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OP10.6 | Ocular Injuries: Classification, Primary Management and Referral — SDL Guide (Part 2)

Closed Globe Injuries: Blunt Trauma

Blunt (closed globe) injuries transmit a concussive force wave through the eye, causing damage at multiple levels. The severity ranges from superficial corneal abrasion to catastrophic posterior segment damage.

Hyphaema: Blood in the anterior chamber from blunt rupture of the iris root blood vessels or angle vessels. Seen as a red fluid level in the anterior chamber. Graded: Grade I (<1/3 of anterior chamber), Grade II (1/3–1/2), Grade III (1/2 to <total), Grade IV (total — '8-ball hyphaema', dark red/black fill). Management: bed rest with 30–45° head elevation (to allow the blood to settle inferiorly and not block the pupil), avoid aspirin and NSAIDs (inhibit platelet function), topical corticosteroids to reduce inflammation. The most dangerous complication is secondary haemorrhage — a rebleed typically on days 2–5, which is often larger and more dangerous than the primary bleed, and may cause corneal bloodstaining or uncontrolled IOP elevation. Refer to ophthalmology; surgical washout for persistent large hyphaema or rising IOP.

Commotio retinae (Berlin's oedema): Retinal whitening caused by disruption of the outer retinal layers from the concussive wave. Appears as a grey-white patch of retinal oedema at the posterior pole or periphery. Usually resolves spontaneously without significant vision loss, but a macular commotio may leave a permanent scotoma. Arrange dilated fundus examination.

Choroidal rupture: A crescent-shaped subretinal scar nasal to the disc, due to rupture of Bruch's membrane and the choroidal vasculature. The rupture itself heals with scarring, but a choroidal neovascular membrane (CNVM) may develop weeks to months later and threaten central vision.

Lens dislocation (subluxation / luxation): The zonular fibres that suspend the lens may rupture with blunt trauma, causing phacodonesis (trembling of the lens on eye movement) and monocular diplopia (subluxation) or complete dislocation into the vitreous or anterior chamber. A dislocated lens in the anterior chamber blocks the pupil and causes acute glaucoma — emergency referral.

Orbital blow-out fracture: A blunt force to the orbit (fist, ball) can cause fracture of the thin floor (or medial wall) of the orbit, with herniation of orbital contents (inferior rectus, orbital fat) into the maxillary sinus. Clinical features: enophthalmos (sunken eye), diplopia on upward gaze (tethered inferior rectus), infraorbital nerve hypoaesthesia (cheek anaesthesia). CT orbit is diagnostic. Surgical repair is needed if diplopia persists or enophthalmos is significant.

Open Globe Injuries: Penetrating and Perforating Wounds

Open globe injuries are among the most vision-threatening presentations in ophthalmology. The hallmark is a full-thickness wound of the eyewall, which may allow extrusion of intraocular contents (vitreous, iris, lens) and permits direct contamination of the eye with microorganisms, leading to endophthalmitis. Immediate, correct first-contact management at the point of injury and at the referring hospital determines the outcome.

Penetrating injuries present with: visible wound in the cornea or sclera, iris tissue prolapsing through the wound (dark uveal tissue may be visible as a brown plug at the wound edge), shallow or flat anterior chamber (if the wound is leaking aqueous), or a low, soft-feeling eye (hypotony) compared to the fellow eye. There may be a small self-sealing wound that is easy to miss — the Seidel test (fluorescein + cobalt blue light) reveals aqueous leakage.

Intraocular foreign body (IOFB) is an especially deceptive injury. A tiny metallic fragment from hammering or grinding operations enters the eye at high velocity through a small self-sealing corneal or scleral wound. The patient may report only mild pain or minimal visual disturbance. On examination the wound may not be visible without careful magnification. The IOFB may lodge in the vitreous, retina, or lens. Immediate X-ray of the orbit (AP and lateral) detects metallic IFOBs; CT scan (NOT MRI — never MRI a suspected metallic IOFB, as the magnet will move the fragment, causing further injury) provides precise localisation. Delayed removal leads to: siderosis bulbi (iron IOFB — rust staining of all intraocular structures, progressive visual loss, ERG changes — develops over months) and chalcosis (copper IOFB — golden deposits on the lens (sunflower cataract), cornea (Kayser-Fleischer-like ring), and retinal degeneration — develops faster, within weeks).

