to describe a case of bilateral and simultaneous central retinal vein occlusion ( rvo ) in a young patient diagnosed with obstructive sleep apnea syndrome ( osas ) . a 38-year - old man with morbid obesity and daytime sleepiness presented with a history of bilateral vision loss . his visual acuity ( va ) was hand movements , and fundus examination ( fe ) revealed bilateral central rvo . laboratory tests for thrombophilia showed increased hematocrit ( 59% ) and high levels of fibrinogen and c - reactive protein . in addition , he received intravitreal ranibizumab . at 10 months after presentation , his va was no light perception in the right eye and hand movements in the left eye . fe revealed bilateral retinal and optic nerve atrophy , and the occurrence of a nonarteritic anterior ischemic neuropathy in the right eye was considered . central retinal vein occlusion ( rvo ) is a common retinal disorder that usually affects individuals 55 of age and , if present in younger individuals , at times hides a procoagulant state [ 1 , 2 ] . central rvo normally occurs unilaterally , but affected patients have an increased risk of developing another vascular occlusion in the fellow eye . on the other hand , recently , rvo has been associated with the obstructive sleep apnea syndrome ( osas ) , a condition characterized by repeated episodes of apnea during sleep that increases the risk of cardiovascular disorders . we report the case of bilateral and simultaneous central rvo in a young patient affected by osas . in august 2012 , a 38-year - old man came to our center with a 5-day history of progressive and bilateral vision loss . his visual acuity ( va ) was hand movements in both eyes . a relative afferent pupillary defect ( rapd ) fundus examination ( fe ) of both eyes revealed vascular congestion and massive pre- and intraretinal hemorrhages in all quadrants ( fig . the right eye 's optic nerve head , posterior pole and macular region were not evaluable due to hemorrhages , while in the left eye severe papilledema , hard exudates and macular edema were noticed . general medical examination revealed morbid obesity with a body mass index ( bmi ) of 45 , untreated hypertension ( 170/100 mm hg ) and type ii respiratory failure . the patient was treated with antihypertensive and antiaggregant drugs and referred to the pneumology and hematology department . after 1 week of presentation , the patient underwent fundus fluorescein angiography ( fa ) ( fig . the patient underwent polysomnography which revealed a pathologic apnea - hypopnea index that led to the diagnosis of osas , and treatment with continuous positive air pressure ( cpap ) was started . laboratory tests for thrombophilia showed increased hematocrit ( 59% ) and high levels of fibrinogen and c - reactive protein ( crp ) . other causes of congenital and acquired hypercoagulability like factor v leiden , mutation g20210a of prothrombin , deficiency of natural anticoagulants and antiphospholipid syndrome were ruled out . after 3 months of antihypertensive treatment , the patient 's blood pressure ranged from 140/90 to 135/80 mm hg . at 3 months from presentation , the patient was treated with 0.5 mg of intravitreal ranibizumab ( lucentis , genentech inc . ) . he did not come to the follow - up visits , but presented again at 10 months from presentation , complaining of poor vision . va was no light perception in his right eye and hand movements in the left eye . spectral domain optic coherence tomography ( sd - oct ) confirmed bilateral macular atrophy ( fig . small remnants of intraretinal fluid not involving the fovea were observed in the right eye ( fig . 5a ) . due to these findings , the occurrence of a nonarteritic anterior ischemic optic neuropathy ( naion ) in the right eye was considered . to our knowledge , this is the second reported case of bilateral and simultaneous central rvo in a patient affected by osas . recently published studies found a high prevalence of rvo in patients affected by sleep apneas [ 5 , 6 ] . these findings can be explained by a broad spectrum of metabolic and hemodynamic changes promoted by osas that can lead to a procoagulant state , facilitating thrombus formation and retinal vascular occlusion . indeed , osas can promote the development of all three factors of the so - called virchow 's triad ( hypercoagulability , hemodynamic changes , endothelial dysfunction ) , and its association with all - cause mortality and cardiovascular disease is well - recognized . our case was diagnosed with type ii respiratory failure , characterized by hypoxemia and hypercapnia , which is characteristic of sleep apnea . cycles of apnea and subsequent intermittent hypoxemia and hypercapnia can result in cerebral vasodilatation and surges in arterial blood pressure . the cerebral vascular system of osas patients is more sensible to arterial pressure changes due to defective mechanisms of autoregulation . rise in intracranial pressure may result in papilledema and high venous pressure on the optic nerve head . in addition , as the central retinal artery and vein share a common adventitial sheath , vasodilatation of the central retinal artery due to hypercapnia may compress the adjacent vein contributing to its occlusion . chronic hypoxemia causes an increase of hematocrit and , as a consequence , of blood viscosity to compensate for a lower arterial oxygen tension . osas also promotes an inflammatory state and , as a result , the level of acute - phase proteins is increased [ 9 , 10 ] . in