Sudden infant death syndrome, child sexual abuse, and child development

Since the introduction of the Back to Sleep Campaigns, there has been a dramatic reduction in sudden infant death syndrome in this country. Steven Blatt and Victoria Meguid review the literature surrounding sleep position. Investigators have continued efforts to find other modifiable risk factors of sudden infant death syndrome. A prospective study of more than 33,000 neonates found a link between a prolonged QT electrocardiogram interval and sudden infant death syndrome. Also discussed are investigations seeking to explain the relationship between smoking and sudden infant death syndrome. Ann Botash, Florence Jean-Louis and Mongkae Ploy Siripornsawan review the latest thinking on genital warts and their relation to specific viral etiologies and child sexual abuse. Other symptoms and signs of sexual abuse are the focus of a number of articles that can help the practitioner care for these unfortunate children. Catherine Church reviews medication options for children diagnosed with pervasive developmental disorders or autism spectrum disorders. Finally, in this article, risperidone, fluoxetine and naltrexone are reviewed.     

Neonatal long QT syndrome and sudden cardiac death

Neonatal sudden cardiac death most often results from cardiac electrical diseases, cardiomyopathies, or sudden infant death syndrome. In infants without a known premortem diagnosis or abnormalities identified at autopsy, sudden infant death syndrome accounts for the vast majority of sudden deaths. Potential cardiac causes of some sudden infant death syndrome cases may include malignant brady- or tachyarrhythmias and congenital long QT syndrome. The possible mechanisms include abnormal brain stem respiratory control of arousal, dysautonomia and malignant cardiac bradyarrhythmias or tachyarrhythmias. Screening for neonatal sudden cardiac death may not be feasible, but hopefully through careful review of history, physical examination, and family health history, and judicious diagnostic testing, can the risk of cardiac sudden death be reduced. Further comprehension of the genetic basis of inherited arrhythmia disorders may help elucidate the mechanisms of arrhythmogenesis and etiologies of sudden infant death. Prevention and treatment of these disorders may also be improved through more detailed understanding of the molecular basis of cardiac electrical pathophysiology.     

֧���ܷη�������������Ժ�����

??There are still problems??including difficulty in feeding baby?? apnea?? stunting on infants with bronchopulmonary dysplasia??BPD?? after being discharged from hospital. The risk of sudden infant death syndrome also increases. Healthcare after discharge from hospital is a continuation after treatment in hospital?? which is important for BPD treatment. Healthcare includes home oxygen after discharge from hospital?? continuing to strengthen infant’s nutrition and feeding guidance?? regular follow-up and prevention of sudden infant death syndrome.     

Distinguishing sudden infant death syndrome from child abuse fatalities

Fatal child abuse has been mistaken for sudden infant death syndrome. When a healthy infant younger than 1 year dies suddenly and unexpectedly, the cause of death may be certified as sudden infant death syndrome. Sudden infant death syndrome is more common than infanticide. Parents of sudden infant death syndrome victims typically are anxious to provide unlimited information to professionals involved in death investigation or research. They also want and deserve to be approached in a nonaccusatory manner. This clinical report provides professionals with information and suggestions for procedures to help avoid stigmatizing families of sudden infant death syndrome victims while allowing accumulation of appropriate evidence in potential cases of infanticide. This clinical report addresses deficiencies and updates recommendations in the 2001 American Academy of Pediatrics policy statement of the same name.     

Has changing diagnostic preference been responsible for the recent fall in incidence of sudden infant death syndrome in South Australia?

