Journal of Sleep Disorders: Treatment and CareISSN: 2325-9639

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Research Article, J Sleep Disor Treat Care Vol: 4 Issue: 2

Obstructive Sleep Apnea during Pregnancy and the Morbidity Outcome

Poj Pinyopornpanish1*, Nuntigar Sonsuwan1 and Supatra Sirichotiyakul2
1Department of Otolaryngology Faculty of Medicine, Chiang Mai University, Thailand
2Department of Obstetrics and Gynecology Faculty of Medicine, Chiang Mai University, Thailand
Corresponding author : Dr. Poj Pinyopornpanish
Department of Otolaryngology Faculty of Medicine, Chiang Mai University, 96/5 Ratchiangsan Rd., Chiang Mai 50100, Thailand
Tel: (66)89-9549797
E-mail: [email protected]
Received: May 11, 2015 Accepted: August 07, 2015 Published: August 11, 2015
Citation: Pinyopornpanish P, Sonsuwan N, Sirichotiyakul S (2015) Obstructive Sleep Apnea during Pregnancy and the Morbidity Outcome. J Sleep Disor: Treat Care 4:2. doi:10.4172/2325-9639.1000158

Abstract

Obstructive Sleep Apnea during Pregnancy and the Morbidity Outcome

Background: There is an increasing concern that obstructive sleep apnea is a risk factor of a poor pregnancy outcome. Our research design used polysomnography, which gives an objective measurement
in defining obstructive sleep apnea in non-high risk pregnancy. This study was carried out to measure the prevalence of obstructive sleep apnea in pregnancy and show whether obstructive sleep apnea is a risk factor of poor pregnancy outcome.
Methods: A prospective cohort study had been carried out at Chiang Mai University Hospital. 50 pregnancy women who received antenatal care at Chiang-Mai University hospital were included in the study. All subjects were assessed by physical examination and polysomnography at GA 28th-32nd weeks and were followed until the end of the pregnancy to see the difference in poor pregnancy outcomes in the obstructive sleep apnea and non-obstructive sleep apnea group.
Results: The prevalence of obstructive sleep apnea in pregnancy was 12%. Obstructive sleep apnea related to overall more poor pregnancy outcomes (RR=7.33(2.45-21.86), p=0.004), more preterm labor (RR=22.0(2.70-178.99), p-0.004), more preeclampsia (p=0.012).
Conclusions: Obstructive sleep apnea was a high risk in pregnancy and should be screened for with multidisciplinary team cooperation, to establish the diagnosis and treatment to enhance maternal and child health

Keywords: OSA; Sleep apnea; Pregnancy; Morbidity; High risk pregnancy

Keywords

OSA; Sleep apnea; Pregnancy; Morbidity; High risk pregnancy

Introduction

Sleep apnea in women occurs at an incidence of approximately 4% and increases during the third trimester of pregnancy [1-3].
The occurrence of obstructive sleep apnea (OSA) during pregnancy has been evaluated based on published case reports with only some of them having polysomnographic documentation of the sleep apnea. Thus, the prevalence of OSA in pregnant women today is not a particularly accurate value, the estimated range being from 6 to 32.2% [1-7].
In pregnant women, obesity is a major cause of sleep breathing disorder (SBD), or OSA [4]. Obese pregnant women are 8.5 times more likely to have SDB than those who are not obese [8]. Greater changes in neck circumference have been associated with a higher prevalence of SDB symptoms [9], and narrowing of the upper airway in the supine position causes more snoring in pregnant women [10]. Especially in high-risk pregnancy, there is 20% of new onset SDB during pregnancy [11].
Several physiological changes during pregnancy may increase upper airway resistance and reduce the cross-sectional area of the airway. Weight gain in pregnancy, abdominal mass loading and elevation of the diaphragm all result in reduced lung volume and reduced functional residual capacity, and tracheal shortening leading to upper airway narrowing. The pharyngeal edema of pregnancy and fat or soft tissue deposition around the upper airways can also lead to airway narrowing [12].
Late pregnancy may be associated with decreased oxygenation in the supine position and the respiratory disturbances during sleep may result in significant reduction of maternal and fetal tissue oxygenation. OSA may cause several adverse outcomes, such as the development of pregnancy induced hypertension (PIH), intrauterine growth retardation, small for gestational age (SGA) and preterm delivery [1-2,13-15]. In a recent study, pregnancy morbidity relating to OSA include preeclampsia (19%), preterm delivery (23%; odd ratio=2.6) and SGA (7%)[14].
Pamidi et al. reported maternal SDB was associated with an increased risk of gestational hypertension and gestational diabetes [16]. Facco et al. found SDB severity in early pregnancy was associated with the risk of developing gestational diabetes in high risk pregnancy woman [17].

