Eye emergencies

• A patient with sudden loss of vision or a painful red eye is a potential emergency until proven otherwise: the goal is to distinguish the vision-threatening causes in the first few minutes and to act, not to make a perfect diagnosis at the bedside. ^[7]
• Acute angle-closure glaucoma (AACG), central retinal artery occlusion (CRAO) and retinal detachment (RD) are the classic "time critical" causes of monocular visual loss; chemical eye injuries and penetrating trauma are the classic time-critical causes of a painful, acutely inflamed eye.
• Laterality (one eye or both) and pain (painful or painless) sort most causes into the right box; a handheld torch, a drop of fluorescein, confrontation fields and a relative afferent pupillary defect (RAPD) check can be done anywhere.
• Do not check intraocular pressure (IOP) if an open globe is suspected; do not give topical corticosteroids or dilate the pupil unless ophthalmology advises.
• Urgent ophthalmology and, for CRAO, urgent stroke pathway activation are the decisions that save sight; ship the patient rather than keep trying to sort it out yourself.

By the end of this page you should be able to:

1. Triage a patient with acute vision loss or a painful red eye using laterality, pain and a short chairside examination.
2. Recognise AACG, CRAO and retinal detachment by their typical stories, and state what must be done in the first minutes and hours.
3. Manage an acute chemical eye injury by irrigation and pH control, and know what follow-up it needs.
4. Recognise, grade and manage a traumatic hyphaema, including who needs screening for sickle cell disease.
5. Recognise an open globe and orbital cellulitis and know when and how to refer.
6. Follow the AAO, RCOphth and StatPearls advice that each condition carries, and name the editions or years you relied on.

This is a decision-and-management page, written for the emergency department or primary-care clinician who meets the patient first. It covers the eye emergencies a medical student is expected to triage, not the full ophthalmological evaluation that happens later in theatre. "Eye emergencies" is a curriculum topic rather than a single disease, so it is organised by presentation (sudden visual loss, chemical injury, trauma) and then by condition.

The American Academy of Ophthalmology (AAO) Preferred Practice Patterns, the Royal College of Ophthalmologists (RCOphth) standards on emergency eye care and the StatPearls chapters are the guideline sources used. They are named where they are relied on. Because the older book chapters do not give a page for any of these topics in the MedGrasp syllabus, no book pages are mapped here. Regional practice notes are given where practice differs.

A practical five-step framework for acute vision loss is described by Maher and colleagues (2026), and the same steps work for the painful red eye too ^[1].

Monocular loss usually comes from disease in front of the chiasm (cornea, anterior chamber, retina, optic nerve). Binocular loss usually comes from behind the chiasm or from a systemic neurologic process, and needs stroke-style thinking ^[1].

Test each eye on its own: patients often close one eye and think vision is lost in both. Homonymous field loss is retro-chiasmal until proven otherwise; a normal anterior segment and quiet eye with such loss points to an occipital infarct ^[1].

Severe pain with nausea, vomiting or haloes points to AACG. Pain on eye movement points to optic neuritis. Surface pain with photophobia points to keratitis or uveitis. Sudden painless loss points to a vascular or retinal cause (CRAO, central retinal vein occlusion, retinal detachment, vitreous haemorrhage, ischaemic optic neuropathy) ^[1].

Ask how fast the loss reached its worst: seconds suggests vascular occlusion or trauma; hours to days suggests infection or inflammation. Ask for flashes, floaters or a curtain or shadow; haloes; transient dimming; jaw claudication or scalp tenderness in a patient over 50 years of age; diabetes or vascular risk factors; recent surgery (post-operative endophthalmitis most often presents within 3 to 5 days of cataract surgery or intravitreal injection); trauma; immunosuppression ^[1].

A useful minimum, with minimal kit, is listed below ^[1].

Fluorescein staining of the surface is essential: it shows corneal epithelial defects, dendritic ulcers of herpetic keratitis, punctate erosions and focal staining of a corneal ulcer; a positive Seidel test confirms an open globe and mandates protection of the eye and urgent referral ^[1].

Do not let investigations delay escalation when red flags exist. The following are time-critical ^[1].

Definition. AACG is an emergency in which the peripheral iris apposes the trabecular meshwork and blocks aqueous outflow, producing a rapid rise in IOP. It is a disease of anatomy (a shallow anterior chamber, a thick or anteriorly placed lens, hyperopia) triggered by pupil dilatation, darkness or drugs with anticholinergic effect (including, for example, many over-the-counter cold preparations).

Presentation. Sudden, often unilateral, severe periocular or orbital pain with blurred vision, haloes around lights, headache, nausea and vomiting. The eye is injected; the cornea is steamy; the anterior chamber is shallow; the pupil is mid-dilated and fixed. Vision can fall to hand movements. It occurs most often in older, hypermetropic patients and in East Asian populations; the anatomical susceptibility is bilateral, so the other eye is at risk ^[1].

