I've just been watching an online presentation from the ATS conference last month. Doug Bradley, from Canada, extracted from the literature what he considered to be the most significant papers from the last year with regards to obstructive sleep apnoea.
The first, as customarily seems to be the case, was from his own lab. This study, published in circulation journal, was looking at whether fluid shift from the legs to the neck, in men with heart failure, during sleep overnight, was associated with obstructive and central sleep apnoea (two different groups of patients). It was demonstrated that this does, in fact, seem to happen. People with heart failure and leg swelling do tend to shift fluid overnight. Their legs get thinner, their necks get fatter and they develop sleep disordered breathing. Worse leg swelling is associated with worse sleep disordered breathing. Patients with more leg swelling are more likely to develop central rather than obstructive sleep apnoea. CPAP therapy makes no difference to the leg oedema but does reduce the neck swelling.
Children with obstructive sleep apnoea often find it difficult to do a sleep study. Access to specialist sleep labs for kids is difficult. For this reason, most ENT specialists in America still perform adenotonsillectomies without sleep studies prior (only 10% of kids having that surgery in the USA have had a sleep study - and I'm sure it's the same here). For that reason, a study published in the blue journal which looked at urinary protein biomarkers of OSA also got a guernsey. This was pretty interesting. There were 9 urinary proteins that are increased in kids with OSA as opposed to snorers and non-snoring controls, and 3 that were reduced. The ability to diagnose OSA in kids with a urine dipstick test may be around the corner - although the point was made that these kids were highly selected, and in particular had no evidence of upper respiratory infection.
Two further studies looked at the impact of exercise on sleep apnoea. The first, also published in the blue journal, put patients through a three month program of exercise of oropharyngeal muscles. The AHI fell by 40% over three months, and the Epworth sleepiness scale score also fell. The second study second study, by the same South American group, looked at patients aged between 42 and 70 years who had both heart failure and sleep apnoea. After a 4 month observation period, 4 months of exercise training ensued. AT the end of that four months the AHI dropped by 40% in the OSA group (but not in patients with CSA) and the nadir oxygen saturation overnight inthe OSA group rose by 5% . All good.
A 5 year follow up study of stroke survivors in Spain evaluated mortality in patients who had moderate to severe OSA and complied with CPAP therapy, as opposed to those who did not. Of 223 patients initially evaluated, 189 were ready to go into the study 2 months after their stroke. Of these, 166 were evaluated and 96 found to have an apnoea-hypopnoea index of more than 20 (an incidence of significant OSA of close to 60% in this population). 28 (29%) of those patients were unable to comply with CPAP - and 68% of those patients died within 5 years. 68 (71%) of the patients complied with CPAP, and only 50% of those patients died within 5 years. Of patients with only mild to moderate OSA (AHI less than 20) the 5 year mortality was 35-40%, which was not significantly higher than patients with no OSA.
CPAP compliance is not great in patients post-stroke OSA. Dr Bradley suggested that part of the reason may be, as shown by researchers in his lab, patients with OSA post stroke are often not sleepy.
Andrew
The first, as customarily seems to be the case, was from his own lab. This study, published in circulation journal, was looking at whether fluid shift from the legs to the neck, in men with heart failure, during sleep overnight, was associated with obstructive and central sleep apnoea (two different groups of patients). It was demonstrated that this does, in fact, seem to happen. People with heart failure and leg swelling do tend to shift fluid overnight. Their legs get thinner, their necks get fatter and they develop sleep disordered breathing. Worse leg swelling is associated with worse sleep disordered breathing. Patients with more leg swelling are more likely to develop central rather than obstructive sleep apnoea. CPAP therapy makes no difference to the leg oedema but does reduce the neck swelling.
Children with obstructive sleep apnoea often find it difficult to do a sleep study. Access to specialist sleep labs for kids is difficult. For this reason, most ENT specialists in America still perform adenotonsillectomies without sleep studies prior (only 10% of kids having that surgery in the USA have had a sleep study - and I'm sure it's the same here). For that reason, a study published in the blue journal which looked at urinary protein biomarkers of OSA also got a guernsey. This was pretty interesting. There were 9 urinary proteins that are increased in kids with OSA as opposed to snorers and non-snoring controls, and 3 that were reduced. The ability to diagnose OSA in kids with a urine dipstick test may be around the corner - although the point was made that these kids were highly selected, and in particular had no evidence of upper respiratory infection.
Two further studies looked at the impact of exercise on sleep apnoea. The first, also published in the blue journal, put patients through a three month program of exercise of oropharyngeal muscles. The AHI fell by 40% over three months, and the Epworth sleepiness scale score also fell. The second study second study, by the same South American group, looked at patients aged between 42 and 70 years who had both heart failure and sleep apnoea. After a 4 month observation period, 4 months of exercise training ensued. AT the end of that four months the AHI dropped by 40% in the OSA group (but not in patients with CSA) and the nadir oxygen saturation overnight inthe OSA group rose by 5% . All good.
A 5 year follow up study of stroke survivors in Spain evaluated mortality in patients who had moderate to severe OSA and complied with CPAP therapy, as opposed to those who did not. Of 223 patients initially evaluated, 189 were ready to go into the study 2 months after their stroke. Of these, 166 were evaluated and 96 found to have an apnoea-hypopnoea index of more than 20 (an incidence of significant OSA of close to 60% in this population). 28 (29%) of those patients were unable to comply with CPAP - and 68% of those patients died within 5 years. 68 (71%) of the patients complied with CPAP, and only 50% of those patients died within 5 years. Of patients with only mild to moderate OSA (AHI less than 20) the 5 year mortality was 35-40%, which was not significantly higher than patients with no OSA.
CPAP compliance is not great in patients post-stroke OSA. Dr Bradley suggested that part of the reason may be, as shown by researchers in his lab, patients with OSA post stroke are often not sleepy.
Andrew
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