The obstructive sleep apnoea hypopnoea syndrome (SAHS) has been recognised for over 30 years and an effective treatment—namely, nasal continuous positive airway pressure (nCPAP)—has been available for almost 20 years. Research into SAHS has risen exponentially during this time, providing us with greater understanding of the epidemiology, pathophysiology, and morbidity associated with the disease. Despite this research, the most cost effective pathway for the diagnosis and management of SAHS has yet to be established and remains the subject of debate.

The gold standard diagnostic test for SAHS is overnight multichannel polysomnography (PSG) which enables detection of obstructive apnoeas, hypopnoeas, and arousals. However, PSG has several drawbacks. It is an expensive system to set up and run. The sleep laboratory is an artificial environment and some patients have a disturbed sleep pattern due to the foreign setting and thus interpretation of the PSG findings in these patients is problematic. The definition and quantification of apnoeas, hypopnoeas, and arousals remain subjects of debate.1-3 The apnoea hypopnoea index (AHI) increases in normal subjects with age, has moderate interobserver variation, and is poorly correlated with symptoms of excessive daytime somnolence.4 ,5 Thus, despite full PSG, identification of those patients with SAHS who benefit from nCPAP remains unclear. It has been argued that SAHS is a clinical diagnosis characterised by daytime somnolence associated with two or more of the following symptoms: loud snoring, choking or gasping during sleep, recurrent nocturnal awakening, unrefreshing sleep, daytime fatigue, and impaired concentration. However, for most physicians this rationale is too imprecise.

Many sleep laboratories use a combination of diagnostic modalities which represent a halfway house between the two extremes of full PSG and a trial of nCPAP—limited channel polysomnography; a combination of video, microphone and oximetry monitoring; pulse transit time; overnight oximetry; and, more recently, nasal pressure monitoring—with variable success.6-11 Recent studies attempting to correlate clinical symptoms and signs with the probability of a positive diagnosis of SAHS have produced encouraging results when used in combination with some of these more limited diagnostic tests.12-14 The simplest test is overnight oximetry which has the advantages of being readily available, relatively inexpensive, and can be performed at home enabling the patient to have a typical night’s sleep. However, it is not possible to differentiate between desaturations occurring secondary to obstructive apnoeas, central apnoeas, primary pulmonary disease, and cardiac disease using overnight oximetry. Thus, its role in the investigation of SAHS is contentious as it is less sensitive and specific than PSG. Several studies of overnight oximetry have shown a moderate positive predictive value but a poor negative predictive value.6-9 Epsteinet al found that overnight oximetry had an unacceptably high false positive rate such that it did not reduce the overall costs of investigation and treatment of patients with possible SAHS, although it is unclear why they had a higher false positive rate than in the other studies.9

In this issue of Thorax Chineret al 15 have once again looked at the validity of overnight oximetry as a screening device, comparing full PSG with overnight oximetry in 275 patients with suspected SAHS. For overnight oximetry the authors defined a significant oxygen desaturation as any fall in oxygen of >4% below baseline values during a six second period and derived an oxygen desaturation index (ODI) as the total number of desaturations during the night divided by the total number of hours in bed. Using ODI values of >5, >10, and >15 they diagnosed 192, 160, and 139 patients, respectively, as having SAHS of whom 14, six, and four subjects, respectively, were false positives when assessed by PSG. These results gave sensitivity and specificity values ranging from 62% to 93% and positive predictive values of 92% to 96%. For the group of patients with ODI values of >5 the 14 false positive patients all had intercurrent diagnoses including chronic obstructive pulmonary disease (COPD), obesity hypoventilation, ischaemic heart disease, and myotonia dystrophica and had significantly lower spirometric values than the true positive population. Using their cut off ODI value of >5 the authors estimate that they would have reduced the number of PSGs performed in their unit by approximately 50%. Interestingly, patients with false negative results tended to have milder disease with respect to severity and duration of symptoms and also AHI as defined by PSG. Unfortunately, the response to treatment of these two patient groups was not investigated. This study differs from previous studies in two potentially important aspects. Firstly, 80% of the subjects investigated by Chineret al had a diagnosis of SAHS which is higher than that documented previously and may explain the greater positive predictive value for overnight oximetry. Secondly, by reducing the oximetry response to six seconds and classifying a desaturation as any fall in Sao ₂ of >4% during this period, the authors proposed that the number of desaturations due to artefact are reduced whilst “true” desaturations are detected thereby increasing sensitivity and specificity. However, this hypothesis was not formally evaluated in the study.

For clinicians struggling to cope with the public sector underfunding of sleep laboratories and the pressure of increasing referrals for investigation of SAHS, this study is very encouraging. Overnight oximetry using a cut off ODI value of >5 appears to be a good positive screening device when taken with other simple measures which are available in all respiratory function laboratories. A combination of clinical predictive factors and overnight oximetry will suffice as an initial screening test for most patients. For those with positive overnight oximetry, spirometric tests should be performed to exclude primary lung disease. It may also be prudent to perform an ECG since left ventricular dysfunction is extremely unlikely with a normal ECG.16 Those patients with normal spirometric and ECG results but abnormal overnight oximetry can thus be started on a trial of treatment. Patients with negative overnight oximetry and a high clinical suspicion of SAHS and those with positive overnight oximetry but abnormal spirometric or ECG results should undergo further investigations as appropriate such as PSG.