Clinical Ophthalmology Interactive Study Guide for PLAB/MRCP/MLA

Ophthalmology Guide

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Acute Red Eye

Acute red eye is one of the most common ophthalmological presentations in primary care and emergency settings. This station covers history-taking, examination techniques, differential diagnosis, and appropriate management of conditions causing red eye – including conjunctivitis, episcleritis, scleritis, acute angle-closure glaucoma, keratitis, and uveitis.

Overview

Acute red eye refers to redness of the eye due to dilation and congestion of conjunctival or deeper blood vessels. It encompasses a spectrum of conditions from benign, self-limiting issues to vision-threatening emergencies. Careful assessment is essential to distinguish between these possibilities and determine appropriate management.

The five major causes of red eye that must be distinguished in clinical practice are conjunctivitis (bacterial, viral, allergic), acute angle-closure glaucoma, acute anterior uveitis, keratitis (including corneal ulcers), and subconjunctival hemorrhage. Each presents with distinct characteristics and requires different management approaches.

💡 PLAB/OSCE Tip

When examining a red eye, always consider the serious “red flags” that require urgent referral: reduced visual acuity, moderate to severe pain, photophobia, corneal involvement, pupillary abnormalities, or systemic symptoms.

🧠 Key Red Eye Mnemonic – “RSVP-C”

Remember these aspects when assessing red eye:

R Redness (distribution and pattern)

S Symptoms (pain, discharge, visual changes)

V Vision check (acuity, affected?)

P Pupils (reactivity, shape, and RAPD)

C Cornea (clarity, fluorescein staining)

Clinical Features & History Taking

A detailed history is crucial in differentiating the causes of red eye:

Onset and duration: Sudden vs. gradual, acute vs. chronic
Pain: Severity, character (gritty, burning, sharp, dull), radiation
Visual changes: Blurring, halos around lights, photophobia
Discharge: Color, consistency, amount (purulent, watery, mucoid)
Associated symptoms: Itching, foreign body sensation, headache
Previous episodes: Recurrent red eye suggests specific conditions
Contact lens wear: Crucial information for risk of infection
Trauma: Recent injury to eye or surrounding structures
Systemic conditions: Autoimmune diseases, diabetes, hypertension

⚠️ Red Flag History Items

Be particularly alert for moderate to severe eye pain, sudden visual loss, photophobia, colored halos around lights, history of trauma, chemical exposure, or recent eye surgery.

Condition	Pattern of Redness	Pain	Discharge	Vision	Pupil
Conjunctivitis	Diffuse, more in fornices	Mild gritty	Variable (depending on type)	Normal	Normal
Acute Angle-Closure Glaucoma	Circumcorneal flush, injected	Severe with headache	None	Reduced, halos	Mid-dilated, fixed
Anterior Uveitis	Circumcorneal (ciliary) flush	Moderate, deep	None or minimal	May be reduced	Miotic, may be irregular
Keratitis/Corneal Ulcer	Circumcorneal	Moderate to severe	Variable	Usually reduced	Normal or miotic
Subconjunctival Hemorrhage	Bright red patch, localized	None	None	Normal	Normal

Examination Technique

A systematic approach to examining red eye ensures complete assessment:

Visual Acuity: Always check and document visual acuity first
External Examination:
- Eyelids: position, closure, entropion/ectropion, lesions
- Conjunctiva: pattern and distribution of injection, follicles, papillae
- Discharge: character, amount
Corneal Assessment:
- Clarity, regularity, fluorescein staining for epithelial defects
- Check for foreign bodies under lids by lid eversion
Anterior Chamber: Depth, presence of cells or flare (in uveitis)
Pupil Examination: Size, shape, reactivity, presence of RAPD
Intraocular Pressure: Using applanation or non-contact tonometry
Fundoscopy: If indicated and possible

💡 Examination Tip

The pattern of redness is diagnostically important. Conjunctival injection is more prominent in the fornices and diminishes toward the limbus, while ciliary injection (seen in more serious conditions) is most pronounced around the corneal limbus.

