Case 1: Central Retinal Artery Occlusion (CRAO) – its a stroke!

A 67-year-old male with a history of hypertension, type II diabetes, and hyperlipidemia presents to the ED with sudden vision loss. He reports waking up 6 hours ago with abrupt, complete vision loss in his right eye. He denies pain, flashes, or previous similar episodes. Vitals are stable. The right eye has no light perception, with a relative afferent pupillary defect (RAPD). Fundoscopy reveals a cherry-red spot at the macula with a pale retina. The left eye appears normal. A CTA of the head and neck identifies 70% stenosis of the right carotid artery. You suspect central retinal artery occlusion (CRAO).

What is CRAO?

It is an acute ischemic event caused by a sudden occlusion of the central retinal artery or one of its branches. This condition shares a common pathophysiology with that of cerebral ischemic strokes; however, it has unique diagnostic and management challenges, unlike cerebral stroke, where we have evidence-based guidelines. The main causes of these occlusions include embolism, thrombosis, vasculitis, and vasospastic events. It is most common in patients 50 to 70 years old with vascular risk factors, and in patients with collagen vascular disease, vasculitis, cardiac valvular abnormality, or sickle cell disease.

Types of CRAO:

1. Non-arteritic and permanent: accounts for over two-thirds of all CRAO cases.

2. Non-arteritic and transient: this is simply a transient ischemic attack, or TIA.

3. Arteritic: due to a systemic inflammatory condition like giant cell arteritis (aka temporal arteritis).

Prevalence of CRAO:

Smith et al. estimated the incidence of CRAO to range from 1 to 10 cases per 100,000 individuals per year, with incidence increasing with age and peaking around 80 years. The review also demonstrated that among patients with the non-arteritic subtype, embolic sources—most commonly from ipsilateral carotid artery stenosis, cardiac valvular disease, or arrhythmias—remain the predominant etiologies of CRAO.

Signs and Symptoms:

Patients with central retinal artery occlusion typically present with sudden, painless vision loss, which usually develops over a matter of seconds. This vision loss may manifest in one of two ways:

• Complete vision loss with only light–dark perception across the entire visual field, or
• Preserved central vision due to the unique vascular supply of the fovea.

On examination, patients often demonstrate a marked reduction in visual acuity and a positive relative afferent pupillary defect (RAPD).

Importantly, in any patient over the age of 50 presenting with sudden vision loss, giant cell arteritis must be considered. While managing CRAO, it is critical to screen for GCA, as it may necessitate urgent initiation of systemic corticosteroids—both to preserve vision in the affected eye and to prevent involvement of the contralateral eye.

Diagnosis:

Although CRAO can have various etiologies, carotid artery stenosis remains the most common, being present in up to 70% of cases. Given this high association, the evidence strongly supports that all patients presenting with acute CRAO should undergo urgent carotid artery imaging.

There are several modalities available to screen for carotid stenosis, including carotid duplex ultrasound, CT/CTA, or cervical MRI. The choice between these often depends on institutional protocols and available resources.

My recommendation is that for any patient presenting with sudden, profound, and painless vision loss, you should strongly consider obtaining a CT/CTA of the head and neck. This helps not only in evaluating for concurrent stroke but also in assessing for underlying carotid stenosis, which may require urgent intervention.

Cardioembolic disease is another common etiology of CRAO, particularly in patients under the age of 40 and those with atrial fibrillation or valvular heart disease. If carotid artery stenosis has been ruled out, the evidence supports pursuing a cardiac workup—specifically a transthoracic echocardiogram and Holter monitoring—to identify a potential embolic source. However, these investigations typically fall outside the scope of emergency department management and are usually arranged by outpatient services or during inpatient follow-up.

Expert Opinion re: Diagnosis:

“As soon as there is suspicion of CRAO, I would recommend ordering CT/CTA head and neck for every patient who comes in with CRAO, mainly to make sure there is no brain involvement (stroke) and to locate the source of the emboli (carotid), and eventually, they will get ECHO to rule out a source from the heart.” –  Dr. Adnan Alawami, Retina Fellow, University of Ottawa

Management:

The management of CRAO is highly time-sensitive, with the primary goal being to restore retinal blood flow and dislodge the obstruction as early as possible. These patients require an urgent ophthalmology consult in the ED, so be sure to involve them early. Additionally, if the patient presents within the first few hours of symptom onset, it’s also reasonable to consult neurology, particularly if you’re considering thrombolytics or stroke team involvement.

