Sleep-disordered breathing during pregnancy is a risk factor for development of hypertensive disorders and gestational diabetes mellitus.
Sleep-disordered breathing (SDB) is a group of disorders characterized by abnormalities in ventilation and respiration. The spectrum ranges from snoring that is considered mild to the most severe form, obstructive sleep apnea (OSA).1 In the obstetric literature, the terms SDB and sleep apnea have been used interchangeably. OSA involves repetitive partial or complete pharyngeal collapse while sleeping, resulting in either apnea or hypopnea.2 These recurrent nocturnal hypoxic events result in arousal from sleep, sleep fragmentation and excessive daytime sleepiness.2-4 In this article we will review what is known about OSA, the associated morbidity and pregnancy management in affected pregnant women.
In the largest prospective study published to date, among the 3,132 nulliparous women who completed objective testing for sleep apnea, prevalence of sleep apnea was estimated to be 3.6% in early pregnancy and increased across gestation with rates as high as 26% in the third trimester. That study confirmed the findings of Pien, et al, who found an increase from 10.5% in the first trimester to 26.7% in the third trimester among a group of women who underwent overnight polysomnography at 2 time points in pregnancy.5
Risk factors for OSA in the general population are well-established and include obesity, older age, African-American race, craniofacial abnormalities, and smoking.6,7 Sleep apnea is associated with Type II diabetes, hypertension and cardiovascular disease.2 Women who have those risk factors before pregnancy may be at risk for sleep apnea. Existing small studies in pregnancy also demonstrate that increasing maternal age, obesity, chronic hypertension, and frequent snoring (> 3x/week) are risk factors for the condition.8-10
Screening for OSA in pregnancy presents a unique challenge. The Berlin questionnaire, Epworth Sleepiness Scale and STOP-BANG questionnaires developed and validated in the general population have not been demonstrated to be useful in the obstetric population, with reported sensitivities and specificities of 36% to 39% and 68% to 77%, respectively. 11-15
The gold standard for diagnosis of sleep apnea is overnight polysomnography.4 However, the test is uncomfortable due to the use of many electrical leads and expensive and inconvenient because of the requirement for the patient to be away from home. Home sleep apnea testing using a portable sleep device presents a more comfortable, affordable and convenient alternative, and it is being used increasingly (Figure 1).4 While home sleep testing is widely accepted, there are limitations, including potential underestimation of sleep apnea severity, which can result in false-negative results.4 If a patient has had a negative home sleep test, and significant clinical suspicion remains, it is recommended that she undergo overnight polysomnography.4
Sleep apnea severity is scored based on the Apnea Hypopnea Index (AHI), a measure of how many apneas (cessation of airflow ≥ 10 seconds accompanied by an arousal or oxyhemoglobin desaturation) and hypopneas (reduction of airflow ≥ 10 seconds accompanied by an arousal or oxyhemoglobin desaturation) are present per hour of sleep. An AHI of 5 to less than 15 is considered mild, 15 to less than 30 is considered moderate, and 30 or greater is considered severe. OSA is defined as having an AHI of 5 or greater with evidence of daytime sleepiness.16
Continuous positive airway pressure (CPAP) is the treatment of choice for mild, moderate, and severe OSA.17 More than 15 randomized clinical trials have demonstrated that treatment of OSA reduces the risks of hypertension, cardiovascular morbidities, and motor vehicle crashes.18-21 Customized oral mandibular repositioning devices are noninvasive and keep the airway open by pulling the lower jaw forward. While they can be an effective treatment for mild to moderate OSA for individuals with good dentition, they are only recommended if a patient cannot tolerate CPAP or desires alternative therapy. However, when it comes to pregnancy, there are few data to direct management. Small studies examined CPAP and used short-term intermediary outcomes, such as maternal blood pressure.22-24 However, with such small sample sizes, they were insufficiently powered to detect an impact of treatment. Therefore, despite the demonstrated increased risk of adverse pregnancy outcomes associated with OSA, we do not have any studies to date that adequately evaluate treatment during pregnancy to show improvement in maternal or neonatal outcome. However, the accepted standard is to offer treatment because there is benefit in the general population.17
The Sleep Disordered Breathing Substudy of the Nulliparous Pregnancy Outcomes Study was a multicenter, prospective cohort study designed to estimate whether SDB during pregnancy is a risk factor for development of hypertensive disorders of pregnancy and gestational diabetes mellitus (GDM). In early and mid-pregnancy, the adjusted odds ratio for preeclampsia when SDB was present was 1.94 (95% CI 1.07–3.51) and 1.95 (95% CI 1.18–3.23), and for GDM was 3.47 (95% CI 1.95–6.19) and 2.79 (95% CI 1.63–4.77). These results support findings from prior smaller cross-sectional and observational studies.10,25-28 Even after controlling for obesity, OSA is also associated with an increased risk of cardiomyopathy (OR, 9.0; 95% CI, 7.5-10.9), pulmonary embolism (OR, 4.5; 95% CI, 2.3-8.9) and in-hospital mortality (OR 5.1 95% CI, 2.4-11.5).29
The adverse fetal and neonatal consequences of sleep apnea in pregnancy are less well delineated. Maternal OSA is associated with a 1.5- to 2-fold increased frequency of low birth weight and small-for-gestational-age infants, both in high-risk women and in an otherwise healthy non-obese cohort.10,30,31 These infants are also more likely to have preterm delivery and neonatal intensive care unit admission (despite similar gestational age at delivery).9 One study following 74 mom-baby pairs 24% of which had OSA noted no difference in general motor scores but an increased frequency of low social development scores in neonates of moms with OSA ( 64% vs. 25%, P = .036 ) at age 12 months.32 There are no studies that indicate an increased risk of fetal death or miscarriage in association with sleep apnea.
