Eduovisual
Special Senses & Otolaryngology
Central retinal artery and vein occlusion
— Presents as sudden, painless, monocular vision loss over seconds, often to counting fingers or light perception.
— Retinal neurons tolerate ischemia for only ~90–240 minutes — irreversible infarction follows. Treat as a time-critical neurologic emergency.
— Vision loss is typically less abrupt, painless, and variable — from mild blur to severe loss depending on ischemic vs non-ischemic subtype.
— Mechanism is virchow-triad-like: stasis from atherosclerotic arterial compression of the adjacent vein, hypercoagulability, endothelial damage.
— Any adult >50 with sudden, painless, unilateral vision loss → CRAO until proven otherwise.
— Patients with HTN, DM, hyperlipidemia, smoking, or atrial fibrillation presenting with monocular visual symptoms.
— Younger patients (<50) with CRVO → think hypercoagulable workup (factor V Leiden, antiphospholipid syndrome, OCPs, hyperhomocysteinemia).
— Concurrent jaw claudication, scalp tenderness, polymyalgia symptoms, or age >50 → giant cell arteritis (GCA) until disproven.
Board pearl: CRAO is treated as an acute ischemic stroke equivalent — the AHA 2021 scientific statement recommends evaluation at a stroke center with stroke-protocol imaging and risk-factor workup, because ~25% have concurrent silent cerebral infarcts on MRI and stroke risk is highest in the first week.
Step 3 management: First action for sudden monocular vision loss in an ED stem is bedside fundoscopy and same-hour ophthalmology consultation, while simultaneously activating a stroke evaluation pathway for CRAO.
— 68-year-old man with HTN, hyperlipidemia, and prior TIA notes the "shade coming down" or curtain effect over the right eye, then complete vision loss within seconds. Painless. Persistent.
— Preceding amaurosis fugax episodes (transient monocular vision loss lasting minutes) in ~10% — these are warning TIAs of the eye and mandate carotid evaluation.
— Often awakens with the deficit or notices it on covering the unaffected eye.
— 60-year-old woman with poorly controlled HTN and open-angle glaucoma reports blurry vision over hours to a day in one eye, sometimes worse on awakening.
— Visual acuity ranges widely — 20/40 in non-ischemic CRVO to counting fingers/HM in ischemic CRVO.
— No pain, no redness, no discharge — distinguishes from angle-closure, uveitis, or keratitis.
— Onset speed (seconds = arterial; hours = venous).
— Pain (absent in both — pain suggests GCA, optic neuritis, angle-closure, or endophthalmitis).
— GCA red flags in any patient >50: new headache, jaw claudication, scalp tenderness, PMR symptoms, fevers, weight loss.
— Cardiovascular risk factors: HTN, DM, dyslipidemia, smoking, AFib, carotid disease, prior stroke.
— Hypercoagulable clues for young CRVO: OCP use, pregnancy/postpartum, prior DVT/PE, recurrent miscarriage, malignancy.
— Glaucoma history (CRVO risk factor — elevated IOP compresses the vein).
— Recent neck manipulation, trauma, or IV drug use (septic emboli, dissection).
— Vision loss <4.5 hours from CRAO onset = potential window for advanced therapy.
— Bilateral simultaneous loss → think GCA, cortical infarct, or methanol — not embolic CRAO.
Key distinction: CRAO = seconds to "blackout"; CRVO = hours to "blurring"; GCA = may mimic either + systemic symptoms + ESR/CRP up. Pain with vision loss → it is not CRAO/CRVO until proven otherwise.
Board pearl: Always ask the patient to cover each eye separately — many patients don't recognize unilateral loss until prompted.
— Pale, edematous retina (ischemic whitening of the inner retinal layers).
— Cherry-red spot at the fovea — the thin foveal retina retains its choroidal blood supply, contrasting against pale surroundings. Appears within hours, fades over days.
— Boxcarring/segmentation of blood column in retinal arterioles (sluggish flow).
— Hollenhorst plaque (refractile cholesterol embolus) may be visible at a bifurcation → points to carotid source.
— Afferent pupillary defect (APD/Marcus Gunn pupil) — virtually always present; sensitive early sign before fundus changes mature.
— Visual acuity typically counting fingers, hand motion, or light perception.
— Diffuse retinal hemorrhages in all four quadrants (dot, blot, and flame).
— Dilated, tortuous retinal veins.
— Cotton-wool spots (nerve fiber layer infarcts) — more numerous in ischemic CRVO.
— Optic disc edema and macular edema.
— APD present in ischemic CRVO; usually absent or mild in non-ischemic.
— Visual acuity each eye (Snellen or near card).
— Pupillary exam with swinging flashlight for APD.
— Confrontation visual fields.
— Intraocular pressure (IOP) — rule out angle-closure (firm globe, fixed mid-dilated pupil, hazy cornea, pain, nausea).
— Extraocular movements, lids, conjunctiva, cornea.
— Temporal artery palpation (tenderness, nodularity, pulselessness → GCA).
