• Clinical assessment of eye injuries involves a thorough history (mechanism of injury, symptoms experienced, past medical and ophthalmic history) and examination (visual acuity, eversion of eye lid, ophthalmoscopy, and slit lamp examination)

May give rise to restricted eye movement and proptosis. These findings may make examination of the underlying structures difficult however more serious underlying injury such as an orbital fracture should be suspected.

Treatment: Elevate the head, instill topical anaesthetic drops. Use Desmares lid retractors to facilitate inspection of the globe. Do not force the eyelid open. In uncomplicated cases the swelling resolves in two to three weeks. Treat with an ice pack, head elevation and reassurance.

Most commonly metallic or glass particles lodging in the corneal surface. Resulting from grinding or hammering. Symptoms include pain, foreign body sensation, and lacrimation. Signs: slit lamp examination may reveal a foreign body, if metallic it may be surrounded by rusty infiltrate.

Treatment: Instill two to three drops of local anaesthetic. Under slit lamp magnification, with the patient focussing on a distant object, remove with a sterile 21g needle, with the doctor’s hand resting on the patient’s cheek to reduce relative movement. Gently prise off the foreign body. Beware: repeated applications of topical anaesthetic slows healing and may result in epithelial toxicity. Once the foreign body is removed, the remaining corneal abrasion is examined and treated with topical antibiotics and an eye patch. Multiple surface foreign bodies may be more easily removed by irrigation or a cotton tipped applicator soaked in local anaesthetic. Some deeply embedded inert foreign bodies such as non-leaded glass may be left in as removal may lead to extensive scarring. In addition, do not remove deep foreign bodies as removal may risk an aqueous leak. Cover the eye with a protective metal shield and refer the patient for surgical management. In the suspicion of penetrating eye injury, careful inspection in the area of the conjunctival laceration is always required to rule out a scleral laceration or an intraocular foreign body. Dilated retinal examination is required to look for retinal damage or intraocular foreign body. Consider a CT scan (axial and coronal views) to exclude an IOFB or a ruptured globe.

A superficial injury resulting from a sharp object, for example a rose thorn. They may produce symptoms of mild pain, eye redness, lacrimation, blepharospasm or a foreign body sensation. Subconjunctival haemorrhages are commonly present. Slit lamp examination with white light may reveal a torn conjunctiva. The edge of the laceration stains brightly with fluorescein dye. Local anaesthetic is instilled and the conjunctiva is gently explored with a moist cotton swab, opened up and sclera exposed, to exclude possible perforation or scleral laceration. Treatment: The conjunctiva has a protective role rather than a structural role. That is why conjunctival lacerations <1cm heal without suturing. Lacerations >1cm or if Tenon’s capsule has been torn, requires suturing with 6.0 or 8.0 Dexon or Vicryl (absorbable sutures) under topical anaesthetic. Use topical antibiotics for 5-7d and an eye patch for 24h. Follow up for large lacerations is in 7d. For full thickness lacerations see ‘ruptured globe’.

Corneoscleral lacerations are partial or full thickness lacerations through the cornea or sclera. They commonly result from adults work related injuries involving small projectile fragments or child injuries caused by pens, needles or sharp toys. The patient may complain of decreased visual acuity, pain, or lacrimation. The globe should be handled cautiously to avoid applying pressure that might rupture a partial thickness laceration or herniate the ocular content of a full thickness laceration. If a ruptured globe is suspected or if signs of perforation become apparent, then no further examination should be done. The eye is lightly padded and protected with a shield and the patient is prepared for further examination and repair in the operating theatre.

Partial thickness laceration. A complete ocular and slit lamp examination is required. Look for signs of perforations (see Ruptured globe). A drop of 2% fluorescein placed on the cornea over a possible entry site will become diluted by the issuing aqueous, turn green and fluoresce (positive Seidel’s test). Applanation tonometry may reveal hypotony. Inspect for a shallow anterior chamber, pupil asymmetry, cataract formation or lens capsule rupture.