OSCE Tips for Red Eye Assessment

In an OSCE station involving red eye, follow this structured approach:

Introduction: Introduce yourself, confirm patient identity, explain the examination
History:
- Onset and duration of redness
- Associated symptoms: pain, visual changes, discharge, photophobia
- Contact lens wear and compliance
- Previous episodes or treatment
- Relevant systemic conditions
Examination Sequence:
- Visual acuity (always start with this)
- External eye inspection
- Corneal examination with fluorescein if available
- Pupil assessment
- Mention intraocular pressure (IOP) measurement
Summary and Management:
- Summarize your findings
- State your differential diagnosis
- Outline appropriate management, including red flags for referral

⚠️ Common OSCE Pitfalls

The most common errors in red eye OSCE stations are:

Forgetting to check visual acuity first
Not asking about contact lens wear
Missing assessment of pupils
Failing to mention when urgent referral is needed

Flashcards: Red Eye Assessment

Click on each card to reveal the answer.

What are the key features of acute angle-closure glaucoma?

(Click to flip)

Answer

Severe pain, reduced vision, halos around lights, fixed mid-dilated pupil, elevated IOP, shallow anterior chamber, and circumcorneal redness.

When should a patient with red eye be urgently referred to ophthalmology?

(Click to flip)

Answer

Reduced visual acuity, severe pain, photophobia with ciliary flush, corneal opacity/ulceration, irregular pupil, recent eye surgery/trauma, or suspicion of angle-closure glaucoma.

How can you distinguish bacterial from viral conjunctivitis?

(Click to flip)

Answer

Bacterial: typically unilateral initially, purulent discharge, crusting. Viral: often bilateral, watery discharge, associated with URTI, preauricular lymphadenopathy, follicles on tarsal conjunctiva.

Red Eye Assessment Quiz

Test your knowledge with these PLAB/OSCE-style questions.

1. A 70-year-old woman presents with a painful red right eye, blurred vision with halos around lights, headache, and nausea. On examination, her pupil is mid-dilated and poorly reactive. What is the most likely diagnosis?

A. Acute angle-closure glaucoma

B. Bacterial conjunctivitis

C. Anterior uveitis

D. Episcleritis

Explanation: The constellation of painful red eye, blurred vision, halos around lights, headache, nausea, and mid-dilated poorly reactive pupil is characteristic of acute angle-closure glaucoma. This is an ophthalmic emergency requiring immediate referral.

2. A 25-year-old contact lens wearer presents with a red, painful right eye with mild photophobia. Examination reveals a small central corneal epithelial defect that stains with fluorescein. Vision is slightly reduced. What is the most appropriate management?

A. Topical chloramphenicol and review in 1 week

B. Topical steroid drops

C. Urgent referral to ophthalmology

D. Artificial tears and continued contact lens use

Explanation: A contact lens wearer with a painful red eye, corneal epithelial defect, and reduced vision needs urgent ophthalmological assessment due to the high risk of microbial keratitis (corneal ulcer), which can rapidly progress to sight-threatening complications.

Sudden Visual Loss

Sudden visual loss is a concerning symptom that may indicate serious underlying pathology. This station focuses on the structured approach to evaluating patients presenting with acute or sudden deterioration in vision, from history-taking to examination techniques and urgent management decisions.

Overview

Sudden visual loss is defined as an acute deterioration in vision occurring over seconds, minutes, hours, or days. The speed of onset, persistence, and associated symptoms provide crucial diagnostic clues. This presentation requires careful assessment and may represent true ophthalmic emergencies requiring immediate intervention.

Causes of sudden visual loss can be broadly categorized as:

Vascular: Central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), anterior ischemic optic neuropathy (AION), amaurosis fugax
Inflammatory/Infectious: Optic neuritis, uveitis, endophthalmitis
Mechanical: Retinal detachment, vitreous hemorrhage
Pressure-Related: Acute angle-closure glaucoma
Neurological: Stroke, intracranial hemorrhage, compressive lesions

💡 Clinical Pearl

While assessing sudden visual loss, think about the anatomical location: is it an anterior segment problem, retinal issue, optic nerve pathology, or a neurological cause? The pattern of visual loss and associated findings will help localize the pathology.

