Common presentations for the eye and eyelids:
• Black eye (periorbital haematoma)
• Dry eyes
• Foreign body sensation
• Loss of vision (painful)
• Loss of vision (painless)
• Painful eye
• Red eye (painful)
• Red eye (painless)
• Swollen (puffy) eyelids.
Common problems and their causes
Irrespective of the presenting complaint, a detailed history is required. The two main symptoms to ask about are pain and visual disturbances.
Ask about the following specific symptoms.
• Establish the extent of reduced visual acuity, e.g. from blurring to total loss of vision
• Any unusual visual experiences, e.g. floaters, photopsia, shadows/scotoma, distortion
• Any diplopia.
• The mechanism of injury—was the injury of low velocity (grinding) or high velocity (hammering, drilling)? Sharp or blunt injury? Size of the offending object.
• Was eye protection used?
• Presence of chemical or organic matter.
Previous ocular history
• Previous ocular surgery (recent and old)
• Pre-existing ocular conditions, e.g. squints, glaucoma
• Any refractive error or amblyopia (lazy eye/poor vision since childhood)
• Does the patient wear contact lens?
Examination of the eye and eyelids
Corneal abrasions (loss of corneal epithelium) are very painful and can prevent examination. Patients often have intense blepharospasm. If this is present and there is no contraindication, place a few drops of topical anaesthetic (e.g. oxybuprocaine). Rapid pain relief is almost diagnostic. This can then be followed by a drop of 2% fluorescein. All but the smallest of abrasions can be seen as a green patch on the corneal surface. Be careful when looking—a total corneal epithelial defect (due to chemical injury) can be missed easily as the whole cornea is then stained.
Options include a Snellen chart, Sheridan–Gardner chart (designed for children, disabled people, those with learning difficulties, or patients who do not speak your language) or a Kay picture chart for children who cannot read. Use a pinhole if spectacles are not available.
The vision is recorded as a fraction. The numerator (upper number) is usually 6 (i.e. the test is usually performed at 6 m). The denominator (lower number) corresponds to the line on the chart the patient could read. Start at the top of the chart, where the letters are biggest and work your way down the chart to the smallest size, testing one eye first and then the other. If the patient only manages to read the top line (60 line), the vision is recorded as 6/60. This means that the patient was tested at 6 m yet could only read the line a normal person should have managed to read at 60 m.
If the patient fails to read the top line, try to ascertain if they can count fingers at 1 m (counting finger vision). Failing that, ascertain if the patient can see movements of hand in front of the eye (hand movement vision). Failing that, test the vision with a light source (light perception or no light perception vision). Test each eye separately.
If the Snellen chart is not available, a mini Snellen chart can be used with the patient wearing their reading glasses.
Test with Ishihara colour plates. Test each eye separately. Colour vision defects are common in men and affect one in eight males (most commonly confusing reds and greens). Loss of colour perception can be a manifestation of optic nerve pathology, e.g. optic nerve compression after trauma and optic neuritis.
Test each eye separately. Test each quadrant (four quadrants) in turn with your fingers or a hatpin.
Assessment of these is vital in assessing optic nerve and retinal function. Ask the patient to look in the distance. Use a bright torch. Assessment includes both the afferent (sensory) and efferent (motor) visual pathways. Normally the pupils of both eyes should respond identically to a light stimulus, regardless of which eye is being stimulated. Light entering one eye produces a constriction of the pupil of that eye (direct response), as well as a constriction of the pupil of the unstimulated eye (consensual response).
Afferent pupillary defect (APD)
This is recorded if a bright light in one eye fails to constrict either pupil (i.e. no stimulus is reaching the midbrain). If one of the pupils constricts, then it is likely that either a pupillary defect (sphincter muscle tear or topical dilating drops), or efferent pathway defect is responsible for the abnormality.
Relative afferent pupillary defect (RAPD)
An important test of the afferent pathway is the ‘swinging light test’ or RAPD test. In the swinging flashlight test, a light is alternately shone into the left and right eyes with delay of 1 second. Normally there should be equal constriction of both pupils, regardless of which eye the light is shone into. This indicates an intact direct and consensual pupillary light reflex. When the test is performed in an eye with an APD, light shone into the affected eye will result in only mild constriction of both pupils. This is due to a decreased response to light from the afferent defect. Light shone into the unaffected eye will cause a normal constriction of both pupils. Thus, light shone in the affected eye will produce less pupillary constriction than light shone in the unaffected eye. This test is undertaken because an APD may be subtle and the pupil may react sluggishly.
Ask the patient to look straight and then follow a target to the eight positions of gaze. Report if the patient sees double vision at any stage.
Observe for any restricted range of eye movement.
The eyelids should be examined with good illumination. Look first at (1) the relative height of the two eyelids and (2) the surface and edge of the eyelids (skin and lashes). The relative heights are best observed casually, rather than under a bright light. If the difference between each palpebral fissure is >2 mm in height, there may be pathology. However, many patients may have a 1 mm difference. When a difference is observed, try to determine which eyelid is abnormal: the upper or lower. If the upper eyelid exposes the white sclera above the limbus in the 12 o’clock position, it is abnormally high (lid retraction). If the upper eyelid covers the pupil, it is abnormally low (ptosis). Extra skin from the upper lid may be seen sagging over the lid margin. This can partially block vision. If it does not, it is a cosmetic issue only.
If a superficial conjunctival foreign body is suspected, the upper eyelid may need eversion. Never evert the upper eye lid if a penetrating injury or corneal thinning (from ulceration) is suspected.
• Instil a drop of local anaesthetic and fluorescein dye.
• Ask the patient to look down.
• With one hand, hold the eyelashes of the upper eyelid between thumb and index finger.
• With the other hand, place a cotton bud (or paper clip or other small blunt object) along the lid, midway from its margin.
• Evert the eyelid over the cotton bud.
• If a foreign body is seen, gently remove it with a moistened cotton bud.
• On completion, ask the patient to look up and the eyelid will return to its normal position.
Look at the lower lid. Sometimes the edge can be turned inwards (entropion) or outwards (ectropion). When the lid is turned inwards, the lashes can rub directly on the cornea. When turned outwards, the cornea can become exposed and dry.
Following injury, the eyelids should both be examined for lacerations (noting position, length, and depth). If a wound is present, care must be taken to look for underlying globe damage and retained foreign body. Consider also the possibility of penetrating orbital and brain injuries. When opening a swollen eyelid, do not press on the eye, as this can cause or exacerbate globe injury. The direction of applied force should be up and down towards the orbital rims. Remember that medial canthal injuries can involve the lacrimal drainage system.
Slit-lamps provide a superior, magnified, and three-dimensional view of ocular contents. Use of these requires training.
• Examine systematically from anterior to posterior.
• Eyelids: lid margins for lacerations.
• Conjunctiva: subconjunctival haemorrhage/follicles. If blood is reported in the tear film after trauma in the absence of a lid laceration, then at least a conjunctival laceration must have occurred to account for the blood. Consider globe damage.
