Ocular and medical emergencies in practice: module 13 part 2: clinical optometry course code: C-13104/OD.
There are some ocular emergencies which are visually threatening and must be appropriately managed to prevent irreversible blindness. There are also some medical emergencies which can present with ocular signs and, if mismanaged, can result in death of the patient. It is paramount that the attending optometrist is alert to these conditions and administers appropriate action. This article discusses the most likely conditions to be encountered by an optometrist in practice.
It is important that ocular injuries are accurately assessed and the findings documented; good clinical records are vital from a medico-legal standpoint. A system for classifying ocular trauma has been developed and is termed the Birmingham Eye Trauma Terminology System (BETTS). In this system, there is standardisation of terminology. An injury is termed 'closed globe' if there is no full thickness wound of the eyeball. The term 'ocular contusion' is also used in such cases. In an 'open globe' injury, there is a full thickness wound present. A partial thickness wound of the eyewall is termed a 'lamellar laceration'.
When the eyeball is struck by a blunt object such as a squash ball, it will cause a rupture of the eyewall rather than a wound injury. When a blunt object strikes the eye, there is a resultant increase in intraocular pressure (IOP) and the eye will split at its weakest point. Certain patients are more vulnerable to blunt object injury than others. Patients with a history of extracapsular cataract surgery have larger incisions compared to those who have had phacoemulsification surgery and are more prone to rupture along these healed surgical lines. In addition, patients who have had radial keratotomies have an increased risk of corneal perforation following blunt injury compared to patients who undergo LASEK for refractive correction.
The term penetrating injury refers to an injury where there is only an entrance wound. An example of a penetrating injury would be a hammering injury where a foreign body enters and remains in the eye (Figure 1). In a perforating injury, there is both an entry and exit wound caused by the same agent--eg a bullet which passes though the eyeball and lodges in the brain. A bullet can also cause extensive facial lacerations (Figure 2).
Common cases of minor trauma include a subtarsal foreign body and corneal foreign bodies and abrasions. A subtarsal foreign body typically occurs after walking past a building site on a windy day. The patient complains of ocular discomfort and the superior bulbar conjunctiva will be injected. The cornea may show diffuse staining or characteristic linear erosions. The patient should have a topical anaesthetic instilled (such as proxymethacaine, amethocaine or tetracaine) and the subtarsal foreign body should then be removed by everting their upper lid. The patient should be advised that when the topical anaesthetic wears off, they will still experience a foreign body sensation until the cornea has completely healed.
A corneal abrasion often occurs following a scratch or injury to the eye. Typically, the patient strikes the eye with a hairbrush or fingernail--often the culprit is their own toddler. The patient experiences intense pain secondary to denudation of the corneal epithelium. Because of this, patients should receive topical anaesthesia in advance of an ocular examination. On examination, the cornea will stain with fluorescein. The treatment of a corneal abrasion is to administer lubricants, a topical antibiotic and a cycloplegic for pain relief. A double pad is useful to aid healing where the extent of the erosion is large. Arc eye is essentially bilateral simultaneous corneal abrasions--this form of photokeratitis can occur during welding and after skiing secondary to prolonged exposure to high concentrations of ultraviolet light. It is managed as a superficial corneal abrasion.
A corneal foreign body may occur following angle grinding. The metal particle strikes the eye and lodges in the cornea. If the foreign body is not immediately removed, an iron rust ring develops around the particle. When treating such patients, it is important to ascertain how the injury occurred as well as performing a full dilated ophthalmic examination to exclude an intraocular foreign body. If the corneal foreign body is relatively superficial, it is often possible to dislodge it using a cotton bud under topical anaesthesia.
A 19-gauge green needle is used to dislodge foreign bodies which are more deeply embedded and a mechanical rust ring remover is helpful in clearing the cornea of residual rusting. The patient is then treated with topical lubricants, antibiotics and if required, cycloplegics.
It is important in any case of trauma to rule out an ocular perforation and exclude an intraocular foreign body. A history of hammering would heighten suspicion of a high velocity injury. All patients with a high index of suspicion for an intraocular foreign body should have radiological investigation. X-rays are performed in upgaze and downgaze to detect intraocular metallic particles and fluorescein 2% dye is useful to detect Seidel positivity--aqueous leakage from a corneal wound is seen to dilute the topical dye. In addition, the anterior chamber shallows when there is a full thickness leaking wound. If a patient is Seidel positive, the IOP should not be checked and no external pressure should be placed on the eye.
