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


Retinal Vein Occlusions

Retinal vein occlusions are a common cause of sudden, painless loss of vision, but can also have a more gradual onset. Vein occlusions are classified as either central (CVO) or branch (BVO) vein occlusions. CVOs generally occur in the vicinity of the lamina cribrosa in the optic nerve head. BVOs usually occur at the sites of arterio-venous crossings in the retina.

The extent of visual loss is extremely variable, especially in CVO. The extent of visual field affected in BVO corresponds to the area of affected retina. The most impressive fundal finding in both conditions is the presence of multiple intraretinal haemorrhages of varying severity. In the case of BVO these haemorrhages occur in the area drained by the affected venule. In the case of CVO the entire retina is affected. Cotton wool spots may occur. The obstruction site may be evident in BVO. Swelling of the optic disc frequently occurs in CVO.

Vein occlusions sometimes present with vitreous haemorrhage secondary to optic disc or retinal neovascularisation or with neovascular glaucoma because of neovascularisation of the anterior chamber angle.

While no emergency management is required, consultation with an ophthalmologist must be arranged to monitor and treat neovascularisation and macular oedema. Follow up with the patient's primary care physician is also warranted to minimise risks such as hypertension and diabetes. In the case of bilateral simultaneous CVO and CVO in people under the age of 60 years a review of possible haematological and inflammatory causes of venous thrombosis and obstruction should be performed. An internist should take a careful history and perform a physical examination and laboratory work-up should be directed by the findings on history and examination. The basic work-up could include a complete blood count, erythrocyte sedimentation rate, fasting plasma homocysteine levels, anti-nuclear antibody and anti-phospholipid antibody levels.

Central Retinal Artery Occlusion

Central retinal artery occlusion (CRAO) presents with unilateral, acute, painless loss of vision. Often, patients may reveal a history of amaurosis fugax.[10] Embolus from the heart, aorta or carotid arteries, giant cell arteritis (GCA) (see below), other collagen vascular diseases, and hypercoaguability disorders are all causes of acute CRAO.

On examination, white retinal oedema and a cherry-red spot in the macula can be detected. There is attenuation of the retinal arterioles and box-car-shaped blood columns may be observed.

Ocular massage has been documented to lead to resolution of CRAO in some instances. Therefore CRAO is a true emergency. Acute, painless loss of vision must be triaged at high priority and ocular massage should be performed immediately once the diagnosis is made. There is no other proven treatment for CRAO. Irreversible damage to the retina occurs within a few hours of the initial occlusion, and hence the window for intervention is short. Ocular decompression by anterior chamber paracentesis sometimes leads to dislodgement of the embolus so that it moves distally in the vascular tree where it may cause less visual loss. This should be performed by an ophthalmologist. Arterial thrombolytics are under investigation for treatment of this condition but are not recommended at this time.[10]

Blood tests, such as complete blood count, a hypercoaguability work-up, erythrocyte sedimentation rate and C-reactive protein (CRP) should be performed. Carotid artery duplex Doppler ultrasonography and complete cardiac evaluation should be performed to determine whether there is a treatable embolic source.

Retinal Tear

Tears in the retina can be precursors to retinal detachment, as they allow fluid from the vitreal cavity to enter the potential space between the retina and retinal pigment epithelium. They require semi-urgent evaluation and treatment. Retinal tears typically present with photopsia or multiple floaters. The photopsia represent the sensory perceptions because of retinal traction. Floaters may occur when a retinal tear crosses and damages a retinal vessel resulting in a vitreous haemorrhage. Retinal tears are diagnosed ophthalmoscopically. An ophthalmoscopic examination for suspected retinal tear is not complete without circumferential scleral depression by an ophthalmologist. Where the view of the retina is impaired, typically because of vitreous haemorrhage, ultrasonographic examination is required. Retinal tears are most commonly treated by an ophthalmologist using laser retinopexy or cryotherapy. The referral should be made within 24 h.

Retinal Detachment

There are three types of retinal detachment classified by aetiology: rhegmatogenous retinal detachment is due to a tear or break in the retina; exudative retinal detachment occurs when inflammatory, neoplastic or other exudative processes cause fluid to leak into the subretinal space and tractional retinal detachment where neovascular membranes, most commonly because of proliferative diabetic retinopathy, pull the retina forward.

Retinal detachment most commonly presents with loss of vision or a visual field defect described as a 'veil' or 'fog'. Acute traction on the retina often gives the appearance of flashing lights or photopsia. A torn retinal blood vessel can lead to vitreous haemorrhage which presents with floaters. Visual acuity and visual field should be determined. The diagnosis of retinal detachment is made on ophthalmoscopy or by B-scan ultrasonography if no clear view to the retina is available.


Endophthalmitis refers to an infection of the contents of the eye. The infection may enter the eye as a result of surgery, trauma, haematogenously or secondary to infection of a trabeculectomy bleb or of the cornea or sclera. Acute endophthalmitis presents with rapidly deteriorating vision and pain. Decreased visual acuity, hypopyon and vitritis are the most common signs.

Early identification of endophthalmitis and immediate referral to an ophthalmologist will increase the probability of saving the patient's eye. The ophthalmologist will obtain a sample of intraocular fluid to send for immediate bacterial and fungal culture. Most cases of endophthalmitis are treated with intravitreal antibiotic injections. Vitrectomy surgery is usually reserved for cases in which the visual acuity is light perception.

Common organisms cultured in endophthalmitis cases include Staphylococcus epidermidis, Staphylococcus aureus, and Streptococcal species, while traumatic endophthalmitis is more often associated with Bacillus species, S. epidermidis, gram-negative species, and mixed flora. Infection of a trabeculectomy bleb is associated with Streptococcal or gram-negative bacterial infections.

Most cases of endophthalmitis are treated with intravitreal vancomycin and ceftazidime. In most cases, intensive topical steroids (prednisolone acetate), topical fortified antibiotics (vancomycin and tobramycin), and atropine should be administered, while trauma patients may benefit from tetanus toxoid as well.[6] The Endophthalmitis Vitrectomy Study did not demonstrate any value in treating endophthalmitis with intravenous antibiotics.[11]


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as: