You are reading 1 of 2 free-access articles allowed for 30 days
The prevalence of obstructive sleep apnea-hypopnea (OSAH) syndrome, which is defined as the combination of an Apnoea/Hypopnea Index (AHI) AHI >5/hour in conjunction with significant daytime sleepiness, in the general population is estimated at prevalence of 4 per in men and 2 per cent in women. However, specific populations are at higher risk for Obstructive Sleep Apnoea Syndrome (OSAS).
What specific patient populations are at high risk for OSAS?
Not every patient with OSAS is obese, but it is the main risk factor and at least 80 per cent of OSAS patients are obese. The prevalence of obstructive sleep apnoea (OSA) in morbid obesity (BMI >40) is estimated to be as high as 90 per cent, with an average higher OSA severity when compared to less-obese patients. A 10 per cent weight gain in OSAS patients predicts a 32 per cent increase in AHI, probably by increasing peripharyngeal fat accumulation.
In patients with severe, drug-resistant hypertension, defined as a clinic blood pressure of >140/90mmHg, while taking a combination of three or more antihypertensive drugs, titrated to maximally-recommended doses, up to 83 per cent have been found to suffer from OSA (defined by an AHI of >10/hour). A non-dipping or reversed pattern on a 24-hour blood pressure monitor is suspicious for OSA in any patient with hypertension.
Epidemiological studies have identified a strong association of OSA and atrial fibrillation (AF), with an increased risk for AF that is two-to-four times that of those without sleep-disordered breathing (SDB). Gami et al estimated that 48 per cent of patients with AF (n=115) referred for cardioversion had OSA.
In the Sleep Heart Health Study, comprising 6,424 men and women, subjects with significant OSA were more likely to have heart failure (HF), independent of other known risk factors. In a large case series of patients with HF undergoing polysomnography, OSA was detected in 37 per cent of 450 subjects studied. Central sleep apnoea is as common in HF.
Similar to heart failure, nocturnal rostral fluid shift plays an important part in the pathogenesis. A recent Swiss, multi-centre study found a 56 per cent OSA prevalence (AHI ≥15/h), which was largely previously underdiagnosed.
Are there any reliable clinical screening tools for sleep apnoea?
Up to 90 per cent of sleep apnoea sufferers in Ireland are undiagnosed; commonly, it is the bed partner who initiates the referral to a sleep clinic and the collateral history is often useful. The patient often underestimates the daytime symptoms, either due to lack of perception or due to concerns regarding consequences, such as driving licence issues in professional drivers.
The most widely-used questionnaire is the Epworth Sleepiness Scale (ESS), grading the likelihood of falling asleep in eight different situations.
It is important to note, though, that a normal ESS does not exclude the presence of sleep apnoea and individual clinical features alone are poorly predictive of OSA.
The Berlin questionnaire is more complex and has been well validated in several populations. It has a high specificity of up to 97 per cent for identifying OSA with a respiratory disturbance index of >15 per hour, however with low sensitivity of only 54 per cent.
The STOP-BANG questionnaire (Table 1) is simple, with eight questions including anthropometric data, such as BMI and neck circumference, and has been shown to have a much improved sensitivity of up to 87 per cent for moderate-to-severe OSA in 4,770 participants who completed polysomnograms in the baseline evaluation of the Sleep Heart Health Study. With the highest score of 8, the probability of sleep apnoea is 81.9 per cent.
I recommend combining these questionnaires with an assessment of the upper airway anatomy. A simple tool for this is the Mallampati Score, originally developed to predict the difficulty placing an endotracheal tube. (see image above).
What is the optimal diagnostic test for sleep apnoea and is there a role for ambulatory sleep studies?
The gold standard for the diagnosis of sleep apnoea remains polysomnography (PSG) in a sleep laboratory.
Limited sleep studies (no EEG, EOG or EMG) require less set-up and can potentially be carried out ambulatory in the patient’s own home. The main drawback of limited studies is that sleep stages and actual sleep time versus wakefulness cannot be assessed. This can lead to a significant underestimation of the sleep apnoea severity. Accidental disconnection of sensors with the subsequent need for repeat studies is common.
Ambulatory, limited studies have the advantage of being more representative of the real-life sleep situation at the patient’s home and cost savings and greatly reduced waiting times will make them an increasingly used alternative.
It is very important to insist that an experienced sleep technician score both full PSG and limited sleep studies manually.
Technology is moving on, though, and there are novel, contactless devices emerging, such as the SleepMinder Device, which has shown a high correlation with PSG in the detection of OSA and even periodic limb movements. The device, originally developed in Dublin, is using very low electromagnetic radiation and detects body movement by measuring the Doppler effect.
