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Obstructive sleep apnea in pregnancy

Obstructive sleep apnea in pregnancy
Literature review current through: Jan 2024.
This topic last updated: Dec 19, 2023.

INTRODUCTION — Obstructive sleep apnea (OSA) refers to apneas and hypopneas (absent or severely reduced airflow, respectively) that occur during sleep despite respiratory effort. Central sleep apnea (CSA) is defined by episodes of cessation of airflow due to absent breathing effort. Collectively, OSA and CSA are referred to as sleep-disordered breathing (SDB).

While the diagnosis and management of OSA are similar in pregnant and nonpregnant patients, some aspects are unique to pregnancy. This topic will focus on these unique details. Discussions regarding the diagnosis and management of OSA and CSA in nonpregnant patients are reviewed separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults" and "Obstructive sleep apnea: Overview of management in adults" and "Central sleep apnea: Risk factors, clinical presentation, and diagnosis" and "Central sleep apnea: Treatment".)

PREVALENCE — The prevalence of objectively determined OSA in pregnant patients is poorly studied. Rates range from 3 to 27 percent and vary depending on gestational age and method used to diagnose OSA [1,2]. Rates may be higher than those reported in the nonpregnant population of reproductive-age females, where the prevalence of OSA has been estimated to be 0.7 to 6.5 percent [3-6].

In one prospective study of 105 pregnant patients who underwent polysomnography, the prevalence of OSA (defined as apnea-hypopnea index [AHI] ≥5 events/hour of sleep) was 10.5 percent in the first trimester and rose to 26.7 percent in the third trimester [1]. Among the 28 patients with OSA in the third trimester, the disorder was mild (AHI 5 to 14) in 23 patients, moderate (AHI 15 to 29) in 4 patients, and severe (AHI ≥30) in 1 patient.

In the largest cohort study to date that included over 3300 patients (with a substantive proportion of Black and Hispanic females) undergoing level 3 home sleep apnea testing, the prevalence of gestational OSA in early pregnancy (between 6 and 15 weeks of gestation) and mid-pregnancy (between 22 and 31 weeks of gestation) was 3.6 and 8.3 percent, respectively [2].

In a prospective cohort study including 100 pregnant patients between 10 to 20 weeks gestation undergoing screening with home sleep apnea testing, patients with chronic hypertension had higher rates of OSA compared with controls matched for body mass index (BMI; 64 versus 38 percent, odds ratio [OR] 2.9, 95%CI 1.3–6.7) [7]. After controlling for age, prevalence of OSA was also higher in patients >25 years with chronic hypertension (OR 2.6, 95% CI 1.1–6.7).

PATHOGENESIS — In addition to pathogenetic factors that contribute to the development of OSA in nonpregnant patients (see "Pathophysiology of upper airway obstruction in obstructive sleep apnea in adults"), numerous hormonal and physiologic changes occur in pregnancy which may also contribute to the development and severity of OSA in pregnant patients, including the following:

Narrow oropharynx – Oropharyngeal diameter appears to narrow and the Mallampati score increases as pregnancy progresses [8,9]. Although the role of airway narrowing in OSA has not been studied in pregnancy, there is a link between OSA and smaller internal size of the airway in the general population. (See "Approach to the difficult airway in adults for emergency medicine and critical care", section on 'M: Mallampati score'.)

In healthy nonpregnant individuals, studies have shown that fluid displacement from the legs into the neck reduces upper airway size and increases upper airway collapsibility [10,11]. Fluid shifts induced by prolonged sitting and recumbency have been strongly related to the degree of OSA [12], although other data have found that such rostral fluid shifts do not increase the frequency of obstructed breathing events [13]. Given that maternal blood volume increases, on average, 40 to 45 percent during pregnancy above nonpregnant levels [14], recumbency has the potential to adversely affect upper airway function and possibly contribute to OSA.

Reduced nasal patency – Nasal patency is reduced during pregnancy secondary to hyperemia and edema of the nasal mucosa [15]. Changes in the nasal mucosa may be due to increased blood flow and variations in circulating levels of estrogen and progesterone. Increased nasal congestion may lead to increased upper airway resistance and more negative intra-pharyngeal pressure with inspiration, in turn predisposing patients in late pregnancy to airway narrowing, and possibly snoring and obstructed breathing during sleep.

Hormonal changes – Increase in progesterone levels during pregnancy leads to increased tidal volume and results in increased minute ventilation [16], either due to direct effects on respiratory drive or enhanced sensitivity of the brain's respiratory center to carbon dioxide [17]. Increased ventilatory drive during pregnancy may enhance loop gain (the ratio of a corrective ventilatory response to a disturbance); if the response exceeds the disturbance (ie, loop gain >1), then self-sustaining periodic breathing with central apneas may result. Alternatively, lower progesterone levels have been observed in pregnant patients with OSA compared with patients without OSA, suggesting that progesterone may play a protective role against OSA [18]. (See "Treatment-emergent central sleep apnea", section on 'Pathogenesis'.)