— Blood pressure both arms, irregular pulse (AFib), carotid auscultation for bruits, cardiac exam for murmurs (endocarditis, valvular source), neuro exam (concurrent stroke).
— Document NIHSS — CRAO patients warrant stroke-protocol assessment.
Board pearl: A cherry-red spot is not pathognomonic — also seen in Tay-Sachs, Niemann-Pick, Sandhoff, and central retinal artery occlusion. Context (acute monocular vision loss in adult) is what makes it CRAO.
Step 3 management: Document an APD finding within minutes — it is the most reliable early bedside sign before mature fundus changes appear.
— ESR and CRP — both elevated in GCA (ESR often >50 mm/hr; CRP more sensitive). A normal ESR with elevated CRP still warrants concern.
— CBC — thrombocytosis supports GCA; anemia in malignancy/inflammation.
— BMP, glucose, HbA1c — diabetes screening and AKI risk.
— Lipid panel.
— Coagulation studies (PT/INR, aPTT) — baseline and if anticoagulation considered.
— Troponin if concurrent chest symptoms or AFib with rapid rate.
— Non-contrast CT head to rule out hemorrhage if any neurologic symptoms or if considering thrombolysis pathways.
— CTA head and neck to identify carotid stenosis, dissection, aortic arch atheroma. Carotid stenosis >50% on the symptomatic side is found in ~30–40% of CRAO patients.
— MRI brain with DWI — up to 25% have concurrent ischemic cerebral lesions, often clinically silent. Per AHA 2021, MRI within 24 hours is reasonable.
— Echocardiogram (TTE first, TEE if suspicion remains) — valvular vegetations, LA thrombus, PFO, aortic atheroma.
— Same vascular risk factor labs.
— IOP measurement (glaucoma is the leading modifiable CRVO risk factor).
— In patients <50 or with recurrent/bilateral CRVO: hypercoagulable panel — antiphospholipid antibodies, factor V Leiden, prothrombin G20210A, protein C/S, antithrombin III, homocysteine, JAK2 if polycythemia suspected.
Board pearl: Do not wait for biopsy to treat suspected GCA. Start high-dose IV methylprednisolone when GCA causes visual loss; temporal artery biopsy within 1–2 weeks remains diagnostic and is not invalidated by early steroids.
CCS pearl: Order ESR, CRP, CBC, CTA head/neck, MRI brain, ECG, echo, lipid panel, HbA1c, and ophthalmology consult as a bundle in the first 30 minutes for CRAO.
— In acute CRAO, OCT shows hyperreflectivity and thickening of the inner retinal layers (nerve fiber, ganglion cell, inner plexiform).
— Weeks later, OCT shows inner retinal thinning/atrophy — a permanent imaging signature.
— In CRVO, OCT quantifies macular edema — the parameter that drives anti-VEGF re-injection decisions.
— In CRAO: delayed arterial filling and prolonged arteriovenous transit time.
— In CRVO: delayed venous filling, capillary nonperfusion (defines ischemic subtype if >10 disc areas of nonperfusion).
— Differentiates ischemic vs non-ischemic CRVO — critical because ischemic CRVO has a 60% risk of neovascular glaucoma within 100 days ("100-day glaucoma").
— Gold standard for GCA confirmation. 3–5 cm segment because of skip lesions.
— Sensitivity ~70–90%; bilateral biopsy increases yield modestly.
— Do not delay steroid initiation while awaiting biopsy.
— CTA head/neck is first-line in ED.
— Carotid Doppler ultrasound is acceptable if CTA contraindicated (contrast allergy, AKI).
— MRA is alternative.
— TTE for initial screen.
— TEE if TTE negative and high suspicion for cardioembolic source (endocarditis, LAA thrombus, PFO with paradoxical embolism, aortic arch atheroma).
— If initial ECG and telemetry are negative but embolic CRAO is suspected, 30-day event monitor or implantable loop recorder mirrors cryptogenic stroke workup to detect paroxysmal AFib (CRYSTAL-AF logic).
— Order before starting anticoagulation when possible — heparin alters antithrombin levels and warfarin alters protein C/S.
— Lupus anticoagulant testing is unreliable on DOAC or heparin.
Key distinction: Non-ischemic CRVO = better acuity, no APD, <10 disc areas nonperfusion → low neovascularization risk. Ischemic CRVO = poor acuity, APD present, extensive nonperfusion → high neovascular glaucoma risk → close monthly follow-up with gonioscopy.
Board pearl: OCT is the fastest, noninvasive bedside confirmation of inner retinal ischemia in ambiguous CRAO presentations.
— Time of onset is the single most important variable. Establish "last known well" exactly as in stroke.
— <4.5 hours: Consider IV tPA (alteplase) at stroke center — evidence is evolving (REVISION trial pending; observational data suggest benefit). AHA 2021 statement says it is reasonable to consider at experienced centers.
— >4.5 hours but acute: Conservative/supportive measures; some centers attempt them in earlier windows too, though evidence is weak.
