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.