Chen et al. (2009) described a preterm infant (33 weeks) born to an alcoholic mother. At birth, the infant showed facial dysmorphic features, optic atrophy, and sensorineural hearing loss characteristics of the fetal alcoholic syndrome (FAS). When the infant developed respiratory distress syndrome (RDS), it was put to CPAP therapy. On the 7th day, the infant developed focal clonic fits, CT brain scanning showed scattered air collections in both cerebral hemispheres. Brain CT scanning repeated after two days displayed widespread bilateral cerebral infarcts. The infant received supportive treatment and three months later in a follow up visit, the child showed marked delayed development and problematic epilepsy.
Unlike uncontrolled diabetes and multiple pregnancies, maternal alcohol abuse during pregnancy is not a specific risk factor to developing RDS (Agrons et al, 2005). In a systematic literature review, Peadon et al (2009) did not recognize cerebral air embolism as a sequel in FAS, in an earlier review, Osborn et al (1993) did not point to cerebral air embolism in cases of FAS. On the other hand, air embolism may occur in neonates with RDS during mechanical ventilation with low birth weight infants at greater risk for air leak and embolism (Agrons et al, 2005). Although CPAP is a practical method for premature infants, yet it does not allow administration of surfactant, besides it carries greater risk for air embolism than intubated premature infants subjected to mechanical ventilation (Fantz, 2009). Neuroimaging studies in FAS cases have the advantages of studying the different patterns of structural abnormalities accompanying FAS (Spadoni et al, 2007). Although in the paper at hand, massive air embolism is more likely to be a sequel of CPAP therapy rather than FAS, neuroimaging studies can provide characterization of the effects of prenatal alcohol especially if large samples are studied (Spadoni et al, 2007).
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