Retinal Artery Occlusion Treatment & Management
- Author: Benjamin Feldman, MD; Chief Editor: Robert E O'Connor, MD, MPH more...
No specific prehospital treatment is available for retinal artery occlusion. The prognosis for visual recovery is related directly to the promptness in treatment; thus, rapid transport to the ED is essential.
Emergency Department Care
The 2 phases of ED care must occur. The first phase involves rapid detection and treatment of visual loss. The second phase involves a thorough investigation for the cause of visual loss.
No randomized controlled trials to support one treatment modality over any others are underway, but anecdotal reports and case series have suggested many modalities of treatment.
Immediate lowering of IOP to a target pressure of 15 mm Hg using medical management, ocular massage, and anterior chamber paracentesis
Apply direct pressure for 5-15 seconds, then release. Repeat several times.
Increased IOP causes a reflexive dilation of retinal arterioles by 16%.
A sudden drop in IOP with release increases the volume of flow by 86%.
Ocular massage dislodges the embolus to a point further down the arterial circulation and improves retinal perfusion.
Anterior chamber paracentesis
Advocated when visual loss has been present for less than 24 hours
Early paracentesis is associated with increased visual recovery.
Slit-lamp removal of 0.1-0.4 mL of aqueous humor via tuberculin syringe and a 27-gauge needle may decrease IOP to 3 mm Hg.
Decrease in IOP is thought to allow greater perfusion, pushing emboli further down the vascular tree.
See Medication for details and mechanisms of action for medications.
Start timolol early in the treatment of CRAO, as this is readily available in most emergency departments. Acetazolamide and mannitol should also be used when CRAO is suspected because there are few downsides to starting these medications early.
In carbogen therapy (5% carbon dioxide, 95% oxygen), carbon dioxide dilates retinal arterioles, and oxygen increases oxygen delivery to ischemic tissues.
Thrombolytics may be useful if initiated within 4-6 hours of visual loss, but they may not be much help if the embolus is cholesterol, talc, or calcific. Thrombolytics are introduced via the proximal ophthalmic artery, delivering increased concentrations directly to the retinal artery and minimizing systemic complications. Results of noncontrolled retrospective studies have been mixed. As of 2007, a European controlled study is underway.
Hyperbaric oxygen (HBO) therapy may be beneficial if initiated within 2-12 hours of onset of symptoms. Institute treatment with other interventions first; transport to a chamber may usurp precious time. Results from noncontrolled studies have been mixed. A 2001 controlled study in Israel showed a benefit in the treatment group. In this study, all patients were treated within 8 hours of symptom onset.
Treatment with IV thrombolytics as with cerebral infarction has been discussed[6, 7, 8] but currently is not the standard of care.
Immediate evaluation is imperative for any patient with acute CRAO.
Ophthalmologists can decide with which further treatment (eg, thrombolytics, hyperbaric oxygen, retrobulbar block) to proceed.
Early treatment (< 2 h from onset of symptoms) with HBO may be associated with increased visual recovery, but HBO can be considered if the duration of visual loss is less than 12 hours. Inhalation of 100% oxygen at 2 atm can provide an arterial pO2 of 1000-1200 mm Hg, resulting in a 3-fold increase in oxygen diffusion distance through ischemic retinal tissues. Some studies show a 40% improvement of 2 or more levels of visual acuity.
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