🧠 Key Mnemonic for Sudden Visual Loss – “VIPER”

Remember these causes when assessing sudden visual loss:

V Vascular (CRAO, CRVO, AION)

I Inflammatory (optic neuritis, uveitis)

P Pressure (acute glaucoma)

E External/Mechanical (retinal detachment)

R Retina/Neurological (stroke, compressive lesions)

Clinical Features & Key Differentials

A focused history is essential in narrowing the differential diagnosis:

Onset and progression: Seconds, minutes, hours, days
Pattern: Total, partial (visual field defect), central, peripheral
Unilateral vs. bilateral: Helps distinguish certain conditions
Associated symptoms: Pain, photophobia, floaters, flashes, headache
Past ocular history: Previous episodes, known eye disease
Medical history: Vascular risk factors, inflammatory conditions

Condition	Onset	Visual Loss Pattern	Associated Symptoms	Key Examination Findings
Central Retinal Artery Occlusion	Seconds to minutes	Profound, painless	None typically	Pale retina, cherry-red spot, box-car segmentation
Central Retinal Vein Occlusion	Hours to days	Variable severity	Usually painless	“Blood and thunder” fundus, dilated tortuous veins, widespread hemorrhages
Retinal Detachment	Hours (may have preceding flashes/floaters)	Visual field defect corresponding to detachment area	Flashes, floaters, shadow/curtain in vision	Elevated grey retina, possible tear visible
Acute Angle-Closure Glaucoma	Hours	Blurred, halos	Severe pain, headache, nausea	Red eye, mid-dilated pupil, corneal edema, elevated IOP
Optic Neuritis	Days	Central vision affected	Pain on eye movement	RAPD, normal or swollen disc (or normal in retrobulbar neuritis)

⚠️ Urgent Presentations

Central retinal artery occlusion is a true ocular emergency with a narrow treatment window (generally <6 hours). Immediate referral is necessary as interventions like ocular massage, IOP-lowering medications, or hyperbaric oxygen may be attempted to restore retinal circulation.

Examination Technique

A systematic ophthalmological examination is crucial in cases of sudden visual loss:

Visual Acuity: Document vision in both eyes (counting fingers, hand movements, light perception if severely reduced)
Visual Fields: Confrontation testing can detect gross defects
Pupil Assessment: Size, shape, reactivity, presence of RAPD (critical for optic nerve pathology)
External Examination:
- Red flag signs: proptosis, lid retraction, chemosis
- Conjunctival and scleral appearance
Anterior Segment:
- Corneal clarity
- Anterior chamber depth and cells
- Iris and pupil
Intraocular Pressure: Particularly important if acute glaucoma is suspected
Fundoscopy:
- Optic disc appearance (color, margins, cup-to-disc ratio)
- Retinal vessels (arterial narrowing, venous dilation, AV nicking)
- Retinal appearance (hemorrhages, exudates, cherry-red spot, pale retina)
- Macula (edema, holes, degeneration)
- Peripheral retina (evidence of detachment)
Neurological Assessment: Brief cranial nerve examination if neurological cause suspected

💡 Examination Tip

The relative afferent pupillary defect (RAPD) is a critical finding in unilateral or asymmetric optic nerve disease. To test for RAPD, perform the swinging flashlight test, moving the light quickly between both eyes while observing for pupillary constriction.

OSCE Tips for Sudden Visual Loss Assessment

Follow this structured approach to excel in OSCE stations on sudden visual loss:

Introduction: Introduce yourself, establish rapport, explain the purpose of the assessment
History:
- Clear timeline of visual loss (onset, progression)
- Determine pattern (total vs. partial, unilateral vs. bilateral)
- Ask about eye pain, flashes, floaters, headaches
- Vascular risk factors: hypertension, diabetes, smoking, hyperlipidemia
- Past ocular and medical history
- Medications (particularly anticoagulants, vasodilators)
Examination Sequence:
- Visual acuity measurement (both eyes)
- Visual field testing by confrontation
- Pupillary assessment (especially RAPD)
- External eye and anterior segment examination
- Fundoscopy (describe technique)
- Brief neurological examination if relevant
Summarize and Plan:
- Present a concise summary of findings
- Give differential diagnoses in order of likelihood
- Outline immediate management plan (emphasize urgency if appropriate)
- Specify what investigations would be appropriate

⚠️ OSCE Communication Tips

When presenting findings to the examiner, use the structure:

“Based on the history of [key features] and examination findings of [key signs], my differential diagnoses are…”
“This is a [urgent/semi-urgent/routine] case requiring [specific management steps]”
“My immediate management would include [specific actions]”

Always acknowledge the impact of visual loss on the patient and address their concerns with empathy.

