Flaig Christian
Landeskrankenhaus Bludenz, Emergency Medicine, Spitalgasse 13, 6700 Bludenz, Austria.
Med Hypotheses. 2007;68(6):1276-86. doi: 10.1016/j.mehy.2006.10.019. Epub 2006 Dec 4.
Despite extensive research, a link between the assumed mechanisms of death and known risk factors for sudden infant death syndrome (SIDS) has not yet been established. Modifiable risk factors such as prone sleeping position, nicotine exposure and thermal stress and non-avoidable risk factors like male gender and some risky socio-economic conditions could be detected, but the etiology of SIDS remains unknown. In many SIDS cases histopathological findings suggest an involvement of vital autonomic control functions and unidentified trigger factors seem to play a role. From a hypothetical point of view, a developmental sympatheticovagal imbalance of the cardiovascular reflex control could cause a predisposition for SIDS. An assumed gastroesophageal trigger impulse is possibly developed during the first weeks of life and could lead to the infant's vagal reflex death. Air swallowed during feeding escapes through the esophagus while the infant is sleeping. The temporarily bloated esophagus exerts pressure on neighboring mediastinal baroreceptors, which is potentially misinterpreted as a rise in arterial pressure. The following cardiodepressoric baroreceptor reflex could lead to arterial hypotension, bradycardia and cardiac arrest. Sleeping in prone position may create an increased thoracic pressure on mediastinal baroreceptors, causing a more pronounced vagal reflex and an increased likelihood of SIDS. Prone position in connection with soft objects in the infant's sleeping environment potentially generates an increased oculobulbar pressure, resulting in an additional cardiodepressoric condition (Aschner-Dagnini phenomenon). From the sixth month of life onwards the sympatheticovagal balance seems to have matured sufficiently to compensate the life-threatening challenges in most infants. Insufficient postprandial burping could either create another independent modifiable risk factor or present the missing link to a common trigger mechanism for SIDS. Further investigations may possibly lead to the explicit recommendation to burp all infants sufficiently and repeatedly before sleep.
尽管进行了广泛研究,但假定的死亡机制与已知的婴儿猝死综合征(SIDS)风险因素之间的联系尚未确立。可以检测到一些可改变的风险因素,如俯卧睡眠姿势、接触尼古丁和热应激,以及不可避免的风险因素,如男性性别和一些危险的社会经济状况,但SIDS的病因仍然不明。在许多SIDS病例中,组织病理学结果表明重要的自主神经控制功能受累,且不明触发因素似乎起了作用。从假设的角度来看,心血管反射控制的发育性交感迷走神经失衡可能导致SIDS易感性。假定的胃食管触发冲动可能在生命的最初几周形成,并可能导致婴儿迷走神经反射性死亡。喂食时吞咽的空气在婴儿睡觉时通过食管排出。暂时膨胀的食管对邻近的纵隔压力感受器施加压力,这可能被误判为动脉压升高。随后的降压压力感受器反射可能导致动脉低血压、心动过缓和心脏骤停。俯卧睡眠可能会增加纵隔压力感受器的胸内压力,导致更明显的迷走神经反射和更高的SIDS可能性。婴儿睡眠环境中俯卧姿势与柔软物体相结合,可能会增加眼球压力,导致额外的降压状况(阿施纳-达尼尼现象)。从生命的第六个月起,交感迷走神经平衡似乎已充分成熟,足以补偿大多数婴儿面临的危及生命的挑战。餐后打嗝不足可能会产生另一个独立的可改变风险因素,或者是SIDS常见触发机制中缺失的环节。进一步的研究可能会明确建议在婴儿睡前充分且反复地帮其打嗝。