— All CRAO patients regardless of window: Full stroke workup, admission or observation, secondary prevention initiation.
— Ocular massage — digital pressure to dislodge embolus and lower IOP.
— IOP-lowering agents — topical timolol, IV acetazolamide, mannitol.
— Anterior chamber paracentesis by ophthalmology.
— Carbogen (95% O₂ / 5% CO₂) inhalation or hyperbaric oxygen — HBO may help if available within ~6–24 hours by maintaining choroidal oxygen diffusion to inner retina.
— These measures do not restore vision reliably and should never delay stroke pathway activation.
— Not a stroke emergency in the same time-critical sense.
— First-line therapy = intravitreal anti-VEGF (ranibizumab, aflibercept, bevacizumab) for macular edema and to prevent/treat neovascularization.
— Intravitreal corticosteroids (dexamethasone implant, triamcinolone) are alternatives.
— Panretinal photocoagulation if anterior segment neovascularization develops.
— Treat underlying HTN, glaucoma, diabetes.
— IV methylprednisolone 1 g daily × 3 days, then oral prednisone 1 mg/kg/day taper over a year.
— Add low-dose aspirin to reduce ischemic complications.
— Consider tocilizumab (IL-6 inhibitor) as steroid-sparing per GiACTA trial.
Step 3 management: For a 70-year-old with sudden monocular vision loss, jaw claudication, and ESR 95 — the first order is IV methylprednisolone, not a CT or biopsy. Vision in the second eye is at imminent risk.
Board pearl: CRAO without GCA → stroke pathway. CRAO with GCA → steroids first, stroke pathway second.
— IV tPA (alteplase 0.9 mg/kg, max 90 mg) — at stroke-capable centers, within 4.5 hours, after excluding hemorrhage and standard contraindications (recent surgery, active bleeding, BP >185/110 uncontrolled, INR >1.7, etc.). Class IIb recommendation; benefit suggested in pooled analyses (~odds of visual recovery ~2–3× higher when given <4.5 h).
— Aspirin 325 mg loading, then 81 mg daily — secondary prevention.
— High-intensity statin (atorvastatin 80 mg or rosuvastatin 40 mg) — initiate in ED for any atherosclerotic embolic source.
— Antihypertensive optimization — but avoid aggressive BP lowering acutely (permissive HTN principle from stroke care).
— Anticoagulation (apixaban, rivaroxaban, warfarin) if AFib or cardioembolic source confirmed.
— Methylprednisolone 1 g IV daily × 3 days, then prednisone 1 mg/kg/day PO (max 60–80 mg), slow taper over 12+ months guided by symptoms and ESR/CRP.
— Aspirin 81 mg daily unless contraindicated.
— Tocilizumab 162 mg SC weekly as steroid-sparing adjunct.
— PPI, calcium 1000–1200 mg, vitamin D 800 IU, bisphosphonate for steroid-induced GI and bone protection.
— PJP prophylaxis (TMP-SMX) if on prednisone ≥20 mg for ≥4 weeks.
— Glucose monitoring and BP checks for steroid effects.
— Intravitreal anti-VEGF — aflibercept 2 mg or ranibizumab 0.5 mg monthly initially, then PRN/treat-and-extend (CRUISE, COPERNICUS, GALILEO trials).
— Intravitreal dexamethasone implant (Ozurdex) — alternative; watch for cataract and IOP rise.
— Topical glaucoma therapy if IOP elevated.
— No role for systemic anticoagulation in routine CRVO — risks outweigh benefits unless a separate indication exists.
— Treat underlying HTN, hyperlipidemia, DM, OSA aggressively.
Board pearl: Systemic anticoagulation is not standard for either CRAO or CRVO without a defined embolic/thrombophilic indication. Antiplatelet therapy and risk-factor modification are the backbone.
Step 3 management: In acute CRAO, simultaneously order alteplase eligibility checklist, aspirin 325 mg, atorvastatin 80 mg, NPO, BP parameters, stroke neurology consult, and ophthalmology consult.
— Performed at bedside: firm digital pressure on closed lid for 10–15 seconds, release for 5 seconds, repeat for several minutes.
— Theoretical goal: dislodge embolus distally and reduce IOP, increasing perfusion pressure.
— Low-risk, low-evidence; widely done but should not delay definitive therapy.
— Ophthalmology procedure: 30-gauge needle removes 0.1–0.2 mL of aqueous humor, abruptly lowering IOP and theoretically increasing perfusion pressure gradient.
— Risks: lens trauma, endophthalmitis, hyphema.
— Selective catheterization of the ophthalmic artery with local tPA delivery.
— EAGLE trial (2010) showed no benefit over conservative therapy and higher complication rates — largely abandoned.
— Current AHA statement does not recommend IAT outside trials.
— Mechanism: dissolved O₂ in plasma supplies inner retina via choroidal diffusion despite arterial occlusion, "bridging" until reperfusion.
— Best evidence for treatment <24 hours of onset, with measurable visual improvement in observational series.