CLINICAL MANIFESTATIONS — The clinical manifestations of OSA are similar in pregnant and nonpregnant patients (table 1) and are described in detail separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)

However, some features overlap with those of normal pregnancy. For example, sleepiness is widely reported by pregnant patients, especially during the first trimester. Pregnancy-related causes of maternal awakening and arousal include fetal movement, urination urge, nocturnal dyspepsia, and leg cramps. All of these symptoms are common in late pregnancy and contribute to sleep fragmentation [3,19]. Thus, what is considered "normal" versus "abnormal" sleepiness in this population is not clear.

DIAGNOSTIC EVALUATION

Differential diagnosis — The differential diagnosis of OSA in pregnancy is similar to that in nonpregnant patients; many of these symptoms (eg, excessive daytime sleepiness, gastroesophageal reflux disease) are also common in normal pregnancy. The differential diagnosis of daytime sleepiness and OSA are provided separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Differential diagnosis' and "Approach to the patient with excessive daytime sleepiness".)

When to suspect OSA — We maintain a high level of clinical suspicion for OSA in pregnant patients. When suspected, we refer the patient to a sleep specialist for evaluation. Data suggest that clinicians perform poorly when evaluating pregnant patients for OSA. In one cross-sectional survey, only 5 percent of patients were asked about snoring by their provider at a prenatal visit; of these patients, 32 percent reported snoring [20].

It is prudent during at least one prenatal visit that such patients be asked about the quality, quantity, and nature of their sleep. In our practice, the following factors raise the suspicion for OSA and prompt further evaluation by a sleep specialist [1,21-24]:

Symptoms or signs suggestive of OSA (table 1), particularly, habitual loud snoring, apneic symptoms (eg, choking or gasping that wake patients from sleep), apneas witnessed by a bed partner or roommate, symptoms of excessive daytime sleepiness (eg, drowsy driving), obesity, excessive gestational weight gain, narrow oropharynx, and large neck circumference (table 1 and table 2). (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Clinical features'.)

Frequent snoring (self-reported snoring ≥3 days per week).

Risk factors for OSA (eg, older age [eg, >35 years], increased body mass index [BMI], chronic hypertension, obesity-related comorbid conditions). These are discussed in detail separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Risk factors and associated conditions'.)

Data that support these risk factors for OSA in pregnant patients are limited.

In one study of nulliparous pregnant patients, logistic regression modeling found that older age, higher BMI, and frequent snoring achieved good prediction of prevalent and incident sleep-disordered breathing (SDB; sensitivity 46 to 61 percent, specificity 90 percent) [25].

Another model utilizing BMI, age, and presence of tongue enlargement (BATE) had a sensitivity of 76 to 79 percent with 82 percent specificity and was particularly accurate in Black patients [26].

In a prospective study including 72 pregnant patients undergoing two level-3 sleep studies performed between 12 to 22 weeks and 32 to 38 weeks of gestation, those with class III obesity compared with those without obesity had higher rates of OSA (38 and 50 percent versus 3 and 9 percent, respectively) [23]. Age was also an independent risk factor.

In our practice, we do not use screening questionnaires (eg, STOP-Bang, Berlin) to evaluate pregnant patients for OSA. While screening questionnaires are inexpensive and easy to administer, they are poorly predictive in the nonpregnant population, and their weaknesses may be even more prominent in pregnant patients [24,27-31]. In a prospective study including 288 pregnant patients evaluated with six OSA screening tools (Berlin, American Society of Anesthesiologists checklist, STOP, STOP-BANG, Flemons Index, and Epworth Sleepiness Scale), the overall predictive ability of the screening tools for OSA was only modest [28]. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Screening questionnaires'.)

Objective testing (home or in-laboratory) — For most pregnant patients in whom we suspect OSA, we prefer full-night, attended, in-laboratory polysomnography (PSG), which is the diagnostic gold standard for OSA. However, similar to nonpregnant patients, for patients in whom uncomplicated OSA is suspected (ie, absence of other conditions (table 3) that can affect breathing during sleep) and in whom the pretest probability is estimated as moderate or severe, unattended home sleep apnea testing (HSAT) with a type 3 device is a reasonable alternative to in-laboratory PSG. (See "Home sleep apnea testing for obstructive sleep apnea in adults", section on 'Type 3 devices (portable devices)'.)

In our practice, we also typically use HSAT to evaluate pregnant patients for OSA when PSG is not initially approved due to insurance restrictions or declined by the patient. If home testing does not demonstrate OSA but clinical suspicion remains high or comorbidities exist that may result in SDB, we generally pursue PSG. Indications for HSAT and PSG in nonpregnant patients are provided in the table (table 4) and details that inform this choice are also provided separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults" and "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Selecting home or in-laboratory testing'.)

