16: Eyes

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Section 16 Eyes

Edited by Peter Cameron

16.1 Ocular emergencies 568

16.1 Ocular emergencies

David V. Kaufman, James K. Galbraith, Mark J. Walland

Injuries

1 Always assess and record vision.

2 Gentle examination with magnification is essential.

3 X-ray/computerized tomography where bony or penetration injury is suspected.

4 The principal first-aid measure for caustic burns is free irrigation with water, with subsequent removal of any particulate matter.

Painful loss of vision

1 Bacterial keratitis requires intensive, specific, topical antibiotic therapy.

2 Acute primary angle closure produces a rock-hard, inflamed eye with a fixed, mid-dilated pupil.

Painless loss of vision

1 It is imperative to test the pupils for a relative afferent pupillary defect, which is an objective sign of neuroretinal dysfunction.

2 Central retinal artery occlusion requires attempts to lower intraocular pressure acutely and immediate referral to an ophthalmologist is required.

3 Elderly patients with acute visual failure have giant cell arteritis until proven otherwise, and need oral steroid cover until the diagnosis is excluded.

4 Recent onset of distorted vision requires ophthalmic review within 1–2 days to exclude exudative age-related macular degeneration.

5 New onset of floaters, particularly in association with flashes, requires early ophthalmic review to exclude retinal detachment.

6 Local ocular pathology does not cause a visual field defect respecting a vertical midline.

Introduction

Ocular emergencies are common. A relatively trivial traumatic presentation may mask a more serious underlying injury. Similarly, a relatively transient episode of visual loss with no abnormality found on examination may indicate potentially life-threatening cerebrovascular disease. Therefore, all eye presentations in an emergency department (ED) should be carefully evaluated with the necessary equipment.

Basic sight testing equipment should include a Snellen 6-m chart and a black occlusive paddle with multiple pinhole perforations. A slit-lamp biomicroscope is needed for examination of the anterior segment and the removal of foreign bodies.

OCULAR TRAUMA

History

Ocular injuries, however trivial, are a frightening experience for the patient, who may have a deep-rooted fear of blindness. The incidence of injuries varies with the environment and protective measures taken. The major injuries result from blunt trauma or penetrating injuries to the globe, with or without the retention of a foreign body. Mechanical interference with eye movement may result from orbital injury, either haematoma or interference with muscle function. Similarly, neurotrauma may disturb the visual pathways or ocular motor nerves.

It is necessary to elicit a history of the patient’s prior visual status, including the wearing of glasses or contact lenses and ocular medication.

Examination

Visual acuity

After an eye toilet to remove any debris from the eyelids, vision is tested by a distance Snellen chart, if necessary using a pinhole device as a rough focusing aid. Vision less than 6/60 Snellen may be graded by the patient’s ability to count fingers at a measured distance, discern hand movements or to project the direction of a light from various angles. The eye not being tested must be completely shielded by an opaque occluder.

It is essential to assess early whether the patient has sustained a relatively minor superficial injury or a severe injury which may be either blunt or penetrating. Reassurance and extreme gentleness in examining the eye, using topical anaesthetic, will allow a more definite assessment to be made in the ED. With penetrating trauma, any external pressure on the eye may result in ocular structures being squeezed out of the wound, drastically worsening the prognosis.

To open lids that are adherent due to blood or discharge, gently bathe with sterile saline. Wipe the eyelid skin dry and apply gentle distractive pressure to skin below the brow and below the lower lid, i.e. over bony orbital rim to open the lids. Note that no pressure should be applied to the globe.

Investigation

All patients in whom a penetrating injury is suspected require X-ray or computerized tomography (CT) scanning to exclude a radio-opaque intraocular foreign body (IOFB). If there is any possibility of metallic IOFB, magnetic resonance imaging (MRI) scans are contraindicated. When an adequate examination cannot be made, or where occult perforation is suspected, examination under anaesthesia is mandatory.

Management of specific injuries

Superficial injury

Corneal abrasion

The corneal epithelium is easily dislodged by a glancing blow from fingers, twigs, stones or a paper edge. The trauma produces an acute sensation of a foreign body, with light sensitivity and excessive tearing.

After fluorescein staining, the size of the epithelial defect is recorded. Antibiotic ointment (chloramphenicol) is instilled and an eye pad applied if local anaesthetic is used. The condition heals spontaneously within 24–48 h. Large abrasions produce reflex ciliary spasm, which may require short-acting mydriatics such as homatropine 2% in addition to oral analgesia to relieve the pain.

