Thirty articles were included. These reported 13 crossover RCTs (n=329), 8 parallel-group RCTs (n=254), one non-RCT (n=15), 11 clinical series with an historical control (n = about 200) and one case report.
Only 3 of the included studies were rated as providing level I evidence; the majority of the other evidence was level II or IV (see Other Publications of Related Interest). The main findings for each of the questions addressed are summarised here. Can APAP effectively reduce the apnoea plus hypopnea index (AHI) in OSA patients? APAP reduced the AHI to acceptable levels (less than 10 per hour) in more than 80 to 95% of the OSA patients studied in 16 RCTs, one non-randomised trial and 9 clinical series. The RCTs, however, were not designed to answer this question and none had a placebo control group. None of the studies included patients with significant central apnoea, and most excluded patients with congestive heart failure or chronic lung disease.
Can APAP reduce the AHI as well as conventional CPAP, in laboratory titration or as chronic treatment? Is the mean pressure lower on APAP devices?
In 12 RCTs, one non-RCT and 3 clinical series, similar AHIs were shown on treatment nights with APAP compared with nights on fixed CPAP. The mean or median treatment pressure was lower with APAP than with CPAP in 9 studies, and was higher in one study.
Can APAP effectively improve sleep quality and subjective and objective measures of daytime sleepiness in OSA patients?
Eleven RCTs, one non-RCT and 4 clinical series found some evidence that APAP improved sleep quality. An improvement in subjective measurement of daytime sleepiness, assessed using the Epworth Sleepiness Scale (ESS), was found with both APAP and CPAP in 4 crossover and 3 parallel-group RCTs; these also found no significant difference between APAP and CPAP. The only non-RCT found no improvement in ESS after one month' APAP when compared to baseline. The objective measures of daytime sleepiness reported were sleep latency (Multiple Sleep Latency Test improved in one clinical series) and the maintenance of wakefulness test latency (similarly improved with APAP and CPAP in 2 parallel-group RCTs).
Can APAP prevent significant nocturnal oxygen desaturation?
The evidence from various studies, which used different indices of arterial oxygen saturation, suggests that APAP prevents significant oxygen desaturation in most patients with OSA.
Are all APAP technologies equally effective?
No studies that met the inclusion criteria compared different APAP technologies.
Is APAP effective in determining an optimal fixed CPAP pressure for chronic fixed CPAP treatment during an attended or unattended APAP titration? Does APAP titration affect acceptance or adherence?
Four RCTs (2 of attended titration, one unattended, 1 partially attended) and 3 clinical series (one attended, 2 unattended) found that APAP could be used to select a fixed CPAP pressure that reduced the AHI to less than 10 per hr in up to 95% of the patients studied. One RCT suggested that using APAP to define a fixed pressure for treatment, rather than traditional CPAP, decreased the percentage of patients who declined to continue CPAP treatment at 6 weeks.
Does auto-CPAP increase the acceptance or utilisation with positive pressure treatment when used as long-term treatment for OSA?
The available evidence was inconsistent.
Are there safety considerations in selecting patients for auto-CPAP titration or treatment?
Only 2 studies specifically addressed safety. One was a case report that described the appearance of central apnoeas that occurred as pressure was increased during APAP titration. In one clinical series, complications including central apnoea with arrhythmia and hypoxemia were reported in 6 out of 21 patients with congestive heart failure or lung disease undergoing CPAP titration; however, the device used was not a true APAP unit.