Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
The cause (or causes) of SIDS is still unknown. Despite the dramatic decrease in the incidence of SIDS in the United States in recent years, SIDS remains one of the leading causes of death during infancy beyond the first 30 days after birth. It is generally accepted that SIDS may be a reflection of multiple interacting factors.
Infant development: A leading hypothesis is that SIDS may reflect a delay in the development of nerve cells within the brain that are critical to normal heart and lung function. Research examinations of the brain stems of infants who died with a diagnosis of SIDS have revealed a developmental delay in formation and function of several serotonin-binding nerve pathways within the brain (serotonin is an example of a brain chemical known as a neurotransmitter that is important for brain function). These pathways are thought to be crucial to regulating breathing, heart rate, and blood pressure responses.
The hypothesis is that certain infants, for reasons yet to be determined, may experience abnormal or delayed development of specific, critical areas of their brain. This could negatively affect the function and connectivity to regions regulating arousal.
Arousal, in this context, refers to an infant's ability to awaken and/or respond to a variety of physiological stimuli. For example, a child sleeping facedown may move his or her face into such a position so that the nose and mouth are completely obstructed. This may alter the levels of oxygen or carbon dioxide in the infant's blood. Normally, these changes would trigger arousal responses, prompting the infant to move his or her head to the side to alleviate this obstruction.
In addition, other normally protective responses to stressful stimuli may be defective in infants
who are vulnerable to SIDS. One such reflex is the
laryngeal chemoreflex. This reflex results in changes in breathing, heart rate, and blood pressure when portions of the airway are stimulated by fluids like saliva or regurgitated stomach contents. Having saliva in the airway may activate this reflex, and swallowing may be important to keep the airway clear. When an infant is in the facedown position, the rate of swallowing is decreased. Protective arousal responses to these laryngeal reflexes are also diminished in active sleep in the facedown position.
Rebreathing asphyxia: When a baby is facedown, air
movement around the mouth may be impaired. This can cause the baby to
re-breathe carbon dioxide that the baby has just exhaled. Soft bedding and
gas-trapping objects, such as blankets, comforters, water beds, and soft
mattresses, are other types of sleep surfaces that may impair normal air
movement around the baby's mouth and nose when positioned facedown.
Hyperthermia (increased temperature): Overdressing, using excessive coverings, or increasing the air temperature may lead to an increased metabolic rate in these infants and eventual loss of breathing control. However, it is unclear whether the increased temperature is an independent factor or if it is just a reflection of the use of more clothing or blankets that may act as objects obstructing the airway.
Sudden infant death syndrome (SIDS) is defined as the sudden death of an infant younger than 1 year that remains unexplained after a thorough case investigation, including the performance of a complete autopsy, examination of the scene of death, and review of the clinical history.