Materials and Methods

Type of research: Prospective cohort study.
Population: pregnant women who received antenatal care services in Chiang-Mai University Hospital.
Duration: from October 2012 to April 2013.
Consent and Ethics
Informed consent was obtained from all individual participants prior to inclusion in the study. Research was approved by the Institution Review Board (Research Ethics Committee 3, Faculty of Medicine, Chiang-Mai University).
Inclusion criteria
• Pregnant women: aged 18-40 years who received antenatal care at Chiang Mai University Hospital.
• Gestational age between 28th and 32rd weeks.
The subject must not have used any other drugs than the supplements provided by the hospital.
Exclusion criteria
• Patient with other high-risks in pregnancy, ie DM, Chronic hypertension, Heart disease, Short stature, Thyrotoxicosis, SLE, Thalassemia.
• Subjects that had an alcohol or smoking habit.
Variables in the study
Basic information: age, history of pregnancy, Epworth sleepiness scale (ESS)
The degree of OSA: The apnea-hypopnea index (AHI) is calculated by dividing the number of respiratory events by the duration of sleep in hours. The AHI is used to measure sleep apnea severity. OSA severity is graded according to the American Academy of Sleep Medicine standards: AHI less than 5 events per hour of sleep is normal, 5-14.9 events per hour of sleep is mild, 15-29.9 events per hour of sleep is moderate, and greater than 30 events per hour of sleep is severe. The diagnosis is made by polysomnography
The incidence of reported complications in obstetrics is as follows:
Preterm birth: delivered before the gestational age of 37 weeks
Preeclampsia: the blood pressure is higher than or equal to 140 mmHg for systolic pressure or 90 mmHg for the diastolic pressure, and proteinuria (≥ 300 mg in 24 hours)
Cesarean section, according to medical indications: difficult birth, necessity to terminate the pregnancy
Small for gestational age: the fetal presentation of weight less than the 10th percentile of the gestational age
• Other complications: premature rupture of membrane, antepartum hemorrhage, the death of the fetus in utero, fetal distress etc.
The size of the neck, chest and abdominal circumferences, which are measured in centimeters in supine position
Friedmann tongue position (FTP), Tonsil grading.
Assessment
All subjects were measured to assess OSA by polysomnography at the gestational stage of 28th- 32rd weeks. If OSA was diagnosed by polysomnography, the patient would be given a consultation by the snoring clinic.
The clinical outcome was measured by the incidence of any poor pregnancy outcomes in obstetrics during the pregnancy until the end of pregnancy. The variables between the OSA and non-OSA group were compared using age, height, BMI and neck and chest circumference using the T-test. A Mann-Whitney U test was used to compare gestational age, body weight gained during pregnancy, abdominal circumference, oxygen saturation, FTP, tonsil grading and ESS. Fisher’s exact test was used for poor pregnancy outcomes. The statistical significance of each was determined by a p-value of less than 0.05.

