• high dietary intake of lutein/zeaxanthin ³—carotenoids in plants with orange, red or yellow colour, fish and green leafy vegetables. Also high intakes of omega-3 polyunsaturated fatty acids may decrease the incidence of nuclear cataract and higher intake of protein may decrease the risk of posterior subcapsular cataract.²

RED EYE

Red eye is very common and covers a broad spectrum of anterior segment diagnoses.

Conjunctivitis

Conjunctival inflammation is the predominant feature. Patients present with a red eye and mucopurulent discharge. The eyelids commonly become ‘stuck together’ overnight and difficult to open on waking. Ocular discomfort varies from surface irritation (e.g. sandiness/grittiness) to pain.

Signs include generalised conjunctival erythema, swelling and discharge. The conjunctiva develops distinct papillae (lymphoid tissue with a central vascular core) or follicles (collection of chronic inflammatory cells), depending on the aetiology. Vision is usually unaffected.

The multiple aetiologies, often separable by history, symptoms and discharge, include those described below.

Common

Bacterial conjunctivitis

(Staphylococcus epidermidis/aureus, Streptococcus pneumoniae, Haemophilus influenzae)

The conjunctiva appears ‘beefy red’ with yellow/green and mucopurulent discharge.

Treatment—antibiotic drops (e.g. chloramphenicol) initially every 2 hours during waking hours if severe, then q.i.d. for 1 week. Heat and lubricants can relieve symptoms. Antibiotic ointment can be used at bedtime.

The second eye usually becomes involved within a few days. Complete resolution is common within 1–2 weeks.

Viral conjunctivitis (predominantly adenovirus)

Follows contact with an affected person in epidemics, less commonly after a viral illness. Patients present with very red eye(s), lid swelling, watering and photophobia, and discomfort may be severe.

On examination there is marked conjunctival erythema and a clear watery discharge, pseudomembranes and subconjunctival haemorrhages if severe, and tender pre-auricular and cervical lymphadenopathy.

Treatment is symptomatic—cold or warm compresses and lubricant tear drops. For most patients this is adequate.

The condition is typically unresponsive to antibiotics and often worse in the first 3–7 days before slow resolution, which takes 2–3 weeks. It is rarely complicated by corneal inflammation (keratitis), which may lead to a longer duration and visual compromise through corneal scarring. These patients need to be referred to an ophthalmologist, who may prescribe weak steroid drops.

FIGURE 28.3 Red eye flow chart

Allergic conjunctivitis

This is usually seasonal (often with hay fever) or there is a known history of allergy. Patients present with red eyes, swollen eyelids, itching and watering. Conjunctival erythema is mild and pink, rather than red. The discharge may be whitish mucus, or clear and watery.

Treatment—involves flushing out the allergen with frequent use of unpreserved lubricant drops.

If severe, the patient should be referred to an ophthalmologist for anti-inflammatory and mast cell stabiliser drops such as fluorometholone and olopatadine or ketotifen.

The prognosis is usually good: most patients do not require long-term medication.

Uncommon

Patients with the conditions described below should be referred to an ophthalmologist for diagnosis, swabs and treatment co-managed with a sexually transmitted disease specialist.

Chlamydia

(Chlamydia trachomatis)

Patients complain of longstanding ocular symptoms, unresponsive to different treatments. A history of sexually transmitted disease is not always apparent, and the patient may be asymptomatic.

On examination there is conjunctival erythema, eyelid swelling, mucopurulent discharge and pre-auricular lymphadenopathy.

Treatment—includes systemic antibiotics (e.g. doxycycline for 3–6 weeks).

Gonorrhoea

(Neisseria gonorrhoeae)

While men may have urethral discharge, it is often asymptomatic in women.

The ocular symptoms and signs are florid. Patients present with red eye and creamy discharge. On examination there is profuse, thick, white purulent discharge and pre-auricular lymphadenopathy.

Keratitis occurs in severe infection and is vision threatening. It requires urgent referral to an ophthalmologist and hospital admission for intravenous antibiotic (e.g. ceftriaxone).

Prevention

This must be reinforced by the general practitioner. Infective conjunctivitis is highly contagious: make patients aware of this!

FIGURE 28.4 Infective conjunctivitis

Patients should avoid touching their eyes and avoid sharing towels and pillow cases. They should wash their hands frequently, and every time after touching their face or eyes.

