Symptoms of sleep-disordered breathing, such as snoring, flow limitation and apnoeas are thought to be more common during pregnancy.  However, there are little data on the foetal outcomes of polysomnographically confirmed obstructive sleep apnoea (OSA) in pregnancy.

 The objective our research was to determine whether OSA during pregnancy is associated with i) acute foetal compromise, as evidenced by foetal heart rate decelerations on continuous foetal cardiotocography during periods of maternal upper airway obstruction and hypoxia; and ii) chronic foetal compromise, as evidenced by a fall in foetal growth trajectory on serial third trimester ultrasound examinations, altered cord blood levels of foetal growth regulators, and birth outcomes.

 Preliminary questionnaires were used to identify women as potential OSA cases and controls.  Late in the third trimester, a sleep study with synchronised foetal heart rate monitoring was performed. Cord blood was collected at delivery and analysed for foetal growth markers.  Foetal growth trajectory across the third trimester was determined by performing serial ultrasound examinations. 

 Forty-one women completed the study, ten of whom had confirmed OSA (apnoea hypopnoea index ≥ 5/hr).

Acute compromise: one case of an abnormal CTG occurred in a woman with OSA and a growth-restricted foetus.  In most women, no foetal heart rate abnormalities were detected, despite moderate OSA associated with significant maternal oxygen desaturation.

Chronic compromise: Among women with OSA, 50% were found to have impaired foetal growth, compared with 19% of controls (p = .07).  In addition, insulin growth factor-I (IGF-I), a key endocrine regulator of foetal growth, was significantly decreased in infants of mothers with OSA compared to BMI-matched controls (p = .03).  A corresponding increase in the insulin like growth factor binding proteins 1 and 2 (IGF-BP1 and IGF-BP2) was also observed (IGF-BP1 – p = .004; IGF-BP2 – p = .06).  In terms of birth outcomes, gestation was significantly reduced in mothers with OSA (M = 38.5 ± 0.9 weeks) compared to the control group (M = 39.4 ± 1.3 weeks, p = .048).  However, infants of mothers with OSA did not differ from the controls on customised birth weight centile (44.2% ± 31.4% vs. 54.1% ± 28.7%, p = .36) and Apgar scores at both 1 minute (8.4 ± 0.8 vs. 8.3 ± 1.3, p = .88) and 5 minutes (9.1 ± 0.3 vs. 9.0 ± 0.9, p = .81).

 We concluded that sleep-disordered breathing during pregnancy may be associated with acute and chronic foetal compromise, even in otherwise uncomplicated pregnancies.  If a link between OSA and increased foetal risk can be established, effective treatment of OSA with continuous positive airway pressure (CPAP) may be able to attenuate adverse perinatal outcomes and is the focus of our ongoing research.