Blurred vision and angle closure glaucoma Flashcards

1
Q

What is a blurred vision?

A

Blurred vision - a single image that is seen indistinctly. Establish whether this is at distance, near or both.

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2
Q

What are other interpretations of blurred vision?

A

A decrease in peripheral vision - the patient may describe bumping into things or frequent scrapes when parking the car.

Alteration of a clear image - e.g., micropsia/macropsia (image appears smaller or bigger) or metamorphopsia (distorted image).
Interference with a clear image (e.g., floaters, flashes of light - photopsia).

Diplopia - monocular (the double vision remains when the uninvolved eye is occluded); binocular (the vision returns to normal on covering one eye), horizontal, vertical, oblique.

Other disturbances of vision - e.g., iridescent vision (haloes, rainbows), dark adaptation problems or night blindness (nyctalopia), colour vision abnormalities.

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3
Q

What should you ask in the hx of blurred vision?

A

Note whether it is unilateral or bilateral.

Ask whether it was sudden or gradual in onset. If sudden, ask what the patient was doing at the time; ask what they have done recently that may have affected the eyes - eg, DIY, trauma. If gradual, ask over what period of time it has developed.

Note whether it has happened before. Note when, and what happened. Ask whether it has been diagnosed.

Establish whether there are any associated factors. Examples include any of the other visual phenomena described above, pain (distinguish between ocular pain and pain in the head), associated ocular complaints (eg, red-eye, discharge, abnormal appearances) or systemic complaints (eg, headache, other neurological problems, generalised malaise).

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4
Q

What are the causes of unilateral, sudden and painful blurred vision?

A

Trauma

Orbital cellulitis: the area surrounding the eye will be hot, red, swollen and tender and the patient will be systemically unwell.

Endophthalmitis: associated with accidental or surgical trauma which may be recent or old but may also be endogenous. Look for the painful red eye, reduced visual acuity and a hypopyon.

Corneal problems: trauma, infection, severe dry eye or exposure keratopathy, contact lens problems.

Anterior uveitis: red-eye associated with photophobia, headache - may be previous episodes.

Acute angle-closure glaucoma: often precipitated when the pupil is in mid-dilation (e.g. watching television in dim conditions), often associated with systemic malaise (headache, nausea, vomiting).

Arteritic anterior optic neuropathy - giant cell arteritis (temporal arteritis): (patients >50 years old) - the pain is often more a headache than acute eye pain; other features include jaw claudication, scalp tenderness, polymyalgia rheumatica ± anorexia, weight loss, fever.

Optic neuritis: (can be bilateral) can be a very painful presentation of multiple sclerosis - look for pain, particularly on moving the eye. There may be other focal neurological symptoms.

Migraine: when there are scintillations, the pain in the head often appears when the visual disturbance is ebbing or has disappeared.

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5
Q

What are the causes of unilateral, sudden and painless blurred vision?

A

Vitreous haemorrhage: may also present as sudden floaters.

Central retinal artery occlusion presents with painless, almost instantaneous, reduction of vision in one eye.

Central retinal vein occlusion frequently presents with loss of vision or blurred vision, often starting on waking.

AMD - in the majority of cases, this is the ‘dry’ form which is associated with a progressive decrease in visual acuity. However, in about 10% of cases, the ‘wet’ form occurs where a neovascular membrane forms which may be susceptible to bleeding, so causing a dramatic and rapid loss of vision.

Retinal detachment tends to produce a ‘curtain’ coming across the visual field rather than blurring of vision.

Intermediate or posterior uveitis - this tends to present with marked floaters ± blurring of vision rather than the painful red eye characteristic of anterior disease.

Anterior ischaemic optic neuropathy - look for a relative afferent pupillary defect, a pale and oedematous optic disc, flame-shaped haemorrhages and possibly an altitudinal visual field defect.

Hydrops - acute corneal oedema may arise in a number of conditions such as keratoconus.

Cerebrovascular disease - this usually causes visual disturbance in both eyes but should be considered when a patient presents with unilateral blurred vision.

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6
Q

What are some causes of vitreous haemorrhage?

