In the United States alone, over 1.5 million people suffer eye injuries per year and over 40 000 of these injuries are associated with some degree of permanent visual loss. When eye infections and other non-traumatic eye emergencies are also taken into account, these numbers are more than quadrupled. In the acute setting, differentiation between the potentially blinding eye injury and a less severe problem must be made: physicians must be able to identify the true ocular emergency, initiate appropriate care, and know when to obtain further consultation.

A good history is important in evaluating eye emergencies, as it is with any other medical problem. The presence of altered vision, pain, swelling, haemorrhage, or discharge must be ascertained. Any history of trauma is fully reviewed to establish the exact mechanism of injury. The past ocular history may also be very important, as it relates to pre-existing visual acuity loss, eye disease, or eye trauma.

The emergency eye examination is divided into six sections: vision, lids/orbit, anterior segment, pupils and extraocular movement, posterior segment, and intraocular pressure. Since some serious eye problems are not readily apparent, a systematic progression through all six sections of the eye examination is required in every emergency evaluation.

Documentation of visual acuity for each eye separately is crucial for proper diagnosis, case management, and medical/legal documentation. The only indication for delaying visual acuity assessment is when a chemical burn requires emergency irrigation: vision is tested after completion of this procedure. The patient should be asked to read a standard eye chart. If this is not possible, the patient is asked to count the fingers on the examiner's hand, detect hand movement, or perceive light. The precise level of visual acuity performance is recorded. Visual field testing by assessing the patient's response to hand movement in the four peripheral quadrants of vision is appropriate for patients with altered vision, head trauma, or other neurological complaints.

The lids are assessed for completeness of elevation and closure, marginal integrity, swelling, and colour. Foreign bodies on the surface of the eye are often hidden under the inner surface of the upper lid or in the cul-de-sac formed by the reflection of upper lid and globe conjunctivia. Examiners must be able to evert the upper lids to inspect for such foreign bodies. Simple eversion of the upper lid is performed by instilling a topical anaesthetic and asking the patient to look down. A cotton applicator tip is placed beneath the orbital rim and the eye lashes are grasped with the other hand: the eyelid is flipped over the applicator stick which serves as a fulcrum. Many foreign bodies will be found on the everted lid surface. Following trauma, examination of the orbit should include palpation for subcutaneous emphysema and defects in the orbital rim. Areas of hypaesthesia are established, as well as the presence of exophthalmos or enophthalmos.

The sclera and conjunctivia are inspected for foreign bodies, lacerations, discharge, swelling, and vascular injection. The cornea should be clear and lustrous. The light reflex from a hand-held flashlight should be crisp and sharp. Any alteration in the light reflex implies corneal pathology. Instillation of topical fluorescein will help to confirm the presence of a corneal abrasion. The anterior chamber is the aqueous filled space between the cornea and iris/lens diaphragm. It is inspected for the presence of blood (hyphaema) or pus (hypopyon). The iris is evaluated for alteration in shape or contour: it may protrude from the eye in full thickness globe lacerations. The lens is situated in the pupillary axis behind the iris diaphragm. It is normally clear and any opacification implies cataract formation.

The pupils should be black, round, equal, and reactive to light. Any non-black pupil implies opacification in the media of the anterior chamber, lens, or vitreous. Pupillary eccentricity may occur after trauma and is often associated with serious ocular damage, such as a ruptured globe. Abnormal pupillary reaction to light or size may be important clues to the presence of intracranial pathology in patients with head trauma. Critical assessment for an afferent pupillary defect (Marcus-Gunn pupil) is important in any case of trauma or reduced vision. Extraocular movement is checked by determining the extent of excursion in the four cardinal positions of gaze—up, down, right, and left.

The posterior segment, which includes the vitreous, retina, and optic nerve, is assessed by direct ophthalmoscopy. Pupillary dilation facilitates examination and can best be accomplished by topical application of tropicamide 1 per cent eyedrops in combination with phenylephrine 2.5 per cent eyedrops. Dilation should be used with caution in patients with a history of head trauma because of the need to monitor pupillary signs. The risk of precipitating angle closure glaucoma is very small with pupillary dilation and should not prevent the use of mydriatic drops if important information can be gained by their use.

