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Am Fam Physician. 2020;102(9):539-545

This clinical content conforms to AAFP criteria for CME.

Author disclosure: No relevant financial affiliations.

Central retinal artery occlusions, chemical injuries, mechanical globe injuries, and retinal detachments are eye emergencies that can result in permanent vision loss if not treated urgently. Family physicians should be able to recognize the signs and symptoms of each condition and be able to perform a basic eye examination. Patients with a central retinal artery occlusion require urgent referral for stroke evaluation and should receive therapy to lower intraocular pressure and vasodilating agents to minimize retinal ischemia. Chemical injuries require immediate irrigation of the eye to neutralize the pH of the ocular surface. A globe laceration or rupture is common in patients with a recent history of trauma from a blunt or penetrating object. Physicians should administer prophylactic oral antibiotics after a globe injury to prevent endophthalmitis. The eye should be covered with a metal shield until evaluation by an ophthalmologist. Patients with symptomatic floaters and flashing lights should be referred to an ophthalmologist for a dilated funduscopic examination to evaluate for a retinal tear or detachment.

Central retinal artery occlusions (CRAOs), chemical injuries, mechanical globe injuries, and retinal detachments are ocular emergencies that have the potential to cause permanent vision loss if they are not promptly recognized and treated (Table 1114 ). Family physicians should be familiar with the signs and symptoms associated with each condition and be able to perform a basic eye examination. American Family Physician's topic module on eye and vision disorders discusses other urgent ocular conditions (

EmergencySigns and symptomsInitial evaluationOphthalmic management
Central retinal artery occlusionAcute, painless loss of vision; amaurosis fugax; retinal whitening with foveal cherry-red spotAssess visual acuity; perform dilated funduscopic examination
Presence of a cherry-red spot in the fovea; unilateral, painless vision loss of hand motion or light perception; evaluate for stroke; echocardiography; electrocardiography; carotid artery ultrasonography; obtain erythrocyte sedimentation rate and C-reactive protein level; immediately refer to an ophthalmologist1
Nonarteritic causes: treat with digital massage, anterior chamber paracentesis, systemic acetazolamide, pentoxifylline (Trental), intra-arterial thrombolysis
Arteritic causes: treat with a high dose of systemic steroids24
Chemical eye injuryEye pain; decreased vision; conjunctival redness or ischemia; corneal clouding or abrasionAssess visual acuity; examine cornea for clarity and conjunctiva for hyperemia; determine the chemical agent
Immediately irrigate eye with normal saline or lactated Ringer solution with at least 2 L of fluid; immediately refer to an ophthalmologist5
Topical antibiotics and artificial tears for mild ocular burns; topical antibiotics, artificial tears, steroids, ascorbate, citrate drops, or amniotic membrane tissue for severe burns6,7
Mechanical globe injuryDecreased vision; conjunctival or corneal laceration; subconjunctival hemorrhage; ocular foreign body; hyphema or shallow anterior chamber; irregular shaped pupil or iris prolapseAssess visual acuity, pupils, cornea, and anterior chamber
Decreased visual acuity, irregular shaped pupil, iris prolapse through corneal or scleral laceration, presence of penetrating foreign body
Place metal shield over eye; provide antiemetics and systemic antibiotics (levofloxacin [Levaquin], ceftazidime [Fortaz], or vancomycin); update Tdap vaccine; immediately refer to an ophthalmologist810
Evaluate for orbital fractures and intraocular foreign bodies with computed tomography; schedule immediate surgical repair of laceration; monitor for endophthalmitis and sympathetic ophthalmia8
Posterior vitreous detachment, retinal tear, retinal detachmentSudden onset of flashing lights and floaters in one eye; peripheral or central visual field defectAssess visual acuity; perform confrontational visual field testing and dilated funduscopic examination
Decreased visual acuity, constricted visual fields, or patients with risk factors including myopia, age ≥ 50 years, prior detachment in the contralateral eye, prior ocular surgery, or family history may represent a retinal tear or detachment; refer to an ophthalmologist within 24 hours11,12
Unaffected visual acuity, full confrontational visual fields, or no known risk factors may represent a posterior vitreous detachment; refer to an ophthalmologist within a few days12
Observe for posterior vitreous detachment and instruct patient to seek prompt reevaluation for increased floaters, flashing lights, or a new peripheral visual field defect
Laser for small retinal tear; surgical repair with pneumatic retinopexy; scleral buckle or vitrectomy for retinal detachment11,13,14

Central Retinal Artery Occlusion


A 76-year-old man presents with acute, painless vision loss in his left eye during the course of 10 minutes. His visual acuity is light perception. Confrontational visual fields reveal a dense scotoma, and a penlight examination shows an afferent pupillary defect.


The annual incidence of a CRAO is approximately one in 100,000 people with a mean age in their early 60s.15 CRAO is caused by an inflammatory, embolic, or thromboembolic obstruction of the central retinal artery that supplies the macula and central retina. Most CRAOs are nonarteritic and are caused by platelet fibrin thromboemboli in the setting of atherosclerotic disease. Risk factors include hypertension, diabetes mellitus, carotid artery disease, coronary artery disease, and tobacco use.16 Arteritic CRAO accounts for less than 5% of cases and is often attributed to giant cell arteritis.16


Patients with a CRAO commonly present with rapid, painless vision loss and an afferent pupillary defect. Dilated funduscopic examination usually shows retinal whitening with a cherry-red spot in the fovea (Figure 1). A Hollenhorst plaque (i.e., white punctate-appearing cholesterol emboli) may be visible at the branching points of blood vessels on the optic nerve.


The standard initial treatment includes ocular massage, anterior chamber paracentesis, vasodilating agents to minimize retinal ischemia, and ocular hypotensive agents including acetazolamide; however, they do not affect the natural course of the disease.2 The administration of pentoxifylline (Trental; three 600-mg tablets per day) has the potential to improve retinal blood flow.3 Intra-arterial thrombolysis has produced favorable outcomes compared with standard therapy.4

Patients diagnosed with a CRAO should be evaluated for possible stroke because of the elevated risk of a subsequent ischemic event. Echocardiography and electrocardiography can be used to determine cardiac function, and carotid artery ultrasonography to assess for stenosis.1

An erythrocyte sedimentation rate and C-reactive protein level should be obtained for patients older than 50 years with symptoms of fever, fatigue, jaw tenderness, scalp tenderness, and weight loss in whom giant cell arteritis is suspected. If the patient's levels are elevated, systemic steroids are recommended. Patients younger than 50 years should receive a hypercoagulable workup to assess for antiphospholipid antibody syndrome and other hypercoagulable diatheses.1


There are no proven therapies that improve vision outcomes after a nonarteritic CRAO. Most patients have a final visual acuity of 20/400 or worse.17 Follow-up should include screening for cerebrovascular complications.

Chemical Injury


A 34-year-old man presents with eye pain, tearing, and decreased vision in his right eye two hours after spraying liquid fertilizer on plants. His visual acuity on presentation is 20/200, and a penlight examination shows swollen upper and lower eyelids, conjunctival injection, and an opaque cornea.


Chemical eye injuries occur when the ocular surface is exposed to an acid or alkali in the form of a liquid, powder, or gas. The severity of the injury is dependent on the chemical's pH concentration and the duration of contact with the ocular surface.18 Chemical burns may cause ischemic damage to conjunctival vessels and corneal limbal stem cells, resulting in conjunctival scarring and corneal opacification. Alkali burns are more common because of the prevalence of alkali in household cleaning agents and are more harmful than acid burns because alkali agents penetrate the ocular surface more quickly.19,20

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