Anatomical deformities of the upper airway can play a role in the pathogenesis of airway closure in OSA. Deformities of craniofacial and soft-tissue structures obstruct the upper airway at various levels, especially the retropalatal and retroglossal regions.[8,9,10] Some of the abnormalities include retrognathia, tonsillar hypertrophy, and macroglossia.[11] These findings underscore the importance of physical examination in patients with suspected OSA. To diagnose the cause of OSA in patients with a craniofacial abnormality, imaging studies are required, including lateral cephalograms.[12]
OSA is uncommonly associated with hypothyroidism, acromegaly, and renal failure. It is reasonable to obtain a thyroid profile in patients with suspected hypothyroidism.[13]
No specific blood tests are available to diagnose OSA. Measurement of erythropoietin, A1c, and C-reactive protein can help assess the severity of the disease, but the utility of these tests is unclear.[14] Spirometry and the flow-volume curve have been shown to be very nonspecific for OSA. The sawtooth sign has been demonstrated in a few patients with OSA.[15]
Clinical findings alone do not establish a diagnosis of OSA.[16] The STOP-Bang (snoring, tiredness, observed apnea, high blood pressure, BMI, age, neck circumference, and male gender) Questionnaire and Epworth Sleepiness Scale can be used to screen patients with signs and symptoms of OSA before referral to sleep apnea testing.[17,18]
Polysomnography is considered the criterion standard test for the diagnosis of OSA; it uses electroencephalography, electromyography, electro-oculography, electrocardiography, and pulse oximetry.[1] Airflow and respiratory efforts are also measured.[19] Two types of polysomnography procedures are used: (1) a full-night study, in which the study is performed on one night and positive airway pressure titration is performed on another night, and (2) a split-night study, in which both the study and pressure titration are performed in one night.[20]
Home sleep testing can be offered to patients who have a high pretest probability of moderate to severe OSA.[21,22] Such patients include those who have excessive daytime sleepiness and any two of the three criteria of habitual loud snoring; apnea, gasping, and choking, which are witnessed during sleep; and hypertension.[22]
OSA is diagnosed by calculating the apnea-hypopnea index, which represents the hourly average of apneic episodes associated with hypoxemia during sleep. The index is considered positive if there are more than 14 events per hour in an asymptomatic patient and more than four events per hour in a symptomatic patient.[23,24]
OSA has an enormous impact on the cardiovascular system. If left untreated, OSA can lead to numerous complications, including systemic hypertension, coronary heart disease, heart failure, pulmonary artery hypertension,[25] and atrial fibrillation.[26,27,28]
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Cite this: Asim Kichloo, Nadir Siddiqui, Nazir Lone, et. al. A Woman With AF After Husband’s Death, Grandkids’ Drug Abuse - Medscape - Nov 16, 2022.
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