Treatment: The goals are to prevent infection, promote stromal healing, minimize scarring or surface irregularities and prevent irregular astigmatism. Shallow lacerations are treated with cycloplegics (5% homatropine), prophylactic antibiotics (0.3% gentamicin) and a patch. Occasionally therapeutic soft contact lenses (TSCL) are used for 2-4 weeks until healing is complete. Long partial thickness corneal lacerations accompanied by a wound gape are often sutured closed in theatre. Daily follow-up is required until healing is complete.

Full thickness lacerations (see ruptured globe). Full thickness lacerations that do not violate the limbus, do not have uveal or vitreous incarceration, are small (<3mm) and are self healing, may respond to non-operative measures such as TSCL to support the wound as it heals. Aqueous humour suppressants (acetazolamide, topical beta-blockers), antibiotics (0.3% ciprofloxacin) and cycloplegics (2% cyclopentolate1) are used. Cyanoacrylate tissue adhesive is useful for non-self sealing puncture wounds less than 2mm, or in the visual axis (sutures would impinge vision).

Require a complete ocular examination including a dilated retinal examination. Suspicion of an orbital foreign body, ruptured globe or significant orbital trauma requires a CT Scan (axial and coronal views with 1.5cm cuts). Simple skin lacerations in the periorbital area are cleaned with Betadine. The wound is irrigated with a syringe containing saline. Search for a foreign body. Isolate a surgical field with sterile drapes. Cover the eye with a protective shield. Suture the various lacerations as follows:

Simple skin lacerations use interrupted stitches under direct vision with fine non-absorbable 6.0 nylon. Remove sutures in 4 days. Deep lacerations of the eyelid are closed in two layers. Interrupted 6.0 absorbable sutures (Vicryl) are used to close the deeper tarsal layer without breaching the conjunctiva. Cut close to the knot. The superficial orbicularis and skin are closed with interrupted 6.0 non-absorbable sutures (nylon).

Eyelid margin lacerations must be accurately apposed to prevent deformity. Repair is carried out under sterile conditions using an operating loupe. Repair of the lid margin takes place prior to the skin repair. The lid margin is aligned using absorbable 6.0 suture (Vicryl), which is passed subcutaneously through the orbicularis muscle and the tarsal plate. A single throw is placed to test correct alignment. Two further subcutaneous absorbable sutures, 6.0 Vicryl, are placed in a similar way further away from the lid margin and spaced at regular intervals. Once tied, the suture ends are left long. The skin is sutured from lid margin downwards, (using two layers if the laceration is deep). The long ends of the three eyelid margin sutures are tied under the knot of the uppermost skin suture to prevent the suture ends from rubbing against the cornea. Topical antibiotics are applied and a course of systemic antibiotics in the case of contamination (dicloxacillin) or human/animal bites (cephalexin). Potentially contaminated wounds may benefit from a delayed wound closure of 2 days. Eyelid marginal sutures are removed in 10-14 days and skin sutures 4-6 days.

Complex eyelid lacerations are those associated with severe ocular trauma (e.g. ruptured globe), involve the lacrimal apparatus, the levator aponeurosis producing ptosis or the superior rectus muscle exposing orbital fat, avulsion of the medial canthus tendon, associated with intraorbital foreign body and those involving extensive tissue loss or distortion of the anatomy. Treatment: require complex surgical repair.

Presence of an IOFB must be excluded in all ocular injuries. A history of hammering metal-on-metal is highly suggestive. IOFB’s cause ocular damage by disrupting the normal anatomy, introducing infection, scar tissue formation and inflammatory reactions to the retained foreign body. Symptoms include pain or decreased vision. Clinically detectable signs may be absent, however if history is highly suggestive of a penetrating injury, it is important not to cause further damage by doing a rigorous examination. Signs suggestive of a penetrating injury: hyphema, subconjunctival hemorrhage, irregular pupil, anterior or posterior segment inflammation, decreased intraocular pressure, or a hole in the iris seen by retroillumination. Slit-lamp examination; search the anterior chamber and iris for a foreign body and look for an iris transillumination defect (direct a small beam of light through the pupil and look at the iris for a red reflex). Examine the lens for disruption, cataracts, or IOFB’s.

