Ocular Stroke (Central Retinal Artery Occlusion) and Temporal Arteritis¶

Sudden, painless blindness or severe visual dimming in one eye is a time-critical neuro-ophthalmic vascular emergency clinically equivalent to an acute ischemic brain stroke. When a blood clot, cholesterol crystal, or autoimmune arterial inflammation blocks the blood supply to the retina (Central Retinal Artery Occlusion [CRAO] or Branch Retinal Artery Occlusion [BRAO]) or the optic nerve head (Anterior Ischemic Optic Neuropathy [AION] caused by Giant Cell Arteritis [GCA / Temporal Arteritis]), oxygen-starved nerve cells begin dying irreversibly within 90 to 240 minutes. Even if the blackout in one eye lasts only 2 to 15 minutes and then clears completely (Amaurosis Fugax, a retinal transient ischemic attack), up to 25 percent of patients already have concurrent silent cerebral infarctions on brain MRI and face an immediate risk of a disabling hemispheric stroke or bilateral blindness. Calling emergency services immediately, transporting directly to a Designated Stroke Center (never waiting for a routine optometrist appointment), and starting immediate intravenous thrombolysis or high-dose intravenous corticosteroids within hours determines whether sight and brain function are saved.

Do this now¶

1. Cover one eye at a time to confirm whether the visual blackout is in ONE eye (monocular) or BOTH eyes (binocular), and write down the exact minute the vision changed ("Last Known Well" time). Hospital stroke teams and neuro-ophthalmologists need the exact minute symptoms started to calculate the 4.5-hour intravenous thrombolysis window.
2. Monocular blackout (only the left eye OR only the right eye is dark/missing a half when the other eye is covered): Indicates an arterial blockage in front of the optic chiasm (Central Retinal Artery Occlusion, Branch Retinal Artery Occlusion, Ophthalmic Artery Occlusion, or Giant Cell Arteritis Optic Neuropathy).
3. Binocular half-field loss (both the left eye AND the right eye cannot see the left side or right side of the room): Indicates an occipital lobe brain stroke (homonymous hemianopia) behind the optic chiasm.
4. Screen every patient aged 50 or older immediately for the "Giant Cell Arteritis (Temporal Arteritis) Red Flag Triad": Ask the patient right now:
5. "Have you had a new headache, temple ache, or tender scalp when brushing your hair or resting on a pillow?"
6. "Does your jaw, tongue, or face ache, cramp, or get tired after chewing food for a minute (jaw claudication)?"
7. "Have you had stiff, aching shoulders or hips in the morning (polymyalgia rheumatica), unexplained fatigue, night sweats, or brief episodes of double vision or chalky vision dimming?"
8. If ANY answer is YES in an adult aged \(\ge 50\text{ years}\): Tell paramedics and the emergency room triage nurse immediately that you suspect Arteritic Ischemic Optic Neuropathy from Giant Cell Arteritis so they administer high-dose intravenous methylprednisolone (\(500\text{ to }1,000\text{ mg}\) IV) immediately before waiting for blood tests or biopsy to save the fellow eye.
9. Call your local emergency number immediately and request transport to a Designated Stroke Center Hospital with an Emergency Department. Dial 911 in the United States and Canada, 112 across the European Union, 999 in the United Kingdom, or see all emergency numbers. State clearly: "The patient has sudden painless vision loss in one eye; we suspect an acute Ocular Stroke (Central Retinal Artery Occlusion) or Giant Cell Arteritis."
10. Position the patient appropriately while waiting for the ambulance:
11. For suspected non-arteritic CRAO / Embolic Eye Stroke (no head trauma or severe heart failure): Lay the patient completely flat on their back (supine, \(0\text{ degrees}\)) with their head flat. Lying flat increases gravitational arterial perfusion pressure to the ophthalmic and central retinal arteries, helping push blood past the clot or through tiny cilioretinal collateral vessels.
12. If the patient has concurrent shortness of breath or suspected brain hemorrhage: Elevate the head slightly to \(15\text{ to }30\text{ degrees}\).
13. Check for concurrent FAST brain stroke signs and carotid dissection warning signs. Check for facial droop, arm weakness, or slurred speech (see stroke guide). If a younger patient (under age 50) develops sudden one-eye vision loss paired with new pain on one side of the neck or face and a slightly drooping eyelid with a smaller pupil on that same side (Horner syndrome) after neck trauma, chiropractic manipulation, heavy lifting, or coughing, suspect an Internal Carotid Artery Dissection.
14. Do NOT aggressively press on or massage the eyeball, do NOT breathe into a paper bag, and keep the patient Nothing by Mouth (NPO). While older medical books mentioned forceful eyeball massage or paper-bag rebreathing, the American Heart Association (AHA) advises against untrained bystander ocular compression or hypercarbia because they have zero proven benefit, can damage the eye or trigger cardiac ischemia, and delay emergency stroke-center thrombolysis.