While awaiting ophthalmology, there are several interventions that have been proposed in the ED setting. It’s important to note, however, that none of these have been definitively shown to improve visual outcomes—but I’ll walk you through them regardless.

1. Ocular massage:

• Aims to mechanically dislodge the embolus.
  • How do you perform it? Apply firm digital pressure using your index finger over the closed eyelid for about 10 to 15 seconds, then release. This is repeated in cycles. The theoretical benefit is that the transient rise and fall in intraocular pressure may help move the embolus distally into a smaller retinal branch, potentially limiting the extent of ischemia.

2. Anterior chamber paracentesis:

• Works by lowering intraocular pressure (IOP), thereby increasing the perfusion gradient to the retina.
• However, this procedure is performed exclusively by ophthalmology.

3. Inhalation of 95% O₂ and 5% CO₂:

• This technique aims to increase intra-arterial CO₂ levels, which in turn can cause vasodilation of the retinal arteries and potentially enhance blood flow to the retina.
• If you’re practicing in a community setting and advanced therapies aren’t readily available, you can ask the patient to breathe into a paper bag for about 10 minutes. This can help elevate CO₂ levels and induce arterial vasodilation as a temporary measure.

How about IV thrombolysis?

Although CRAO may theoretically respond to thrombolytic therapy, particularly if administered within the first 4.5 hours of symptom onset, current evidence has not demonstrated any meaningful improvement in outcomes. Schumacher et al. conducted an RCT comparing intra-arterial tPA to conservative treatment in 84 CRAO patients presenting within 20 hours. At one month, both groups showed improved visual acuity, but no significant difference was found (p = 0.69). Due to a high risk of symptomatic intracranial hemorrhage and no visual benefit, the trial was terminated early after the first interim analysis. The study did not support the use of intra-arterial tPA for acute CRAO.

Another meta-analysis of observational studies evaluating IV thrombolysis for CRAO suggested a modest benefit when IV tPA is administered within 4.5 hours, showing an absolute risk reduction of 32.3% and a number needed to treat (NNT) of 4. However, it’s important to note that none of the included studies evaluated TNK, which is now the standard thrombolytic agent for cerebral strokes at most centers across Canada.

Since thrombolysis hasn’t shown consistent benefit, what about hyperbaric oxygen therapy?

Hyperbaric oxygen (HBO) has been proposed as a potential therapy for CRAO, based on its theoretical ability to directly oxygenate the retina and mitigate ischemia. However, the evidence remains limited, relying mostly on retrospective studies, with no robust prospective trials or randomized controlled studies to support its efficacy as a standard treatment.

The proposed therapeutic effects of hyperbaric oxygen therapy (HBO) in CRAO are based on two main mechanisms:

1. Enhanced oxygen delivery to ischemic retinal tissue through the choroidal collateral circulation, which remains patent even when the central retinal artery is occluded. Animal studies have shown that under hyperbaric conditions, this collateral flow can meet 100% of the retina’s metabolic oxygen requirements.

2. HBO may also contribute to reducing retinal edema and limiting ischemia-reperfusion injury once recanalization occurs, thereby preserving retinal function.

Masters et al. conducted a retrospective review of 39 CRAO patients treated with HBO twice daily for five days. They found that 72% showed visual improvement, with a mean gain of 5 Snellen lines. Patients treated within 12 hours had the greatest benefit, averaging 6 lines of improvement. Though small and single-center, the study’s findings are promising and support further research into early HBO therapy for CRAO.

Expert Opinion re: Management:

“Unfortunately, no strong evidence of any treatment. We usually start them on ASA loading dose and then refer them to the Stroke Prevention Clinic. If within <12 hours, I would personally send them to ED for urgent CT/CTA. And of course, if there is any suspicion of GCA, I would order ESR/CRP/CBC and treat with 1g Solumedrol (methylpred).” — Dr. Adnan Alawami, Retina Fellow, University of Ottawa

 