Results

Demographic data
There were 1552 new patients in the antenatal care unit, 77 of those were volunteers. After the exclusion of women, 8 with known high risk pregnancy issues and 19 patients who did not have the support of their family, 50 pregnant women (which were non high risk pregnancy) were available to be included in the study.
For all participants, age was 27 ± 5 (18-39) years; GA was 30 ± 2 (28-32) weeks, height was155.6 ± 5.4 (145.0-167.0) cm, BMI prior to pregnancy 20.44 ± 2.63 (15.20-27.34) kg/m2 (Table 1).
Table 1: Clinical and demographic data between the non-OSA and OSA group.
Relationship of participant parameters and OSA occurrence
OSA was found in 6 (12%) of the 50 participants; all had mild OSA. There was a statistically significant difference in only FTP between the OSA and non-OSA groups (Tables 1 and 2). FTP gr III or greater was the most appropriate cut off point to screen for OSA in pregnancy with a sensitivity of 66.7% and a specificity of 84.1%.
Table 2: Clinical and demographic data between the non-OSA and OSA group.
The clinical and demographic data among OSA and non-OSA group was shown in Table 1. The only statistically different parameter of both group was AHI (p<0.001).
Between the variables, there was a significant difference of FTP grading (P=0.030) while tonsil grading and ESS in both group showed no statistically significant difference. The distribution of the grading is shown in Table 2.
Relationship of OSA and poor pregnancy outcomes Poor pregnancy outcomes were found in 4 women (66.67%) in the OSA group (in total 6), and 4 women (9.09%) in the non-OSA group (in total 44), as shown in Table 3 and 4. The risk ratio was 7.33 (2.45-21.86) (p=0.004) (Table 4, Figure1).
Figure 1: Percentage of poor pregnancy outcomes between non-OSA and OSA groups.(SGA=small for gestational age, *= statistically significant).
Table 3: Clinical and demographic data between the non-OSA and OSA group.
Table 4: Clinical and demographic data between the non-OSA and OSA group.
Preterm labor was found in 3 women (50.0%) in the OSA group (in total 6), which is more than that found in the non-OSA group, there being only one (2.27%) in the non-OSA group (in total 44), with the risk ratio at 22.0(2.70-178.99) (p=0.004). Preeclampsia was also found in 2 women in the OSA group but the risk ratio cannot be calculated because there was no occurrence of this in the non-OSA group.
The need for a Cesarean section and incidence of SGA also occurred more in the OSA group, with the risk ratio at 2.44 (0.30- 19.89) times more than the non-OSA group (p=0.411); and at 7.33(1.26-42.82) times of non-OSA group (p=0.066), respectively.
Analysis of all parameters that related to poor pregnancy outcomes
Multivariate logistic regression was used for the analyses and indicated that AHI was the only common cause of poor outcomes, preterm labor and preeclampsia (Table 4). The other factors, such as the ESS, tonsil grading, FTP, BMI prior to pregnancy, weight gain during pregnancy, neck, chest, abdominal circumference, minimum oxygen saturation and average oxygen saturation, were not found to show any statistical correlation with a poor pregnancy outcome. However, tonsil grading was the other common cause associated with preeclampsia and SGA.