Emergency triage decision tree: Sudden painless vision loss & Temporal Arteritis¶

Use this clinical flowchart to classify monocular vs. binocular ischemic vision loss and activate the exact hospital stroke or steroid protocol within minutes.

flowchart TD
    Start["Sudden Painless Vision Loss,<br/>Visual Field Blackout, or Transient Dimming"] --> CoverTest{"Cover Each Eye Separately:<br/>Is Vision Lost in ONE Eye or BOTH Eyes?"}

    CoverTest -->|"BOTH EYES lose the exact same<br/>Left Half or Right Half of vision"| Occipital["HOMONYMOUS HEMIANOPIA<br/>(Acute Posterior / Occipital Brain Stroke):<br/>Call 911 / 112 / 999 Immediately for Stroke Center"]

    CoverTest -->|"ONE EYE ONLY (Monocular Vision Loss):<br/>Lesion is in the Retina, Optic Nerve,<br/>or Ipsilateral Carotid/Ophthalmic Artery"| AgeCheck{"Check Age & Giant Cell Arteritis<br/>(Temporal Arteritis) Red Flags:<br/>Is Patient Age >= 50 Years WITH<br/>Temple Headache, Scalp Tenderness,<br/>Jaw Pain when Chewing, or Shoulder Stiffness?"}

    AgeCheck -->|"YES (Age >= 50 + ANY GCA Symptom,<br/>or Chalky/Altitudinal Vision Loss):<br/>SUSPECT GIANT CELL ARTERITIS<br/>(Arteritic AION or Arteritic CRAO)"| GCAProtocol["IMMEDIATE 'SAVE THE SECOND EYE' PROTOCOL:<br/>1. Call 911 / 112 / 999 -> Emergency Department NOW<br/>2. Administer Stat High-Dose IV Methylprednisolone<br/>   (500 to 1,000 mg IV/day x 3 days) IMMEDIATELY<br/>   (Do NOT delay steroids for ESR/CRP labs or biopsy)<br/>3. Order Stat ESR, CRP, Platelets + Temporal Ultrasound/Biopsy"]

    AgeCheck -->|"NO GCA Symptoms<br/>(or Patient Under Age 50)"| DurationCheck{"Did Vision Return to 100% Normal<br/>Within 2 to 15 Minutes,<br/>or is Vision STILL Dark/Missing?"}

    DurationCheck -->|"Vision Returned Completely in 2 to 15 Min<br/>('Window Shade Pulled Down & Lifted Up'):<br/>AMAUROSIS FUGAX (Retinal TIA)"| TIAProtocol["ACUTE RETINAL TIA EMERGENCY:<br/>1. Do NOT stay home (High risk of brain stroke in 24-72h)<br/>2. Go to Designated Stroke Center Emergency Room NOW<br/>3. Needs stat Brain MRI (DWI), Carotid CTA/Ultrasound,<br/>   ECG/Holter for AFib, Dual Antiplatelets, & Statin"]