• Cornea: clarity, arcus senilis, foreign bodies, keratic precipitates, prolapsed tissues, e.g. iris or uveal tissues which normally appears dark in colour.
• Intraocular pressure (IOP): this is approximately between 10 and 20 mmHg. If you cannot measure this, assess the IOP using your fingers to see if the globe is hard. This can help diagnose acute glaucoma. Ask the patient to close the eye and look down. Using your two index fingers, press through the upper eyelid to feel the consistency of the eyeball. Compare it with your own eye. In postoperative patients or if globe rupture/penetrating injury is suspected, the IOP should not be assessed this way, as pressure on the eyeball can open up the wound or further expulse the ocular contents.
• Anterior chamber: this should be deep and clear. Blood and inflammatory debris can settle and form a fluid level called hyphaema and hypopyon, respectively.
• Iris: should be round and reactive to light. Any irregularity in shape is abnormal. Look for defects in in the iris periphery (called a dialysis). This indicates significant trauma with avulsion of the iris root from the ciliary body.
• Lens: this should be clear. Any opacity in the lens is known as a cataract.
See Figure 10.1.
Look for the red reflex and examine the optic disc and retina. A poor red reflex indicates opacity in the media (cataract, vitreous haemorrhage). Visualize the disc (if you do not see the disc, follow the branching of the vessels towards the disc). Once on the disc, assess its margin (distinct or blurred), rim colour (pale or hyperaemic), cup (full or empty), and blood vessels (congested, pulsating, or attenuated).
Papilloedema is suspected if the margin is blurred, colour hyperaemic, cup is full, and vessels congested. The rest of the fundus is examined by rotating the ophthalmoscope to view different quadrants and macula.
Assessing a child in distress can be difficult. Obtain a detailed history from an adult witness if possible. If this is not available, always suspect an injury being the cause of a red or painful eye.
Assess the visual acuity—fixing and following objects of interest, reaching out for objects of interest or the Sheridan-Gardner test, depending on the age and verbal ability of the child. Test each eye in turn if possible. Note the following:
• General observation, e.g. periorbital redness or bruising.
• Test pupil responses.
• Test for red reflexes.
• If globe injury is suspected, do not try to pry the eyelids open as this can exacerbate a perforating eye injury.
• If periorbital bruising is present, especially if associated with injuries in other part of the body, suspect non-accidental injury.
• If the eyelid is red, tender, and swollen, especially if the child is febrile, suspect periorbital cellulitis.
• If a purulent discharge is present in the eye(s) in a baby in the first month of life, suspect ophthalmia neonatorum as a cause for the red eye(s). This should be investigated for gonorrhoea or chlamydia.
• If a white pupil or leucocoria is present (absent red reflex), congenital cataract and retinal abnormalities (retinoblastoma, Coat’s disease, toxoplasma) must be ruled out.
• A white blowout fracture should be suspected if there are signs of a sunken globe, minimal periorbital haemorrhage, or restricted eye movements (especially if associated with severe pain on eye movements). The child is often distressed and vomiting.
• If an eyelid laceration is present, always consider the possibility of a penetrating injury no matter how small the size of the laceration, e.g. a toddler falling on a pencil and penetrating the orbit.
Ocular assessment in the unconscious patient
Visual acuity testing and colour perception are reliable tests in the early recognition and documentation of loss of vision. However, they require a patient who is fully awake and cooperative. Unfortunately, visual assessment in the unconscious patient is extremely difficult. It is in these patients that early and possibly treatable threats to sight may be easily overlooked. Initial clinical assessment therefore usually relies on the assessment of pupillary size, reaction to light and careful assessment of globe tension by palpation, if there is proptosis. The presence of a RAPD is regarded as a sensitive clinical indication of visual impairment. Initial fundoscopy is difficult to perform without dilating the pupil, (which would be contraindicated in an unconscious head-injured patient), but should be attempted anyway. Fundoscopy can also appear misleadingly normal, as the optic nerve takes time to atrophy. However it may be possible to detect intraocular haemorrhage, retinal oedema/detachment, and avulsion or swelling of the optic disc. If fundoscopy is not possible, the red reflex should at least be checked and compared between each eye.
Never press on the globe if a rupture or perforation is suspected.
• ESR/CRP in inflammatory conditions, notably suspected temporal arteritis.
• Eye swabs are required in suspected chlamydial or unusual infections.
Plain orbital X-rays may reveal fractures and retained foreign bodies but CT scan is the investigation of choice if the history suggests a likely presence.
CT scan is the investigation of choice for complex trauma and foreign body detection and localization. MRI is useful in the assessment of the globe, optic nerve, and in the assessment of orbital swellings/masses.
This can often detect an intraocular foreign body (IOFB), haemorrhage, retinal detachment, and define globe integrity. Ultrasound B-scan may be required to show scleral thickening in posterior scleritis.
Portable tonometry can be used to measure the IOP in suspected glaucoma and following trauma. Handheld IOP-measuring devices are now available and reported to be reliable.
This measures the amount of moisture bathing the eye. This test is useful for determining the severity of conditions resulting in dry eyes.
Tear breakup time test
This measures the time it takes for tears to break up in the eye. The tear breakup time can be determined after placing a drop of fluorescein in the cul-de-sac.
These can be broadly divided into:
• Lid trauma
• Perforating/penetrating (sharp) trauma
• Blunt trauma—closed globe injury or ruptured globe.
Open globe injury
This refers to a full-thickness wound in the corneoscleral wall of the eye. This may be caused by blunt trauma (globe rupture) or by a sharp object (laceration or penetrating/perforating injury, with or without a retained IOFB).
Closed globe injury
This does not have a full-thickness wound in the eye-wall and includes lamellar lacerations, superficial foreign bodies, and contusion of the globe. Generally speaking, initial poor visual acuity, presence of an RAPD, and posterior involvement of the eye, carry a bad prognosis. This holds true for both closed and open globe injuries.
Vision-threatening globe injuries may not always be obvious and a high index of suspicion is required. Lid laceration, subconjunctival haemorrhage, bruising, and oedema are all commonly associated and should lead to suspicion.
Penetrating/perforating globe injuries
With penetrating trauma, the globe is disrupted by a full-thickness entry wound. This may be associated with prolapse of the ocular contents. In perforating trauma, the globe is disrupted by a through and through injury, with both an entrance and exit wound. This is a severe injury. These injuries are usually caused by a sharp object causing full-thickness penetration into the cornea or sclera. There may also be a retained IOFB. Blood-stained tears may indicate the possibility of an open globe injury. The eye can look collapsed—uveal tissue, retina, and the vitreous gel may be seen prolapsing. A hyphaema and vitreous haemorrhage are usually present and the lens may be damaged and cataractous. The IOP is low and aqueous fluid may be seen leaking from the wound if fluorescein drops are instilled.
• Visual loss depends on size, location, and extent of injury.
