婴儿猝死综合征的病因

<正>婴儿猝死综合征(Sudden Infant Death Syndrone,SIDS)又名威胁婴儿生命症(Apparent Life Threatening Event,ALTE),是指1岁以内的婴儿平素体健,无明显病因突然死亡,而死后尸解找不到明显的致病因素。SIDS是引起活婴死亡的重要因素,发病率约为1.2‰～1.45‰,发病年龄<1岁,其中以1～4个月(占70.7％)多见,以冬季和早春发病多。目前认为SIDS的病因是多因素的,现将国外目前关于SIDS的病因研究进展综述如下。     

婴儿猝死综合征病因研究近况

婴儿猝死综合征 (ｓｕｄｄｅｎｉｎｆａｎｔｄｅａｔｈｓｙｎｄｒｏｍｅ ,ＳＩＤＳ)是指外观健康的婴儿无明显诱因突然死亡 ,经尸检、病史回顾仍难以完全解释其病因的临床综合征。自 6 0年代起 ,各国学者对其病因进行广泛研究并提出众多学说 ,如 :过热、早产、自主神经功能紊乱、胃食管反流误吸、低血糖等。近年来 ,国外学者对其病因又提出新的见解 ,现综述如下。1　俯卧睡眠俯卧睡眠与ＳＩＤＳ的关系经大样本回顾性研究表明两者间存在显著相关性 ,俯卧睡眠被认为是ＳＩＤＳ高危因素之一[1～ 4] 。Ｓｋａｄｂｅｒｇ等[1 ] 报道挪威 1987～ 1…     

婴儿猝死综合征病因分析

近年来国内外对婴儿猝死已引起重视。凡乳儿、婴儿突然意外死亡虽尸检仍不能解释其致死原因的病例称为“婴儿猝死综合征”．又称“摇篮死亡”。该病近年来发病正在大幅度上升，成为4周-1岁婴儿死亡的主要原因。尸检中无法解释死因，发生该病倾向的婴儿体重增加很慢，有反射及肌张力的异常，呼吸不平稳，爱哭以及神经过敏。一般认为在出生后第一周内没有死亡的，死亡年龄在一周-1岁之间，尤以2—4个月时摄多。本文对有关本病的病因及发病机理作一探讨分析。     

婴儿猝死综合征与法医学的研究进展

婴儿猝死综合征(sudden infant death syndrome, SIDS),以往在欧美也称之为摇篮死(crib death).自1970年第二届国际婴儿猝死原因会议后,已普遍采用婴儿猝死综合征这一名称.日本厚生省SIDS研究小组对其定义为:由无法根据婴幼儿健康状况和既往史预测,也无法根据死亡前状况和尸检证实的原因而引起婴幼儿突然死亡的症候群.     

婴儿猝死综合征1例

孕妇 ,3 0岁 ,因停经 40 + 1周 ,双下肢水肿 1个月而入院。诉述 4个半月出现胎动 ,定期检查 ,均正常。 1月前出现双下肢水肿 ,伴血压升高 ,往健。入院查体 :T、P、R均正常 ,BP 1 8.6/ 1 2 .5kPa,一般情况可 ,心肺未见异常。PV :宫高 2 7cm ,腹围 1 0 2cm ,LOA位 ,胎心 1 40次 /分 ,律齐 ,头先露 ,浮。尿常规示蛋白 ( +)。入院诊断 :①孕40 + 1周G1P0 ;②妊娠高血压综合征 (中度 )。入院后引产 ,因宫口开大 3cm时胎头高浮且产瘤形成 ,以“相对性头盆不称、妊娠高血压综合征” ,行剖宫产术娩出一 3 40 0g男婴 ,Apgar评 3分 ,立即清理呼…     

成年人意外猝死与婴儿猝死综合征类似

研究发现,许多看似健康的成年人有可能意外死亡,其表征类似于婴儿猝死综合征。据来自于英国爱心基金会医疗主管与负责此项目研究的主要人员之一Tim Bowker博士报道,毫无原因地突然倒下并最终死亡的成年人数“远高于官方公布的统计数字”;如同婴儿猝死综合征一样,该死亡被称作为“成年人猝死综合征”。     

睡眠姿势及环境与婴儿猝死综合征

目的：探讨睡眠姿势及环境与婴儿猝死综合征的关系。方法：查阅，分析，归纳多篇国外献，结果：婴儿睡眠姿势，环境与婴儿猝死综合征存在相关性。结论：婴儿俯卧睡眠，过热、被动吸烟为婴儿猝死综合征的高危因素。     