While guidelines from the American Academy of Sleep Medicine (AASM) recommend against the use of home sleep apnea testing for OSA diagnosis in patient groups with comorbidities, pregnancy is not specified as a contraindication [32]. Similarly, the AASM recommends that HSAT be used only in populations with substantive data on sensitivity and specificity [33]. Although substantive data on the value of HSAT in pregnancy are not available, limited data do suggest some value during pregnancy [34,35]. For example, in an observational study that demonstrated increased risk for adverse outcomes among patients with gestational OSA, HSAT was used to identify pregnant patients with OSA, suggesting that this methodology may be sufficiently sensitive to identify clinically significant cases of OSA in pregnant patients [36]. In a subsequent prospective study of 92 pregnant patients with suspected OSA, the apnea-hypopnea index (AHI) was similar when HSAT was compared with PSG (performed within the same week) [37]. Based on an AHI threshold of ≥5 events/hour, HSAT had a positive-predictive value of 85 percent and a negative-predictive value of 92 percent [37].

DIAGNOSIS AND CLASSIFICATION OF SEVERITY — The diagnostic criteria for OSA in pregnant patients are similar to those in nonpregnant patients. Patients who meet criteria are traditionally classified as having mild, moderate, or severe disease on the basis of the apnea-hypopnea index (AHI) and symptoms. However, while we typically use these criteria and classification system, there are no studies describing normative data in pregnant patients. Further details on diagnostic criteria and classification are provided separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnosis'.)

ANTEPARTUM MANAGEMENT — Our management strategy is based on our experience, indirect data from nonpregnant patients in whom efficacy is proven, and limited evidence that treatment during pregnancy impacts maternal or neonatal morbidity. In the absence of scientific evidence, clinicians have used their own protocols [38] or followed the published recommendations for treatment in the nonpregnant population [39-42].

Management of OSA — Patients who are pregnant and have OSA should be managed by a sleep medicine specialist. Most patients are managed in a similar fashion to those who are not pregnant. This includes patient education, behavior modification (eg, avoidance of sedatives and alcohol), and positive airway pressure (PAP), the latter of which is the mainstay of therapy for most patients with moderate to severe OSA. Behavior modification, indications for PAP (typically auto-adjusting PAP [APAP]), PAP titration modules, and target goals for PAP are discussed separately. (See "Obstructive sleep apnea: Overview of management in adults", section on 'General issues for all patients' and "Obstructive sleep apnea: Overview of management in adults", section on 'Positive airway pressure (PAP) therapy' and "Mode selection for titration of positive airway pressure in adults with obstructive sleep apnea" and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea".)

Pregnancy-specific management issues are discussed in the sections below.

Behavior modification — Recommendations for behavior modifications are similar to nonpregnant patients (eg, avoidance of sedatives and alcohol). However, the exception is weight loss. Weight loss, which has been demonstrated to improve comorbid conditions and decrease the overall apnea-hypopnea index (AHI), is not typically recommended in pregnancy due to the potential for harm (eg, increased risk of having a small for gestational age of the newborn). However, we encourage patients to achieve gestational weight gain at the lower limit of the range recommended by the Institute of Medicine, which, may benefit an individual's risk for pregnancy related morbidity from worsening OSA control. (See "Gestational weight gain", section on 'Recommendations for gestational weight gain'.)

The impact of incidental weight loss (eg, from hyperemesis gravidarum) on OSA control has not been studied.

Positive airway pressure — PAP therapy is the mainstay of OSA treatment. The following are pregnancy-specific issues that need to be considered when managing pregnant females with PAP for OSA.

Indications – Indications for PAP therapy are the same as for nonpregnant patients (ie, patients with moderate to severe OSA and patients with mild OSA who have select indications listed in the algorithm (algorithm 1)). However, for pregnant patients with mild OSA, in addition to all the usual indications for PAP therapy (eg, physiologic sequalae of OSA), we also use PAP therapy if the patient has recurrent oxyhemoglobin desaturations to <90 percent. The rationale is the potential for adverse effects of hypoxemia on the fetus. For patients with mild OSA who develop adverse outcomes associated with OSA (eg, hypertensive diseases of pregnancy including preeclampsia; gestational diabetes), a trial of CPAP therapy is also appropriate [43]. Indications in nonpregnant patients are discussed separately. (See "Obstructive sleep apnea: Overview of management in adults", section on 'Indications'.)

Modality selection – For patients with OSA who are pregnant and who need PAP therapy, we prefer to use APAP rather than fixed-level continuous PAP (CPAP). The rationale for this approach is that for some patients, OSA control may worsen over the course of pregnancy (eg, due to upper airway changes during pregnancy or weight gain) resulting in a higher pressure requirement [44]. Thus, the use of APAP avoids the need for a formal retitration study. When prescribing APAP, we use the results of the original PAP titration study (if performed) as a guide to the range of pressures to be prescribed.