Intraocular pressure is measured if the differential diagnosis of the presenting complaint includes acute glaucoma. The intraocular pressure should not be measured if a ruptured globe is suspected. Intraocular pressure is most accurately measured by slit lamp applanation tonometry or hand-held Schiotz tonometry. In addition, the extremely firm eye of a patient with acute glaucoma and markedly elevated intraocular pressure can readily be detected by comparing the tactile pressures of the globes. Tactile intraocular pressures are established by palpating the globes through closed eyelids.

Radiographic evaluation of the orbit is helpful in patients with suspected ruptured globes, intraocular or intraorbital foreign bodies, orbital fractures, orbital haemorrhage, orbital abcess, or abnormal globe position. For assessment of fractures and radioopaque foreign bodies, the prefered imaging series includes posteroanterior and lateral views, with Caldwell, Waters, and base projections. CT scanning has superseded plain radiographic evaluation in many cases and should be used whenever possible.

The one ocular emergency that requires immediate treatment is a chemical burn of the eye. Immediate irrigation is the treatment of choice. Although the full effects of chemical burns may take days or weeks to become manifest, the damage itself occurs within the first minutes to hours after the chemical injury. Alkaline burns are often more dangerous than acid burns, because of more rapid penetration of ocular tissues by alkaline agents.

Chemical burns are treated most effectively by irrigation at the site of injury. When a telephone call is received regarding such an injury, the caller should be instructed to start irrigation immediately with the nearest irrigation source available. If trained emergency personnel are not present at the site of injury, copious irrigation should be performed for 5 min, and the patient should then seek help at an emergency centre. Instillation of topical anaesthetic drops makes the patient comfortable and allows more effective irrigation to be performed. The eyelids are retracted and any particulate chemical matter is removed. A continuous flow of normal saline through an intravenous tubing set is directed across the ocular surface. Neutralizing solutions to negate the alkalinity or acidity of the offending chemical are not required. After completion of irrigation and removal of particulate matter, the ocular surface pH is checked and confirmed to be normal. A topical cycloplegic agent to reduce ciliary muscle spasm and a topical antibiotic are instilled. This is followed by application of a sterile eye patch. Prompt referral to an ophthalmologist is recommended as patients with severe burns (Fig. 1) 2331 may require admission to hospital for medical and/or surgical management.

Thermal injuries commonly involve the face and ocular adnexae. Fortunately, the blink reflex and Bell's reflex which turns the eye upward when the lids close, usually protect the globe. Thermal corneal abrasion occurs occasionally and these injuries are best treated with a topical cycloplegic agent and topical antibiotic. Routine burn care is required for the skin of the lids and periorbital tissues. Emphasis is directed towards minimizing scarring during the healing process so that subsequent cicatricial changes in the lid do not result in ocular exposure or misdirection of eyelashes.

If lid closure is compromised, either acutely or chronically, a moist chamber must be provided to protect the exposed cornea. Failure to maintain hydration of an abraded cornea can result in perforation within hours to days. To achieve moist chamber protection, lubricate the surface of the eye with ophthalmic ointment or drops. If necessary, apply sterile Vaseline to the skin of the orbital rim and place a polyethylene sheet (Saran Wrap) over the orbital area. Skin grafting and lid tarsorraphy may be needed at a later date to establish proper lid position and adequate globe protection.

A full thickness corneoscleral laceration is a surgical emergency, but it is not always easy to make the diagnosis. Vision may be excellent, and the external appearance of the globe may be normal. The history often provides clues to the diagnosis of an occult globe rupture or intraocular foreign body. Suspect a ruptured globe whenever a patient has been engaging in activities involving metal-on-metal contract. A history of penetrating trauma or significant blunt trauma should raise the suspicion of globe rupture. Because the sclera is thinnest underneath the rectus muscles, blunt injury can cause rupture and scleral dehiscence in these areas.

Important signs may herald the presence of a ruptured globe (Fig. 2) 2332. A large subconjunctival haemorrhage with swelling may overlie a scleral rupture. Uveal prolapse, indicated by the presence of pigmented iris or ciliary body on the surface of the globe, confirms globe rupture. A traumatic hyphaema should be considered a ruptured globe until proven otherwise. An irregular or pear-shaped pupil often points in the direction of a corneoscleral laceration. Any focal opacification of the lens may represent foreign body penetration. Such focal changes may stand out as white changes against the black pupillary space when examined with a penlight, or as a dark silhouette against the brighter red reflex of the fundus when the eye is examined with a direct ophthalmoscope.

