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Hyperbaric oxygen in the treatment of acute retinal artery occlusion.
Diving and Hyperbaric Medicine : the Journal of the South Pacific Underwater Medicine Society 2017 December
INTRODUCTION: Acute retinal artery occlusion (ARAO) is a major cause of sudden, painless visual loss, often leaving no useful vision in the affected eye. Its incidence is cited at 0.85 per 100,000 persons per year but may be higher because of under-reporting. The natural history is difficult to study, but a spontaneous resolution rate of < 1-8% for acute, non-arteritic ARAO has been cited. Occurrence in an only eye is devastating for the patient. There is currently no consensus regarding management of ARAO and little evidence to support any treatment modality. Despite only limited case series, hyperbaric oxygen treatment (HBOT) is recommended for ARAO by the Undersea and Hyperbaric Medical Society (UHMS) and by the European Committee for Hyperbaric Medicine.
METHODS: Between early 2003 and December 2012, all ARAO patients presenting to Christchurch Hospital were referred for consideration of HBOT. These 31 consecutive patients' medical records were reviewed retrospectively. The time delay from onset of visual loss to commencing HBOT; the presenting visual acuity; various demographic data; the HBOT administered and the outcome visual acuity were documented.
RESULTS: All 31 patients underwent at least one HBOT (median 4, range 1-7) at a pressure of 203-284 kPa for 1.5 to 2.0 h. One patient's treatment was terminated after 60 min at their request; another declined further HBOT and one suffered middle ear barotrauma. Thirteen patients also received anticoagulants at the discretion of the referring ophthalmologist. Twenty three patients had temporarily improved vision with the first HBOT. Seven patients had permanent, good visual recovery (6/18 or better; Snellen chart); and two only modest improvement (6/60). All nine patients who improved permanently were treated within 10 hours of symptom onset.
CONCLUSIONS: Where available, HBOT is indicated for ARAO. Our protocol may not have been aggressive enough and the UHMS protocol is recommended. A multi-centre, randomised controlled trial is feasible, but would be logistically difficult and expensive and may be ethically unsupportable given the lack of alternative, effective treatments.
METHODS: Between early 2003 and December 2012, all ARAO patients presenting to Christchurch Hospital were referred for consideration of HBOT. These 31 consecutive patients' medical records were reviewed retrospectively. The time delay from onset of visual loss to commencing HBOT; the presenting visual acuity; various demographic data; the HBOT administered and the outcome visual acuity were documented.
RESULTS: All 31 patients underwent at least one HBOT (median 4, range 1-7) at a pressure of 203-284 kPa for 1.5 to 2.0 h. One patient's treatment was terminated after 60 min at their request; another declined further HBOT and one suffered middle ear barotrauma. Thirteen patients also received anticoagulants at the discretion of the referring ophthalmologist. Twenty three patients had temporarily improved vision with the first HBOT. Seven patients had permanent, good visual recovery (6/18 or better; Snellen chart); and two only modest improvement (6/60). All nine patients who improved permanently were treated within 10 hours of symptom onset.
CONCLUSIONS: Where available, HBOT is indicated for ARAO. Our protocol may not have been aggressive enough and the UHMS protocol is recommended. A multi-centre, randomised controlled trial is feasible, but would be logistically difficult and expensive and may be ethically unsupportable given the lack of alternative, effective treatments.
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