Investigations: Plain radiology is indicated for all ocular injuries involved in hammering or chiseling injuries involving metallic bodies (PA and lateral views ) and CT scan or ultrasound for non-metallic bodies ( MRI scan is contraindicated for metallic bodies). Treatment: transfer the patient supine. Nil by mouth. Place a protective shield over the involved eye and cover the contralateral eye with soft conjugate movement. In addition, note tetanus prophylaxis, culture entry site and give IV antibiotics. Surgical removal of the IOFB is always indicated. Surgical repair involves suturing the entry site and the planned removal of the foreign body (FB) at a later date. Metallic FB’s require removal within 24h. Anterior FB’s are removed by corneal section and if the lens involved, lensectomy. Posterior FB’s are removed by FB forceps following a vitrectomy. Inert FBs such as glass, stone, and plastics may not need removal but simply observed periodically for signs of inflammation.

• Do not cause further damage with a rigorous examination if clinical history is highly suggestive of penetrating injury
• X-ray is indicated for all injuries involving metallic particles

A ruptured globe is a full-thickness traumatic disruption of the sclera or cornea resulting from blunt forces causing an abrupt rise in intraocular pressure. Usually arising from work related injuries, violence or sports, the globe decompresses and ruptures through the weakest point, the insertion of the extra-ocular muscles or the corneo-scleral junction. Diagnosis is usually obvious but may be occult. Symptoms and signs suggestive of globe rupture include pain, deceased visual acuity (a normal visual acuity is rarely present in a globe rupture), extensive subconjunctival haemorrhage (often involving 360 degrees of bulbar conjuctiva), a deep or shallow anterior chamber, hyphaema, low IOP (however IOP can be normal or high), irregular pupil, iridodialysis, cyclodialysis, lens subluxation, commotio retinae, retinal tears, vitreous haemorrhages, obvious corneal or scleral lacerations or intraocular contents may be outside the orbit. Treatment: it is an ophthalmological emergency. Further examination is avoided once diagnosis of ruptured globe is made. Avoid manipulating the eye as pressure on the globe may risk extrusion of the intraocular contents and introduce infection. Protect the eye with a shield, bed rest, NBM , systemic antibiotics to prevent endophthalmitis (cephazolin and gentamicin), tetanus toxoid prn, anti-emetics and analgesia.(topical agents are contraindicated), and consent for the operative procedure. Radiological studies: plain radiographs will detect radio-opaque metal FBs. CT scan (axial and coronal sections 1.5mm apart). Radiolucent materials (wood and plastic) may be detected by MRI and may localize the rupture and exclude an IOFB. Surgical repair involves exploration and repair of various damaged tissues according to a plan formulated prior to operating. Vitreous haemorrhages may predispose to proliferative vitreoretinopathy with scar formation and contraction. A vitrectomy can remove this stimulus and improve anatomical and visual outcome. Extensive injuries to the anterior segment may require secondary reconstruction. Enucleation is indicated as a last resort in the case of continued deterioration of the visual function. The various reconstructive procedures are beyond the scope of this book.