Immediate management. The goals are to lower the pressure fast and to break the attack, then to create a permanent bypass.

• Medical (under ophthalmology guidance): topical IOP-lowering agents (a beta-blocker, an alpha-agonist and/or a prostaglandin analogue), a systemic carbonic anhydrase inhibitor (for example acetazolamide) and, where appropriate, an osmotic agent (intravenous mannitol, monitoring renal function). Pupillary constriction with a miotic (pilocarpine) is used once the pressure has begun to fall; it is less effective at very high pressures.
• Definitive: a laser peripheral iridotomy in the affected eye, and usually in the fellow eye prophylactically.
• Positioning and analgesia: the patient should lie supine; control pain and vomiting; avoid anything that keeps the pupil dilated.

Evidence and editions used. The AAO Preferred Practice Pattern on Primary Angle-Closure Disease (most recent edition available open-access at the time of writing) is the standard referenced by this page; among open-access summaries, an Australian Prescriber review on adult glaucoma management and the acute-vision-loss review above were consulted for general classes and safety rather than dosing. If you cannot confirm a dose against a current guideline or drug label, do not write it and use your local formulary ^[4][1].

Definition. CRAO is an acute ischaemic event of the inner retina from occlusion of the central retinal artery or one of its branches. It is a stroke equivalent: the retina and brain share the same vasculature, and a CRAO should trigger the same risk-factor search as a cerebral ischaemic event ^[1].

Presentation. Sudden, painless, profound monocular visual loss over seconds. Visual acuity is often reduced to counting fingers or worse. On fundoscopy the retina is pale and oedematous with a cherry-red spot at the macula; box-carring (segmentation) of the blood in the retinal arterioles may be visible. A relative afferent pupillary defect is common. Not all patients have the classic fundus; if the presentation is right but the view is poor, act anyway.

Management in the first hours. Treat CRAO with the urgency of a stroke. Management varies and is controversial; there is no universally accepted protocol, and the evidence is low grade ^[2].

• Activate the stroke pathway and arrange urgent ophthalmology. Many patients (up to two-thirds) have underlying cardiovascular or cerebrovascular disease, so cardiac and carotid evaluation should follow ^[1].
• Consider immediate, evidence-discussed temporising measures that you can do while awaiting the specialist: ocular massage (repeated intermittent digital pressure on the globe), IOP-lowering measures to improve perfusion, and re-breathing into a paper bag (hypercapnia causes vasodilatation). None of these is proven to restore vision; they must never delay referral.
• Thrombolysis and thrombectomy. Intravenous and intra-arterial thrombolysis, and mechanical embolectomy in selected cases, are practised in some centres and are not universally recommended; decisions belong to the stroke and ophthalmology teams. Hyperbaric oxygen is used in some protocols for branch and central occlusion.
• History matters. Ask about giant cell arteritis in any patient 50 years or older with headache, jaw claudication or scalp tenderness: vision in the second eye can be lost within hours, and emergency high-dose corticosteroids must not wait for a biopsy result.

Guideline sources. StatPearls (Tripathy, Shah and Waymack, 2024) describes the entity, its emergency classification and its standard evaluation; the AAO EyeNet review of CRAO emergency protocols discusses time-critical approaches; the open-access Cureus review by Lakkis and colleagues (2025) summarises current practice ^[2][4][5].

Definition. A separation of the neurosensory retina from the retinal pigment epithelium, allowing fluid to accumulate in the subretinal space.

Types. Rhegmatogenous RD is the common form, usually preceded by a posterior vitreous detachment with a retinal tear; tractional RD (proliferative diabetic retinopathy, trauma); exudative RD (inflammatory, neoplastic, vascular). The common teaching point is that sudden new floaters, flashes and a descending curtain mean rhegmatogenous RD or its precursor.

Presentation. Flashes (photopsia), a sudden shower of floaters, and a shadow or curtain moving across the visual field. Pain is absent. Central vision is spared while the fovea is attached (macula-on) and collapses once the fovea detaches (macula-off). Patients often describe "a cobweb", "a veil" or "a curtain".

Management. Macula-on detachment is the surgical emergency of the eye: same-day ophthalmology, because once the fovea detaches visual recovery is permanently worse. Macula-off detachment still needs prompt repair (days, not weeks), with posturing over a break, laser retinopexy or cryotherapy to the tear, and a surgical procedure (pneumatic retinopexy, scleral buckle or vitrectomy) chosen by the vitreoretinal surgeon.

Low-resource note. Dilated fundoscopy is not always available. If the story (flashes, floaters, curtain, loss of a wedge of field) is strong, arrange same-day ophthalmology regardless of whether a tear is visible at the bedside; B-scan ultrasound through the lids can show a detached retina when the fundus view is obscured by haemorrhage or cataract ^[1].

