Eye Examination & Vision Assessment

Written by: Andrew Swampillai from Leicester, Northampton and Rutland Deanery,

Introduction
Examination of the eyes is a popular OSCE station in many medical schools but one that is often taught haphazardly on Ophthalmology placements. The examination of the ocular structures and function need not frighten the medical student and is similar in structure to examination of other systems of the body. The student or junior doctor should bear in mind that the eye is the only organ that can be examined from both inside and outside and so detection of ocular problems need not be onerous.

Assessment of the eyes and vision consists of two main components: history taking (covered in the article on Ocular History Taking) and anatomical/functional testing. Following these steps will ensure that the eyes are examined in a systematic and thorough manner. As with all examinations, not all these tests are needed and history taking will be the guide as to what ocular functions need to be assessed. This list is not meant to be exhaustive but should help guide you in terms of directing your differential diagnosis of common ocular problems that present in general practice and eye casualty.

ASSESSMENT OF VISION AND OCULAR FUNCTION

The examination of ocular function can be broadly categorised into four parts: 1. 2. 3. 4. Visual acuity Visual fields Pupillary reactions Extraocular movements

For this you will need: Snellen chart with pinhole aperture Pen torch Red hat pin Occluder for cover testing

Visual acuity
Visual acuity is tested by use of the Snellen chart. This is a board that consists of high contrast letters, decreasing in size as one reads the letters to the bottom. Depending on which Snellen chart is used, the patient will be positioned at 3 or 6 metres. Each row is denoted a number from 6 to 60 and corresponds to the distance from which a normal eye, i.e. one without refractive errors, could read that row of letters e.g. a row denoted 12, means that a normal eye can read that row at 12 metres.

To examine a patient, test each eye separately by asking the patient to cover one eye with their hand or by using a hand-held occluder. If a patient wears spectacles, then these should be worn. Ask the patient to read down to the lowest row of letters that they can see clearly. Then test each eye again with the pinhole. The use of the pinhole should give a more accurate reading of their visual acuity, as any true refractive errors not corrected by the patients spectacles will be eliminated by the pinhole. Visual acuity is recorded as the distance at which the patient is positioned from the chart (numerator)

over the number of the lowest line read (denominator). For example, if a patient read to line 12 and was positioned at 6 metres, their visual acuity is recorded as 6/12.

Normal visual acuity is defined as 6/6. Sometimes if a patient reads a row but gets one or two letters incorrect, the visual acuity can be recorded with a negative value; for example, if a patient reads to the line 12 but reads two letters incorrectly, their visual acuity is recorded as 6/12-2. For anymore than two letters misread, the the previous line read correctly should be recorded as the true visual acuity.

If a person cannot read any lines, counting fingers (CF) can be tried by asking the patient to see how many fingers they can see you holding at 1 metre. If this is unsuccessful, proceed to elicit whether the patient can percieve hand movements (HM). If this also proves to be unsuccessful, test light perception by use of a pen torch. If the patient sees nothing at all, then the visual acuity should be recorded as NPL (no perception of light).

Other tests of visual acuity For patients who are illiterate, a Snellen chart of randomly arranged capital letter 'E' can be used. Like the normal Snellen chart, these are arranged in decreasing order of size and in different directions. The patient is asked which direction the letter 'E' is facing.

For paediatric patients, there are a variety of assessment tools to test visual acuity: Infants up to 2 years: Cardiff cards Toddlers 2-3 years: Kay's pictures Young children 4-5 years: Sheridan-Gardiner test

Visual fields
Confrontational visual field testing is a relatively simple method and relies on comparing the patient's visual fields with your own. Sit in front of the patient about 1 metre away. Ask the patient to cover one eye with their hand. If the patient covers their left eye, cover your own left eye i.e. the contralateral eye, with your hand as well. Ask the patient to focus on your face and not move their eyes anywhere else, otherwise the test is void. Placing your arm to the outside, maintain an equidistance between yourself and the patient. Hold a random number of fingers and ask the patient how many fingers you are holding. Do this another two times in each quadrant. N.B. this will involve you swapping your hands to keep the same eye covered.

A more accurate way of doing this is by use of a white hat pin. If a visual defect is present, work towards the centre to see if the defect passes away. Repeat the test again for the other eye.

Pupillary reactions
Testing pupillary reactions requires a dimly light room, to avoid interference from daylight. The patient should focus on a target, so as to eliminate the accommodation reflex. A pen torch is used and should be positioned from just below, to prevent causing any discomfort to the patient by suddenly shining a bright light directly onto their eyes.

Direct light response First check pupillary response to light by slowly introducing the light from the pen torch onto that eye (direct light response). Normal response is constriction of the pupil. Failure for this to happen is known as an afferent pupillary defect and indicates a pathology with the corresponding optic nerve. Check the response of the other eye (to assess the consensual response).

