Author(s): Tristan McMullan and David Sprigings
The visual pathway extends from the cornea to the occipital cortex (Figure 19.1). Visual loss may indicate ocular, intracranial or systemic disease that requires prompt intervention to preserve sight. Clinical assessment (Table 19.1; Figure 19.2) will narrow the differential diagnosis and determine further management.
Giant cell arteritis should be considered in any patient over 50 with new-onset visual symptoms: it can present with transient visual loss in one eye (amaurosis fugax), persistent visual loss due to retinal or optic nerve ischaemia (may rarely affect both eyes) or diplopia.
Sudden loss of vision typically (but not exclusively) reflects vascular disease, and gradual loss of vision, a non-vascular disorder (Table 19.2).
Loss of vision in one eye indicates disease of that eye or optic nerve.
Bilateral visual loss occurs with systemic disease or focal disorders involving the visual pathway from the optic chiasm back to the occipital cortex.
Patients may report loss of vision in only one eye, even though both eyes are affected. With a homonymous hemianopia, the patient may only be aware of the visual loss in the eye with the temporal field defect, despite having a nasal visual field defect in the fellow eye.
Sudden painless persistent loss of vision is usually due to ischaemia/infarction or haemorrhage at some point along the visual pathway, but is also a feature of retinal detachment (Table 19.3). Sudden transient loss of vision has a range of ocular, vascular and neurological causes (Table 19.4).
Central or Peripheral Visual Field?
Central blurring or vision loss is typical of macular pathology (e.g. diabetic maculopathy).
Monocular peripheral visual loss may be due to a retinal vascular event (e.g. branch retinal vein occlusion, branch retinal artery occlusion), other retinal disease (e.g. retinal detachment) or optic nerve disease (e.g. ischaemic optic neuropathy, optic neuritis, or asymmetric or monocular glaucoma).
Pain in the eye usually indicates anterior eye disease (e.g. keratitis, anterior uveitis, primary angle-closure glaucoma). Optic neuritis and giant cell arteritis can cause visual loss, which may or may not be associated with pain in the eye.
Painless loss of vision is typical of cataract, retinal disorders and disorders of the visual pathway.
A careful drug history is essential as many drugs can cause transient or persistent visual loss (Table 19.5).
Suspected Giant Cell Arteritis
If there is persistent visual loss, seek urgent advice from an ophthalmologist. Methylprednisolone IV can be given.
If there has been transient visual loss, give prednisolone 60 mg PO. The patient should be reviewed by an ophthalmologist the same day. In addition to prednisolone, start aspirin 75 mg daily, unless there are contraindications such as active peptic ulceration or a bleeding disorder. Start a proton pump inhibitor (e.g. omeprazole 20 mg daily) for gastrointestinal protection. Assess osteoporotic fracture risk, and prescribe bone protection therapy if indicated.
Central and Branch Retinal Artery Occlusion
See urgent advice from an ophthalmologist.
Complete a full cardiovascular examination and record an ECG. Assess cardiovascular risk factors. Arrange an echocardiogram and carotid duplex scan to determine if there is an embolic source. Check full blood count, C-reactive protein ESR, blood glucose, biochemical profile and lipids.
Central and Branch Retinal Vein Occlusion
Complete a full cardiovascular examination and record an ECG.
Consider diabetes and hyperviscosity syndromes (check full blood count and serum protein electrophoresis). In younger patients consider thrombophilia (Table 56.1). Hypertension is the main risk factor but screen for other cardiovascular risk factors. Consider antiplatelet therapy if not contraindicated.
Arrange follow-up with an ophthalmologist.
Seek urgent advice from an ophthalmologist.
In most patients with optic neuritis complicating multiple sclerosis, symptoms resolve spontaneously, with recovery starting within ten days and usually complete by six weeks. Corticosteroid therapy (methylprednisolone IV) may accelerate recovery but does not alter long-term outcomes.
Complete a full cardiovascular examination and record an ECG. Assess cardiovascular risk factors. Arrange an echocardiogram and carotid duplex scan to determine if there is an embolic source. Check full blood count, C-reactive protein ESR, blood glucose, biochemical profile and lipids.
Consider/exclude giant cell arteritis (Chapter 99).
Give antiplatelet therapy if not contraindicated.
See Chapter 66 for further management of amaurosis fugax/transient ischaemic attack. Seek urgent advice from a stroke physician.
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