Chloral hydrate sedation for magnetic resonance imaging in newborn infants.

BACKGROUND: The aim of this study was to look for clinically significant adverse effects of chloral hydrate used in a large cohort of infants sedated for magnetic resonance imaging. METHOD: Case notes of infants who underwent magnetic resonance imaging (MRI) scanning from 2008 to 2010 were reviewed, with patient demographics, sedation dose, comorbidities, time to discharge, and side effects of sedation noted. RESULTS: Four hundred and eleven infants (median [range] postmenstrual age per weight at scan 42 [31(+4) -60] weeks per 3500 g [1060-9900 g]) were sedated with chloral hydrate (median [range] dose 50 [20-80] mg·kg(-1)). In three cases (0.7%), desaturations occurred which prompted termination of the scan. One infant (0.2%) was admitted for additional observation following sedation but had no prolonged effects. In 17 (3.1%) cases, infants had desaturations which were self-limiting or responded to additional inspired oxygen such that scanning was allowed to continue. CONCLUSION: When adhering to strict protocols, MRI scanning in newborn infants in this cohort was performed using chloral hydrate sedation with a relatively low risk of significant adverse effects.

Perinatal infections, prematurity and brain injury.

PURPOSE OF REVIEW: The association between perinatal infection and brain injury is widely accepted but a cause-and-effect relationship has not yet been proven. This article summarizes available evidence and current primary publications for debate. RECENT FINDINGS: Work completed during the review period has reinforced current understanding of perinatal infection, prematurity and brain injury. In animal experiments: lipopolysaccharides have been further implicated in brain injury, not only as a cause of brain injury but also as mediators of preconditioning and protection. Recent studies suggest that cerebral injury following low-dose lipopolysaccharide administration may become compensated in adulthood. Other studies have emphasized the complexity of the response by showing that plasma cytokine levels may not reflect those in the central nervous system or inflammatory events in the brain. SUMMARY: Perinatal infection and maternofetal inflammation is strongly associated with preterm birth. Inflammation probably represents an important mechanism for cerebral damage, and both overt lesions and maldevelopment can result. Epidemiological data and multiple animal models to link infection, inflammation and brain damage exist, but proof of causation is elusive.