Flashcards: Sudden Visual Loss

Click on each card to reveal the answer.

What are the classic fundus findings in CRAO?

(Click to flip)

Answer

Pale retina, cherry-red spot at the fovea, attenuated arterioles, and “box-car” segmentation of blood in retinal vessels.

What are the key symptoms of retinal detachment?

(Click to flip)

Answer

Photopsia (flashes of light), floaters, peripheral visual field defect described as a “curtain” or “shadow” extending from the periphery, and painless vision loss.

In which condition is the swinging flashlight test most useful?

(Click to flip)

Answer

Optic neuritis, where a positive RAPD (relative afferent pupillary defect) is a key diagnostic finding. The affected pupil will dilate instead of constricting when light is swung from the unaffected to the affected eye.

Sudden Visual Loss Quiz

Test your knowledge with these PLAB/OSCE-style questions.

1. A 75-year-old man with hypertension and diabetes presents with sudden, painless loss of vision in his right eye 2 hours ago. Visual acuity is hand movements in the right eye. Fundoscopy reveals a pale retina with a cherry-red spot at the macula. What is the most appropriate immediate management?

A. Oral acetazolamide and review in 24 hours

B. Topical steroids and mydriatics

C. Arrange for a routine ophthalmology referral

D. Immediate ophthalmology referral as an emergency

Explanation: This presentation is consistent with central retinal artery occlusion (CRAO), which is an ophthalmic emergency. Immediate referral is necessary as interventions need to be attempted within hours to potentially salvage vision. Treatment may include ocular massage, IOP-lowering medications, and possibly thrombolysis in select cases.

2. A 32-year-old woman presents with gradually worsening blurred vision in her right eye over 3 days. She reports pain on eye movement. Visual acuity is 6/60 in the right eye, with a right RAPD. Fundoscopy may be normal or show mild disc swelling. Which investigation would be most appropriate?

A. MRI brain and orbits

B. Carotid Doppler ultrasound

C. Temporal artery biopsy

D. Fluorescein angiography

Explanation: This presentation is typical of optic neuritis (inflammation of the optic nerve). MRI brain and orbits is the most appropriate investigation to confirm the diagnosis, assess for demyelinating lesions elsewhere in the CNS, and evaluate for multiple sclerosis, as optic neuritis can be the presenting feature of MS.

Case 1: Acute Angle Closure Glaucoma

A 65-year-old woman presents to the emergency department with severe right eye pain, headache, nausea, and blurred vision with halos around lights for the past 6 hours. This case explores the presentation, assessment, and management of acute angle closure glaucoma, a true ophthalmic emergency.

Case Presentation

Patient: Mrs. Sarah Johnson, 65-year-old female
Presenting Complaint: Severe right eye pain with headache, nausea, and blurred vision for 6 hours
HPC: Patient reports sudden onset of severe right eye pain radiating to the right side of her head. She describes seeing halos around lights and experiencing progressively worsening vision. She has also had three episodes of vomiting. Symptoms started while watching television in a dimly lit room.

Past Medical History: Hypertension, Hyperlipidemia
Medications: Amlodipine 5mg daily, Simvastatin 20mg nocte
Family History: Mother had glaucoma
Social History: Lives alone, independent with ADLs

💡 Key Thought

Acute angle closure glaucoma is an ophthalmic emergency requiring immediate intervention to prevent permanent vision loss. The classic symptom triad includes eye pain, reduced vision, and halos around lights, often with associated headache, nausea, and vomiting due to the extremely high intraocular pressure.

