Obstructive Sleep Apnea-Hypopnea Syndrome

So now I heat my bedroom with a thermostatically controlled electric fan heater, with my bedroom door closed, so it is not running constantly, or all of the time and hey presto, I don't have Sleep Apn

My Care Focus: Obstructive Sleep Apnea-Hypopnea Syndrome

Kevin Fernando, MBChB

Disclosures

August 15, 2024

This transcript has been edited for clarity.

In this podcast, I'm going to talk about what we need to know in primary care about obstructive sleep apnea-hypopnea syndrome (OSAHS), which is a commonly missed diagnosis.

OSAHS is part of the spectrum of sleep-related breathing disorders, ranging from simple intermittent snoring to severe obesity hypoventilation syndrome (what we previously called pickwickian syndrome), which is characterized by obesity, daytime hypercapnia, elevated carbon dioxide levels in the blood, and sleep-disordered breathing.

OSAHS is a sleeping giant. If untreated, OSAHS is associated with neurocognitive impairment; an increased risk for cardiometabolic disorders, including type 2 diabetes and hypertension; and an increased risk for all-cause death. You can see that OSAHS is a condition that impacts both quality and quantity of life. Additionally, people living with OSAHS are 10 times more likely to be involved in a road traffic accident, so this is a condition that, when it remains undiagnosed, may affect the community, too.

How common is OSAHS? OSAHS affects around 6%-13% of adults in the UK, so it is as common as type 2 diabetes but remains underdiagnosed in primary care. Around 1 in 4 of "tired all the time" presentations in primary care are secondary to OSAHS, sedative medications such as amitriptyline, or insomnia disorders.

What happens during OSAHS? Normal sleep requires an unobstructed pathway from the nasal pharynx to the lung. Anything that obstructs the airway — for example, a deviated nasal septum, chronic rhinitis or sinusitis, enlarged tonsils, or obesity — results in repeated narrowing or closure of the upper airways, which leads to upper airway resistance and impedance of airflow.

This in turn can lead to fragmented sleep and shallow breathing (hypopnea), or episodes of complete cessation of breathing (apnea) — hence, the terminology OSAHS (obstructive sleep apnea-hypopnea syndrome). The resulting hypoxemia triggers the central nervous system to wake the individual, reopen their airway, and start breathing again.

In severe cases, OSAHS can lead to hypercapnia, as mentioned, and obesity-hypoventilation syndrome. This fragmented sleep leads to autonomic nervous system dysfunction — in particular, sympathetic nervous system stimulation — and this is thought to be what drives the increased risk for cardiometabolic disease and death.

Who is likely to be affected by OSAHS? The risk for OSAHS is increased in people living with overweight or obesity; type 2 diabetes; cardiac arrhythmias, particularly fibrillation; stroke or transient ischemic attack; chronic heart failure; moderate or severe asthma; polycystic ovary syndrome; Down syndrome; hypothyroidism; and treatment-resistant hypertension.

Interestingly, the link between OSAHS and type 2 diabetes is bidirectional. Past studies have demonstrated that OSAHS was independently associated with an increased risk of developing type 2 diabetes, and patients with insulin-treated type 2 diabetes had a significantly increased risk for OSAHS, especially women.

It is postulated that the intermittent hypoxemia and recurrent arousals in OSAHS can stimulate the autonomic nervous system, leading to increased catecholamine production, which impairs glucose metabolism, reduces insulin sensitivity, and ultimately induces beta-cell dysfunction in the pancreas.

Conversely, insulin resistance has been demonstrated to reduce the ventilatory response. Additionally, systemic inflammation and neuropathy in type 2 diabetes may weaken respiratory muscles and tone, leading to OSAHS.

We should consider checking a regular A1c level in all of our patients living with OSAHS, and we should consider screening for OSAHS in our patients living with type 2 diabetes, particularly those living with overweight or obesity, too.

