly, 5.0% of control A infants (n = 21) and 2.2% of control B infants (n = 9) had been immunized within 24 hours of the maternal interview, which represents the comparable time frame for the age-matched control infants. These results confirm the earlier preliminary findings from the NICHD SIDS Cooperative Epidemiological Study and suggest that DTP immunization is not a significant factor in the occurrence of SIDS.

Black or African American↗
PubMed1996

An analysis of sudden infant death syndrome in aboriginal infants.

The purpose of this case-control study was to identify antenatal and perinatal risk factors for sudden infant death syndrome (SIDS) in Aboriginal infants in Western Australia (WA). Cases were all Aboriginal infants born in WA from 1980 to 1990 inclusive and classified as dying from SIDS in WA. Controls consisted of a matched group and a random group both selected from liveborn Aboriginal infants born from 1980 to 1990. Multivariate modelling showed that SIDS in Aboriginal infants was strongly related to young maternal age (< 20 years, odds ratio (OR) = 2.89), high parity (parity > 3, OR = 4.40) and being small-for-gestational age (OR = 3.36) but was not associated with single marital status (OR = 0.95) or male sex (OR = 0.97). Although the study was based on routinely collected data, results do highlight some important groups for SIDS prevention. To gain further knowledge in terms of SIDS in Aboriginal infants, there is an urgent need to collect information concerning infant care practices in the Aboriginal community.

Adult↗
PubMed2002

Congenital myasthenic syndrome associated with episodic apnea and sudden infant death.

The sudden infant death syndrome has multiple etiologies. Some congenital myasthenic syndromes can cause sudden infant death syndrome by apnea, but the frequency of this etiology is unknown. We report here a young patient with sudden respiratory crises culminating in apnea followed by recovery, against a background of no or variable myasthenic symptoms without dyspnea. One sib without myasthenic symptoms and one sib who only had mild ptosis died previously during febrile episodes. Studies reported by us elsewhere traced the proband's illness to mutations in choline acetyltransferase. Here, we describe in detail the morphologic investigations and electrophysiologic findings, which point to a presynaptic defect in acetylcholine resynthesis or vesicular filling, in the proband. Analysis of DNA from a sib who previously died of sudden infant death syndrome revealed the same choline acetyltransferase mutation. Thus, mutations in choline acetyltransferase may be a cause of sudden infant death syndrome as, theoretically, could other presynaptic myasthenic disorders.

Acetylcholine↗
PubMed1985

Neuronal development in the medullary reticular formation in sudden infant death syndrome and premature infants.

Morphological and morphometrical development of the neurons in the medullary reticular formation was observed in control, sudden infant death syndrome (SIDS) and prematurely born infants, using Golgi stains. With increasing gestational age, in controls dendrites became long, spines increased and the distribution of spines assumed a mature pattern. The number of spines reached a peak at 34 to 36 weeks gestation and after birth it decreased rapidly. Term and prematurely born SIDS infants showed a persistence of reticular dendritic spines. On the other hand, ventilator-dependent prematurely born infants had decreased numbers of dendritic spines with thin dendrites and long, thin spines. Persistence of reticular dendritic spines in SIDS infants may suggest incomplete development to the mature, higher level of respiratory control. Spine abnormalities in the ventilator-dependent prematurely born infants may indicate secondary neuronal changes in the reticular formation.

Dendrites↗
PubMed1978

Ambulatory and in-hospital continuous recording of sleep state and cardiorespiratory parameters in 'near miss' for the sudden infant death syndrome and control infants.

Electrophysiologic and cardiorespiratory events were studied polygraphically and by ambulatory monitoring in 'near miss' for sudden infant death syndrome (SIDS) and normal control infants 1-4 months old. The data show that 'near miss' babies typically have many apneic periods in their sleep, particularly apneas lasting 10 sec or longer. These tend to decrease with age. They have longer lasting apneas than controls, although the latter have respiratory pauses lasting less than 10 sec, in particular during rapid eye movement (REM) sleep. An upper respiratory infection (URI) in 'near miss' infants clearly appears to be a risk factor which will be studied further both in-hospital and at home using a monitoring technique with our Medilog ambulatory system.

Ambulatory Care↗
PubMed1990

Are race and length of gestation related to age at death in the sudden infant death syndrome?