Orbital fractures

Orbital ‘blowout’ fractures strictly only involves the orbital floor and spares the orbital rim. Caused by direct impact of a blunt object just larger than the orbital rim (human fist, squash ball) forcing the eye back into the orbit causing a sudden raise in the IOP and a blowout fracture at the weakest part of the orbit, the thin orbital floor. Herniation of the intraorbital contents into the bony defect may occur. Clinical features include pain (especially on attempted vertical eye movement due to entrapment of the inferior rectus and inferior oblique muscle). For the same reason there is restriction on eye movement particularly elevation and diplopia more marked on vertical gaze. Paraesthesia around the cheek and upper lip below the eye due to damage of the infraorbital nerve. Enopthalmos (measured by an exopthalmometer once swelling has subsided) due to orbital herniation into the maxillary sinus. Other signs may include epistaxis, eyelid oedema and ecchymosis, and subcutaneous emphysema may occur on sneezing or blowing ones nose. Ophthalmological examination includes careful evaluation for rupture, hyphaema or microhyphaema, traumatic iritis, retinal or choroidal damage. IOP should be measured. CT scan of the orbits and brain (axial and coronal views) is indicated if diagnosis is uncertain or surgical repair considered. Treatment: commence broad-spectrum oral antibiotics, instruct the patient not to blow his/her nose, ice packs to the orbit for 24-48h. Less severe cases are treated conservatively. Surgical repair at day 5-10 for more severe injuries, significant entrapment of soft tissues (persistent diplopia), cosmetically unacceptable enophthalmos (greater than 2mm). Patients are followed up and monitored for the development of associated ocular injuries (e.g., orbital cellulitis, angle-recession glaucoma, and retinal detachment).

Medial wall orbital fractures are less common and may give rise to subcutaneous emphysema around the nose and eyelid. Epiphora if the nasolacrimal duct is involved. Weakness of lateral eye movement and diplopia occur if the medial rectus muscle is entrapped. Plain radiographs may show herniated contents in the maxillary sinus and air in the orbit. CT scans provide more information. Treatment: antibiotics to prevent orbital cellulitis, eye padding, patient instructed not to blow nose. Surgical correction is indicated if the medial rectus muscle is entrapped in the fracture.

Traumatic hyphaema is the presence of blood in the anterior chamber of the eye caused by tearing of small ciliary or iris vessels from blunt or penetrating injuries. They are classified according to the percentage of anterior chamber filled with blood. A total hyphaema is often referred to as an “eight ball hyphaema”. Symptoms include a dull ache and reduced visual acuity that improves as the blood settles. Signs: layering of blood inferiorly in the upright patient. A force large enough to produce a hyphema may cause other injuries; angle recession, lens subluxation and peripheral retinal tears.

Complications: rebleeding most commonly between 24-48h, elevated IOP (secondary to red blood cells obstructing the outflow canal of Schlemm), synechiae formation, and permanent corneal blood staining (facilitated by raised IOP). Investigations: measure IOP using applanation tonometry (if very low, suspect a ruptured globe). B-scan ultrasound to exclude retinal detachment. Treatment: aims to decrease risk of future bleeding, reduce complications and screen for other ocular injuries. Most hyphemas spontaneously re-absorb within a week. Mydriatics are used to increase patient comfort and to prevent the formation of synechiae. Anti-emetics, mild analgesia and avoid aspirin, cover the eye with a protective shield. Treat raised IOP>25mm Hg with topical beta-blockers (0.5% timoptol) , acetazolamide or IV mannitol if IOP>35mm Hg. If the IOP remains high, the hyphaema should be treated surgically . Once the hyphema has cleared the drainage angle should be examined by gonioscopy to exclude recession. Some patients may require admission, however compliant patients with small hyphemas may be treated as an outpatient. 1% Atropine daily, slit-lamp examinations and IOP measurement.

A sudden increase in pain or decrease in vision should alarm the patient to return for re-evaluation.

Inflammation of the anterior chamber (iris and ciliary body) as a result of blunt trauma. Symptoms include pain, photophobia, and blurred vision. Inspection may reveal pupillary constriction secondary to spasm or a dilated pupil from traumatic mydriasis. Slit-lamp examination reveals perilimbal injection, white cells and flare reaction. The IOP may be reduced if the inflamed ciliary body is producing less aqueous humour, or increased IOP secondary to inflammatory obstruction of the draining trabecular meshwork.. Other conditions associated an anterior chamber reaction must be suspected such as a traumatic corneal abrasion, traumatic hyphaema, and traumatic retinal detachment. Treatment: cycloplegic agents (2% cyclopentolate).until inflammation subsides. Use steroid drops (1% prednisone acetate). At 1 month perform ophthalmoscopy and gonioscopy to exclude angle recession and retinal breaks or disruption.