• Lid lacerations, bruising, and subconjunctival haemorrhage.
• Direct ophthalmoscopy: look for loss of red reflex (cataract or vitreous haemorrhage), check pupil reactivity.
• Cornea and sclera: a wound may be seen and the eye may look collapsed, uveal tissues (iris) and vitreous may be seen prolapsing.
• Examine anterior chamber: look for hyphaema, cataract, irregular or distorted pupil, collapsed or flat anterior chamber.
• IOP may be low and the eye may feel soft.
• Instil a drop of fluorescein and look for leaking fluid (Siedel sign).
• Examine the retina if possible, looking for IOFB, vitreous haemorrhage, retina injury.
See Figure 10.2.
These injuries can be deceptive. In cases of small high-velocity objects (such as metal and glass chips) the eye may appear intact and a small entry wound overlooked. The history is therefore important. Care must be taken not to apply pressure to the eye as this can further expulse the ocular contents. The possibility of associated brain injury should also be borne in mind. If intraocular blood or lid oedema prevent examination, ultrasound or CT scan can detect IOFB, retinal detachment, and globe integrity.
• Analgesia and antiemetics as required.
• A hard plastic shield should be taped over the eye to protect it.
• Check tetanus status.
• NBM (in case surgery is needed under general anaesthesia).
• Refer urgently for surgical repair (undertaken as soon as possible).
• The use of oral ciprofloxacin is thought to reduce the risk of endophthalmitis.
• Prognosis depends on visual acuity at presentation, size, and location of defects (large/posterior defects carry poor prognosis). Corneal scarring, glaucoma, cataract, and retinal detachment are the main complications leading to poor vision.
Blunt trauma can result in intraocular damage with an intact eyeball, or cause a ruptured globe. This is a similar type of injury as seen when a tomato is dropped from a height—the impact may only cause bruising of the fruit or cause rupture of its skin. Anteroposterior compression of the eye during trauma expands the globe at the equator. This is the mechanism of tearing of structures within the eye. The force of trauma may not appear to be severe but an object small enough to fit within the bony orbital rim will transmit all its energy to the eyeball.
In blunt trauma, visual acuity is usually reduced without an APD. The patient may report floaters and that the vision has improved since the incident. This is because any intraocular blood has settled at the bottom of the eye with the patient in an upright posture.
• Look for associated lid laceration, bruising and subconjunctival haemorrhage.
• Look for iris sphincter muscle tears, iris dialysis, hyphaema, and a displaced or subluxated lens.
• Check IOP. This can be high if blood blocks the trabecular meshwork in the drainage angle.
• Look for posterior segment complications of trauma—vitreous haemorrhage, choroidal ruptures, retinal commotio, and retinal tears leading to a retinal detachment.
• If the view of the fundus is poor, an ultrasound scan can detect globe rupture, retinal tears, and detachment.
If the eye appears soft or collapsed in the setting of blunt trauma, a globe rupture must be excluded. With closed globe injuries, the eyelid injuries and subconjunctival haemorrhage can be similar to those of open globe injuries. However, the globe shape looks normal.
• If a rupture is suspected, or vision is affected, refer urgently.
• Control inflammation, pain, and IOP—steroid drops, cycloplegic, and antihypertensive drops need to be initiated.
• With minor injuries careful follow-up is needed to assess for late complications—retinal detachment, glaucoma, cataract, and retinal membrane formation.
• Prognosis is generally good and depends on whether any of the above-listed complications arise.
• Choroidal rupture and retinal detachment involving the macula carry the worst prognosis.
Ruptured globe is defined as the loss of integrity of the eyeball following blunt trauma (Figure 10.3). The bony orbit offers protection to the eye but is deficient anteriorly. This is even more significant in individuals with prominent eyes, as they are more susceptible to blunt trauma. Interpersonal violence and falls are the commonest causes of globe rupture. There is a history of significant blunt ocular trauma, usually with an object small enough to fit within the bony orbital rim, e.g. knuckles, squash ball, or the edge of an object. Previous ocular surgical history is important as any scar is a potential site of rupture. Patients present with severe pain and sudden loss of vision. Visual acuity is usually down to perception of light with APD. An associated lid laceration and bruising may be seen. A subconjunctival haemorrhage is invariably present. Uveal tissue, retina, and the vitreous gel may be prolapsing out of the eye. The eye is collapsed, and if the rupture is posterior, the anterior chamber looks very deep. The lens may be displaced and a hyphaema is usually present. The IOP is very low and eye movements are reduced.
If severe lid bruising and oedema are present, it will be difficult to examine the eye. Care must be taken not to press on the eye in an attempt to open the lids, as this will further expulse ocular contents. If severe lid oedema prevents examination and a rupture is suspected, then an ultrasound or CT scan can detect globe integrity.
• Analgesia and antiemetics should be given as required. Globe injuries can be painful and vomiting is common (uncontrolled vomiting can further expulse ocular contents).
• A hard plastic shield should be taped over the eye to stop eye-rubbing, especially in children.
• Check tetanus status.
• Refer urgently. Primary surgical repair should be arranged as soon as possible.
• Oral ciprofloxacin may be used to prevent endophthalmitis.
• Prognosis is generally poor, depending on the site and extent of rupture (posterior rupture and large defects carry the worst prognosis).
Traumatic optic neuropathy (TON) occurs in approximately 0.5–5 % of closed head injuries. These can sometimes be relatively trivial in nature. Visual loss is permanent in approximately half. Injuring forces transferred to the optic canal results in damage to the optic nerve. Stretching, contusion, or shearing forces can injure the nerve as it passes through the relatively thick bony canal into the orbit. Deceleration injuries and blunt trauma to the face and head are the common causes of TON. Motor vehicle collisions, falls, and assault account for the majority of cases. Displaced fractures around the orbital apex together with bleeding and oedema compress the nerve.
• The diagnosis of TON is a clinical one.
• Loss of consciousness is commonly associated.
• Visual loss is usually sudden and profound although it can be moderate and delayed.
• There is decreased visual acuity and a relative APD.
• When the eye appears normal but there is reduced vision and an APD, injury to the nerve near the optic canal should be suspected.
• Optic nerve avulsion, or nerve compression resulting in nerve head swelling or central artery and vein occlusion are readily recognizable on fundoscopy.
TON needs immediate referral. Treatment has long been controversial and may be medical or surgical:
• Medical treatment aims to reduce oedema and inflammation however the role of high dose steroids is controversial with a growing consensus against this.
• Surgical decompression is even more controversial. It may be indicated for optic nerve haematoma or if a bony fragment is seen (on CT) to be impinging on the optic nerve.
This is an area where part of the corneal epithelium is deficient. The patient complains of pain, watering, and has a foreign body sensation. They have difficulty keeping the eye open. Usually there is a history of trauma or contact lens wear. The eyelids may be in spasm and the conjunctiva is injected. With topical anaesthesia, the vision is normal. The area of abrasion stains with fluorescein.