    DurationCheck -->|"Vision Remains Dark (Complete Blackout)<br/>or Missing Top/Bottom Sector:<br/>SUSPECT CENTRAL OR BRANCH RETINAL<br/>ARTERY OCCLUSION (CRAO / BRAO)"| CRAOProtocol["ACUTE OCULAR STROKE ('CODE STROKE'):<br/>1. Call 911 / 112 / 999 -> Designated Stroke Center NOW<br/>2. Lay patient FLAT on back (0 degrees) to boost perfusion<br/>3. Note exact minute of onset (< 4.5 hour IV tPA window)<br/>4. If neck pain + small pupil/droopy lid -> Check Carotid Dissection"]

Pathophysiology: How the eye's dual blood supply works and why minutes matter¶

The eye is supplied by the ophthalmic artery, which is the very first major branch off the internal carotid artery just as it enters the skull from the neck. Because the ophthalmic artery branches directly off the internal carotid artery, anything happening in the arteries of the eye is a direct window into the arteries of the brain and heart.

Inside the eye socket, the ophthalmic artery splits into two completely separate vascular systems that feed different layers of the retina and optic nerve:

1. The Central Retinal Artery (CRA) System (Feeds the Inner Retina):
2. The central retinal artery pierces the center of the optic nerve and branches across the inner surface of the retina into four quadrants (superior temporal, inferior temporal, superior nasal, and inferior nasal branches).
3. It is an anatomical end-artery with zero collateral connections in 70 to 85 percent of humans.
4. (Anatomical exception: About 15 to 30 percent of people are born with an extra accessory vessel called a cilioretinal artery coming from the choroidal circulation that feeds the central macula. In a lucky patient with a cilioretinal artery who suffers a CRAO, their entire peripheral vision goes black, but a tiny pinhole island of 20/20 central reading vision survives.)
5. The Short Posterior Ciliary Arteries (SPCAs) System (Feeds the Optic Nerve Head & Outer Retina):
6. Two to three main posterior ciliary trunks divide into 10 to 20 tiny short posterior ciliary arteries that form a vascular ring around the head of the optic nerve and feed the choroid (which nourishes the outer photoreceptor rods and cones, including the central fovea).
7. Why Giant Cell Arteritis loves the Short Posterior Ciliary Arteries: The internal elastic lamina of the short posterior ciliary arteries and superficial temporal arteries is the #1 target of the autoimmune giant-cell attack in Temporal Arteritis, explaining why Giant Cell Arteritis causes devastating optic nerve head infarction (Arteritic Anterior Ischemic Optic Neuropathy [A-AION]) in 80 percent of visual cases and Arteritic CRAO in 10 to 15 percent.

The Retinal Ischemic Survival Clock (Why 90 to 240 Minutes is the Threshold)¶

Classic primate neuro-ophthalmology experiments (Hayreh et al.) and human stroke trials establish the exact biological survival clock of retinal ganglion cells when the central retinal artery is clamped shut: - 0 to 90 minutes of complete occlusion: Retinal tissue is stunned (ischemic penumbra), but full or near-full visual recovery is possible if blood flow is restored immediately. - 90 to 240 minutes (1.5 to 4 hours): Progressive, patchy infarction of the inner retinal ganglion cell layer occurs; partial recovery is still possible with emergency reperfusion. - Beyond 240 minutes (4+ hours) of complete total occlusion: Massive, irreversible necrosis of the inner retina occurs, leaving permanent profound visual loss (usually counting fingers [CF], hand motion [HM], or light perception [LP] only) unless a cilioretinal artery or incomplete blockage preserved a penumbra.