Swinging flashlight response Shine light onto one eye for about 3 seconds and then rapidly alternate to the other eye and back. A normal response should be brisk constriction of each pupil as light is shone onto the eye, with a consensual response seen in the other eye i.e. constriction. An abnormal response can be seen when light is shone onto the diseased eye - a dilation process ensues. This is known as a relative afferent pupillary defect (Marcus Gunn Pupil) and indicates that the sensory (afferent) stimulus sent to the midbrain is impaired.

Light-near dissociation reflex This test is performed in a well lit room and tests for the accommodation reflex. This is done by asking the patient to focus on an object or a wall in the distance. Inform the patient that you will soon bring a hat pin/tip of a pen into their visual field but not to look at this unless told to do so. Introduce this object into their line of vision and ask the patient to now focus on the object, observing their pupils. A normal response is pupillary constriction as the eye accommodates to focus. Failure to do this is termed light-near dissociation.

More information on pupillary disorders can be found in the article on Pupillary Abnormalities.

Extraocular movements
To perform this test, you should know which nerves innervate which eye and how each extraocular muscle works: Cranial Nerve IV (Trochlear): innervates the superior oblique Cranial Nerve VI (Abducens): innervates the lateral rectus Cranial Nerve III (Oculomotor): innervates all the remaining muscles (i.e medial rectus, inferior oblique, superior rectus and inferior rectus)

Each eye is connected to six different extraocular muscles. The functions of each muscle are: Superior oblique: Depresses the eye when looking medially Inferior oblique: Elevates the eye when looking medially

Superior rectus: Elevates the eye when looking laterally Inferior rectus: Depresses the eye when looking laterally Medial rectus: Adduction when pupil moving along horizontal plane Lateral rectus: Abduction when pupil moving along horizontal plane

A simple and well known mnemonic to remember the innervations of the extraocular muscles is "SO4, LR-6, everything else-3" (Superior Oblique - cranial nerve 4, Lateral rectus - cranial nerve 6, all other muscles - cranial nerve 3).

Sit up close, in front of the patient. Tell the patient that you are going to stabilise their head, by gently place your hand underneath their chin. With the other hand, ask the patient to focus on your index finger and follow it with their eyes only. You should trace an imaginary 'H' shape and look at how both eyes move. Check for any nystagmus or inability of one eye to move in accordance with your finger (palsy). Ask the patient if there was any diplopia when looking in any particular way.

Specific information on nerve palsies can be found in the article on Extraocular nerve palsies.

Optic nerve function

Testing for pathology at the level of the optic nerve can only be done after tests for visual acuity and RAPD have been carried out. The main way to assess optic nerve function is to test for colour impairment/ This is primarily done by use of the Ishihara colour plates, which test primarily for redgreen colour defects. The Ishihara test conists of using a book of plates with a circle of dots with varying size and colour. Within the circle is a seprate entity of dots that form a random number or alphabet. These figures will be visible to those with normal colour vision but not to those with redgreen defect. There are usually 15 plates in total and th examiner will flick through each plate, giving a 5 second delay between each plate. A colour defect will become apparent after the use of a few plates. A score of 13+/15 is considered normal. If there is no access to the Ishihara colour plates or the patient is illiterate, a brightly coloured object (red) can be used. If the patient says that the colour appears washed out, this should alert the examiner to optic nerve pathology.

EXAMINATION WITH THE SLIT LAMP

The examination of the eyes should be methodical so as to not miss out any areas of potential pathology. For this reason, most doctors in eye casualty examine the eyes "front to back" - i.e. from lids to optic nerve.

Eyelids
This ideally should be performed with the use of a slit lamp. Examine both upper and lower eyelids, making sure to compare one with the other. Note the position of the eyelids for drooping (unilateral or bilateral? Complete or incomplete?). Are the eyelids unusually everted or inverted? Are the eyelashes normal (presence of crusting or aberrant eyelashes)? Is there any presence of swelling or erythema? Has the patient sustained a laceration (consider if the cornea is involved)? Any unusual lumps or bumps? If you suspect that a foreign body is under the eyelids, you will need to evert these to gain as much access possible. It is good practice to do this with the use of a local anaesthetic but this is not always necessary. Gain consent first from the patient and warn them that you will fold back their

eyelids for a few seconds to examine inside. To do this, ask the patient to look down. With the base of your thumb and index finger, grab hold of the edge of the eyelid, folding it over a cotton bud to expose the tarsus and fornix. Clean out any foreign body that is not embedded too deeply.