• Chloramphenicol drops or ointment should be prescribed four times daily for 5 days.
• Ensure that there is no opacity of the cornea (which indicates a secondary infection of the underlying stroma) and that there are no foreign bodies.
• Although an eye pad is not essential, it helps keep the eye closed and patients tend to feel more comfortable. It can be kept on for 1 day.
• No contact lens should be worn for 2 weeks and after the patient has seen his/her own optician.
• If the patient is very distressed, cycloplegic drops and oral analgesia will provide some relief until abrasion heals.
Abrasions usually heal rapidly and the patient should be a lot more comfortable in 2 days. Refer only if a secondary corneal ulcer or a recurrent erosion syndrome develops. Long-term use of lubricating eye ointments, bandage contact lens, and occasionally surface treatment by needle puncture or laser may then be required.
This is a specific condition caused by ultraviolet injury from welding, tanning lamps, and high-altitude snow (sometimes seen in inexperienced skiers who don’t wear sunglasses). Ultraviolet light causes oedema and sloughing of the corneal epithelium leading to punctate erosions or abrasions. Patients complain of pain, tearing, blepharospasm, photophobia, and blurred vision several hours after exposure. Treatment is similar to an abrasion.
These require careful assessment and often referral to an appropriate specialty (ophthalmology, oculoplastics, plastics, maxillofacial), depending on local protocols. The main concerns here are:
• The possibility of an associated, yet hidden globe injury
• Loss of function of the eyelids following treatment
• Injuries to the lacrimal drainage system.
Assess the eye carefully. A normal appearance does not rule out a serious injury. The mechanism of injury may provide clues to possible globe problems. Small lid lacerations may conceal a large retained foreign body. Always consider retained foreign bodies and image accordingly. Damage to the canalicular system can occur with injuries to the medial aspect of the lid margins. Suspected canalicular injuries should be referred. Conjunctival, corneal, and scleral lacerations, hyphaema, lens dislocation, and globe rupture must all be excluded. Upper lid injuries may affect the levator muscle and its function should be noted. Penetrating globe, orbital, and cranial injuries must be excluded in all penetrating lid lacerations.
Inability to effectively close the eyelids quickly results in drying of the cornea, ulceration, and potentially loss of sight. Even relatively minor eyelid lacerations may predispose to this and may be easily overlooked. Avulsion of the eyelids is a rare but devastating injury and extremely difficult to reconstruct.
• Visual acuity, visual fields, ocular movements, the pupil, and the fundus should all be examined
• The position, length, and depth of the wound(s) should be documented.
• Medially sited eyelid injuries can damage the lacrimal drainage system and require special attention.
• Upper lid injuries may affect the levator muscle and its function should be noted.
• Neurological examination is required if penetrating brain injury is suspected. Even small lid lacerations may be the entry wound for a significant penetrating injury.
Plain orbital films may reveal fractures and retained foreign bodies, but CT scan is the investigation of choice.
Lid lacerations not involving the lid margin
Eyelids have an excellent blood supply and delayed primary closure is not necessary. Simple lacerations can be explored and cleaned under local anaesthesia and closed in layers as with any laceration. Eyelid function (protecting the globe) is the primary consideration. Begin with irrigation, antisepsis (non-irritant to the globe), and a check for retained foreign bodies. Superficial lacerations of the eyelid, not involving the eyelid margin, may be closed with running or interrupted 6-0 suture (Prolene®, Ethilon®, Vicryl®, etc.).
Deep lacerations should include the orbicular muscle and skin in the repair. Care must be taken to ensure suture ends do not rub the cornea and cause abrasions. Many shallow cuts can be apposed without sutures; they scab over and heal extremely well. If skin is missing, seek advice on possible reconstruction. Antibiotic ointments may be prescribed. Skin sutures can be removed in 5 days.
Complex lacerations (including any involving the lid margin, lateral and medial canthal regions, medial third of the lids, and levator muscle) must be referred for repair. These lacerations can disrupt the lacrimal drainage system and functional integrity of the lid. As the lid is very vascular, even necrotic-looking tissue can survive and thus no tissue should be excised.
Lid lacerations involving the lid margin
These usually require referral to a specialist. Primary closure is often possible if there is <25% tissue loss. Irregular edges may be excised (minimally) by creating a pentagonal wedge, removing as little tissue as possible. A 4-0 silk or nylon traction suture is placed in the eyelid margin 2 mm from the wound edges and 2 mm deep and is tied in a slipknot. Symmetric suture placement is critical to obtain good alignment. Approximately 2 or 3 absorbable Vicryl® 5-0 or 6-0 sutures are placed internally to approximate the tarsal plate. The skin and conjunctiva should not be included in this internal closure. Ensure that the wound edges are everted. Skin can be closed with 6-0 nylon/Prolene®/Vicryl® sutures. Skin sutures are removed in 5–7 days.
If there is tissue loss >25% this will require a flap or graft and is best managed by a specialist. In the upper eyelid, if orbital fat is seen, or if ptosis is noted, damage to the orbital septum and levator aponeurosis should be suspected.
If an eyelid is avulsed, the missing tissue can be sometimes reattached if soaked in diluted antibiotic solution, wrapped in moistened sterile gauze, and preserved in ice. Refer urgently. If necrosis is present, minimal debridement should be undertaken to prevent further tissue loss.
Timing of repair of lid lacerations depends on the general condition of the patient and the presence of other injuries. Repair can be safely deferred up to 48 hours (so long as the eye is protected), if other injuries take precedence. However, if unprotected, the cornea can dry very quickly. Under these circumstances, until the defect is repaired, eyelid remnants should be pulled over the globe and supported to provide corneal cover. If a delay in repair is expected, the wound should be cleaned and irrigated with saline. Superficial foreign bodies should be removed. Copious amounts of saline irrigation under light pressure (using a 20 mL syringe and 18-gauge cannula) can be used to wash out foreign bodies and reduce microbial load. IV antibiotic cover (e.g. co-amoxiclav 500 mg three times daily) is needed for all bite injuries and contaminated wounds.
Chemicals that have a pH different to that of the eye (pH = 7.4) can cause a burn. Domestic and industrial accidents are the commonest causes of chemical burns to the eye. Alkalis cause more damage than acids, as they dissolve lipid membranes and penetrate deeper. Loss of vision results from severe dry eyes and scarring. Complications include cataract formation, glaucoma, and uveitis. Patients present with severe pain, blepharospasm, watering, and variable reduction in vision.
• If the chemical is a dry powder, quickly brush as much of this off as possible. Once you start irrigating any residual powder will dissolve producing more active agent.
• Irrigate with copious amounts of saline (litres) as soon as possible. This must continue until the pH is normal before anything else is done (it is not unusual to use over 5 L).
• It is important to irrigate the fornices as residual chemicals tend to settle here.
• Try to obtain the pH of the chemical and establish the baseline pH of both eyes.
• Apply local anaesthetic drops if necessary.
