Pregnancy and Sleep Apnoea

Recent studies suggest that sleep-disordered breathing increases the risk of pregnancy induced hypertension  and is associated with adverse maternal and fetal outcomes. The incidence of obstructive sleep apnea-hypopnea syndrome is 2 to 5% in the general female population; however, the incidence in pregnant women is unknown. Below is a case study that investigated sleep apnoea events during pregnancy.

Case Study

A 26-year-old woman, 10 weeks of gestation, was seen in a chest clinic with increasing sleepiness and daytime fatigue. Her partner noticed loud snoring during this pregnancy with witnessed apnea episodes during sleep. She was sleeping 8 hours every night and waking about four to five times to go to the bathroom. Her medical problems included depression, migraine headaches, hypertension, and a history of pre-eclampsia (pregnancy related hypertension).

Physical Examination

Her Epworth sleepiness scale score was 12/24. Her body mass index was 33 kg/m2 with a neck size of 15.75 inches. Her oropharynx was congested and narrowed (Mallampati grade 4). The rest of the physical examination findings were unremarkable.

Laboratory Data

Below are the results of an overnight polysomnogram (sleep study).

REM=Rapid Eye Movement; PLMS = Periodic Limb Movements While Sleeping; SaO₂ = Arterial Oxygen Saturation

Diagnosis: Moderate obstructive sleep apnoea-hypopnoea syndrome in pregnancy

Treatment: Nasal continuous positive airway pressure therapy (CPAP)

Clinical Course

Treatment with CPAP was offered, but she refused it. Later, recurrent pre-eclampsia developed in the patient at 37 weeks of gestation, for which bed rest was advised. However, due to the persistence of pre-eclampsia, labor was induced, and the patient delivered a 2300g healthy baby girl. The patient lost a considerable amount of weight postpartum, with a significant improvement in snoring and apneas during sleep.

General Background

The physiologic changes of pregnancy (ie, progressive weight gain and upward displacement of the diaphragm) predispose women to obstructive sleep apnea (OSA). 

Oestrogen induces increased blood flow and oedema of the nasopharyngeal mucosa. This causes narrowing of the upper airway, with increased resistance to airflow. Progesterone has some protective effect by increasing respiratory drive and minute ventilation (breathing rate and volume). However, the increased ventilatory drive can lead to instability in the respiratory control pathways, thereby predisposing the patient to OSA. 

Upward displacement of the diaphragm decreases the lung capacity by 20%, in addition to the normal decline in lung capacity during sleep. Due to this reduction the traction on the trachea and pharynx that is exerted by lung inflation decreases, thereby enhancing the collapsibility of the upper airway. 

Episodes of apnea coupled with low oxygen reserves during pregnancy increase the risk of maternal hypoxemia (low oxygen) and compromise oxygen delivery to the foetus. 

Symptoms of OSA include night-time snoring, witnessed apneas, gasping, and choking sensations during sleep. During the day, patients complain of nonrefreshing sleep, excessive daytime sleepiness, morning headaches, fatigue, impaired concentration, and personality changes.

Some studies have suggested that sleep-disordered breathing is associated with adverse pregnancy outcomes, such as pregnancy-induced hypertension, preeclampsia and foetal growth retardation.

What is the Mechanism?

It has been postulated that intermittent maternal drop in blood oxygen levels induced by sleep-disordered breathing can cause placental lack of oxygen, triggering oxidative stress and blood vessel ‘endothelial’ activation. Oxidative stress and endothelial dysfunction are implicated in the pathogenesis of pregnancy-induced hypertension. The absence of nocturnal dipping in systolic BP is seen in women with preeclampsia and in those with OSA, suggesting a common link between the two. 

Although no specific guidelines exist for screening pregnant patients for OSA, pregnant women with excessive daytime somnolence, loud snoring, and witnessed apneas should be evaluated for OSA with polysomnography. It is also prudent to obtain a meticulous sleep history in women who gain excess weight during pregnancy and in obese patients in whom gestational hypertension or preeclampsia develops. Uncomplicated snoring, pregnancy-induced hypertension, or intrauterine growth retardation alone, in the absence of sleep apnea symptoms, are insufficient indications for ordering polysomnography. 

The treatment guidelines for pregnant women with OSA are similar to those for the general population, as the data in pregnant women are limited. 

An important goal in pregnant women is the avoidance of maternal hypoxemia (drop in blood oxygen levels). Patients with severe sleep apnea (apnea-hypopnea index [AHI], > 30), mild-to-moderate sleep apnea (AHI, 5 to 30) with clinical symptoms, or recurrent oxygen desaturations of < 90% should receive treatment. 

Nasal continuous positive airway pressure (CPAP) is the first-line therapy. A recent study showed that CPAP was safe and well tolerated in pregnant women. 

In pregnant women with pre-existing OSA, symptom recurrence should be assessed, especially if there is excess weight gain or gestational hypertension. A repeat sleep study or the titration of CPAP pressure would be indicated if insufficient treatment is suspected. 

OSA precipitated by pregnancy usually improves following delivery, as nasopharyngeal oedema resolves and excess weight is lost. The postpartum withdrawal of CPAP therapy with follow-up for symptom recurrence can be attempted in patients with mild-to-moderate pregnancy-associated sleep apnea. If symptoms recur, a repeat sleep to assess the baseline AHI is indicated. 

For severe pregnancy-associated sleep apnea, therapy should be continued and a repeat sleep study obtained when the patient's weight returns to 10 to 15% of baseline. This would be to establish a baseline AHI and the clarification for continued therapy. Patients with preexisting OSA can safely return to pre-pregnancy therapy when their weight returns to 10 to 15% of baseline, with close follow-up for symptom recurrence.

Summary

1. OSA can complicate pregnancy given the risk factors of weight gain, the upward displacement of the diaphragm, and hormonal-induced hyperemia of the nasopharyngeal passages.

2. Preliminary evidence has suggested that sleep-disordered breathing confers the risk of hypertensive disorders of pregnancy and is associated with adverse maternal and foetal outcomes.

3. There are no specific guidelines for screening pregnant women for OSA. In women with preexisting obesity in whom gestational hypertension or preeclampsia develops, there should be a high index of suspicion for sleep-disordered breathing.

4. Nasal CPAP is the standard treatment. Postpartum withdrawal of therapy with close monitoring of symptoms can be attempted, especially if weight returns to baseline levels.

Dr Andrew Scott

Thoracic and Sleep Physician

Thoracic and Sleep Group Queensland (TSGQ)

References

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