Data to support this approach are limited. In one prospective study including 12 pregnant patients with sleep-disordered breathing (SDB), an increase in CPAP pressure of 1 to 2 cm H2O was required in half of the patients over the course of pregnancy [44].

Mode selection and titration modules for PAP therapy are described separately. (See "Mode selection for titration of positive airway pressure in adults with obstructive sleep apnea" and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Auto-titrating continuous positive airway pressure (APAP)'.)

Efficacy and safety – Data describing the efficacy of PAP in pregnant females are limited [43-45]. In general, PAP improves sleepiness, snoring, and fatigue, similar to that seen in the nonpregnant population.

However, the impact on other clinically relevant outcomes such as blood pressure control is unclear. In one prospective study including 11 pregnant patients with OSA and severe preeclampsia, APAP resulted in a reduction in mean nocturnal blood pressure [45], although, study limitations warrant cautious interpretation of this study.

Trials examining the effect of PAP therapy on outcomes including blood pressure and cardiovascular risk are in progress [46,47].

In our experience adverse effects are similar to those in the general population. Limited data suggest that the theoretical concern for decreased cardiac output due to the applied positive intrathoracic pressure from PAP therapy is not clinically important. In a randomized trial including 24 patients with severe preeclampsia, cardiac output but remained at baseline when the patients were treated with APAP but decreased during sleep (from 7.7 L/min to 5.7 L/min) in those who were not treated with APAP [48]. However, these data may not apply to pregnant patients with OSA who do not have preeclampsia. (See "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea", section on 'Side effect management'.)

Follow-up and adherence – Regardless of the selected modality, we follow-up patients within one to two weeks after initiation of PAP therapy and regularly thereafter (eg, every one to three months during pregnancy) so that adherence to and efficacy of PAP treatment can be assessed and adjusted as needed.

It is estimated that only 50 percent of all patients are adherent to PAP therapy. While rates of nonadherence have not been formally studied in pregnant patients, our experience suggest that it may be similar to the general population. Pregnant patients in our clinics often cite nasal congestion and lack of symptomatic improvement as reasons for nonadherence. The approach to nonadherence is discussed separately. (See "Obstructive sleep apnea: Overview of management in adults", section on 'Follow-up' and "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea".)

Treatments of limited benefit

Mandibular advancement devices — Customized oral mandibular advancement devices are noninvasive devices that keep the airway open by pulling the lower jaw forward. They can be used when PAP fails or is poorly tolerated or as first-line therapy in selected patients [49,50].

While they can be effective at improving OSA control in nonpregnant patients, only 35 to 40 percent of patients achieve a reduction in the degree of OSA to normal levels (ie, AHI <5 events/hour), and oxyhemoglobin saturation levels often do not return to normal [51]. The potential for fetal hypoxemia, the multiple fittings that can be needed to initiate oral appliance use, the time it takes to fabricate the device, and the potential need for frequent refitting due to gestational weight gain, make this treatment impractical for pregnant patients as initial therapy for OSA. However, when patients who are being treated successfully with an oral mandibular advancement device become pregnant, it is reasonable to continue using the device as long as OSA symptoms remain well-controlled. Recurrence of symptoms (eg, snoring, witnessed apneas) while using an oral device may indicate that the oral appliance needs to be further advanced or that switching to PAP therapy is needed. (See 'Positive airway pressure' above.)

No mandibular advancement device data exist in pregnant patients with OSA, but clinical trials are in progress. Data that support oral devices in the general population are described separately. (See "Oral appliances in the treatment of obstructive sleep apnea in adults".)

Surgery — Surgical treatments for mild to moderate OSA, such as uvulopalatopharyngoplasty, generally achieve a reduction in AHI to the normal range in less than half of nonpregnant patients with OSA [52]. However, in pregnant patients, given the relative lack of efficacy and the potential for adverse consequences associated with surgery and anesthesia (which are likely to be magnified during pregnancy), surgeries for OSA are generally not suitable approaches. The surgical treatment of OSA is discussed separately. (See "Surgical treatment of obstructive sleep apnea in adults".)

Treatments not used: Pharmacologic therapy — Wakefulness promoting agents (eg, modafinil) are sometimes used in nonpregnant patients with adequately-treated OSA who have persistent, burdensome daytime sleepiness and in whom alternative causes of daytime sleepiness have been excluded.

However, in pregnant patients, we advise against the use of wakefulness-promoting agents and we discontinue these agents if patients are already taking them prior to becoming pregnant. The rationale for this approach is that two wakefulness promoting agents (modafinil and armodafinil), have been shown to be associated with an increased risk of major congenital anomalies [53-55]. We also extend this recommendation to lactating individuals since limited data suggest that modafinil may be present in breast milk and the effects in infants are unknown [56]. The pregnancy and lactation risks of solriamfetol are unknown [57].

When these agents are discontinued, patients should be warned about increased sleepiness and should take appropriate precautions, such as when driving.