• Note vision, epithelial defects, corneal clarity, cataract, and residual particulate matter.
• Immediate referral to ophthalmology is then made, once the pH has come back to normal.
• Further management with involves antibiotics, steroids, potassium ascorbate, cycloplegia, and vitamin C.
• Patients usually require admission especially if both eyes are involved and vision is impaired.
The prognosis can be extremely poor. This depends on the pH of the chemical and the extent damage. Hence first-aid treatment received on site and in casualty is vitally important.
The red eye
This usually refers to injection and prominence of the superficial blood vessels of the conjunctiva or sclera. This is different from the subconjunctival haemorrhage seen in trauma. There are many causes.
If an obvious cause is absent carefully examine the following.
• Visual acuity: any reduction indicates serious ocular disease, notably keratitis, iridocyclitis, and glaucoma.
• Eyelids: blepharitis, entropion, ectropion, trichiasis.
• Conjunctiva: conjunctivitis, subconjunctival haemorrhage.
• Ciliary flush: this is a ring of redness spreading out from around the cornea of the eye. Seen in corneal inflammation, iridocyclitis, or acute glaucoma.
• Sclera: episcleritis (usually sectoral and relatively painless), scleritis (usually painful and tender).
• Cornea: look for corneal foreign body, contact lens, and corneal opacities. Stain with fluorescein and look for corneal staining (abrasion, ulcer, punctate staining). Corneal opacities are the fourth leading cause of blindness.
• Anterior chamber: look for cells, hyphaema, hypopyon, and depth of anterior chamber. A shallow chamber may indicate a predisposition to narrow-angle glaucoma. Any ‘red eye’ with a shallow anterior chamber suggests acute glaucoma.
• Pupil: in iridocyclitis, the involved pupil will be smaller than the uninvolved one, due to spasm of the sphincter muscle of the iris. With AACG, the pupil is generally fixed in mid-position, oval, and responds sluggishly to light, if at all.
• IOP should be measured. This is mostly normal or low in iritis. It is elevated only in herpetic uveitis (which is not common). In traumatic perforating ocular injuries, the IOP is usually low.
Glaucoma is a common condition with an estimated prevalence in the over 40s of 1%. It is usually asymptomatic. It comprises a group of eye diseases in which there is damage to the optic nerve head and visual field loss, usually associated with abnormally elevated IOP (although a significant number of patients can have normal eye pressures). If left untreated this will ultimately lead to loss of vision.
IOP is normally maintained by a balance between formation of aqueous within the eye and its subsequent drainage via a trabecular network of tissues at the ‘drainage angle’. Increase in IOP usually occurs as a result of obstruction to the outflow of the aqueous. Obstruction can occur if the periphery of the iris becomes displaced forwards so that it covers the drainage angle of the anterior chamber. This results in angle closure and affects patients whose angle is very narrow. This will result in ‘closed’-angle glaucoma. In open-angle glaucoma, pathological changes occur within the microstructure of the drainage system and so obstruct the outflow of aqueous. In these cases the angle is not closed but remains ‘open’.
Acute angle-closure glaucoma
AACG occurs when sudden closure of the drainage angle leads to a rapid rise in the IOP. Patients with narrow drainage angles are predisposed to this when the pupil dilates. This bunches up the peripheral iris over the angle and blocks it. The increasing size of the lens in the ageing eye also pushes the iris forward, which further narrows the angle. Hence the condition mainly affects the elderly. Long-sighted patients are also at risk, as they have smaller eyes and therefore narrower angles.
Patients present with a short history of increasing eye pain. This becomes very severe. They also complain of nausea, vomiting, reduced vision, and haloes seen around lights. Some patients may be mistakenly diagnosed as having an abdomen problem, due to severe nausea and vomiting. The cornea becomes cloudy and the pupil unreactive and mid-dilated. The globe becomes hard to palpation. Both eyes have shallow anterior chambers. There may have been previous milder attacks during the night when the pupil naturally dilates. These may have resolved spontaneously.
• Refer immediately to ophthalmology, as the pressure in the eye must be reduced urgently.
• IV acetazolamide 500 mg stat, topical apraclonidine 1% three times daily, timolol 0.25% twice daily may also be given to reduce the pressure (if there are no systemic contraindications).
• Dexamethasone 0.1% four times daily is used to control inflammation.
• Pilocarpine 1% is given to the opposite eye to prevent acute closure.
• Laser peripheral iridotomies may be performed to prevent an attack of angle closure.
• In resistant cases, administration of IV mannitol or oral glycerine can reduce the IOP by drawing fluid out of the eye. Caution must be observed in patients with heart failure.
• If the pressures are controlled quickly, the prognosis is good.
Open-angle glaucoma is the commonest form of glaucoma. It is an insidious, slowly progressive disease, which occurs bilaterally and with no symptoms until considerable visual impairment has occurred. Early diagnosis is therefore imperative and may be achieved by regular screening of the over 50s or those with a known family history.
Treatment can be both medical and surgical, the medical treatments aim to increase the outflow and/or suppress the secretion of aqueous. Surgical treatment aims to create an alternative outflow for the aqueous or partially destroy ciliary body to reduce inflow.
In secondary glaucoma, the raised IOP is secondary to a local cause such as iritis, injury, rubeosis (iris neovascularization due to diabetes or central retinal vein occlusion), and inappropriate use of steroid eye- drops. Treatment involves controlling the underlying factors and then medical or surgical treatment of glaucoma, as appropriate. Secondary glaucomas generally have a poorer prognosis.
Congenital glaucoma may present at birth or in the ensuing months and years. The condition is caused by the abnormal development of the drainage angle, which results in raised IOP. This in turn causes the immature eye to enlarge. This is referred to as buphthalmos, which literally means ‘ox eye’. Treatment is almost invariably surgical. Urgent ophthalmic referral is required.
This is a condition in which the cornea becomes inflamed. It is usually painful and often associated with blurred vision. The patient may also describe feelings of itchiness each time they blink. Two types are generally described:
• Superficial keratitis. This involves the superficial epithelium of the cornea. After healing, there is usually no scarring.
• Deep keratitis. This involves the deeper layers of the cornea and therefore heals with scarring. This can permanently impair vision if it is on visual axis. Treatment involves topical corticosteroid eyedrops.
Keratitis has multiple causes.
Herpes simplex keratitis (dendritic keratitis) is a viral infection of the cornea with herpes simplex virus. It frequently leaves a ‘dendritic ulcer’. Herpes zoster keratitis is another cause.
Bacterial infection of the cornea can follow from an injury or from wearing contact lenses. Common organisms are Staphylococcus aureus and Pseudomonas aeruginosa, respectively.
This is a protozoal infection of the cornea. It is a rare but severe complication of contact lens wear caused by washing and storing lenses in water or swimming and bathing with contact lenses in the eye. The infection is extremely difficult to diagnose and treat. Therefore the disease is usually diagnosed late and runs a long course with severe inflammation.