Discussion

Pregnancy might be associated with a more frequent OSA prevalence. The majority of the studies carried out to date were, however, assessed using questionnaires, which may not be as precise as with polysomnography [6]. Thus in this study polysomnography was used.
It should be noted that the polysomnography was used at the junction of the 2nd and 3rd trimester of the pregnancy, even though there have been reports of greater OSA in the 3rd trimester, potentially leading to an increase in complications. Therefore, this study monitored OSA in the junction between the 2nd and 3rdtrimesters so the findings would be less confounded with such complications.
Our study reveals the prevalence of OSA was 12% in pregnant women compared to that of earlier reports, which was between 6 and 32.2% [1-7]. We studied in non-high risk pregnancy and found that there was a normally distributed BMI range prior to pregnancy, none of the patients being obese. Louis [5,14] commented that obesity related to comorbidities such as chronic hypertension, diabetes, weight gain and older age, all of which were also risk factor of OSA; however, with a population limited only to those with obesity, the conclusion could not be determined in those with non-obesity. Thus our study could possibly be used to partially answer the question of OSA in non-obese pregnant women.
The difference between those with OSA and non-OSA is only in FTP. Thus in normal pregnancy the FTP could be a factor used to advice for screening of OSA in pregnancy. After we calculated for sensitivities and specificities of all grades of FTP, the most powerful cut off point for screening was FPT gr III or greater (sensitivity 66.7%, specificity 84.1%)
Overall, poor pregnancy outcomes had a higher incidence in the OSA group. These were preterm labor and preeclampsia. In this study, we calculated the number associated with OSA in each outcome, the number associated with complications being just 2 patients with preterm birth. However, this number could not be calculated for preeclampsia due to there being no occurrence in the non-OSA group. If calculated, OSA could possibly be related to preeclampsia at 3.55 times more than those with non-OSA [5]. According to metaanalysis of Pamidi reported that maternal SDB was associated significant with gestational hypertension, preeclampsia (pooled adjusted odds ratio 2.34; 95% CI 1.60-3.09)[16]
We found that the risk ratio for preterm labor in OSA was19.3, more than that quoted in the Louis [14] study with an odd ratio of only 2.6. Kelestimur [15] explained that OSA might be a cause of increasing hypoxia, and more hypoxia may cause higher levels of oxytocin, which stimulates contractions of the uterus, leading to preterm labor. More hypoxia also leads to vascular injury and higher blood pressure as well as the occurrence of hypertension in cases of OSA. This may explain the reflex which brings on preeclampsia.
These conditions could be compensatory mechanisms by the maternal body to facilitate the transport of oxygen to peripheral tissues. The detection of OSA and treatment could help patients avoid suffering poor pregnancy outcomes such as preterm labor and preeclampsia.
The 4 SGA cases (2 being OSA and the other non-OSA) were not statistically different. However, previous research by Fung [7] showed a relationship between OSA and SGA with an odd ratio 6, reporting that a fetus with severe growth restriction had an acute response to maternal oxygen-desaturation, but most of the fetuses were well protected from transient maternal hypoxia although those with uteroplacental insufficiency were not.
We suggest that OSA in pregnancy could cause hypoxia which possibly increases uteroplacental blood flow. Desaturation may induce a response from the body of the mother by increasing the blood supply to her body and placenta; this will lead to higher blood pressure or preeclampsia giving greater oxygenation to the fetus in those mothers. But in those with decompensation this may cause SGA. Kelestimur’s study [15] in rats found that oxytocin increased during hypoxia (Figure 2).
Figure 2: Hypothesis of the development of poor pregnancy outcomes in OSA.
After determining the difference between the variables by multivariate regression on the incidence of poor pregnancy outcomes, the current study found that OSA was the single common factor causing statistically significant differences for overall poor pregnancy outcomes (preterm labor and preeclampsia).
The benefit of treatment with nocturnal nasal CPAP(continuous positive airway pressure) machine in preeclampsia showed improvement in fetal movement [18] and cardiac output [19]
In our study, we did not find patients with severe OSA. To our knowledge, there is no definite guideline for OSA in pregnancy. Surveillance and cautious early management in obstetrics is recommended. Therefore, future research should be evaluated in group with OSA, providing treatment to reduce the incidence of OSA and poor pregnancy outcomes.

Conclusion

OSA in pregnancy has an impact on the occurrence of poor pregnancy outcomes such as preterm labor and preeclampsia. The study then suggests an increasing awareness of OSA as a potential high-risk during pregnancy, and therefore, highly recommends investigation by polysomnography.
Obstetricians should suspect OSA and refer patients to specialists for a sleep study to investigate whether the patient has OSA or not. Treatment during pregnancy needs to be established with collaboration between the multidisciplinary team to enable care for both the mothers and babies.

Acknowledgments

We wish to thank Ms. Kittika Kanjanarattanakorn, statistician, Mrs. Rochana Phuackchantuck, statistician, We thank two anonymous reviewers for their comments that helped to improve a previous version of the manuscript.

Funding

The study was supported by The Unit of Snoring and Sleep apnea; Otolaryngology department; Chiang-Mai University

Compliance with Ethical Standards

The study had been approved by “Research Ethics Committee 3, Faculty of Medicine, Chiang-Mai University”

Inform Consent

Informed consent was obtained from all individual participants prior to their inclusion in the study.

Disclosure of potential conflict of interest

All authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest (such as honoraria; educational grants; participation in speakers’ bureaus; membership, employment, consultancies, stock ownership or other equity interest; and expert testimony or patent-licensing arrangements), or non-financial interest (such as personal or professional relationships, affiliations, knowledge or beliefs) in the subject matter or materials discussed in this manuscript.