Bruising and irritation of the iris sphincter can cause constriction. Small tears in the sphincter muscle fibres can cause dilatation. These defects may resolve over days or be permanent if the muscle fibres are damaged. Treatment is supportive and it is important to inform the patient of pupil asymmetry to avoid unnecessary investigations later.

Avulsion of the iris from its root, giving rise to separation of the iris from the sclera may result from blunt trauma. No specific treatment is required however ophthalmological referral is mandatory, as this condition may appear as a second pupil and can cause monocular diplopia or the cosmetic defect requiring surgical correction.

Acute glaucoma may result from blunt injuries disrupting the canal of Schlemm and narrowing the angle of the anterior chamber. Lens swelling or dislocation, which can impede the outflow of aqueous humour and give rise to an acute elevation of IOP. Treatment is with miotics to increase the angle, topical beta-blocking agents (timolol), acetazolamide to decrease aqueous formation, and in the last instance mannitol.

Traumatic cataract may result from a blunt or penetrating injury. Disruption of the lens capsule will cause the stromal cells to absorb fluid, swell and cloud obscuring vision. Mild injuries lead to small anterior lens opacities that may not progress. More severe trauma may lead to either central posterior opacities which progress or peripheral lens opacities , which tend to be static. Treatment involves observing the cataract progression and allowing retinal pathology to settle for 6 months followed by lens replacement if sight is limited.

Lens subluxation or dislocation results from a severe blunt force applied to the globe in an antero-posterior direction causing stretching of the equatorial region and tearing of the zonule fibres. If more than 25% of these fibres are ruptured then the lens becomes unstable and may give rise to subluxation/dislocation of the lens into the anterior or posterior chamber. Anterior dislocation may give rise to acute angle closure glaucoma and surgery is indicated. Posterior dislocation of the lens into the vitreous may be asymptomatic and requires conservative treatment. A possible sign present is trembling or shimmering of the iris with rapid eye movements termed iridodonesis. If complicated by secondary glaucoma, uveitis, vitreous inflammation, or cataract formation giving rise to visual loss, lens replacement will be necessary.

May occur secondary to tearing of retinal vessels in blunt trauma. One must also suspect retinal and choroidal tears. Symptoms include floaters, and dark streaks that move with the eye (blood in the vitreous humour). Signs include inability to view the fundus and loss of the red light reflex. Ultrasound and indirect ophthalmoscopy are used to evaluate the retina and choroid. Treatment: head elevation, and ophthalmological referral. Delayed vitrectomy is indicated if blood does not resolve, to avoid scarring and retinal traction injury.

Localized crescent shaped tear in the choroid are a result of antero-posterior compression of the globe and occur in the posterior pole (crescenteric shape) or peripherally (radial shape). The patient may complain of decreased visual acuity. Occasionally associated with macular oedema, and complicated by choroidal haematomas which may give rise to vitreous hemorrhages, or choroidal neovascular membrane (CNVM). Fluorescein angiography may confirm the choroid rupture or delineate a CNVM. Treatment: No specific treatment other than observation. Should the patient complain of further loss of vision or angiography delineates CNVM near the fovea laser photocoagulation may be offered.

Direct blunt trauma giving rise to the mechanical disruption of the retinal photoreceptors and diffuse retinal oedema. Symptoms may be decreased vision if oedema located near the macular or asymptotic. Fundoscopy reveals confluent areas of retinal whitening in which retinal vessels are clearly demarcated. Retinal detachment or retinal artery occlusion must be excluded. Treatment: no specific treatment required and usually resolves spontaneously. Patients re-examined in 2 weeks and instructed to return if experience floaters, flashing lights or decreased vision.

