Obstructive sleep apnoea – debunking the myths

PREOPERATIVE ASSESSMENT OF OBSTRUCTIVE SLEEP APNOEA

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P Robinson
Royal Adelaide Hospital, Adelaide, SA

This talk will focus on the medical assessment of Obstructive Sleep Apnoea (OSA) from my perspective as an adult Respiratory and Sleep Physician.

Why is it important to identify patients with OSA preoperatively? While it seems intuitive, there are only limited data which demonstrate an increased risk of postoperative cardiac and respiratory complications as well as an increased length of stay in patients with OSA (1)

How then to identify patients with OSA preoperatively? The gold standard for the diagnosis of OSA remains an overnight polysomnogram(PSG) in an inpatient sleep laboratory. This is an expensive, time consuming process which is not practicable for every patient suspected of suffering with OSA. However, if there is a strong suspicion of OSA and the proposed surgery is high risk, then a full PSG should be obtained beforehand and appropriate treatment instituted.

There have been numerous attempts to validate simpler diagnostic tools which include various combinations of clinical history and examination findings, more specific questionnaires and limited monitoring such as overnight oximetry. Important symptoms include witnessed snoring and apnoeas and abnormal daytime sleepiness. Discriminatory examination criteria are age, sex, body mass index (BMI), neck circumference (greater than 45 cm) and pharyngeal anatomy.

Validated questionnaires include the Epworth Sleepiness Scale and the Berlin Questionnaire. In one study, all patients with severe OSA had an Epworth score above 10 (2). A multivariate apnoea index combining relevant symptoms, age, sex and body mass index showed that at least one-third of full PSG could have been averted (3). Overnight oximetry can also identify patients with moderate to severe OSA with 84% accuracy (4). This accounted for 1/3 of all patients referred to this sleep centre. Other investigations which might be included in specific patients include radiological assessment of the upper airway and nasendoscopy under sedation.

There is ongoing discussion about in hospital versus in the home sleep studies. The pace of advancing technology has outstripped the medical profession’s ability to validate and the health industries ability to fund these new methods. However, there is little doubt that accurate PSG will be performed in the home setting in the near future (5).

What are the physiological and biochemical mechanisms contributing to OSA?

The two primary forces tending to collapse the upper airway are the intraluminal negative pressure generated by the diaphragm during inspiration and the extraluminal pressure resulting from tissue and bony structures surrounding the upper airway. The extraluminal pressure is increased by fat deposition around the pharynx or by abnormal bony structure such as a recessed mandible. One study showed that Asian patients had more severe OSA for a given BMI than Caucasians, postulating that this was due to anatomical differences in the upper airway.

Forces tending to keep the upper airway patent include the pharyngeal dilator muscles and longitudinal traction on the airway resulting from lung inflation. Genioglossus is the best studied and probably most important pharyngeal dilator muscle. Neuromuscular control is reduced during sleep, especially in REM sleep, further contributing to upper airway collapse (6).

Normally, ventilatory control (largely driven by O2 and CO2 chemoreceptors) is less stable during sleep than wakefulness. This instability can be magnified by OSA setting up a negative feedback loop which, it is postulated, can become self-perpetuating (6).

In addition to these physiological mechanisms, there is increasing interest in biochemical abnormalities in fat metabolism (eg leptin, reactive oxygen species) but it is not clear whether these are pathogenetic for OSA or an epiphenomenon associated with obesity (7).

How should OSA be managed, once identified? Splinting of the upper airway with positive air pressure is now the definitive treatment for OSA. CPAP provides immediate, effective treatment and is now well tolerated with good long term compliance. Most current CPAP units have in-built pressure sensors to detect snoring or apnoeas (fluctuating or absent pressure) coupled to a sophisticated algorithm to adjust the delivered pressure. Nasal and full-face masks have improved but remain problematic for some patients and this treatment still suffers from the perception of being uncomfortable and ugly! In addition to controlling the apnoeic events and restoring normal respiration and sleep, there is evidence that CPAP can control end organ effects such as cardiac disease (8) and stroke (9).

Intraoral devices which position the mandible forward have also been shown to be effective, mainly in patients with mild OSA (10).

Surgical treatment remains controversial. There are numerous case reports but no adequate comparative trials have been conducted to verify surgical treatment. Several different operations are being offered to reduce the bulk of upper airway soft tissue or reposition the tongue or bony structures. An important subgroup is the younger patient with enlarged tonsils, some of whom have severe OSA and clearly benefit from adenotonsillectomy.

Management of obesity is central to treating OSA but a detailed discussion is beyond the scope of this talk.

I will complete this presentation with a case report of a young man presenting with moderately severe OSA. Further investigation showed enlarged tonsils as well as obesity. Points for discussion include appropriate diagnostic investigations and his treatment options. Should he use CPAP prior to surgery? Does he need surgery at all? What are his anaesthetic risks?

Time of Presentation<
Saturday 13 May 2006 - 1530-1700

References

1. Cartagena R. Preoperative evaluation of patients with obesity and obstructive sleep apnoea. Anesthesiology Clin N Am 2005;23:463-478.
> 2. Johns M. Daytime sleepiness, snoring, and obstructive sleep apnoea. The Epworth sleepiness scale. Chest 1993;103:30.<br> 3. Maislin G, Pack A, Kribbs N, A survey screen for prediction of apnea. Sleep 1995;18:158-166.
> 4. Antic N, Catcheside P, Hansen C, Utility of a new high sampling rate oximeter and dip-rate software at diagnosing moderate-severe OSA in the attended and unattended setting. TSANZ abstract presentation 2005.<br> 5. Pack A. Advances in sleep-disordered breathing. Am J Respir Crit Care Med 2006;173:7-15.
> 6. White D. Pathogenesis of obstructive and central sleep apnea. Am J Respir Crit Care Med 2005;172:1363-1370.<br> 7. Phillips C, Grunstein R. Obstructive sleep apnoea: time for a radical change? Eur Respir J 2006;27:671-673
> 8. Marin J, Carrizo S, Vicente E. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnooea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365:1046-1053.<br> 9. Yaggi H, Concato J, Kernan W. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med 2005; 353:2034-2041.
> 10. Mehta A, Qian J, Petocz P. A randomized, controlled study of a mandibular advancement splint for obstructive sleep apnoea. Am J Respir Crit Care Med 2001; 163: 1457-1461.<p>