Last updated on:February 3rd, 2021
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This is a common and important symptom, as untreated OSA can lead to accidents due to extreme daytime sleepiness.
This is due to the interrupted sleep patterns of these patients resulting in non-restorative sleep.
Patients may be blissfully unaware of this important symptom; it often has to be elicited from their partner or family members.
This is due to the obstruction of airflow during sleep that is caused by the recurrent collapse of the velopharyngeal or oropharyngeal airway.
Apneic episodes during sleep
The patient's partners and family members may complain of cessation of breathing during sleep. This may trigger awakening with sudden gasping.
This too is because of airflow obstruction during sleep.
Male gender increases the risk of OSA. The cause for this is not entirely clear but is thought to be due to anatomical reasons.
Dull, holocephalic headaches on waking are a recognized symptom of OSA. The exact cause for this is unclear. Potential etiologies include night-time hypercapnia with vasodilation; an increase in intracranial pressure; and/or sleep disturbances.
OSA can impact attention, memory, visuospatial function, and executive function. The exact cause for this is unclear.
There is an association between OSA and depression. The exact cause for this relationship is unclear, but is thought to be due to fragmented sleep.
There may be a genetic predisposition to OSA through inherited craniofacial structure abnormalities.
Obesity is a known risk factor for OSA. This is thought to be due to fat deposition around the airway, leading a to greater risk of pharyngeal airway collapsibility, and functional impairment of the upper airway muscles.
These include an abnormal maxillary or mandibular size and tonsillar or adenoid hypertrophy. All of these abnormalities increase the risk of airway obstruction.
Hypertension is common amongst patients with OSA. The exact mechanism of this relationship is thought to be multifactorial, relating to oxidative stress, endothelial dysfunction and activation of the sympathetic and renin-angiotensin-aldosterone systems.
Signs of pulmonary hypertension or cor pulmonale
These may include a right ventricular heave, a loud or palpable P2, a prominent jugular venous pressure or peripheral edema. This is thought to be due to pulmonary vasoconstriction in the setting of alveolar hypoxia.
Narcolepsy can present with sleepiness and fatigue.
The presence of cataplexy, hypnagogic hallucinations and sleep paralysis can help differentiate this from OSA. A polysomnogram can differentiate between these two entities.
Central sleep apnea
This can present similarly with episodes of apnea and daytime somnolence; and it is associated with underlying congestive cardiac failure, renal disease, and cerebrovascular disease.
CSA is differentiated from OSA by the lack of respiratory effort. A polysomnogram can assist in making the diagnosis.
Periodic limb movements
This can lead to recurrent movements of the limbs causing sleep fragmentation and daytime sleepiness.
This can be differentiated on the polysomnogram.
This can mimic OSA and be differentiated on the polysomnogram.
Gastroesophageal reflux disease
This can mimic OSA by presenting with a choking sensation. This can be differentiated via polysomnogram and by demonstrating response to a proton pump inhibitor.
Nocturnal asthma can mimic OSA by presenting with nocturnal dyspnea and choking. This can be differentiated via a polysomnogram, which would be normal in nocturnal asthma.
A polysomnogram is required for the diagnosis of OSA. An in-laboratory polysomnogram is the gold standard for diagnosis, but home testing can be considered in select patients.
More than five episodes of predominantly obstructive respiratory events per hour of sleep is required for the diagnosis, in addition to the symptoms as described above. The most common measure of obstructive respiratory events is the apnea-hypopnea index (AHI).
The severity is then graded depending on the number of obstructive respiratory events per hour of sleep. They are classified into:
Several clinical prediction tools have been developed to screen for OSA. These include: the STOP-BANG questionnaire, sleep apnea clinical score, Berlin questionnaire, and Epworth sleepiness scale.
Of these, the STOP BANG questionnaire may have the highest sensitivity. This consists of eight questions, namely:
A score of 3 or more puts the patient at high risk of OSA; and these patients should be strongly considered for confirmatory testing with a polysomnogram.
It is important to note that these tools are for screening purposes only. A polysomnogram is still required for the formal diagnosis of OSA.
Screening for associated conditions
Patients with OSA have a higher prevalence of type 2 diabetes, dyslipidemia, and hypertension. Screening for these conditions should be considered and their cardiovascular risk profiles should be optimized.
The diagnosis of OSA should be explained to the patient, particularly with regards to the natural history and consequences of untreated OSA. This is also an important comorbidity to be aware of perioperatively, due to the risk of difficult ventilation/intubation and postoperative airway obstruction.
All patients should be counselled about restrictions on driving and operating heavy machinery if their OSA is not appropriately controlled. This is particularly relevant in high risk occupations (i.e., taxi drivers, forklift operators, truck drivers). Sleepiness accounts for a significant percentages of motor vehicle accidents and untreated OSA is a significant risk factor.
Positive airway pressure therapy
There is good evidence that continuous positive airway pressure can improve OSA symptoms, reduce motor vehicle accidents, improve blood pressure and overall quality of life. However, the effect on mortality is still controversial at this point.
Non-adherence is a common issue amongst patients, and many patients do not tolerate the mask. Patients should be followed up closely initially to address these issues.
The importance of weight loss should be emphasized to all patients with OSA. This can result in a reduction in the apnea-hypopnea index, alleviate daytime sleepiness, and reduce overall cardiovascular risk.
Exercise is an important adjunct in the management of OSA, and there is evidence that it improves OSA symptoms independent of the degree of weight loss.
Avoidance of alcohol
Alcohol consumption can worsen OSA due to its effect on depressing the central nervous system.
Avoiding certain medications
Medications that depress the central nervous system should be avoided, such as benzodiazepines and certain antidepressants.
There are a wide variety of oral appliances that aim to maintain upper airway patency. These include mandibular advancement splints and tongue retaining devices. These work by either holding the tongue more anteriorly or by protruding the mandible anteriorly. They can be very effective in the right patients.
Upper airway surgery
In specific circumstances, upper airway surgery can be considered. This is applicable to patients who have failed other therapies and have a surgically correctable cause for their airway obstruction, such as tonsillar or adenoid hypertrophy, or craniofacial abnormalities.
Uvulopalatopharyngoplasty (UPPP) is the most common surgery performed for OSA; in this, excess tissue from the soft palate and pharynx is removed.