Sudden Infant Death Syndrome - Mechanism (pathophysiology)

Current thinking regarding the mechanism of SIDS is focused on disordered regulation of the cardiorespiratory systems. The primary area of physiological regulation in humans is within the brain stem, which is located anatomically at the base of the brain. Abnormal findings on autopsy (as described in the above section), combined with clinical observations of abnormal regulatory control, support the view that delayed maturation or disruption of brain stem function results in the infant's lack of ability to respond when breathing and circulation patterns are insufficient to maintain life.

Several areas of respiratory regulation have been studied. Abnormalities of breathing patterns—such as recurrent brief apneic episodes, prolonged apneic An infant sleeping in a car seat attached to a Sudden Infant Death Syndrome (SIDS) monitor. There are documented incidences of SIDS occurring even when the infants were being properly monitored, the machinery was fully functioning, and the resuscitative efforts were started promptly and correctly. This suggests that while abnormal breathing patterns are found in infants who subsequently die of SIDS, this is probably not the primary mechanism. (David H. Wells/Corbis) event, and periodic breathing—have been observed in infants who later died of SIDS. The ability to electronically monitor and record breathing patterns in infants sparked enthusiasm for screening and monitoring of infants felt to be at high risk for SIDS.

However, experience has proven this intervention is not reliable in detecting which infants with abnormal breathing patterns will actually subsequently die of SIDS. In addition, multiple false alarms from the monitoring equipment resulted in high noncompliance rates in the home setting.

Diminished respiratory responsiveness to excessive buildup of carbon dioxide (hypercarbia) or to excessively low levels of oxygen (hypoxia) has also been found in infants at risk for SIDS. Nevertheless, the ability to discriminate between these infants and those not at risk who may have similar diminished responsiveness is lacking as of 2001.

A third respiratory regulation control mechanism is the arousal response. When experiencing hypocarbia or hypoxia, a normal sleeping infant will arouse and increase respiratory efforts in response to this life-threatening situation. Infants lacking sufficient arousal responsiveness will continue sleeping, becoming progressively more hypoxic, resulting in cardiorespiratory failure and sudden death.

Other mechanisms that are thought to be associated with the occurrence of SIDS include abnormal cardiac rhythms and increased body and/or environmental temperatures. It is likely that the pathophysiology of SIDS involves complex interactions between abnormal regulatory control systems and epidemiological risk factors such as poor intrauterine growth, exposure to smoking, prone sleep positioning, and prematurity.