Apnea of prematurity (AOP) remains one of the common diagnoses in neonatal intensive care units, especially with the increased survival of extremely premature infants. Multiple definitions exist for AOP, depending on the medical society. It has been defined by the American Academy of Pediatrics Committee of the Fetus and Newborn as the presence of respiratory pauses for more than 20 s or shorter pauses associated with cyanosis or desaturations or bradycardia less than 100 bpm in infants less than 37 weeks gestational age.¹ The control of breathing is a complex process, which includes interaction between multiple peripheral and central receptors, neurons, and the respiratory center in the bulbo-pontine region, which is responsible for rhythmogenesis. AOP is the best single indicator of the immaturity of this process.² An increasing number of apnea days has previously been shown to be associated with worse clinical outcomes, including abnormal neurodevelopment, which might be related to intermittent hypoxic episodes and bradycardia during those events.

Methylxanthines and non-invasive respiratory support have been the mainstays of the management of AOP. Caffeine citrate is the only Food and Drug Administration-approved medication for the treatment of AOP. However, despite these interventions, the severity of AOP can progress to needing invasive mechanical ventilation and its untoward consequences. In most cases, sensory tactile stimulation, in addition to supplemental oxygen, terminates the episode. The mechanism by which tactile stimulation stimulates respiration is unclear, but it is postulated that it does so by producing non-specific excitatory neuronal impulses that result in respiratory stimulation together with activating the reticular formation of the brain stem, leading to arousal.³ In addition, limb motion has been shown to increase respiratory rates even during sleep through proprioceptive afferents, which coordinate respiratory generation and locomotion.⁴ Moreover, the effect of mechanical stimulation on the respiratory centers depends on the nerves that are stimulated. Various sensory receptors are present throughout the skin, each type responding to a different degree of stimulus, indicating that the location and degree of tactile stimulus can lead to a different response.^5,6

早产儿呼吸暂停 (AOP) 仍然是新生儿重症监护病房的常见诊断之一，特别是随着极早产儿存活率的增加。 AOP 存在多种定义，具体取决于医学会。美国儿科学会胎儿和新生儿委员会将其定义为胎龄小于 37 周的婴儿出现超过 20 秒的呼吸暂停或与发绀或饱和度降低或心动过缓 (低于 100 bpm) 相关的较短呼吸暂停。¹呼吸的控制是一个复杂的过程，包括多个外周和中枢受体、神经元以及负责节律发生的球桥区呼吸中枢之间的相互作用。 AOP 是这个流程不成熟的最佳单一指标。²先前已证明，呼吸暂停天数增加与较差的临床结果相关，包括神经发育异常，这可能与这些事件期间的间歇性缺氧发作和心动过缓有关。

甲基黄嘌呤和无创呼吸支持一直是 AOP 治疗的支柱。柠檬酸咖啡因是唯一经美国食品和药物管理局批准用于治疗 AOP 的药物。然而，尽管采取了这些干预措施，AOP 的严重程度仍可能发展到需要有创机械通气及其不良后果。在大多数情况下，除了补充氧气之外，感觉触觉刺激也可以终止发作。触觉刺激刺激呼吸的机制尚不清楚，但据推测，它是通过产生非特异性兴奋性神经元脉冲来实现的，这些非特异性兴奋性神经元脉冲导致呼吸刺激，同时激活脑干的网状结构，从而导致觉醒。³此外，事实证明，即使在睡眠期间，肢体运动也可以通过协调呼吸产生和运动的本体感觉传入来增加呼吸频率。⁴此外，机械刺激对呼吸中枢的影响取决于受刺激的神经。皮肤各处存在各种感觉受体，每种类型对不同程度的刺激做出反应，表明触觉刺激的位置和程度可以导致不同的反应。^5,6