Comprehensive comparison of the 5 major ischemic ocular emergencies¶

Use this clinical table to distinguish embolic CRAO, branch retinal artery occlusion, amaurosis fugax, arteritic optic neuropathy (Giant Cell Arteritis), and non-arteritic optic neuropathy:

Condition 1: Central and Branch Retinal Artery Occlusion (CRAO & BRAO)¶

Why the American Heart Association mandates a "Code Stroke" for CRAO¶

Historically, patients who lost vision in one eye went to an optometrist or eye clinic first, where hours or days were spent doing eye exams before anyone checked their brain or neck arteries. In 2021, the American Heart Association (AHA) and American Stroke Association (ASA) issued a landmark Scientific Statement transforming CRAO care globally: 1. CRAO is an Acute Ischemic Stroke: Because the retina is embryologically part of the central nervous system and fed by the internal carotid artery, an occlusion of the central retinal artery is literally an ischemic stroke of the retina. 2. 1 in 4 CRAO Patients Has a Concurrent Silent Brain Stroke Right Now: Diffusion-weighted brain MRI (DWI) studies prove that 19 to 25 percent of patients presenting with acute CRAO or BRAO have simultaneous acute ischemic strokes in the cerebral hemisphere caused by a shower of clots breaking off the same carotid plaque or heart chamber, even when the patient has zero arm weakness or speech trouble. 3. Intravenous Thrombolysis Window (\(\le 4.5\text{ Hours}\)): When a patient with non-arteritic CRAO arrives at a Designated Stroke Center within 4.5 hours of symptom onset, after an immediate non-contrast head CT rules out brain bleeding and labs rule out Giant Cell Arteritis, stroke neurologists and ophthalmologists can administer intravenous tissue plasminogen activator (alteplase or tenecteplase). Clinical meta-analyses show that IV thrombolysis given within 4.5 hours significantly increases the rate of meaningful visual recovery compared to conservative observation.

What is the "Cherry-Red Spot" on an eye exam?¶

When an emergency physician or ophthalmologist looks into an eye with CRAO using an ophthalmoscope or fundus camera within hours of the attack: - The inner layers of the retina (fed by the blocked central retinal artery) swell with intracellular water (cytotoxic edema), turning opaque milky white. - However, the dead-center bullseye of the macula (the foveola) is anatomically paper-thin and contains no inner retinal ganglion layers, it is nourished entirely by the underlying choroid (fed by the intact posterior ciliary arteries). - Because the bright red vascular choroid shines right through the thin transparent center while surrounded by a halo of milky-white infarcted retina, it creates the classic "Cherry-Red Spot" of Central Retinal Artery Occlusion.

Why you must NOT rely on home "Ocular Massage" or "Paper-Bag Breathing"¶

Older textbooks suggested pressing forcefully on the closed eyeball (digital ocular massage) or breathing into a brown paper bag (carbogen therapy) for CRAO. - Modern Clinical Verdict (AHA & AAO): Both practices are discouraged for bystanders. Forceful eyeball pressing can rupture an eye with recent surgery, worsen a retinal detachment, or trigger a vagal bradycardia reflex (oculocardiac reflex). Breathing into a paper bag causes systemic hypoxia in older patients without improving retinal survival. The single effective pre-hospital action is laying the patient flat on their back and calling 911 / 112 / 999 for immediate Stroke Center transport.

Special Cause in Adults Under Age 50: Internal Carotid Artery Dissection¶

If a younger adult (aged 20 to 50) develops sudden monocular vision loss or amaurosis fugax, ask if they have neck pain, a one-sided headache, or facial ache, and check their eyelids and pupils in dim light: - A tear in the inner lining of the internal carotid artery in the neck (Internal Carotid Artery Dissection), often triggered by neck whiplash, yoga hyperextension, chiropractic manipulation, heavy lifting, or violent coughing, stretches the sympathetic nerve fibers wrapped around the outside of the carotid artery wall. - This produces ipsilateral Horner Syndrome (a slightly drooping upper eyelid [ptosis] and a smaller constricted pupil [miosis] on the same side as the neck pain) alongside retinal or cerebral emboli. Immediate CT angiography (CTA) of the head and neck in the emergency department confirms the dissection.