Examination Findings

Visual Acuity:

Right eye: 6/60 (not improving with pinhole)
Left eye: 6/9 (improves to 6/6 with pinhole)

External Examination:

Right eye: Conjunctival injection, particularly circumcorneal (ciliary flush)
Right cornea appears hazy/edematous
Right pupil mid-dilated (5mm) and non-reactive to light
Left eye appears normal

Intraocular Pressure (IOP):

Right eye: 58 mmHg (normal: 10-21 mmHg)
Left eye: 16 mmHg

Gonioscopy: (Would be performed by ophthalmologist)

Right eye: Closed angle in all quadrants
Left eye: Narrow but open angle

Fundoscopy:

Limited view of right fundus due to corneal edema
Left fundus normal with cup-to-disc ratio of 0.3

Pathophysiology

Acute angle closure glaucoma occurs when the drainage angle between the iris and cornea becomes suddenly and completely blocked, preventing aqueous humor from exiting through the trabecular meshwork. This causes a rapid rise in intraocular pressure.

The mechanism typically involves:

Anatomical predisposition: Eyes with shallow anterior chambers and narrow angles are at risk
Precipitating factors: Pupillary dilation (dark environments, emotional stress, certain medications) causes the peripheral iris to bunch up and block the drainage angle
Progressive angle closure: As pressure rises, the iris is pushed further against the trabecular meshwork, worsening the blockage

Risk factors include:

Advanced age (typically over 50)
Female gender
Hyperopia (farsightedness)
Asian or Inuit ethnicity
Family history of angle closure
Certain medications (anticholinergics, sympathomimetics, tricyclic antidepressants)

Immediate Management

Acute angle closure glaucoma requires urgent treatment to reduce intraocular pressure and preserve vision:

Medical Therapy (initiate immediately):
- Topical beta-blockers (e.g., timolol 0.5%): Reduces aqueous production
- Topical alpha-agonists (e.g., apraclonidine 1%): Reduces aqueous production
- Topical prostaglandin analogues (e.g., latanoprost): Increases uveoscleral outflow
- Topical pilocarpine 2-4%: Constricts pupil to pull iris away from angle (after IOP starts to decrease)
- Oral/IV acetazolamide 500mg: Reduces aqueous production
- Oral/IV osmotic agents (e.g., mannitol): Further reduces IOP in severe cases
- Analgesia and antiemetics as needed
Definitive Treatment:
- Laser peripheral iridotomy (LPI): Creates a small hole in the peripheral iris to allow aqueous flow from posterior to anterior chamber, bypassing the pupillary block
- Performed once the acute attack is controlled and cornea clears
- Prophylactic LPI in the fellow eye is also indicated due to high risk (estimated 40-80% risk of attack in untreated fellow eye)
Alternative Surgical Options:
- Surgical peripheral iridectomy: If laser not possible
- Lens extraction: May be considered especially if cataractous

Follow-Up & Prognosis

Follow-up:

Regular IOP monitoring initially (hours to days)
Gonioscopy to reassess angle status
Visual field testing to assess for damage
Optic nerve monitoring
Long-term follow-up for glaucoma monitoring

Prognosis:

Depends on duration and severity of attack
Prompt treatment (within hours) generally leads to good outcomes
Delayed treatment may result in permanent visual field defects, optic nerve damage, or even blindness
Up to one-third may develop chronic glaucoma requiring long-term medication

Patient Education:

Importance of compliance with medications
Need for prophylactic treatment of the fellow eye
Recognition of warning symptoms for recurrence
Avoidance of medications that can trigger angle closure (e.g., certain antihistamines, decongestants)

OSCE Approach to Acute Angle Closure Glaucoma

In an OSCE station involving suspected acute angle closure glaucoma:

1. Initial Assessment:

Introduce yourself, confirm patient identity, and explain examination
Take focused history: onset, severity of pain/vision loss, halos, associated symptoms
Ask specifically about risk factors and precipitating events

2. Examination Sequence:

Visual acuity assessment (affected and unaffected eye)
Inspect for red eye, corneal haziness, and mid-dilated fixed pupil
State that you would check intraocular pressure (describe tonometry)
Mention examining the anterior chamber depth (Van Herick technique)
Carefully assess pupillary responses
Attempt fundoscopy (noting it may be difficult due to corneal edema)

