Introduction

Ophthalmological problems are best dealt with by ophthalmic urgent care. They have the skills and equipment to perform a comprehensive eye examination. The most important part of any eye exam is detecting reversible reductions in vision. An assessment of acuity must always be made. The red eye and the blind eye are easy enough to diagnose. It is surprising how patients with structural brains lesions do not appreciate their hemianopia even when gross. Occasionally a red eye can be associated with systemic disease. The headache and painful IIIrd nerve signifying an expanding saccular aneurysm about to rupture is an important diagnosis not to miss. Horner’s syndrome is a useful sign in stroke medicine and apical lung tumours. Those with suspected amaurosis fugax (transient monocular blindness) need an antiplatelet and referral to TIA services. Giant cell arteritis (GCA) mustn’t be missed – steroids must be started to preserve vision in the unaffected eye to prevent complete blindness.

Causes

• Arteritic anterior ischaemic optic neuropathy: arteritic ‘inflammatory’ AION usually due to GCA. Occlusion of posterior ciliary artery which supplies optic nerve. Usually painless. ↑ESR/CRP. Aged >50. Temporal artery tenderness. Headache, jaw claudication. Usually unilateral but may proceed to complete visual loss in both eyes. Afferent pupillary defect. Start steroids: PREDNISOLONE 1 mg/kg if suspected. Section 13.4 on GCA below.
  
• Non-arteritic anterior ischaemic optic neuropathy: atherosclerotic or thromboembolic occlusion of posterior ciliary artery which supplies optic nerve. Usually painless, associated with arteriosclerotic vascular disease, older males. Usually unilateral but may proceed to complete visual loss in both eyes. Atrial fibrillation. Main issue is differential from GCA. Afferent pupillary defect. Treat as for stroke disease. Echo for embolic source. ECG for AF. Carotid doppler may show plaques or stenosis on affected side; assess and manage vascular risk factors.
  
• Central retinal artery occlusion: sudden severe visual loss in seconds. Afferent pupillary defect. May be complete or affect branches. Retina is pale and white with a cherry-coloured spot at macula. Associated with vascular risk factors. If seen within first hour, sudden pressure and release to the globe may dislodge embolism or propel it peripherally. Refer all patients who present with retinal artery occlusion within 24 hours of the symptoms to ophthalmologist to attempt dislodging the embolus causing the occlusion. After 24 hours from onset refer them to an ophthalmologist within one week who may refer on to TIA clinic. Should have carotid dopplers and ESR/CRP to exclude GCA. Give steroids immediately if GCA suspected. IV thrombolysis has been trialled and looks promising but awaits further evidence. A recent review suggests that a clinical trial of early systemic fibrinolytic therapy for CRAO is warranted within a 4.5 h window and that conservative treatments are futile and may be harmful. [JAMA Neurol 2015;72:1148.]
  
• Central/branch retinal vein occlusion (CRVO/BRVO): sudden or gradual painless visual loss in seconds. Afferent pupillary defect. May be complete or affect branches. Fundi – Retina is red with haemorrhage with bloody venous infarction and engorged dilated retinal veins. Associated with HTN, DM, atherosclerosis, and glaucoma are major risk factors for the development of CRVO/BRVO in older patients. Others are vasculitis and thrombophilia. If seen within first hour sudden pressure and release to the globe may dislodge embolism or propel it peripherally. Several trials support the use of vascular endothelial growth factor (VEGF) inhibitors and intravitreal corticosteroids for the treatment of macular oedema in CRVO and BRVO. A fluorescein angiogram shows delayed filling in venous phase. Rare causes: Behçet’s syndrome, antiphospholipid syndrome, and protein C deficiency, sarcoidosis
  
• Retinal detachment: painless progressive visual loss depending on retinal area detached. If macula affected then central vision is lost. May see floaters and describe flashes of light. Fundoscopy shows pigmented cells in vitreous. Retinal detachment or break. In retinal detachment, the inner sensory retina detaches from the underlying pigmented epithelium of the retina. Patients also describe a shadow or curtain that comes across their field of vision. The most common cause of retinal detachment is a tear or hole in the retina that may be secondary to a posterior vitreous detachment or an ocular trauma.
  
• Corneal ulcer: severe pain, red eye and visual loss (see Red eye, Section 13.2).
  
• Acute angle closure glaucoma: PAIN + RED EYE + VISUAL LOSS (see Red eye, Section 13.2).
  
• Occipital stroke: may give only clinical finding as visual loss. Haemorrhagic or infarction. May give homonymous hemianopia but bilateral strokes may occur depending on aetiology. Section 11.19. Bilateral occipital lesions. Anton’s syndrome: blind patient maintains they can see. A form of visual anosognosia.
  
• Occipital/parietal/temporal tumour: visual loss and hemianopia progressive +/− headache.
  
• Optic neuritis: eye movements may be painful. May be seen as a first presentation of multiple sclerosis or NMO. Often young and more commonly female. Monocular blindness comes on over hours so more subacute than acute. Afferent pupillary defect. Vision worse with heat. Variable defects and scotomas. Altered colour perception initially. Optic disc may be normal or swollen. Some recovery over 2–6 weeks with residual temporal pallor. Discuss high dose IV methylprednisolone with neurology.
  
• Vitreous haemorrhage: may be due to proliferative retinopathy. Blood may obscure retina and loss of red reflex and afferent pupillary defect.
  
• Pituitary apoplexy: sudden headache and visual loss and possible IIIrd nerve palsy. Steroids for acute pituitary insufficiency and urgent neurosurgical decompression if vision affected (Section 5.9).

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