Condition 2: Amaurosis Fugax (Transient Monocular Vision Loss / Retinal TIA)¶

Why "vision returning to normal in 5 minutes" is still a 911 / 112 / 999 emergency¶

Amaurosis fugax ("fleeting darkness") occurs when a fragment of cholesterol (a Hollenhorst plaque) or a platelet-fibrin micro-clot breaks loose from a plaque in the internal carotid artery of the neck (or from the heart in atrial fibrillation), lodges briefly in the central retinal artery, and then breaks apart within 2 to 15 minutes: - Patients describe it as "a dark window shade pulling smoothly down over ONE eye" until the eye is gray or black, lasting 3 to 10 minutes, and then lifting back up until vision is 100 percent normal. - The Trap: Because vision returns to normal after 5 minutes with zero pain, many people brush it off as eye strain or a migraine and stay home. - The Reality: Amaurosis fugax is a Retinal Transient Ischemic Attack (TIA). Without emergency hospital evaluation, dual antiplatelet therapy (aspirin + clopidogrel), high-intensity statin therapy, and urgent carotid endarterectomy or stenting (if carotid narrowing is \(70\%\text{ to }99\%\)), the next clot that breaks off hours later can plug the middle cerebral artery, causing permanent paralysis and loss of speech.

How to tell Amaurosis Fugax apart from a benign Visual Migraine Aura or Papilledema¶

Condition 3: Giant Cell Arteritis (GCA / Temporal Arteritis) in Adults Aged 50 and Older¶

Why Giant Cell Arteritis is the most preventable cause of bilateral total blindness¶

Giant Cell Arteritis (GCA), also known as Temporal Arteritis, is an autoimmune granulomatous vasculitis of medium and large arteries that occurs exclusively in adults aged 50 years and older (peaking between ages 70 and 85).

In GCA, immune T-cells and giant cells infiltrate the wall of extracranial branches of the carotid and vertebral arteries: - The artery wall swells inward (intimal hyperplasia) until the central channel clots shut. - When this inflammatory occlusion strikes the short posterior ciliary arteries or central retinal artery, the optic nerve head dies of sudden oxygen starvation (Arteritic Anterior Ischemic Optic Neuropathy [A-AION]), leaving the eye completely dark in over 50 percent of cases. - The "Fellow Eye" Clock: Once the first eye loses vision from GCA, that first eye rarely recovers significant sight. However, if high-dose corticosteroid therapy is delayed, 30 to 50 percent of patients suffer an identical attack in their SECOND (remaining) eye within 24 hours to 7 days, leaving them permanently blind in both eyes. Untreated GCA can also inflame the vertebral and internal carotid arteries (causing brainstem strokes) and the thoracic aorta (causing aortic dissection).

Complete Red Flag Symptom Checklist for Giant Cell Arteritis (Age \(\ge 50\))¶

Because 20 percent of patients with visual loss from GCA have "occult GCA" (minimal headache, with only subtle jaw or systemic symptoms), check every item on this list in any adult over 50 with a visual change:

• 1. Jaw Claudication (Most Specific Symptom of GCA, present in ~50%): Ask the patient: "When you chew chewy food like meat or crusty bread for 1 to 2 minutes, do your jaw muscles or tongue start aching, cramping, or feeling exhausted so you have to stop chewing and rest?" This happens because the facial and maxillary arteries supplying the chewing muscles and tongue are narrowed by arteritis, causing exercise-induced muscle ischemia.
• 2. New-Onset Localized Headache (Present in 70% to 80%): A new throbbing, boring, or burning ache over one or both temples, the forehead, or the back of the head in an older adult.
• 3. Scalp Tenderness and Abnormal Temporal Artery: Brushing hair, resting the head on a pillow, or wearing eyeglasses feels sore on the scalp. Running a finger gently over the superficial temporal artery (in front of the ear and above the temple) reveals a thickened, nodular, tender artery with a weak or absent pulse.
• 4. Premonitory Visual Warning Signs: Brief 5-minute dimming spells (amaurosis fugax) or transient diplopia (double vision, present in 10% to 15%) caused by ischemia of the eye muscles.
• 5. Polymyalgia Rheumatica (PMR) and Constitutional Symptoms (Present in 40% to 50%): Symmetric morning stiffness and aching across both shoulders, neck, and hips lasting more than 45 minutes after waking, accompanied by low-grade fever, night sweats, anorexia, or unintentional weight loss.