Corneal foreign body

Small ferrous particles rapidly oxidize when adherent to the corneal epithelium, producing a surrounding rust ring within hours. The rusted particle requires removal under adequate topical anaesthesia using a slit-lamp microscope. An adherent rust ring may be loosened by the application of antibiotic ointment and padding for 24 h, after which it is easily shelled out with the edge of a fine hypodermic needle. Mechanical dental burrs may cause large areas of epithelial removal and delay return to work. Wooden splinters are particularly dangerous as they may easily penetrate the eye and cause violent suppuration. In all suspected foreign body injury, the upper and lower lids should be everted and examined with suitable lighting and magnification. The conjunctival fornices may be swept gently with a moist cotton bud under topical anaesthesia.

Penetrating injury

A careful history is important in assessing penetrating injury, including prior visual status and the use of contact lenses or spectacles. Occupational trauma may be due to high-speed penetrating metal fragments. Agricultural trauma often involves heavily contaminated implements.

Examination of the eye involves the instillation of sterile topical anaesthetic drops, followed by a gentle eye toilet removing debris, clot and glass from the face and lids. The lids should be opened without pressure (Fig. 16.1.1). The penetration may be evidenced by an obvious laceration or presence of prolapsed tissue with collapse of the globe. Conjunctival oedema (chemosis) and low intraocular pressure (IOP) may indicate an occult perforation or bursting injury.

Fig. 16.1.1 Emergency department diagnosis of penetrating injury. FB, foreign body.

When a penetrating injury is either suspected or established, the patient must be transferred without delay to a centre where appropriate surgical facilities are available. During transport, the eye should be covered with a sterile pad and a plastic cone. Vomiting should be prevented with antiemetics, and the fasted patient given intravenous fluids as necessary.

Penetrating trauma involving the cornea has the best prognosis. Lens involvement requires removal of the traumatized lens and usually a staged implantation of an intraocular lens. Posterior segment trauma involving tears or perforation of the choroid and retina requires staged vitreo–retinal surgery and has a guarded prognosis. Uncommonly, penetrating trauma excites an autoimmune reaction resulting in a destructive inflammation involving the uninjured fellow eye – sympathetic ophthalmitis. Long-term follow-up of all penetrating ocular trauma is mandatory.

Blunt trauma

Concussion of the globe may cause tearing of the iris root, resulting in blood in the anterior chamber. A hyphema greater than one-third of the anterior chamber usually indicates some damage to the drainage angle, and may also be associated with concussive lens damage. Uninterrupted absorption of the hyphema is essential, and is aided by sedation and an admission to hospital. The affected eye is padded and the patient nursed semirecumbent to encourage sedimentation of the blood in the anterior chamber to clear as much of the angle as possible. A hyphema may cause considerable pain due to raised IOP. To lower the pressure, oral or intravenous acetazolamide 500 mg initially is required.

Pain is relieved by paracetamol or narcotics, with antiemetics if necessary. Aspirin in any form should be avoided as it increases the risk of secondary haemorrhage. The patient should remain in bed until the blood has completely cleared from the anterior chamber. Bleeding recurs in up to 10% of patients, usually due to early mobilization in those with extensive iris damage. Total hyphema has a poor prognosis because of secondary glaucoma, field loss and corneal opacification. When angle damage occurs, long-term follow-up after hyphema is required to determine whether the IOP is raised. The fundus requires careful examination after the hyphema has cleared completely, to exclude a traumatic retinal tear, which may be heralded by sudden onset of flashes and floaters.

Chemical burns

Chemical trauma requires priority assessment on arrival at an emergency centre.

Alcohol and solvent burns occur from splashes while painting and cleaning. Although the epithelium is frequently burnt, it regenerates rapidly. The condition is very painful initially, but heals with topical antibiotic and patching for 48 h.

Alkali and acid burns are potentially more serious because of the ability of the burning agent to alter the pH in the anterior chamber of the eye and inflict chemical damage on the iris and lens. Caustic soda, lime and plaster, commonly used in industry, may inflict painful, deep and destructive ocular burns. Splashes of acids, such as sulphuric and hydrochloric, if concentrated, will cause equally destructive injury.

The first principle of management at the injury site is copious irrigation of the eyes for at least 10 min with running water. Assessment of the ocular burn should be done using topical anaesthetic drops and fluorescein staining to determine the area of surface injury. The eyelids should be everted and the fornices carefully examined and swept gently with a cotton bud to ensure there is no particulate caustic agent remaining.

Chemical burns where the epithelium is intact or minimally disturbed can usually wait 24 h before review by an ophthalmologist. Burns involving more than one-third of the epithelium and the corneal edge, with any clouding of the cornea, are potentially more serious as subsequent melting of the cornea by collagenase action may ensue. These burns should all be further irrigated in the ED with a buffered sterile solution such as lactated Ringer’s (Hartmann’s). The irrigation should continue until the tears are neutral to litmus testing.