Patients should be given a medical certificate for a week, or while the eyes are red and discharging, occasionally longer in the case of viral conjunctivitis.

Sexually transmitted infection requires co-management and education with a specialist in this field.

Blepharitis

Blepharitis is a very common condition, with flaky deposits and crusting on the eyelashes. Patients complain of gritty, sandy and irritated eyes. Deposits and oil droplets can be seen with magnification or, if severe, with the naked eye, over the meibomian gland orifices.

An ophthalmologist usually diagnoses these patients and the treatment needs to be reinforced by the general practitioner.

Lid and lash hygiene techniques involve washing the eyelashes with baby shampoo, with eyes closed, and topical lubricants. As this is often ongoing, the frequency of washing is tailored to control the symptoms.

If severe or associated with acne rosacea, the ophthalmologist may prescribe doxycycline 50 mg daily for at least 6 weeks. Tetracycline antibiotics alter the lipid chemistry of the eyelid glands and the protective effect may last for up to a year.

Chalazion

A chalazion is an eyelid inflammatory mass caused by blockage of meibomian glands.

Treatment—massage with a hot wash cloth, and lid and lash hygiene as above. Surgical incision and curettage under local anaesthetic if conservative treatment fails.

Episcleritis and scleritis

Episcleritis and scleritis are inflammatory conditions affecting the episclera and the sclera.

FIGURE 28.5 Blepharitis

FIGURE 28.6 Eyelid chalazion and lid margin stye

Episcleritis causes a tender red eye. The redness is over the bulbar sclera and maybe localised, sectoral or diffuse. There are no other ocular signs. It is rarely associated with an underlying systemic condition. Symptomatic treatment with lubricants and/or non-steroidal anti-inflammatory drops leads to complete resolution.

Scleritis is uncommon and characterised by a deep, severe ocular pain. This needs to be referred to an ophthalmologist for management, as it may be vision threatening. Scleritis may be associated with autoimmune disease (rheumatoid arthritis, Wegener’s granulomatosis, systemic lupus erythematosus, scleroderma) and treatment may involve systemic immunosuppression.

Pterygium and pinguecula

A pathologically identical, fleshy conjunctival overgrowth changes from pinguecula to pterygium when it extends onto the cornea.

Damage occurs to the conjunctival basal cells as a result of sun exposure.

Patients present with ocular irritation, redness and, rarely, altered vision from corneal indentation, impingement on the visual axis or dry eye.

Treatment—ocular lubricants and protection from sun exposure. Patients should be encouraged to wear a hat and wraparound sunglasses. Patients predisposed to pterygium (blue eyes, fair complexion) are also at increased risk of skin cancers and should be warned about this.

FIGURE 28.7 Episcleritis

FIGURE 28.8 Pterygium

If symptoms are severe and unresponsive to lubricants, the ophthalmologist may prescribe a weak steroid for a short time to control inflammation, or recommend surgical excision. The pterygium is excised and a conjunctival graft is sutured onto the defect to decrease the chance of recurrence. Surgery has a high success rate.

Occasionally, precancerous dysplasia and frank squamous cell carcinoma may mimic a pterygium.

Corneal disease

Abrasion, foreign body

A corneal abrasion, usually from trauma, is an epithelial defect that stains with fluorescein.

Check the cornea for a foreign body. A metallic foreign body rapidly forms a rust ring and requires prompt removal with adequate anaesthesia, movement control, magnification and illumination.

Patients present with a history of trauma and a painful, watery and red eye. Depending on the location of the defect (central or peripheral) and the size, vision might be affected.

Treatment—prevention and detection of infection while healing occurs, usually within several days. A topical antibiotic (e.g. gtt chloramphenicol q.i.d.) is used until healing is complete. Daily follow-up may be necessary until resolution. Lubricant drops should be used for at least a month to minimise risk of recurrent corneal erosion.

Keratitis (bacterial, viral)

A corneal abscess usually follows corneal trauma, except in contact lens wearers, where microtrauma routinely occurs during insertion and removal; this favours bacterial infection.

A corneal abscess is seen as an area of white cell infiltrate, with an overlying epithelial defect and an inflammatory reaction in the anterior chamber (even to the extent of hypopyon). It is usually extremely painful and if not treated promptly may result in permanent visual loss, secondary to scarring, especially if central.

