While control of breathing and sleep state maturation becomes more normal as preterm infants approach term postconceptual ages, there is some evidence for residual effects of prematurity. Two early cross-sectional studies in late preterm infants demonstrated minor increases in the number of short (2–15 s) central pauses in former late preterm infants [11], and shorter but similar numbers of pauses in preterm compared to term infants [12]. Neither study reported an increase in the number of prolonged apneas or apneas that resulted in significant cardiorespiratory consequences. Both of these studies assessed breathing during sleep only at a single time point.

Albani et al. prospectively studied a small group (n = 12, 50 % male) of late preterm (mean gestational age 35 weeks, range 32.2–36.6) infants and term (n = 21, 48 % male) infants with sequential polysomnograms (PSGs) at 40, 52, and 64 postconceptual weeks to characterize the number, duration, and character (obstructive, central, mixed) of apneas [13]. All infants in both groups were apparently healthy, and did not have evidence of apnea of prematurity requiring pharmacological treatment, bronchopulmomary dysplasia or other pulmonary disease, or intracranial hemorrhage. Apnea was defined as a pause of 3 s or greater, and classified as central if no respiratory effort was recorded, obstructive if respiratory effort was recorded, and mixed if both patterns were present in either order. Apnea density (number per unit time), duration, character, and the presence of periodic breathing were measured. Compared to term infants, preterm infants had significantly increased density of apneas at the 40-week recording (126 vs. 49 per 100 min recording, p < 0.05). Most of the observed differences were attributable to a higher density of obstructive/mixed apneas in NREM/quiet sleep among the preterm infants. At the 52-week postconceptual age recording, term infants had higher apnea density overall (50 vs. 20 per 100 min, p < 0.05), driven largely by findings in REM sleep, and there were no differences at 64 weeks postconceptual age in apnea density or type. Apneas in both groups were very rare during the final recording. The majority of preterm infants demonstrated periodic breathing at 40 weeks (75 % vs. 42 % term, p < 0.05), primarily during NREM sleep. Periodic breathing was rare in both groups during subsequent recordings. Somewhat surprisingly, two of the preterm infants died during the study; both deaths were attributed to sudden infant death syndrome (SIDS), one at 44 weeks after one PSG and one at 56 weeks after two PSGs. The infant who died at 44 weeks was described as having more frequent and longer apneas (obstructive and mixed) and more periodic breathing than the other preterm and term infants. The second infant was similar to preterm peers. This study, although small, suggests that variations in breathing during sleep in preterm infants in the immediate postnatal period largely resolve shortly after postconceptual term ages are reached in healthy late preterm infants. These findings cannot be extrapolated to children born extremely prematurely or with significant lung disease, and are limited by the very small sample size. Research studies also have shown that the presence and severity of bronchopulmonary dysplasia (BPD) may be associated with the severity of alterations in control of ventilation [14, 15]; therefore, BPD may influence propensity for persistent sleep-related breathing disturbances in preterm infants.

SIDS is defined as the unexplained death of a child during sleep before 1 year of age. While the precise pathophysiology and etiology of SIDS remain elusive, and is likely multifactorial, it is thought to be a disorder of respiratory control and arousal. Infants born prematurely are at increased risk for SIDS. Early descriptions of the relationship between preterm birth and SIDS suggested that rates rise substantially with increasing prematurity (1.06 deaths/1000 live births at term vs. 3.52 deaths/1000 live births at 24–28 weeks gestation) and that the peak age at death was 4–6 weeks earlier in preterm children [16]. Despite a decrease in overall rates of SIDS with the “Back to Sleep” campaign, preterm birth remains a risk factor for SIDS. In one population-based case-control study in five regions in England, preterm birth (<37 weeks gestation) was associated with a 3.44 (2.47–4.79) increased odds of SIDS, although this relationship was attenuated and no longer significant after multivariate adjustment [17]. Other studies, however, have found higher rates of SIDS in children born preterm in multivariate analyses that include adjustment for maternal smoking, markers of socioeconomic status, and race, including a study of linked US birth and death records from 1996 to 1998 [18]. In this study, adjusted odds ratios for SIDS in children born preterm compared with those born at 40–41 weeks gestation ranged from 1.52 (1.42–1.63) for children born at 36–37 weeks gestation to 2.88 (2.57–3.23) for children born at 28–32 weeks gestation. Halloran and colleagues also found that the postnatal age at death was slightly later in preterm infants than term infants (16 vs. 12 weeks), with a second peak at approximately 28 weeks in those born extremely prematurely (22–27 weeks gestation), although postconceptional age at death was earlier in preterm infants [18]. Similar to the findings by Malloy and Hoffman [16], when analyzed by postconceptional age, very preterm infants died, on average, more than 6 weeks earlier than term infants (46 vs. 54 weeks postconceptual age). The increased prevalence of SIDS in children who were born prematurely suggests that there are sustained abnormalities in respiratory control in some cases, although non respiratory (cardiac) differences may also play a role. Instability of central chemoreception, responses to carbon dioxide and hypoxia, and the impact of early chronic intermittent hypoxemia on the autonomic nervous system have all been implicated (reviewed in [4, 19]). Shared risk factors for prematurity and SIDS (maternal inflammation, nicotine exposure) have also been suggested to explain the association [19].

SDB is a term that broadly describes abnormal breathing and/or gas exchange during sleep, and encompasses a spectrum of severity from primary snoring to upper airway resistance syndrome (UARS) to obstructive sleep apnea syndrome (OSAS). Untreated SDB is associated with behavioral and neurocognitive effects across its spectrum [20], and metabolic and cardiovascular effects in its more severe form [21]. The prevalence of snoring, as reported by caregivers, is highly variable depending on the definition used, but a meta-analysis of studies that included over 95,000 children (0–19 years of age) worldwide found the prevalence to be 7.45 % (95 % CI 5.75–9.61 %) [22]. Most studies suggest an OSAS prevalence of 4–11 % using questionnaires and 1–4 % using PSG in otherwise healthy children [22], with a peak prevalence occurring between ages 2 and 6 years. A second increase in prevalence is likely in adolescence, associated with obesity. Many studies have demonstrated prematurity to be a risk factor for obstructive sleep-disordered breathing during childhood [23–25]. However, these associations vary by age group. A longitudinal birth cohort showed that the association between SDB and prematurity was present in early childhood, but not during adolescence, when obesity emerged as a strong risk factor [26].

The pathophysiology of OSAS is complex, and reviewed in detail elsewhere [27]. While the defining feature is the partial or complete collapse of the upper airway during sleep, there are multiple factors that likely contribute to upper airway obstruction, including soft-tissue hypertrophy (adenoids, tonsils, airway fat deposition), skeletal craniofacial features, pharyngeal and laryngeal tone, lower respiratory tract neuromuscular tone, arousal threshold, and control of breathing [27, 28]. Gas exchange abnormalities due to lower respiratory tract disease, upper airway inflammation due to gastroesophageal reflux, or swallowing disorders may influence the development or presentation of OSAS. Premature birth may influence several of these factors, most notably ventilatory control, airway tone, craniofacial growth, lower airway disease, and increased risk for obesity in some premature populations. As these influences seem to change with age, we will discuss the relationship between prematurity and SDB by age category. When possible, differences in children with and without BPD will be discussed.