More serious caustic injuries have shown a significant improvement in outcome with the introduction of 10% citrate and ascorbate drops, commencing 2-hourly for 48 h and reducing over the week, in combination with 1 g oral ascorbic acid daily. This regimen has an inhibitory effect on corneal melting. Topical antibiotic (chloramphenicol) and soluble steroids such as prednisolone phosphate 0.5% decrease inflammation.

Initial treatment of caustic injury:

• Immediate flooding of the eye with fresh water for 10 min.

• Transfer to medical centre.

• Assess visual acuity in both eyes.

• Ascertain chemical agent and time of injury.

• Sterile topical anaesthetic, e.g. tetracaine (amethocaine).

• Stain with fluorescein.

• Examine the cornea and conjunctiva.

• Evert lids and sweep tarsal plate with cotton bud.

• Reirrigate.

A minor injury is defined as less than one-third epithelial loss and a clear cornea. A major injury is a large epithelial defect, a conjunctival burn and a hazy media.

For major injury commence ascorbic acid 1 g daily and 10% topical ascorbate hourly.

Prevention

Children are constantly exposed to domestic hazards, particularly household utensils with sharp points and caustic substances in spray cans, which need to be kept out of reach. The well-known workshop injuries caused by iron fragments created while hammering or chipping, exploding car batteries and carbonated drinks bottles cause significant trauma. Protective glasses – preferably polycarbonate – may provide protection in racquet sports. Contact lenses do not protect.

Australian seatbelt legislation has markedly reduced the incidence of penetrating eye injuries in road trauma, but eye problems still occur from violent head and facial trauma in addition to the neurological complications of head injury.^1,²

ACUTE INFLAMMATORY CONDITIONS

Acute primary angle-closure (glaucoma)

Acute primary angle-closure (APAC) is characterized by an acute impairment of the outflow of aqueous from the anterior chamber in an anatomically predisposed eye. This results in a rapid and severe elevation in IOP. Normal IOP lies between 10 and 21 mmHg, but in cases of APAC can rise to >60 mmHg. This is manifested as severe pain, blurring of vision and redness. The pain may be severe enough to cause nausea and vomiting, and may be poorly localized to the eye. Visual disturbance can be preceded by halos around lights, and in established cases is due to corneal oedema. Relative hypoxia of the pupillary sphincter due to elevated pressure results in a pupil unresponsive to light stimulation. The pupil is classically fixed and mid-dilated. The associated inflammation induces congestion of conjunctival and episcleral vessels. The term ‘acute angle-closure glaucoma’ is no longer regarded as appropriate, as there may be no optic nerve head cupping or visual field loss – the features that define glaucoma – at the acute presentation.

Treatment of APAC is aimed at lowering the IOP and allowing the flow of aqueous from the posterior to the anterior chamber. Acetazolamide 500 mg i.v. and/or topical apraclonidine or brimonidine may be effective in acutely lowering the pressure and thereby reducing pain. If ineffective, subsequent constriction of the pupil with 2% pilocarpine, a parasympathomimetic, may alleviate the forward bowing of the iris, relieve the pupil block and re-establish aqueous flow and angle drainage. One drop is initially instilled every 5 min for 15 min, and then half-hourly. If the pressure is very high, however, the ischaemia induced will render the pupillary sphincter unresponsive to the pilocarpine. In these cases it may be necessary to move to early laser treatment.

A peripheral iridotomy (PI) is performed using the yttrium:aluminium:garnet (YAG) laser to allow aqueous permanently to bypass the pupil and remove the risk of further episodes of APAC. This may be done acutely or electively. The anatomical predisposition to APAC is usually bilateral, and a PI is also performed in the other eye as an elective procedure. Until this is done, miotics are instilled (G. pilocarpine 2% qid) in the unaffected eye to avoid the risk of APAC.

Early YAG laser PI in the affected eye may be hampered by corneal oedema. Argon laser peripheral iridoplasty may be used in the acute phase for resistant attacks, or where corneal oedema precludes YAG laser PI.^3,⁴

Acute iritis

Acute iritis (AI) is an inflammatory response in the ciliary body and the iris. As part of this response there is an increase in vascular dilatation and permeability, with release of inflammatory mediators and cells that can damage intraocular structures.

Acute iritis (AI) is usually an idiopathic condition with no systemic cause or association. Less commonly, associated conditions may include HLA B27-related disease, sarcoidosis, inflammatory bowel disease, including ulcerative colitis and Crohn’s disease, connective tissue disorders such as ankylosing spondylitis and ocular infection, including herpetic disease or toxoplasmosis. A complete history will often give clues to these associations.