If a ruptured globe is suspected, stop the examination and place a protective shield over the eye. Do not patch the eye: the pressure of an eye patch may forcefully extrude intraocular contents. Avoid any further ocular manipulation and do not proceed with periocular surgery. Tetanus prophylaxis is indicated. An immediate referral to an ophthalmologist is indicated for urgent surgical repair. If there is likely to be any delay in surgical repair, topical antibiotic drops (not ophthalmic ointments) may be placed in the eye. Intravenous therapy with antibiotics effective against both Gram-positive and Gram-negative organisms is indicated. Radiographic and CT studies should be performed if intraocular foreign bodies are suspected.

Microsurgical repair represents definitive treatment. Repair aims to restore normal ocular architecture and minimize scarring in the visual axis. Prompt treatment restores useful vision in many eyes. One rare, but important, potential complication of corneoscleral lacerations is sympathetic ophthalmia, a bilateral granulomatous uveitis. Patients suffering penetrating ocular trauma should be carefully evaluated during the first 14 days following injury. If there is no potential for restoration of vision in the injured eye, its removal should be considered in order to guard against the development of sympathetic ophthalmia in the fellow eye.

Blunt or penetrating trauma may tear iris vessels, resulting in hyphaema (a layering of blood in the anterior chamber): the presence of hyphaema confirms serious eye damage. Associated glaucoma, lens injury, or posterior segment damage are present in 25 to 30 per cent of these patients. Globe rupture must also be considered. Protection of the eye with a shield and immediate ophthalmic consultation are mandatory. Elevation of the patient's head promotes dependent settling of the blood and facilitates further evaluation. Surgical exploration may occasionally be needed to rule out rupture of the globe.

Many patients with hyphaema are treated with topical cycloplegic agents, topical and/or systemic, and systemic antifibrinolytic agents. Activity restriction and globe protection are required during the first 5 days, because this is the critical time for rebleeding. Rebleeding may be associated with glaucoma and corneal blood staining and is associated with reduced visual prognosis.

Blunt orbital trauma commonly results in lid swelling and ecchymosis. It occasionally causes orbital fractures, retrobulbar haemorrhage, and globe rupture. The uncomplicated ‘black eye’ characterized by swelling, ecchymosis, and subconjunctival haemorrhage is best treated with cold compresses and non-aspirin-containing pain relief. Rarely, haemorrhage occurs in the retrobulbar space, resulting in proptosis and elevated intraocular pressure. A retrobulbar haemorrhage with compromised visual function is treated with topical &bgr;-blockers and intravenous carbonic anhydrase inhibitors to reduce intraocular pressure. Patients may also benefit from intravenous osmotic agents, such as 25 per cent mannitol. Surgical decompression of the orbit may be needed if medical measures are not effective.

Fractures resulting from blunt trauma most commonly involve the thin inferior or medial orbital walls. Signs of possible orbital fracture include restricted eye motility, enophthalmos, epistaxis, hypaesthesia over the infraorbital nerve distribution, palpable orbital rim stepoff fractures, orbital emphysema with crepitance, and cerebrospinal fluid rhinorrhoea. Definitive diagnosis requires radiographic confirmation (Fig. 3) 2333. CT scanning has largely replaced X-ray tomography in determining the extent of inferior blow-out fractures. Supportive treatment of orbital fractures includes cold compresses and analgesics that do not contain aspirin. Systemic antibiotics may be indicated because of the associated sinus trauma. Eye and ENT consultation is indicated. Orbital fractures are rarely surgical emergencies: if surgery is indicated, it is often best performed 4 to 10 days after the injury.

Profound visual loss following blunt orbital trauma may be caused by an optic nerve injury. Such patients may benefit from intensive systemic corticosteroids or immediate surgical decompression of the optical canal.

As with orbital trauma, the physician evaluating lid lacerations must consider the possibility of deeper penetration. In many cases, the diagnosis and treatment of occult globe injury takes precedence over the more readily apparent lid laceration.

Superficial lacerations not involving the lid margin should be cleaned and debrided of foreign material. Tetanus prophylaxis is indicated. Surgical repair is directed at maintaining full lid function and good cosmesis. Traction on the lid margin should be avoided to minimize lid margin distortion.