Things to consider: Droopy eyelids (ptosis): Horner's syndrome, Myasthenia Gravis, Bell's palsy, Blepharochalasis, Myotonic dystrophy Eyelid folding: (inwards) Entropion, (outwards) Ectropion Eyelashes: (growing inwards) Trichiasis Inflammation: Blepharitis Swelling/Erythema: Orbital cellulitis Laceration: refer immediately to eye casualty Lumps or bumps: Chalazion, Sebaceous Cyst, Basal cell carcinoma, Squamous cell carcinoma

Lacrimal system
Examining the lacrimal system begins with inspecting the eyelids as mentioned above. Check for whether entropion and ectropion are present, as these interfere with drainage through the puncta (minute orifices from which the canaliculi begin). Entropion particularly poses a problem as the eyelid is everted, causing the lower punctum to be turned away from the ocular surface and hence lead to epiphora (overspill of tears). Examine the punctum under the slit lamp to check for any stenosis caused by scarring or papillomas. The medial canthus should be examined in detail for any unusual erythematous swellings and discharge (dacrocystitis). Patients who complain of sore-gritty eyes with a foreign body sensation should be checked for dry eyes. To do this, the eyes should be stained by fluorescein eye drops by asking the patient to look up and inserting a drop into the lower fornix. The patient then blinks to spread the fluorescein across the ocular surface. Slit lamp settings are then adjustered to cobalt blue light and the patient's eyes are examined with this light shining on them to give a luminous green appearance. Dry eyes may reveal mucin strands and punctate epithelial erosions on the cornea. The tear film should be assessed by asking the patient to blink with the fluorescein and measuring how long the film takes to break - normal timing is at least 10 seconds. N.B. The Schirmer's test is no longer used in most ophthalmic departments.

Conjunctiva
Be sure to examine both the upper and lower fornices in both eyes. This is done by everting the eyelids as described previously. Assess the colour of the conjunctiva. Check for any follicles or papillae. Be also sure to check for any foreign bodies that may be stuck in the folds of the conjunctiva.

Things to consider: Colour: mild pink/perilimbal injection (uveitis), deep red (subconjunctival haemorrhage) Discharge: watery (viral conjunctivitis), mucoid (vernal conjunctivitis), purulent (bacterial conjunctivitis) Papillae: allergic/bactrial conjunctivitis Follicles: viral conjunctivitis Pinguecula: translucent yellowish deposits at the limbus Pterygium: fibrovascular opacity growing over cornea to the nasal limbus

Cornea

It is best to check corneal sensation before instilling any fluorescein drops, which contain local anaesthetic. This can be done by assessing sensation on both sides by lightly touching the surface with a wisp of cotton. A brisk blink reflex should follow. Then fluorescein can instilled and the cornea examined under blue light to see if any epithelial loss (ulcer or abrasion) is present. Penetrating injuries should be carefully ruled out by the Seidel test: application of 10% fluorescein to the suspected site of injury will change the fluorescein from a brownish to a light orange colour due to dilution with aqueous.

Things to consider: Shape: abnormally steep (keratoconus), abnormally flat (cornea plana) Ulcers: Herpes simplex (dendritic), Mooren's (peripheral), Dellen (saucer shaped) Bacterial keratitis: redness, photophobia, pain, foreign body sensation Viral keratitis: corneal anaesthesia Fungal keratitis: usually the same presentation as bacterial. May be diagnosed following keratitis presumed to be bacterial, but which is not responding to treatment

Anterior chamber
The presence of pus in the anterior chamber (hypopyon) can indicate inflammation i.e. uveitis or something more sinister such as endophthalmitis. Uveitis can be confirmed by angling the slit lamp light at 30 degrees to the cornea. Flare (cloudiness - like a beam of light passing through a smokey room) is usually indicative. Blood settling in the inferior aspect of the chamber (hyphaema) is usually caused by trauma. The iris should also be assessed for discrepancy in colour (heterochromia) and any suspicious lesions such as iris melanomas. In glaucoma suspects, gonioscopy is performed to view the iridocorneal angle by use of a "three way mirror" or goniolens, but this is outside the scope of this article. Pupil sizes should be noted for discrepancy (anisocoria). The size may also be distorted in acute angle aclosure glaucoma (oval) or anterior synechiae (general shape distortion).

Lens
The lens should ideally be examined in a dilated patient. Depending on the patient, you may see eyes with normal lens (phakic) or artificial lens (pseudophakic). Patients may be aphakic due to a number of conditions. Early signs of cataracts can be spotted with experience. Usually a dimming of the red reflex when the ophthalmoscope is held around arm's length from the patient's eye is a give away, especially in the elderly patient. Slit lamp examination can reveal which type of cataract has formed. Sometimes the lens maybe displaced in a number of congenital conditions. Examining the red reflex in young children and infants can be difficult and should be attempted with the parent holding the child in place and encouraging them to look towards the light of the ophthalmoscope. In some cases, the paediatric ophthalmologist will opt for the use of cyclopentolate 0.5% (a mydriatic and cycloplegic) to help dilate the pupil. Any paediatric patient with a 'white pupil' (leukocoria) should be referred immediately for further investigations.