All contact lens wearers with an acute red eye should be referred to an ophthalmologist that day.

Depending on the size and location of the abscess, an ophthalmologist will perform corneal scrapings to send for urgent microscopy, culture and sensitivity testing. After this, antibiotic treatment with fortified and broad-spectrum antibiotics is commenced. As drops are administered every 15 minutes including overnight, these patients usually require hospital admission.

Prognosis is variable, depending on the organism isolated and abscess location. Pseudomonas, common in contact lens wearers, is extremely aggressive.

Prevention of corneal infection is achieved through patient education, nightly contact lens removal and cleaning with an approved sterilising agent. Contact lenses should be checked regularly for deposits and tears prior to insertion and should be removed from the eyes immediately when ocular pain, redness or decreased vision occurs.

Viral keratitis, usually due to herpes simplex virus (HSV) or herpes zoster virus (HZV), forms a dendrite (branching structure) on the cornea that stains with fluorescein. Corneal sensation is absent when tested with a wisp of cotton, and vision is reduced.

These viruses have a number of ocular (e.g. conjunctivitis, keratitis, uveitis, scleritis, glaucoma, retinitis) and systemic (e.g. cranial nerve palsy, meningitis, stroke) complications.

Avoid and remove all steroid drops if you suspect viral keratitis.

FIGURE 28.9 Bacterial keratitis with abscess

Patients should be referred to an ophthalmologist for assessment and treatment with topical aciclovir 5 times a day. Steroid drops may be added by an ophthalmologist, once the infection is controlled, to minimise scarring.

If the condition is systemic or the patient is immunosuppressed, oral aciclovir/famciclovir/valaciclovir is indicated.

Trauma

Chemical injury

The eyelids, conjunctiva and cornea are commonly affected. Alkali injuries may continue to penetrate deeper tissues even after removal of the toxin.

Treatment should be initiated immediately—lavage with normal saline until pH is neutral. Local anaesthetic may be required. Transfer to hospital with continued irrigation if necessary en route.

Carefully remove particulate matter with a moist cotton bud, check conjunctival fornices to their depths. Assess the depth and extent of injury. Patients with severe injuries are hospitalised and treated with intensive drops to prevent infection and scarring while promoting healing.

Blunt trauma

Blunt trauma sends a shock wave though the globe, which may affect all ocular structures. A systematic examination, from anterior (corneal abrasion, hyphaema, traumatic mydriasis, uveitis) to more posterior (cataract, vitreous haemorrhage, commotio retinae, choroidal rupture, retinal detachment, optic nerve avulsion, ruptured globe) will reveal the damage sustained. Any patient with a history of significant trauma or any signs should be referred to an ophthalmologist. Place a protective shield over the eye without pressure, once the eyelids have been closed gently. Complications (e.g. glaucoma) may occur decades later.

FIGURE 28.10 Corneal dendrite stained with fluorescein

Penetrating eye injury

Patients present with a history of trauma with a sharp object or a small high-speed projectile (e.g. hammering metal on metal). Suspect a penetrating injury or intraocular foreign body from grinding or hammering metal. The signs maybe subtle, but vision is reduced and the iris appears abnormal.

If a ruptured globe, penetrating eye injury or intraocular foreign body is suspected:

• Do not press on the globe.

• Protect the eye with a plastic shield.

• Give analgesia, antiemetic, antibiotic and tetanus booster as appropriate.

• Keep patient fasted.

• Refer to an ophthalmologist as soon as possible for examination, imaging and surgical repair.

Uveitis

Uveitis is inflammation of the uveal tract of the eye, affecting the iris (anterior uveitis), ciliary body (intermediate uveitis) or choroid (posterior uveitis).

FIGURE 28.11 Anterior uveitis with red eye and miosis

Anterior uveitis or iritis is the most common. The patient presents with red eye, photophobia, ocular pain and decreased vision.

On examination there is decreased visual acuity, ciliary injection (perilimbal redness) and pupillary constriction (miosis). Slit lamp examination reveals anterior chamber cells and flare (white blood cells and protein).

FIGURE 28.12 Loss of vision flow chart

Half of anterior uveitis cases are idiopathic.

