EM@3AM – Central Retinal Artery Occlusion
- Jul 8th, 2017
- Erica Simon
Author: Erica Simon, DO, MHA (@E_M_Simon, EMS Fellow, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)
Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.
A 56-year-old female with a history of HTN, HLD, and CAD (CABG x2) presents to the emergency department immediately following the sudden loss of vision in her right eye. She denies recent trauma, headache, slurred speech, motor and sensory deficits. She denies eye pain. She does not wear contact lenses or glasses. The patient reports an eye examination within the previous year, stating “my eyes have been perfectly fine.”
Initial VS: BP 123/76, HR 66, T 99.9F Oral, RR 12, SpO2 97% on room air.
Pertinent physical exam findings:
HEENT: EOMI; OD: afferent pupillary deficit; fundoscopic examination: OD: macular edema; fovea: cherry red spot.
Cardiovascular: S1, S2, regular rate and rhythm. No carotid bruits.
What’s the next step in your evaluation and treatment?
Answer: Central Retinal Artery Occlusion (CRAO)1-4
- Epidemology: Typically occurs in older adults with atherosclerotic disease.1,2 Incidence reported as 1 in 100,000 persons residing in the U.S.3
- Etiology:1 Embolism from a carotid artery plaque is the most frequent cause.
- Clinical Manifestations:2 Painless, monocular vision loss.
- Evaluation and Treatment:
- Obtain visual acuity (usually significantly reduced in the affected eye (> 20/200)).2,3
- Perform a thorough H&P.
- History: question specifically regarding HTN, hyperlipidemia, CAD, or history of stroke.
- Occular exam: afferent pupillary deficit may be present.
- Fundoscopic exam: edema and opacfication of the superficial retina with a “cherry red” spot localized to the fovea (+/- segmentation or “boxcarring” of the retinal vasculature).
- Consult ophthalmology.
- Dislodgement of the embolus by direct digital pressure followed by a sudden release, dilation of the artery to promote forward flow (increasing intra-arterial pCO2 with an inhaled mixture of 95% O2 and 5% CO2), reduction of IOP (timolol, etc.), sublingual isosorbide dinitrate (increase blood oxygen to dilate the retinal arteries), and hyperbaric oxygen therapy have demonstrated limited benefit.2
- The efficacy of the aforementioned interventions, utilized as monotherapy or combination therapy, varies from 6-49%.3
- Intra-arterial thrombolysis may be considered on a case-by-case basis in conjunction with a ophthalmologist:
- Retrospective case-control studies have demonstrated a potential role for intra-arterial thrombolysis performed within 4 hours of symptom onset.4
- Open-label observational trials have shown intra-arterial fibrinolysis to be effective in CRAO, with up to 60-70% of treated patients experiencing improvement in visual acuity.3
- The evaluation of CRAO in a patient < 50 years of age should include: an assessment for hypercoaguability, vascultis, and myeloproliferative disorders.2,3
- CRAO is the ocular equivalent of a stroke and requires medical management/optimization.3
- Freund K, Sarraf D, Meiler, W, Yannuzzi L. Retinal Vascular Disease. in The Retinal Atlas. 2nd ed. Philadelphia, Saunders. 2017; 493-650.
- Guluma K, Lee J. Ophthalmology. In Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia, Elsevier. 2018. 790-819.e3.
- Varma D, Cugati S, Lee A, Chen C. A review of central retinal artery occlusion: clinical presentation and management. Eye (Lond). 2013; 27(6):688-697.
- Arnold M, Koerner U, Remonda L, Nedeltchev K, Mattle H, et al. Comparison of intra-arterial thrombolysis with conventional treatment in patients with acute central retinal artery occlusion. J Neurol Neurosurg Psychiatry. 2005; 76:196-199.
For Additional Reading:
Acute Visual Loss in the Emergency Department: Pearls and Pitfalls