Things to consider: Dimmed red reflex: cataract (nuclear, cortical or subcapsular) Displaced lens (ectopia lentis): Marfan's, Homocystinuria, Weill-Marchesani, Ehlers-Danlos, Refsum Leukocoria: retinoblastoma, congenital cataracts, Coat's disease

Fundus
The examination of the fundus can be carried out in the primary care setting with the use of a direct ophthalmoscope. More detailed examinations will need the use of a slit lamp or an indirect ophthalmoscope; where a light source is attached to a head-set worn by the ophthalmologist, who holds a lens piece to focus into the eye. The indirect method is useful because it gives a wider view of inside the eye, all the way to the ora serrata (periphery of the retina). Examination with the direct ophthalmoscope should be be started off by warning the patient that you will get very close to them and that they should stare into the distance, unless otherwise told. The red reflex should be attained first by standing at a distance. Then examining with your right eye, advance on the right side of patient, coming up close to their face until you can see the retina and the blood vessels. It is best practice to divide the retina into four quadrants and examine the blood vessels as they come out of the optic disc. To visualise the macula, ask the patient to look directly into the light (making sure that the source is not too bright for them). The macula is two disc diameters to the temporal side. With the slit lamp, a handheld lens (usually 97 diopters) is used to look into the fundus. The image produced will be inverted e.g. a lesion noted through the slit lamp on the inferior side is in reality located in the superior edge. The patient can look in different directions for the ophthalmologist to see different areas of the retina.

Things to consider: Haemorrhages: retinal vein occlusion, diabetic retinopathy, hypertensive retinopathy, retinal detachment, macular degeneration Hard exudates: diabetic retinopathy Cotton wool spots (soft exudates): diabetic retinopathy, hypertensive retinopathy Roth spots: usually pathognomonic of bacterial endocarditis but can be found in leukaemia, diabetes and pernicious anaemia Pale retina: retinal artery occlusion Optic disc: pallor (optic atrophy), oedema (papilloedema), cupping (glaucoma)

AGE RELATED MACULAR DEGENERATION

Age-related macular degeneration (ARMD) is a term used to describe a characteristic pattern of macular change and central visual loss, thought to be associated with the natural ageing process. Commonest cause of irreversible visual loss in the developed world Burden of disease with ARMD likely to increase with an ageing population

PATHOGENESIS
Normal Structure and Function The relevant layers at the back of the eye are: Photoreceptor layer: outermost part of the neuroretina, composed of rods (light perception) and cones (colour perception) Retinal pigment epithelium (RPE) Bruch's membrane Choroid: highly vascular layer providing nutrition to the outer layers of the retina, including the photoreceptor layer

The RPE is a single layer of cells, with microvilli that project in and around the outersegments of the photoreceptors i.e. it is in close association with the neuroretina, but is only loosely attached. The RPE is essential for normal retinal function by carrying out the following tasks: Phagocytosis of redundant external segments of photoreceptors. Recycling of vitamin A and therefore helping regeneration of rhodopsin and cone opsin Absorption of light scattered by the sclera to allow better image formation (RPE cells contain melanin) Facilitating nutrient and waste transfer between the retina and choroid (RPE cells are held together by tight junctions and therefore form part of the blood-retinal barrier)

Bruch's membrane refers to the joint basement membrane of the RPE and the choroid. This contributes to the diffusion barrier between choroidal blood vessels and the retina.

Pathological changes

The progression from normal macula, to dry ARMD through to wet AMD is variable - only 10% of patients will develop wet changes in their lifetime. The risk factors involved in determining progression are as yet uncertain, however the following have been suggested: Increasing age Family history Smoking: single greatest modifiable risk factor in progression Drusen type: soft drusen (larger >63um, ill-defined borders) is more strongly associated with progression from ARM to ARMD than hard drusen (small, well-defined). Increasing number and confluence of drusen also increases risk. Oxidative stress: some evidence that vitamin/mineral supplementation slows progression Cardiovascular risk factors: recent studies have linked poorly controlled hypertension, sedentary lifestyle, obesity, etc with increased risk of progression to wet ARMD.

CLINICAL PRESENTATION
Classic patient: Elderly, caucasian, positive family history

Smoking history (link to progression) Changes tend to be bilateral but asymmetrical

Symptoms: 1. Decreased vision: blurred central vision or central scotoma (more advanced). Usually gradual onset, but may notice more rapid deterioration with wet ARMD (during episodes of haemorrhage/macular oedema). 2. Metamorphopsia/visual distortion: patients may describe certain parts of their visual field appearing bigger (macropsia) or smaller (micropsia) Functionally, as ARMD affects central vision, patients complain of difficulty reading, watching TV, differentiating colours and recognising faces.

Signs: 1. Reduced visual acuity 2. Reduced visual fields: central scotoma + loss of colour saturation/contrast perception 3. Amsler grid: this is a useful tool to quantify and qualify the degree of visual impairment caused. It refers to a grid of vertical and horizontal black lines on a white background, which appear distorted/blurred/darkened in areas corresponding to the patient's scotoma. 4. Ophthalmoscopy: absent foveal reflex drusen (discrete yellow lesions) hypo/hyperpigmented areas (atrophic change) wet changes: haemorrhages, neovascularisation

INVESTIGATION
A good history and examination is usually sufficient to diagnose ARMD. However, the following imaging techniques help (1) confirm diagnosis; (2) identify early wet changes and (3) act as a baseline to monitor disease progression and/or response to treatment.

