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The eye lies in the bony orbit of the skull and is covered by the eyelid, which protects it from foreign bodies and keeps the anterior surface moist by maintaining the tear film. The upper lid is elevated by two muscles: the levator palpebrae superioris, innervated by cranial nerve III; and Müller’s muscle, innervated by sympathetic nerves. The orbicularis oculi muscle closes both upper and lower eyelids and is innervated by cranial nerve VII.
The orbit also contains the six extraocular muscles responsible for eye movement; the lacrimal gland; blood vessels; autonomic nerve fibres; and cranial nerves II, III, IV and VI, cushioned by orbital fat ( Fig. 8.1 ).
The conjunctiva is a thin mucous membrane lining the inner aspects of the eyelids and the anterior surface of the eyeball. It is reflected at the superior and inferior fornices. The conjunctiva is coated in a tear film that protects and nourishes the ocular surface.
The eyeball is normally approximately 25 mm in diameter and comprises three layers (see Fig. 8.1 ). These are:
Outer fibrous layer: this includes the white sclera and the clear cornea anteriorly.
Middle vascular layer (uveal tract): anteriorly, this consists of the ciliary body and the iris, and posteriorly, the choroid.
Inner neurosensory layer (retina): the retina is a thin layered structure responsible for transducing light to neurological signals. There are two main types of photoreceptors: cones function maximally under photopic (light) conditions and enable colour vision while rods are primarily used in scotopic (dark) conditions. Cones are concentrated at the centre of the retina and are most highly concentrated at the centre of the macula (the fovea). Photoreceptors transduce light into neuronal signals that pass via bipolar cells and ganglion cells to the nerve fibre layer of the inner retina before entering the optic nerve.
Six extraocular muscles are responsible for eye movement: (1) the superior rectus, (2) medial rectus, (3) lateral rectus, (4) inferior rectus, (5) superior oblique and (6) inferior oblique. Each muscle is responsible for a specific vector of eye movement ( Fig. 8.2 ). They work together to move the eye in other directions.
Cranial nerve III innervates the superior rectus, medial rectus, inferior oblique and inferior rectus muscles. Cranial nerve IV innervates the superior oblique muscle, and cranial nerve VI innervates the lateral rectus muscle. The cranial nerves originate in the midbrain and pons and pass through the cavernous sinus ( Fig. 8.3 ). Examining for eye movement deficits reveals cranial nerve deficits. For instance, a complete loss of cranial nerve III results in a loss of function of the superior rectus, inferior oblique, medial rectus and inferior rectus. If cranial nerves IV and VI are intact, the lateral rectus and the superior rectus continue to pull the eye inferiorly and laterally. This gives the classical ‘down and out’ resting position of an eye with cranial nerve III palsy.
The major refractive elements of the eye are the tear film, cornea and crystalline lens. The cornea accounts for approximately two-thirds of the refractive power of the eye while the lens provides additional controllable refraction, allowing light to focus onto the retina at varying focal lengths. When light is precisely focused at the retina, the eye is called emmetropic ( Fig. 8.4A ). When the focus point falls behind the retina, the result is hypermetropia (see Fig. 8.4B , long-sightedness). When the focal point is in front of the retina, the result is myopia (see Fig. 8.4C , short-sightedness). These refractive errors can be corrected with lenses or partially corrected with a pinhole (see Fig. 8.4D ).
The visual pathway connects the eye to the brain and consists of the retina, optic nerve, optic chiasm, optic tracts, lateral geniculate bodies, optic radiations and visual cortex. Deficits in the visual pathway lead to specific field defects ( Fig. 8.5 ).
The pupil controls the amount of light entering the eye. The intensity of light determines the pupillary aperture through autonomic reflexes. The parasympathetic pathway controlling pupillary constriction is shown in Fig. 8.6A ; the sympathetic pathway controlling pupillary dilatation is shown in Fig. 8.6B .