This follows infection of a blackfly bite. This is also known as ‘river blindness’.
This is due to dryness of the cornea caused by incomplete or inadequate eye-lid closure.
Keratitis due to intense ultraviolet radiation exposure (e.g. snow blindness or arc eye.)
This depends on the cause of the keratitis:
• Infectious keratitis can progress rapidly, and generally requires urgent antibacterial, antifungal, or antiviral therapy. Aciclovir is the mainstay of treatment for herpes simplex virus.
• Contact lens wearing should be prohibited.
• Steroids should not be used for infective keratitis.
This is inflammation of the uveal tract of the eye (the pigmented layer—the iris, ciliary body, and choroid). If only the iris is involved, it is called iritis or anterior uveitis. Uveitis can be associated with systemic inflammatory diseases, such as sarcoidosis, SLE, and various arthritides.
Patients usually have a dull ache over the eye and may have blurred vision and floaters. Photophobia can be severe. Conjunctival injection, either ciliary (around the cornea) or generalized is often present. On slit-lamp examination, inflammatory cells can be seen in the anterior chamber, which can stick to the corneal endothelium (keratic precipitates) or form a hypopyon. The pupils may be irregular and immobile if the iris adheres to the lens (due to posterior synechiae). Vitritis and yellow retinal infiltrates may be present on fundoscopy in posterior uveitis.
Refer as soon as possible to ophthalmology. Investigation is not required initially if the patient is otherwise well. Steroids (topical, local injections, and systemically, depending on severity) and cycloplegics must be started under ophthalmology supervision. Generally the prognosis is very good but uveitis can be chronic and recurrent.
Scleritis and episcleritis
This is an inflammation of the scleral or episcleral layer of the eye. It may be associated with systemic and connective tissue diseases, such as rheumatoid arthritis and SLE. Onset is generally over a few days. Usually there is unilateral aching in the eye associated with sectoral (localized) injection of the eye. Scleritis is much more severe and can cause reduced vision, chemosis, proptosis, and pain on eye movement. Episcleritis should not affect any eye functions. Exudative retinal detachment, disc oedema, and vascular occlusions can occur with scleritis. Secondary uveitis and keratitis may occur. Ultrasound B-scan may be required to show scleral thickening in posterior scleritis.
Episcleritis is generally self-limiting over a period of around 4 weeks and can be managed conservatively if mild. Episcleritis and mild scleritis respond well to NSAIDs (e.g. ibuprofen 400 mg three times daily for 4 weeks). Moderate to severe scleritis usually requires systemic and topical steroids under ophthalmology supervision. The prognosis is very good for episcleritis and depends on system associations for scleritis.
Refer as soon as possible for scleritis. Although this is not required for episcleritis, refer in severe or non-resolving cases and when diagnosis is in doubt. Local irritation from lashes and foreign bodies need to be excluded if there is sectoral injection of the eye with a gritty sensation.
Surface foreign bodies occur on the cornea, conjunctiva, or under the lids (Figure 10.4). Slow velocity (grinding, welding, and wind-borne) foreign bodies do not have the force to penetrate the eye and only embed themselves superficially in the epithelium. There is a foreign body sensation or grittiness in the eye, watering, and variable photophobia. A clear history of a foreign body may not always be present or it may precede symptoms by hours. On examination the vision is normal, unless the foreign body is on the visual axis. The eye is injected and may be in spasm until anaesthetic drops are instilled.
Foreign bodies in and around the eye can be divided into:
• Subtarsal foreign bodies
• Corneal foreign bodies
• Intraorbital foreign bodies
• Intraocular foreign bodies.
• Instil local anaesthetic drops.
• Everting the lids is essential.
• Foreign bodies can sometimes be seen more readily if fluorescein drops are instilled.
• Surface foreign bodies should be directly visible and do not require radiological investigation.
• A moistened cotton bud is effective for removing most conjunctival and subtarsal foreign bodies. However, a green needle used with a slit-lamp is often needed for corneal foreign bodies.
• Prescribe chloramphenicol ointment four times a day for 5 days and padding for the first day.
• Referral is not required unless a rust ring remains on the cornea or an infected corneal ulcer has developed under the foreign body.
IOFBs that have penetrated the eye as a result of high-velocity injuries are discussed under penetrating injuries. IOFBs usually occur due to high-velocity injury like gunshot injury or industrial accidents. CT scan is the investigation of choice for foreign body detection and localization. Referral to ophthalmologist is necessary.
These can develop within hours from the iron in a metallic foreign body. Removal may be deferred for a day or so, to allow the ring to become more superficial. Antibiotic ointment may help to prevent infection. Rings persisting for >72 hours should be removed or referred. See Figure 10.5.
Contact lens-related problems
Contact lenses are widely used by many patients but are not looked after, replaced, and cleaned properly. This can lead to sight-threatening complications. Contact lenses can be hard, gas permeable, or soft. The latter can be flexed between fingers and generally speaking are more comfortable than the others. Many soft lenses are disposable and are therefore thrown away after each use. Hence they are less likely to get infected or build-up lipoprotein deposits that can reduce oxygen permeability, comfort, and clarity. Extended-wear lenses (worn for weeks) and lenses designed for yearly disposal are more likely to cause problems.
Over-wear is by far the commonest cause of problems. This leads to hypoxia and damage to the epithelium of the cornea. Epithelial microcyst formation, abrasions, blood vessel growth, and increased risk of microbial keratitis can occur.
• What type of lens is worn?
• How old is the lens?
• How old is the lens case and solutions? (Look at how clean/dirty the case is.)
• What cleaning regimen is used?
• Does the patient ever clean the lens in water, or swim with the lenses in?
• How many hours and continuous days are lenses worn?
• Pre-existing eye diseases. Dry eyes, blepharitis, and corneal scarring increase infection risk.
These are usually caused by over-wear and hypoxic damage to the epithelium, which swells and easily sloughs off when the lens is removed.
Contact lens intolerance
The patient complains of increased discomfort and redness leading to reduced wear time. The commonest reason is dry eyes. Artificial tear drops (preservative free) may alleviate the problem. Other reasons for intolerance are build-up of deposits on lens, lens solution allergy, and giant papillary conjunctivitis (large papillae are seen under the upper lids). This is an allergic response to lens deposits or mechanical irritation.
Conjunctivitis and microbial keratitis need to be referred promptly as serious complications can arise.
• General advice on contact lens care, cleaning, and avoiding over-wear must be emphasized.
• Dry eyes can be managed with artificial tears suitable for the type of lens being worn.
• Abrasions can be treated chloramphenicol four times daily for 5 days.
• No lens should be worn for at least 2 weeks after the eye has settled and after the patient has seen their optician for a check-up to assess suitability to continue wear.
• All infections should be referred to an ophthalmologist.
Loss of vision
Loss of vision can have many causes, some obvious, others less so. It can occur instantly or over a brief period of time. Although all require urgent referral to an ophthalmologist, some conditions are treatable and therefore need rapid diagnosis. The key elements in the history are:
• Speed of onset of symptoms.