Critical diaphragm failure in sudden infant death syndrome

Sudden infant death syndrome (SIDS) is the leading cause of death in infants between the ages of 1 and 12 months in developed countries. SIDS is by definition a diagnosis of exclusion, and its mechanism of action is unknown. The SIDS-Critical Diaphragm Failure (CDF) hypothesis postulates that the cause of death in SIDS is respiratory failure caused by CDF. Four principal risk factors contribute to CDF in young infants: undeveloped respiratory muscles, non-lethal infections, prone resting position, and REM sleep. Even relatively minor infections can cause an acute and significant reduction in diaphragm force generation capacity that in conjunction with other risk factors can precipitate CDF. CDF-induced acute muscle weakness leaves few, if any pathological marks on the affected tissue.Understanding the underlying mechanism of SIDS may help in formulating new approaches to child care that can help to further reduce the incidence of SIDS.     

Critical diaphragm failure in sudden infant death syndrome

Abstract

Sudden infant death syndrome (SIDS) is the leading cause of death in infants between the ages of 1 and 12 months in developed countries. SIDS is by definition a diagnosis of exclusion, and its mechanism of action is unknown. The SIDS–Critical Diaphragm Failure (CDF) hypothesis postulates that the cause of death in SIDS is respiratory failure caused by CDF. Four principal risk factors contribute to CDF in young infants: undeveloped respiratory muscles, non-lethal infections, prone resting position, and REM sleep. Even relatively minor infections can cause an acute and significant reduction in diaphragm force generation capacity that in conjunction with other risk factors can precipitate CDF. CDF-induced acute muscle weakness leaves few, if any pathological marks on the affected tissue.Understanding the underlying mechanism of SIDS may help in formulating new approaches to child care that can help to further reduce the incidence of SIDS.     

Multiple serotonergic brainstem abnormalities in sudden infant death syndrome

Context  The serotonergic (5-hydroxytryptamine [5-HT]) neurons in the medulla oblongata project extensively to autonomic and respiratory nuclei in the brainstem and spinal cord and help regulate homeostatic function. Previously, abnormalities in 5-HT receptor binding in the medullae of infants dying from sudden infant death syndrome (SIDS) were identified, suggesting that medullary 5-HT dysfunction may be responsible for a subset of SIDS cases. Objective  To investigate cellular defects associated with altered 5-HT receptor binding in the 5-HT pathways of the medulla in SIDS cases. Design, Setting, and Participants  Frozen medullae from infants dying from SIDS (cases) or from causes other than SIDS (controls) were obtained from the San Diego Medical Examiner's office between 1997 and 2005. Markers of 5-HT function were compared between SIDS cases and controls, adjusted for postconceptional age and postmortem interval. The number of samples available for each analysis ranged from 16 to 31 for SIDS cases and 6 to 10 for controls. An exploratory analysis of the correlation between markers and 6 recognized risk factors for SIDS was performed. Main Outcome Measures  5-HT neuron count and density, 5-HT_1A receptor binding density, and 5-HT transporter (5-HTT) binding density in the medullary 5-HT system; correlation between these markers and 6 recognized risk factors for SIDS. Results  Compared with controls, SIDS cases had a significantly higher 5-HT neuron count (mean [SD], 148.04 [51.96] vs 72.56 [52.36] cells, respectively; P<.001) and 5-HT neuron density (P<.001), as well as a significantly lower density of 5-HT_1A receptor binding sites (P.01 for all 9 nuclei) in regions of the medulla involved in homeostatic function. The ratio of 5-HTT binding density to 5-HT neuron count in the medulla was significantly lower in SIDS cases compared with controls (mean [SD], 0.70 [0.33] vs 1.93 [1.25] fmol/mg, respectively; P = .001). Male SIDS cases had significantly lower 5-HT_1A binding density in the raphé obscurus compared with female cases (mean [SD], 16.2 [2.0] vs 29.6 [16.5] fmol/mg, respectively; P = .04) or with male and female controls combined (mean [SD], 53.9 [19.8] fmol/mg; P = .005). No association was found between 5-HT neuron count or density, 5-HT_1A receptor binding density, or 5-HTT receptor binding density and other risk factors. Conclusions  Medullary 5-HT pathology in SIDS is more extensive than previously delineated, potentially including abnormal 5-HT neuron firing, synthesis, release, and clearance. This study also provides preliminary neurochemical evidence that may help explain the increased vulnerability of boys to SIDS.      

Association of respiratory virus infections with sudden infant death syndrome

From September, 1974, to September, 1979, 488 cases of sudden infant death syndrome (SIDS) in Melbourne were studied for evidence of viral infection. One hundred and eighty-eight infants (39%) yielded one or more viruses, with respiratory viruses being detected in 102 cases (21%). Further evidence of a respiratory virus association with SIDS was obtained by comparing the monthy respiratory virus isolation rates at the Royal Children's Hospital from 1973 to 1979 with the incidence of SIDS in the same period. A highly significant correlation was obtained between these isolation rates and the incidence of SIDS, which suggests that respiratory viruses play a role in SIDS in Melbourne.     