— Reasonable at HBO-capable centers; access often limits use.
— Performed in clinic under topical anesthesia and sterile prep with povidone-iodine.
— Anti-VEGF or dexamethasone implant.
— Risks: endophthalmitis (~1 in 3000), retinal detachment, IOP elevation, cataract.
— Patients counseled to report pain, redness, decreased vision, photophobia immediately post-injection.
— Reserved for CRVO with anterior segment or retinal neovascularization.
— Ablates ischemic peripheral retina to reduce VEGF drive.
— If CTA reveals symptomatic carotid stenosis ≥50% ipsilateral to CRAO, carotid endarterectomy (CEA) within 2 weeks is indicated (NASCET data extrapolated — CRAO/amaurosis is a stroke-equivalent event).
— Carotid artery stenting is alternative in select cases.
CCS pearl: After acute CRAO management, order CTA neck → if ≥50% symptomatic stenosis → vascular surgery consult for CEA within 14 days. Delay beyond 2 weeks loses the maximal stroke-prevention benefit.
Board pearl: Intra-arterial thrombolysis is a distractor answer on Step 3 — pick IV tPA at experienced centers within 4.5 h, or supportive care + secondary prevention.
— Higher prevalence of GCA — threshold for ESR/CRP and empiric steroids should be low. GCA incidence rises sharply after age 70; women > men 3:1.
— Polypharmacy review before adding aspirin, statins, anticoagulants — check for NSAIDs, SSRIs (bleeding synergy), anticholinergics.
— Fall risk before initiating antihypertensive intensification.
— Cognitive screening to ensure ability to comply with eye-injection follow-up and steroid taper.
— Bone health: any patient starting long-term prednisone for GCA needs DEXA, calcium, vitamin D, and bisphosphonate initiation per ACR glucocorticoid-induced osteoporosis guidelines (≥7.5 mg/day for ≥3 months in adults ≥40).
— Contrast considerations for CTA: weigh contrast-associated AKI risk against need for vascular imaging. eGFR <30 → IV hydration, consider MRA (gadolinium) or carotid Doppler.
— Acetazolamide (for IOP lowering) requires dose reduction; avoid if CrCl <10.
— DOACs for AFib: apixaban preferred in CKD (small renal clearance fraction); dabigatran avoided in CrCl <30.
— Statin dosing generally unchanged but monitor for myopathy.
— NSAIDs avoided — relevant if GCA patients tempted to self-medicate headaches.
— Warfarin requires more cautious titration; INR less reliable in cirrhosis.
— Statins — atorvastatin and rosuvastatin both have hepatic clearance; avoid in active liver disease or decompensated cirrhosis; mild elevations of transaminases are not a contraindication.
— Tocilizumab contraindicated in active hepatitis; screen HBV/HCV before initiation.
— Acetaminophen-based analgesia preferred over NSAIDs in cirrhosis at reduced doses.
— Visual loss is often permanent in CRAO — discuss expectations honestly. Avoid aggressive interventions if frailty index is high and benefit is marginal.
— Falls and depression rise after monocular vision loss — proactive screening in elderly.
Board pearl: In any patient >50 with vision loss, send ESR and CRP before deciding on disposition. Missing GCA risks the contralateral eye within days.
Step 3 management: Initiate glucocorticoid-induced osteoporosis prophylaxis at the same visit that prednisone is prescribed — do not defer to outpatient.
— Retinal vascular occlusion in pregnancy is rare but suggests antiphospholipid syndrome (APS), preeclampsia, HELLP, amniotic fluid embolism, or peripartum cardiomyopathy with embolism.
— Workup includes APS antibodies (lupus anticoagulant, anticardiolipin, anti-β2 glycoprotein I), BP and proteinuria for preeclampsia, echo for cardiomyopathy.
— Treatment caveats:
— IV tPA in pregnancy is relative contraindication — case-by-case at stroke center.
— LMWH preferred over warfarin (teratogenic 6–12 weeks; fetal bleeding 3rd trimester) when anticoagulation is indicated.
— Aspirin 81 mg is safe in pregnancy and is mainstay for APS prevention.
— Anti-VEGF intravitreal therapy is generally avoided in pregnancy (theoretical placental VEGF concerns); steroid implants or laser preferred.
— Postpartum hypercoagulability persists ~6 weeks — maintain vigilance.
— Differential: sickle cell disease/trait, congenital hypercoagulability, congenital heart disease with paradoxical embolism, vasculitis (Behçet, SLE), trauma, leukemia/hyperviscosity, mitochondrial disease (MELAS), homocystinuria.
— Mandatory workup: hemoglobin electrophoresis, echo with bubble study, full thrombophilia panel, ANA, homocysteine, urine amino acids.
— Hypercoagulable evaluation mandatory — factor V Leiden, prothrombin G20210A, protein C/S, antithrombin III, antiphospholipid antibodies, homocysteine, JAK2 V617F (polycythemia vera), paroxysmal nocturnal hemoglobinuria flow cytometry if hemolysis present.
