Discussion
We report a case of CRAO occurring after AF ablation. In this case, sudden visual loss in the left eye occurred and did not improve well with treatment.
CRAO can be caused by retinal artery embolism or hemodynamically-induced retinal ischemia. The risk factors for CRAO are shown in Table 2.3-5 AF was a cause of CRAO. A previous study using implantable loop recorders reported that 15% of CRAO patients had subclinical AF.8
There have been few reports of ophthalmic complications of AF ablation. Although a previous study showed one patient developed a unilateral quadrantopsia consistent with a retinal artery embolus after catheter ablation,9 there have been no reports about CRAO with complete unilateral visual loss. To our knowledge, this is the first case report to describe CRAO following AF ablation.
Ischemic damage to the retina is irreversible within 4 hours of the onset of CRAO,3 therefore prompt management is important. Common treatments for CRAO are shown in Table 3.3,10-18 Ocular massage was performed because the embolus in the central retinal artery was expected to be dislodged.3 As medical therapies, vasodilators such as nitroglycerine and anticoagulant such as heparin have been used; however, there is no evidence that these agents are effective. A recent study showed that digital subtraction angiography–guided superselective ophthalmic artery or selective carotid thrombolysis with urokinase and papaverine was an effective treatment method for CRAO.12
Another study showed that alprostadil infusion resulted in significant visual improvement in patients with CRAO.11 In this study, the logarithm of the minimum angle of resolution best corrected visual acuity significantly improved from 2.73 to 1.48 at 1 month after the onset of CRAO, and all 6 patients experienced vision improvement.11 Our use of alprostadil for 3 d somewhat improved peripheral vision.
We needed a long procedural time in this case. Therefore an embolic event was more likely to occur because long left atrium dwell time exposed this patient to thrombus formation on catheters.19 The differential diagnosis in this case is air embolism vs. thromboembolism. In this case, the body mass index was high and glossoptosis with conscious sedation tended to occur irrespective of using noninvasive positive pressure ventilation. This condition induced a long apnea and might be a cause of an air embolism. Deep sedation with a laryngeal mask airway might be a preventive method. If possible, avoiding a long procedural time, which is a risk factor for complication,20 might also prevent complications.
To minimize the risk of permanent visual loss from CRAO, operators suspecting it should closely cooperate with an ophthalmologist to diagnose this disease as soon as possible.