[FIGURE 1 OMITTED]
A shield should be applied but if no shield is available, the eye should not be padded while transferring the patient. When referring a patient to hospital where surgery may be required (in order to remove an intraocular foreign body or to suture a ruptured globe) the patient should be advised to fast, as these cases are typically performed under general anaesthesia. It is paramount that in such cases, the ocular foreign body is not removed. Although the patient may be distressed to have a fish hook embedded in their cornea, when there is suspicion of a full thickness corneal laceration, such objects should only be removed in the controlled environment of an operating theatre.
Other alerting signs of an intraocular foreign body include focal transillumination of the iris and cataract (a particle may traverse the lens). In addition, gonioscopy should also be performed because foreign bodies may otherwise lie undetected in the trabecular meshwork. It is important that all intraocular metallic foreign bodies are removed as they place the eye at high risk of developing the devastating condition of ocular siderosis (chalcosis if copper is the foreign body) in later years. Some objects such as glass and eyelashes are inert and may not cause any inflammatory reaction. Vegetable matter has the potential to cause fungal endophthalmitis.
Blunt trauma to the eye can have devastating effects (Figures 3 and 4). The smaller the object and the higher the velocity at impact, the greater the trauma to the eye. A squash ball has the potential for greater injury than a football as a football will be deflected back from the orbital rim. A squash ball will cause a direct contusional injury with the eyeball. When assessing such an injury, it is useful to work systematically from anterior to posterior. The eyelids and surrounding skin are often bruised (Figure 5) and Arnica (a homeopathic remedy) is useful in reducing such swelling.
A blunt injury may be severe enough to cause an orbital floor blow out fracture. The globe is displaced inferiorly and the perimuscular fat tethers the globe into position. The patient is unable to gaze superiorly and may also experience diplopia in the primary position. There may be infraorbital anaesthesia secondary to neural damage and surgical emphysema secondary to subcutaneous air, typically from the ethmoidal sinuses. (1) Any patient with such a fracture needs a full medical assessment as a matter of urgency.
[FIGURE 2 OMITTED]
Blunt injuries may cause bleeding of the structures of the anterior segment resulting in a hyphaema (Figure 6). If blood fills the globe, it is termed an 'eight ball hyphaema' and this requires surgical evacuation of the clot. A simple hyphaema is treated with bed rest and cycloplegics to prevent the formation of synechiae. Patients should not be administered aspirin for pain relief as this exacerbates a secondary bleed--patients should take paracetamol. Complications of a hyphaema include raised IOP and corneal staining. Blunt trauma to the pupillary sphincter will result in an irregular pupil and an iridodialysis (disinsertion of the iris from the scleral spur) may occur. (2) The intraocular lens may opacify causing a cataract or become dislocated or subluxed. In addition, the extraocular muscles may become avulsed following blunt trauma or assault (Figure 7). (3) Complications of blunt trauma to the posterior segment include vitreous haemorrhage, retinal tears, commotio retinae and choroidal rupture. Commotio retinae is caused by neuro-retinal injury resulting in a cloudy swelling (4). It has a grey/white appearance and tends to resolve without sequelae.
Choroidal rupture is generally concentric with the optic disc and may be associated with retinal haemorrhages. Patients should be carefully examined to detect peripheral retinal tears and advised of the symptoms of a retinal detachment.
