Bilateral RAO is extremely rare and constitutes less than 2% of cases of RAO [9]. In this current study bilateral RAO accounted for 1.8% of cases of RAO seen in our centre. Similarly, Schmidt et al. reported a prevalence less than 2% (0.5%) in a retrospective study of patients with non-inflammatory RAO in Germany [16]. Hayreh et al. on the contrary reported a much higher incidence of 13.7% in a prospective study on RAO in Iowa, USA over a period of 27 years [5]. The majority of patients in this study were males, which is consistent with findings from earlier studies on RAO [5,15-17]. The mean age in our cohort of patients (58.3 years), however, contrasts with higher mean ages of 66 years and 74 years reported in patients with RAO in Germany [16] and America [17] respectively. These findings, though suggestive of RAO occurring at an earlier age in Indian patients, needs to be interpreted with caution considering the small number of cases in this study. A review of all cases of RAO seen in our centre will determine if this is the case. Most cases of RAO in this study were nonsimultaneous, and the median interval for involvement of the fellow eye was 90 days. Even though bilateral RAO is extremely rare, patients need to be aware of not only the risk of subsequent cerebral stroke and ischemic heart disease, but also of the fellow eye suffering a similar event.
Systemic cardiovascular diseases have a well-known association with RAO [5]. Arterial hypertension, diabetes mellitus, hyperlipidaemia, carotid artery disease, coronary artery disease, transient ischaemic attack, cerebrovascular accident, and tobacco smoking have been described as significantly more common among these patients than in the general population [5,18]. Most of the patients in this current study had more than one risk factor with hypertension being the most common. This is consistent with the findings by Schmidt et al [16]. Twenty percent of patients in this study had a history of stroke while an additional 60% of brain MRI/CT scans revealed areas of infarction in the brain. In a case-control study on the correlation of the history of stroke and RAO by Xiao et al, 40% of patients with RAO had a stroke prior to developing the arterial occlusion while another 22% had areas of infarction in the brain on cranial MRI/CT scan [19]. Abnormal findings were noted on echocardiography and carotid Doppler in 50% and 25% respectively of patients that had these procedures in this study. In contrast, Xiao et al found more patients with abnormalities on carotid ultrasound, 89% as against 32% with abnormalities on echocardiography [19]. Acute pancreatitis which was seen in one patient in this study has been associated with bilateral RAO [20]. It is postulated that arterial occlusion occurs as a result of complement activation with subsequent leukoembolization [20]. Aggressive management of modifiable risk factors is essential in preventing a repeat arterial occlusion in the fellow eye following a unilateral RAO as well as other life threatening vascular events.
Visual outcome was poor in the majority of eyes in this study which is in agreement with previous studies. Several factors play a crucial role in determining the visual outcome of CRAO, and these include duration of retinal ischaemia, type of CRAO, cause of CRAO, site of occlusion in the central retinal artery, residual retinal circulation, and presence and area of supply by a patent cilioretinal artery [21]. The duration of RAO is, however, almost always the principal determining factor in the production of irreversible retinal damage, that is, the longer the ischemia, the more marked the retinal damage, and the worse the visual outcome [21]. The majority of patients in this study presented after 24 hours of loss of vision with a mean duration 6.9 days in eyes with acute RAO. This is higher than 3.4 days reported by Xiao et al [19]. Retinal artery occlusion is an ocular emergency, and any intervention is best done within four to 6.5 hours which is the retinal ischaemia tolerance time, before irreversible damage occurs [22,23]. A recent review by Tobalem et al., however, suggests that this critical time limit for inner retinal non-perfusion has been greatly overestimated, and that irreversible retinal ganglion cell death occurs after 12-15 minutes of complete CRAO in humans [24]. Patients with unilateral RAO, therefore, should be made to understand the importance of prompt presentation to the hospital if loss of vision occurs in the fellow eye.
Ocular neovascularization (ONV) is an important complication of CRAO and is a less-frequent complication of BRAO. Patients with ocular ischaemic syndrome, and type 2 diabetes are particularly at risk of developing this complication following occlusion of the central retinal artery [21,25]. About 13% of eyes had ONV in this current study which compares favourably with 14.5% reported by Mason et al [25]. However, neovascular glaucoma was reported in only one (4%) of these eyes in this current series in contrast to 83% reported by Mason et al [25].
Our study had a few limitations including its retrospective nature, and incomplete data in some case files. The sample size was small but this is not unconnected with the rarity of the condition. It was also difficult to determine if the simultaneous cases were truly simultaneous as these patients were seen within seven days to a month of development of visual loss.
In conclusion, bilateral RAO is very rare and usually nonsimultaneous with a median interval of 90 days for involvement of the fellow eye. The majority of patients presented outside of the window period for any meaningful intervention even when the fellow eye developed the same symptoms. Patients with previous unilateral RAO, therefore, need to be educated not only about the potentially fatal complications that could be associated with the condition, but also the possibility of the fellow eye suffering a similar event, and the importance of prompt presentation to the hospital if this occurs. This along with management of associated risk factors may go a long way in preventing catastrophic visual loss in probably the only seeing eye.