Potential asphyxia and brainstem abnormalities in sudden and unexpected death in infants.
OBJECTIVE
Sudden and unexplained death is a leading cause of infant mortality. Certain characteristics of the sleep environment increase the risk for sleep-related sudden and unexplained infant death. These characteristics have the potential to generate asphyxial conditions. We tested the hypothesis that infants may be exposed to differing degrees of asphyxia in sleep environments, such that vulnerable infants with a severe underlying brainstem deficiency in serotonergic, γ-aminobutyric acid-ergic, or 14-3-3 transduction proteins succumb even without asphyxial triggers (e.g., supine), whereas infants with intermediate or borderline brainstem deficiencies require asphyxial stressors to precipitate death.


METHODS
We classified cases of sudden infant death into categories relative to a "potential asphyxia" schema in a cohort autopsied at the San Diego County Medical Examiner's Office. Controls were infants who died with known causes of death established at autopsy. Analysis of covariance tested for differences between groups.


RESULTS
Medullary neurochemical abnormalities were present in both infants dying suddenly in circumstances consistent with asphyxia and infants dying suddenly without obvious asphyxia-generating circumstances. There were no differences in the mean neurochemical measures between these 2 groups, although mean measures were both significantly lower (P < .05) than those of controls dying of known causes.


CONCLUSIONS
We found no direct relationship between the presence of potentially asphyxia conditions in the sleep environment and brainstem abnormalities in infants dying suddenly and unexpectedly. Brainstem abnormalities were associated with both asphyxia-generating and non-asphyxia generating conditions. Heeding safe sleep messages is essential for all infants, especially given our current inability to detect underlying vulnerabilities.
Department of Pathology, Enders Building Room 1112, Boston Children's Hospital, 61 Binney St, Boston, MA 02115. hannah.kinney@childrens.harvard.edu.
Bradley B
BB
Randall
David S
DS
Paterson
Elisabeth A
EA
Haas
Kevin G
KG
Broadbelt
Jhodie R
JR
Duncan
Othon J
OJ
Mena
Henry F
HF
Krous
Felicia L
FL
Trachtenberg
Hannah C
HC
Kinney
D048948:14-3-3 Proteins / Q000378:metabolism*; D001237:Asphyxia / Q000150:complications*; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D001933:Brain Stem / Q000378:metabolism*; D016022:Case-Control Studies; D002851:Chromatography, High Pressure Liquid; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D016684:Prone Position; D044282:Receptor, Serotonin, 5-HT1A / Q000378:metabolism*; D011963:Receptors, GABA-A / Q000378:metabolism*; D012044:Regression Analysis; D012307:Risk Factors; D012701:Serotonin / Q000378:metabolism*; D012890:Sleep; D013398:Sudden Infant Death / Q000209:etiology*; D016683:Supine Position
D048948:14-3-3 Proteins; D015415:Biomarkers; D011963:Receptors, GABA-A; D044282:Receptor, Serotonin, 5-HT1A; D012701:Serotonin
14-3-3 proteins; GABA receptors; bed-sharing; prone sleep; serotonin; sudden infant death syndrome