Sudden Infant Death Syndrome

Kinney and Thach (Aug. 20 issue) review the putative terminal respiratory pathway associated with the sudden infant death syndrome (SIDS), and they indicate a life-threatening event and failure of arousal as the first steps in the respiratory pathway to SIDS. The authors mention only central cortical and subcortical structures involved in arousal mechanisms, without referring to peripheral arterial chemoreceptors as the carotid body, the role of which in arousal from asphyxial events is widely accepted. Prematurity and exposure to smoke also increase the risk of SIDS and adversely affect the response of the peripheral arterial chemoreceptors. These chemoreceptors undergo structural and functional development during the postnatal period, with a gradual increase in hypoxic sensitivity. Prematurity causes intrinsic abnormalities of the response of the peripheral arterial chemoreceptors, which may be further worsened by prematurity-associated intermittent hypoxic events or oxygen therapy. Intermittent hypoxia may cause hypersensitivity of the peripheral arterial chemoreceptors, which may increase the risk of SIDS, precipitating unstable respiration through apneic responses after sighs or brief arousals.2-4 Conversely, exposure to hyperoxia has been reported to cause hyposensitivity of the peripheral arterial chemoreceptors, possibly leading to an ineffective response. Perinatal exposure to nicotine also blunts the function of the peripheral arterial chemoreceptors through changes in expression of neurotransmitters and neuromodulators.