Affiliation:
1. Pediatric Neurology Division, Childrens Hospital Los Angeles, Keck School of Medicine, Los Angeles, California; and Department of Neurology, University of Southern California, Los Angeles, California
Abstract
Three infants with infant botulism are presented to illustrate how atypical, early, and severe features may obscure or delay diagnosis. Two boys aged 6 weeks and 20 days, respectively, presented with rapid deterioration after brief periods of poor feeding, one with an apparent life-threatening event at home and the other with a full cardiopulmonary arrest. Initial abnormal laboratory findings of coagulopathy suggested sepsis in the first infant. In the second infant, severe acidosis and hypoglycemia suggested an underlying metabolic disorder. A third infant, aged 1 month, was hospitalized originally with an admitting diagnosis of “pharyngitis” resulting from his inability to take adequate feedings. He received intravenous fluids and antibiotics. One week later he suffered a respiratory arrest. Laboratory findings of severe hyponatremia and acidosis at the time of his arrest suggested a metabolic etiology. Even retrospectively, none of these infants had the typical initial complaint of constipation, and none were noted to have ptosis or facial weakness before catastrophic collapse. However, in each case, the parent had initially brought the child to the physician for “poor feeding” or “poor suck,” which was not recognized by medical personnel as a result of bulbar weakness. Ultimately, all 3 infants were found to have infant botulism. All 3 had received antibiotics before catastrophic collapse, possibly contributing to the rapidity of the deterioration. Each recovered, although the delay in diagnosis made them ineligible for treatment with botulism immunoglobulin.
Publisher
American Academy of Pediatrics (AAP)
Subject
Pediatrics, Perinatology and Child Health
Cited by
33 articles.
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