To guide your ophthalmic history, remember the anatomy of the eye. This will enable you to work from ‘front to back’ to include or exclude differential diagnoses.
Start the ophthalmic history with open questions so the patient can describe their symptoms in their own words. Use the patient’s description to inform more directed questions later.
Specific visual symptoms prompt specific sets of directed questions. The most common symptoms are described below.
Loss or reduced vision is the most common change. Patients often describe blurred vision. Ocular disease is the most common cause of a change in vision. Any intraocular condition that prevents light from activating retinal photoreceptors or the signal from photoreceptors reaching the optic nerve can cause altered vision. Rarely, damage to the extraocular visual pathway may cause altered vision (see Fig. 8.5 ).
When patients present with a change in vision, ask:
Was the onset of visual change sudden or gradual? Sudden or gradual visual loss leads to specific differential diagnoses ( Box 8.1 and Fig. 8.7 ; Box 8.2 and Fig. 8.8 ). If sudden, then enquire about possible causes (e.g. trauma, foreign body, chemical injury).
Cause | Clinical features | Cause | Clinical features |
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Unilateral | |||
Giant cell arteritis |
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Vitreous haemorrhage |
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Central retinal vein occlusion |
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Wet age-related macular degeneration |
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Retinal detachment |
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Anterior ischaemic optic neuropathy |
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Central retinal arterial occlusion |
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Optic neuritis/retrobulbar neuritis |
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Corneal disease |
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Amaurosis fugax |
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Bilateral | |||
Giant cell arteritis |
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Cerebral infarct |
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Raised intracranial pressure |
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Migraine |
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Cause | Clinical features |
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Refractive error |
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Glaucoma |
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Cataract | |
Diabetic maculopathy |
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Compressive optic neuropathy |
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Retinitis pigmentosa |
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Dry age-related macular degeneration |
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Does the vision change affect one or both eyes? Sudden onset of bilateral change in vision suggests a post chiasmal cause.
Is the change in vision associated with any additional features (e.g. haloes, flashing lights, floaters, distortion, discharge, red eye, pain)? Haloes are bright or rainbow-coloured rings seen surrounding a light source. They occur when there is corneal oedema and are most commonly associated with angle-closure glaucoma. Flashes and floaters result from a disturbance of the vitreous–retinal interface, most commonly due to a posterior vitreous detachment. This usually occurs with age as the vitreous degenerates, liquefies and peels away from the retina, resulting in floaters. Detachment sometimes causes retinal traction, resulting in flashing lights. More rarely, posterior vitreous detachment causes a retinal tear (releasing cells seen as floaters), which may progress to retinal detachment with visual field loss. Distortion is most commonly seen in diseases of the macula, such as age-related macular degeneration, epiretinal membrane, vitreous traction on the retina or central serous retinopathy.
Does the change in vison affect part or whole of the visual field? If part, which part? Specific types of visual field loss may point to retinal disease, such as macular degeneration, optic nerve disease such as glaucoma or visual pathway defects (see Fig. 8.5 ).
Ask:
Can you describe the nature of the pain?
How severe is it?
Did anything cause the pain?
Is pain exacerbated or relieved by anything?
Any other associated features (e.g. change in vision, red eye, discharge, photophobia, watering eye)?
The most common cause of a painful eye is corneal irritation from a foreign body or infection. The cornea is one of the most highly innervated parts of the body. When the corneal nerves are activated, a patient experiences foreign body sensation, pain, reflex watering and photophobia. There are, however, many other causes of a painful eye. Box 8.3 summarises the history and examination findings associated with a painful eye.