Chemical burns present an ocular emergency in which the optometrist is at the front line of treatment. Appropriate management of this condition from presentation has a direct impact on the long-term outcome of the patient. Common products containing alkalis include cleaning products and fertilisers (ammonia), drain cleaners and airbags (sodium hydroxide), cement, plaster, mortar (lime) and fireworks (magnesium hydroxide). Common products containing acids include battery acid (sulfuric acid) and bleach (sulfftrous acid). Whether presenting with an alkali or an acid burn, all patients should have copious irrigation to remove the chemical. Patients should receive topical anaesthesia before such irrigation. Ideally, the eye should be irrigated with a sterile balanced buffered solution, such as normal saline solution or Ringer's lactate solution. Immediate irrigation with even plain tap water is preferred, if these are not available. The irrigation solution must contact the ocular surface. This is best achieved with a special irrigating tubing (eg, Morgan lens) or a lid speculum. Irrigation should be continued until the pH of the ocular surface is neutralised, usually requiring 1-2 litres of fluid. It is also important to evert the eyelids and remove any particulate matter from the subtarsal space. If not removed, the residual particles can serve as a reservoir for continued chemical release and injury. Alkalis saponify (hydrolyse esters to form alcohol and carboxylic acid) cell wall protein in cell walls so therefore can cause extensive penetrating damage. Alkalis penetrate into and through the cornea and into the anterior segment. Subsequent hydration of glycosaminoglycans results in stromal haze. Hydration of collagen causes fibril distortion and shortening, leading to trabecular meshwork alterations that can result in increased IOP. Acids dissociate into hydrogen ions and anions in the cornea. The hydrogen molecule damages the ocular surface by altering the pH, while the anion causes protein denaturation, precipitation and coagulation. Protein coagulation generally prevents deeper penetration of acids and is responsible for the ground glass appearance of the corneal stroma following acid injury. Hydrofluoric acid is an exception; it behaves like an alkaline substance because the fluoride ion has better penetrance through the stroma than most acids, leading to more extensive anterior segment disruption. Chemical injuries cause ischaemia of the peripheral cornea by damage to blood vessels. The degree of limbal ischaemia (blanching) is perhaps the most significant prognostic indicator for future corneal healing because the limbal stem cells are responsible for repopulating the corneal epithelium. In general, the greater the extent of blanching, the worse the prognosis. However, the presence of intact perilimbal stem cells does not guarantee normal epithelial healing. Extensive burns can even cause perforation of the globe. Both acid and alkali chemical burns are a true ocular emergency, which must take precedent over all other waiting patients.
Acute angle closure glaucoma
Acute angle closure glaucoma occurs when a shift in aqueous humor outflow leads to structural changes in the eye and a consequent rise in IOP. The most common pathological mechanism is pupillary block--the shift in the transpupillary aqueous humor outflow produces a rise in pressure in the posterior chamber. Because of this, the peripheral iris is pressed against the trabecular meshwork and Schwalbe's line. This obstruction of the trabecular outflow causes a rise in IOP to levels up to 80 mmHg.
Patients complain of a rapidly progressive deterioration in vision with pain and redness in the affected eye. Nausea and vomiting, may be associated with this condition. The eye is injected, there is corneal oedema and a shallow anterior chamber. The pupil is mid-dilated and often oval in shape and the disc is hyperaemic. The lens may develop discrete opacities termed glaucomflecken. The glaucomatous attack can be broken by miotics and carbonic anhydrase inhibitors and at a later stage bilateral laser iridotomies are created. The pupil may retain an anomalous shape and there may be areas of iris atrophy.
Central retinal artery occlusion
A central retinal artery occlusion (CRAO) is an ophthalmic emergency, which if treated appropriately may restore vision. The incidence of retinal arterial occlusion is estimated to be 0.85/100,000 per year. (5) CRAO results in abrupt and massive visual loss, with visual outcomes of 6/60 or lower. CRAO appears to be more common in males than females at a ratio of 2:1 and is usually diagnosed too late for effective therapeutic intervention. The time required for irreversible loss of vision in an experimental model of CRAO was less than 250 minutes. (6) CRAO mainly affects older people, with a mean age of 60 years at presentation. In many cases, retinal arterial obstruction is associated with general cardiovascular disease risk factors: hypertension (60%), smoking, diabetes (25%) and hypercholesterolemia. Giant cell arteritis (GCA) may present in elderly people as a CRAO.
[FIGURE 3 OMITTED]
Retinal arterial occlusion is characterised by a sudden, painless loss of vision. The visual defect is unilateral. Sometimes patients note the visual defect on waking up in the morning, which may be due to reduced retinal perfusion secondary to nocturnal hypotension. Some patients may report antecedent episodes of transient visual disturbance.