Use of these agents in nonpregnant patients with OSA and pregnant patients with narcolepsy are discussed separately. (See "Evaluation and management of residual excessive sleepiness in adults with obstructive sleep apnea" and "Treatment of narcolepsy in adults", section on 'Pregnancy and lactation'.)

Management of OSA-related pregnancy issues — As OSA is associated with increased maternal and fetal morbidity (see 'Maternal outcomes' below and 'Fetal outcomes' below), we perform the following in pregnant patients with OSA:

Monitor blood pressure and urine protein during routine prenatal care visits. (See "Prenatal care: Second and third trimesters", section on 'Routine ongoing assessments'.)

First- or early second-trimester testing for gestational diabetes with a glucose-tolerance test to detect asymptomatic diabetes. For those with an initially negative screen, we also perform repeat screening at 24 to 28 weeks gestation. (See "Gestational diabetes mellitus: Screening, diagnosis, and prevention", section on 'Screening for overt diabetes in early pregnancy'.)

Ultrasonography to estimate fetal weight every three to four weeks starting at 28 weeks gestation to detect fetal growth abnormalities. This management is similar to patients with chronic hypertension in pregnancy. (See "Chronic hypertension in pregnancy: Prenatal and postpartum care", section on 'Screening for fetal growth restriction'.)

Fetal surveillance (ie, nonstress test and amniotic fluid index, biophysical profile) as indicated for OSA-associated comorbid conditions. There are no data to support fetal surveillance solely for isolated sleep apnea.

INTRAPARTUM MANAGEMENT — Our approach to intrapartum management of patients with OSA is as follows:

We instruct patients who have been using positive airway pressure (PAP) devices or an oral appliance for OSA, to bring their devices when they present to the Labor and Delivery unit. The device is not needed while awake but is encouraged during sleep.

If not already consulted prenatally, we consult anesthesia early in the patient's labor. Early placement of regional anesthesia may prevent the need for general anesthesia if emergency cesarean birth becomes necessary. Regional anesthesia in this population may also avoid general anesthesia-associated maternal morbidity and mortality [58] and avoid the potential need for opioids to manage labor pain. (See 'Postpartum management' below and "Surgical risk and the preoperative evaluation and management of adults with obstructive sleep apnea".)

We continuously monitor oxygenation during labor with a pulse oximeter. If desaturation is observed (eg, <90 percent), we perform a comprehensive clinical evaluation to determine the etiology. This evaluation should focus on respiratory causes of hypoxemia and any potentially life-threatening causes (eg, pulmonary embolus, amniotic pulmonary embolism, aspiration, pneumothorax, cardiogenic pulmonary edema, cardiac arrythmia). (See "Evaluation and management of the nonventilated, hospitalized adult patient with acute hypoxemia".)

For patients who undergo cesarean birth, intrapartum management of OSA is similar to that in nonpregnant patients, the details of which are discussed separately. (See "Intraoperative management of adults with obstructive sleep apnea".)

POSTPARTUM MANAGEMENT

Identification of those at risk – Scoring systems that assess the risk of perioperative complications in patients at risk for OSA may be helpful in identifying nonpregnant patients at increased risk for postdelivery complications but their use may be limited in pregnant patients [28]. These are described separately. (See "Postoperative management of adults with obstructive sleep apnea", section on 'Postoperative complications' and "Surgical risk and the preoperative evaluation and management of adults with obstructive sleep apnea", section on 'Perioperative complications' and "Surgical risk and the preoperative evaluation and management of adults with obstructive sleep apnea", section on 'Initial assessment'.)

Management – Following delivery (vaginal or cesarean birth), we apply the same principles of management as nonpregnant patients with OSA in the postoperative setting. This involves management in the upright position, pain control with the avoidance of opioids, and resumption of airway management as soon as is feasible with whatever device was in place prior to delivery (eg, positive airway pressure [PAP], oral device). Consulting with a sleep medicine specialist, if not already done, is also appropriate. In addition, patients with OSA should be counseled about the risks of excessive sleepiness for the safe provision of breast feeding and childcare. Further details on the postoperative management of patients with OSA are provided separately. (See "Postoperative management of adults with obstructive sleep apnea", section on 'General strategies' and "Postoperative management of adults with obstructive sleep apnea", section on 'Positive airway pressure therapy' and "Breastfeeding: Parental education and support", section on 'Maternal exhaustion'.)

Limited data in pregnant patients support this approach. In a study of 20 postpartum patients with moderate to severe OSA (ie, apnea-hypopnea index [AHI] >15/h), elevated upper body positioning reduced the AHI from 7.7±2.2/h to 4.5±1.4/h [59]. (See "Postoperative management of adults with obstructive sleep apnea".)

Follow-up – All pregnant patients diagnosed with OSA should be followed postpartum by a sleep medicine specialist for reassessment of OSA severity (eg, re-evaluation of PAP prescription requirements, oral appliance prescription, weight management).

