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At least 145 records · Page 8Linked to original sources
PubMed2001

Sudden unexpected infant deaths in Dundee, 1882-1891: overlying or SIDS?

Using a cohort study of all deaths in infants under 12 months in Dundee born between 1882-91 we set out to compare the aetiology of sudden unexpected infant deaths in Dundee at the end of the 19th Century with the aetiology of present day Sudden Infant Death Syndrome (SIDS). During 1882-1891, 361 infants died suddenly and unexpectedly and without obvious cause while in bed with their parents. The sex ratio of deaths was even (0.51 male) whereas the typical male fraction of SIDS today is 0.61. The mean age at death was almost two and one-half weeks younger in the Dundee cohort than for SIDS in modern Scotland. The infants in the Dundee cohort were discovered more frequently early in the morning than is typical. Their social class distribution was different in that no overlying cases were found in the higher classes whereas SIDS affects all classes. The overlying rate for illegitimate infants was lower than that reported for SIDS today. The epidemiological characteristics of the Dundee cohort and of those dying from present day SIDS differ considerably. The Dundee cohort apparently died from overlying rather than from SIDS as it is classified today. Present day advice that co-sleeping is safe should be given more cautiously until the safety of co-sleeping is resolved. It might be prudent to inform parents that co-sleeping is a risk factor for SIDS and that it should therefore be avoided.

Asphyxia↗
PubMed1974

Hypoxemia and the sudden infant death syndrome.

Infants with known chronic hypoxemia before death retained a large proportion of the brown fat cells that are normally replaced by white fat cells after birth. Many of these hypoxemic infants also had an abnormal retention of extramedullary hematopoiesis. These same abnormalities were found in many victims of the sudden infant death syndrome.

Adipose Tissue↗
PubMed1995

Epidemiology of sudden infant death syndrome (SIDS) for Kentucky infants born in 1990: maternal, prenatal, and perinatal risk factors.

Using state vital statistics data for infants born to Kentucky residents in 1990, a nonconcurrent prospective study design was used to evaluate various risk factors for infant mortality from Sudden Infant Death Syndrome (SIDS). For comparison, an identical analysis was performed for infant mortality from all causes combined, including SIDS. The following factors were considered as potential risks: infant low birthweight, maternal age at delivery, maternal education, maternal cigarette and alcohol use during pregnancy, prenatal care, maternal race, method of delivery, premature birth, sex of the child, and multiple (twin or more) birth. A categorical analysis was used to calculate an adjusted relative risk for each potentially significant (p < 0.10) risk factor. Potentially significant adjusted relative risks for SIDS are maternal age under 20 (1.73, p < or = 0.08), maternal years of education (0.80 for one year, p < 0.01), maternal cigarette use (1.92 for one pack per day, p < 0.01), Cesarean delivery (2.09, p < or = 0.01), and premature birth (1.76, p < or = 0.08). Potentially significant adjusted relative risks for infant death from all causes are low birthweight (5.93, p < 0.01), maternal age over 35 (1.54, p < or = 0.05), maternal years of education (0.94 for one year, p < or = 0.02), marginal prenatal care (1.47, p < or = 0.01), premature birth (1.47, p < 0.01), and female sex (0.82, p < or = 0.05). Given this data, there may be unique risk factors for SIDS. The implications of these findings are discussed.

Adult↗
PubMed2002

The contribution of prone sleeping position to the racial disparity in sudden infant death syndrome: the Chicago Infant Mortality Study.

BACKGROUND: Rates of sudden infant death syndrome (SIDS) are over twice as high among African Americans compared with Caucasians. Little is known, however, about the relationship between prone sleeping, other sleep environment factors, and the risk of SIDS in the United States and how differences in risk factors may account for disparities in mortality. OBJECTIVE: To assess the contribution of prone sleeping position and other potential risk factors to SIDS risk in a primarily high-risk, urban African American population. DESIGN, SETTING, AND POPULATION: Case-control study consisting of 260 infants ages birth to 1 year who died of SIDS between November 1993 and April 1996. The control group consists of an equal number of infants matched on race, age, and birth weight. Prospectively collected data from the death scene investigation and a follow-up home interview for case infants were compared with equivalent questions for living control participants to identify risk factors for SIDS. MAIN OUTCOME MEASURES: Risk of SIDS related to prone sleeping position adjusting for potential confounding variables and other risk factors for SIDS, and comparisons by race-ethnicity. RESULTS: Three quarters of the SIDS infants were African American. There was more than a twofold increased risk of SIDS associated with being placed prone for last sleep compared with the nonprone positions (odds ratio [OR]: 2.4; 95% confidence interval [CI]: 1.6-3.7). This OR increased after adjusting for potential confounding variables and other sleep environment factors (OR: 4.0; 95% CI: 1.8-8.8). Differences were found for African Americans compared with others (OR: 1.8; 95% CI: 1.2-2.6 and OR: 10.3, 95% CI: 10.3 [3.2-33.8, respectively]). The population attributable risk was 31%. Fewer case mothers (46%) than control mothers (64%) reported being advised about sleep position in the hospital after delivery. Of those advised, a similar proportion of case mothers as control mothers were incorrectly told or recalled being told to use the prone position, but prone was recommended in a higher proportion of black mothers (cases and controls combined) compared with nonblack mothers. CONCLUSIONS: Prone sleeping was found to be a significant risk factor for SIDS in this primarily African American urban sample, and approximately one third of the SIDS deaths could be attributed to this factor. Greater and more effective educational outreach must be extended to African American families and the health personnel serving them to reduce prone prevalence during sleep, which appears, in part, to contribute to the higher rates of SIDS among African American infants.