Hospital Emergency Protocol for Suspected Giant Cell Arteritis¶

According to the joint clinical practice guidelines of the American College of Rheumatology (ACR), European Alliance of Associations for Rheumatology (EULAR), and British Society for Rheumatology (BSR): 1. Start High-Dose Corticosteroids IMMEDIATELY Upon Clinical Suspicion (Before Biopsy or Labs Return): - If ANY visual symptoms are present (vision loss, amaurosis fugax, or double vision): Administer intravenous methylprednisolone \(500\text{ to }1,000\text{ mg}\) IV per day for 3 consecutive days, followed by high-dose oral prednisone (\(1\text{ mg/kg/day}\), typically \(60\text{ to }80\text{ mg}\) daily) and consideration of tocilizumab. - If cranial GCA symptoms are present WITHOUT visual symptoms yet: Start oral prednisone \(40\text{ to }60\text{ mg}\) daily immediately. 2. Never Delay Steroids Waiting for a Temporal Artery Biopsy or Ultrasound: The inflammatory changes and giant cells inside the temporal artery wall persist for 10 to 14 days after starting high-dose steroids, while delaying steroids by even 12 hours can cost the patient their remaining eye. 3. Blood Tests Ordered Immediately in the ER: Erythrocyte Sedimentation Rate (ESR), C-Reactive Protein (CRP), and Complete Blood Count (CBC) (checking for reactive thrombocytosis with platelets \(>400,000/\mu\text{L}\)).

Exact communication script for 911 / 112 / 999 and hospital triage¶

Because painless vision loss makes the outside of the eye look 100 percent normal (white sclera, clear cornea), triage staff at general hospitals can underestimate its urgency unless you use the exact stroke and vasculitis terminology:

• For Suspected Central Retinal Artery Occlusion (CRAO) Within 4.5 Hours:

  "I need an emergency ambulance at [Exact Address]. The patient is a [Age]-year-old [male/female] who developed sudden, complete, painless blindness in the [left/right] eye at [Exact Minute of Onset]. According to American Heart Association guidelines, we suspect an acute Ocular Stroke (Central Retinal Artery Occlusion) and need immediate Code Stroke transport to a Designated Stroke Center within the 4.5-hour intravenous thrombolysis window."

• For Suspected Giant Cell Arteritis (Temporal Arteritis) in an Adult Aged 50+:

  "Emergency triage: this [Age]-year-old patient has sudden vision loss [or double vision / transient dimming] in the [left/right] eye accompanied by [new temple headache / scalp tenderness / jaw pain when chewing food]. We suspect Arteritic Ischemic Optic Neuropathy from Giant Cell Arteritis and need immediate emergency physician evaluation for stat high-dose intravenous methylprednisolone (500 to 1,000 mg IV) RIGHT NOW to prevent permanent blindness in the fellow eye."

• For Resolved Amaurosis Fugax (Retinal TIA):

  "The patient is a [Age]-year-old who experienced a complete painless blackout ('window shade') in the [left/right] eye lasting [Number] minutes at [Time] today. Even though vision has returned to normal, this is Amaurosis Fugax, an acute Retinal TIA, and requires immediate Stroke Center emergency evaluation, brain MRI, carotid artery imaging, and ECG."