Principle. Alkalis (lime, cement, ammonia, lye) are worse than acids. Acids are precipitated by tissue proteins and largely stop at the surface; alkalis saponify lipids and penetrate. Every minute counts: irrigate before you do anything else, including taking a history or checking visual acuity.

What to do.

1. Protect yourself (gloves, eye protection) and remove any contact lenses and particulate matter if it comes away easily. Never pull on adherent particles.
2. Anaesthetise the eye (topical anaesthetic).
3. Irrigate copiously with any available sterile balanced fluid: sterile saline or Ringer's lactate is ideal; tap water or any clean water is acceptable if nothing else is available. Evert the lids and irrigate the fornices.
4. Check the pH in the conjunctival sac after irrigation and continue until the pH is normal (around 7). Check again some minutes later; pH can rebound.
5. Document the agent, the estimated time of exposure, the irrigation, and the final pH.
6. After irrigation: antibiotic ointment, cycloplegic, and lubrication as advised; escalate. Topical corticosteroids, if used, are prescribed by ophthalmology (to limit scarring) and must not be used without excluding infection.
7. Surgery (limbal stem-cell and ocular surface reconstruction) is a specialist decision for severe grades.

Low-resource note. If sterile irrigation fluid is not available, clean tap water is used instead and irrigation continues for a prolonged period, because under-irrigation is the usual error. ^[3]

Corneal abrasion is a loss of the corneal epithelium, classically from a fingernail, a foreign body, a contact lens or an accidental swipe. It is intensely painful, with photophobia, tearing and (with fluorescein) a linear or punctate epithelial defect. Management: remove the foreign body if it is superficial, irrigate, provide analgesia (topical NSAID drops for a short period are widely used, with care about toxicity if prolonged), consider a short course of topical antibiotic, and avoid contact lens wear until healed. A topical corticosteroid is not appropriate for a simple abrasion.

Contact lens wearers demand a lower threshold: a painful red eye in a contact lens wearer is keratitis until proven otherwise. They need urgent slit-lamp examination by ophthalmology and usually empirical anti-pseudomonal cover as directed by the specialist.

Corneal ulcer (keratitis) is a microbial invasion of the corneal stroma. Clues: a white infiltrate, overlying epithelial defect, anterior chamber reaction, pain out of proportion, and (in herpetic disease) a dendritic branching ulcer. Management depends on organism class: bacterial ulcers are treated with intensive broad-spectrum topical antibiotics (often fortified aminoglycoside plus a fluoroquinolone), fungal ulcers with antifungals, and herpetic ulcers with antiviral therapy; acanthamoeba in contact lens wearers is treated with antiseptic agents. Steroids are never started before the infection is controlled. Swab and culture if possible; admit if severe, central or sight-threatening.

Important exam trap. A "red eye" after blunt trauma with a small infiltrate and a foreign-body sensation may be a corneal foreign body retained in the tarsal conjunctiva: evert the upper lid ^[1].

Definition and grading. Hyphema is blood in the anterior chamber from a tear of iris or ciliary-body vessels. It usually follows blunt trauma; grading runs from grade I (less than one-third of the anterior chamber) to grade IV (total, "eight-ball").

Clinical impact. Poor visual outcome after traumatic hyphema is more often due to the accompanying injury (corneal laceration, retinal detachment) than to the blood itself, but hyphema alone is responsible in 8 to 33% of cases ^[3].

Principles of management (current practice varies widely; the Cochrane review found no single regimen clearly superior) ^[8].

• Topical steroids: routinely used by most centres (94.4% for gross hyphema, 80.6% for microhyphema), usually prednisolone, typically for about 2 to 3 weeks including taper. Their benefit for final visual acuity is uncertain ^[3].
• Topical cycloplegics (atropine 1%, or cyclopentolate 1 to 2%) are used at over 90% of centres: they relieve pain and spasm, prevent synechiae and improve the view of the posterior segment. No effect on re-bleed rates has been shown ^[3].
• Antifibrinolytics (tranexamic acid, epsilon-aminocaproic acid) have a moderately re-bleed-lowering effect in some, but not all, analyses and were not used by any of the responding centres in the IGATES survey; their systemic use is contraindicated where thromboembolism is a risk ^[3].
• Anticoagulant and antiplatelet drugs: about 40% of centres stop them when the patient's clinician advises it ^[3].
• Activity and posture: head elevation and sleeping upright (86% of centres) and partial bed rest (58%); shielding of the eye (53%); complete bed rest only in a minority ^[3].
• IOP and surgery. Raised IOP is the main indication for anterior chamber washout. Many centres wash out at lower pressures in patients with sickle cell disease (for example above 24 mmHg for 1 to 2 days) than in patients without (for example above 50 mmHg for 2 to 5 days). Classical surgical indications (Read, 1975) include corneal blood staining, total hyphema with IOP above 50 mmHg for 5 days, or failure of a large clot to reduce by half within 5 days with IOP above 25 mmHg ^[3].
• Sickle cell disease or trait. SCD/ SCT status increases re-bleed and raised-IOP risk; only about one centre in six screens every hyphema patient, but screen when suggested by ethnicity, family history or raised IOP. SCD should lower your threshold for surgical washout ^[3].
• Follow-up: most centres see patients within 48 hours; follow-up continues until resolution. ^[3]