— OCP and smoking — discontinue OCPs; aggressive smoking cessation.
— Consider occult malignancy (Trousseau-like phenomenon) if otherwise unexplained.
— Recreational stimulants (cocaine, methamphetamine) — vasospastic CRAO.
— More commonly cause proliferative sickle retinopathy and branch retinal vein occlusion, but CRAO/CRVO can occur with crisis.
— Manage with hydration, oxygen, exchange transfusion if severe.
Key distinction: In an adult <50 with CRVO, the workup pivots from "atherosclerosis" to "thrombophilia + glaucoma + OCP/smoking." Missing APS risks recurrent thromboses elsewhere.
Board pearl: A young woman on OCPs with CRVO → discontinue OCPs immediately and screen for APS.
— Most CRAO patients end up with counting fingers or worse in the affected eye. Only ~15–20% recover useful vision.
— Spontaneous improvement, when it occurs, happens within days; lack of improvement by 1 week is essentially permanent.
— Cilioretinal artery sparing (present in ~15–30% of eyes) preserves central foveal vision and confers a much better acuity outcome — look for the spared "wedge" on fundoscopy.
— ~25% have acute ischemic cerebral lesions on MRI at presentation.
— Risk of overt stroke is highest in the first 7 days post-CRAO — drives the urgency of stroke workup and secondary prevention initiation in the ED.
— Long-term stroke risk remains elevated for years.
— Complication of ischemic CRVO (and less commonly ischemic CRAO).
— Retinal ischemia drives VEGF release → iris and angle neovascularization (rubeosis iridis) → secondary angle closure → painful, blinding glaucoma.
— Peak incidence ~3 months post-occlusion.
— Requires monthly gonioscopy and IOP checks for at least 6 months.
— Treatment: PRP, anti-VEGF, IOP-lowering drops, glaucoma surgery.
— Major cause of vision loss; treated with intravitreal anti-VEGF or steroid implant. Often chronic, requiring serial injections.
— Late complications of untreated neovascularization.
— In GCA, the second eye is at risk within 1–2 weeks if untreated — devastating consequence.
— Idiopathic CRVO in the fellow eye occurs in ~5–10% over 5 years.
— tPA bleeding: intracranial hemorrhage ~1–6% (mostly minor for ophthalmic doses in ICH-screened patients).
— Long-term steroids: hyperglycemia, HTN, osteoporosis, infection, AVN, psychiatric effects.
— Intravitreal injection complications: endophthalmitis (~0.03–0.05% per injection — vision-threatening), retinal detachment, IOP spikes, cataract.
— Depression, anxiety, driving restrictions, fall risk, occupational impact.
Board pearl: A patient with prior CRAO who develops a TIA or stroke within days is the classic Step 3 stem — emphasizes that CRAO is part of a systemic atherothrombotic disease.
Step 3 management: Schedule CRVO patients for gonioscopy at 1 month, then monthly for at least 6 months to detect early rubeosis.
— Ophthalmology — bedside or telemedicine — for confirmation, IOP management, and procedural decisions.
— Stroke neurology / neurology — for CRAO, to coordinate tPA eligibility and stroke workup.
— Rheumatology — if GCA is suspected/confirmed, for taper management and steroid-sparing agents.
— Admit CRAO patients for expedited stroke workup (CTA, MRI, echo, telemetry) mirroring TIA admission criteria.
— Patients with completed workup, no concurrent stroke, and stable risk factors may transition to observation status and discharge with rapid outpatient follow-up within 24–48 hours — depends on institutional pathways.
— CRVO patients typically managed entirely outpatient unless there is concurrent acute systemic illness (acute thrombotic event, GCA, hypertensive emergency).
— Post-tPA monitoring for 24 hours (neuro checks, BP control).
— Concurrent large-vessel cerebral occlusion requiring thrombectomy.
— Hypertensive emergency.
— GCA with airway-threatening (rare) or systemic vasculitic complications.
— Endocarditis with embolic phenomena.
— Symptomatic carotid stenosis ≥50% → CEA within 14 days.
— Aortic arch or great vessel pathology requiring intervention.
— AFib initiation/optimization of anticoagulation.
— Endocarditis management.
— Patent foramen ovale closure decision (in young CRAO without other source).
— Confirmed thrombophilia in young patient — duration and intensity of anticoagulation.
— JAK2-positive polycythemia vera or essential thrombocythemia.
— At centers with HBO capability and acute CRAO within ~24 hours — early consult while workup proceeds.
— Ensure scheduled ophthalmology follow-up within 1 week for CRAO (or sooner for CRVO with macular edema).
— Communicate medication starts (statin, antiplatelet, anticoagulant, steroid) and monitoring plans to PCP.
CCS pearl: For CRAO, the typical CCS sequence is: ED stabilization → telemetry admission → CTA, MRI, echo, ESR/CRP → ophthalmology + stroke neurology consults → secondary prevention meds → carotid surgery consult if stenosis → discharge with 1-week ophtho follow-up and 1–2 week stroke clinic follow-up.
