Obstructive Sleep Apnoea During Pregnancy Requiring Tracheostomy

Hastie, Stewart J.; Prowse, K; Perks, W H; Atkins, Jessica; Blunt, V. A. W.

doi:10.1111/j.1479-828x.1989.tb01768.x

Cited by 34 publications

(18 citation statements)

References 10 publications

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“…Case studies have reported that, when women with SDB received treatment before the third trimester, they delivered infants with normal birth weight and high Apgar scores [4,98,119]. However, causality has not been established.…”

Section: Adverse Pregnancy Outcomes: Possible Biological Pathwaysmentioning

confidence: 99%

Sleep-disordered breathing and pregnancy: potential mechanisms and evidence for maternal and fetal morbidity

Izci‐Balserak

Pien

2010

Current Opinion in Pulmonary Medicine

105

106

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Purpose of review This article reviews current data on pathophysiologic mechanisms by which sleep-disordered breathing during pregnancy may cause harm, and explores biological pathways for associated adverse maternal and fetal outcomes, especially pregnancy-induced hypertension and gestational diabetes. Recent findings Accumulating data indicate that snoring and sleep apnea during pregnancy are likely to increase the risk for gestational hypertension and preeclampsia. Several new studies have observed that sleep-disordered breathing and short sleep duration also increase the risk of gestational diabetes, similar to observations in the general population. There are varying levels of emerging evidence for potential mechanisms, including oxidative stress, increased sympathetic activity and inflammation, adipokine levels and insulin resistance, linking sleep-disordered breathing events during pregnancy to adverse outcomes. Summary Sleep-disordered breathing and adverse maternal–fetal outcomes such as preeclampsia and gestational diabetes share a number of mechanistic pathways, and growing data in pregnant women indicate that snoring and sleep apnea increase the risk of these and other complications for both the mother and the fetus. Nevertheless, direct evidence of the pathophysiologic mechanisms by which sleep-disordered breathing during pregnancy exerts negative effects remains sparse.

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Section: Adverse Pregnancy Outcomes: Possible Biological Pathwaysmentioning

confidence: 99%

Sleep-disordered breathing and pregnancy: potential mechanisms and evidence for maternal and fetal morbidity

Izci‐Balserak

Pien

2010

Current Opinion in Pulmonary Medicine

105

106

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“…To date, studies of OSA during pregnancy have predominantly been case reports, [27][28][29][30][31][32][33] with few longitudinal studies and no population based epidemiological studies. Thus, while it is known that the prevalence of OSA in women of reproductive age is approximately 5%, 34 the true prevalence of OSA in pregnancy is unclear.…”

Section: Snoringmentioning

confidence: 99%

“…27 35 42 Those pregnant patients with OSA who had infants of normal birth weight tended to have been diagnosed before the third trimester and started on treatment (either with tracheostomy or nasal CPAP). [28][29][30] However, at the individual level, the immediate fetal effects are unclear. A case report of severe OSA during pregnancy revealed normal fetal heart rate reactivity on cardiotocographic (CTG) recording, even during maternal apnoeic episodes with associated severe oxyhaemoglobin desaturations.…”

Section: Snoringmentioning

confidence: 99%

Sleep disordered breathing and pregnancy

Edwards

Middleton²,

Blyton³

et al. 2002

Thorax

111

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“…All previously reported fetuses survived. One had a birthweight below the tenth centile for gestational age 4 and in all other cases the birthweight was below the 25 th centile including three cases where there was maternal diabetes mellitus 12,14 .…”

Section: Discussionmentioning

confidence: 90%

Obstructive sleep apnoea and fetal death: successful treatment with continuous positive airway pressure

Brain¹,

Thornton

Sarkar³

et al. 2001

British Journal of Obstetrics and Gynaecology

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Case reportA 22 year old moderately overweight woman, with spina bi®da and an ileourinary conduit, booked at 11 weeks in her second pregnancy. She had reduced mobility due to leg weakness, but no kyphoscoliosis or restrictive lung disease from chest wall deformity. Her ®rst pregnancy had resulted in a ®rst trimester miscarriage. Her systolic/diastolic blood pressure at booking was 120/ 80mmHg. Proteinuria on dipstick testing was 11, persisting throughout her pregnancy. Urine culture repeatedly showed sterile pyuria, presumably both related to the ileal conduit.At 24 weeks of gestation she developed hypertension, which was treated with labetalol 400mg twice daily. There was urinary protein of 1.6g/L. She had no headache, visual disturbance, epigastric pain or hyper-re¯exia. The platelet count was 199 X 10 9 /L, and serum urate 0.38 mmol/L (NR 0.14-0.38). An ultrasound scan at 26 weeks of gestation showed a growth restricted fetus (head circumference 231mm, approximately 50 th centile, abdominal circumference 192mm, approximately 10 th centile) with a reduced volume of amniotic¯uid and reversed end-diastolic¯ow velocities in the umbilical artery. The fetal cardiograph was normal for 26 weeks of gestation with short term variation of 5.5 ms. Seventy-two hours later the fetus had died and labour was induced of a female weighing 600g (, 10 th centile for gestational age).Serology for toxoplasmosis, cytomegalovirus, rubella IgM and lupus anticoagulant were all negative. A postmortem was declined, but a skeletal survey estimated maturity at 23 weeks of gestation and revealed no other abnormality.During her admission for induction of labour she snored loudly and pulse oximetry during sleep revealed repeated drops in peripheral oxygen saturation to a nominal value of 40%. She admitted that she often felt fatigued during the day and was prone to falling asleep in inappropriate circumstances.Physical examination revealed a large neck, an oropharynx crowded with large tonsils and a low soft palate. Sleep studies con®rmed severe obstructive sleep apnoea with an apnoea index of 29.9 (number of apnoeic episodes per hour, normal range ,5-10) and an apnoeahypopnoea index of 30 (number of apnoeic plus hypopnoeic episodes per hour, normal range ,15). Apnoeas were associated with drops in peripheral oxygen saturation to as low as 20%. Treatment with nocturnal nasal continuous airways pressure (nCPAP) reduced the apnoea index to 1.7 and the apnoea-hypopnoea index to 4.3 with a signi®cant reduction in peripheral desaturation. Her partner also had obstructive sleep disorder and already had been treated with nCPAP. She remained hypertensive and was treated with labetalol 200mg daily.Three months later she again conceived and continued to use nCPAP at night throughout the pregnancy. Her systolic/diastolic blood pressure was at booking 110/80 mmHg on 100mg labetalol daily and a urine dipstick revealed 1 proteinuria. A routine ultrasound scan at 20 weeks was normal. Sleep studies at 26 weeks of gestation showed an apnoea index of 0.4 and a...

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Obstructive Sleep Apnoea During Pregnancy Requiring Tracheostomy

Abstract: The case is presented as an unusual example of the benefit of tracheostomy during pregnancy in a patient with obstructive sleep apnoea syndrome.

Cited by 34 publications

References 10 publications

Sleep-disordered breathing and pregnancy: potential mechanisms and evidence for maternal and fetal morbidity

Sleep-disordered breathing and pregnancy: potential mechanisms and evidence for maternal and fetal morbidity

Sleep disordered breathing and pregnancy

Obstructive sleep apnoea and fetal death: successful treatment with continuous positive airway pressure

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