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Step 2 CK · Ophthalmology & ENT

Eye Trauma & Ocular Emergencies

Irrigate, shield, or cut: the right first move saves sight

Ophthalmology & ENT·Urgent Eye Conditions·6 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy
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Chemical injury

Why alkali is worse. Alkalis such as lye (sodium hydroxide in drain and oven cleaners), ammonia and lime (calcium hydroxide in cement and plaster) saponify cell-membrane lipids, producing liquefactive necrosis that keeps penetrating into the anterior chamber and the limbus. Most acids, such as sulfuric acid from car batteries, denature surface proteins into a coagulum that limits their depth; hydrofluoric acid is the exception and penetrates like an alkali.

Alkali versus acid injury
FeatureAlkaliAcid
ExamplesLye, ammonia, lime in cement or plasterSulfuric (battery), hydrochloric
NecrosisLiquefactive (saponification)Coagulative (protein precipitation)
DepthDeep, into anterior chamber and limbusUsually superficial (hydrofluoric acid excepted)
PrognosisWorse: scarring, glaucoma, cataractBetter with prompt irrigation

Treatment comes before examination. This is the one eye emergency in which visual acuity waits.

  1. Irrigate at onceTap water at the scene; normal saline or lactated Ringer in the ED, often several liters.
  2. Make it tolerableTopical anesthetic plus a lid speculum or Morgan irrigating lens.
  3. Clear the fornicesEvert the lids and sweep out retained particles such as lime, which keep releasing alkali.
  4. Check pHPause for 5–10 minutes, test the fornix, and continue until pH is 7.0–7.5.
  5. Then examineVisual acuity, slit lamp with fluorescein, IOP and urgent ophthalmology.

Aftercare and sequelae. Ophthalmology typically prescribes a topical antibiotic, a cycloplegic and a short, supervised course of topical steroid. Severity tracks corneal haze and limbal ischemia, and late complications include corneal scarring and vascularization, limbal stem cell failure, symblepharon, glaucoma and cataract.

A pale, quiet-looking eye after an alkali burn is not reassuring: blanched limbal vessels mean ischemia of the corneal stem cell niche and a severe injury.

Open globe injury

Recognition. An open globe is a full-thickness wound of the cornea or sclera, from blunt rupture or a sharp laceration. Suggestive signs are a peaked or teardrop pupil pointing toward the wound, 360° bullous hemorrhagic chemosis, an abnormally shallow or deep anterior chamber, hyphema, dark uveal tissue prolapsing through the wound and marked vision loss. In the Seidel test, fluorescein diluted by leaking aqueous streams bright green under cobalt-blue light.

Intraocular foreign body. Hammering or grinding metal throws tiny high-velocity fragments that can enter the eye through a pinpoint wound. Thin-cut noncontrast CT of the orbits localizes them; MRI is contraindicated when a ferromagnetic fragment is possible. Soil-contaminated injuries raise the risk of Bacillus cereus endophthalmitis.

Management. Place a rigid shield (never a pressure patch), elevate the head of the bed, keep the patient NPO, and give analgesia and antiemetics, because vomiting and Valsalva can extrude intraocular contents. Update tetanus, start IV antibiotics against endophthalmitis (vancomycin plus ceftazidime, or a fluoroquinolone), and arrange emergent surgical repair.

With a suspected open globe, do not measure IOP, press on the eye, instill drops, perform B-scan ultrasound or remove an impaled object.

Sympathetic ophthalmia. Weeks to months after a penetrating injury, uveal antigens exposed in the injured eye can trigger bilateral granulomatous uveitis that threatens the uninjured eye.

Hyphema and traumatic iritis

Hyphema. Blunt trauma tears vessels of the iris root or ciliary body, and blood layers in the anterior chamber. Elevate the head of the bed 30–45° so blood settles and clears the visual axis, apply a rigid shield, restrict activity, and give a cycloplegic and topical steroid as directed by ophthalmology, with daily IOP checks. Use acetaminophen rather than NSAIDs, and avoid aspirin and anticoagulants, because rebleeding risk peaks around days 2–5.

Sickle hemoglobin. Screen at-risk patients with a sickle solubility test or hemoglobin electrophoresis. In sickle cell disease or trait, rigid sickled cells clog the trabecular meshwork, IOP spikes, and the optic nerve is injured at lower pressures. Avoid carbonic anhydrase inhibitors and hyperosmotic agents, whose acidosis and hemoconcentration promote sickling, and keep a low threshold for surgical washout.

Late complications of hyphema include corneal blood staining and angle-recession glaucoma years later, so these patients need yearly eye exams.

Traumatic iritis. One to three days after blunt injury, anterior uveitis causes deep aching pain, photophobia (including consensual photophobia when light enters the uninjured eye), tearing, ciliary flush and a small sluggish pupil, with cells and flare on slit lamp. A cycloplegic relieves ciliary spasm and prevents posterior synechiae; a topical steroid is added once ophthalmology excludes an epithelial defect or infection.

Orbital trauma

Blowout fracture versus retrobulbar hemorrhage
FeatureOrbital floor blowout fractureRetrobulbar hemorrhage
MechanismFist or ball larger than the orbital rimBleeding into the closed orbit; trauma, surgery, anticoagulation
Key signsUpgaze diplopia, infraorbital numbness, enophthalmos, emphysemaProptosis, tense orbit, vision loss, RAPD, IOP often >40 mmHg
DiagnosisNoncontrast CT of the orbitsClinical; do not wait for CT
TreatmentNo nose blowing; repair for entrapment, persistent diplopia, large defect or enophthalmosEmergent lateral canthotomy with cantholysis

Blowout fracture. A sudden rise in orbital pressure breaks the thin orbital floor (maxillary bone) or medial wall (lamina papyracea). Periorbital ecchymosis, diplopia on upgaze from inferior rectus entrapment, numbness of the cheek, upper lip and upper teeth from infraorbital nerve (V2) injury, enophthalmos once swelling subsides, and orbital emphysema are typical. Nose blowing forces air into the orbit and should be avoided. Surgery within about 2 weeks is reserved for persistent diplopia, large floor defects or enophthalmos, and every patient needs an ophthalmologic exam to exclude globe injury.

Trapdoor fracture in children. A child's elastic floor can snap back and trap the inferior rectus with little external bruising (the "white-eyed blowout"). Traction on the muscle triggers the oculocardiac reflex, carried by the trigeminal nerve (V1) and returned by the vagus, causing bradycardia, nausea, vomiting, syncope or even asystole. Emergent surgical release prevents muscle ischemia.

Retrobulbar hemorrhage. Blood trapped behind the globe raises pressure in a compartment bounded by bone and the orbital septum, compressing the optic nerve and its blood supply. Proptosis, lids that resist retropulsion, pain, falling acuity, a relative afferent pupillary defect and restricted motility make the diagnosis. Perform bedside lateral canthotomy with inferior cantholysis immediately, ideally within about 90–120 minutes before ischemic damage becomes permanent; IV acetazolamide, mannitol and topical timolol are adjuncts.

UV keratitis

Photokeratitis. Ultraviolet light from unprotected arc welding ("welder's flash"), snow or water glare, or tanning lamps injures the corneal epithelium. Symptoms begin 6–12 hours later, often waking the patient at night, with severe bilateral pain, tearing, photophobia and blepharospasm; fluorescein shows diffuse punctate staining. The epithelium heals in 1–2 days with oral analgesics, a cycloplegic, lubricants and antibiotic ointment, and contact lenses stay out until healing is complete.

Never send a patient home with topical anesthetic drops: repeated use delays epithelial healing and can lead to corneal ulceration.