3. Communication of Findings and Plan:

Clearly state your diagnosis: “Based on the acute onset of severe eye pain, reduced vision, halos around lights, corneal edema, fixed mid-dilated pupil, and elevated IOP, this is acute angle closure glaucoma.”
Emphasize urgency: “This is an ophthalmic emergency requiring immediate treatment to preserve vision.”
Outline immediate management plan with medication doses
Explain need for definitive treatment with peripheral iridotomy
Mention prophylactic treatment for the fellow eye

4. Patient Communication:

Use clear, non-technical language to explain the condition
Emphasize the seriousness but reassure that prompt treatment improves outcomes
Explain that both eyes will need treatment to prevent future attacks

⚠️ Common OSCE Pitfalls

Avoid these common mistakes in AACG OSCE stations:

Failing to recognize the urgency of the condition
Not checking visual acuity in both eyes
Forgetting to mention prophylactic treatment of the fellow eye
Using pilocarpine before IOP is reduced (can worsen block initially)
Not identifying precipitating factors in history
Failing to explain the long-term follow-up needed

Flashcards: Acute Angle Closure Glaucoma

Tap each card to reveal the answer.

What is the classic clinical triad in AACG?

(flip for answer)

Answer

Eye pain, reduced vision, and halos around lights.

Why should pilocarpine be delayed in initial AACG treatment?

(flip for answer)

Answer

When IOP is very high, pilocarpine may worsen pupillary block by increasing iris-lens contact. It should be used after initial pressure reduction.

Why is prophylactic treatment of the fellow eye necessary?

(flip for answer)

Answer

There is a 40-80% risk of the fellow eye developing an acute attack if left untreated due to similar anatomical predisposition.

Acute Angle Closure Glaucoma Quiz

Test your understanding:

1. Which of the following is NOT typically seen in acute angle closure glaucoma?

A. Mid-dilated, fixed pupil

B. Corneal edema

C. Hypotony (low intraocular pressure)

D. Ciliary flush (circumcorneal injection)

Explanation: AACG is characterized by markedly elevated IOP, not hypotony. Typical IOP is often >40-50 mmHg. The other findings (fixed pupil, corneal edema, and ciliary flush) are classic features of AACG.

2. Which medication should be administered first in acute angle closure glaucoma?

A. Pilocarpine 4% eye drops

B. Acetazolamide 500mg IV/oral and beta-blocker eye drops

C. Atropine 1% eye drops

D. Steroid eye drops

Explanation: Initial management focuses on rapidly lowering IOP with acetazolamide and beta-blockers. Pilocarpine is useful but should be delayed until some pressure reduction has occurred. Atropine would worsen the condition by dilating the pupil further. Steroids are not indicated in the initial management.

Case 2: Central Retinal Artery Occlusion

A 72-year-old man with hypertension and atrial fibrillation presents with sudden, painless, complete vision loss in his right eye that occurred 2 hours ago. This case explores the presentation, assessment, and management of central retinal artery occlusion (CRAO), an ophthalmic emergency with a narrow therapeutic window.

Case Presentation

Patient: Mr. Robert Thompson, 72-year-old male
Presenting Complaint: Sudden, painless, complete vision loss in the right eye for 2 hours
HPC: Patient was watching television when he experienced sudden, complete loss of vision in his right eye. He describes it as “like a curtain coming down.” There was no pain, flashes, or floaters. He has had no headache, jaw claudication, or other systemic symptoms.

Past Medical History: Hypertension, Atrial fibrillation, Hypercholesterolemia, Previous TIA 2 years ago
Medications: Apixaban 5mg BD, Bisoprolol 5mg daily, Atorvastatin 40mg daily, Lisinopril 10mg daily
Family History: Father had stroke at age 70
Social History: Ex-smoker (quit 10 years ago), consumes alcohol socially

💡 Key Point

Central retinal artery occlusion (CRAO) is an ophthalmic emergency characterized by sudden, painless, severe vision loss typically in one eye. It represents the ocular equivalent of a stroke and has a very narrow therapeutic window (generally under 6 hours). This patient’s vascular risk factors (hypertension, AF, previous TIA) make him a classic candidate for this condition.

