1. Ptosis (drooping of one or both upper eyelids).

2. The colour of the sclerae:

TABLE 13.2 Causes of uveitis

Iritis (anterior uveitis)     Idiopathic     Generalised disease        • Seronegative spondyloarthropathies        • Inflammatory bowel disease        • Diabetes mellitus        • Granulomatous disease—e.g. sarcoidosis        • Infections—e.g. gonococcal, syphilis, toxoplasmosis, brucellosis, tuberculosis

Choroiditis (posterior uveitis)     Idiopathic     Generalised disease        • Diabetes mellitus        • Granulomatous disease—e.g. sarcoidosis        • Infections—e.g. toxoplasmosis, syphilis, tuberculosis, toxocaral infection

The uveal tract consists of the anterior uvea (iris) and posterior uvea (ciliary body and choroid).

Look from behind and above the patient for exophthalmos, which is prominence of the eyes. If there is actual protrusion of the eyes from the orbits, this is called proptosis. It is best detected by looking at the eyes from above the forehead; protrusion beyond the supraorbital ridge is abnormal. If exophthalmos is present, examine specifically for thyroid eye disease: lid lag (the patient follows the examiner’s finger as it descends—the upper lid lags behind the pupil), chemosis (oedema of the bulbar conjunctiva), corneal ulceration and ophthalmoplegia (weakness of upward gaze). Look then for any corneal abnormalities, such as band keratopathy or arcus senilis.

3. Look for corneal ulceration which may be obvious if severe. A drop of sterile fluorescein will stain corneal ulcers.

4. Proceed then as for the cranial nerve examination—that is, testing visual acuity, visual fields and pupillary responses to light and accommodation. Interruption of the sympathetic innervation of the eye at any point results in Horner’s syndrome (partial ptosis and a constricted but reactive pupil). Perceptible anisocoria (inequality of the diameters of the pupils) has been found in 20% of normal people. Remember also that elderly people quite often have imperceptible pupillary light reactions.

5. Test the eye movements (Figure 13.4). Look also for fatiguability of eye muscles by asking the patient to look up at a hat-pin or finger for about half a minute. In myasthenia gravis the muscles tire and the eyelids begin to droop.

6. Test colour vision if acuity is not poor. Ishihara test plates (where coloured spots form numbers) can be used. Red desaturation (impaired ability to see red objects) can occur with optic nerve disease. Red-green colour blindness affects 7% of males (X-linked recessive).

7. Test the corneal reflex. Consider the possibility that the patient may have a glass eye. This should be suspected if visual acuity is zero in one eye and no pupillary reaction is apparent. Attempts to examine and interpret the fundus of a glass eye will amuse the patient but are always unsuccessful.

8. Perform fundoscopy. Successful ophthalmoscopy requires considerable practice. It is important that it be performed in reduced ambient lighting so that the patient’s pupils are at least partly dilated and the examiner is not distracted. It can be easier to perform the examination, especially of the fundi, through the patient’s spectacles. Otherwise, the patient’s refractive error should be corrected by use of the appropriate ophthalmoscope lens. The patient should be asked to stare at a point on the opposite wall or on the ceiling and to ignore the light of the ophthalmoscope. Patients will often attempt to focus on the ophthalmoscope light and should be asked not to do this.

Begin by examining the cornea. Use your right eye to examine the patient’s right eye, and vice versa. Turn the ophthalmoscope lens to +20 and examine the cornea from about 20 cm away from the patient. Look particularly for corneal ulceration. Turn the lens gradually down to 0 while moving closer to the patient. Structures, including the lens, humour and then the retina at increasing distance into the eye, will swim into focus.

Examine the retinas (Figure 13.5; see also Figure 11.8, page 336). Focus on one of the retinal arteries and follow it into the optic disc. The normal disc is round and paler than the surrounding retina. The margin of the disc is usually sharply outlined but will appear blurred if there is papilloedema or papillitis, or pale if there is optic atrophy. Look at the rest of the retina, especially for the retinal changes of diabetes mellitus or hypertension.

There are four types of haemorrhages: streaky haemorrhages near the vessels (linear or flame-shaped); large ecchymoses that obliterate the vessels; petechiae, which may be confused with microaneurysms; and subhyaloid haemorrhages (large effusions of blood which have a crescentic shape and well-marked borders; a fluid level may be seen). The first two types of haemorrhage occur in hypertensive and diabetic retinopathy. They may also result from any cause of raised intracranial pressure or venous engorgement, or from a bleeding disorder. The third type occurs in diabetes mellitus, and the fourth is characteristic of subarachnoid haemorrhage.

There are two main types of retinal change in diabetes mellitus: non-proliferative and proliferative. Non-proliferative changes include: (1) two types of haemorrhages—dot haemorrhages, which occur in the inner retinal layers, and blot haemorrhages, which are larger and occur more superficially in the nerve fibre layer; (2) microaneurysms (tiny bulges in the vessel wall), which are due to vessel wall damage; and (3) two types of exudates—hard exudates, which have straight edges and are due to leakage of protein from damaged arteriolar walls, and soft exudates (cottonwool spots), which have a fluffy appearance and are due to microinfarcts. Proliferative changes include new vessel formation, which can lead to retinal detachment or vitreous haemorrhage.

Hypertensive changes can be classified from grades 1 to 4:

It is important to describe the changes present rather than just give a grade.

Inspect carefully for central retinal artery occlusion, where the whole fundus appears milky-white because of retinal oedema and the arteries become greatly reduced in diameter. This presents with sudden, painless unilateral blindness, and is a medical emergency.

Central retinal vein thrombosis causes tortuous retinal veins and haemorrhages scattered over the whole retina, particularly occurring alongside the veins (‘blood and thunder retina’). This presents with sudden painless loss of vision which is not total.

Retinitis pigmentosa causes a scattering of black pigment in a criss-cross pattern. This will be missed if the periphery of the retina is not examined.

In retinal detachment, the retina may appear elevated or folded. The patient describes a ‘shade coming down’, flashes of light or showers of black dots. A diagnosis requires immediate referral to try to prevent total detachment and irrevocable blindness.

White spots occur in choroiditis which when active have a fluffy edge (e.g. in toxoplasmosis, sarcoidosis).

Finally, ask the patient to look directly at the light. This allows the examiner to locate and inspect the macula. Macular degeneration is the leading cause of blindness; central vision is lost. Drussen formation occurs in macular degeneration—small deposits are seen under the epithelium in the central retina. Macular degeneration may occur secondary to an atrophic or neovascularisation process.

9. Palpate the orbits for tenderness. Auscultate the eyes with the bell of the stethoscope—the eye being tested is shut while the other is open and the patient is asked to stop breathing. Listen for a bruit that may be a sign of an arteriovenous malformation or a vascular tumour.

10. Feel for the pre-auricular node (adenoviral conjunctivitis).