Emergency eye trolley setup

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 focussing aid. Vision less than 6/60 Snellen may be graded by the patient’s ability to count fingers (CF) at a measured distance, discern hand movements (HM) or to project the direction of a light (PL) from various angles. The eye not being tested must be completely shielded by an opaque occluder.

Investigation

All patients in whom a penetrating injury is suspected require X-ray or computed tomography (CT) scanning to exclude a radiopaque 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.

Penetrating injury

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. Extruded tissue or projectiles should not be removed: intraocular contents will surely follow. Removal can only be undertaken in the controlled environment of an operating theatre. Prognosis depends on the extent of globe disruption.

Blunt injury

Concussion of the globe may cause tearing of the iris root, resulting in blood in the anterior chamber (hyphaema). A hyphaema 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 hyphaema is essential and is aided by sedation and an admission to hospital. Traditional treatment is to pad the affected eye and to nurse the patient semirecumbent to encourage sedimentation of the blood in the anterior chamber to clear as much of the angle as possible. A hyphaema may cause considerable pain due to raised IOP. To lower the pressure, oral or intravenous acetazolamide 500 mg initially is required. Atropine drops to ‘splint’ the ocular interior are logical but theoretically risk a re-bleed with the initial dilating effect.

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 hyphaema has a poor prognosis because of secondary glaucoma, field loss and corneal opacification. When angle damage occurs, long-term follow up after hyphaema is required to determine whether the IOP is raised. The fundus requires careful examination after the hyphaema has cleared completely, to exclude a traumatic retinal tear, which may be heralded by sudden onset of flashes and floaters.

Smaller hyphaemas may be managed on an outpatient basis, perhaps with rest at home and the use of atropine drops and can be considered only if daily IOP monitoring is not required.

Chemical burns

The first principle of management at the location where the injury was sustained is copious irrigation of the eyes for at least 10 min with running water. Chemical trauma requires priority assessment on arrival at an emergency centre and immediate irrigation if this has not been done or was inadequate.

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.

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 (e.g. chloramphenicol) is used; topical steroid is used under ophthalmic supervision.

Flash burns

Exposure of the eyes to prolonged or severe ultraviolet radiation results in widespread punctate epithelial loss from the corneal surface. This is most frequently seen in welders who have not used sufficient eye protection while working or workers who have been inadvertently adjacent to welding. Patients complain of moderate to severe ocular discomfort with excessive watering and foreign body sensation. This usually occurs some hours after exposure to the inciting ocular radiation.

Ocular examination shows widespread punctate fluorescein staining, usually with no ulceration and no evidence of foreign body present. It is usual to elicit a history of exposure to welding. Other instances in which excessive ultraviolet radiation may be encountered are in alpine snowfields and tanning beds.

Treatment is supportive with oral analgesia and explanation of the cause and likely time course. The symptoms generally settle within 24–48 h as the epithelium recovers. While local anaesthetics give short-term relief, it is not appropriate to use these as a treatment.

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 (crowded) eye. This results in a rapid and severe elevation in IOP. Usual 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 IV 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.