A

It may arise as a result of diabetic retinopathy, a retinal break or detachment, retinal vein occlusion and, occasionally, a posterior vitreous detachment or age-related macular degeneration (AMD). Also, consider it in trauma, subarachnoid or subdural haemorrhage, intraocular tumours and sickle cell disease. It can occur in other more unusual situations too.

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7
Q

What are the systemic causes of blurred vision?

A

Giant cell arteritis (temporal arteritis)

Papilledema - optic disc swelling secondary to raised intracranial pressure may give rise to headache rather than eye pain. Visual abnormalities tend to be transient initially.

Amaurosis fugax - this characteristically presents as a curtain across the vision and may be associated with intraocular emboli, atrial fibrillation and carotid bruits.

Migraine prodrome - this may occur in some people without the following headache. It is usually unilateral but may progress to be homonymous.

Toxic illness - it is apparent that the patient is pyrexial and unwell.

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8
Q

What are the causes of bilateral, sudden and painful blurred vision?

A

Arc eye, as in welders. There will probably be a history of welding a number of hours earlier with inadequate protection and often the patient will offer the diagnosis.

Beware of malignant hypertension in the susceptible patient who develops rapidly progressing blurring of vision bilaterally (not necessarily equally). Pain tends to be in the form of headaches.

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9
Q

What are the causes of bilateral, sudden and painless blurred vision?

A

Papilloedema.

Cerebrovascular disease may lead to damage to the visual pathways and optic cortex. There may or may not be macular sparing. Visual disturbance is often homonymous

Drugs - anticholinergic drugs but also sedative drugs like antipsychotics and anticonvulsants. The onset of effect of these drugs can be quite slow.

Refractive errors tend to change very slowly over years but, in poorly controlled diabetes mellitus, they may change more rapidly. Drugs like steroids and anticholinergics can also have this effect.

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10
Q

What are the causes of bilateral/unilateral, gradual and painless blurred vision?

A

Glaucoma - this is characterised by asymptomatic but progressive peripheral visual field loss which is usually bilateral but asymmetric.

Refractive errors - hormonal changes, such as occur during pregnancy, can affect the refractive error but this reverts on restoration of baseline hormone levels. Progression of corneal disease such as dystrophies or keratoconus can also cause gradual visual loss.

Cataracts - the patient may also complain of dulling of colours (and may be noted by relatives to have a predilection for very bright or gaudy colours!). Think of cataracts in patients with diabetes and those on systemic steroids and immunosuppressants (eg, transplant patients).

AMD - dry form.

Cystoid macular oedema - this may occur as a result of surgery, inflammation or vascular disease.

Diabetic maculopathy - ischaemia may lead to gradual decrease in visual acuity whereas oedema tends to result in more acute visual distortion.

Genetic disease - there are many degenerative conditions that can cause blurring of the vision. These may affect the elements of the visual media (eg, the cornea in keratoconus) or the retina (eg, Best’s disease).

Drug toxicity - for example, hydroxychloroquine, methanol, ethambutol and, more recently, it has been described with COX-2 inhibitors.

Other toxic agents - including exposure to organophosphates.

Inflammatory optic neuropathies - these tend to be associated with systemic diseases such as sarcoid, vasculitis or syphilis.

Chronic eye strain - as with excessive use of computers under adverse conditions, may produce blurred vision.

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11
Q

What are the causes of unilateral, gradual and painful blurred vision?

A

Neoplastic or inflammatory disease of the orbit and globe.

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12
Q

What are the causes of medically unexplained vision loss?

A

This can occur in four circumstances:

  • Organic disease has not been diagnosed.
  • The patient is a malingerer with secondary gain.
  • The visual loss is psychosomatic.
  • Münchhausen’s syndrome (or fabricated or induced illness by carers - formerly known as Münchhausen’s syndrome by proxy).

Note: deciding that there is no underlying organic disease is difficult and not advisable without a specialist opinion. You may note some features or be aware of some aspects of the patient’s situation that raise the question in your own mind and, depending on circumstances, it may be worth mentioning these to the ophthalmology team.

Malingerers tend to have a unilateral visual loss, whereas functional loss tends to be bilateral.

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13
Q

What is the management of blurred vision?

A

As a rule of thumb, acute, painful conditions warrant same day referral. A suspected case of giant cell arteritis (temporal arteritis) - where the patient doesn’t necessarily have eye pain - and central retinal artery occlusion also need prompt referrals.