Associations include:

• systemic diseases

• ankylosing spondylitis (most common) and other HLA B27 positive disease

• sarcoidosis

• juvenile rheumatoid arthritis

• infectious diseases

• HIV medications (rifabutin, cidofovir)

• ocular syndromes

• trauma.

The general practitioner should be involved in the systemic work-up of a uveitis patient. Investigations include blood tests (antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), ESR, C-reactive protein, syphilis test, rheumatoid factor, HLA B27, HIV) and a chest X-ray (tuberculosis and sarcoidosis).

Ocular treatment, initiated by an ophthalmologist, involves steroids and mydriatics. The iris is dilated to prevent central posterior internal adhesions.

In the absence of systemic disease, most patients achieve complete resolution following an episode of acute anterior uveitis. An appropriate referral should be made to a physician if an underlying cause is found or if anterior uveitis becomes recurrent or chronic.

Acute angle closure

Acute angle closure occurs in the presence of an anatomically narrow anterior chamber angle. It is more common in older individuals (larger crystalline lens), females (smaller eyes) and especially people of Chinese descent. It is often precipitated in semi-dark conditions, when the pupil is mid-dilated.

FIGURE 28.13 Acute angle closure

Warning signs may precede full closure: intermittent episodes of ocular pain and redness, with blurred vision and coloured rings around lights. In an acute angle closure crisis, pain is often severe and there may be nausea and even vomiting. Vision blurs as the cornea becomes cloudy, there is perilimbal injection, the pupil is mid-dilated and non-reactive to light, and digital eye pressure is extremely high.

Refer the patient urgently for treatment, to minimise irreversible damage to the anterior and posterior segments of the eye.

Definitive treatment eliminates pupil block and re-establishes aqueous outflow through the trabecular meshwork. A hole is made in the peripheral iris with a laser (laser iridotomy). After the attack has been broken, the patient is assessed and treated if needed, as per primary open-angle glaucoma (see below).

LOSS OF VISION IN THE WHITE EYE

Loss of vision is a common presentation to the general practitioner. On examination the external eye appears normal. Speed of referral to an ophthalmologist depends on the duration and onset of symptoms. Sudden visual loss should be referred promptly and is usually due to a vascular or retinal cause.

Gradual vision loss (BCVA) can be due to cataract and, more rarely, glaucoma. A slow onset of loss may be discovered suddenly by a patient (usually by covering the other eye for the first time).

Cataract

Cataract is opacification of the crystalline lens. It is most commonly related to age (‘senile’ cataract). Other types are congenital, drug-related (steroids, amiodarone, chlorpromazine, anti-glaucoma drops), traumatic, and related to ocular (e.g. uveitis, retinitis pigmentosa) and systemic diseases (e.g. diabetes, atopy, neurofibromatosis, myotonic dystrophy).

Many causes for senile cataract have been investigated, without a single cause found. Sunlight exposure may contribute. Wearing sunglasses and a hat is a relatively simple protective measure. Diet has also been extensively studied, with varied results. In a recent paper, high dietary intake of lutein/zeaxanthin and vitamin E seem to be partly protective.³ Smoking is an independent risk factor.

Visual complaints from cataracts depend on morphology, location and type of lens opacities present. There is commonly a decrease in visual clarity (distance and near, and not correctable with glasses), foggy or misty vision, glare especially associated with driving at night (from oncoming car headlights) and a paradoxical improvement in near vision (nuclear sclerosis increases lens dioptric power, thus possibly facilitating close work focus).

On examination there is decreased BCVA and opacity on red reflex in the visual axis.

A dilated slit lamp examination determines the type, severity and associated ocular conditions requiring management. An assessment is made of the need for and risks of surgery for that individual eye and patient.

Cataracts do not ‘damage’ the eye unless they precipitate angle closure or are allowed to become hypermature. A decision to extract a cataract depends on the patient’s symptoms, visual needs and lifestyle. Poor vision in the elderly is related to depression and an increased risk of falls.

Any surgical procedure should be conducted only when the possible benefits outweigh the risks to an individual patient. In cataract surgery, the cataractous lens is removed and replaced by an artificial one. This is usually conducted under assisted local or topical anaesthesia and most patients are awake but comfortable.

