Opthalmology Flashcards
Acute angle closure glaucoma
Glaucoma is a group of disorders characterised by optic neuropathy due, in the majority of patients, to raised intraocular pressure (IOP). It is now recognised that a minority of patients with raised IOP do not have glaucoma and vice versa.
In acute angle-closure glaucoma (AACG) there is a rise in IOP secondary to an impairment of aqueous outflow. Factors predisposing to AACG include:
hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age
Features
severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain
Management
urgent referral to an ophthalmologist
management options include reducing aqueous secretions with acetazolamide and inducing pupillary constriction with topical pilocarpine
Peripheral iridotomy is the definitive treatment for AACG
Important for meLess important
All of them are treatment options for acute angle closure glaucoma. However, the question is asking the DEFINITIVE treatment and the definitive treatment for AACG is a laser peripheral iridotomy to produce an extra pathway in the iris for aqueous to flow from the posterior chamber into the anterior chamber in order to be drained into the angle.
Topical beta blockers such as timolol work by decreasing production of aqueous. Topical alpha agonists such as brimonidine work by decreasing production of aqueous and increasing drainage. Topical prostaglandin analogues such as latanoprost work by increasing the outflow of aqueous. Topical carbonic anhydrase inhibitors such as dorzolamide work by decreasing production of aqueous. They can all be used to control the intraocular pressure in glaucoma patients. However, they are not definitive treatments for AACG.
Age related macular degeneration
Age-related macular degeneration is the most common cause of blindness in the UK. Degeneration of the central retina (macula) is the key feature with changes usually bilateral. ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography.
Traditionally two forms of macular degeneration are seen:
dry (90% of cases, geographic atrophy) macular degeneration: characterised by drusen - yellow round spots in Bruch’s membrane
wet (10% of cases, exudative, neovascular) macular degeneration: characterised by choroidal neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis
Recently there has been a move to a more updated classification:
early age-related macular degeneration (non-exudative, age-related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE)
late age-related macular degeneration (neovascularisation, exudative)
Age-related macular degeneration (ARMD) is the commonest cause of visual loss in elderly persons in the developed world. It affects 30-50 million people worldwide.
Epidemiology
population estimates suggest a male to female ratio of 1:2
the average age of presentation is greater than 70 years of age
Risk factors
Advancing age itself is the greatest risk factor for ARMD. The risk of ARMD increases 3 fold for patients aged older than 75 years, versus those aged 65-74.
Smoking is another key risk factor in the development of ARMD, current smokers are twice as likely as non-smokers to have ARMD related visual loss, and ex-smokers have a slightly increased risk of developing the condition, (OR 1.13).
Family history is also a strong risk factor for developing ARMD. First degree relatives of a sufferer of ARMD are thought to be four times more likely to inherit the condition.
Other risk factors for developing the condition include those associated with increased risk of ischaemic cardiovascular disease, such as hypertension, dyslipidaemia and diabetes mellitus.
Patients typically present with a subacute onset of visual loss with:
a reduction in visual acuity, particularly for near field objects
difficulties in dark adaptation with an overall deterioration in vision at night
fluctuations in visual disturbance which may vary significantly from day to day
they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects
Signs:
distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
Investigations:
slit-lamp microscopy is the initial investigation of choice, to identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD. This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.
ocular coherence tomography is used to visualise the retina in three dimensions, because it can reveal areas of disease which aren’t visible using microscopy alone.
Treatment:
the AREDS trial examined the treatment of dry ARMD in 3640 subjects. It showed that a combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.
Vascular endothelial growth factor, (VEGF) is a potent mitogen and drives increased vascular permeability in patients with wet ARMD. A number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss. Evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible. Examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.
Laser photocoagulation does slow progression of ARMD where there is new vessel formation, although there is a risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.
Allergic conjunctivitis
Allergic conjunctivitis may occur alone but is often seen in the context of hay fever
Features
Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis)
Itch is prominent
the eyelids may also be swollen
May be a history of atopy
May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)
Management of allergic conjunctivitis
first-line: topical or systemic antihistamines
second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil
Anterior uveitis
Anterior uveitis is one of the important differentials of a red eye. It is also referred to as iritis. Anterior uveitis describes inflammation of the anterior portion of the uvea - iris and ciliary body. It is associated with HLA-B27 and may be seen in association with other HLA-B27 linked conditions (see below).
Features
acute onset
ocular discomfort & pain (may increase with use)
pupil may be irregular and small
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired
Associated conditions
ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen
Management
urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops
Argyll-Robertson pupil
Argyll-Robertson pupil is one of the classic pupillary syndrome. It is sometimes seen in neurosyphilis. A mnemonic used for the Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
Features
small, irregular pupils
no response to light but there is a response to accommodate
Causes
diabetes mellitus
syphilis
Mydriasis
Causes of mydriasis (large pupil)
third nerve palsy
Holmes-Adie pupil
traumatic iridoplegia
phaeochromocytoma
congenital
Drug causes of mydriasis
topical mydriatics: tropicamide, atropine
sympathomimetic drugs: amphetamines, cocaine
anticholinergic drugs: tricyclic antidepressants
Ptosis + dilated pupil = third nerve palsy; ptosis + constricted pupil = Horner’s
Horner’s syndrome
Features
miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)
Distinguishing between causes
heterochromia (difference in iris colour) is seen in congenital Horner’s
anhidrosis: see below
Central lesions
Anhidrosis of the face, arm and trunk
Stroke
Syringomyelia
Multiple sclerosis
Tumour
Encephalitis
Holmes-Adie pupil
Holmes-Adie pupil is a benign condition most commonly seen in women. It is one of the differentials of a dilated pupil.