Objective: An apparent decrease in deaths attributed to sudden infant death syndrome (SIDS) has been noted in a number of diverse geographical areas during the past several years. At the same time the definition of SIDS has been in a state of flux and some observers have raised the possibility that the fall in SIDS deaths is due to diagnostic transfer rather than to a genuine decrease in numbers. The present study was undertaken to investigate this possibility.
Methodology: All sudden and unexpected deaths in infants under 1 year of age in South Australia during a 10 year period from 1984 to 1993 were reviewed.
Results: The number of deaths due to SIDS fell from 40 in 1984 to 17 in 1993, with a maximum of 52 cases per year in 1987. In contrast, the number of cases of sudden death not due to SIDS remained under 10 per year. The overall infant death rate also fell, while the total number of births per year remained relatively unchanged.
Conclusions: The lack of major change in sudden infant death rates from other causes, combined with the fall in SIDS deaths, is not supportive of diagnostic transfer being a major determinant of the declining SIDS death rate. Therefore, other factors are likely to be responsible for the falling SIDS rate in this population.     

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.     

The frequency of a disease-causing point mutation in the gene coding for medium-chain acyl-CoA dehydrogenase in sudden infant death syndrome

A number of rare inherited metabolic disorders are known to lead to death in infancy. Deficiency of medium-chain acyl CoA dehydrogenase has, on clinical grounds, been related particularly to sudden infant death syndrome. The contribution of this disorder to the etiology of sudden infant death syndrome is still a matter of controversy. The present study investigated 120 well-defined cases of sudden infant death syndrome in order to detect the frequency of the most common disease-causing point mutation in the gene coding for medium-chain acyl-CoA dehydrogenase (G985) compared with the frequency in the general population. A highly specific polymerase chain reaction assay was applied on dried blood spots. No over-representation of homo- or heterozygosity-for G985 appears to exist in such a strictly defined population, for which reason it may be m'bre relevant to look at a broader spectrum of clinical presentations of inherited metabolic disorders and examine a wider range of sudden death in infancy.     

Sudden infant death syndrome in twins

The incidence of sudden infant death syndrome is higher among twins than it is among singleton infants. Incidence of sudden infant death syndrome in twins in South Australia, is discussed, as well as some features of these twins and the health of the cotwins. The literature concerning the status of the cotwin is reviewed.     

Sudden infant death syndrome among Asians in California

We analyzed California linked birth and infant death records for 1978 to 1985 to determine the ethnic-specific incidence of sudden infant death syndrome in five Asian-American subgroups, and to assess the association of sudden infant death syndrome with cultural assimilation. The overall incidence of sudden infant death syndrome for these groups was 1.1/1000 live births (194 cases). The ethnic-specific incidence was statistically associated with the immigration status of each ethnic group, as measured by the proportion of all live births for which the mother was born in the United States, with a higher incidence for groups that have been in the United States for the longest period. A logistic model was used to examine simultaneously the association of sudden infant death syndrome with maternal ethnicity, ethnic homogeneity or heterogeneity of the parents, and maternal birthplace (United States, or elsewhere). The logistic analysis did not yield statistically significant evidence to support cultural assimilation as a factor in the incidence of sudden infant death syndrome for these groups. This finding may be due to small sample size and inadequate indicators of assimilation. It may also be that other factors relating to immigration and selective migration affect the incidence of sudden infant death syndrome among Asian-Americans.     

Effect of sleeping position on nasal patency in newborns

Sleeping posture has been implicated in the pathophysiology of sudden infant death syndrome. The effect of supine and lateral sleeping positions on nasal patency was investigated using acoustic rhinometry in 11 healthy newborns. The implications of the findings in sudden infant death syndrome are discussed.     

Risk of sudden infant death syndrome in subsequent siblings

To determine the risk of recurrence of sudden infant death syndrome in families, we studied 251,124 live births by linked birth and death certificates from Oregon for a 10-year period. We found five recurrences among 385 subsequent siblings, for a rate of 13/1000 live births and a relative risk of 6. When the recurrences were adjusted separately for birth order and maternal age, the risk was still five times that expected (p less than 0.001). Families with infant deaths from causes other than sudden infant death syndrome had similar recurrence rates, suggesting that the phenomenon was not specific to sudden infant death syndrome. The overall mortality rate for subsequent siblings after a sudden death event totaled 20.8/1000. We believe that a risk of 2%, although small in the design of studies of infants at risk for sudden infant death syndrome, is not trivial in the counseling of parents.     