Board pearl: Treat CRAO like a TIA admission, not like a routine eye complaint.
— Sectoral, not global, vision field defect (altitudinal or wedge).
— Fundus shows pale wedge along arteriolar distribution.
— Same embolic workup as CRAO; visual prognosis better.
— Sectoral hemorrhages and edema along a venous distribution, typically at AV crossings (HTN drives arteriolar compression of vein).
— More common than CRVO; better prognosis.
— Same anti-VEGF management for macular edema.
— Proximal to CRAO — affects both inner retina (CRA territory) and choroid (ciliary territory).
— Severe vision loss (often no light perception).
— No cherry-red spot (because choroid is also ischemic — nothing red to show through).
— More common in GCA than embolic disease.
— Sudden painless vision loss, often altitudinal field defect (typically inferior).
— Disc edema with peripapillary hemorrhages, normal macula.
— Patients have "disc at risk" (small cup-to-disc ratio); often awaken with deficit.
— Risk factors: HTN, DM, OSA, sildenafil use, nocturnal hypotension.
— No effective acute treatment; treat risk factors; aspirin debated.
— Pale, swollen disc ("chalky white disc"); severe vision loss.
— Systemic GCA symptoms; ESR/CRP markedly elevated.
— Immediate IV steroids; biopsy within 1–2 weeks.
— Sudden vision loss with normal fundus initially (lesion behind globe); APD present.
— Often perioperative (prone spine surgery, cardiac surgery) or GCA-related.
— Mixed picture with both pallor and hemorrhages.
— Suggests inflammatory/infiltrative process (orbital cellulitis, mucormycosis, syphilis).
Key distinction: CRAO = pale retina + cherry-red spot + APD; CRVO = hemorrhages everywhere + tortuous veins; AION = disc edema + altitudinal defect; OAO = no light perception + no cherry-red spot.
Board pearl: A chalky white swollen disc in an elderly patient with vision loss = arteritic AION until proven otherwise — start steroids before biopsy.
— Painful unilateral vision loss with halos, headache, nausea, vomiting.
— Firm globe, mid-dilated fixed pupil, hazy cornea, IOP often >40 mm Hg.
— Treat with topical beta-blocker, alpha-agonist, prostaglandin, pilocarpine, oral/IV acetazolamide, mannitol; definitive laser peripheral iridotomy.
— Painless vision loss with flashes, floaters, curtain or veil in the visual field.
— Dilated exam shows retinal tear or detachment; urgent ophthalmology referral.
— Sudden floaters and vision loss; loss of red reflex; no view of fundus.
— Causes: proliferative diabetic retinopathy, retinal tear, trauma, Terson syndrome (SAH).
— Pain with eye movement, central scotoma, dyschromatopsia (red desaturation), APD.
— Younger patients (20–40), often female; MS association.
— MRI orbits and brain; IV methylprednisolone per ONTT.
— Visual loss preserves pupillary response (no APD), often bilateral homonymous deficits, may have other neurologic signs.
— MRI confirms; manage as stroke.
— Normal exam, normal APD, inconsistent acuity testing; diagnosis of exclusion.
— Methanol — bilateral simultaneous vision loss + metabolic acidosis with high anion gap and osmolar gap. Treat with fomepizole, dialysis.
— Quinine, ethambutol, amiodarone toxicity.
— Transient scintillating scotoma, lasts <60 minutes, reversible.
— Pain, redness, hypopyon, recent intraocular surgery or injection.
— Emergent vitreous tap and intravitreal antibiotics.
— Painful proptosis, ophthalmoplegia, fever; immunocompromised or diabetic; emergent imaging and IV antibiotics/antifungals.
— Pulsatile proptosis, conjunctival chemosis, bruit.
— Cortical vision loss with severe HTN, headache, seizures; MRI shows parieto-occipital edema.
Key distinction: Pain with vision loss takes you off the CRAO/CRVO path → think angle-closure, optic neuritis, GCA, endophthalmitis, orbital cellulitis.
Board pearl: Bilateral simultaneous painless vision loss in a patient with metabolic acidosis = methanol — order osmolar gap and start fomepizole.
— Antiplatelet: aspirin 81 mg daily (or clopidogrel 75 mg if aspirin intolerant). Dual antiplatelet therapy (aspirin + clopidogrel × 21–90 days) considered in select patients per recent stroke evidence (CHANCE/POINT extrapolation).
— High-intensity statin: atorvastatin 40–80 mg or rosuvastatin 20–40 mg, target LDL <70 mg/dL (and arguably <55 mg/dL per ESC and emerging US data for very-high-risk atherosclerosis).
— Antihypertensive optimization: BP target <130/80 per AHA/ACC; ACEi/ARB or thiazide first-line; avoid orthostatic hypotension.
— Diabetes management: HbA1c target individualized (typically <7%); consider GLP-1 RA or SGLT2i if comorbidities favor.
