SANFORD G. DUKE, MD; GREGORY N. POSTMA, MD; WILLIAM F. MCGUIRT, JR, MD; DOUGLAS RIRIE, MD; DAVID B. AVERILL, MD; JAMES A. KOUFMAN, MD

WINSTON-SALEM, NORTH CAROLINA

Laryngopharyngeal reflux in the infant has been proposed as a possible cause of sudden infant death syndrome (SIDS). We investigated the efferent laryngeal and diaphragmatic responses to acid exposure on the laryngeal mucosa using a neonatal canine model. Electromyographic (EMG) recordings from the thyroarytenoid muscle and the diaphragm were measured with hooked-wire electrodes. Reproducible laryngospasm responses occurred in all animals after laryngeal exposure to hydrochloric acid at pH 2.0 or less. Laryngospasm occurred in combination with tachypnea and increased diaphragmatic activity in most of the animals. Laryngospasm was associated with prolonged apnea and total cessation of diaphragmatic EMG activity in 1 animal, and in another, initial tachypnea was followed by erratic diaphragmatic activity and brief apnea. Laryngeal acid exposure (below pH 2.0) causes laryngospasm and may result in paradoxical apneic events in neonatal dogs. Acid-induced, laryngospasm-associated apnea may represent a potential cause of SIDS, and the immature dog appears to be an excellent model for further investigations