For patients diagnosed with gestational OSA, we typically repeat testing (home sleep apnea testing or full-night, attended, in-laboratory polysomnography [PSG]) [24], particularly after losing their pregnancy weight. At our institutions, we generally recommend that this evaluation take place 8 to 12 weeks after delivery. However, it is important to keep in mind weight loss may occur at a slower rate, and thus, postpartum management of OSA needs to be individualized. Specific weight loss strategies may need to be applied which, in addition to improving OSA, may improve their overall health. (See "Obstructive sleep apnea: Overview of management in adults", section on 'Weight loss and exercise'.)

For patients with prepregnancy OSA whose disease severity worsened or improved during pregnancy, the need for repeat testing or switching to APAP is individualized.

Data that describe the course of OSA following delivery are limited. In one longitudinal study including 10 patients who presented with a sleep-related breathing disorder in the third trimester, sleep apnea severity improved after delivery [60]. However, the majority (70 percent) of patients continued to have the disorder up to three months postpartum. This study did not account for possible body position effects on the degree of sleep-disordered breathing (SDB), postpartum weight loss, and changes in body fat composition and distribution, all of which possibly contributed to these findings.

Future pregnancies – There are no data regarding the effect of a subsequent pregnancy on the natural history of OSA or whether the development of OSA during one pregnancy increases the risk of developing OSA in subsequent pregnancies. Similarly, whether a prior history of gestational OSA affects risk for adverse maternal-fetal outcomes in subsequent pregnancies (regardless of whether OSA has recurred) has not been reported. In our experience, patients with OSA and body mass index (BMI) ≥40 kg/m2 have experienced a regression of OSA with substantial weight loss; in the absence of such changes, subsequent pregnancies are also affected by OSA.

OSA may be associated with increased rates of infertility. In a retrospective study, higher rates of OSA were reported in females with infertility compared with matched controls who did not have infertility (1.4 versus 0.6 percent; adjusted odds ratio [OR] 2.1) [61]. While the cause infertility is patients with OSA is uncertain, such patients have an increased prevalence of polycystic ovary syndrome, which is a known cause of infertility [62].

OUTCOMES — While OSA appears to be associated with an increased risk of adverse outcomes in pregnancy [2,22,63-78], data have been hindered by the inclusion of patients with a variety of sleep disorders, lack of adjustment for potential confounders, low numbers, and publication bias. Whether OSA treatment ameliorates these adverse outcomes is unknown.

Maternal outcomes

Severe maternal morbidity — OSA is associated with severe maternal morbidity (SMM). In a study based on maternal discharge codes that included more than 55 million patients, OSA was associated with an increased odds of the following indicators of SMM: eclampsia (odds ratio [OR] 5.4, 95% CI 3.3-8.9), cardiomyopathy (OR 9, 95% CI 7.5-10.9), and pulmonary embolism (OR 4.5, 95% CI 2.3-8.9); in-hospital mortality was also increased (OR 5.3, 95% CI 2.4-11.5) [63]. The findings were confirmed in another, smaller sample of 1.5 million pregnant patients with a discharge diagnosis of OSA [64].

Hypertensive disorders of pregnancy — OSA is associated with the development of both preeclampsia and gestational hypertension [2,63,65]. In a meta-analysis of pregnant patients from 120 observational studies, compared with patients without sleep disturbances, those with objectively diagnosed OSA had an increased risk for preeclampsia (OR 2.36, 95% CI 2-2.79) and gestational hypertension (OR 1.93, 95% CI 1.51-2.46) [66]. This is consistent with data from nonpregnant patients with OSA who also are at increased risk of developing hypertension. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Complications'.)

Gestational diabetes — OSA is associated with the development of gestational diabetes (GDM) [2,67-69]. In a meta-analysis of observational studies, pregnant patients with OSA had an approximately two-fold increased risk of GDM compared with patients without sleep disturbances (OR 1.88, 95% CI 1.47-2.4) [66].

The severity of OSA may be directly associated with higher glucose levels. In one cross-sectional study of 65 pregnant patients with GDM between 24 and 34 weeks of gestation, patients with an apnea-hypopnea index (AHI) ≥30 events/hour of sleep had higher glucose levels during nocturnal and early morning periods compared with those who had an AHI <10 events/hour, even after adjustment for body mass index (BMI) and use of insulin/metformin [70]. Specifically, for every 10-unit increase in AHI, nocturnal and morning glucose levels rose by 3.6 mg/dL (0.2 mmol/L; 95% CI 0.04-0.4) and 4.7 mg/dL (0.26 mmol/L; 95% CI 0.08-0.4), respectively.

Metabolic syndrome — OSA may be associated with metabolic syndrome. In one study of pregnant patients with sleep-disordered breathing (SDB), those with an AHI ≥5 had an increased risk of metabolic syndrome compared with those who had an AHI <5 events per hour (adjusted risk ratio [aRR] 1.4, 95% CI 1.1-1.9) [79]. This risk was even higher in those in whom OSA persisted after delivery (aRR 2.5, 95% CI 1.6-3.8).

