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Ten infants with rapidly developing and severe episodes of hypoxaemia (15-120 s duration) were studied. In infants over 2 months old most episodes occurred when awake, after a sudden noxious stimulus. In younger infants frequent yet undetected episodes occurred during sleep and feeding. Arterial PO2 fell below 20 mm Hg within 20 s, and loss of consciousness, sometimes with convulsions, occurred after 30 s. Clinical observations, measurements of respiratory movements, air flow, oesophageal pressure, external oblique surface electromyogram, and, in two cases, chest fluoroscopy and microlaryngoscopy documented episodes of no inspiratory flow but continued expiratory activity at low lung volume with partial or complete glottic closure. In five infants, episodes continued despite tracheostomy or an indwelling nasotracheal tube. No intracardiac shunt could be demonstrated and the rapid fall in arterial PO2 was attributed to lack of ventilation at a maximum expiratory position in the presence of a rapid recirculation time. In five infants tested there was a low proportion of phosphatidylcholine in the tracheal aspirate. In one infant audible expiratory braking (grunting) was present for most of the awake time. This previously unrecognised mechanism for severe hypoxæmia may be one cause of neurodevelopmental damage and sudden death in infants and young children. © 1985.

Original publication




Journal article


The Lancet

Publication Date





571 - 577