Although uncommon in children, SP appears to be primarily a condition of males and adolescents and appears to be increasing in incidence in this population. According to these data, a large portion of children are being managed without procedural intervention.
This is the first pediatric study on the rate and degree of esophageal displacement from the airway at the level of the cricoid cartilage. Lateral displacement of the esophagus occurred at a significantly greater rate in the younger (45%) compared with the older (15%) children, which was directly opposite of our hypothesis. Of the 36 children (30%) with esophageal displacement, all had displacement to the left of the cricoid cartilage.
Since the 1970s, when inhaled anticholinergic agents were first introduced as adjunct therapies for the immediate treatment of pediatric asthma exacerbations, several trials have shown varying degrees of benefit from their use as bronchodilators in combination with inhaled short-acting beta-adrenergic agonists and systemic corticosteroids. Although other anticholinergics exist, ipratropium bromide (IB) specifically has emerged as the overwhelming choice of pulmonologists and emergency physicians because of its limited systemic absorption from the lungs when given as an inhaled preparation. However, although the varying trials, predominantly in the emergency department setting, have typically shown a trend toward improved outcomes, none has set forth clear dosing protocol recommendations for use by practicing physicians. It is our goal in this review of the available literature on the use of IB, as an adjunct to inhaled short-acting beta-adrenergic agonists, to summarize practical, evidence-based recommendations for use in the pediatric emergency department setting for acute asthma exacerbations. We also hope to better delineate the most effective dosing regimen in those patients who might benefit most from the addition of IB and to explore proposed additional benefits it may have as a modulator of cholinergic-induced effects from high-dose beta-agonist therapy and viral triggers.
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