Cataract surgery is generally safe and successful. Complications occur rarely; the most serious include infection (endophthalmitis), intraocular haemorrhage, retinal detachment and decreased vision in the fellow eye from a very rare autoimmune condition (sympathetic ophthalmia). Other complications (raised intraocular pressure, macular oedema, a second-stage operation if zonules or posterior capsule have torn) may lead to a prolonged and difficult postoperative course but often do not prevent good long-term results.

Most patients will need to use antibiotic and steroid drops for around 1 month postoperatively, and attend follow-up with their ophthalmologist during this time. Even years later, opacification of the ‘bag’ (posterior capsule) in which the artificial lens sits may diminish vision. This is treated with a laser posterior capsulotomy.

FIGURE 28.14 Cataract

The general practitioner and the ophthalmologist together facilitate the patient’s readiness for and recovery from surgery.

Glaucoma

Glaucoma is a group of diseases which cause progressive optic neuropathy. They are classified into primary (absence of other conditions) and secondary (known cause). Open versus angle closure describes aqueous dynamics and depends on the gonioscopic appearance of the anterior chamber drainage angle. The most common type of glaucoma in our community is primary open-angle glaucoma.

Primary open-angle glaucoma

The main risk factors for primary open-angle glaucoma (POAG) are advancing age, family history and an elevated intraocular pressure.

The condition is usually asymptomatic in the early stages. As the glaucoma advances, the patient increasingly loses visual field and may complain of bumping into things or falling. Glaucoma causes irreversible visual loss, and is the leading cause of preventable blindness globally.

The key to management is early diagnosis by opportunistic screening, followed by regular monitoring and appropriate treatment.

Diagnosis is made by optic nerve examination and visual field assessment. In a general practice office, a decrease in visual acuity can be measured (not usually from the glaucoma itself), and a visual field defect elicited if sufficiently extensive. A relative afferent pupillary defect (see pupil examination, earlier) detects optic nerve function asymmetry between the two eyes. This is usually the case in early to moderate glaucoma, and is a very useful way for general practitioners to detect this progressive disease simply and quickly while it is asymptomatic.

FIGURE 28.15 Glautomatous optic disc with inferior and superior rim thinning

An ophthalmologist will measure intraocular pressure, and evaluate and record the appearance of the optic nerve head. Diagnostic tests (perimetry) are performed to determine optic nerve function.

Treatment, initiated by an ophthalmologist, involves intraocular pressure reduction, usually at first with drops, but sometimes with laser trabeculoplasty. There are five classes of ocular hypotensive medications: alpha-adrenergic agonists (brimonidine, apraclonidine), beta-blockers (timolol, betaxolol), carbonic anhydrase inhibitors (topical dorzolamide and brinzolamide, systemic acetazolamide), cholinergics (pilocarpine) and lipid receptor agonists (latanoprost, bimatoprost, travoprost). There are also fixed combinations of timolol with some of these, such as with latanoprost (Xalacom™), with travoprost (DuoTrav™), with bimatoprost (Ganfort™), with dorzolamide (Cosopt™) and with brimonidine (Combigan™).

Medications are tailored to the individual patient. All may have local side effects and many have the potential for systemic side effects, as drops can enter the systemic circulation directly through the nasopharyngeal mucosa. In this way, topical medications can mimic intravenous medications.

To widen the systemic safety of topically applied agents, patients should be guided to adopt the ‘double DOT’ instillation technique (Digital Occlusion of the Tear Duct, and Don’t Open Technique). After instilling drops, the lacrimal sac should be occluded steadily with index finger digital compression and the eye closed for 3 minutes. This reduces systemic absorption by two-thirds. If more than one drug is used, wait at least 5 minutes between drops to obtain maximal advantage from each.

Eye pressure can also be reduced by laser and surgical treatments.

Retinal and vitreous detachment

Posterior vitreous detachment (PVD) is part of normal ageing. As the vitreous liquefies and separates from the retina, a peripheral retinal tear can form. If fluid enters through the tear, a retinal detachment follows.

Vitreous detachment causes floaters, seen as black spots that move with the eye in the vision. Symptoms of retinal detachment include new floaters, flashes of light, decreased vision or a new scotoma (area of missing vision). All patients with these symptoms should be referred that day.