Examination Findings

Visual Acuity:

Right eye: Hand movements only
Left eye: 6/9 (improves to 6/6 with pinhole)

External Examination:

No conjunctival injection
Normal corneal appearance bilaterally
Pupils: Right RAPD present

Intraocular Pressure:

Right eye: 14 mmHg
Left eye: 16 mmHg

Fundoscopy:

Right eye: Diffuse retinal whitening/pallor, cherry-red spot at the fovea, attenuated arterioles, segmentation of blood column in arterioles (“box-car” or “cattle-truck” appearance)
Left eye: Normal fundus with cup-to-disc ratio of 0.3, normal vessels, and healthy macula

Blood Pressure: 168/92 mmHg Heart Rate: Irregular, 84 bpm

Pathophysiology

Central retinal artery occlusion occurs when blood flow through the central retinal artery is suddenly blocked, resulting in ischemia and infarction of the retina. The retina has a dual blood supply – the choroidal circulation supplies the outer retina (including photoreceptors), while the retinal circulation via the central retinal artery supplies the inner retina.

The mechanism typically involves:

Embolic occlusion: Most common cause (often from carotid artery, heart valves, or cardiac chambers)
Thrombotic occlusion: Related to underlying atherosclerotic disease
Inflammatory/vasculitic causes: Less common (e.g., giant cell arteritis)

The classic fundoscopic finding of a “cherry-red spot” occurs because:

The inner retina becomes opaque/whitened due to ischemia
The fovea lacks inner retinal layers and appears red against the pale retina (due to visible choroidal circulation)
Retinal arteries appear narrowed with segmented blood flow (“box-car” appearance)

Risk factors include:

Cardiovascular disease: Hypertension, diabetes, hyperlipidemia
Cardiac sources of emboli: Atrial fibrillation, valvular disease, endocarditis
Carotid artery disease
Hypercoagulable states
Giant cell arteritis (more common in patients >50)
Smoking

Immediate Management

Management of CRAO focuses on emergency interventions to restore retinal circulation and comprehensive vascular risk assessment:

Immediate Ocular Therapy (attempts to dislodge the embolus/improve perfusion):
- Ocular massage: Applying pressure to the eye for 5-15 seconds and then releasing repeatedly to create pressure fluctuations that may dislodge emboli
- IOP lowering: Topical beta-blockers, alpha-agonists, and/or oral/IV acetazolamide to reduce IOP and improve perfusion gradient
- Anterior chamber paracentesis: Rapidly reduces IOP (specialist procedure)
- Breathing 95% oxygen and 5% CO₂ (carbogen): Induces vasodilation and increases oxygen delivery to the retina
- Sublingual glyceryl trinitrate: For vasodilation
Specialist Interventions (if within therapeutic window):
- Intra-arterial thrombolysis: Within 4-6 hours of onset (varies by protocol)
- Hyperbaric oxygen therapy: May be considered in select cases
Vascular Risk Assessment:
- Blood tests: FBC, ESR, CRP (to rule out giant cell arteritis), lipid profile, HbA1c, clotting screen
- ECG and echocardiogram: To identify cardiac sources of emboli
- Carotid Doppler ultrasound: To assess for carotid stenosis
- Consider temporal artery biopsy if suspicion of giant cell arteritis

Follow-Up & Prognosis

Follow-up:

Regular ophthalmological review to monitor for complications:

Neovascularization of iris or retina
Neovascular glaucoma

Ongoing management of vascular risk factors
Multidisciplinary management with stroke physician/cardiologist

Prognosis:

Visual prognosis is generally poor, even with treatment
Most patients are left with counting fingers vision or worse
Better outcomes may be seen if treatment is initiated within 90-120 minutes
Transient CRAO or presence of cilioretinal artery sparing the macula improves prognosis

Secondary Prevention:

Antiplatelet or anticoagulation therapy as appropriate
Optimal control of hypertension, diabetes, and hyperlipidemia
Carotid endarterectomy if significant stenosis present
Smoking cessation
Regular monitoring of the fellow eye