First-contact management of open globe (the do-nots and do-dos):
- DO: Apply a Fox rigid protective shield over the orbit (do NOT press on the eye). Give IV broad-spectrum antibiotics (ciprofloxacin or cefazolin + gentamicin per local protocol). Keep nil by mouth for emergency surgical repair. Give tetanus toxoid/immunoglobulin as indicated. Transfer urgently to a tertiary ophthalmology centre with a vitreoretinal surgeon.
- DO NOT: Patch with pressure. Remove impaled or embedded foreign objects. Apply eye drops. Perform tonometry. Allow the patient to vomit without anti-emetics (Valsalva manoeuvre from vomiting can extrude intraocular contents).

Chemical Burns: The Alkali-Worse-than-Acid Rule and Immediate Management

Chemical burns to the eye are the most time-critical ocular emergencies. The severity and prognosis depend on: (1) the nature of the chemical (alkali vs acid); (2) the concentration and pH; (3) the duration of contact before irrigation; and (4) how quickly and thoroughly irrigation is performed.

Why alkali is worse than acid — the fundamental mechanism:

Acid burns (sulphuric acid, battery acid, hydrochloric acid): Acids cause coagulative necrosis — they denature and precipitate proteins on contact. This coagulation creates a layer of denatured protein on the conjunctival and corneal surface that acts as a barrier, limiting further penetration of the acid into deeper structures. While acid burns are painful and can be severe, they tend to be somewhat self-limiting in terms of depth of penetration.

Alkali burns (calcium hydroxide/lime, ammonia, sodium hydroxide/lye, potassium hydroxide, cement): Alkalis cause liquefactive (colliquative) necrosis — they saponify the fatty acids of cell membranes (dissolving cell membranes) and hydrolyse proteins. Crucially, NO COAGULATIVE BARRIER forms. The alkali continues to penetrate through the conjunctiva, through the corneal stroma, through the trabecular meshwork, and into the anterior chamber, ciliary body, and even the lens — causing progressive destruction with each minute of contact. The extent of damage continues to increase for hours after initial contact if the chemical is not completely removed. An alkali with pH >12 can achieve intraocular penetration within minutes. Alkali burns are therefore more severe than acid burns of equivalent concentration, and the window for effective irrigation is particularly narrow.

IMMEDIATE COPIOUS IRRIGATION — the single most important action:
The FIRST action for any chemical ocular burn — before examination, before checking visual acuity, before calling the ophthalmologist, before taking the full history — is immediate copious irrigation with whatever fluid is available: tap water, saline, Ringer's lactate, or even drinking water from a bottle. In the pre-hospital setting, the patient should be holding their eye under running tap water. In the casualty setting, attach the eye to continuous IV saline flow using a standard giving set directed at the open palpebral fissure. Irrigate for a minimum of 30 minutes for alkali, and irrigate until the conjunctival pH (tested with litmus paper or pH strips placed in the inferior conjunctival fornix) returns to 7.0–7.4. Do not stop irrigation simply because the time threshold is met — check pH and continue if still alkaline.

Roper-Hall grading of chemical burns (prognosis):
- Grade I: Clear cornea, no ischaemia. Excellent prognosis.
- Grade II: Corneal haze, details visible, <1/3 limbal ischaemia. Good prognosis.
- Grade III: Total corneal epithelial loss, corneal stroma hazy, 1/3 to 1/2 limbal ischaemia. Guarded prognosis.
- Grade IV: Cornea opaque, 1/2 or more limbal ischaemia (porcelain white limbus). Very poor prognosis.

The limbus is a critical anatomical zone — it contains corneal epithelial stem cells. Limbal ischaemia destroys these stem cells, resulting in persistent epithelial defects, neovascularisation, and corneal scarring that are extremely difficult to treat.