Fetal outcomes

Preterm birth — Population-based studies have described an increased frequency of preterm birth in patients with sleep apnea [22,80-83]. In a meta-analysis of observational studies, those with objectively diagnosed OSA had an increased risk for preterm birth compared with patients without sleep disturbances (OR 1.38, 95% CI 1.26-1.51) [66]. However, data are limited by inclusion of studies with different forms of sleep-related breathing disorders, lack of rigorous diagnostic criteria, and lack of adjustment for potential maternal confounders, particularly maternal age and BMI.

Fetal heart rate deceleration — The impact of maternal OSA on fetal heart rate patterns is unclear since studies have reported contrasting findings:

In a cohort study in which 100 pregnant patients underwent simultaneous fetal monitoring and in hospital polysomnography (PSG), apneic episodes were not associated with abnormality of the fetal heart rate tracing [84].

In a cohort study of 40 pregnant patients in the third trimester, the majority (84 percent) of late and/or prolonged fetal heart rate decelerations occurred within 30 seconds after a respiratory event [76]. However, there was a high rate of hypertensive disease, diabetes, and obesity (mean BMI 36 to 37 kg/m2) in this cohort, creating uncertainty about the confounding effects of these comorbidities.

In a prospective study of 84 pregnant patients (mean gestational age 36 weeks) with BMI ≥30 kg/m2 undergoing simultaneous fetal monitoring and laboratory-based PSG, only a minority (1.5 percent) of apnea or hypopnea events were followed by decelerations [85].

At least two other case reports have described an association between OSA and fetal heart decelerations [71,72].

Low birth weight — Although case reports and retrospective studies have described an association between OSA and impaired fetal growth, confounders that affect birth weight negatively (eg, preeclampsia, poor gestational weight gain) and positively (eg, obesity, diabetes, excessive gestational weight gain) were not adjusted for in analyses [73-75,77,80]. In a systematic review evaluating the effects of SDB in pregnancy, those with SDB had a modest increase in low birth weight neonates compared with those without SDB (<2500 g, OR 1.67, 95% CI 1.00-2.78) [22]. By contrast, in subsequent meta-analyses including only studies with objectively assessed SDB, patients with and without SDB had similar rates of small-for-gestational-age [66,86] and large-for-gestational-age neonates [66].

Congenital anomalies — Limited data suggest that OSA may be associated with congenital anomalies. In a population-based study in which over 1,400,000 maternal records were linked to live newborn records, OSA was associated with an increased risk for congenital anomalies (adjusted OR 1.26, 1.11-1.43) [87]. Newborns of mothers with OSA were also more likely to be admitted to the intensive care unit (25.3 versus 8.1 percent).

Fetal death — There are no high-quality data evaluating how maternal OSA affects the risk of fetal demise. One meta-analysis reported an increased risk of stillbirth in pregnant patients with OSA (OR 1.25, 95% CI 1.08-1.45) [66].

SPECIAL CONSIDERATIONS

Snoring — In nonpregnant patients, snoring may be associated with increased upper airway resistance, and/or obstructive apneas and hypopneas. Data in pregnant patients are limited:

Prevalence – The prevalence of snoring in pregnant patients has been estimated to be between 14 and 53 percent and may be higher than that reported in nonpregnant females [8,88-91]. The prevalence of frequent snoring (≥3 nights/week) increases as gestation advances [8,91].

Effect of snoring on outcomes – Observational data are conflicting regarding the effect of snoring on pregnancy and neonatal outcomes [88-90,92-96]. However, patients with a diagnosis of sleep-disordered breathing (SDB) were not excluded from these studies, thereby limiting interpretation of these outcomes.

Maternal outcomes – Higher rates of gestational hypertension [90] and preeclampsia [88,92], have been reported among habitual snorers compared with nonsnorers during pregnancy. However, studies comparing new-onset snoring in pregnancy with chronic snoring as a risk factor for preeclampsia and gestational hypertension have conflicting results [90,93].

Snoring may also increase the risk of gestational diabetes. In a prospective cohort study including over 15,700 females, those who reported habitual snoring were more likely than nonsnorers to develop gestational diabetes (odds ratio [OR] 2.50, 95% CI 1.34-4.67) [95].

Neonatal outcomes – Similarly, while some studies have shown higher rates of small-for-gestational age infants in habitual snorers compared with nonsnorers [88,94], other studies have failed to find significant differences between infants born to snorers and nonsnorers [89,96].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Sleep-related breathing disorders in adults".)

SUMMARY AND RECOMMENDATIONS

Scope – Obstructive sleep apnea (OSA) refers to apneas and hypopneas (absent or severely reduced airflow, respectively) that occur during sleep despite respiratory effort. (See 'Introduction' above.)