Overview
unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light
Holmes-Adie syndrome
association of Holmes-Adie pupil with absent ankle/knee reflexes
Pupil Disorders
Disorder
Notes
Adie pupil
Tonically dilated pupil, slowly reactive to light with more definite accommodation response. Caused by damage to parasympathetic innervation of the eye due to viral or bacterial infection. Commonly seen in females, accompanied by absent knee or ankle jerks.
Marcus-Gunn pupil
Relative afferent pupillary defect, seen during the swinging light examination of pupil response. The pupils constrict less and therefore appear to dilate when a light is swung from unaffected to affected eye. Most commonly caused by damage to the optic nerve or severe retinal disease.
Horner’s syndrome
Miosis (pupillary constriction), ptosis (droopy eyelid), apparent enophthalmos (inset eyeball), with or without anhidrosis (decreased sweating) occurring on one side. Caused by damage to the sympathetic trunk on the same side as the symptoms, due to trauma, compression, infection, ischaemia or many others.
Hutchinson’s
Unilaterally dilated pupil which is unresponsive to light. A result of compression of the occulomotor nerve of the same side, by an intracranial mass (e.g. tumour, haematoma)
Argyll-Robertson pupil
Bilaterally small pupils that accommodate but don’t react to bright light. Causes include neurosyphilis and diabetes mellitus
Blepharitis
Blepharitis is inflammation of the eyelid margins. It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis). Blepharitis is also more common in patients with rosacea
The meibomian glands secrete oil on to the eye surface to prevent rapid evaporation of the tear film. Any problem affecting the meibomian glands (as in blepharitis) can hence cause drying of the eyes which in turns leads to irritation
Features
symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur
Management
softening of the lid margin using hot compresses twice a day
‘lid hygiene’ - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
Cataracts
A cataract is a common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision. Cataracts are the leading cause of curable blindness worldwide.
Epidemiology
Cataracts are more common in women than in men
The incidence of cataracts increases with age. One study found that 30% of individuals aged 65 and over had a visually-impairing cataract in either one or both eyes
Causes
Normal ageing process: most common cause
Other possible causes
Smoking
Increased alcohol consumption
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: hypocalcaemia
Patients typically present with a gradual onset of:
Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights
Signs:
A Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.
Investigations:
Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract
Classification
Nuclear: change lens refractive index, common in old age
Polar: localized, commonly inherited, lie in the visual axis
Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
Management
Non-surgical: In the early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/contact lens, or by encouraging the use of brighter lighting. These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed.
Surgery: Surgery is the only effective treatment for cataracts. This involves removing the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice. Also whether both eyes are affected and the possible risks and benefits of surgery should be taken into account. Prior to cataract surgery, patients should be provided with information on the refractive implications of various types of intraocular lenses. After cataract surgery, patients should be advised on the use of eye drops and eyewear, what to do if vision changes and the management of other ocular problems. Cataract surgery has a high success rate with 85-90% of patients achieving 6/12 corrected vision (on a Snellen chart) postoperatively.
Complications following surgery
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour
Central retinal vein occlusion
Central retinal vein occlusion (CRVO) may be due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis).
Features
sudden painless loss of vision
severe retinal haemorrhages
‘cherry red’ spot on a pale retina
afferent pupillary defect
Central retinal artery occlusion
Central retinal artery occlusion
causes sudden unilateral visual loss
due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
features include afferent pupillary defect, ‘cherry red’ spot on a pale retina
Chorioretinitis
Causes
syphilis
cytomegalovirus
toxoplasmosis
sarcoidosis
tuberculosis
Pizza pie appearance on fundoscopy = chorioretinitis
Corneal ulcer
Corneal ulcers are more common in contact lens users
Features
eye pain
photophobia
watering of eye
focal fluorescein staining of the cornea
Prescribing anaesthetic eye drops for patients with corneal ulcer is not advisable as it may cause more harm- delays healing of the ulcer
Important for meLess important
Oral analgesics should be prescribed for pain relief. All of the other listed options are topical anaesthetic agents. Abuse or long-term use of topical anaesthetics have toxic effects on the cornea and decreases corneal re-epithelialisation. This will prolong the healing time and the eye becomes more susceptible to further infections. It is for this reason most practitioners avoid prescribing topical anaesthetics for regular unsupervised use.
Diabetic retinopathy
Diabetic retinopathy is the most common cause of blindness in adults aged 35-65 years-old. Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes
Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia
In exams you are most likely to be asked about the characteristic features of the various stages/types of diabetic retinopathy. Recently a new classification system has been proposed, dividing patients into those with non-proliferative diabetic retinopathy (NPDR) and those with proliferative retinopathy (PDR):
New classification
Mild NPDR
1 or more microaneurysm
Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots, venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
Severe NPDR
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
Proliferative retinopathy
retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years
Maculopathy
based on location rather than severity, anything is potentially serious
hard exudates and other ‘background’ changes on macula
check visual acuity
more common in Type II DM
Dry eyes
People with dry eye syndrome typically present with feelings of dryness, grittiness, or soreness in both eyes, which worsen through the day, and watering of the eyes, particularly when exposed to wind. Symptoms that are worse on wakening, eyelids sticking together on waking, and redness of the eyelids suggest dry eye syndrome caused by Meibomian gland dysfunction.
There may be no abnormalities on examination. Less commonly people present with a complication of dry eye syndrome, for example, conjunctivitis or ulceration of the cornea, suggested by severe pain, photophobia, marked redness, and loss of visual acuity.
Eyelid hygiene is the most appropriate management step here. Eyelid hygiene helps to control blepharitis. Most people with dry eye syndrome have blepharitis.
Punctate fluorescein staining of the cornea is common in patients with dry eyes