Evidence sources. The IGATES global survey (Miller et al., 2022) and the Cochrane review of medical interventions for traumatic hyphema (Gharaibeh et al., 2019) are the open references used above; the AAO does not publish a Preferred Practice Pattern on traumatic hyphema, so practice varies internationally. ^[3][8].

Principles.

• Do not manipulate, compress or irrigate a suspected open globe beyond what is needed to protect it. Place a rigid shield (not a pad pressed against the eye), check tetanus status, give antiemetics and keep the patient fasting, and image the orbit (CT) for intraocular foreign bodies and fractures.
• Open globe (laceration or rupture) is an emergency surgery case. Signs include an irregular pupil, a shallow or deep anterior chamber, a positive Seidel test, vitreous leakage, extruded uveal tissue and (in the blunt case) an eccentric pupil. CT of the orbits is the imaging test; MRI is avoided when metallic foreign bodies are possible.
• Blunt trauma without rupture can still cause hyphema, lens dislocation, retinal dialysis, angle recession, commotio retinae and traumatic optic neuropathy.
• Intraocular foreign bodies: CT localises them; ultrasound helps when the view is obscured; removal is surgical. Remember siderosis with retained iron.
• Traumatic optic neuropathy: treat the underlying injury; high-dose corticosteroids are controversial and, in many protocols, not used; refer urgently.
• Endophthalmitis after trauma is a surgical emergency; prophylactic antibiotics as directed by the specialist.

Regional note. The EXTRACCT blast-ocular-trauma guideline (2026) and the ED data on ocular trauma remind clinicians that simple primary repair can be done in centres with the right equipment, but that posterior-segment and complex cases must be transferred ^[6].

Orbital cellulitis is an infection of the soft tissues posterior to the orbital septum, most commonly from spread of ethmoid or frontal sinusitis. It is a vision- and life-threatening condition that can progress to cavernous sinus thrombosis, meningitis or cerebral abscess.

Clues. Lid swelling, erythema, pain, proptosis, limited and painful eye movements, fever and reduced vision; leukocytosis occurs in the majority and imaging (CT orbit and sinuses) confirms the diagnosis and shows subperiosteal abscess. Involvement is usually unilateral; bilateral disease is virtually diagnostic of cavernous sinus thrombosis ^[6].

Management. Intravenous antibiotics covering the organisms likely from sinusitis (including anaerobes), sinus drainage if needed, and urgent surgical drainage when there is a large or medial subperiosteal abscess, optic nerve compromise, deterioration after 48 hours of intravenous antibiotics or in children younger than 9 years ^[6].

Cross-check. MedGrasp covers the medical and surgical detail under "Conjunctivitis and orbital cellulitis" (plain text). This page lists orbital cellulitis only as an emergency triage item and refers there for the rest; do not duplicate the full antimicrobial regimens. National antibiogram-based guidelines lead the choice of drug.

• Conjunctivitis and orbital cellulitis
• Childhood vision and hearing disorders
• Retinal detachment (if a dedicated topic exists)
• Acute vision loss (presentation page, where available)
• Sepsis and meningitis for cavernous sinus thrombosis
• Trauma: initial assessment and secondary survey

• Acute vision loss is triaged first by laterality (monocular versus binocular) and then by pain (painful versus painless); these two steps place most causes in the right box.
• CRAO, AACG and retinal detachment are the classic time-critical causes of monocular visual loss; CRAO is a stroke equivalent.
• Chemical burns need irrigation before anything else, with repeated pH checks, because under-irrigation is the commonest error.
• A corneal ulcer in a contact lens wearer is keratitis until proven otherwise and needs urgent specialist examination.
• Hyphema is managed with cycloplegics, steroids, head elevation and shielding; evidence-based benefit is weak, and sickle cell disease lowers the threshold for surgical washout.
• Suspected open globe must not be manipulated, pressed or irrigated beyond protection; shield it and refer.
• Orbital cellulitis is an emergency with risk of cavernous sinus thrombosis; intravenous antibiotics and early imaging are the mainstays.
• Treat the patient and refer early; do not let prolonged examination delay the decision to send.