Sleeping prone and the risk of sudden infant death syndrome.

OBJECTIVE--To critically analyze reports that show a relationship between sudden infant death syndrome (SIDS) and the prone sleeping position in infants. DATA SOURCES--Peer-reviewed articles, published letters, book chapters, and local and national health statistics were used, without time or language restrictions. These studies represented three races, four continents, and seven countries; none was published in North America. STUDY SELECTION--No studies were ignored, but only those with case controls were reviewed in detail; we regarded a recent cohort analytic (prospective) study as particularly strong, in addition to six before-and-after (intervention) trials. DATA EXTRACTION--Hill's criteria for decision making were used to assess the quality and validity of the data. DATA SYNTHESIS--Without exception, all studies demonstrated an increased risk for SIDS associated with the prone sleeping position. The published likelihood ratios (relative risk or odds ratio) for SIDS in the prone position compared with SIDS in any other position ranged from 3.5 to 9.3 in seven studies. Publicity against the use of the prone position has been associated with reduction of SIDS by 20% to 67%, paralleling the reduction in use of the prone position, with no increase in deaths from aspiration or in other diagnostic categories. CONCLUSIONS--We recommended avoidance of the prone sleeping position for infants in the first 6 months of life unless there is a specific medical indication for it. Reports from the Netherlands, Great Britain, Australia, and New Zealand indicate that avoiding the prone position for infants in the first 6 months of life could reduce the number of SIDS deaths by as much as 50%. Unfortunately, these findings have received little attention in North America. We offer here an analysis of these reports so that physicians can assess the evidence and advise parents accordingly.     

Risk factors for sudden infant death syndrome among northern plains Indians

Context  Sudden infant death syndrome (SIDS) is a leading cause of postneonatal mortality among American Indians, a group whose infant death rate is consistently above the US national average. Objective  To determine prenatal and postnatal risk factors for SIDS among American Indians. Design, Setting, and Participants  Population-based case-control study of 33 SIDS infants and 66 matched living controls among American Indians in South Dakota, North Dakota, Nebraska, and Iowa enrolled from December 1992 to November 1996 and investigated using standardized parental interview, medical record abstraction, autopsy protocol, and infant death review. Main Outcome Measures  Association of SIDS with maternal socioeconomic and behavioral factors, health care utilization, and infant care practices. Results  The proportions of case and control infants who were usually placed prone to sleep (15.2% and 13.6%, respectively), who shared a bed with parents (59.4% and 55.4%), or whose mothers smoked during pregnancy (69.7% and 54.6%) were similar. However, mothers of 72.7% of case infants and 45.5% of control infants engaged in binge drinking during pregnancy. Conditional logistic regression revealed significant associations between SIDS and 2 or more layers of clothing on the infant (adjusted odds ratio [aOR], 6.2; 95% confidence interval [CI], 1.4-26.5), any visits by a public health nurse (aOR, 0.2; 95% CI, 0.1-0.8), periconceptional maternal alcohol use (aOR, 6.2; 95% CI, 1.6-23.3), and maternal first-trimester binge drinking (aOR, 8.2; 95% CI, 1.9-35.3). Conclusions  Public health nurse visits, maternal alcohol use during the periconceptional period and first trimester, and layers of clothing are important risk factors for SIDS among Northern Plains Indians. Strengthening public health nurse visiting programs and programs to reduce alcohol consumption among women of childbearing age could potentially reduce the high rate of SIDS.      

Defects of metabolism of fatty acids in the sudden infant death syndrome

Two hundred consecutive cases of the sudden infant death syndrome were reviewed for the presence of fat in the liver; 14 showed diffuse panlobular microvesicular fatty change indistinguishable from that found in Reye's syndrome. Samples of frozen liver were available in five of the 14 cases; histochemical analysis showed well preserved cytochrome oxidase and succinate dehydrogenase activity in all five, uncharacteristic of Reye's syndrome. Fatty acyl-coenzyme A dehydrogenase activity in the liver was assayed biochemically in two of the same five cases with severe hepatic fatty infiltration; both showed a defect in medium chain acyl-coenzyme A dehydrogenase activity using the substrate octanoyl-coenzyme A. Both cases also showed cerebral oedema in association with fatty infiltration of renal tubules, myocardium, and skeletal muscle, characteristic of Reye's syndrome. It is concluded that diffuse panlobular microvesicular fatty change of the liver in victims of the sudden infant death syndrome, although essentially non-specific, indicates that the state of mitochondrial enzymes should be investigated.