our patient , chronic high serum levels of fibrinogen and crp were reported . fibrinogen is an independent risk factor for cardiovascular disease and an important mediator in the coagulation process , as it can promote platelet aggregation and formation of fibrin clots . crp is an acute - phase protein and does not only mediate inflammation , but also plays an active role in the coagulation cascade and can be considered an independent risk factor for thrombotic events . crp can decrease the activity of tissue plasminogen by the activation of plasminogen activator inhibitor-1 with a subsequent decrease of the fibrinolytic activity . platelet activity can also be stimulated by cathecolamines , which have increased levels in sleep apnea due to an enhanced sympathetic activation in response to the nocturnal desaturation of oxyhemoglobin . in patients affected by osas , other metabolic and biochemical alterations have been found . for instance , an increase in concentration of clotting factors ( xiia and viia ) was described in two clinical trials . however furthermore , osas is strongly related with systemic hypertension , a major risk factor for rvo . a large community - based study demonstrated that patients with osas have a two - fold increase in odds ratio for presenting hypertension . at presentation , our patient had uncontrolled hypertension which may have contributed to the development of central rvo . finally , at 10 months after presentation , our patient presented important optic nerve atrophy in his right eye , along with a va of no light perception . such findings are possible but infrequent in central rvo and , considering the rapd observed at presentation , we can not discard that a naion could have occurred in the right eye . in fact , naion has been recently associated with osas [ 14 , 15 , 16 ] . a cross - sectional study by mojon et al .   found a significantly higher prevalence of osas in patients affected by naion ( 71% ) compared to matched controls ( 18% ) . later , a prospective study by palombi et al .   confirmed this finding and reported a relative risk for naion patients to have a osas of 4.9 compared to the general population , suggesting a clinically significant association between the two conditions . however , direct damage of the optic nerve due to osas - induced hypoxia , altered vascular autoregulation and vascular compression may contribute to the development of this condition [ 14 , 15 , 17 , 18 ] . in our case , an early diagnosis of naion was not formulated . a rapd is a common finding in central rvo , and the evaluation of the optic nerve head was not possible due to massive retinal hemorrhages . color vision assessment and peripheral visual field test , recommended in the evaluation of central rvo and naion , were programmed but not carried out due to very poor patient compliance . our patient was treated with cpap , which can reduce the deleterious effects of intermittent hypoxemia during sleep and improve levels of inflammatory markers , and antihypertensive drugs . on the other hand , no effective medical treatment is established to prevent or treat rvo , and the role of cpap in preventing naion is controversial [ 16 , 20 ] . therefore , identifying and treating any underlying condition is important in order to reduce the risk of rvo and , as the consequences of osas are systemic , it is important to remark that a multidisciplinary approach is required for optimal management of these patients . the evolution of the bilateral and simultaneous central rvo in our case was unfavorable , despite all our efforts . considering that the consequences of central rvo , especially if bilateral , can be very invalidating , it is critical to identify persons who are at higher risk . until recently , osas was not associated with rvo and few studies on this issue have been published [ 3 , 4 , 5 , 6 ] . in addition , with the exception of a cohort study by chou et al . , well - designed epidemiological studies investigating whether rvo is more frequent in osas patients are lacking . nevertheless , despite the scarce scientific evidence , in our opinion , ophthalmologists should consider osas patients at high risk for rvo . considering that osas can promote a procoagulant state , affected patients may develop rvo more frequently than the normal population .
purposeto describe a case of bilateral and simultaneous central retinal vein occlusion ( rvo ) in a young patient diagnosed with obstructive sleep apnea syndrome ( osas).case reporta 38-year - old man with morbid obesity and daytime sleepiness presented with a history of bilateral vision loss . 
 his visual acuity ( va ) was hand movements , and fundus examination ( fe ) revealed bilateral central rvo . 
 general medical examination revealed untreated hypertension and type ii respiratory failure . 
 laboratory tests for thrombophilia showed increased hematocrit ( 59% ) and high levels of fibrinogen and c - reactive protein . 
 other causes of congenital and acquired hypercoagulability were ruled out . 
 pathologic polysomnography led to the diagnosis of osas . 
 the patient was treated with antihypertensive drugs and continuous positive air pressure . 
 in addition , he received intravitreal ranibizumab . at 10 months after presentation , his va was no light perception in the right eye and hand movements in the left eye . 
 fe revealed bilateral retinal and optic nerve atrophy , and the occurrence of a nonarteritic anterior ischemic neuropathy in the right eye was considered .