Adolescent↗
PubMed1991

Does breastfeeding protect against sudden infant death syndrome?

Sudden Infant Death Syndrome (SIDS), the leading cause of infant death from one to six months in the developed world, strikes approximately two infants per 1000 live births in the U.S. The characteristics of the infants who die suddenly and unexpectedly are non-specific; none are universal except for the age distribution. Therefore, an infant is recognized to have died from SIDS only after thorough examination fails to demonstrate any other cause for the death. It is the purpose of this paper to review the most populat hypotheses of the causes of SIDS and try to explain through published scientific findings how breastfed infants appear to be protected from this condition. Many hypotheses have been proposed to explain SIDS. Some deficiencies/problems are related to the infant, such as a defect in sleep and/or breathing control, severe infant botulism, infections, reactions to immunizations, hypersensitivity to cow's milk, "maternal deprivation syndrome." Other causes are attributed to maternal circumstances, such as lower socioeconomic status, prenatal health, smoking, and the winter season. Additional suggestions of potential causes of SIDS include baby's thiamine deficiency, and hormonal and/or biochemical imbalance. The occurrence of most of these circumstances can be associated with a lack of breastfeeding. Because SIDS occurs much less frequently in breastfed infants, it is speculated that breastfeeding protects infants against SIDS. However, scientific literature lacks uniformity in the definitions of breastfeeding (whether partial and exclusive). This specification is necessary to select control infants to elucidate the well documented substantial lower rate of incidence of SIDS in breastfed babies.

Breast Feeding↗
PubMed2000

Association of IL-10 genotype with sudden infant death syndrome.

Sudden infant death syndrome (SIDS) is a major cause of infant death of unknown etiology. We propose that SIDS results from a genetically determined imbalance in the production of inflammatory and anti-inflammatory cytokines in response to the infant's microbial flora. We were especially interested to know the relationship between SIDS and genetically determined higher or lower production of IL-10, an anti-inflammatory cytokine. Biallelic polymorphisms in the promoter region of the IL-10 gene associated with higher or lower production of IL-10 were determined in a SIDS and in a control group using a sequence-specific oligonucleotide approach. One particular allele of the IL-10 gene, the IL-10-592*A allele, was significantly associated with SIDS. Indeed, 70% of the SIDS babies carried the IL-10-592*A allele (p = 0.007 compared with control). In addition, there was a significant reduction in the frequency of homozygosity for the allele IL-10-592*C (p = 0.001 compared with control). Carrying the A allele (either A/A or A/C) had an odds ratio of 3.3 (95% confidence interval 1.4-8.0). In the same patients there was no association with other IL-10 gene polymorphisms nor with other cytokine (TNF-alpha, TGF-beta 1) genotypes, emphasizing the particular relationship between SIDS and the IL-10-592*A allele.

Alleles↗
PubMedDate not supplied

[Infant botulism and sudden infant death syndrome].

Infant botulism represents a distinct entity of botulism. Ingestion of the ubiquitously present spores of Clostridium botulinum leads to germination of the organism and neurotoxin production in the infant intestine. Symptoms typically develop gradually in contrast to classical food botulism in which an acute onset of symptoms shortly after the ingestion of preformed toxin in a food is characteristic. Microbiologically, the diagnosis is established by identification of Clostridium botulinum organism and toxin in stool specimen. However, positive results in these tests provide only indirect evidence for the clinical relevance of the neurotoxin since asymptomatic carriers have been found. The toxin irreversibly blocks the release of acetylcholin from the motoric end plate which results in muscle weakness and paralysis. Depending on the amount of toxin produced, infant botulism exhibits a broad clinical spectrum ranging from oligosymptomatic forms to a fulminant course with acute respiratory failure within hours leading to sudden death. Unrecognized mild forms or beginning muscle weakness can be a co-factor for other risk factors of sudden infant death (SIDS). In studies analyzing infants who died from SIDS, botulism bacteria or toxin were found in up to 20 % of cases. Infant botulism therefore represents an important differential diagnosis of unexplained and inconclusive muscular hypotonia in the first year of life.