Frequently asked questions¶

Why does the outside of the eye look completely white and normal during an ocular stroke (CRAO) or temporal arteritis?¶

The blood vessels that make the surface of the eye look red during pink eye or glaucoma are superficial conjunctival and episcleral vessels on the front of the eyeball. In Central Retinal Artery Occlusion and Giant Cell Arteritis, the arterial blockage occurs deep inside the back of the eye socket in the tiny central retinal artery or short posterior ciliary arteries feeding the retina and optic nerve, so the front of the eye remains completely white and painless while the retina inside is starving for oxygen.

How do I check at home if sudden blurry vision is in one eye (monocular) or both eyes (binocular)?¶

When one eye suddenly loses vision or develops a dark shadow, the human brain tries to merge the normal image from the good eye with the dark image from the bad eye, which makes the person feel as though both eyes have gone blurry or dizzy. Always cover your left eye completely with the palm of your hand to test your right eye alone, and then cover your right eye to test your left eye alone; this immediately reveals whether the blackout is strictly in one eye or affecting the left or right half of both eyes.

Why is jaw pain when chewing food (jaw claudication) the most important warning sign of Giant Cell Arteritis?¶

Unlike temporomandibular joint (TMJ) arthritis, which hurts the moment you open your mouth or bite down on something hard, jaw claudication in Giant Cell Arteritis is caused by autoimmune inflammation narrowing the arteries that supply blood to your chewing muscles and tongue. Because the muscles cannot get enough oxygen during repetitive exercise, your jaw feels fine on the first bite of food, develops a deep cramping ache or exhaustion after chewing for 60 to 90 seconds, and feels better as soon as you stop chewing; recognizing this symptom and going to the ER for steroids prevents sudden blindness.

If my vision went dark in one eye for 5 minutes and then came back 100 percent normal, why can't I just wait to see my eye doctor next week?¶

A 5-minute painless blackout in one eye (amaurosis fugax) means a blood clot or cholesterol crystal broke off from a narrowed carotid artery in your neck or from your heart, plugged your eye's main artery, and then broke apart. Up to 1 in 4 patients with retinal artery events already have silent new stroke spots on a brain MRI, and the risk of a massive, permanently paralyzing brain stroke is highest during the first 24 to 72 hours after that warning episode, requiring an immediate hospital Stroke Center visit.

Sources checked¶

• American Heart Association (AHA) and American Stroke Association (ASA, United States): Management of Central Retinal Artery Occlusion: A Scientific Statement From the American Heart Association (Mac Grory et al., Stroke 2021; establishing CRAO as a Code Stroke emergency, the \(\le 4.5\text{ hour}\) IV tPA protocol, and discouragement of delays from conservative ocular massage).
• American College of Rheumatology (ACR, United States) and European Alliance of Associations for Rheumatology (EULAR): 2021 ACR/Vasculitis Foundation Guideline and EULAR Recommendations for the Management of Giant Cell Arteritis (immediate IV methylprednisolone \(500\text{ to }1,000\text{ mg/day}\) for visual loss prior to temporal artery biopsy or ultrasound).
• British Society for Rheumatology (BSR, United Kingdom) and National Institute for Health and Care Excellence (NICE, United Kingdom): Guideline on Diagnosis and Treatment of Giant Cell Arteritis and NICE NG128: Stroke and Transient Ischaemic Attack in Over 16s (amaurosis fugax urgent TIA pathway).
• American Academy of Ophthalmology (AAO, United States): Preferred Practice Pattern (PPP): Retinal and Ophthalmic Artery Occlusions.
• Royal College of Ophthalmologists (RCOphth, United Kingdom): Ophthalmic Services Guidance: Management of Acute Retinal Arterial Occlusion and Giant Cell Arteritis.

Related guides¶

• Sudden vision loss, retinal detachment, and acute angle-closure glaucoma
• Stroke recognition (FAST) and emergency response
• Orbital cellulitis, swollen eye infections, and cavernous sinus thrombosis
• Aortic dissection and ruptured abdominal aortic aneurysm
• Heart attack recognition and first aid