MANAGEMENT
Aims: (1) preventing progression of disease (2) minimising functional impairment/improving vision-related quality of life

Dry ARMD: Most active interventions for ARMD are only indicated in patients with wet changes. The mainstay of treatment of dry ARMD is watchful waiting and symptom management (discussed later). Observation: 6-24 month follow-up with community optometrists to monitor changes/progression to wet ARMD. Patients may be given a copy of the Amsler grid for selfmonitoring and asked to report any new visual symptoms developing in between visits. Vitamin supplementation (lutein): may be recommended in patients with advanced dry ARMD who are at high risk of progression to wet ARMD. The evidence base for effectiveness is currently under debate. Consequently, these have to be purchased individually by the patient, as they cannot currently be prescribed on the NHS. Smoking cessation: lowers rate of progression in both dry and wet ARMD.

Wet ARMD A number of new therapies have been developed to limit neovascular changes. It must be noted that these do not affect areas of established scarring and fibrosis, so patients may still be left with residual visual loss.

Visual rehabilitation / Symptom management The measures described above are aimed at preventing progression of disease. However, a number of patients will have some degree of irreversible visual loss, that may cause significant functional impairment. Visual loss may be due to progressive geographic atrophy in dry ARMD, or complications of wet ARMD including subretinal haemorrhage, retinal detachment and scar formation. Needs are specific to each patient and must be identified and managed on an individual basis. Some available options include:

Low vision aids, magnifiers Training in eccentric focusing (using peripheral vision to carry out tasks like reading/watching TV that normally involve central vision) Driving: as peripheral vision is spared, most patients with ARMD can continue to drive. However, legally they are required to undergo a DVLA-organised visual field assessment to ensure that the central visual field loss is not severe enough to cause difficulty. Blind registration: a few patients with advanced disease will require to be registered blind, particularly those with long-standing progressive changes.

Allergic Eye Diseases

Written by: Tasleema Begum (Manchester University)

Quick anatomical review

In the context of allergic eye disease the most important parts of the eye to consider are the external aspects of it that are easily accessible to the surrounding environment and hence able to come into contact with various allergens that may cause disease in susceptible patients.

Figure 1: Anatomy of the eye

The diagram above shows some important anatomical parts of the eye. Most allergic conditions of the eye affect the:

Conjunctiva -This is a thin membrane consisting of stratified columnar epithelium which lines the sclera (bulbar conjunctiva) and the eyelids (tarsal conjunctiva). It is richly vascularised and innervated and is responsible for the production of a mucinous solution that contributes to the tear film that is responsible for the protection of the cornea and sclera.

Cornea - This is a clear and transparent avascular structure that occupies the central part of the eye and is responsible for 78% of the focusing power of the eye. It is highly innervated and consists of various layers that allow it to function properly. Endothelial cells of the inner layer continuously pump fluid out of the cornea to ensure clarity is maintained and the right amount of refraction takes place.

Epidemiology
About 20% of the UK population are affected by allergies and of these patients 20% of them experience problems pertaining to the eye. 50% of those seeking help for allergies present with ocular symptoms and allergic eye disease accounts for 15% of GP consultations relating to eye problems.

Classification
The different types of allergic disease consist of: 1. 2. 3. 4. 5. Acute Allergic Conjunctivitis (AAC)/ Ocular urticaria Simple Allergic Conjunctivitis (SAC) seasonal or perennial Vernal Keratoconjuctivitis (VKC) Atopic Keratoconjuctivitis (AKC) Giant Papillary Conjunctivitis (GPC)

AAC This occurs in response to direct exposure to a large amount of airborne or hand borne allergens

Figure 2: Acute Allergic Conjunctivitis

SAC This can be either seasonal or perennial. Seasonal conjunctivitis occurs in response to an allergic reaction to grass, pollen and fungal spores and affects people mainly in spring or summer. Perennial conjunctivitis affects patients all year round and is a reaction to everyday allergens such as animal danders and dust mites.

Figure 3: Simple Allergic Conjunctivitis

VKC This is most common in Arabs and Afro-Caribbeans and is usually more severe in the spring and warm windy conditions. It affects males more commonly and is a condition that affects

children above the age of 5 years. It almost always resolves by puberty. There is intense itching with a stringy mucoid discharge and closer inspection reveals a cobble stoning appearance and white Trantas dots on the upper papillae due to infiltration of inflammatory cells in the palpebral type, while white mucoid nodules around the limbus appear in the limbal type. There is a risk of visual loss if this condition is not adequately managed due to corneal involvement and scarring. Suspect this condition in a patient who is not responding to standard treatment of conjunctivitis and referral to an ophthalmologist is required.

Figure 4: Limbal type Vernal Keratoconjunctivitis

Figure 5: Palpebral type Vernal Keratoconjunctivitis

AKC This is an adult form of VKC and most commonly affects young adult males who present with intense itching and watery discharge. They usually have a history of atopic dermatitis and involvement of the eyelids with thick crusty scarring. These patients may be susceptible to concurrent infections such as Herpes Simplex Virus as are those with VKC. There is a higher rate of corneal involvement than with VKC and some signs of photophobia and visual blurring.