Acetylcholine↗
PubMed1997

Suspended rocking cradles, positional asphyxia, and sudden infant death.

OBJECTIVE: To describe the risk of unexpected death in infants who are placed in suspended rocking cardles. MAIN OUTCOME MEASURES: Ten cases of sudden infant death and 5 cases of infant asphyxia with successful resuscitation reported to the Consumer Product Safety Commission were analyzed. The death scene investigation reports and autopsy material were made available for evaluation. All 15 cases implicated a suspended head-to-toe rocking cradle. RESULTS: Infants were aged 3 months or younger and were found in the facedown prone position when discovered. The cradle was tilted at greater than 5 degrees, and the head was wedged at one end of the cradle. A locking pin was not used in 14 cases. Ten of the 15 infants died. The autopsy reports listed sudden infant death syndrome as the cause of death. CONCLUSIONS: Suspended rocking cradles represent a potentially lethal sleeping environment and should not be used without a locking pin in place. Infants should be placed in the supine position for sleep.

Asphyxia↗
PubMed1988

Models of mystery: physician and patient perceptions of sudden infant death syndrome.

Sudden infant death syndrome or SIDS is the term applied to unexplained infant deaths. This syndrome is distinguished by a lack of knowledge about its cause, pathophysiology, and possibilities for prevention. Given these uncertainties, SIDS provides an opportunity to investigate what types of explanatory models are constructed by physicians and patients when relatively little is known about a condition, and how these models may be translated into clinical practice. Interviews about SIDS were conducted with members of a Pediatric Pulmonary Section and their high risk patients, and the clinical interactions between the staff and families were observed. The pulmonary model focused on physiological causes which might affect respiration, and reflected uncertainty in both content and variability. Parents largely accepted the respiratory hypothesis, although they also considered nonphysiological causes. They tended to manage the uncertainty by focusing on ways to prevent SIDS and by believing they could predict which babies might die. However, observations of clinical interactions revealed that very little of the uncertainty as perceived by either the staff or the parents was discussed. The staff is able to emphasize hope for a particular patient, despite the uncertainty that surrounds SIDS, by following an explicit protocol which states how to handle a child despite the theoretical unknowns, and focusing on the knowns about the particular baby's condition.

Adult↗
PubMed2002

Synergistic effect of influenza a virus on endotoxin-induced mortality in rat pups: a potential model for sudden infant death syndrome.

Sudden infant death syndrome is the most common cause of postneonatal infant mortality in the developed world. It is a diagnosis of exclusion with peak age of incidence between 2 and 6 mo. Fifty to 63% of these infants have a preexisting upper respiratory tract infection before death. We hypothesized that the immature immune system may be altered by a primary infection, preventing a protective response after secondary challenge. To mimic dual infection, we used a nonlethal strain of a rat-adapted influenza A virus and a sublethal dose of endotoxin to establish a model that results in pathology and death in 12-d-old rat pups similar to that seen in infants dying of sudden infant death syndrome. Mortality only occurred when specific criteria such as timing between infectious insults and developmental age of the pup were met. Results suggest that mortality is caused by a rapid systemic shock event rather than lung-specific damage. Gross pathologic findings such as lung petechiae and liquid blood around the heart on necropsy were consistent with those seen in infants dying of sudden infant death syndrome. Histopathologic lesions including subendocardial hemorrhage and mild cortical thymocyte necrosis were found with greater severity and frequency in dually challenged animals. Macrophage subpopulation in rat-adapted influenza A virus-inoculated animals was significantly elevated in the spleen at the time of death. Our model suggests that the developing immune system can be primed to respond in an exaggerated way to a second immune challenge resulting in unexpected death.

Animals↗
PubMed2006

Sudden infant death syndrome.

Sudden infant death syndrome (SIDS) continues to be the most common cause of postneonatal infant death. SIDS is a complex, multifactorial disorder, the cause of which is still not fully understood. However, much is known now about environmental risk factors, some of which are modifiable. These include maternal and antenatal risk factors such as smoking during pregnancy, as well as infant-related risk factors such as non-supine sleeping position and soft bedding. Emerging evidence also substantiates an expanding number of genetic risk factors. Interactions between environmental and genetic risk factors may be of critical importance in determining an infant's actual risk of SIDS. Although no practical way exists to identify which infants will die of SIDS, nor is there a safe and proven prevention strategy even if identification were feasible, reducing exposure to modifiable risk factors has helped to lower the incidence of SIDS. Current challenges include wider dissemination of guidelines to all people who care for infants, dissemination of guidelines in culturally appropriate ways, and surveillance of SIDS trends and other outcomes associated with implementation of these guidelines.