Rates of OSA in pregnant patients may be higher than that reported in the nonpregnant population. Hormonal and physiologic changes that occur in pregnancy may contribute to the development and worsening severity of OSA in such patients. (See 'Prevalence' above and 'Pathogenesis' above.)

Clinical manifestations of OSA are similar in pregnant and nonpregnant patients (table 1). The clinician should have a lower than usual threshold to suspect OSA in pregnancy since the symptoms of OSA and pregnancy overlap. (See 'Clinical manifestations' above and "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)

Diagnostic evaluation – Our approach is the following (see 'Diagnostic evaluation' above):

For most pregnant patients with suspected OSA, we perform full-night, attended, in-laboratory polysomnography (PSG) since PSG is the diagnostic gold standard for OSA. Unattended home sleep apnea testing (HSAT) may be a reasonable alternative for patients in whom PSG is not initially approved due to insurance restrictions or declined by the patient, although a negative HSAT may not confidently exclude OSA, especially when the suspicion remains for the diagnosis. (See 'Diagnostic evaluation' above and 'Objective testing (home or in-laboratory)' above.)

The diagnostic criteria for OSA in pregnant patients are similar to those in nonpregnant patients and are discussed separately. (See 'Diagnosis and classification of severity' above and "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnosis'.)

Management – Pregnant patients with OSA should be managed by a sleep medicine specialist. Most patients are managed in a similar fashion to those who are not pregnant with the following exceptions (see 'Management of OSA' above and "Obstructive sleep apnea: Overview of management in adults"):

While weight loss has been demonstrated to decrease the number of apnea/hypopnea episodes in nonpregnant patients, we do not typically advise weight loss in pregnancy. Rather, we encourage patients to achieve gestational weight gain at the lower limit of the recommended range which may benefit an individual's risk for pregnancy related morbidity from worsening OSA control. Further details are provided separately. (See 'Behavior modification' above and "Gestational weight gain".)

For pregnant patients with OSA, positive airway pressure (PAP) therapy is the mainstay of treatment and is similar to that in nonpregnant patients (algorithm 1). (See 'Positive airway pressure' above and "Obstructive sleep apnea: Overview of management in adults", section on 'Positive airway pressure (PAP) therapy'.)

-For patients with mild OSA, we suggest PAP therapy for those with recurrent oxyhemoglobin desaturations <90 percent (Grade 2C).

-We suggest auto-adjusting continuous PAP (APAP) rather than fixed-level continuous PAP (CPAP) (Grade 2C). APAP avoids the need for a repeat titration study since OSA control may worsen over the course of pregnancy necessitating an increase in PAP. PAP improves sleepiness, snoring, and fatigue in pregnant patients but the impact on other clinically relevant outcomes (eg, blood pressure control) is unclear.

Mandibular devices and surgery are not pragmatic approaches to treating gestational OSA. For pregnant patients with OSA, use of wakefulness promoting agents (eg, modafinil and armodafinil) are contraindicated due to the risk of fetal harm. (See 'Treatments of limited benefit' above and 'Treatments not used: Pharmacologic therapy' above.)

Trimester-specific management issues include the following:

Antepartum – Antepartum surveillance with monitoring of blood pressure and urine protein during routine prenatal care visits, first- or early second-trimester testing for gestational diabetes, ultrasonography to estimate fetal weight every three to four weeks starting at 28 weeks gestation, and standard fetal surveillance as indicated for comorbid conditions. (See 'Management of OSA-related pregnancy issues' above.)

Intrapartum – Patients are encouraged to use their PAP or oral device for use during sleep when in the Labor and Delivery unit. We consult anesthesia early (for placement of regional anesthesia), continuously monitor oxygenation with pulse oximetry, and clinically evaluate for desaturation events. For patients who undergo cesarean birth, intrapartum management of OSA is similar to that in nonpregnant patients, the details of which are discussed separately. (See 'Intrapartum management' above and "Intraoperative management of adults with obstructive sleep apnea".)

Postpartum – Postpartum management includes ensuring the upright position, pain control with the avoidance of opioids, prompt resumption of airway management (eg, PAP, oral device), and follow-up with a sleep medicine specialist to reassess OSA severity and need for PAP as pregnancy weight is lost. Further details in nonpregnant patients are provided separately. (See 'Postpartum management' above and "Postoperative management of adults with obstructive sleep apnea".)

Outcomes – OSA is associated with increased maternal and fetal morbidity. Adverse maternal outcomes include severe maternal morbidity, gestational hypertension, preeclampsia, and gestational diabetes. Adverse fetal outcomes are less clear but may include preterm birth, fetal heart rate decelerations, congenital anomalies, and fetal death. Whether OSA treatment ameliorates these adverse outcomes is unknown. (See 'Outcomes' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Robert C Basner, MD, who contributed to earlier versions of this topic review.

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Topic 14202 Version 60.0

References

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