Figure 6: Atopic Keratoconjunctivitis

GPC This is characterised by the presence of large papilla on the conjunctiva of the upper eyelids in response to foreign objects, especially contact lenses.

Figure 7: Giant Papillary Conjunctivitis

Pathogenesis

Type 1 hypersensitivity This is responsible for SAC which is often quite easily managed as well as GPC which usually affects contact lens wearers. Some people may have a type I hypersensitivity reaction to cosmetics that also involves the skin and is known as dermatoconjuctivitis. Type I hypersensitivity reactions involve IgE mediated mast cell degranulation and is the mechanism that underlies conditions such as asthma and eczema. There is an initial sensitisation to an allergen and then mast cell activation on re-exposure which comprises an immediate and late phase reaction.

Type 4 hypersensitivity This is responsible for VKC and AKC and consists of both an IgE mediated response as well as a CD4+ T-cell mediated reaction. These conditions are usually more severe and accompanied by the risk of having vision affected due to corneal involvement. Eosinophils produce major basic protein which is responsible for the corneal inflammation (keratitis) seen in VKC and AKC.

Clinical features
Common: Soreness Redness Stringy discharge Visual acuity is preserved Itchy

Rare: Swelling of the eyelids Chemosis Photophobia

Differential diagnoses includes bacterial and viral conjunctivitis as well as dry eye syndrome and other eye pathologies that cause red eyes such as acute glaucoma and anterior uveitis. Features that are useful in distinguishing allergic eye conditions from others is that allergies are usually itchy and patients often have a personal or family history of other atopic conditions such as hay fever and eczema.

Management
The main aim is to provide symptom relief and control the release of mediators and inflammation. Simple measures Allergen avoidance, cool soothing, lubricating eye drops

Topical treatment Antihistamines: e.g Antazoline, Azelastine, and Emedastine. These are very effective in reducing the itching, but should not be used for longer than six weeks Decongestants: oxymetazdine and tetrahydrozoline hydrochloride. These are useful for reducing the redness of eyes. Mast cell stabilisers: Sodium cromoglicate, Nedocromil and Lodoxamide. The most effective mast-cell stabilizer, which also has antihistamine properties, is olopatadine while Ketotifen also has an anti-eosinophillic activity which makes it very effective. Anti inflammatories: NSAIDs may provide relief from the swelling and redness Steroids: These are reserved for more serious conditions such as VKC and AKC and in those in whom the symptoms are not resolving. They should be avoided in people with bleeding tendencies, cataracts and glaucoma and require an ophthalmologists supervision.

Oral treatment: this is used in those who are not responding to topical therapy Antihistamines: e.g Cetirizine, Loratidine and Fexofenodine Anti inflammatory eg. Diclofenac, ketorolac and flurbiprofen Immunosuppressant e.g ciclosporin and tacrolimus. These may become necessary for the treatment of VKC and AKC

Other treatment: may consist of antibiotic, antiviral or anti-fungal treatment if there is coexisting infection.

Most allergic eye diseases respond well to simple home treatments or over the counter medication, but if there is any pain, visual loss or symptoms lasting longer than 24 hours then medical advice should be sought. The main complications with severe allergies consist of corneal ulcerations and pain with the possibility of a decrease in visual acuity.

Introduction
A cataract is opacity within the lens of the eye, and may affect either one or both eyes. The opacity changes the transparency and refractive index of the lens, resulting in the blurring of a persons vision. According to the World Health Organisation (WHO, 2007), cataracts account for 47.9% of blindness worldwide. The reported prevalence of childhood cataracts ranges from 1-15 per 10,000 children.

Types of Cataract
Nuclear Cataract

Cortical Cataract

Subcapsular Cataract

This occurs at the centre of the lens, and interferes with distance vision. It is the most common type of cataract, and is usually the result of advancing age.

This begins at the outer rim of the lens, and gradually works towards the centre of the lens. It resembles the spokes of a wheel. It is most commonly found in patients with diabetes.

This affects the back of the lens, causing glare and blurring of vision. It is the most rapidly progressing type of cataract. Risk factors for the development of a subcapsular cataract are use of steroids, diabetes, and myopia.

Aetiology

Risk Factors
The following are associated with acquired cataract in developed nations:

Age (above 60 years of age) Smoking Physical trauma Alcohol consumption Sunlight exposure Low educational levels Poor lifestyle habits inclusive of malnutrition and physical inactivity Metabolic syndrome Diabetes mellitus Systemic corticosteroid use and possibly prolonged administration of high doses of inhaled corticosteroids

Pathogenesis
The lens of the eye is composed of specialised cells arranged in a highly ordered and complex manner. These cells are stratified epithelia and have a very high content of cytoplasmic protein; the crystallins. These proteins, along with the complex structure, impart transparency to the lens.

Unlike other epithelia, the lens does not shed nonviable cells. As such, it is particularly susceptible to the degenerative effects of aging on cell structure. The exact pathogenetic mechanisms of this are not known. It has, however been observed that most of the risk factors identified are environmental stressors that lead to the formation of toxins or the impairment of antioxidants.