• Whether it is binocular or monocular.
• Whether it is associated with pain or headache.
• Associated systemic risk factors (hypertension, diabetes, hypercholesterolaemia).
• Ocular history.
• Whether the patient is on anticoagulants.
To aid in diagnosis, loss of vision can be classified into painful and painless.
Painful loss of vision
• Arteritic anterior ischaemic optic neuropathy—temporal arteritis
• Optic neuritis
• Chemical burns
• Corneal ulcers
• Blunt and penetrating ocular trauma
• Uveitis—especially posterior and intermediate uveitis
• Scleritis—especially posterior scleritis
• Orbital cellulitis
• Herpes zoster ophthalmicus
• Retrobulbar haemorrhage
• Endophthalmitis—exogenous and endogenous.
In painful loss of vision, acute angle-closure glaucoma must be ruled out.
• Examine the cornea to rule out corneal pathology, e.g. corneal ulcers. Consider chemical keratitis and blunt/penetrating injury.
• Exclude uveitis.
• Consider arteritic anterior ischaemic optic neuropathy secondary to temporal arteritis or giant cell arteritis in anyone over 50—ask about headaches, jaw claudication, malaise, weight loss, and appetite loss. Palpate for tenderness and non-pulsating superficial temporal arteries. Examine pupils for relative afferent pupil defect and look for signs of swollen optic disc. Urgently check the ESR and CRP, which are usually raised in this condition.
• Optic neuritis is commonly associated with demyelinating disease (MS). It is usually associated with unilateral loss of vision deteriorating over a few days, reduced colour and light perception, pain on eye movements, and is typically seen in young (20–50 years old) females. Examine for reduced visual acuity, red colour desaturation, RAPD, central field defects, and a swollen optic disc.
• If the patient has undergone recent eye surgery (e.g. cataract surgery, trabeculectomy, vitrectomy, penetrating trauma), or received a recent injury consider exogenous endophthalmitis as a diagnosis. In addition to pain and reduced vision, the eye is red, there is fibrin in the anterior chamber, a hypopyon, and loss of red reflex (red reflex may be present early)—urgent referral to ophthalmologists is mandatory.
Painless loss of vision
• Amaurosis fugax—TIA involving the optic nerve
• Retinal artery occlusion—central or branch
• Retinal vein occlusion—central or branch
• Non-arteritic anterior ischaemic optic neuropathy
• Retinal detachment
• Vitreous haemorrhage
• Neurological diseases—occipital cortex strokes, lesions involving the visual pathways.
Retinal detachment is the separation of the retina from the underlying retinal pigmented epithelium as a result of fluid gathering between the two layers. The majority of cases follow vitreous degeneration and its shrinkage, resulting in vitreous separation from the retina (posterior vitreous detachment). If there are abnormal adhesions between the two, the retina can tear as the vitreous shrinks, allowing fluid to gather beneath it. This is the commonest form of retinal detachment. Less commonly, ocular vascular abnormalities, cancers, or fibrosis in the vitreous (advanced diabetic retinopathy) can cause detachment. Trauma, short-sightedness (myopia) and family history are risk factors.
The main clinical features are:
• Flashing lights (like lightning).
• Floaters (dots, lines, spider’s web or flies floating in front of vision) occur because the collapsed strands of vitreous gel are moving around within the eye and cast a shadow on the retina.
• Shadowing (dark curtain covering a part of vision).
There is usually a short history of hours to days. There may be reduced vision if the macula is involved. Examine the visual acuity, visual fields, and pupils (an APD may be detected if a significant portion of the retina is detached). Fundoscopy reveals an elevated retina with or without folds.
If the patient presents at the retinal-tear stage, laser or cryotherapy can be utilized to ‘weld’ the retina down around the tear to stop fluid leaking underneath it. Surgery is often required to flatten the retina if a significant detachment has occurred. The prognosis depends on the cause and extent of detachment. If the macula is unaffected, prognosis for vision is good.
Most patients with flashes and floaters only have a vitreous detachment. It is, however, difficult to predict which ones go on to develop retinal detachment from the history alone. Therefore all need urgent ophthalmology review.
Optic neuritis is an inflammatory optic neuropathy. It is commonly associated with demyelinating disease (MS). However viral infections, compressive lesions, or systemic diseases such as sarcoidosis need to be borne in mind. Usually there is unilateral loss of vision deteriorating over a few days, reduced colour and light perception, typically in the young (20–50 years old) patients. Periocular pain, especially on eye movement, is often present. Examine for reduced visual acuity, red colour desaturation, RAPD, and central or para-central field defects. Swelling of the optic nerve and other focal neurological defects (e.g. weakness) may be present. During the acute attack, vision deteriorates for 1 week and then gradually resolves over the ensuing 3 months to near normal. Investigations should be directed towards this diagnosis if systemic or other neurological associations are present, or if the clinical picture is atypical.
In an acute attack of demyelinating optic neuritis, a course of IV steroids followed by oral steroid has been shown to speed recovery and reduce recurrence in the short term. However, the long-term prognosis is not altered. With other causes, the systemic associations dictate prognosis. Prognosis is best for post-viral optic neuritis. Refer as soon as possible to a neuro-ophthalmologist or neurologist.
Retinal artery occlusion
An occlusion of the central retinal artery or any of its branches can result from an embolus or thrombosis. Less common causes are temporal arteritis and collagen vascular diseases. There is sudden unilateral painless loss of vision, which may be severe and total (central retinal artery occlusion, CRAO) or partial with sectoral field defect (branch retinal artery occlusion, BRAO). The patient may have a history of ischaemic heart disease, diabetes, stroke, amaurosis fugax (sudden loss of vision which resolved within 24 hours), and smoking. The following features are noticed on examination:
• CRAO: visual acuity is at best counting fingers or light perception. There is RAPD, narrow arteries, and a white oedematous retina with a cherry-red spot at the macula. If the patient has a cilioretinal artery (separate artery to the macula from the choroidal circulation, found in 20% of the population), central vision is spared in CRAO. The patient may have 6/6 vision with restricted fields.
• BRAO: vision is variably reduced (depending on how much the macula is affected). The pupils usually react normally and there is sectoral whitening of retina and arterial attenuation.
Refer immediately to ophthalmology. Get an ESR and CRP urgently to exclude temporal arteritis. A full cardiovascular work-up can be done, routinely including fasting glucose, cholesterol, triglyceride, ECG, and carotid Dopplers.
The aim of management is to try and dislodge the embolus by reducing the eye pressure within 24 hours of occlusion. The simplest method is ocular massage but IV acetazolamide 500 mg stat or paracentesis (fluid drainage from the anterior chamber) is more effective, although the latter can cause severe complications. The above measures generally have a poor success rate. Usually the occlusion is not reversible and the visual loss is permanent.
Temporal arteritis must be excluded in all patients >50 years.