“In all patients with CRAO, a CT/CTA and stroke workup should be completed because you need to identify if there is a critical carotid stenosis on the ipsilateral side of the CRAO, as that would need DAPT load and admission for consideration of stenting or carotid endarterectomy. Those could go either to vascular surgery or to neurology. As endarterectomy is still first-line treatment, it would be a first call to vascular surgery, then neurology if they feel that the anatomy isn’t favorable or there are patient concerns that they wouldn’t tolerate the procedure (anesthetic considerations, stroke on imaging, bilateral stenosis, stenosis too high, etc). “Essentially, most stroke physicians would consider TNK but only hyper-early. It’s not really studied in the thrombolytic trials, but most people would only consider it in the first couple hours of symptoms.”  Dr. Emma Ferguson, EM and Stroke Staff, The Ottawa Hospital” — Dr. Emma Ferguson, EM and Stroke Staff, The Ottawa Hospital

Case 2: Central Retinal Vein Occlusion (a DVT!)

A 65-year-old male with a history of hypertension, type II diabetes, and hyperlipidemia presents to the ED with sudden vision changes. He reports noticing blurred vision and a dark haze in his left eye over the past 24 hours, which has progressively worsened. He denies pain, flashes, or prior similar episodes. Vitals are stable. Visual acuity in the left eye is 20/200, with no relative afferent pupillary defect (RAPD). Fundoscopy of the left eye reveals extensive retinal hemorrhages in all quadrants, dilated and tortuous veins, and macular edema. The right eye is normal. A CTA of the head and neck shows no significant stenosis or embolic source.

The pathogenesis of CRVO is thought to follow Virchow’s triad—vessel wall damage, venous stasis, and hypercoagulability. It typically results from one of three mechanisms: thrombus formation within the retinal vein, compression of the retinal vein by an atherosclerotic central retinal artery, or inflammation leading to secondary venous occlusion.

Types:

• Perfused (non-ischemic): characterized by retinal vessel dilation and edema.
• Non-perfused (ischemic): presents with sudden, painless vision loss in one eye. 

Risk Factors:

•  Age is the most significant risk factor, with over 90% of CRVO cases occurring in patients older than 55.
• Hypertension is present in up to 73% of CRVO patients over 50 and in about 25% of younger patients. Poor blood pressure control may increase the risk of CRVO recurrence in the same or contralateral eye.
• Elevated cholesterol is also associated with CRVO, with total cholesterol levels >6.5 mmol/L found in up to 35% of cases.
• Diabetes is present in approximately 10% of CRVO cases in individuals over 50 years old.
• Oral contraceptive use is the most common associated risk factor in younger female patients.
• Vasculitis
• Hyperviscosity
• Smoking 

Signs and Symptoms:

• Non-ischemic CRVO typically presents with sudden, unilateral blurred vision that is often mild. Symptoms may be worse upon waking and tend to improve throughout the day.
• Ischemic CRVO presents with sudden, painless, and severe visual impairment.
• Approximately 7% of patients with unilateral CRVO will develop the condition in the opposite eye within five years.
• Visual acuity in the affected eye is often significantly reduced (worse than 20/200).
• Ipsilateral afferent pupillary defect.

On fundoscopic examination, the eye often appears strikingly congested, with a classic “blood and thunder” appearance—characterized by widespread retinal hemorrhages in all quadrants.

As an emergency physician, how should you manage this condition, and what should be your next step?

Expert Opinion: “Once suspected, you can send the patient to ophthalmology clinic. These cases can be seen non-urgently within 1 week.” — Dr. Adnan Alawami, Retina Fellow, University of Ottawa

Should anticoagulation or antiplatelets be initiated in the ED?

The evidence for their use in CRVO is mixed and limited. Most studies have shown no significant difference in visual acuity between patients who received these agents and those who did not.

Expert Opinion: “I wouldn’t recommend starting LMWH. No evidence suggests that LMWH would work unless there is an underlying thrombophilia.” — Dr. Adnan Alawami, Retina Fellow, University of Ottawa

Case 3: Ischemic Optic Neuritis (ION)

A 72-year-old female with a history of hypertension and hyperlipidemia presents to the ED with sudden vision loss in her right eye. She reports waking up this morning with severe vision impairment that has progressively worsened over several hours. She also complains of a two-week history of scalp tenderness, fatigue, and a dull, constant headache over her right temple. Additionally, she notes jaw pain while chewing and general malaise. Vitals are stable, but she appears fatigued. Visual acuity in the right eye is reduced to hand motion only, with a relative afferent pupillary defect (RAPD). Fundoscopy of the right eye reveals a pale, swollen optic disc. The left eye is normal. Palpation of the right temporal artery reveals tenderness and decreased pulsation. Blood tests show an elevated ESR (105 mm/hr) and CRP (30 mg/L).

