Case 1: 85/F living alone ^[1]:

• PMH: dry eyes on lubricating eyedrops
• One hour ago, both eyes (OU) very painful after putting "usual eyedrops"
• Rinse with tap water
• Immediate action: Irrigate and check pH

The next slide reveals the error: a White Flower topical liniment labelled “for external use only” was stored beside a similarly sized lubricant bottle. Both eyes were exposed. This is a medication-storage and packaging lesson as well as a burn case: bring the bottle or a photograph of its label, but do not delay first aid while identifying every ingredient.

For an isolated chemical splash, start irrigation immediately after scene safety and removal of contaminated contact lenses or clothing. A simultaneously obvious penetrating injury or embedded object changes the problem: do not remove the object or pressurise the globe; obtain emergency ophthalmic/trauma direction ^[7].

Chemical burn of the eye — epidemiology ^[1]:

• Workplace injuries: predominantly young men
• Household injuries: predominantly young children (1–2 years old)

Severity of injury depends on ^[1]:

1. Chemical: type (acid vs alkali) and concentration
2. Duration of exposure: time from injury to first aid (irrigation)
3. Area of involvement
4. Depth of penetration

A specific high-yield example from the slides: Cement/concrete has pH 12–14 (containing lime / calcium hydroxide) — this is an alkali and therefore extremely dangerous ^[1].

Acid burn vs Alkali burn ^[1]:

Fluorescein stain + Cobalt blue light ^[1]:

Fluorescein is a vital dye that stains areas of epithelial loss. When viewed under cobalt blue light, denuded epithelium fluoresces bright green. This is how you map the extent of corneal epithelial damage in chemical burns (and corneal abrasions, ulcers, etc.).

The first image shows a broad inferotemporal epithelial defect; cobalt-blue illumination makes the same green-staining area more conspicuous. By day 3, the green defect has largely closed. Fluorescein marks missing epithelium, not the chemical itself and not the full depth of injury. Surface closure does not prove that limbal, stromal, trabecular or lens injury is absent.

Emergency management ^[1]:

• Immediate copious irrigation (do not wait)
• Aim to eliminate the causative agent
• Target pH 7.0–7.2
• Wait 5–10 minutes then recheck pH

Practical irrigation sequence:

1. Protect staff and the other eye; remove contact lenses and brush away dry particulate chemical before flooding when this can be done safely.
2. Use any immediately available clean, non-toxic fluid; isotonic saline or lactated Ringer's is comfortable, but tap water is preferable to delay.
3. A topical anaesthetic and irrigation device may help, but neither should postpone the first flush.
4. Direct flow from nasal to temporal side, irrigate the fornices and remove retained particles. There is no magic litre count: several litres and 30 minutes or more may be required.
5. Pause for at least 5 minutes, then recheck both eyes. Continue until a physiological pH (about 7.0–7.2) remains stable ^[7]. Do not try to neutralise an acid with alkali or vice versa.

Roper-Hall Classification ^[1]:

How to read the photographs: progressive stromal haze obscures the iris, while white, avascular perilimbal conjunctiva represents limbal ischaemia. Do not grade from epithelial-defect size alone. More limbal injury means fewer surviving epithelial stem-cell niches and a worse healing prognosis.

The four-panel sequence shows a green epithelial defect shrinking circumferentially from surviving limbus. The chronic-stage panels show the consequence of severe limbal failure: persistent epithelial defect, fibrovascular pannus, corneal opacity and surface neovascularisation. Roper–Hall remains exam-friendly, while the Dua system records clock hours of limbal involvement and percentage conjunctival involvement more granularly ^[7].

After irrigation, urgent ophthalmic management is tailored to grade and IOP. It may include preservative-free lubrication, prophylactic topical antibiotic while epithelium is absent, cycloplegia, a specialist-directed topical corticosteroid regimen, and—when stromal melt is a concern—ascorbate, citrate or a tetracycline. Severe burns may need amniotic membrane or later ocular-surface/limbal reconstruction. These are not a fixed emergency-department prescription bundle; repeated epithelial, limbal, corneal and pressure assessment determines treatment ^[7].

Full thickness wound ^[1]:

• Laceration: caused by a sharp object
• Rupture: caused by blunt force

This is the fundamental distinction in open globe injuries. A laceration has a clean, well-defined wound from a sharp instrument (knife, glass, wire). A rupture occurs when blunt force (e.g., fist, ball, fall) raises intraocular pressure to the point that the globe wall gives way at its weakest point.

The Birmingham Eye Trauma Terminology System first asks whether the cornea or sclera has a full-thickness wound:

Do not use “penetrating” as a synonym for every open globe. The diagram's branches encode mechanism and wound pattern.

Blunt force ^[1]:

• Results in peripheral volume displacement with increased "wedge pressure"
• The area of least resistance is most affected:
  • Lens (zonular dehiscence → subluxation/dislocation)
  • Iris root (iridodialysis)
  • Trabecular meshwork (traumatic glaucoma)
  • Retina at vitreous base (retinal dialysis → detachment)
  • Thinnest sclera posterior to muscle insertion (rupture site)

How to read the blunt-force diagram: anteroposterior compression displaces globe volume equatorially. The anterior “hydraulic wedge” can injure the iris root and angle; posterior traction can produce retinal dialysis at the vitreous base; pressure may rupture thin sclera behind a rectus insertion. Lens-zonule damage, angle recession, retinal dialysis and posterior scleral rupture are therefore linked consequences of the same deformation. A normal-looking cornea does not exclude an occult posterior rupture.

Assessment of ocular mechanical trauma ^[1]:

Is it likely to be an open globe injury? Consider:

• Mechanism of injury: sharps, high impact force, severe injury (e.g., multiple trauma, serious head injuries)
• Foreign body in high-velocity injuries (e.g., hammering, drilling, explosion)
• Risk factors: prior eye surgeries (old surgical wounds are weak points), lack of protective eyewear, contamination

Physical examination may not always be feasible at bedside ^[1]:

• Difficult if soft tissue swelling, profuse bleeding, or pain → do not force open
• Must be very gentle
• Avoid manipulation that exerts pressure on the eye (e.g., lid retraction, putting lid speculum, direct contact with globe)
• Do not remove any protruding foreign body or tissues from the eye

The two gross-swelling photographs are a safety test, not a diagnosis challenge. Severe lid oedema, bleeding and a protruding object can make the globe impossible to inspect. Inability to see the eye is not permission to force it open; preserve the object in place, shield without pressure and use mechanism plus imaging/specialist assessment.

Signs of open globe ^[1]:

• Obvious corneal or scleral lacerations
• Uveal prolapse (dark brown/black tissue protruding through the wound — this is iris/ciliary body/choroid)
• Peaked pupil (iris tissue plugging the wound distorts the pupil toward the laceration site)
• Volume loss (the eye is soft/hypotonus because aqueous/vitreous has leaked out)
• Protruding foreign body
• Bullous subconjunctival haemorrhage (may mask an underlying scleral rupture)

The image grid demonstrates four distinct clues: dark uveal tissue prolapsing through a wound; an embedded metallic object that must be left in situ; a teardrop pupil pointing toward the wound; and 360° raised haemorrhagic chemosis concealing the sclera. None should prompt bedside probing.

Other signs of ocular injury ^[1]:

• Hyphaema: blood in the anterior chamber (visible as a fluid level or diffuse red tinge)
• Iridodialysis: disinsertion of the iris root from the ciliary body
• Lens subluxation/dislocation: disrupted zonular fibres → lens shifts or falls into vitreous
• Aphakia: absence of the lens (traumatic extrusion through wound or dislocation into vitreous)

In the companion image grid, the horizontal blood level is hyphaema; the peripheral black crescent at a torn iris root is iridodialysis; a visible lens edge with an aphakic crescent indicates lens subluxation; and the final eye lacks a lens in the pupillary axis. These are consequences of blunt-force deformation, not proof by themselves that the globe wall is intact.