Acute anterior iritis is generally unilateral, although bilateral involvement is seen. It is characterized by pain, redness and visual disturbance. The pain is constant and exacerbated by light owing to movement of the inflamed iris. Dilatation of the conjunctival and episcleral vessels is apparent, particularly in the vessels adjacent to the corneal limbus, often referred to as limbal flush. Visual acuity can be reduced by varying degrees depending on the severity of inflammation. The pupil is constricted due to irritation.

Examination of the anterior segment with the slit lamp will reveal evidence of increased vascular permeability, seen as fibrin clumps, flare and inflammatory cells in the aqueous released from the vessels. In some cases small collections of neutrophils can be seen aggregating on the posterior surface of the cornea as keratic precipitates (KP). In cases of severe inflammation, cells can accumulate in the inferior anterior chamber and a sediment level can be seen as a hypopyon. The IOP may be raised.

Treatment of AI is directed towards resolution of the inflammatory response and limiting the ocular effects of this response. The mainstay of treatment is intensive, topical steroid eye drops (prednisolone acetate 1%, up to hourly in severe cases). In severe cases, orbital steroid injections or oral steroids may be necessary. Mydriatic eye drops (G. homatropine 2% qid) are used to break any lens–iris adhesions and to limit the extent of permanent adhesions. In ‘splinting’ the iris these drops also provide pain relief by limiting pupil movement.

As the degree of inflammation decreases on slit-lamp examination, the topical treatment is decreased in frequency. The long-term use of topical steroid drops is not without risk, and can be associated with the development of glaucoma, cataract and concurrent ocular surface infection, such as herpes simplex keratitis.

Acute infectious keratitis

The surface of the eye is protected by several mechanisms from penetration by infectious agents, both bacterial and viral. The flow of tears over the surface washes debris away and contains antibodies and lysozymes. The smooth surface of the corneal epithelium hinders the adherence of infectious agents, and the rapid repair of any defect in the epithelium limits the likelihood of penetration by such agents. If these defenses are impaired in any way there is the possibility of penetration into the corneal stroma, and active infection may occur.

Bacterial keratitis is characterized by a focus of infection with an associated inflammatory response. Patients complain of pain, redness, watering and a decrease in visual acuity. Fluorescein staining shows an area of ulceration over the infection, which appears as an opacity or area of whiteness within the cornea. Marked conjunctival and episcleral injection results in a unilateral red eye. Evidence of intraocular inflammation is usually present, with cells and flare being seen in the anterior chamber on slit-lamp examination. In severe cases, a collection of inflammatory cells can be seen in the inferior part of the anterior chamber as sediment, called a hypopyon.

The most important aspect of management is to identify the infectious agent and to commence appropriate antibiotic treatment. A specimen is taken via a scraping for microbiological assessment, including Gram staining and culture. Under topical anaesthetic, using a preservative-free single-use dispenser of benoxinate or tetracaine (amethocaine), a sterile 23G needle is used to gather a small specimen. This is transferred directly to glass slides and also plated on to HB and chocolate agar plates for culture. Fungal cultures may be indicated. Antibiotic therapy is not delayed until the results are available, but is commenced on a broad-spectrum basis, such as the intensive use of a fluoroquinolone eye drop (e.g. G. ciprofloxacin) on an hourly basis. Daily monitoring with slit-lamp examination is mandatory and severe infections require hospital admission. This regimen can be modified when culture and sensitivity results are available. It is sometimes necessary to add a topical steroid when the active infection is under control, to limit the amount of inflammation and vascularization – and hence damage – to the cornea.

Herpes simplex infection of the cornea usually presents initially as an infection of the epithelial cell layer, although with recurrent episodes stromal involvement may be seen. It is most often a unilateral infection. As with other herpetic infections it is not possible to eradicate the virus, but limitation of inflammatory-mediated damage is important. Patients complain of foreign body sensation, redness, watering and a variable decrease in visual acuity. On examination the areas of infected epithelium can be seen as a branching irregularity or dendrite on the surface of the eye. Multiple dendrites may be scattered over the surface, particularly in immunocompromised patients. These are best seen when the cornea is stained with fluorescein or Rose Bengal stains and viewed under the slit lamp.

Treatment is directed to clearing the virus from the cornea to promote epithelial healing and limit stromal involvement and damaging corneal inflammation. An antiviral ointment, aciclovir, is instilled five times daily until there is resolution of the epithelial lesions, and then ceased as long-term usage may be toxic to the unaffected corneal epithelium. Steroid eye drops are contraindicated except under the strict supervision of an ophthalmologist.