Risk factors for SIDS in Japan: A record-linkage study based on vital statistics

This study examines the effect of items as reported on birth certificates on sudden infant death. We linked infant death certificates with birth certificates for the infants born in 1989 to residents of the Tohoku, Tokai and Kyushu regions in Japan (n = 409 679), that is, about one-third of the infants born in Japan that year. The mortality rate from sudden infant death, including 88 deaths from sudden infant death syndrome (SIDS) and 17 deaths from instantaneous death, was 25.6 per 100 000 live births. Elevated risk of sudden infant death was associated with low birthweight, late birth order, illegitimacy, male gender and young maternal age. These results correspond to previous studies from Western countries, suggesting a similar pattern for SIDS in Japan.     

Congenital long QT syndrome in newborns]

The perinatal manifestations of the long QT syndrome are rare, but early diagnosis and therapy are necessary to prevent sudden death. CASE REPORTS: A long QT syndrome was diagnosed in two neonates who presented with foetal bradycardia. In one case, a mutation in the gene KCNQ1 was identified, and a long QT syndrome was diagnosed in the mother and two brothers of the neonate. On beta-blocker therapy, one infant became free of long QT syndrome related symptoms, but a sudden death of the second infant occurred. CONCLUSION: The long QT syndrome should be considered in the differential diagnosis of foetal bradycardia. Early treatment of the neonate and his family may prevent ventricular arrhythmias and sudden death.     

An update on the approach to apparent life-threatening events

PURPOSE OF REVIEW: Apparent life-threatening events are an ongoing diagnostic dilemma for clinicians. Since most apparent life-threatening event episodes occur in infants under 6 months of age, they can generate considerable anxiety in parents and providers. This review will discuss issues to consider in the evaluation of infants after an apparent life-threatening event. To ensure proper management, a systematic approach should be taken to attempt to determine the cause of the event. RECENT FINDINGS: More recent literature suggests that infants with apparent life-threatening events frequently present without signs or symptoms of illness. Obtaining a careful history and physical examination is essential in determining the cause of the event. In this article, we will review the most current literature and discuss the American Academy of Pediatrics new recommendations on sudden infant death syndrome prevention. SUMMARY: After a careful review of the literature, prone sleeping is one of the biggest risk factors for sudden infant death syndrome. The association between apparent life-threatening events and sudden infant death syndrome remains to be explored further, but current evidence suggests minimal risk after an apparent life-threatening event episode. This article will help clinicians prepare for this difficult challenge by providing up-to-date information and identifying problems to be addressed in future research.     

Identifying infants at risk for sudden infant death syndrome

PURPOSE OF REVIEW: This review examines recent research relevant to the underlying pathophysiology and risk factors for sudden infant death syndrome. RECENT FINDINGS: Current research focuses on the linkage between known risk factors and vulnerability, genetic contributions, and the role of dysfunctional brainstem neurotransmission in the pathogenesis of this syndrome. While social inequalities, prematurity, maternal smoking, infant sleeping practices and sleep environment, arousal failures and environmental pollutants remain important risk factors, new evidence is emerging that certain genetic polymorphisms may contribute to vulnerability. New neuropathological studies have provided strong support for abnormal brainstem serotonergic function. Since serotonin influences a wide range of physiological systems including breathing, the cardiovascular system, temperature, and sleep-wake cycles, this finding strongly supports the hypothesis that sudden infant death syndrome is the result of dysregulation of the autonomic nervous system and provides biological plausibility for certain risk reduction strategies. SUMMARY: Despite a putative diagnostic shift, sudden infant death syndrome remains the most common cause of death from 1 month to 1 year of age. Recent studies confirmed established risk factors and have suggested new genetic vulnerabilities. Finally, new evidence supports a key role for abnormalities in brainstem serotonin systems in the pathophysiology of this syndrome.     

