## 1 Introduction  
Sleep apnea is a common condition in the category of sleep disorders. The complexity and relevance of early diagnosis and treatment is motivated by several complications it can cause. Obstructive sleep apnea is one of the most common chronic respiratory diseases with a prevalence of 3-7% in the adult population, along with other obstructive pulmonary diseases such as asthma (7.7%) and chronic obstructive pulmonary disease (11.7%) [1; 2]. As one of the characteristic mechanisms of sleep apnea syndrome, hypoxia is a condition that can progress with cardiovascular, neurological, or ophthalmic complications [1; 2]. Sleep apnea syndrome is classified into three types depending on its production mechanism: obstructive, central, mixed. Obstructive sleep apnea syndrome (OSAS) is characterized by the collapse of the upper airways (CAS) that causes full or partial lapse of air flow, followed by a decrease in oxygen saturation of the arterial blood, and disruption of sleep stages by short awakenings. Mixed sleep apnea syndrome is characterized by episodes of central apnea and obstructive sleep apnea within the same episode [2]. In central SAS (SASC) disorders occur in the respiratory centers, so the impulse is transmitted to the respiratory muscles causing insufficient ventilation.  
The severity of OSAS can be estimated using the apnea-hypopnea index (AHI), apnea being defined by a total obstruction of the upper airways, while hypopnea by a partial one. Thus, AHI highlights the number of episodes of apnea/hypopnea, being able to establish the lack of pathology (AHI \(<\) 5/h) or its presence (AHI \(\geq\) 5/h), the latter being classified as mild (AHI: 5-15/h), moderate (AHI: 15-30/h) and severe (AHI \(>\) 30/h) SAS [3]. Investigations for OSAS diagnosis are drowsiness questionnaires, pulmonary function tests, ENT examination, printing cardio-respiratory polysomnography or multichannel respiratory polygraphy called sleep study (gold standard in diagnosis), cardiac examination, vigilance tests, sleep latency tests [2; 3]. Favoring factors in the onset or progression of SAS have been mentioned in the literature: obesity (the main risk factor), gender, alcohol (depression of the upper respiratory tract muscles selectively and negatively influences the response to awakening at the end of each apnea), physiological (short neck) or pathological structural anatomical defects (adenotonsillar hypertrophy, retrogation and macroglossia, size reduction of the upper respiratory tract that may be caused by obesity, and pathology in which there is an increase in adipose tissue deposition in the soft tissues of the pharynx), snoring determined by the pathways narrowing that occurs years before the onset of the pathology) and cardiovascular risk factors: essential hypertension, insulin resistance, pathological glucose tolerance test, dyslipidemia [4].  
Among the most common eye events we mention are floppy-eyelid syndrome, glaucoma, central serous chorioretinopathy, non-arteritic anterior ischemic optic neuropathy (NAION), central vein occlusion of the retina, diabetic retinopathy, macular disease, keratoconus, papillary conjunctivitis, corneal punctate epitheliopathy, recurrent corneal erosion, keratitis, dry-eye syndrome [3; 5]. During episodes of apnea hypoxemia and transient hypotension occur, sometimes oxyhemoglobin desaturation drops below 30%, these being proposed as an etiological mechanism for the advancement of glaucoma and NAION complications after ischemic optic nerve injury [6].