Bedding and Linens↗
PubMed2003

Relation of beta-casomorphin to apnea in sudden infant death syndrome.

Sudden infant death syndrome (SIDS) is the most common cause of death in infants and its pathogenesis is complex and multifactorial. The aim of this review is to summarize recent novel findings regarding the possible association of beta-casomorphin (beta-CM) to apnea in SIDS, which has not been widely appreciated by pediatricians and scientists. beta-CM is an exogenous bioactive peptide derived from casein, a major protein in milk and milk products, which has opioid activity. Mechanistically, circulation of this peptide into the infant's immature central nervous system might inhibit the respiratory center in the brainstem leading to apnea and death. This paper will review the possible relationship between beta-CM and SIDS in the context of passage of beta-CM through the gastrointestinal tract and the blood-brain barrier (BBB), permeability of the BBB to peptides in infants, and characterization of the casomorphin system in the brain.

Animals↗
PubMed1996

Vulnerability of the infant brain stem to ischemia: a possible cause of sudden infant death syndrome.

In infants, extreme extension or rotation of the head can occlude one or both vertebral arteries. We sought to determine whether small communicating arteries or asymmetric vertebral arteries could predispose the brain stem to ischemia should such head movements occur. In 68 infants, the carotid, posterior communicating, precommunicator posterior cerebral, basilar and vertebral arteries were fixed in formalin, embedded in resin, the circumferences measured by image analysis, and the relative conductance of blood in each artery per gram of brain calculated. Conductance in the vertebrobasilar and carotid systems lagged behind increases in brain weight during the postnatal growth spurt. In 81% of infants, conductance through the communicating arteries was less than 25% of basilar artery conductance. Conductance in one vertebral artery was less than half that of the contralateral artery in 41% of infants. In conclusion, the lag in available blood flow and small communicating and asymmetric vertebral arteries may predispose the infant brain stem to ischemia if one or both vertebral arteries are occluded by head rotation or extension. Because these head movements are likely to be accentuated in the prone sleeping position (a risk factor for sudden infant death syndrome), we suggest that vertebral artery occlusion may underlie some cases of sudden unexpected infant death.

Age Factors↗
PubMed2002

[Sudden infant death syndrome].

Sudden infant death syndrome (SIDS) is a disease of unknown cause. The occurrence of SIDS is rare during the first month of life, increases to a peak between 2 and 4 months old, and then declines. The following have been consistently identified across studies as independent risk factors for SIDS: prone sleep position, sleeping on a soft surface, maternal smoking during pregnancy, young maternal age, bedsharing, prematurity and/or low birth weight, and male sex. Although the cause of the sudden infant death syndrome is multifactorial, contemporary hypotheses include defects in arousal or cardiorespiratory control. The interesting is hypothesis that prolongation of the QT interval may have a role in the pathogenesis of SIDS.

Birth Order↗
PubMed1988

Nonnatural death masquerading as SIDS (sudden infant death syndrome).

This article relates our experiences with accidental and homicidal deaths in reported sudden infant death syndrome (SIDS) cases. Our intent is to alert personnel in medical and health-related professions as well as death investigators (coroners, law enforcement officials, etc.) that a thorough scene investigation and history need to be obtained when a child's death has been reported, since this may modify the type of autopsy to be performed. It should not be assumed that all children less than 1 year of age who die suddenly die from SIDS.

Accidents, Home↗
PubMedDate not supplied

[Sudden infant death syndrome (SIDS)].

Sudden Infant Death Syndrome (SIDS) is the term first proposed in 1969 for a distinctive subgroup of unexpected infant deaths occurring during the first months of life, with relatively consistent clinical, epidemiological and pathological features, which remain unexplained after a thorough case investigation, including a complete autopsy, examination of death scene and review of clinical history. Sudden infant death unnecessary means SIDS. According to definition, SIDS remains a diagnosis of exclusion, distinguished from others only by subjective and permissive variables. Despite the vague and permissive nature of the definition, epidemiological studies identified some risk factors as prematurity and social disadvantage. Nevertheless, the most interesting findings are those related to environmental and care features, as drug addiction and/or smoke exposition during pregnancy, sleep position of the infant, environmental temperature, parental bed sharing and breast feeding. Those factors play a variable role, but their correction reduced SIDS incidence. Sudden infant death is a diagnosis made by expert pathologists with pediatrician's and investigator's advice, based primarily on autopsy findings and death scene investigation performed through the severe application of investigative protocols.

Female↗