Revisiting Postoperative Vision Loss following Non-Ocular Surgery: A Short Review of Etiology and Legal Considerations

Central retinal artery occlusion (CRAO) is an ophthalmic emergency and the ocular analogue of cerebral stroke. Best evidence reflects that over three-quarters of patients suffer profound acute visual loss with a visual acuity of 20/400 or worse. This results in a reduced functional capacity and quality of life. There is also an increased risk of subsequent cerebral stroke and ischaemic heart disease. There are no current guideline-endorsed therapies, although the use of tissue plasminogen activator (tPA) has been investigated in two randomized controlled trials. This review will describe the pathophysiology, epidemiology, and clinical features of CRAO, and discuss current and future treatments, including the use of tPA in further clinical trials.

Opinion statement Central retinal artery occlusion (CRAO) is an ocular emergency and is the ocular analogue of cerebral stroke. It results in profound, usually monocular vision loss, and is associated with significant functional morbidity. The risk factors for CRAO are the same atherosclerotic risk factors as for stroke and heart disease. As such, individuals with CRAO may be at risk of ischemic end organ damage such as a cerebral stroke. Therefore, the management of CRAO is not only to restore vision, but at the same time to manage risk factors that may lead to other vascular conditions. There are a number of therapies that has been used in the treatment of CRAO in the past. These include carbogen inhalation, acetazolamide infusion, ocular massage and paracentesis, as well as various vasodilators such as intravenous glyceryl trinitrate. None of these “standard agents” have been shown to alter the natural history of disease definitively. There has been recent interest shown in the use of thrombolytic therapy, delivered either intravenously or intra-arterially by direct catheterisation of the ophthalmic artery. Whilst a number of observational series have shown that the recovery of vision can be quite dramatic, two recent randomised controlled trials have not demonstrated efficacy. On the contrary, intra-arterial delivery of thrombolytic may result in an increased risk of intracranial and systemic haemorrhage, while the intravenous use of tissue plasminogen activator (tPA) was not shown to be efficacious within 24 h of symptom onset. Nevertheless, both of these studies have shown one thing in common, and that is for treatment to be effective in CRAO, it must be deployed within a short time window, probably within 6 h of symptom onset. Therefore, while CRAO is a disease that does not have a treatment, nevertheless it needs to follow the same principles of treatment as any other vascular end organ ischaemic disease. That is, to attempt to reperfuse ischemic tissue as quickly as possible and to institute secondary prevention early.

Perioperative visual loss (POVL), a rare, but devastating complication, can follow non-ocular surgery. Highest rates of visual loss are with cardiac and spine surgery. The main causes of visual loss after non-ocular surgery are retinal vascular occlusion and ischaemic optic neuropathy. This review updates readers on the incidence, suspected risk factors, diagnosis, and treatment of POVL due to these conditions.