OSCE Approach to Central Retinal Artery Occlusion

In an OSCE station involving suspected CRAO:

1. Initial Assessment:

Introduce yourself, confirm patient identity, and explain examination
Take focused history: exact time of onset, complete vs. partial vision loss, painless nature
Ask about vascular risk factors: hypertension, diabetes, smoking, previous TIA/stroke
Medication history: focus on anticoagulants/antiplatelets, vasodilators
Age >50: ask about GCA symptoms (headache, jaw claudication, scalp tenderness)

2. Examination Sequence:

Visual acuity assessment
Pupillary responses: check for RAPD
Intraocular pressure measurement
Dilated fundoscopy (describe technique)
Describe key findings: retinal pallor, cherry-red spot, attenuated arterioles, box-car segmentation
Check vital signs: BP, heart rate, rhythm
Mention examination of carotid arteries for bruits

3. Communication of Findings and Plan:

Clearly state your diagnosis: “Based on the sudden onset painless vision loss and characteristic fundus findings of retinal pallor, cherry-red spot, and box-car segmentation, this is a central retinal artery occlusion.”
Emphasize urgency: “This is an ophthalmic emergency with a narrow therapeutic window of approximately 4-6 hours.”
Outline immediate management plan:
- Ocular massage
- IOP-lowering medications
- Consider anterior chamber paracentesis
- Supplemental oxygen/carbogen
Discuss urgent investigations:
- FBC, ESR, CRP (particularly if >50 years)
- ECG, echocardiogram
- Carotid Doppler
Mention referral to stroke services: “CRAO is an ocular stroke and requires same-day stroke workup”

4. Patient Communication:

Explain the condition as an “eye stroke” for patient understanding
Discuss visual prognosis honestly but sympathetically
Emphasize the importance of identifying and managing the underlying cause to prevent further vascular events

⚠️ Common OSCE Pitfalls

Avoid these common mistakes in CRAO OSCE stations:

Not documenting precise time of symptom onset (crucial for management decisions)
Forgetting to check and document RAPD
Missing the assessment for giant cell arteritis in older patients
Failing to mention the need for urgent stroke workup
Not recognizing the systemic implications beyond the eye
Providing unrealistic expectations regarding visual recovery

Flashcards: Central Retinal Artery Occlusion

Tap each card to reveal the answer.

What causes the cherry-red spot in CRAO?

(flip for answer)

Answer

The fovea lacks inner retinal layers, allowing the choroidal circulation to show through as a red spot against the surrounding pale, ischemic retina.

What is “box-car” or “cattle-truck” segmentation?

(flip for answer)

Answer

The fragmentation of the blood column in retinal arterioles seen in CRAO, appearing as alternating dark (blood) and light (plasma) segments.

What is the approximate therapeutic window for CRAO?

(flip for answer)

Answer

Approximately 4-6 hours from symptom onset, with better outcomes if treatment is initiated within 90-120 minutes.

Central Retinal Artery Occlusion Quiz

Test your understanding:

1. Which of the following is NOT a typical finding in acute central retinal artery occlusion?

A. Cherry-red spot at the macula

B. Relative afferent pupillary defect

C. Tortuous, dilated retinal veins

D. Box-car segmentation of blood in retinal arteries

Explanation: Tortuous, dilated retinal veins are a characteristic finding in central retinal VEIN occlusion (CRVO), not CRAO. In CRAO, the retinal arteries are typically attenuated (narrowed), while the veins appear normal or slightly narrowed.

2. A 75-year-old patient presents with sudden vision loss in one eye. On examination, there is a cherry-red spot at the macula. Which of the following would be most appropriate as first-line management?

A. Arrange routine ophthalmology appointment within 2 weeks

B. Start topical steroid drops

C. Immediate ocular massage and IOP-lowering treatments

D. Arrange for outpatient carotid Doppler next day

Explanation: CRAO is an ophthalmic emergency. First-line management involves attempts to dislodge the embolus and improve retinal perfusion through ocular massage and IOP-lowering treatments. These should be initiated immediately, as there is a narrow therapeutic window (generally 4-6 hours).