Check the guidance from the DVLA regarding a patient’s ability to drive. This will depend on the nature of the visual problem and the underlying cause.

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14
Q

What is angle-closure glaucoma?

A

Angle-closure glaucoma (ACG) is a condition of acutely raised intraocular pressure (IOP) associated with a physically obstructed anterior chamber angle.

It is divided into primary and secondary types and the distinction is important as the treatments vary. Both primary and secondary types may cause acute painful attacks or chronic asymptomatic disease.

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15
Q

How does the aqueous humor flow in the normal eye?

A

In the normal eye, aqueous humor is produced by the ciliary body behind the iris and flows through the pupil to drain into the trabecular meshwork which lies around the circumference of the angle between the iris and the cornea.

This junction of the iris and cornea at the periphery of the anterior chamber is the anterior chamber angle.

Occasionally, the iris can become apposed to the trabecular meshwork and so block off the aqueous drainage. This results in a rise in IOP which causes a number of symptoms and signs, depending on the type of angle closure.

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16
Q

What is primary acute angle-closure glaucoma?

A

Angle-closure can arise as a consequence of the anatomy of the eye: some people’s angles are naturally very narrow which makes the angle more vulnerable to blocking off.

Severe hypermetropes fall into this category. In this case, the condition is known as primary AAC.

Narrow angles are not present in young people. The lens grows as we age and in some people this pushes the iris forwards, narrowing the angle.

17
Q

What are the risk factors for primary acute angle-closure glaucoma?

A

Risk factors include family history, advanced age and Asian or Inuit ethnicity.

Other susceptible patients include those with a thin iris, a thick lens and a shorter axial length of the eyeball (front to back).

The ocular shape is to some extent hereditary, so there may be a familial tendency.

Pupillary dilation with topical mydriatics can push the iris into the angle and precipitate AAC in anyone with narrow angles.

Some systemic drugs which dilate the eye, such as alpha-adrenergic agonists used in urinary incontinence, can produce the same effect.

18
Q

What is secondary acute angle-closure glaucoma?

A

Angle-closure can also occur as a result of forces exerted on the iris either anteriorly (e.g., secondary to peripheral anterior synechiae pulling the iris up) or posteriorly (e.g., the lens bulging forward as a result of swelling).

Secondary closure can also arise through blockage, as a result of the trabecular meshwork being blocked by matter such as blood (from a hyphaemia), blood vessels (from poorly controlled advanced diabetic eye disease) or proteins (as seen in hypertensive uveitis).

19
Q

What are the stages of acute angle-closure glaucoma?

A

Latent - there are anatomical predispositions present.

Subacute - there may be mild symptomatic episodes which suggest incomplete angle closure and which have spontaneously resolved.

Acute - the most likely to present in primary care.

Chronic

Absolute - the end stage of untreated disease (an irreversibly severely sight impaired eye).

AAC is an emergency - prompt diagnosis and treatment are essential to save sight and prophylactic measures will be needed to prevent an attack in the fellow eye.

20
Q

What is the presentation of acute angle-closure glaucoma?

A

Pain - this is severe and rapidly progressive. It may be confined to the eye but more usually spreads around the orbit with an associated frontal or generalised headache.

Blurred vision (rapidly progressing to visual loss).

Coloured haloes around lights. Transient blurring of vision and haloes around light, suggest mild, subacute attacks.

Systemic malaise - nausea and vomiting are common and may be the main presenting feature in some patients - particularly where obtaining a history is a problem (e.g., the demented elderly patient).

Attack precipitants - a common aetiology of AACG (75% of occasions) is pupillary block. The mid-dilated pupil snags on to the lens, so causing a build-up of aqueous beneath it which further pushes the iris forward, so eventually blocking off the trabecular meshwork. It is therefore not uncommon to hear that the attack came on in situations where there was mid-dilation of the pupil - e.g., during a moment of stress or excitement, whilst watching TV in dim lighting conditions or after topical mydriatics or systemic anticholinergics. The same situation can occasionally occur in older people after general anaesthetic - the lens can accumulate fluid and, in the predisposed individual, bulge forward so also causing a pupillary block.

