Benzyl alcohol is normally oxidized rapidly to benzoic acid, conjugated with glycine in the liver, and excreted as hippuric acid. However, this metabolic pathway may not be well developed in premature infants. The
Benzyl Alcohol may therefore have been metabolized to benzoic acid, which could not be conjugated by the immature liver but accumulated, causing metabolic acidosis (2).
These reports of neonatal toxicity from benzyl alcohol are highly noteworthy. However, caution must be exercised in attributing individual illness to
Benzyl Alcohol since many of the described clinical features commonly occur in neonates seriously ill from other causes. Newborns most likely to receive large volumes of flush solutions, relative to body weight, are the very small, sick premature infants who already have a high risk of mortality. Thus, mortality potentially attributable to
Benzyl Alcohol should also be assessed by a careful comparison of neonatal mortality in newborns receiving large amounts of non-bacteriostatic flush solutions and medications with comparable newborns receiving large amounts of bacteriostatic solutions and medications. Retrospective analyses of newborns who received saline flushes with
Benzyl Alcohol and survived are also needed to establish whether a dose-response relationship exists between clinical and laboratory findings and the intensity of exposures to benzyl alcohol, and to identify more completely the pathologic and clinical features of toxicity in newborns.