Treatment-resistant hypertension also presents a fascinating relationship with OSAHS, which has changed my practice, to be honest. The prevalence of OSAHS is 30%-50% in hypertensive individuals, 70%-85% in those with resistant hypertension, and over 90% in those with refractory hypertension.

Next time you're adding in a fourth-line antihypertensive drug, such as spironolactone, think to yourself, could this individual have underlying OSAHS? This has been a real practice-changing message for me.

When should we suspect OSAHS? Sleepiness is often, obviously, a feature, but be aware that OSAHS can be associated with insomnia and sleep disruption. Other features of possible OSAHS include snoring, witnessed apneic episodes, unrefreshing sleep, waking headaches, excessive sleepiness, tiredness or fatigue, nocturia, choking during sleep, and cognitive dysfunction or memory impairment.

If an individual has two or more of these possible features of OSAHS, take a sleep history and formally assess for OSAHS. We commonly use the Epworth Sleepiness Scale in primary care, but remember, this scale is helpful to assess sleepiness rather than to diagnose OSAHS. We should not use the Epworth Sleepiness Scale alone to determine whether referral to a sleep clinic is required.

We should also use the STOP-BANG questionnaire, which is an acronym for snoring loudly, tired during the day, observed apneic or choking episodes, high blood pressure, BMI over 35, age over 50, neck size over 16 in or 40 cm, and male gender. If the individual answers yes to five to eight of these questions, this suggests a high risk for OSAHS.

Management of OSAHS is largely driven by our sleep clinics, with consideration of continuous positive airway pressure (CPAP). CPAP maintains a patent airway and stops episodes of apnea or hypopnea. CPAP can improve sleepiness, alertness, and overall quality of life. Of course, CPAP also mitigates the risk for future adverse cardiometabolic complications.

What can we do in primary care to aid management? We can reinforce relevant lifestyle modifications, such as weight loss to reduce adipose tissue in the pharynx, which will in turn reduce airway narrowing. We can counsel about reducing alcohol intake, because alcohol causes relaxation of muscles in the neck and pharynx, worsening airflow obstruction.

Smoking leads to inflammation of the respiratory mucosa, adding to airway narrowing. Signposting to smoking cessation services is important on many levels. Lastly, advise on practical measures when sleeping. Sleeping in a lateral and not supine position is helpful to reduce nasopharyngeal collapse. This is easier said than done, but some of my patients sleep with a small backpack or use extra pillows to stay lateral. We should also undertake a medication review and stop any sedative medication or muscle relaxants, especially benzodiazepines.

Finally, a few pointers about driving, sleepiness, and OSAHS. Driving licensing rules, of course, vary across the world. However, OSAHS itself is not the problem; tiredness and sleepiness are. Our patients are responsible for deciding whether they are too tired or sleepy to drive. It doesn't matter if they have suspected OSAHS, were up all night with a new baby, or were binge-watching the latest Netflix series through the night. If they are likely to be too sleepy to the point where their driving might be impaired, they must not drive.

If the sleep clinic diagnoses OSAHS but says that the sleepiness during waking hours is not excessive, then your patient can continue to drive. If, however, the sleep clinic diagnoses moderate or severe OSAHS with excessive sleepiness, your patient must not drive until the sleep clinic is satisfied that CPAP or other treatment has the sleepiness under control.

Finally, the Sleep Apnoea Trust is a UK-based patient support charity working to improve the lives of people living with OSAHS, their partners, and their families. They have some great resources on their website for patients and also for us as healthcare professionals.

Medscape

Me: So i'm a Type 2 Diabetic and i've had Sleep Apnea for the past 25 years or so although I've not addressed it, as it seems to only occur during the winter months for me - which got me thinking. So now I heat my bedroom with a thermostatically controlled electric fan heater, with my bedroom door closed, so it is not running constantly, or all of the time and hey presto, I don't have Sleep Apnea any more - Fancy that!!

My Sleep Apnea got so bad, I would wake up not breathing sometimes and I'd hit my chest with my fist, repeatedly, to get my lungs working again - and I'm stil lhere to tell the story too.