References

  1. LoubeDI, Poceta JS, Morales MC, Peacock MD, Mitler MM (1996) Self-reported snoring in pregnancy association with fetal outcome. Chest 109:885-889.

  2. Franklin KA, Holmgren PA, Jonsson F, Poroma N, Stenlund H, et al. (2000) Snoring, pregnancy- induced hypertension and growth retardation of the fetus. Chest 117:137-141.

  3. Bourjeily G, Raker CA, Chalhoub M, Miller MA (2010) Pregnancy and fetal outcomes of symptoms of sleep-disordered breathing. EurRespir J 36:849-855.

  4. Olivarez SA, Maheshwari B, McCarthy M, Zacharias N, Casturi L, et al. (2010) Prospective trial on obstructive sleep apnea in pregnancy and fetal heart rate monitoring. Am J Obstet Gynecol 202:552-557.

  5. Louis J, Auckley D, Miladinovic B,Shepherd A, Mencin P, et al. (2012) Perinatal outcomes associated with obstructive sleep apnea in obese pregnant women. Obstet Gynecol 120:1085-1092.

  6. Ko HS, Kim MY, Kim YH, Lee J, Park YG, et al. (2013) Obstructive sleep apnea screening and perinatal outcomes in Korean pregnant women. Arch Gynecol Obstet 287:429-433.

  7. Fung AM, Wilson DL, Lappas M, Howard M, Barnes M, et al. (2013) Effects of maternal obstructive sleep apnoea on fetal growth: a prospective cohort study. PLoS One 8:e68057.

  8. Maasilta P, Bachour A, Teramo K, Polo O, Laitinen LA (2001) Sleep-related disordered breathing during pregnancy in obese women. Chest 120:1448-1454.

  9. Hedman C,Pohjasvaara T, Tolonen U, Suhonen-MalmAS, Myllyla VV (2004) Effects of pregnancy on mother’s sleep. Sleep Med 3:37-42.

  10. Bradley TD, Brown IG, Grossman RF,Zamel N, Martinez D, et al. (1986) Pharyngeal size in snorers, nonsnorers, and patients with obstructive sleep apnea. N Engl J Med 315:1327-1331.

  11. Facco FL, Ouyang DW, Zee PC, Willium AG (2014) Sleep Disordered Breathing in a High-risk Cohort Prevalence and Severity across Pregnancy. Am J Perinatol31:899-904.

  12. Kapsimalis F, Kryger M (2007) Obstructive sleep apnea in pregnancy. Sleep Med Clin 2: 603-613.

  13. Pien GW, Schwab RJ (2004) Sleep disorders during pregnancy. Sleep 27:1405-1417.

  14. Louis JM, Auckley D, Sokol RJ, Mercer BM (2010) Maternal and neonatal morbidities associated with obstructive sleep apnea complicating pregnancy. Am J Obstet Gynecol 202:261.

  15. Kelestimur H, Leach RM, Ward JP, Forsling ML (1997) Vasopressin and oxytocin release during prolonged environmental hypoxia in the rat. Thorax 5 2:84-88.

  16. Pamidi S, Pinto LM, Marc I, Benedetti A, Schwartzman K, et al. (2014) Maternal sleep-disordered breathing and adverse pregnancy outcomes: a systematic review and metanalysis. Am J Obstet Gynecol 210:52.e1-52.e14.

  17. Facco FL, Ouyang DW, Zee PC,Strohl AE, Gonzalez AB, et al. (2014) Implication of sleep-disorder breathing in pregnancy. Am J Obstet Gynecol210:559.e1-559.e6.

  18. Blyton DM, Skilton MR, Edwards N, Hennesy A, Celermajer DS, et al. (2013) Treatment of sleep disordered breathing reverses low fetal activity level in preeclampsia. Sleep 36:15-21.

  19. Bylton DM, Sulivan CE, Edward N (2004) Reduced nocturnal cardiac output associated with preeclampsiais minimized with the use of nocturnal nasal CPAP. Sleep 27:79-84.

Track Your Manuscript

Recommended Conferences

8th International Conference on Epilepsy & Treatment

Amsterdam, Netherlands