— Anticoagulation if AFib (CHA₂DS₂-VASc ≥2 in men, ≥3 in women) or cardioembolic source: apixaban, rivaroxaban, dabigatran, edoxaban, or warfarin per indication.
— Smoking cessation: counseling + pharmacotherapy (varenicline, bupropion, NRT).
— Lifestyle: Mediterranean or DASH diet, ≥150 min/week moderate exercise, weight management, limit alcohol.
— Prednisone taper over 12–24 months guided by clinical symptoms and ESR/CRP.
— Tocilizumab as steroid-sparing.
— Aspirin 81 mg daily.
— Bone protection (calcium, vitamin D, bisphosphonate, DEXA).
— PJP prophylaxis if prednisone ≥20 mg ≥4 weeks.
— Glucose, BP, lipid monitoring; immunizations (avoid live vaccines while immunosuppressed; encourage inactivated flu, COVID, pneumococcal, shingles recombinant).
— Treat HTN to <130/80, lipids per ASCVD risk, diabetes per A1c goals.
— Address OSA — increasingly recognized CRVO risk factor; screen with STOP-BANG.
— Glaucoma management — IOP control with topical therapy.
— Smoking cessation.
— Anti-VEGF treat-and-extend with serial OCT.
— Aspirin only if separately indicated (no proven CRVO-specific benefit).
— CEA within 14 days for symptomatic ≥50% stenosis (men) and ≥70% (women per some guidelines); ongoing antiplatelet/statin.
Step 3 management: A CRAO discharge order set must include aspirin, statin, BP medication, smoking cessation referral, ophthalmology follow-up in 1 week, stroke clinic follow-up in 2 weeks, and a PCP visit within 7–14 days.
Board pearl: CRAO is a secondary prevention opportunity — patients leave with at minimum antiplatelet + statin + BP optimization, even if vision is unrecoverable.
— Ophthalmology: 1 week post-event for CRAO; CRVO patients typically monthly during anti-VEGF treatment phase, then extended intervals.
— PCP: within 7–14 days for medication titration, BP/lipid/glucose review.
— Stroke clinic / neurology: 2–4 weeks for CRAO.
— Vascular surgery: within 1–2 weeks if carotid intervention indicated.
— Rheumatology: monthly initially for GCA taper.
— BP: home log, target <130/80.
— Lipid panel: 4–12 weeks after statin start, then annually; target LDL <70.
— HbA1c: every 3 months until at goal, then every 6 months.
— ESR/CRP monthly during GCA taper.
— CBC, CMP, lipids, glucose for steroid monitoring.
— IOP and gonioscopy monthly × 6 months for CRVO (rubeosis surveillance).
— OCT for macular edema response to anti-VEGF.
— DEXA baseline and yearly on chronic prednisone.
— INR if on warfarin (target 2–3 for AFib); periodic CBC for DOACs and renal function quarterly.
— Low-vision rehabilitation referral for any patient with persistent monocular vision loss — magnifiers, lighting, occupational therapy.
— Driving counseling — per state law; one-eyed patients may continue driving if visual field and acuity meet criteria, but require adaptation period.
— Depression screening — PHQ-9 at follow-up visits; vision loss is a major risk factor.
— Fall prevention: home safety assessment, PT consult.
— Occupational accommodations — communicate with employer where appropriate.
— Patient education on second-eye warning signs: sudden vision change, new floaters, eye pain, GCA symptoms (new headache, jaw pain) → ED immediately.
— Smoking cessation at every visit (5 A's).
— Diet, exercise, weight, alcohol — document and re-engage.
— Medication adherence checks — aspirin, statin, BP meds are lifelong.
— Expect multiple intravitreal injections; explain endophthalmitis warning signs (pain, redness, vision drop within days of injection) and 24/7 contact pathway.
Step 3 management: At the post-CRAO PCP visit, recheck BP, lipids, HbA1c, medication adherence, smoking status, depression (PHQ-9), and confirm scheduled ophthalmology and stroke clinic follow-up — a classic transition-of-care checklist.
Board pearl: Low-vision rehabilitation is underutilized — refer every patient with permanent acuity loss, not just the legally blind.
— tPA for CRAO is an off-label, evidence-evolving indication. Patients (or surrogates) must be informed of:
— Uncertain benefit vs ICH risk (~1–6%).
— Possibility of no visual recovery despite treatment.
— Alternatives (conservative measures, no treatment).
— Document shared decision-making explicitly. If patient lacks capacity (e.g., aphasia from concurrent stroke), engage surrogate per state hierarchy.
— State-specific. Many states mandate physician reporting of conditions that impair driving; others rely on patient self-reporting.
— Counsel monocular patients about adjustment period and field testing; document the conversation.
— California, Pennsylvania, Oregon, and several others have specific reporting statutes — know your jurisdiction.
— The most dangerous gap is between ED discharge and outpatient follow-up. Patients with CRAO are at peak stroke risk in the first 7 days.
