Common Ophthalmic Emergencies

G. D. Khare; R. C. Andrew Symons; D. V. Do


Int J Clin Pract. 2008;62(11):1776-1784. 

In This Article

Cornea and Anterior Chamber

Microbial Keratitis

Bacterial keratitis often presents with a painful red eye and a mucopurulent discharge. Slit-lamp examination usually reveals a corneal epithelial defect and an inflammatory infiltrate of the corneal stroma. Signs of severe infection include an anterior chamber inflammatory reaction and hypopyon. Common offenders include Staphylococcus, Streptococcus and Pseudomonas species. Staphylococcal infections often present with a focal stromal infiltrate or abscess, while streptococcal keratitis is often very purulent or crystalline. Pseudomonal keratitis is common in the setting of prolonged contact lens use and often presents with an acute suppurative infiltrate.

Complete history of contact lens use and general eye care should be assessed. Slit-lamp examination with fluorescein stain can help determine any amount of epithelial loss and further characterise corneal infiltrate. Corneal and contact lens smears for bacterial, fungal, acanthamoebal and viral cultures should be performed to determine treatment.

For vision-threatening infections, fortified tobramycin alternating with fortified cefazolin should be given as eye drops every hour. Broad-spectrum antibiotics such as intensive fluoroquinolone drops can be given for uncomplicated cases of community acquired bacterial keratitis. Topical corticosteroids may help reduce inflammation after anti-bacterial therapy has been. A patch should never be placed over an eye considered to be infected as this reduces the removal of pathogens by the tear-film.[6]

Ocular pain in a contact lens wearer should always be treated with caution. Contact lens wear can damage the ocular surface mechanically, immunologically, by hypoxic stress, by exposure to toxins in lens care media, and by providing a foreign body which can increase risk of development of infections. In particular, contact lens wearers have an increased risk of infection by Pseudomonas species, Acanthameba and Fusarium.[7] Pain in contact lens wearers should generally be referred to an ophthalmologist.

Herpetic keratitis usually presents with a watery, red eye and decreased visual function. Slit-lamp examination using fluorescein classically demonstrates a dendritic ulcer. A viral swab should be collected, as documentation of herpes simplex infection may be important in subsequent management. Ophthalmic referral is necessary to start anti-viral therapy.

Corneal Foreign Body

Corneal foreign bodies present with pain, foreign body sensation and often with decreased vision. Slit-lamp examination reveals a foreign body on the surface of the cornea. Evaluation should rule out the possibility of a full-thickness corneal laceration. Most corneal foreign bodies can be removed at the slit lamp using topical anaesthesia and a 27-gauge needle by a skilled ophthalmologist or physician. Prophylaxis of microbial keratitis is usually accomplished using erythromycin ointment. Pain control may include the use of a pressure patch, non-narcotic analgesics and cold compresses.

Corneal Abrasion

Foreign body sensation in the absence of a corneal foreign body is often because of a corneal abrasion. This can usually be diagnosed at the slit lamp, and fluorescein dye can often aid in determining the area of abraded corneal epithelium. It is important to evert the upper and lower eyelids to detect a foreign body that may be causing the abrasion. Topical antibiotic eyedrops or ointment is usually recommended to prevent infection.

Chemical Injury

Chemical injuries range in severity from superficial punctuate keratitis to corneal opacification with limbal ischemia. Acids and irritants can damage the cornea and conjunctiva. However, the most feared chemical insult to the cornea is an alkali burn, and these injuries should be managed with particular care. Ideally the management of corneal burns begins at the site of injury, where copious irrigation with tap water should be employed. In the emergency room irrigation should be commenced immediately with saline or Ringer lactate. In the case of an alkali burn the irrigation should continue for at least 30 min, or until the inferior cul-de-sac reaches a neutral pH of 7.0 by litmus paper test. Acids and alkali should never be used to neutralise each other.

After irrigation examination should include visual acuity and a slit-lamp examination to assess conjunctival and corneal damage. Lid eversion must be performed to search for foreign bodies. IOP may be increased and therefore should be checked.

Any foreign bodies or residual chemical crystals should be removed. Necrotic tissue should be debrided. Any conjunctival adhesions should be gently broken with a glass rod covered with antibiotic ointment. Depending on the injury it may be appropriate to treat with a topical antibiotic such as erythromycin, prednisolone acetate 1%, a cyclopegic agent such as atropine or homatropine. Additional lubrication using artificial tears and oral pain medication are used as needed. Significant intraocular hypertension should be treated. An ophthalmologist should assess all alkali injuries as well as severe chemical injuries from any other cause. There is some evidence that more severe alkali burns may benefit from a regime of intensive topical steroids, ascorbate and citrate.[8] The long-term visual rehabilitation of a severe corneal burn is complex and is usually managed by a corneal specialist.

Acute Angle Closure Glaucoma

Acute ocular hypertension or 'glaucoma' presents with ocular pain, decreased vision, frontal headache, nausea and coloured halos around lights. IOP is increased and slit-lamp examination sometimes shows corneal microcystic oedema. The most common cause of acutely raised IOP is acute angle closure. Most cases are related to narrow anterior chamber angles, often because of increased lens thickness. Other important causes of angle closure, which are important to differentiate so that appropriate cause specific treatment may be initiated are, neovascular glaucoma and some cases of uveitic glaucoma. Patients may have acutely increased IOP, corneal microcystic oedema and a shallow anterior chamber in both eyes. East Asians and the Inuit are genetically predisposed to shallow anterior chambers with narrow angles. It is sometimes triggered by mydriatic use. Complete evaluation and treatment of angle closure glaucoma require immediate ophthalmic referral. Peripheral iridotomy in the affected eye and usually also in the fellow eye are required in cases of anatomically narrow angles.


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