Pulse-oximetry alone is not recommended as a screening tool, but it can be highly suggestive of OSA in selected patients with a very high pre-test probability and no relevant comorbidities.
Are there alternatives if the patient is intolerant of CPAP?
Fortunately, the use of a Continuous Positive Airway Pressure (CPAP) machine is not always necessarily the first-line treatment in all cases. Compliance with CPAP improves with good patient education. In addition, I encourage patients to join support groups such as the Irish Sleep Apnoea Trust (ISAT), which also has excellent educational materials on its website.
At least 20 per cent of patients are not adhering to CPAP therapy long-term. There are, however, a number of treatment alternatives.
Some patients will be lucky enough to have positional OSA, with most of the sleep-disordered breathing occurring in supine position and the AHI in lateral position is normal or only in the mild range of disease. There are a number of treatment options, ranging from the low-tech good old-fashioned tennis ball method, to more sophisticated special pillows, to the more expensive high-tech option of electronic vibratory alarms worn across the chest or around the neck.
Mandibular advancement devices (MAD)
MAD are well established in the treatment of non-apnoeic snorers and in mild-to-moderate OSA, often even as first-line therapy, with compliance rates similar to CPAP therapy. Once the patient is accustomed to the MAD and any necessary titration has taken place, the patient should undergo a repeat sleep study with the MAD in situ to confirm that the AHI is reduced to an acceptable level.
Upper airway (UA) surgery
The results of UA surgery in unselected OSAS patients are generally poor. Procedures include uvulopalatopharyngoplasty (UPPP), which involves excision of the tonsils and posterior soft palate/uvula, and closure of the tonsillar pillars or maxillo-mandibular advancement surgery (MMA).
There is a role for surgery in defined cranio-facial abnormalities that lead to a reduced UA size. There is little doubt that isolated nasal procedures to improve nasal obstruction have no significant effect on the AHI; they can, however, have a role to improve tolerance of CPAP or MAD.
Bariatric surgery can be considered in patients with a BMI >=40 or >=35 in patients with comorbidities such as OSAS, diabetes mellitus or hypertension. In addition to the wide-ranging metabolic effects of gastric sleeve resection or Roux-en-Y gastric bypass, these are extremely effective in reducing OSA severity. The AHI decreases by about 75 per cent, with about two-thirds of the patients being cured of OSA. Many patients though will have to remain on CPAP, despite the often massive weight loss, albeit at a lower pressure level. Systematic follow-up sleep studies post-op are therefore essential, while the optimal time point post-op is still controversial.
Implantable hypoglossal nerve stimulation systems (HGNS) have been developed as a treatment for obstructive sleep apnoea. They stimulate the hypoglossal nerve during inspiration and recruit the lingual musculature, leading to decreases in pharyngeal collapsibility during sleep. Reported results from smaller, non-randomised, industry-sponsored studies are promising, but optimal patient selection still needs to be established. Best results appear to be achieved in less-severe patients with mainly hypopneas and lack of concentric pharyngeal collapse on sleep endoscopy.
Does CPAP therapy reduce the cardiovascular risk in patients with OSA?
The large, multi-centre, randomised, controlled SAVE trial, recently published in NEJM, showed no effect of CPAP therapy on the composite primary end-point, namely death from cardiovascular causes, myocardial infarction, stroke or hospitalisation for unstable angina, HF or transient ischaemic attack. The average CPAP use in this study was, however, low with 3.3 hours per night, which may explain the negative outcome.
An earlier randomised study which involved greater CPAP use (6.9 vs. 5.2h/night) improved cardiovascular outcomes.
In a large, long-term, prospective observational study published in 2015, severe OSA significantly increased the risk of fatal and non-fatal cardiovascular events. The patients with sufficient CPAP use of more than four hours per night, however, had similar cardiovascular mortality and morbidity rates to healthy individuals.
There is a large body of evidence that CPAP therapy results in a relatively small but significant decrease in blood pressure.
Patients with OSA also have a 25 per cent greater risk of AF recurrence even after catheter ablation than those without OSA, according to a meta-analysis of six studies with 3,995 patients from 2011.
Patients with OSA who were treated appropriately with CPAP had an 82 per cent lower rate of recurrence than patients who did not receive treatment.
In heart failure patients with OSA, CPAP improves left ventricular ejection fraction, exercise capacity and quality of life. Large randomised, controlled trials showing a mortality benefit are lacking, but uncontrolled studies suggest that untreated OSA is associated with greater mortality in HF.