Alexander K.C. Leung, MD
Department of Pediatrics
University of Calgary
Calgary, Alberta, Canada T2N 1N4
Robert Van Howe, MD
Michigan State University College of Human Medicine
Marquette, MI 49855
Dr Brooks notes that in our article we mention that obstructive sleep apnea (OSA) is one of the common reported causes of secondary nocturnal enuresis (SNE).1 He also writes that OSA is associated with both primary nocturnal enuresis (PNE) and SNE and references his study to support this statement.2 Dr Brooks studied 160 children, 4 years of age or older, who were referred for possible sleep-disordered breathing (SDB) and found a high prevalence of nocturnal enuresis (NE). OSA was associated with both PNE and SNE.2 OSA is a recognized cause of SNE. When OSA is the only cause of SNE, successful treatment of the OSA leads to resolution of the SNE. OSA might be a contributing factor in the pathogenesis of PNE but is an unlikely cause. Children with PNE have always wet at night, and their problem therefore antedates the typical onset of symptoms of SDB, which correlate with adenoidal growth and are maximal in the kindergarten-aged child. We heartily support Dr Brooks' suggestion that all patients with NE should be screened by history for symptoms suggestive of SDB and that treatment should be offered when appropriate. Notwithstanding, we routinely counsel our patients that treatment of the SDB might not lead to resolution of the wetting. Both SDB and NE are common problems, often associated but not so commonly related in a cause-and-effect manner. Many patients with both SDB and NE undergo adenotonsillectomy (T/A) but experience improvements only in the SDB. We routinely counsel the families of such children that T/A should be offered only with the anticipation of an improvement in the SDB and not with any expectation that the NE will resolve. Unless there is a clear history that identifies the onset of SNE with that of the SDB, we do not recommend T/A or any other therapy for SDB as a specific treatment for NE. In the study we performed, we routinely screened patients for symptoms of SDB but identified only 2. One patient with PNE already had an established diagnosis of SDB and was undergoing treatment with continuous positive airway pressure, but the therapy had not had any influence on the NE. The second patient had SNE, and we referred the patient to a specialist in SDB in children.
REFERENCES
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