Clinical Presentation: Symptoms and Signs

Opacification of lens is painless, progressive, and highly variable

Often bilateral but asymmetrical Common complaints include problems with night driving, reading road signs, and reading fine print "Myopic shift" (an increase in nearsightedness) happens prior to opacification of lens Cataracts may present as immature (transmits red reflex), mature (does not transmit red reflex), or hypermature (cortex of lens has liquefied and lens nucleus is mobile within capsule) Mature and hypermature cataracts can give rise to secondary glaucoma that is associated with a red and painful eye (unlike many other glaucoma's)

With regards to the presentation of congenital cataracts: Approximately one-third of congenital cataracts in children are inherited, one third are associated with systemic diseases, and one-third are idiopathic or sporadic.

Parent's observation of cataract Visual behaviour that deviates from normal Asymmetry of red reflex identified on Bruckner testing (simultaneous red reflex test) Leukocoria (white pupillary reflex) Nystagmus Strabismus (Squint) Photophobia Delayed development Family history of hereditary cataracts Genetic disorder associated with cataracts

Cataracts detected in infants and young children must be referred to a specialist as soon as possible in order to allow for normal visual development and to prevent blindness.

Differential Diagnosis
Macular degeneration Presbyopia Retinal disease Retinoblastoma (in children)

Diagnosis

Slit lamp examination

The slit lamp is a binocular microscope

Provides a three dimensional view of the eye

A beam or "slit" of light is used as opposed to diffuse light

Height and width can be adjusted

Anatomic features of the eye can be accentuated

Provides greater magnification and illumination than most handheld devices

Is used to diagnose a number of traumatic and non-traumatic disorders, including cataract

Posterior capsular opacification on retroillumination with slit lamp

Prevention
There is no proven therapy to prevent either cataract formation or its progression once it has developed. However, the following have been observed to be of benefit in decreasing risk: Eating a healthy diet Eating a diet rich in lutein and zeaxanthin Smoking cessation Postmenopausal oestrogen use (longer than 10 years) Vitamin supplementation

Management

Phacoemulsion

Most widely used

Most effective

Safest

The hard lens nucleus is liquefied by an ultrasonic probe

Fragments are aspirated, along with soft lens fibres

Replacement lens (folded) is placed into empty capsular bag where it gradually unfolds

The incision made through lens capsule heals on its own

Complications that may result from surgery

Early complications

Rupture of posterior capsule (3%)

Trauma to iris Prolapsed iris Wound gape Haemorrhage in anterior chamber Rupture of lens capsule with loss of vitreous Vitreous haemorrhage Choroidal haemorrhage Post-operative endophthalmitis Late Complications

Opacification of posterior capsule (20%)

Cystoid macular oedema Uveitis Retinal detachment Open and closed angle glaucoma Age-related macular degeneration

Postoperative thickening of the lens capsule frequently occurs over time causing gradual deterioration of vision. This can be treated by splitting the capsule with a laser.

Prognosis
Postoperatively 95% of patients that have no other complications achieve a corrected acuity of 6/12.

The major risk factors that affect prognosis are diabetes and diabetic retinopathy. Diabetes causes fluctuating blood glucose levels. Occasionally, high blood glucose levels cause oedema and subsequent swelling of the lens. When the blood glucose diffuses, the swelling in the lens also reduces. This repeated action causes cataracts.

In paediatric cataracts, visual acuities of 20/20 to 20/40 may be achieved if cataracts are diagnosed and treated early.

Summary
Cataracts are lens opacities that can range in severity from unnoticed dots to total fogging of vision. Cataracts are by far the commonest cause of preventable blindness worldwide.

Age-related causes are most common, although there are also familial or congenital causes. Gradual painless deterioration of vision is the most common symptom reported, with other possible co-existing symptoms such as glare and problems with night driving dependent on the type of cataract.

Early symptoms can be alleviated with spectacles, but to correct vision, surgery is required. Surgery involves the insertion of an intraocular lens to replace the affected one. The exact technique used is determined by the aetiology and density of the cataracts. Phacoemulsification (a form of small incision surgery) is the most frequently used technique. Further investigations such as blood glucose, serum calcium, and liver biochemistry should be considered in order to diagnose any possible underlying metabolic disorder.

It is also worth noting that cataracts may not always be bilateral, and hence, eyes may be managed and treated individually according to the severity of the cataract within each eye.

he cornea is a transparent, avascular structure. It consists of 5 layers (illustrated below in figure 1): A Anterior Epithelium: Non-keratinised stratified squamous epithelium. Cells migrate from the basal layer upwards and from the periphery to the centre B Bowman's membrane C Stroma: Connective tissue layer, type 1 collagen D Descemet's Membrane E Endothelium: Actively pumps water and ions from the stroma to control corneal hydration and transparency. If damaged, these cells do not regenerate and corneal decompensation occurs where the cornea becomes white and cloudy

Nerve Innervation: Trigeminal nerve (CN V) - Ophthalmic Branch (CN V1) - Long Ciliary nerves

Functions: Refracts light with the lens to focus light onto the retina. Protects the internal ocular structures

Layers of the cornea

Summary of Corneal Pathologies

Corneal Pathologies
Inflammation Corneal oedema, cellular infiltration and ciliary congestion

Infectious Keratitis: The epithelial layer acts as a barrier to infection. Disruption of this barrier and predisposing factors such as abnormal lid anatomy, trauma, contact lens wear and corneal paraesthesia can lead to infection.

