Driving and obstructive sleep apnoea.

Driving is a skill requiring many simultaneous cerebral activities, mainly eye-hand coordination with accurate speed and direction computations. This high level of activity requires full concentration, as evidenced by the higher accident rates in those who use mobile phones while driving. There is very good evidence that inadequate sleep is an important cause of fatigue-related driving accidents, possibly causing up to 20% of all accidents. Most of these sleep-related accidents are due to lifestyle issues such as driving without having had adequate sleep, and happen at times when vigilance is naturally low (eg, in the afternoon and at night). Furthermore, accidents are extremely expensive to society, with fatal accidents costing over £1 million. For nearly 20 years the part played by sleep disorders—particularly obstructive sleep apnoea (OSA)—has been recognised. OSA can grossly fragment sleep and produces excessive daytime sleepiness that is likely to cause the increased road traffic accident rates seen in patients with OSA. However, it is not entirely clear what aspects of sleep fragmentation in OSA lead to poorer driving ability: is it just sleepiness and inevitable ‘‘microsleeps’’ at the wheel or is there also general impairment of driving skills including eye-hand coordination such as occurs with excess alcohol? The evidence suggests mixed effects during simulated driving. As with arguments over OSA and cardiovascular risk, there may be confounders influencing any apparent relationship between OSA and driving accidents. For example, obesity itself is a cause of excessive sleepiness without necessarily the presence of OSA. Obesity may influence mechanical aspects of driver ability such as proper scanning of the road (particularly to the sides), as well as fully effective braking and steering in hazardous situations. Other risk factors for OSA such as alcohol consumption may also be important confounders. In certain studies the occurrence of an accident or near-accident may have provoked investigation for sleep apnoea and falsely raised the apparent association. Given the highly plausible hypothesis that OSA causes accidents, what studies are available which demonstrate a cause and effect relationship? A recent meta-analysis reviewed the 40 or so relevant studies in this area, both in commercial and non-commercial drivers. The original cohort studies on patients with OSA were sometimes small, often had relatively unmatched controls and were based on self-reported accidents rather than an objective record. These studies suggested that the excess accident rate was as high as four times the rate in controls. George and Smiley were the first to study over 1000 patients and controls using objective data from a central accident record system. An increased accident rate was found in patients with OSA, but only at the more severe end of the spectrum (apnoeahypopnoea index (AHI) .40) where the rate was about double the control figure. A more recent cohort study from Japan also found a dose-response effect of both AHI and Epworth Sleepiness Scale (ESS) in a group of 448 subjects attending a sleep laboratory, with an accident rate nearly three times higher in those with AHI .30 than in those with AHI ,5. Case-control studies starting with patients having accidents (n = 102) rather than OSA suggested that those with OSA were 4–7 times more likely than control subjects (n = 152) to have had an accident, despite controlling for some potential confounders. However, there seemed to be no AHI ‘‘dose-response’’ effect or relation to sleepiness but, interestingly, recent alcohol consumption was a synergistic factor with OSA. A Spanish study also found a more than twofold higher accident rate in 60 patients with OSA compared with 60 control subjects, but again there was no dose-response effect either with the AHI or subjective sleepiness as measured using the ESS. Cross-sectional studies on normal populations have also shown an association with sleep apnoea. In the Wisconsin cohort study (n = 913) there was a small increase in the accident rate (particularly considering multiple accidents) over 5 years in those with an AHI .15. Single accidents rates showed no real ‘‘dose-response’’ effect with AHI. Cross-sectional studies are prone to the effect of confounding variables and therefore randomised and controlled intervention studies would be more robust. However, it would be unethical to run such a study and expect a control group of untreated symptomatic patients to continue driving, awaiting their accidents. What is the best that has been possible? An early study looked at patients with OSA and compared 36 subjects compliant with continuous positive airway pressure (CPAP) with 14 non-compliant with CPAP (control subjects). A sevenfold higher rate compared with the average rate in the area was found before treatment, which only subsequently fell to below local area rates in the patients compliant with CPAP. However, numerous studies have shown that patients non-compliant with medical advice are different from compliant patients, and this is therefore an important confounder. George performed a similar study comparing driving accident rates before and after prescribed CPAP for subjects with OSA versus matched controls using independent records of the actual accidents. The accident rate was about three times higher than control levels before treatment, falling to control levels after treatment but only in those compliant with CPAP. A significant problem with these studies is that the diagnosis of OSA itself may be effective in reducing accident rates by alerting the patients (and relatives) to the extra risk, leading to a more responsible attitude to driving when sleepy. An alternative approach to understanding the accident risk—and perhaps the mechanism of any increased risk—has been the use of driving (or, more usually, steering) simulators. These clearly demonstrate impaired steering ability compared with control subjects, with increased wandering from the road and delayed responses to additional distracting events. 19 The poorer performance of patients with OSA appeared to be a combination of increasing sleepiness as well as poor eye-hand coordination. Simulated steering ability has also been shown, in randomised controlled trials of patients with moderate to severe OSA, to improve in those treated with CPAP but not in those treated with ineffective sham CPAP. Correspondence to: Professor J Stradling, Sleep Unit, Oxford Centre for Respiratory Medicine, Churchill Hospital, Oxford OX3 7LJ, UK; [email protected] Editorials