Management of OSA in pregnant women should continue through the postpartum period and should be multidisciplinary (Table 1). Women with known OSA who become pregnant should be evaluated by a sleep medicine specialist. Goals of the visit should include optimization of CPAP settings to help a patient achieve a normalized AHI and oxygenation. Obstetric providers should be acutely aware of the risk of hypertensive disorders and diabetes. Management should focus on early detection or prevention of these conditions.
Women who are undiagnosed but suspected of having OSA should be referred to a sleep medicine specialist for evaluation. Situations where a suspicion of sleep apnea may arise include, but are not limited to, maternal symptoms of excessive daytime sleepiness, witnessed apneas, or observed maternal hypoxia in the absence of cardiorespiratory pathology. A sleep medicine provider can evaluate the patient and make recommendations regarding diagnosis and management throughout pregnancy and in the postpartum period. In the absence of pregnancy-specific data to direct treatment, we suggest treatment for all women with OSA. An individualized plan can be developed with the sleep medicine provider.
Women with OSA are also more likely to have comorbid conditions that predispose them to cesarean deliveries.9 The described perioperative risks include the need for conversion to general anesthesia and difficult airway intubation. A preoperative airway assessment and early evaluation by anesthesiology for placement of regional anesthesia and pain algorithms that maximize the use of nonopioid medications may be beneficial for these women.33,34 There are no clear guidelines for postpartum management. Because of risk of postoperative respiratory suppression, it is recommended that patients at increased risk of respiratory compromise from OSA have continuous pulse oximetry monitoring after discharge from the recovery room and that it be maintained as long as the patients remain at increased risk.35 If frequent or severe airway obstruction or hypoxemia develop during the monitoring period, CPAP or noninvasive positive pressure ventilation should be considered.35
During the postpartum period, all women diagnosed with or suspected of having OSA should be managed in a way similar to the general population.17 The American Academy of Sleep Medicine suggests that they be evaluated by a sleep medicine provider to allow for reassessment of OSA severity and overall management/treatment strategy.17 Weight loss and bariatric surgery are important tools for treatment of sleep apnea in obese women.
In conclusion, obstructive sleep apnea in pregnancy is a prevalent and under-recognized disorder that carries implications for both mother and fetus. Increased awareness with appropriate diagnosis, treatment, and perioperative management could improve outcomes in these pregnancies. <
Disclosures The authors report no potential conflicts of interest with regard to this article.
1. Chervin RD, Guilleminault C. Obstructive sleep apnea and related disorders. Neurologic clinics. 1996;14(3):583-609.
2. Jordan AS, McSharry DG, Malhotra A. Adult obstructive sleep apnoea. Lancet. 2014;383(9918):736-747.
3. Alam I, Lewis K, Stephens JW, Baxter JN. Obesity, metabolic syndrome and sleep apnoea: all pro-inflammatory states. Obesity reviews : an official journal of the International Association for the Study of Obesity. 2007;8(2):119-127.
4. Kapur VK, Auckley DH, Chowdhuri S, et al. Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: An American Academy of Sleep Medicine Clinical Practice Guideline. Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2017;13(3):479-504.
5. Pien GW, Pack AI, Jackson N, Maislin G, Macones GA, Schwab RJ. Risk factors for sleep-disordered breathing in pregnancy. Thorax. 2014;69(4):371-377.
6. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. American journal of respiratory and critical care medicine. 2002;165(9):1217-1239.
7. Punjabi NM. The epidemiology of adult obstructive sleep apnea. Proceedings of the American Thoracic Society. 2008;5(2):136-143.
8. Facco FL, Ouyang DW, Zee PC, Grobman WA. Development of a pregnancy-specific screening tool for sleep apnea. Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2012;8(4):389-394.
9. Louis J, Auckley D, Miladinovic B, et al. Perinatal outcomes associated with obstructive sleep apnea in obese pregnant women. Obstet Gynecol. 2012;120(5):1085-1092.
10. Pamidi S, Pinto LM, Marc I, Benedetti A, Schwartzman K, Kimoff RJ. Maternal sleep-disordered breathing and adverse pregnancy outcomes: a systematic review and metaanalysis. Am J Obstet Gynecol. 2014;210(1):52.e51-52.e14.
11. Netzer NC, Stoohs RA, Netzer CM, Clark K, Strohl KP. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Annals of internal medicine. 1999;131(7):485-491.
