International Journal of Clinical Practice
Common Ophthalmic Emergencies
G. D. Khare; R. C. Andrew Symons; D. V. Do
Int J Clin Pract. 2008;62(11):1776-1784.
Abstract and Introduction
Epidemiology of Emergency Room Presentations
Cornea and Anterior Chamber
Optic Nerve and Neurological
Giant cell arteritis is an autoimmune disorder in the elastic lamina of arteries, causing luminal obstruction and ischaemia.[2] GCA causes a rapidly progressive, irreversible optic neuropathy. The headache that accompanies GCA is typically associated with scalp tenderness because of superficial temporal arteritis and with jaw claudication during chewing. Systemic symptoms such as fatigue and malaise, chills and loss of weight are common. GCA commonly occurs in association with polymyalgia rheumatica. Transient visual obscurations maybe a symptom of impending optic neuropathy. Arteritic ischaemic optic neuropathy presents with acute, unilateral visual loss that quickly becomes bilateral. Other ophthalmic manifestations include CRAO and palsies of the third, fourth and sixth cranial nerves.
When GCA presents with a headache it must be diagnosed and treated so that optic neuropathy can be avoided. Therefore the suspicion of the diagnosis of GCA must be entertained whenever a patient over the age of 50 years present with a temporal headache. When the presentation is of unilateral arteritic ischaemic optic neuropathy then treatment must be started in an attempt to protect the other eye from developing a vascular occlusion. Work-up should include a comprehensive eye examination. In cases of arteritic anterior ischaemic optic neuropathy, a relative afferent pupillary defect is present and the optic disc is swollen. Retinal cotton wool spots may be present.[10] Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are usually elevated. Temporal artery biopsy is diagnostic, and may be performed up to a week after initiation of steroid therapy. GCA causing an optic neuropathy is treated with intravenous methylprednisolone.
Cavernous Sinus Thrombosis
Cavernous sinus thrombosis can present with bilateral chemosis, eyelid oedema, eye movement abnormalities and proptosis. Often, patients develop fever, nausea and altered consciousness. The thrombosis usually results from extension of an infection (usually S. aureus), or aseptically from trauma or surgery.
The ophthalmic examination should focus on identifying any cranial nerve palsies, with particular attention devoted to observing pupillary reflexes for an APD, extraocular motility, trigeminal nerve function, ptosis, exophthalmia and resistance to retropulsion. CT scan or magnetic resonance imaging (MRI) of the sinuses, orbit and brain can help diagnose this condition. Two to three sets of peripheral blood cultures as well as a culture from the source of infection should be obtained to help define treatment.
Co-management with paediatricians or internists is usually appropriate. Management generally includes hospitalisation, intravenous fluid replacement, and intravenously administered antibiotics for several weeks. Nafcillin (or vancomycin if patient is penicillin allergic) plus ceftazidime can be used initially until culture results are obtained. For non-infectious causes, systemic anti-coagulation or aspirin is recommended.
The classic triad presentation of Horner's syndrome is unilateral ptosis, meiosis and facial anhidrosis. The meiosis often presents as anisocoria, most apparent in dim light, with the smaller pupil on the affected side. Causes of Horner's syndrome include internal carotid dissection, trauma, cluster headaches, herpes zoster infection, Pancoast tumour and stroke.
The most important diagnosis to make or exclude in an emergent fashion is internal carotid artery dissection. This diagnosis may be excluded using catheter angiography, CT angiography, or a combination of MRI and magnetic resonance angiography. Combined carotid artery MRI and magnetic resonance angiography (MRA) are now favoured by many practitioners as they are minimally invasive and highly sensitive.[12]
Third Nerve Palsy
A third nerve palsy presents with diplopia and ptosis. It may be accompanied by periocular pain, which is particularly frequent in cases of aneurysmal compression. The affected eye will have impaired motility, and appear turned down and out, especially in cases of nerve compression, and will often have a dilated pupil that is minimally reactive to light. The most common causes of third nerve palsy are microvascular infarcts, typically occurring in people with diabetes, hypertension or atherosclerosis, and a berry aneurysm, usually of the posterior communicating artery (PCA). Other causes of this condition include brain tumour, uncal herniation and pituitary apoplexy.
Work-up should include a complete history including risk factors for GCA, known cancer or central nervous system mass, hypertension, diabetes mellitus and recent infections. Blood pressure should be measured. A complete ocular examination, including pupillary reflexes, extraocular motility and visual fields should be performed, along with a full neurologic examination, assessing all other cranial nerves. In cases of non-pupil sparing third nerve palsy a gadolinium-enhanced MRI/MRA is best able to image a mass or aneurysm impinging on cranial nerve III (CN III). PCA aneurysms should be referred urgently to a neurosurgeon. Non-pupil sparing third nerve palsies where an aneurysm is not detected should be further evaluated by a neurologist or neuro-ophthalmologist. Other tests may include ESR, and fasting blood sugar and glycosylated haemoglobin.
Homonymous Hemianopia
Patients with homonymous hemianopia present with bilateral loss of vision of either the right or left visual field, but have normal pupillary responses. This disorder can be due to any unilateral lesion of the optic tract posterior to the optic chiasm. Stroke, tumour, haemorrhage, demyelinating disease and infection such as Progressive Multifocal Leukoencephalopathy (PML) may also present with homonymous hemianopia.[10] A homonymous quadrantanopia has similar localising significance, but is most likely to be secondary to a lesion of the optic radiations.
This presentation calls for complete ocular and neurologic examination, including MRI of the brain, and evaluation of stroke risk factors. Emergent ECG should also be performed to rule out myocardial infarction or atrial fibrillation.[10] Where an acute cerebral vascular accident (CVA) is diagnosed it should be managed urgently by an internist or neurologist.
Int J Clin Pract. 2008;62(11):1776-1784. © 2008 Blackwell Publishing
G. D. Khare,1 R. C. Andrew Symons,2 D. V. Do 2
1Johns Hopkins University School of Medicine, Baltimore, MD
2Wilmer Eye Institute, Johns Hopkins Hospital, Baltimore, MD
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