In a CRAO, the blockage may occur at any point between the origin at the ophthalmic artery and the optic disc head. However, usually the blockage occurs at the level of the lamina cribrosa. Vision is usually reduced to the level of counting fingers or hand movements, unless there is a separate cilioretinal artery supplying the macula. A relative afferent papillary defect is usually present and the retina may initially appear normal. However, within a few hours, the nerve fibre layer becomes thickened with retinal whitening particularly in the macula. A cherry red spot develops at the fovea where the choroid is still visible. Emboli may be seen in the central retinal artery in about a quarter of cases. Retinal arteries become thin and attenuated and may have breaks in the column of blood (boxcarring or cattle-trucking).
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The management of acute retinal arterial occlusion is difficult and the outcomes are often disappointing. There are no proven treatments. This is because retinal arterial occlusions are relatively rare events, so studies have been either retrospective or small case series without a randomly allocated control group. The aim of the treatment is to restore the retinal blood supply as soon as possible, increase oxygen delivery to the retina or limit the damage from hypoxia. For treatment to have any prospect of success, it must be started immediately. If a patient with a CRAO presents within 24 hours, it is reasonable to attempt several of the non-invasive treatments described below. In some ophthalmic centres, if a CRAO is diagnosed within a few hours of onset, more invasive treatments may be performed.
The simple act of lying the patient fiat increases retinal perfusion pressure. Ocular massage may also be useful as it has been reported to occasionally help to dislodge an embolus. Pressure is applied to the globe with the eyelids closed for 10 seconds and then suddenly released. This cycle is repeated for up to 15 minutes. An emergency anterior chamber paracentesis may be performed to rapidly reduce the IOP. In addition, drugs to lower the IOP (eg, oral acetazolamide) are given to try to augment the effect of massage or anterior chamber paracentesis, in the hope of dislodging an embolus and improving the retinal perfusion. Improved retinal blood flow may be achieved by vasodilatation of the vessels and this can be achieved by asking the patient to re-breathe into a paper bag.
A retinal detachment is a detachment of the neurosensory retina from the retinal pigment epithelium through influx of fluid into the subretinal space. A rhegmatogenous retinal detachment is produced by a full-thickness defect. It is an ophthalmological emergency, which can lead to blindness if untreated. The most common causes are agerelated destruction and liquefaction of the vitreous body. The vitreous detachment following degeneration can cause holes and tears through traction on the peripheral retina, allowing the liquid part of the vitreous to penetrate and separate the neurosensory layer from the pigment epithelial layer. Other predisposing factors are high myopia, cataract surgery and ocular trauma. The incidence of rhegmatogenous retinal detachment is 0.01%. It is diagnosed most frequently between the ages of 50 and 70 years. The risk of rhegmatogenous retinal detachment in the opposite eye is 10%. The most important symptoms are photopsia, floaters and an absolute scotoma. Clinically, the detached retina shows a whitish and creased surface. Retinal defects, pigment cells and erythrocytes are found in the vitreous body often with subnormal IOP.
If the macula is still attached, it is considered an ophthalmic emergency. If the retinal detachment is complete and has been present for weeks or months, surgical intervention is not urgent. A retinal tear is always treated as an emergency as if left untreated, it will eventually progress to a retinal detachment.
Patients with bacterial corneal ulcerations need urgent referral. These include contact lens wearers or immunocompromised individuals such as diabetic patients. The presence of a hypopyon requires emergency intervention. Pseudomonal infection can progress rapidly and result in corneal perforation within 48 hours.
Patients with a history of penetrating keratoplasty must be assumed to be rejecting their graft until proven otherwise. They require urgent referral for further assessment and immunosuppression.
A herpetic corneal ulcer should receive topical antiviral therapy to reduce scarring and visual loss. If there is an associated anterior chamber reaction, the patient should be dilated by the referring optometrist both for analgesia and to reduce the formation of posterior synechiae.
Other ocular emergencies include blebitis and postoperative endophthalmitis. Blebitis occurs in patients who have had a trabeculectomy with formation of a filtering bleb. When the bleb becomes infected, the eye is red and the bleb has a milky appearance. It is an ophthalmic emergency as the infecting organisms can quickly access the intraocular cavities.
Any patient with a history of recent ophthalmic surgery (eg, postoperative cataract or post intravitreal injection) who presents with a red and painful eye should be treated as a potential case of endophthalmitis and be urgently referred back to the treating surgeon. The sooner that intravitreal antibiotics are administered to these patients, the better the visual outcome.
Giant cell arteritis
Temporal arteritis refers to inflammation of the superficial temporal artery and is a feature of GCA. GCA causes inflammation of large to medium sized arteries and typically involves the superficial temporal, ophthalmic, posterior ciliaries and proximal section of the vertebral artery. Arteritic occlusion of these vessels can result in blindness. There may also be concomitant arteritis of the aorta and other arteries resulting in dissecting aneursyms, aortic incompetence, myocardial infarction, brain stem stroke and renal failure. It is for this reason that GCA is classified not only as a neuro-ophthalmic emergency but as an acute medical emergency that can result in death. The presentation of GCA may be abrupt or insidious and typically occurs during the seventh or eighth decade of life. Constitutional symptoms include anorexia, fever, malaise, depression, myalgias, night sweats and weight loss. The hallmark symptom of GCA is a recent-onset localised headache, usually to the temporal or occipital area. This headache occasionally may be diffuse or bilateral. When palpating, the superficial artery is tender, inflamed and nodular.
As the arteritis advances, no pulse can be palpated. Patients commonly complain of scalp tenderness which is elicited when combing hair. They may suffer jaw claudication as a consequence ofischaemia to the muscles of mastication--chewing therefore becomes painful. Visual symptoms are present in about 33% of patients. Ophthalmic presentations of GCA include arteritic anterior ischaemic optic neuropathy (AAOIN), which may be preceded by amaurosis fugax. Any new onset nerve palsy in the elderly patient should be considered GCA until ruled out. In GCA associated AAION, the optic nerve appears swollen and chalky white with splinter haemorrhages. There is an associated profound reduction in visual acuity. If GCA is clinically suspected, it is important that patients are immediately referred to Accident and Emergency for clinical workup and treatment with systemic steroids. If a patient has presented with AAION in one eye, their fellow eye is at high risk of becoming affected. Unfortunately cases of bilateral blindness are not uncommon--65% of untreated patients become bilaterally blindwithinweeks. The diagnosis of GCA is made by a number of criteria including an elevated erythrocyte sedimentation rate (ESR), C reactive protein (CRP) and positive temporal artery biopsy. (7)
[FIGURE 5 OMITTED]
Surgical (compressive) third nerve palsy
Patients presenting with a dilated, unreactive pupil involving third nerve palsy must be presumed to have an intracranial aneurysm until proved otherwise. The patient may have a history of associated headache and examination may reveal a ptosis secondary to weakness of the levator palpebrae superiorus. The eye will be diverged and inferiorly directed. There will be weakness of adduction secondary to palsy of the medial rectus. The superior rectus and inferior rectus are weak and the superior oblique remains unopposed so there is ocular intorsion on downgaze. Disruption of the pupillary parasympathetic supply results in a fixed dilated pupil. The patient may not have any visual difficulties as the ptosis masks their diplopia.
An intracranial aneurysm of the posterior communicating artery in the Circle of Willis must be ruled out. The patient should be immediately referred for a neuro-surgical workup.
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If a patient is noted to have bilateral disc swelling, papilloedema as a result of raised intracranial pressure must be suspected and excluded. In cases of papilloedema, the patient may complain of headache and nausea. The patient may also experience transient visual obscurations as well as horizontal diplopia, which is a consequence of involvement of the abducens nerve. Patients with raised intracranial pressure tend not to exhibit spontaneous venous pulsations at the optic disc and the blind spot is enlarged. The patient requires neuro-imaging and assessment to rule out an intracranial tumour. The term papilloedema is reserved for optic disc swelling in the presence of raised intracranial pressure.
It is important to distinguish orbital or postseptal cellulitis, which is a medical emergency, from preseptal cellulitis. The clinical picture is characterised by severe general malaise, exophthalmos, a motility deficit and considerable lid and conjunctival swelling. Along with persistent loss of function due to damage to the optic nerve, there is a risk of cavernous sinus thrombosis leading to death. The treatment consists of prompt broad-spectrum systemic antibiotics and often debridement of the paranasal sinuses is required. Subperiosteal abscesses of the orbit usually have to be drained. The most common bacteria are Staphylococci, Streptococci and Haemophilus species. Orbital cellulitis is more common in children than in adults.