Occurs after a penetrating or non-penetrating trauma to the globe. Forces produce a sudden deformation of the vitreous and retinal damage occurs in areas of strong adhesion, such as the anterior vitreous base. Retinal breaks may be horse shoe shaped tears, which may lead to retinal detachment. Retinal dialysis is the separation of the peripheral retina located most commonly in the infra-temporal quadrant. Less commonly progresses to retinal detachment and often settles spontaneously. Breaks and dialysis progress to retinal detachment when vitreous fluid enters the subretinal space. Clinically presents with floaters, photopsia, visual acuity loss (with macula involvement) and field reduction. Treatment: retinal breaks and dialysis are treated with photocoagulation as prophylaxis to retinal detachment. Scleral buckling surgery is indicated for breaks associated with retinal detachment.

Avulsion of the optic nerve behind the optic nerve head results from the shearing forces from blunt trauma. There is either little or no light perception. Examination reveals a total afferent pupillary defect, as shown by no direct or consensual response when light is shone in the affected eye, but an intact response when light is shone in the normal eye (Marcus Gunn). Fundoscopy reveals retinal infarction and large blot haemorrhages. The patient is informed of a poor visual prognosis.

Optic neuropathy may result from compression by haemorrhage, bone, or perineural oedema and laceration of the nerve may result from bone fracture or foreign body. Clinically presents with diminished visual acuity especially colour and exhibits a relative afferent pupillary defect. Fundoscopy shows retinal vein congestion and diminished retinal artery circulation. CT scan is used to detect a FB or to determine the cause of the neuropathy. Treatment: surgical intervention may be indicated with diminished visual acuity with neural decompression but is only successful within the first few hours.

• An ocular emergency. Successful recovery depends on early treatment by an eye surgeon

Probably the most devastating injury to befall an eye is contamination with alkaline substances. These include caustics, concrete or cement and ammonia based liquids.

Such an injury, usually an industrial accident, represents a true ocular emergency. The pH is over 8 and the chemical rapidly passes through the ocular tissues causing thrombosis and tissue necrosis. Pain is extreme and the associated blepharospasm makes treatment difficult.

Emergency treatment consists of immediate irrigation with whatever water is available. The eye is anaesthetized with tetracaine 0.5%, and irrigation is continued with N. Saline until the pH approaches a neutral level. All particulate matter such as concrete must be removed from the fornices, under general anaesthetic if necessary.

Examination of the eye at this stage may show the white necrotic patches of the sclera and conjunctival fornices together with clouding of the corneal stroma.

Alternatively the appearance of a red injected eye is a good and healthy sign. The use of mydriatics and antibiotics is standard. In addition, solutions containing ascorbic acid and steroids is controversial. Prognosis is general poor.

In distinction to alkali injuries, acids cause much less devastating results. The corneal epithelium coagulates and falls off resulting in a large ulcer. The sclera remains viable. Treatment is basic and in the main, recovery is good by comparison.

In this modern day, many synthetic or acrylic compounds are used in industry. In all cases treatment is similar and traditional. Water is ubiquitous as a means of treatment. Cyanoacrylate (Super Glue) causes a dramatic event usually in children who, trying to remove the top of the tube, squirt the rapidly drying liquid into the eye. Fortunately the event cause relatively little injury as the glue does not stick to wet surfaces (cornea), but to the dry lid margins. Separation of the lids manually, leaves the lashes in the coagulum but very little other damage.

Patients exhibiting poor prognostic indicators should be informed of their diminished possibility of return of vision. The most important prognostic indicator is the visual acuity at initial assessment Other poor indicators are presence of an afferent pupillary defect, blunt trauma, immediate loss of vision after the trauma, large scleral lacerations ,and those extending more posteriorly. Penetrating BB gun injuries also have a poor prognosis.

• Many eye injuries are preventable. Simple measures such as education are usually all that is necessary