Several types of lacerations call for particular care and handling (Fig. 4) 2334. First any laceration extending into the medical third of the upper or lower lid may involve the tear drainage canalicular system. Surgical repair must include co-optation of the severed canaliculi. Second, deep lacerations of the superior portion of the orbit may involve the lid elevator (levator aponeurosis) resulting in an inability to raise the lid. To avoid ptosis, the levator aponeurosis tear must be recognized and repaired at the time of initial injury. Third, lacerations with fat prolapse imply deep penetration through the orbital septum. These lacerations are associated with a higher incidence of globe penetration, foreign bodies, lid functional impairment, and infection. Fourth, full thickness lacerations involving the lid margin must be repaired in layers: tarsus, subcutaneous tissues/orbicularis muscle, and skin. Improper closure may lead to notching of the lid margin, impaired lid function, and long-term breakdown of the ocular surface. Fifth, avulsion injuries often require repair based upon skin flap mobilization and skin grafts. Any piece of avulsed lid tissue should be saved for potential use in skin grafting.

Corneal abrasions rarely threaten vision, but result in significant patient complaints because of foreign body sensation, tearing, and light sensitivity. A topical anaesthetic promptly relieves the pain; topical fluorescein highlights the area of cornea affected (Fig. 5) 2335. Foreign bodies must be searched for by everting the upper lid. A foreign body on the conjunctival surface may be removed by irrigation or with a cotton swab. Foreign bodies on the surface of the cornea are best removed using the magnification of loupes or a slit lamp. A 25-gauge needle or spud is used to flip the foreign body off the surface of the cornea. Residual rust rings may require more manipulation.

Patients with corneal abrasions following removal of foreign bodies require treatment with topical antibiotic and cycloplegic drops. A pressure patch is applied to maintain lid closure. Most corneal defects heal by epithelial migration under the closed lid within 24 h. Systemic analgesics may be necessary. Topical anaesthetics should never be prescribed for home use by the patient because a painless epithelial defect may develop to an infected corneal ulcer.

The most important considerations in the differential diagnosis of the red eye are conjunctivitis, iritis, corneal infection, and acute glaucoma.

Conjunctivitis or ‘pink eye’ is the most frequent cause of red eye presenting to the physician. Infectious conjunctivitis may be caused by bacteria or viruses: both are associated with tearing, ocular injection, discharge with crusting of the lids, and mild discomfort. More exuberant mucopurulent discharge is characteristic of bacterial infections; palpable preauricular nodes are common in patients with viral infections. The corneas are clear on penlight or slit lamp examination. Moist compresses and topical antibiotics are used to treat both forms of conjunctivitis. Gram-positive organisms are the most common causes of bacterial conjunctivitis and this must be kept in mind when selecting antibiotics.

Neonatal conjunctivitis is a potentially serious concern because of the possibility of gonococcal infection: Neisseria gonorrhoeae is the only bacterial species that can penetrate intact corneal epithelium. A minor external conjunctivitis can turn into a virulent endophthalmitis which is vision threatening. Topical and systemic therapy, including possible hospital admission, most be co-ordinated by the ophthalmologist and pediatrician.

Allergic conjunctivitis is seasonal in presentation and associated with itching, tearing, and ocular injection. Discharge tends to be less prominent. These patients are best treated with cold compresses and a topical vasoconstrictor combining an ocular decongestant and antihistamine.

Iritis is a term used for intraocular inflammation, in contrast to an external infection such as conjunctivitis. Patients often complain of blurred vision and light sensitivity. The eye is red but the injection tends to be accentuated in the circumcorneal area. The pupil is often constricted when compared to the fellow eye. The cornea is generally clear, but may be hazy if the intraocular pressure is elevated. Definitive diagnosis requires a slit lamp to detect inflammatory cells in the anterior chamber. Treatment includes topical cycloplegics and topical steroids. Topical corticosteroid treatment should never be initiated without discussion with an ophthalmologist. Short-term steroid treatment can unmask latent Herpes simplex keratitis; in the long term it can cause glaucoma or cataract.

Corneal infection manifests as a focal infiltrate in the normally clear and lustrous cornea. The patient has a sensation of a foreign body and an altered corneal reflex on penlight examination. This is a vision threatening emergency and Gram stains and cultures must be performed on specimens taken from the involved area to determine whether the infection is bacterial, viral, or fungal in origin.