ACUTE VISUAL FAILURE

Introduction

Acute visual failure is any acute change in visual acuity, visual field or colour vision. Effective emergency management depends upon rapid recognition of those conditions for which acute therapy is available (Table 16.1.1). Some conditions have no effective therapy, or are more appropriately managed on an outpatient basis.

Table 16.1.1 Acute visual failure for which acute therapy is available

Condition	Therapy
Central (or branch) retinal artery occlusion	Acetazolamide Pulsed ocular compression Anterior chamber paracentesis

Anterior ischaemic optic neuropathy Steroids Exudative age-related macula degeneration

anti-VEGF injections

Retinal detachment Surgery

Clinical assessment

History

Particular attention should be paid to the rapidity of onset, degree and location in space of visual loss, previous episodes and associated symptoms. Most of the sinister causes of acute visual failure are painless (Table 16.1.2).

Table 16.1.2 Symptoms significant for cause in acute visual failure

Symptom	Condition
Floaters (if recent onset)	Posterior vitreous detachment Vitreous haemorrhage Retinal detachment

Flashes (especially temporal)

Retinal detachment

Shadow (billowing curtain/cloud)

Retinal detachment

Vitreous haemorrhage

Distortion Exudative macula disease Amaurosis fugax

Retinal artery occlusion

Anterior ischaemic optic neuropathy

Pain on eye movement Optic neuritis Visual field loss Horizontal hemifield

Anterior ischaemic optic neuropathy

Branch retinal vein occlusion

Branch retinal artery occlusion

Vertical hemifield (bilateral) Retrochiasmal CVA/compression Whole-field (unilateral)

Vitreous haemorrhage

Central retinal artery occlusion

Anterior ischaemic optic neuropathy

Central retinal vein occlusion

Bilateral total loss of vision

Bilateral occipital infarction

Toxic (methanol/quinine)

One should distinguish on history between acute onset and acute discovery of visual loss, as a patient may discover decreased vision from, for example, cataract, or retinal venous occlusion, by inadvertently covering one eye for the first time.

Examination

Testing of the visual acuity and visual field will clarify uni- or binocular involvement.

Examination of the pupils is mandatory before pharmacological dilation. Test for a relative afferent pupillary defect (RAPD), one of the few objective signs. When required, pupils will dilate in 10–15 min with tropicamide 1.0% drops, which last 1–2 h.

Bilateral vision loss

Bilateral visual field loss usually implicates a retrochiasmal – and, therefore, non-ocular – cause. This visual field defect will, however, respect a vertical midline. In contrast, the retinal nerve fibre layer and retinal vascular elements within the eye are distributed around a horizontal midline, and may thus involve a superior or inferior (i.e. horizontal) hemifield. Localized ocular pathology does not cause a visual field defect respecting a vertical midline.

Bilateral acute, complete, visual failure is uncommon. Bilateral occipital infarction may present with bilateral blindness, but pupil responses would be expected to be intact. Rapidly progressive bilateral sequential visual loss from temporal arteritis is occasionally encountered. Other prechiasmal causes of bilateral, simultaneous, ocular involvement include toxic causes, such as poisoning with either quinine or methanol, where the patient presents with bilateral blindness and fixed, widely dilated pupils. Visual recovery in these cases is variable, and the efficacy of a range of therapeutic interventions is controversial.⁵^–⁷

Central retinal artery occlusion

The history is typically of sudden, painless loss of vision in the affected eye over seconds. This may have been preceded by episodes of transient loss of vision (amaurosis fugax) in the previous days or weeks. Mean age of presentation is in the 60s. Men are more frequently affected, and the history may include evidence of previous cardiac or cerebrovascular disease. Systemic arterial hypertension and diabetes mellitus are often coexistent. Carotid disease is frequently implicated, with emboli often being the cause of the obstruction, but their absence does not preclude the diagnosis, as the obstruction may lie behind the lamina cribrosa.

The visual acuity is drastically reduced, often to the level of light perception, with a RAPD present on the affected side. Fundus examination shows creamy-white retinal oedema (cloudy swelling) with a central red fovea – the ‘cherry-red spot’ – caused by the absence of oedema in the thinner retina at the fovea. The arterioles may be attenuated, with segmentation (‘cattle-trucking’) of the blood column. An embolus may be seen at any point along the retinal arterioles, from the disc to the periphery.

