Southall D P, Talbert D G, Johnson P, Morley C J, Salmons S, Miller J, Helms P J
Lancet. 1985 Sep 14;2(8455):571-7. doi: 10.1016/s0140-6736(85)90583-5.
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 hypoxaemia may be one cause of neurodevelopmental damage and sudden death in infants and young children.
对10例迅速发展且严重低氧血症发作(持续时间15 - 120秒)的婴儿进行了研究。2个月以上的婴儿,大多数发作发生在清醒时,由突然的有害刺激引发。较小的婴儿在睡眠和喂食期间频繁出现未被察觉的发作。动脉血氧分压在20秒内降至20毫米汞柱以下,30秒后出现意识丧失,有时伴有惊厥。临床观察、呼吸运动测量、气流、食管压力、腹外斜肌表面肌电图,以及两例胸部荧光透视和显微喉镜检查记录到无吸气气流但在低肺容量时呼气活动持续且声门部分或完全关闭的发作。5例婴儿尽管进行了气管切开术或留置鼻气管导管,发作仍持续。未发现心内分流,动脉血氧分压迅速下降归因于在快速再循环时间存在的情况下,处于最大呼气位置时缺乏通气。在5例接受测试的婴儿中,气管吸出物中磷脂酰胆碱比例较低。1例婴儿在大部分清醒时间都有可闻及的呼气制动(呼噜声)。这种先前未被认识的严重低氧血症机制可能是婴幼儿神经发育损伤和猝死的原因之一。