Symptoms associated with PVD usually settle spontaneously within months. However, the retina needs to be checked for tears and holes—these can be treated with laser. Retinal detachment often requires surgery.

FIGURE 28.16 Dry macular degeneration with drusen and atrophy

Age-related macular degeneration

There are two types, based on morphology. Dry or atrophic type comprises 80–90% of cases, and is characterised by retinal drusen (deposits of lipid waste products) and areas of atrophy. This leads to a gradual decline in central vision.

Wet or neovascular type occurs in only 10–20% of cases, but is responsible for most severe and sudden visual loss. Retinal features include choroidal neovascular membrane formation, areas of haemorrhage and scarring.

Patients present with a decrease in reading vision, not correctable with reading glasses, distortion of straight lines (metamorphopsia) or missing letters (scotoma) and difficulty recognising faces. These symptoms can occur gradually over years as in the dry form, or suddenly over days in the wet variety.

There is no specific treatment for dry macular degeneration but much research is being conducted in this area. Treatment targets other reversible ocular conditions contributing to visual loss, such as cataract, and monitoring for neovascular changes. Education is provided regarding risk factors, provision of visual aids, support groups and information (see below).

Wet ARMD needs early referral, diagnosis and intervention. Retinal bleeding commonly obscures the neovascular membrane. Ocular coherence tomography (OCT) and fluorescein angiography permit diagnosis and guide management. Neovascular membranes are classified according to proximity to the fovea (subfoveal, juxtafoveal and extrafoveal), type of vascular pattern (e.g. classic or occult) and size.

Juxtafoveal or extrafoveal membranes may be treated with thermal argon laser, as the resulting scotoma is not at the centre of vision.

Subfoveal and some juxtafoveal lesions can be treated with intravitreal injections of an antivascular endothelial growth factor (anti-VEGf). These agents may maintain or even improve vision, and have revolutionised management over the past few years. Injections may be needed every 4–6 weeks while the vascularisation process is active; monitoring is lifelong. The most serious risk of intravitreal injections is intraocular infection (endophthalmitis), with a reported prevalence of less than 1%.

Early diagnosis and treatment in wet ARMD is essential to improve prognosis. Patients are asked to monitor their central vision daily, using an Amsler grid: they look steadily at the central dot, one eye at a time, with reading glasses on, noting any new or changed patches of metamorphopsia. In this way, even mild retinal oedema can be recognised early by the apparent distortion of lines and areas of absent lines. If this occurs, treatment should be initiated within a few days.

The important risk factors for ARMD are increasing age, smoking and family history. Cardiovascular risk factors such as hypertension also contribute.

There are no definitive dietary guidelines. A healthy diet low in animal fat and high in fish is recommended. A variety of vegetables of different colours, especially green leafy ones, may be beneficial.

FIGURE 28.17 Amsler grid

Specific ARMD vitamin formulations are available over the counter, and these may help to slow the progression of already established ARMD; however, they have not been shown to affect early disease or prevent disease occurring.

The Age-Related Eye Disease Study (AREDS)⁴ found that a combination of antioxidant vitamins plus zinc helped slow the progression of intermediate macular degeneration to an advanced stage, which is when most vision loss occurs. The US National Eye Institute recommends that people with intermediate ARMD in one or both eyes or with advanced ARMD (wet or dry) in one eye but not the other take this formulation each day.⁵ However, this combination of nutrients did not help prevent ARMD, nor did it slow progression of the disease in those with early ARMD. The doses of nutrients are:

• vitamin C (500 mg per day)

• vitamin E (400 IU per day)

• beta-carotene (15 mg per day, or 25 000 IU of vitamin A)

• zinc (80 mg per day)

• copper (2 mg per day, to prevent copper deficiency that can occur when taking extra zinc).

Any patient already taking other supplements needs to consider correct total doses of nutrients. Beta-carotene increased the rate of lung cancer in smokers and for this reason has been omitted in commonly available commercial preparations.

A patient qualifies for a blind pension if ‘legally blind’—this means BCVA of 6/60 in the better eye and/or less than 10 degrees of visual field around fixation in both eyes. All medical practitioners caring for a patient should be aware of community support available from government departments and non-government organisations, and should ensure that the patient is receiving appropriate assistance, not only financially, but also to maintain their safety and maximise their visual performance and, thus, their independence and dignity.