Acute treatment proceeds on the assumption that the cause is embolic. The principles of therapy are, therefore, to vasodilate the retinal arterial circulation in order to promote dislodgement of the embolus from a proximal position and encourage its movement downstream to a less strategic site. All the measures currently used are directed to lowering the IOP, thereby relieving the compressive effect on the intraocular vasculature. Intravenous or oral acetazolamide 500 mg will lower IOP within 15–30 min; pulsed ocular compression (‘ocular massage’) involves cyclical sustained compression of the globe for 10–15 s before sudden release of this compression, continuing for 5–10 min. The release of pressure may result in a momentary marked increase in the perfusion pressure gradient and dislodge an embolus. Definitive reduction of IOP is achieved with anterior chamber paracentesis by the removal of aqueous from the eye (see section on Anterior chamber paracentesis). Visual outcomes are generally poor in central retinal artery occlusion (CRAO), but occasional successes justify aggressive intervention if the patient presents within 12 h.

Intra-arterial fibrinolytic therapy is a promising technique that is not widely available at present and requires the services of an experienced interventional neuroradiology team.⁸^–¹¹ The place of hyperbaric therapy is uncertain at this time.¹² The use of carbogen gas (95% oxygen/5% carbon dioxide) is now largely historical.

Non-acute management must include attempts to define the embolic source. Investigations may include Doppler and cardiac ultrasound, and perhaps angiography (including aortic arch studies), as well as assessment of cardiac and cerebrovascular risk factors. An erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) should exclude temporal arteritis – which causes 5% of cases of CRAO – as a non-embolic cause.

Anterior chamber paracentesis

The eye is anaesthetized with topical, unpreserved drops from single-use dispensers – tetracaine 1%. The fornices and globe are prepared with a drop of 10% povidone-iodine. An assistant is useful to steady the patient’s head at the slit lamp. With toothed forceps to provide counterpressure opposite the site of entry into the anterior chamber, a 27 G needle on an insulin syringe with the plunger removed is inserted parallel to the iris plane: if the eye is phakic (i.e. natural lens present), then the needle course must be only over the iris, below the margin of the pupil, to avoid contact with the lens. Aqueous will drain along the barrel of the syringe and should be allowed to continue until the cornea starts to wrinkle. The needle is then withdrawn, taking great care not to allow the needle point to tip backwards against the lens in the softened eye. The entry wound is self-sealing. Antibiotic drops such as chloramphenicol should be commenced and used four times a day for 4 days. Vision will be worse immediately after the procedure.

Central (branch) retinal vein occlusion

Central or branch retinal vein occlusion may present as a painless blurring of vision that is not sudden. Patients are usually in the older age group, often with systemic hypertension, diabetes mellitus and glaucoma. Visual acuity varies with severity, as does the presence of an RAPD. The characteristic fundus appearance is of extensive intraretinal haemorrhage with a variable number of cotton wool spots. There may be disc oedema, with venous tortuosity and a generally congested appearance.

There is no emergency management specific to the vein occlusion that will positively influence the visual outcome, and the patient should therefore be referred to the next ophthalmic outpatient clinic. Systemic hypertension and raised IOP rarely require acute control.

Anterior ischaemic optic neuropathy

Arteritic anterior ischaemic optic neuropathy (AION) is the feared visual loss of giant cell (temporal) arteritis (GCA). The patient is commonly mid-70s or older, and more often female. Presentation is with profound vision loss in one eye. This may have been preceded by premonitory visual obscurations or double vision, to which the patient may not have ascribed significance. Systematic questioning may reveal specific features such as jaw claudication, headache, scalp tenderness, anorexia, malaise, weight loss or night sweats, and there may be a history of polymyalgia rheumatica in up to 50% of cases. Giant cell arteritis is a systemic illness with the potential for devastating visual loss, as well as long-term life-threatening non-ophthalmic complications.

Vision may be reduced at presentation to the level of perception of light only. An RAPD will be present. Total field loss in the affected eye is usual. Fundus examination will almost invariably show disc oedema, but the fundus may be otherwise normal. Evidence of decreased acuity, colour vision deficits and disc oedema should also be sought in the other eye. Palpation of the temporal arteries will often be abnormal, with the pulses perhaps absent or the arteries thickened and tender.

Clinical suspicion requires blood to be drawn for ESR and CRP. Treatment should then be started on an urgent basis and must not be delayed or deferred until after temporal artery biopsy. The biopsy will remain positive for at least several days despite steroids. Elevation of both ESR and CRP is highly specific for a diagnosis of GCA, but does not avoid the need for biopsy.¹³ Urgent referral to an ophthalmologist is required.

Prednisolone 1 mg/kg daily is an accepted dose, although recent experience has suggested that ‘pulse’ methylprednisolone 500 mg i.v. daily or twice daily over 1–2 h is safe and more efficacious in suppressing the inflammation, and this has become standard therapy in a number of centres. This is generally used for 3 days, and oral prednisolone is then substituted.¹⁴^–¹⁶ Treatment will be prolonged (at least 6 months) and should be undertaken in cooperation with a physician. Attention should also be directed to the avoidance of steroid complications in this aged patient group.