Although race and preterm delivery are known to be associated with sudden infant death syndrome (SIDS), the relationships between age at death from SIDS and these factors have not been well described. To examine these relationships, we used linked infant birth and death records for the cohort of 1,204,375 White and 283,776 Black postneonates who were born from 1979 to 1981 in five states: California, Georgia, Missouri, South Carolina and Tennessee. Deaths attributable to SIDS occurred to 1404 White postneonates and to 696 Black postneonates. Although postneonatal SIDS rate among Black infants was twice that of White infants, the relative risk was smaller among infants with gestations of less than 35 weeks. For White postneonates, the median postneonatal age at death sharply declined for gestations from 28-29 weeks to 36-37 weeks and levelled off for longer gestations. For Black postneonates, the results do not support an association between length of gestation and age at death. The findings suggest that practitioners investigating approaches to avert SIDS need to maintain their interventions to an older age among White preterm infants. Researchers investigating the causes of SIDS need to consider the relationship between length of gestation and age at death from SIDS as well as possible developmental differences between White and Black preterm infants.

Black or African American↗
PubMed1988

Intrathoracic petechial hemorrhages: a clue to the mechanism of death in sudden infant death syndrome?

(1) Intrathoracic petechiae are characteristic of most SIDS cases, and tend to be more numerous in these cases than in deaths from other causes, including mechanical asphyxia. (2) Their localization suggests that intrathoracic negative pressure plays a role in their genesis. (3) Several human and animal studies suggest that petechiae arising from the pulmonary circulation may differ from those originating from systemic vessels in the thorax. (4) Experimental studies suggest that vigorous respiratory efforts are responsible for their formation. This would seem to exclude respiratory paralysis as a mechanism for most SIDS deaths. (5) These petechiae are not consistent with cardiac arrest or failure as the primary agonal event in SIDS. (6) The fact that petechiae are more prominent in SIDS than in other deaths adds to the evidence that SIDS is not a "wastebasket" diagnosis, despite the imperfection of existing diagnostic criteria. (7) These petechiae do not prove that the final mechanism of most SIDS deaths is upper airway obstruction. However, they do provide substantial support for that thesis.

Animals↗
PubMed1983

Elevation of postmortem triiodothyronine in sudden infant death syndrome and in infants who died of other causes: a marker of previous health.

We measured serum concentrations of thyroxine (T4), triiodothyronine (T3), reverse T3, free T4, thyroid-stimulating hormone, and cortisol in 62 victims of sudden infant death syndrome (SIDS) in 30 infants who died of known causes and in 15 living controls. The mean T3 value was elevated in 69% of those with SIDS. 37% of the others who died, and in no control infants. After excluding those who died of known cause who had abnormal thyroid function (abnormal postmortem concentrations of T4, free T4, or reverse T3), the T3 values were elevated in 63% of those remaining. When the data were analyzed on the basis of case histories and autopsy findings, those infants who were in good health and died suddenly of accidental causes had an elevation in mean T3 similar to that seen in SIDS victims; those who died under conditions known to alter thyroid metabolism did not. The T4, free T4, reverse T3, thyroid-stimulating hormone, and cortisol values were not useful in differentiating those with SIDS from the living controls, or those who were healthy at the time of death. We were unable to find any difference in T3 serum concentrations between the total group who had SIDS and those who had SIDS with minor infections, with petechiae on intrathoracic organs, with premature birth, or those who were resuscitated. Our data point out the importance of using appropriate controls when evaluating SIDS. The normal reverse T3 values in SIDS, as well as confirmation of the normal T4 and free T4 values, constitute evidence against chronic persistent alveolar hypoventilation or prolonged episodes of hypoxia immediately preceding death from SIDS.

Female↗
PubMedDate not supplied

Cardiovascular causes for sudden infant death.

Although sudden infant death syndrome (SIDS) is a cause for sudden infant death, other causes should be ruled out before diagnosing SIDS. Cardiac causes for sudden infant death include viral myocarditis, congential heart disease particularly congential aortic stenosis, endocardial fibroelastosis, and anomalous origin of the left coronary artery from the pulmonary artery. Other cardiac conditions that may result in sudden death include rhabdomyomas of the heart in tuberous sclerosis and conduction system disorders. The most frequent conduction system disorders resulting in sudden death include histiocytoid cardiomyopathy, congential heart block that may be associated with maternal lupus erythematosus, arrhythmogenic right ventricular dysplasia, noncompaction of the left ventricle, and long QT syndromes.

Arrhythmias, Cardiac↗