Hyphaema deserves special mention: It is one of the most common findings in blunt ocular trauma. A small hyphaema (microhyphaema or < 1/3 anterior chamber) may resolve spontaneously. A total hyphaema (8-ball hyphaema) is a vision-threatening emergency because blood blocks aqueous outflow → acute IOP elevation → optic nerve damage, and blood staining of the cornea. Patients with sickle cell trait/disease are at particularly high risk of complications from even small hyphaemas because sickled red cells block the trabecular meshwork more easily.

Management of open globe injury ^[1]:

• Emergency ophthalmology consultation
• Urgent surgical repair as soon as the patient can safely undergo it (the lecture uses “within 24 hours”)

Pre-operative measures ^[1]:

• NPO (nil by mouth — patient needs general anaesthesia for repair)
• Bed rest — avoid cough or straining (any Valsalva raises IOP → may extrude intraocular contents)
• Pain management — reduces patient distress and involuntary straining
• Treat nausea and prevent vomiting — vomiting dramatically raises IOP
• ±Tetanus prophylaxis — especially for contaminated wounds, soil/vegetable matter
• Eye shield after initial examination — rigid, non-contact shield that protects the eye from inadvertent pressure

Eye shield: rigid, non-contact ^[1]

The eye shield is a critical concept: it is NOT an eye pad (soft gauze pad that contacts the eye). A rigid shield (e.g., a plastic or metal cup) rests on the bony orbital rim and does not touch the globe, preventing any external pressure that could worsen an open globe injury.

Additional pre-operative measures include prompt broad-spectrum systemic antibiotic prophylaxis according to the local open-globe pathway, an antiemetic, analgesia, tetanus assessment and head elevation. Do not instil drops or ointment, perform a Seidel test, measure IOP or manipulate the wound once an open globe is obvious unless the ophthalmic team specifically directs it [6,8].

Blunt trauma to the orbit commonly causes orbital blowout fractures — the orbital floor (maxillary bone) and medial wall (lamina papyracea of the ethmoid) are the thinnest walls. Entrapment of the inferior rectus muscle in a floor fracture → restriction of upgaze → diplopia. On CT, you see a "trapdoor" defect in the orbital floor with herniation of orbital fat ± muscle into the maxillary sinus, and there may be a fluid level in the sinus (blood).

Clinical clues: infraorbital numbness (infraorbital nerve runs along the orbital floor), enophthalmos (sunken eye from expanded orbital volume), subcutaneous emphysema (communication with paranasal sinuses).

Retrobulbar haemorrhage after trauma can cause orbital compartment syndrome — a true ophthalmic emergency. The orbit is a closed bony cone; blood accumulating behind the globe raises intraorbital pressure → compresses the optic nerve and central retinal artery → irreversible blindness within 60–120 minutes.

Management: immediate lateral canthotomy with inferior cantholysis by a trained clinician when the clinical diagnosis is made; do not wait for CT in a threatened eye. The aim is to release the lateral canthal tendon and decompress the orbit while definitive ophthalmic/trauma care is arranged.

Blunt or penetrating injury can damage the optic nerve directly or indirectly. Suspect it with otherwise unexplained visual loss, dyschromatopsia, field loss and RAPD after trauma. Urgently exclude globe, orbital compartment and compressive/vascular injuries. The AAO evidence review found no consistent benefit from systemic corticosteroids or optic-canal decompression for indirect traumatic optic neuropathy; observation versus intervention is a specialist, case-specific decision, not a reflex megadose-steroid order ^[10].

The most feared complication of open globe injury is bacterial or fungal infection within the eye, especially after a contaminated wound or retained organic IOFB. Reduced vision, hypopyon and vitritis are major clues; pain may be variable. It requires emergency ophthalmic sampling and intravitreal therapy, with vitrectomy selected by the treating team.

A rare bilateral granulomatous panuveitis can follow penetrating trauma or intraocular surgery. The historic “enucleate within 14 days” rule is not evidence-based prophylaxis: contemporary reviews and a 2023 meta-analysis do not show that primary eye removal reliably prevents sympathetic ophthalmia. Primary repair and globe preservation are usually attempted when feasible; removal of an unsalvageable, blind painful eye is an individual multidisciplinary decision [11,12].