Non-arteritic AION is classically seen in males in the late 50s and 60s, who have a history of cardiac or vascular disease, hypertension, diabetes or smoking. The presentation may be similar to that seen with GCA – although the visual acuity and field loss may not be as profound and the specific systemic symptoms are absent – so that management must be as for arteritic AION until GCA is excluded.

Retinal detachment

Retinal detachment is usually a result of retinal hole formation, with seepage of fluid into the subretinal space and lifting of the retina. This may occur as a result of trauma, but is more often seen in an older age group as a result of vitreous traction in spontaneous posterior vitreous detachment (PVD), and is predisposed to by high myopia (short-sightedness). Exudative retinal detachment is less common and is associated with underlying pathology.

Posterior vitreous detachment

Shrinkage and detachment of the vitreous is common in the older population, and produces a new onset of floaters – wispy spots, threads or ‘spider webs’ in the vision. As part of this process, vitreous traction on the retina may produce flashes of light (photopsia) seen particularly in the temporal periphery of vision in that eye. These flashes can usually be distinguished from the visual aura of migraine. While PVD is usually not serious in its own right, early elective ophthalmic review is required as it is not possible to exclude related changes predisposing to retinal detachment without dilated examination of the retinal periphery.

Retinal detachment

With a history of flashes and floaters, the presence of pigmented cells (‘tobacco dust’) in the anterior vitreous should alert one to the possibility of a retinal hole and subsequent retinal detachment. A detached retina shows a visual field defect, which will be described as a shadow or curtain, corresponding to the area of detachment, i.e. inferior field defect equals superior retinal detachment. Vision loss is painless. There may be an RAPD, depending on the amount of retina involved. Treatment will usually require surgery. If the visual acuity is normal, the macula is likely to be still attached and referral to an ophthalmologist specializing in vitreo-retinal surgery is urgent.

Vitreous haemorrhage

The most common causes are proliferative diabetic retinopathy, chronic branch retinal vein occlusion, posterior vitreous detachment or trauma. Patients with an acute vitreous haemorrhage may have symptoms varying from a few floaters causing blurred vision to a total loss of vision to a level of light perception, depending on the density of the haemorrhage. Any loss of vision is painless. The red reflex may be poor and the view of the retina may be similarly impaired. Media opacities do not affect pupil light reflexes, so there should be no RAPD, unless the underlying retina is damaged or detached.

The patient should be referred for early ophthalmic assessment – urgent if an RAPD is present – which may include B scan ultrasonography to exclude retinal detachment if the retinal view is inadequate. Aspirin should be avoided.

Age-related macular degeneration

In 10–20% of cases of age-related macular degeneration (AMD), an exudative-type disease is seen, and in its most sinister form this will involve subretinal neovascularization (SRNV). These patients may present with painless distortion of vision, particularly metamorphopsia – a complaint that objects that they know to be straight appear curved. Visual acuity is reduced, depending on the stage of the disease; an RAPD is rarely seen owing to the relatively small area of retina involved, which manifests as a central scotoma on field testing. Macular drusen (yellow spots), retinal thickening and haemorrhage may be seen, with at least drusen usually also seen in the fellow eye.

Acute symptoms must not be dismissed. With appropriate treatment, central vision may be preserved in a proportion of these patients. Rapid ophthalmic review is therefore appropriate. Treatment will be undertaken following fundus fluorescein angiography to delineate the subretinal vascular lesion. Laser photocoagulation has been the traditional therapy, but the emergence of verteporfin, and more recently anti-vascular endothelial growth factor (VEGF) agents such as ranibizumab (Lucentis) have revolutionized the treatment options and prognosis. Clinical trials with the anti-VEGF agents are ongoing.^17,¹⁸

Optic neuritis

Optic neuritis classically presents in young females, and may be the first presentation of a demyelinating illness. Visual symptoms are not usually sudden, and presentation is thus seldom acute. The vision declines gradually over days, perhaps to the level of 6/36–6/60, with loss of colour vision being prominent. The common visual field defect is a central scotoma, but many variations are possible, and an RAPD should always be present. If disc oedema is not seen the diagnosis may be retrobulbar neuritis. There may be pain on medial or superior eye movement.

Good spontaneous recovery has made the value of treating optic neuritis controversial: the results of the Optic Neuritis Treatment Trial ¹⁹ would suggest that there is no place for oral prednisolone alone in management. The benefit of ‘pulse’ intravenous methylprednisolone seems restricted to shortening the acute episode, without influencing the possibility of progression to multiple sclerosis or the final visual outcome.²⁰ However, there is usually no role for acute intervention, and referral within a day or two to a neurologist or an ophthalmologist is satisfactory.

