Central apnea after adenotonsillectomy in childhood: case report

Abstract

Obstructive sleep apnea syndrome (OSAS) during childhood has a prevalence of 2–4%, and its main underlying cause is hypertrophy of the upper airway lymphoid tissues [1–3]. In children, central apnea (CA) may be part of OSAS or may occur as a physiological event of wake–sleep transition or REM sleep. However, although CA is considered to be common in healthy children, several authors have detected CA indices generally <1/h even when different criteria are used for the definition of the events [4–7]. The preponderance of CA in the context of OSAS should suggest secondary causes. CA presenting as a periodic breathing pattern is observed at a certain frequency only in premature babies or among children at high altitude. In older children, unless it occurs as a brief phenomenon at the beginning of sleep, a more expressive periodic breathing pattern may be associated with anomalies of the central nervous system [8]. Children with OSAS appear to have a higher central apnea index (CAI) than healthy children. A proposed underlying mechanism is a possible inhibitory action of mechanoceptors of the upper airways on the respiratory center causing CA in the presence of a pharyngeal collapse and obstruction [9]. Another possible mechanism regarding post-movement CA is that these events could be favored by a larger number of arousals induced by obstructive respiratory events [10]. More recently, a new entity called complex apnea syndrome (CAS) was described in adult patients with OSAS after treatment with a positive airway pressure (PAP) device, as the resolution of obstructive apneas is followed by the emergence of central ones [11–17]. CAS can represent a polysomnographic pattern that occurs due to different underlying mechanisms. These mechanisms are believed to involve PAP-dependent aspects like the lung stretch reflex and reduction of the anatomical dead space. Also, PAPindependent mechanisms, such as a possible increment of ventilation due to increased chemosensitivity that could develop over time of recurrent exposure to apnea and hypoxia, might also take part in these events. With increased ventilatory gain, small oscillations of CO2 could generate an over-compensatory response, leading to CA events. Sleep may uncover a high latent chemosensitivity as ventilation becomes more dependent on gas variations and is less modulated by the wakefulness ventilatory drive. Microarousals, while leading to a decreased CO2 tension, could be a trigger for CA. Although this mechanism is present under physiological conditions, only non-repetitive CA events are considered normal. A large number of CA can occur during L. A. de Almeida :A. L. Eckeli :H. H. Sander : R. M. F. Fernandes Department of Neuroscience and Behavioral Sciences— Neurology Division, Ribeirao Preto School of Medicine, University of Sao Paulo, Ribeirao Preto, SP, Brazil