Bacterial corneal infections may progress rapidly and require institution of topical antibiotic therapy, at a frequency up to every 30 min. The incidence of corneal infections has increased with the increasing popularity of extended-wear contact lenses. Gram-negative infections are more common in these patients. If there is any doubt as to the type of corneal infection, broad spectrum topical antibiotics effective against both Gram-negative and Gram-positive organisms should be provided. Herpes simplex keratitis constitutes a special type of corneal infection. Classically, patients have a dendritic pattern of fluorescein staining on the cornea when viewed with a cobalt blue light. These patients require topical antiviral therapy. Topical steroids may exacerbate the problem. Fungal ulcers require topical antifungal therapy. An ophthalmologist should be actively involved in the care of patients with corneal infections.

Acute angle closure glaucoma results from a sudden obstruction of aqueous outflow within the eye. Iris tissue blocks the outflow structures and intraocular pressure rises dramatically. Patients have a deep-seated aching pain which is often severe: this pain may even be referred to the chest and abdomen with associated nausea and vomiting. Vision is reduced because of corneal oedema. There is a mottled light reflex from the oedematous cornea. Elevated intraocular pressure is confirmed by tactile testing or tonometry. The ophthalmologist should be involved as quickly as possible. Initially, medical therapy is instituted, including a topical &bgr;-blocker, topical pilocarpine, and intravenous carbonic anhydrase inhibitors. An oral or intravenous hyperosmotic agent may also be indicated. In most cases, definitive therapy requires creation of a laser or surgical iridectomy to relieve iris pupillary block.

Cellulitis may occur anterior or posterior to the orbital septum. The majority of these infections are due to contiguous sinus disease or associated dacryocystitis. Anterior preseptal cellulitis is associated with swelling, redness, and occasional discharge. Orbital cellulitis, with penetration deep to the orbital septum, may be heralded by decreased vision, impaired ocular motility, an afferent pupillary defect, increasing proptosis, or optic nerve swelling.

All orbital infections should be cultured and Gram-stained as appropriate. Preseptal cellulitis generally responds to warm compresses and topical and oral antibiotics. Orbital cellulitis requires more aggressive systemic treatment, including intravenous antibiotics and more extensive ophthalmological, ENT, and radiographic evaluation to determine the underlying cause. Diabetic, chronically ill, or immunologically compromised patients with cellulitis are at particularly high risk of developing a fungal infection (phycomycosis) that may be fulminating and life-threatening.

Acute, non-traumatic loss of vision generally arises from a problem with the optic nerve or retina. The most important causes of painless loss of vision are central retinal artery occlusion, central retinal vein occlusion, vitreous haemorrhage, and retinal detachment. Painful loss of vision is associated with optic neuritis and temporal arteritis. Optic neuritis, which tends to occur in younger patients, is associated with painful movement of the eye. Temporal arteritis affects a more elderly population and presents with a characteristic unilateral headache.

The two causes of acute loss of vision that require immediate treatment are central retinal artery occlusion and temporal arteritis. Central retinal artery occlusion usually presents as sudden, profound loss of vision in one eye of an elderly patient; it may be intermittent at first. Vision is reduced to counting fingers or to the light perception level, and an afferent pupillary defect is present. Ophthalmoscopic examination reveals narrowed retinal arterioles and a ‘cherry red spot’ macula (Fig. 7) 2337. Emergency treatment is directed at maximizing circulation to the optic nerve and retina. The circulation is enhanced with rebreathing of CO&sub2;, topical &bgr;-blockers, intravenous carbonic anhydrase inhibitors, and intermittent digital massage if retinal emboli are documented. A surgical paracentesis for immediate decompression of the globe may be performed by an ophthalmologist. All patients require neurological evaluation to determine the source of the vascular occlusion.

Temporal arteritis is potentially blinding to both eyes. Patients present with decreased vision and exquisite tenderness over the forehead or scalp. An afferent pupillary defect is present and there may be haemorrhagic optic nerve swelling. Generalized symptoms of polymyalgia rheumatica may be present. If the erythrocyte sedimentation rate is elevated, oral systemic steroids are required. Immediate steroid therapy minimizes the chance of bilateral optic nerve damage. A temporal artery biopsy can subsequently be performed on a more elective basis to confirm the diagnosis.

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