The different types of infectious keratitis have been outlined in the table below and illustrated in figures 2 and 3.

Infective Keratitis

Herpes Simplex epithelial keratitis: dendritic ulcers with terminal bubls staining with fluorescein

Herpes Zoster: punctate epithelial errosions and superficial pseudodendrites

Corneal Dystrophy
Corneal dystrophies refer to inherited conditions that cause progressive corneal opacification with age. They tend to be symmetrical in their eye involvement and are classified depending on the layer of cornea that is involved. 1) Epithelial Dystrophy: Cogans microcystic dystrophy; AD inheritance, most common type of dystrophy, mainly asymptomatic but causes corneal erosions. 2) Bowmans Layer Dystrophy

3) Stromal Dystrophy: Lattice dystrophy; AD inheritance, leads to amyloid deposits in the stroma causing corneal erosions commonly treated with keratoplasty.

4) Endothelial Dystrophy: Fuchs; AD inheritance/sporadic, F>M, onset 50+. Damaged endothelial cells are unable to efficiently pump H20 ions causing corneal oedema. Associated with Bullous Keratopathy where endothelial decompensation occurs secondary to oedema. This can also be caused by intraocular surgery, herpetic keratitis, uveitis or trauma.

Corneal Ectasia
Keratoconus is a bilateral, asymmetrical disorder of conical protrusion of the centre of the cornea.

Associations:

Common in asians Atopy Down's Syndrome Retinitis Pigmentosa Connective Tissue Disease

Symptoms: Blurred vision Diplopia Glare

Signs: Progressive astigmatism and myopia Irregular astigmatism on refraction Munsons sign: protrusion of the lower lid on down gaze caused by coning of the cornea (illustrated in Figure 4)

Investigations: Keratometry: assess degree of astigmatism: high degree of irregular astigmatism Pachymetry: measures corneal thickness: thin cornea Computer assisted topography detects coning

Treatment: Glasses can correct astigmatism Contact lenses: rigid gas permeable lenses or piggyback lenses Corneal graft: full/partial thickness

Keratoglobus: rare bilateral thinning of the entire cornea, highly susceptible to rupture from minor trauma.

Exposure Keratopathy
Exposure keratopathy occurs as a result of inability to close the eyelids which exposes the corneal surface, allowing it to dry out, occasionally leading to infection and even perforation. Associations: Thyroid eye disease Bells palsy Any cause of proptosis

Symptoms: Foreign body sensation Epiphora Burning & irritation

Signs: Poor Bells phenomenon Corneal opacification & ulceration Conjunctival injection

Treatment: Mild: Artificial tears & lubrication may suffice Moderate: Artificial tears & hourly lubrication ointment Severe: Will need antibiotic prophylaxis +/- treatment Taping the eyelids closed at night is a temporary measure and permanent measures include lid tightening procedures & gold-weight insertion into the upper lid.

Corneal Foreign body and Ocular trauma

When describing an anterior segment injury it is important to classify the mechanism and nature of the injury; the terms below are an example of a classification system.

1. 2. 3. 4. 5. 6.

Closed injury: blunt trauma leaving the globe intact Open injury: blunt/penetrating trauma causing full thickness defect in the globe Penetrating injury: single defect on entry of object into the globe, no exit Perforating injury: entry and exit wounds of the penetrating object Laceration: sharp object causing a partial/full thickness wound Rupture: full thickness globe defect, not necessarily at site of trauma but at a weak point in the globe.

Assessment: When assessing the trauma remember to go through the basics of history and examination. Investigations such as a B scan can often be useful in assessing damage to the posterior segment. Management: Conservative: A: Analgesia and anti-emetics B: Antibiotics C: Protective cover and topical cycloplegia Remove foreign bodies with the aid of topical anaesthesia. Observe for infection.

Surgical: (management prior to surgery) A: Analgesia and Anti-emetics B: Antibiotics C: Protective cover Tetanus prophylaxis

Chemical Injury Alkali injuries are more severe than acid injuries as they cause saponification of the cell membrane which results in cellular disruption. Once the surface epithelium has been damaged, the alkali can penetrate further into the stroma. Immediate management: Test the pH of the eye and wash out with normal saline until the pH is neutralised. On examination: Determine the nature of the injury and assess degree of limbal ischaemia and corneal clouding Commence: Oral analgesics and Cyclopentolate Prophylactic topical antibiotics, oral doxycycline Topical steroids Topical ascorbate Preservative free ocular lubricants

NOTE: chemical injuries can lead to many long term complications:

Cataract Secondary glaucoma Dry eyes Corneal opacification/corneal scarring Perforation