Retinal vein occlusion
Occlusion may involve the central retinal vein or any of its branches. The retinal vein and artery share a common sheath. The artery can therefore compress the vein as they cross, leading to stasis and occlusion. The condition generally affects the elderly.
Patients present with unilateral, painless loss of vision developing over a few hours. There may be a history of hypertension, diabetes, glaucoma, hormone replacement treatment, or hypercoagulable state. The vision is variably reduced and there may be an RAPD, visual field defect, and a raised IOP. On fundoscopy, a swollen disc, congested and dilated veins, retinal haemorrhages, and cotton-wool spots are seen in the area supplied by the occluded vein. FBC and coagulation profile should be investigated. A fluorescein angiogram may be performed later.
No treatment is shown to reverse acute vein occlusion. Control of vascular risk factors, hypertension, IOP, and hypercoagulability states aim to protect the second eye. Patients require long-term ophthalmic follow-up to screen for treatable complications (such as neovascularization, macular oedema, and glaucoma). The prognosis depends on the degree and extent of ischaemic damage and ensuing complications. Poor initial vision and an RAPD carry the worst prognosis. Up to 5% of patients can have the second eye affected.
Vein occlusion should be suspected in asymmetrical diabetic retinopathy.
Sudden bleeding into the vitreous can occur for many reasons:
• Retinal tear ± detachment
• Posterior vitreous detachment
• Retinal vein occlusion
• Subarachnoid haemorrhage (Terson’s syndrome).
Patients present with sudden painless loss of vision. There is loss of the red reflex (without the presence of cataract), and fundoscopy is unable to view the retina. Ultrasonography can confirm the diagnosis
Any unexplained vitreous haemorrhage is due to retinal tear(s) until proven otherwise.
Amaurosis fugax is painless and transient monocular visual loss. It can be considered as a type of TIA, during which an embolus obstructs the lumen of the retinal or ophthalmic artery, causing a decrease in blood flow to the retina. The most common source of these emboli is from an atherosclerotic carotid artery. Other pathophysiological mechanisms exist.
Patients present with monocular visual loss that usually lasts for seconds to minutes. The fundus usually appears normal. Check for atrial fibrillation, carotid bruit, and examine for neurological defect elsewhere. FBC, fasting lipids, and blood sugar to rule out diabetes. Other investigations include carotid Dopplers, echocardiography as an outpatient. Commence aspirin if no contraindications and refer to ophthalmology or a TIA clinic.
The main function of the eyelids is to regularly spread the tears and other secretions across the surface of the eye to keep it moist. This keeps the eyes from drying out. The blink reflex protects the eye from foreign bodies. Any disorder of the eyelids affecting these functions can result in irritating symptoms and the risk of corneal injury.
Common eyelid disorders
• Stye (hordeolum) is an infection of the glands by Staphylococcus aureus. The main symptoms are pain, redness of the eyelid margin, and swelling. Styes usually disappear within a week without treatment or with warm water compresses.
• Chalazion is caused by the obstruction of the oil glands. They can be mistaken as styes but they are less painful and it tends to be chronic.
• Blepharitis is a common infective condition that causes inflammation of the eyelids. Treatment includes maintaining good hygiene and warm compresses on the affected eyelid to remove crusts. Antibiotics may be prescribed.
• Ectropion is the turning outwards of the lower lid from globe. It usually results from ageing, but sometimes can be a complication of surgery, injury, or disease. Entropion is where the lid turns inwards.
• Eyelid oedema can occur during an allergic reaction to food, drugs, plants, or secondary to infections.
• Eyelid tumours (e.g. basal cell carcinoma).
• Blepharospasm (eyelid twitching) is involuntary spasm of the eyelids.
• Ptosis is when the upper eyelid droops as a result of weakness of the levator muscle or dysfunction of the nerves to it. It can be part of the normal ageing process or secondary to pathology elsewhere (diabetes, stroke, Horner’s syndrome, myasthenia gravis).
The lacrimal apparatus
The lacrimal drainage system consists of the puncta, canaliculi, lacrimal sac and nasolacrimal duct. Tears are produced by the lacrimal gland and swept over the eye surface with each blink. Tears drain via the lower canaliculus predominantly (70%) and upper canaliculus (30%) by the lacrimal pump mechanism (the action of the eyelids contracting and pumping the tears into the lacrimal sac).
It is important to differentiate between hypersecretion and epiphora as both can present with watery eye.
Reduced tear drainage from lacrimal system obstruction at any point from the punctum, canaliculus, sac, and nasolacrimal duct. Nasolacrimal duct obstruction is the commonest.
Excess production of tears in response to stimulation from corneal irritation (e.g. corneal foreign body), dry eye, or conjunctival irritation (e.g. blepharitis, conjunctivitis).
Epiphora in the presence of patent nasolacrimal drainage pathway without hypersecretion. This can be due to eyelid malposition, e.g. lower lid ectropion (lid turned out), lacrimal pump failure, (facial palsy) punctual, canalicular, and nasolacrimal duct stenosis (without complete obstruction).
This is a dilated lacrimal sac filled with mucous. It can present as a lump around the medial canthus and is often confused with a skin cyst (dermoid, sebaceous). Patients also complain of epiphora. If these get large they can cause considerable distortion of the local anatomy, with canthal drifting. This can then appear like a tumour. Mucocoeles can also become infected (dacryocystitis). Consider this in any patient presenting with an abscess along the side of their nose.
History taking in epiphora
• Is stickiness/watering constant or intermittent? Is it worse outdoors?
• Any inflammation or lump at the medial canthus?
• History of nasal disease, sinusitis, polyps, or nasal trauma.
• Any photophobia, red eye?
• Previous conjunctivitis, eye drops and drugs.
Look specifically for periocular and medial canthus pathology notably eyelid malposition and a mucocoele.
• Fluorescein dye retention test. A drop of fluorescein 2% will rapidly disappear from the conjunctiva if the system is patent. The dye will be retained if blocked.
• Slit lamp examination to exclude corneal causes, blepharitis, punctual stenosis, tear meniscus.
• Probe and syringe/irrigate the lacrimal system (use topical anaesthesia).
• Special clinical tests—Jones’ tests used to confirm and localize functional epiphora are performed by ophthalmologists.
Aetiology of the watery eye
Epiphora secondary to blockage of the nasolacrimal duct and functional epiphora need a non-urgent referral to ophthalmology for surgical management. In cases of entropion (turning in of eyelid) steri-strips can be used temporarily to prevent the eyelid rolling in and causing damage to the cornea with the lashes. Trichiatic lashes (misdirected) can cause corneal abrasion and can be removed.
This is an acute infection of the lacrimal sac. There is usually a pre-existing swelling close to the medial canthus. Patients present with pain, erythema, a watery eye, and oedema.
Management—oral or IV antibiotics depending on the severity. It is important to remember that acute dacryocystitis can cause orbital cellulitis and requires urgent ophthalmology assessment if not responding to oral antibiotics.