ABSTRACT
Purpose: To evaluate the effectiveness of hyperbaric oxygen (HBO2) therapy as a treatment for central retinal artery occlusion (CRAO). Methods: A total of 38 patients who underwent HBO2 for non-arteritic CRAO were identified. Patients with arteritic CRAO, branch retinal artery occlusion, ophthalmic artery occlusion, and other diagnoses were excluded from the analysis. The main outcome measured was the change in visual acuity at the most recent follow-up exam compared to the visual acuity at presentation before the initiation of HBO2 therapy. Results: The overall visual acuity after HBO2 compared with the visual acuity at presentation showed a mean improvement of 0.5 logMAR from 2.2 to 1.7 logMAR (p=0.0003). Patients who presented with hand motion and light perception vision had a mean improvement of 0.4 logMAR (p=0.06) and 0.8 logMAR (p=0.004) after HBO2, respectively. An average visual acuity improvement of 0.5 logMAR (p=0.01) was observed when patients underwent HBO2 earlier than 24 hours of symptom onset. This mean improvement increased to 0.9 logMAR (p=0.009) if HBO2 was initiated within eight hours. Conclusions: HBO2 may be an effective treatment for non-arteritic CRAO, especially if patients are treated early and present with salvageable vision. The time to treatment and the presenting visual acuity may be predictive factors on the visual prognosis following HBO2. Further studies with a prospective design and more patients are necessary to determine the long-term outcomes and the optimal protocol for HBO2 in CRAO patients.
ABSTRACT
PURPOSE OF REVIEW: Nonarteritic anterior ischemic optic neuropathy remains a disease that is poorly understood in many aspects. The clinical presentation may diverge significantly from the classic unilateral, painless, sudden vision loss affecting patients over the age of 50 years. This variability might make nonarteritic anterior ischemic optic neuropathy hard to differentiate from optic neuritis and arteritic ischemic optic neuropathy. The course of nonarteritic anterior ischemic optic neuropathy is also variable, often sequentially affecting the other eye. RECENT FINDINGS: Visual recovery has been reported, but it is not the rule. Multiple risk factors have been proposed, including crowded disc, atherosclerosis, diabetes, hyperlipidemia, hypertension, hypotension, hemoconcentration, hemodilution, and hypercoagulable states. The optic nerve damage in nonarteritic anterior ischemic optic neuropathy appears to result from a perfusion insufficiency in the short posterior ciliary arteries leading to infarction of the retrolaminar portion of the optic disc. The underlying mechanisms are still unclear, however. Multiple medical and surgical treatment options have been investigated, including optic nerve sheath decompression, standard and megadose corticosteroids, levodopa, carbidopa, hyperbaric oxygen, and neuroprotective agents, but no proven effective treatment is currently available. SUMMARY: Intense investigations in humans and animals are under way. Hopefully these studies will enhance our understanding of the risk factors and pathophysiology of nonarteritic anterior ischemic optic neuropathy and aid in developing new strategies for prevention and treatment.