12. Lockhart EM, Ben Abdallah A, Tuuli MG, Leighton BL. Obstructive Sleep Apnea in Pregnancy: Assessment of Current Screening Tools. Obstetrics & Gynecology. 2015;126(1):93-102.
13. Chung F, Subramanyam R, Liao P, Sasaki E, Shapiro C, Sun Y. High STOP-Bang score indicates a high probability of obstructive sleep apnoea. British journal of anaesthesia. 2012;108(5):768-775.
14. Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991;14(6):540-545.
15. Johns MW. Reliability and factor analysis of the Epworth Sleepiness Scale. Sleep. 1992;15(4):376-381.
16. Berry RB, Brooks R, Gamaldo CE, Harding SM, Marcus C, Vaughn B. The AASM manual for the scoring of sleep and associated events. Rules, Terminology and Technical Specifications, Darien, Illinois, American Academy of Sleep Medicine. 2012.
17. Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep M. Clinical Guideline for the Evaluation, Management and Long-term Care of Obstructive Sleep Apnea in Adults. Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2009;5(3):263-276.
18. Buchner NJ, Sanner BM, Borgel J, Rump LC. Continuous positive airway pressure treatment of mild to moderate obstructive sleep apnea reduces cardiovascular risk. American journal of respiratory and critical care medicine. 2007;176(12):1274-1280.
19. Haentjens P, Van Meerhaeghe A, Moscariello A, et al. The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials. Archives of internal medicine. 2007;167(8):757-764.
20. Tregear S, Reston J, Schoelles K, Phillips B. Continuous positive airway pressure reduces risk of motor vehicle crash among drivers with obstructive sleep apnea: systematic review and meta-analysis. Sleep. 2010;33(10):1373-1380.
21. MEHRA R. Sleep apnea ABCs: Airway, breathing, circulation. Cleveland Clinic Journal of Medicine. 2014;81(8):479-489.
22. Blyton DM, Sullivan CE, Edwards N. Reduced nocturnal cardiac output associated with preeclampsia is minimized with the use of nocturnal nasal CPAP. Sleep. 2004;27(1):79-84.
23. Guilleminault C, Palombini L, Poyares D, Takaoka S, Huynh NT-L, El-Sayed Y. Pre-eclampsia and nasal CPAP: part 1. Early intervention with nasal CPAP in pregnant women with risk-factors for pre-eclampsia: preliminary findings. Sleep medicine. 2007;9(1):9-14.
24. Poyares D, Guilleminault C, Hachul H, et al. Pre-eclampsia and nasal CPAP: part 2. Hypertension during pregnancy, chronic snoring, and early nasal CPAP intervention. Sleep medicine. 2007;9(1):15-21.
25. Facco FL, Ouyang DW, Zee PC, Grobman WA. Sleep disordered breathing in a high-risk cohort prevalence and severity across pregnancy. American journal of perinatology. 2014;31(10):899-904.
26. Salihu HM, King L, Patel P, et al. Association between maternal symptoms of sleep disordered breathing and fetal telomere length. Sleep. 2015;38(4):559-566.
27. Luque-Fernandez MA, Bain PA, Gelaye B, Redline S, Williams MA. Sleep-disordered breathing and gestational diabetes mellitus: a meta-analysis of 9,795 participants enrolled in epidemiological observational studies. Diabetes care. 2013;36(10):3353-3360.
28. Facco FL, Parker CB, Reddy UM, et al. Association Between Sleep-Disordered Breathing and Hypertensive Disorders of Pregnancy and Gestational Diabetes Mellitus. Obstet Gynecol. 2017;129(1):31-41.
29. Louis JM, Mogos MF, Salemi JL, Redline S, Salihu HM. Obstructive sleep apnea and severe maternal-infant morbidity/mortality in the United States, 1998-2009. Sleep. 2014;37(5):843.
30. Pamidi S, Marc I, Simoneau G, et al. Maternal sleep-disordered breathing and the risk of delivering small for gestational age infants: a prospective cohort study. Thorax. 2016;71(8):719-725.
31. Ding X-X, Wu Y-L, Xu S-J, et al. A systematic review and quantitative assessment of sleep-disordered breathing during pregnancy and perinatal outcomes. Sleep and Breathing. 2014;18(4):703-713.
32. Tauman R, Zuk L, Uliel-Sibony S, et al. The effect of maternal sleep-disordered breathing on the infant’s neurodevelopment. American Journal of Obstetrics and Gynecology. 2015;212(5):656.e651-656.e657.
33. Saravanakumar K, Rao SG, Cooper GM. Obesity and obstetric anaesthesia. Anaesthesia. 2006;61(1):36-48.
34. Munnur U, de Boisblanc B, Suresh MS. Airway problems in pregnancy. Critical care medicine. 2005;33(10 Suppl):S259-268.
35. Chung F, Memtsoudis SG, Ramachandran SK, et al. Society of anesthesia and sleep medicine guidelines on preoperative screening and assessment of adult patients with obstructive sleep apnea. Anesthesia and analgesia. 2016;123(2):452.