[FIGURE 7 OMITTED]
Orbital cellulitis occurs in the following three situations: (1) extension of an infection from the periorbital structures, most commonly arising from the paranasal sinuses (the face, globe and lacrimal sac may also be a source of infection); (2) direct inoculation of the orbit from trauma or surgery; and (3) haematogenous spread from bacteraemia (bacteria in the blood). In preseptal cellulitis, the globe is white, vision is good and the extraocular movements are full. In orbital cellulitis, the globe is injected, visual acuity and colour vision are compromised and there is proptosis and ophthalmoplegia. The infection can proceed very quickly and therefore it is imperative to initiate an urgent referral and intervention.
The attending optometrist should be proficient in detecting, treating and appropriately referring ocular emergencies. The inappropriate management of these conditions increases the patient's risk of blindness and in some cases may even lead to their death.
MSc in Clinical Optometry
CITY UNIVERSITY and OT have joined forces allowing readers to achieve CET points through to a full Masters in Clinical Optometry. The content of this article is part of the forthcoming Anterior Segment Eye Disease module running May 16-18 2010. Please note that the OT/City exam will run on May 27 2010 and is based on the City CET articles published in 2009--'Diabetes' and 'Vision in the Aged' For further information please contact Dr Michelle L Hennelly by emailing (m.hennelly@city. ac.uk) or call 0207 040 8352.
1 .Which one of the following is FALSE? Giant cell arteritis:
a. is treated with high dose topical steroids
b. is diagnosed by temporal artery biopsy
c. is associated with jaw claudication
d. may be fatal
2. Which one of the following is FALSE regarding complete third nerve palsy?
a. it may be associated with an intracranial aneurysm
b. ptosis is a feature
c. the affected eye is hypertropic
d. the parasympathetic supply to the pupil is interrupted
3. Which one of the following is FALSE? Papilloedema is:
a. associated with headache and nausea
b. associated with transient visual obscurations
c. associated with diplopia
d. synonymous with bilateral optic neuritis
4. Which one of the following is FALSE? Orbital cellulitis may:
a. follow an infected stye
b. follow sinusitis
c. follow preseptal cellulitis
d. be treated with topical antibiotics
5. Signs of a penetrating eye injury do NOT include:
a. a Seidel negative result
b. focal transillumination of the iris
c. intraocular foreign body
d. traumatic cataract
6. Which one of the following is FALSE regarding chemical injuries?
a. injuries should be immediately irrigated with copious fluid
b. alkalis penetrate deeper then acids
c. limbal ischaemia is a poor prognostic sign
d. injuries should be neutralised with acid if the patient has an alkali burn
Course code- C-13104/ OD
7. Which one of the following is FALSE? In acute angle closure glaucoma:
a. the eye is injected
b. vision is reduced
c. there may be an associated posterior capsular cataract
d. there is associated pain
8. Which one of the following is FALSE regarding central retinal artery occlusion (CRAO)?
a. a cherry red spot is a feature of this condition
b. CRAO is associated with painful visual loss
c. CRAO may be preceded by amaurosis fugax
d. CRAO may be treated by emergency paracentesis
9. Which one of the following is FALSE? Treatment of CRAO includes:
a. inhalation of high dose oxygen
b. anterior chamber paracentesis
c. oral acetazolamide
d. ocular massage
10. Which one of the following is FALSE? Rhegmatogenous retinal detachment:
a. is associated with pigmented cells in the vitreous cavity
b. is associated with complaints of photopsia
c. usually affects patients between the ages of 20 and 30 years of age
d. is a feature of high myopia
11. Which one of the following is FALSE? Corneal ulcers:
a. are rapidly progressive in Pseudomonal infections
b. are more common in contact lens wearers
c. may be more aggressive in diabetic patients
d. are treated with topical steroids
12. Which one of the following is FALSE? Endophthalmitis is a recognised complication of:
a. intravitreal injections
b. cataract surgery
d. panretinal photocoagulation
Louise O'Toole FRCSI (Ophth), MRCOphth, MMedSci FEBO
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|Date:||Feb 12, 2010|
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