Cause | History | Examination |
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Blocked gland on lid |
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Corneal foreign body |
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Corneal infection |
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Scleritis |
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Angle-closure glaucoma |
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Conjunctivitis |
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Uveitis |
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Optic neuritis |
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Orbital cellulitis |
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Thyroid eye disease |
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The eye is covered in a network of vessels in the conjunctiva, episclera and sclera. Ciliary vessels are also found around the cornea. Dilatation or haemorrhage of any of these vessels can lead to a red eye. Additionally, in uveitis, acute angle-closure glaucoma and corneal irritation, the ciliary vessels around the cornea become more prominent (‘ciliary flush’). The appearance is distinct from conjunctivitis, in which there is classically a relative blanching of vessels around the cornea.
Ask:
Is there any pain or photophobia?
Is vision affected? If so, how?
Has there has been any recent trauma or foreign body?
Is the eye itchy?
Is there any discharge? If so, what kind (e.g. watery, sticky, clear, yellow)?
Has there been any recent contact lens use?
Box 8.4 summarises the features of the common causes of a red eye on history and examination.
Causes | History | Examination |
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Allergic conjunctivitis |
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Viral conjunctivitis |
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Bacterial conjunctivitis |
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Trauma |
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Acute angle-closure glaucoma |
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Acute anterior uveitis |
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Episcleritis |
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Scleritis |
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Dry eyes |
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Subconjunctival haemorrhage |
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Corneal ulcer/abrasion |
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Orbital cellulitis |
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Thyroid eye disease |
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Ask:
Does the double vision occur with one eye open or only with both eyes open? Binocular double vision is caused by an imbalance in eye movement between the eyes. Monocular diplopia results from intraocular disease in one eye.
What is the character of the double vision (e.g. are images seen side by side, one above the other or at an angle)?
Has there been any recent trauma?
In binocular diplopia, test the eye movements ( Fig. 8.9 ) and use your knowledge of the function of the extraocular muscles (see Fig. 8.2 ) to work out which cranial nerve is affected.
The causes of double vision are summarised in Box 8.5 and Figs. 8.10 and 8.11 .
Monocular |
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Binocular |
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Ocular discharge results from either an increase in production or a decrease in drainage from the ocular surface. Irritation of corneal nerves activates cranial nerve V(I), resulting in a reflex tearing response.
Tears normally drain from the ocular surface through the puncta, small openings to the medial end of the upper and lower eyelid, into the nasolacrimal duct, which opens below the inferior turbinate in the nasal cavity. Consequently, blockage of tear drainage or an abnormal lid position can also result in excessive discharge.
Ask:
Is the discharge clear or opaque? If opaque, what colour?
Is the discharge watery or sticky?
Is the discharge associated with any other features (e.g. pain, foreign body sensation, red eye or itchiness)?
The clinical features of different types of eye discharge are summarised in Box 8.6 .
Causes | Clinical features |
---|---|
Bacterial conjunctivitis |
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Viral conjunctivitis |
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Blocked tear duct |
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Trichiasis/foreign body |
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Allergic conjunctivitis |
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Blepharitis |
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Poor tear film/dry eyes |
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The orbit is enclosed by bone on all sides, except anteriorly. As a result, orbital swelling can lead to the anterior displacement of the globe and proptosis.
Ask if the swelling is:
Unilateral or bilateral?
Acute or gradual in onset?
Associated with pain?
Associated with itch or irritation?
Associated with double vision?
Box 8.7 summarises the common causes of swollen eyes.
Category | Causes | Clinical features |
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Infective |
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Inflammatory |
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Neoplastic |
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Systemic |
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Vascular |
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Pseudoproptosis |
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Ask the patient whether they have any known ophthalmic conditions. Enquire specifically about amblyopia (a reduction in vision in one eye from childhood), as this may limit best-corrected visual acuity. Check whether the patient normally wears glasses or contact lenses, and ask about the last time they had their eyes checked for refractive correction. Also ask about any previous eye surgery, as this may also limit vision.
Focus on systemic diseases that can affect the eyes. In particular:
a history of diabetes or hypertension, especially in the context of visual loss
thyroid disease in the context of red, swollen eyes or double vision.
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