1 What are the roles of hyperbaric oxygen and intra-arterial fibrinolytic therapy in central retinal artery occlusion?

2 What is the appropriate therapy for acute optic neuritis: oral steroid, intravenous steroid or no treatment?

3 What are the long-term results with anti-VEGF treatments for exudative age-related macula degeneration?

1 McCarty CA, Fu CLH, Taylor HR. Epidemiology of ocular trauma in Australia. Ophthalmology. 1999;106:1847-1852.

2 Colby K. Management of open globe injuries. International Opthalmologic Clinic. 1999;39:59-69.

3 Lai JSM, Tham CCY, Chua JK, et al. Laser peripheral iridoplasty as initial treatment of acute attack of primary angle-closure: A long-term follow-up study. Journal of Glaucoma. 2002;11:484-487.

4 Lam DSC, Lai JSM, Tham CCY, et al. Argon laser peripheral iridoplasty versus conventional systemic medical therapy as first line treatment of acute angle closure: a prospective, randomised controlled trial. Ophthalmology. 2002;109:1591-1596.

5 Canning CR, Hague S. Ocular quinine toxicity. British Journal of Ophthalmology. 1988;72:23-26.

6 Bacon P, Spalton DJ, Smith SE. Blindness from quinine toxicity. British Journal of Ophthalmology. 1988;72:219-224.

7 Stelmach MZ, O’Day J. Partly reversible visual failure with methanol toxicity. Australia and New Zealand Journal of Ophthalmology. 1992;20:57-64.

8 Watson PG. The treatment of acute retinal arterial occlusion. In: Cant JS, editor. The ocular circulation in health and disease. St Louis: Mosby Year Book; 1969:243-245.

9 Schmidt D, Schumacher M, Wakhloo AK. Microcatheter urokinase infusion in central retinal artery occlusion. American Journal of Ophthalmology. 1992;113:429-434.

10 Weber J, Remonda L, Mattle HP, et al. Selective intra-arterial fibrinolysis of acute central retinal artery occlusion. Stroke. 1998;29:2076-2079.

11 Beatty S, Au Eong KG. Local intra-arterial fibrinolysis for acute occlusion of the central retinal artery: a meta-analysis of the published data. British Journal of Ophthalmology. 2000;84:914-916.

12 Beirna I, Reissman P, Scharf J, et al. Hyperbaric oxygenation combined with nifedipine treatment for recent-onset retinal arterial occlusion. European Journal of Ophthalmology. 1993;3:89. 84

13 Hayreh SS, Podhajsky PA, Raman R, et al. Giant cell arteritis: validity and reliability of various diagnostic criteria. American Journal of Ophthalmology. 1997;123:285-296.

14 Hayreh SS. Anterior ischaemic optic neuropathy. Differentiation of arteritic from non-arteritic type and its management. Eye. 1990;4:25-41.

15 Liu GT, Glaser JS, Schatz NJ, et al. Visual morbidity in giant cell arteritis. Clinical characteristics and prognosis for vision. Ophthalmology. 1994;101:1779-1785.

16 Cornblath WT, Eggenberger ER. Progressive visual loss from giant cell arteritis despite high-dose intravenous methylprednisolone. Ophthalmology. 1997;104:854-858.

17 Rosenfeld PJ, Brown DM, Heier JS, et al. Ranibizumab for neovascular age-related macular degeneration. New England Journal of Medicine. 2006;355:1419-1431.

18 Brown DM, Kaiser PK, Michels M, et al. Ranibizumab versus verteporfin for neovascular age-related macular degeneration. New England Journal of Medicine. 2006;355:1432-1444.

19 Beck RW, Cleary PA, Anderson MA, et al. A randomized controlled trial of corticosteroids in the treatment of acute optic neuritis. New England Journal of Medicine. 1992;326:581-588.

20 Kapoor R, Miller DH, Jones SJ, et al. Effects of intravenous methylprednisolone on outcome in MRI-based prognostic subgroups in acute optic neuritis. Neurology. 1998;50:230-237.

Further reading

Kanski J. Clinical Ophthalmology. A systematic approach, 6th edn. Butterworth-Heinemann Ltd, Oxford, 2007. (rev)

The Wills eye manual. Office and emergency room diagnosis and treatment of eye disease, 4th edn. Philadelphia: Lippincott Williams and Wilkins, 2004. (rev)

Riordan-Eva P. Vaughan and Asbury’s general ophthalmology, 16th edn. New York: McGraw-Hill Medical, 2003.

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