What is ischemic optic neuritis?

The optic nerve carries signals from the eyes to the brain, which then translates them into the images we see. When blood flow is decreased or blocked, the nerve is deprived of oxygen and nutrients, eventually causing it to malfunction and die. Simply put, ION results from reduced blood flow to the optic nerve, leading to nerve damage.

Types:

Ischemic optic neuropathy is typically classified as either anterior or posterior, depending on the part of the optic nerve affected. The anterior type is further divided into two subtypes: arteritic and non-arteritic. For the purpose of this case, I will focus on arteritic anterior ischemic optic neuropathy.

Arteritic AION:

Essentially, this is a vasculitis of autoimmune etiology affecting branches of the internal carotid artery, particularly the ophthalmic and temporal arteries. It typically occurs in patients over 50 years of age and may present with concurrent symptoms of giant cell arteritis, such as weight loss, malaise, jaw pain, headache, and scalp tenderness.

I chose to focus on this condition because, if left untreated, vision loss may progress to involve both eyes within days to weeks in at least 50% of cases. This underscores the importance of prompt diagnosis and urgent, aggressive treatment.

Diagnosis of Arteritic AION:

The American College of Rheumatology recommends that the presence of at least 3 out of the following 5 diagnostic criteria is sufficient to support the diagnosis. Having 3 positive criteria yields a sensitivity of 93.5% and a specificity of 91.2%:

1. Age > 50
2. New headache
3. Abnormality of the temporal artery (tenderness or pulselessness)
4. ESR > 50 mm/hr
5. Positive temporal artery biopsy

Pearls:

An ESR >50 mm/hr has a sensitivity of up to 90% for diagnosing giant cell arteritis (GCA), but a normal ESR does not rule it out. GCA can still occur in patients with ESR <50 mm/hr, particularly in those with a high pretest probability. In such cases, referral for temporal artery biopsy should still be strongly considered.

Normally, ESR tends to rise with age, and its diagnostic utility improves when interpreted alongside CRP. So, never rely on a normal ESR alone to rule out temporal arteritis, as this may lead to missed diagnoses. Parikh et al. concluded that using both ESR and CRP together offers greater sensitivity for diagnosing GCA than using either test alone, with a combined sensitivity of 99%.

That said, while the combination of ESR and CRP offers excellent sensitivity, any patient with a strong clinical suspicion for GCA should still undergo temporal artery biopsy and may require empirical treatment, regardless of test results. If vision is affected, ophthalmology consultation is warranted; otherwise, rheumatology should be involved for further management.

Physical Examination:

• Large afferent pupillary defect
• Visual loss
• Visual field defect
• Fundoscopy reveals a pale, swollen optic disc

Management:

• If visual involvement: high-dose intravenous methylprednisolone up to 1 gram daily for 3 days, before transitioning to oral steroids.
• Studies have shown that patients treated with high-dose IV methylprednisolone have a greater likelihood of visual improvement, with rates reaching up to 34%.
• In contrast, patients with uncomplicated GCA without visual involvement can be started on oral prednisone at a dose of 60 mg daily, and rheumatology should be consulted for further management.

Expert Opinion re: Management:

“If vision is affected, give IV methylprednisolone 1 g daily for 3–5 days, then transition to oral prednisone 1 mg/kg. Consult ophthalmology in the ED.” — Dr. Adnan Alawami, Retina Fellow, University of Ottawa

Case 4: Acute Angle-Closure Glaucoma

A 58-year-old female with no significant medical history presents to the ED with sudden, severe pain in her right eye, accompanied by blurred vision, nausea, and vomiting that began six hours ago. She reports seeing halos around lights and denies any trauma or similar episodes in the past. Vitals are stable. The right eye is red, with a fixed mid-dilated pupil and corneal haziness. Intraocular pressure (IOP) in the right eye is 52 mmHg (normal: 10–21 mmHg), while the left eye is 14 mmHg. Fundoscopy is difficult due to corneal edema, but the left eye appears normal.

What is AACG?