Knowledge of sudden infant death syndrome prevention strategies in a multicultural, disadvantaged community

AIM: This study assessed levels of maternal knowledge of sudden infant death syndrome prevention strategies in a socio-economically disadvantaged, culturally diverse population. METHODS: Pregnant women (n=233) were asked to name three things they could do to reduce the risk of cot death. Answers were marked in accordance with the US National Institute of Child Health and Development guide-lines. RESULTS: Of women 51.5% could correctly name two or more strategies that could reduce the risk of sudden infant death syndrome. There was significant difference by the woman's country of birth: 68.2% of Australian-born women were able to correctly identify two or more strategies, compared with only 37.3% of those born overseas (P<0.001). Most of the small number of Indigenous women included in the study were able to correctly identify two or more strategies. Year of arrival in Australia, number of previous children, age and level of education were not significantly related to women's knowledge. CONCLUSION: Knowledge of sudden infant death syndrome prevention strategies was poorer in overseas-born women. Practitioners working with disadvantaged, overseas-born women should give consideration to women's knowledge of sudden infant death syndrome prevention if current low rates of sudden infant death syndrome deaths are to be maintained.     

The fifty percent male excess of infant respiratory mortality

AIM: To test whether infant mortality from clearly respiratory causes has a consistent male excess that is different from the male excess in most cardiac conditions. METHODS: Analysis of male excess in infant mortality data from the United States and from north European countries. Data are analyzed for the period 1979-2002 in autopsied and unautopsied cohorts. RESULTS: Several modes of respiratory death in infancy are characterized by an approximate 50% male excess. This common excess is demonstrated in vital statistics for infant respiratory distress syndrome, sudden infant death syndrome, inhalation of food and other objects causing obstruction of respiratory tract or suffocation, congenital pneumonia, viral pneumonia, bronchiolitis and bronchitis, and accidental drowning. Results are presented for these and other respiratory causes of mortality in all United States infant deaths from 1979-1998 and for sudden infant death syndrome from the United Kingdom and Scandinavia. In sudden infant death syndrome, the common male excess appears to exist only for the autopsied post-neonatal cases. Comparisons are made to the male excess mortality from congenital cardiac anomalies showing a similarly large male excess for those conditions resulting in severe hypoxic and ischemic hypoxia. CONCLUSION: Because these respiratory disease conditions are quite different, it is proposed that their common approximately 50% male excess implies a common terminal hypoxic condition and mechanism of death reached via the different pathways. We hypothesize that an unknown X-linkage may be responsible for this consistent male excess in infant mortality.     

Pre- and postnatal medical care and risk of sudden infant death syndrome

The current study investigated whether sufficient attendance at prenatal and postnatal checks affects the risk of sudden infant death syndrome. A case-control study in the Tyrol enrolled 99 infants with sudden infant death syndrome that occurred between 1984 and 1994, and 136 randomly selected control cases. The risk of sudden infant death syndrome was higher in infants whose mothers attended less than five antenatal health checks than in the group with at least five or more visits (OR 5.1; p < 0.01). Babies who received medical help beyond routine health controls had a lower risk than those who did not (OR 0.32; p < 0.001). These differences persisted when social and demographic variables (mother's age at delivery, educational level, marital status, parity and gestational age) were taken into account. Our study identified inadequate antenatal and postnatal care as a risk indicator for sudden infant death syndrome and as a potential target for further educational work. Clinical recommendations should await the results of further evaluations.     

Apnoea and seizures.

We report two infants with near miss sudden infant death syndrome events exhibiting seizure disorders after caffeine treatment, suggesting there is an infant subgroup diagnosed as near miss sudden infant death syndrome who have apnoea possibly with seizures whose seizure threshold may be lowered by central nervous system stimulants like caffeine.