— Mitigation: ensure follow-up appointments are made before discharge (not just recommended); provide written instructions and a 24-hour contact number; medication reconciliation with the patient holding the list; use a closed-loop referral system.
— Failure to send ESR/CRP in a patient >50 with vision loss is a classic malpractice scenario when the contralateral eye later goes blind.
— Document the GCA review of systems and lab results explicitly.
— Sudden visual loss does not impair decisional capacity. Provide consent forms in alternative formats (read aloud, large print) and ensure understanding.
— Intravitreal injection endophthalmitis, post-tPA ICH — per AMA and Joint Commission, prompt, honest disclosure to patient is required.
— Anti-VEGF therapy access varies by insurance — bevacizumab off-label is far less expensive than ranibizumab/aflibercept and has comparable efficacy (CATT, IVAN trials in AMD; SCORE-2 in CRVO). Insurance prior authorization may delay care.
— Address language barriers with certified interpreters — never family members for high-stakes consent.
— Verify TB and HBV status before prolonged immunosuppression; assess osteoporosis baseline; reconcile interacting medications (warfarin, antihyperglycemics, antihypertensives).
— In frail elderly with severe bilateral vision loss and limited prognosis, revisit goals of care, code status, and home-support resources.
Board pearl: A patient >50 with vision loss who is discharged without an ESR/CRP is the Step 3 ethics/safety vignette where the next stem is bilateral blindness — never skip the GCA workup.
Step 3 management: Before discharge, confirm a scheduled follow-up date, written warning signs, medication reconciliation, and patient-teach-back understanding — the safe transition-of-care bundle.
Board pearl: "Painless sudden monocular vision loss + cherry-red spot + APD + age >50 with HTN/AFib" = CRAO → stroke workup, ophthalmology, ESR/CRP, and time-from-onset assessment for tPA candidacy.
— 70-year-old man with HTN, hyperlipidemia, smoking presents with sudden painless complete vision loss in the right eye 2 hours ago. Exam: APD, pale retina with cherry-red spot. Best next step? → Stroke pathway activation, ESR/CRP, CTA head/neck, ophthalmology consult, consider IV tPA at stroke center within 4.5 h.
— 75-year-old woman with new temporal headache, jaw claudication, weight loss, ESR 102, presents with vision loss and pale swollen disc. Best next step? → IV methylprednisolone 1 g now, then temporal artery biopsy within 1–2 weeks. Do not wait for biopsy.
— 62-year-old hypertensive man with gradual blurring over hours; exam shows diffuse retinal hemorrhages in 4 quadrants, dilated tortuous veins, macular edema on OCT. Best initial treatment? → Intravitreal anti-VEGF; control HTN; rule out glaucoma; lipid and diabetes screen.
— 32-year-old woman on OCPs, smoker, with CRVO. Next workup? → Stop OCPs, smoking cessation, hypercoagulable panel (antiphospholipid antibodies, factor V Leiden, prothrombin G20210A, homocysteine).
— 68-year-old with transient 5-minute monocular vision loss, resolved. Best next step? → Urgent CTA carotids, antiplatelet, statin, ED-level workup — this is a TIA equivalent.
— CRAO patient with 80% ipsilateral ICA stenosis on CTA. Best next step? → Carotid endarterectomy within 14 days, continue aspirin + statin.
— Patient with severe eye pain, headache, nausea, mid-dilated fixed pupil, IOP 52. → Acute angle-closure glaucoma, not CRAO.
— IV drug user with fever, new murmur, and acute monocular vision loss with Hollenhorst-like emboli or Roth spots. → Blood cultures, TEE, IV antibiotics — septic embolic CRAO.
— Patient with high anion gap acidosis after homemade alcohol → methanol; treat with fomepizole, dialysis.
— Three months post-ischemic CRVO, patient develops eye pain, IOP 48, iris neovascularization. → Neovascular glaucoma (100-day) — anti-VEGF, PRP, IOP-lowering, glaucoma surgery.
— CRAO patient discharged without ophthalmology follow-up; returns with second-eye involvement and is found to have undiagnosed GCA. → Tests patient safety / system gaps.
Board pearl: When the stem says "age >50 + vision loss," your first reflex on the answer choices should be ESR + CRP + consider empiric steroids — even if other answers look attractive.
Central retinal artery occlusion is a time-critical stroke of the eye demanding immediate fundoscopy, GCA exclusion with ESR/CRP, stroke-pathway workup with CTA and MRI, consideration of IV tPA within 4.5 hours at a stroke center, and lifelong secondary prevention — while central retinal vein occlusion is a subacute thrombotic event managed primarily with intravitreal anti-VEGF for macular edema, aggressive control of HTN/glaucoma/diabetes, and vigilant surveillance for ischemic conversion and neovascular glaucoma.
Board pearl: The single highest-yield Step 3 reflex: age >50 + sudden vision loss = check ESR/CRP and call ophthalmology before you leave the bedside — and treat CRAO as an ischemic stroke equivalent in every other respect.