In simple terms, the eye constantly produces aqueous humor, which flows through a series of pathways. This fluid provides structural support to the eye and delivers oxygen and nutrients to the avascular lens and cornea. Ideally, whatever flows into the eye should also be drained out. The fluid is drained through the trabecular meshwork, which acts as a one-way valve—also known as the drainage angle. This system keeps intraocular pressure at normal levels. If this process is disrupted, fluid accumulates, pressure rises, and the optic nerve may become damaged, eventually leading to blindness.

• IOP is normally between 10 and 20 mmHg.
• IOP is determined by the rate of aqueous humor production relative to its outflow and removal. 

Risk Factors:

• Shallow anterior chamber (which narrows further with aging as the lens enlarges—the most common etiology)
• Tumors
• Neovascular processes 

Signs and Symptoms:

• Acute symptoms are often triggered by pupillary dilation, which can occur in low-light environments or after taking certain medications such as anticholinergics or sympathomimetics.
• Patients typically present with at least two of the following symptoms:
• Acute onset of ocular pain
• Nausea or vomiting
• Intermittent blurring of vision with halos around lights (due to corneal edema)
• Photophobia
• Visual loss
• And with at least three of the following signs:
• IOP > 21 mmHg (often > 40 mmHg)
• Conjunctival injection
• Haziness with fixed mid-dilated pupil
• Shallow anterior chamber

Management:

From an emergency medicine perspective, the primary goal is to lower intraocular pressure (IOP) using two classes of medications:

1. Medications that decrease the production of aqueous humor (“reducers”):
   • a. Prostaglandins (latanoprost 0.005%, 1 drop)
   • b. Topical beta-blocker (timolol 0.5%, 1–2 drops)
   • c. Carbonic anhydrase inhibitor (acetazolamide 500 mg IV or PO)
   • d. Systemic osmotic agent (mannitol 1–2 g/kg IV over 45 minutes, typically reserved if topical medications and acetazolamide are ineffective within 1 hour)
2. Medications that enhance the outflow of aqueous humor (“outflowers”):
   • a. Topical selective alpha-agonists (e.g., brimonidine—alpha-2 specific, 1 drop)
   • b. Miotics (pilocarpine 1–2%)
   • c. Topical steroids (prednisolone acetate 1%, 1 drop every 15 to 30 minutes, four times, then every hour) 

Expert Opinion re: Management:

“Start topical antihypertensive drops (latanoprost, timolol, brimonidine, and dorzolamide—one drop each every 15–20 minutes). Also, give Diamox 250–500 mg PO. This will help to reduce the pressure in the eye and assist with assessment, comfort, and laser management.” — Dr. Adnan Alawami, Retina Fellow, University of Ottawa

hypopion

Repeat every 15-20 minutes

Laser peripheral iridotomy is the definitive treatment for the anatomical abnormalities that lead to elevated IOP. It should ideally be performed by ophthalmology within 24–48 hours, so an ophthalmology consult should be arranged in the ED.

Case 5: Uveitis

A 35-year-old male with a history of ankylosing spondylitis presents to the ED with a three-day history of left eye pain, redness, and photophobia. He denies trauma or vision changes. Vitals are stable. The left eye is red with perilimbal injection, and there is no discharge. Slit-lamp exam reveals anterior chamber cells and flare. Intraocular pressure is normal in both eyes.

What is uveitis?

Uveitis is essentially an autoimmune inflammation of the uvea—the middle layer of the eye that includes the iris, ciliary body, and choroid. The most commonly affected areas are the iris and ciliary body, a condition referred to as anterior uveitis. Recognizing and diagnosing uveitis is crucial to prevent long-term vision loss due to complications such as scarring, iris deformities, and an increased risk of retinal detachment.

The underlying cause of acute anterior uveitis remains unknown in 60–80% of cases. However, uveitis is one of the most common extra-articular manifestations of seronegative arthritis, including ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease–associated arthritis, and reactive arthritis.

Symptoms:

• Patients with anterior uveitis typically present with:
  • A painful red eye, usually worse with eye movements and accommodation
  • Photophobia
  • Occasionally, decreased visual acuity
• These symptoms typically evolve rapidly over a few days.
• On eye examination, conjunctival injection is typically more pronounced around the limbus—the area of the conjunctiva adjacent to the iris. This pattern is known as perilimbal injection or ciliary flush. In contrast, conjunctivitis usually presents with erythema that is more prominent toward the periphery of the conjunctiva.
• On slit-lamp examination, you will observe cells (leukocytes that appear as tiny sparkles) and flare (proteins that create a hazy, smoky appearance) in the anterior chamber.
• In severe uveitis, a layer of pus may form in the anterior chamber—this is called a hypopyon.