Background - a previous history of AACG is infrequent. These attacks are usually the first indication of such a problem.

Slit-lamp examination

Raised IOP

Examination shows a red eye which is more marked around the periphery of the cornea. Shows a hazy cornea and a minimally reactive mid-dilated pupil.

21
Q

How do you diagnose acute angle-closure glaucoma?

A

Diagnosis of AAC is based on at least two of these symptoms:

  • Ocular pain.
  • Nausea/vomiting.

History of intermittent blurring of vision with haloes and at least three of the following signs:

  • IOP greater than 21 mm Hg (clinically this can mean a stony hard pupil).
  • Conjunctival injection.
  • Corneal epithelial oedema.
  • Mid-dilated non-reactive pupil.
  • Shallow chamber in the presence of occlusion.
22
Q

What are the differentials fos acute angle-closure glaucoma?

A
Corneal disorder 
Anterior uveitis 
Scleritis 
Endophthalmitis 
Keratitis 
Trauma
23
Q

What is the initial management of acute angle-closure glaucoma?

A

Refer immediately to save sight.

Initial medical treatment typically involves all topical glaucoma medications that are not contra-indicated in the patient, together with intravenous acetazolamide. Patients are laid supine.

Topical agents include:

  • Beta-blockers - e.g., timolol, cautioned in asthma.
  • Steroids - prednisolone 15 every 15 minutes for an hour, then hourly.
  • Pilocarpine 1-2% (in patients with their natural lens).
  • Phenylephrine 2.5% (in patients who do not have their own lens).

Acetazolamide is given intravenously (500 mg over 10 minutes) and a further 250 mg slow-release tablet after one hour - check for sulfonamide allergy and sickle cell disease/trait. U&E should be monitored.

If there is no response, systemic hyperosmotics (eg, glycerol PO 1 gm/kg of 50% solution in lemon juice or mannitol 20% solution IV 1-1.5 gm/kg) may be added.

Offer systemic analgesia ± antiemetics.

Call duty ophthalmologist. Treatment may be repeated based on the IOP response.

24
Q

What is the definitive treatment of acute angle-closure glaucoma?

A

Surgical treatment:

  • Peripheral iridotomy (PI) - this refers to (usually two) holes made in each iris with a laser, usually at around the 11 and 2 o’clock positions. This is to provide a free-flow transit passage for the aqueous. Both eyes are treated, as the fellow eye will be predisposed to an AAC attack too. This procedure can usually be carried out within a week of the acute attack, once corneal oedema has cleared enough to allow a good view of the iris.
  • Surgical iridectomy - this is carried out where PI is not possible. It is a less favoured option, as it is more invasive and therefore more prone to complications.
  • Lensectomy - one of the few situations, where cataract surgery is performed on an urgent basis, is when the cataractous lens has swollen to precipitate an attack of AAC. The lens is extracted at the earliest opportunity. Beyond this particular situation, there is some debate as to whether a lensectomy should be routinely performed; it is not the routine practice in this country.
25
Q

What are the complications of acute angle-closure glaucoma?

A

These include permanent loss of vision, repetition of the acute attack, attack in the fellow eye and central retinal artery or vein occlusion.

Patients should be informed about the increased risk to first-degree relatives: if they are found to have shallow anterior chambers, they can be offered prophylactic PIs.

26
Q

What is chronic angle-closure glaucoma?

A

Chronic angle-closure glaucoma (COAG) refers to an insidious, progressive closing off of the trabecular meshwork, resulting in scarring and a gradual rise in IOP.

This can arise due to a very gradual thickening of the crystalline lens associated with predisposing anatomy. COAG is a bilateral but usually asymmetric condition, affecting women more commonly, particularly hypermetropes.

Just as in POAG, patients are usually asymptomatic unless the condition is very advanced, in which case there may be decreased acuity or peripheral visual field loss.

Occasionally, in the advanced stages, there may be some redness and ocular discomfort but this is not comparable to the pain of AACG.

Once COAG has been diagnosed, the patient should undergo prompt PIs in both eyes.

Some patients need additional medical therapy with the topical glaucoma drugs used for POAG.

Compliance can be an issue and patient education and eye clinic follow-up are essential.