Management:

These patients require referral to ophthalmology, typically within 24–48 hours.

You can consider administering a drop of a topical cycloplegic (such as Homatropine, 1 drop TID of a 2–5% solution), which also serves as pain control. Their pain is relieved with cycloplegics but not with topical anesthetics. The idea behind using a cycloplegic is to prevent miosis, thereby reducing the pain associated with ciliary muscle spasm.

How about topical steroids?

Steroids are off-limits and should only be used in consultation with ophthalmology. This is due to the risk of worsening an undiagnosed infection or causing a corneal ulcer—either of which could lead to vision loss.

Expert Opinion re: Management:

“I wouldn’t recommend starting any steroid drops, as there could be other underlying pathologies like corneal abrasion, ulcer, HSV, or VZV—conditions that steroids could significantly worsen. Do not give these patients cycloplegics in the ED unless they are known to have recurrent uveitis and their symptoms are consistent with previous episodes. Typically, we can see them on the same day if we are contacted during working hours; otherwise, they can be seen in clinic the following day.” — Dr. Adnan Alawami, Retina Fellow, University of Ottawa.

Case 6: Endophthalmitis

A 62-year-old male with a history of cataract surgery three days ago presents to the ED with sudden onset of worsening vision, eye pain, and redness in his right eye. He also reports mild swelling of the eyelids and sensitivity to light. Vitals are stable. The right eye shows significant conjunctival injection, corneal edema, and a hypopyon visible on slit-lamp exam. Visual acuity in the right eye is limited to hand motion only, while the left eye is normal.

Endophthalmitis is an infection of the globe—and it is a medical emergency!

Risk Factors:

• • Recent intraocular surgery
• • Previous perforated globe
• • Endogenous infection
• Here is a table outlining the types of organisms commonly associated with different eye procedures and those associated with endogenous endophthalmitis:

Signs and Symptoms:

• Ocular pain
• Decreased vision
• Decreased visual acuity
• Chemosis
• Hyperemia of the conjunctiva
• Hypopyon (evidence of intraocular inflammation) 

Does PoCUS have a role in diagnosing endophthalmitis?

PoCUS can be used as a rule-in test to help diagnose endophthalmitis. Shinde et al. presented a case report of a 72-year-old male who presented with eye pain and swelling, initially suspected to have orbital cellulitis. Due to the significant swelling, a proper eye exam was not possible. A clinician used a linear ultrasound probe and identified hyperechoic debris within the eye—findings consistent with an intraocular infection, specifically endophthalmitis. This case highlights how PoCUS can play a critical role in clinical decision-making by identifying pathology that might otherwise be missed, ultimately altering the management plan and improving patient outcomes.

Expert Opinion re: PoCUS and Posterior Chamber Pathologies:

“We’re bad at fundoscopy and eye exams in general, and it’s a much better way to assess posterior chamber pathology. I would be hesitant to use it as a ‘rule-out test’ for endophthalmitis, but it may be useful as a rule-in.” — Dr. Rajiv Thavanathan, EM Staff, The Ottawa Hospital

Management:

• Ophthalmology consult in the ED for intravitreal antibiotics, which is the ideal treatment and typically performed by ophthalmology
• Blood cultures (only if endogenous infection is suspected) 

Do these patients need admission?

Dr. Alawami advises that admission is generally not required, except in cases where there are socioeconomic barriers or if the patient is deemed unreliable for outpatient follow-up.

Is there a role for systemic antibiotics in the ED management of these patients?

Some clinicians still administer them despite the lack of strong supporting evidence. The reality is that systemic antibiotics are largely ineffective and have no role in treating a vitreous infection like endophthalmitis.

Expert Opinion re: Systemic Antibiotics:

“There is no evidence to suggest that IV antibiotics are needed. These patients need intravitreal injections of vancomycin, ceftazidime, and dexamethasone. However, they can sometimes present as orbital cellulitis, and we would recommend IV antibiotics such as third-generation cephalosporins in those cases.” — Dr. Adnan Alawami, Retina Fellow, University of Ottawa

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