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
Episcleritis
Features
red eye
classically not painful (in comparison to scleritis), but mild pain may be present
watering and mild photophobia may be present
phenylephrine drops may be used to differentiate between episcleritis and scleritis. Phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels. If the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
Approximately 50% of cases are bilateral.
Management
conservative
artificial tears may sometimes be used
Episcleritis is a cause of red eye which is classically not painful
Eyelid problems
Eyelid problems commonly encountered include:
blepharitis: inflammation of the eyelid margins typically leading to a red eye
stye: infection of the glands of the eyelids
chalazion (Meibomian cyst)
entropion: in-turning of the eyelids
ectropion: out-turning of the eyelids
Stye
Different types of stye are recognised:
external (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum producing) or glands of Moll (sweat glands).
internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)
management includes hot compresses and analgesia. CKS only recommend topical antibiotics if there is an associated conjunctivitis
A chalazion (Meibomian cyst) is a retention cyst of the Meibomian gland. It presents as a firm painless lump in the eyelid. The majority of cases resolve spontaneously but some require surgical drainage
Topical antibiotics are only recommended for stye if associated conjunctivitis
Herpes zoster ophthalmicus
Herpes zoster ophthalmicus (HZO) describes the reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles.
Features
vesicular rash around the eye, which may or may not involve the actual eye itself
Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement
Management
oral antiviral treatment for 7-10 days
ideally started within 72 hours
intravenous antivirals may be given for very severe infection or if the patient is immunocompromised
topical antiviral treatment is not given in HZO
topical corticosteroids may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review
Complications
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia
This patient may have a corneal abrasion or a dendritic corneal ulcer, particularly given the photophobia. The feathery pattern however points more towards a herpes simplex keratitis. Such a patient should be reviewed immediately by an ophthalmologist. Giving a topical steroid in this situation could be disastrous as it may worsen the infection.
Herpes simplex keratitis
Herpes simplex keratitis most commonly presents with a dendritic corneal ulcer.
Features
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer
Management
immediate referral to an ophthalmologist
topical aciclovir
Herpes zoster ophthalmicus requires urgent ophthalmological review and 7-10 days of oral antivirals
Hypertensive retinopathy
The table below shows the Keith-Wagener classification of hypertensive retinopathy
Stage I
Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring
Stage II Arteriovenous nipping
Stage III
Cotton-wool exudates
Flame and blot haemorrhages
IV
Papilloedema
Eye Infections
Toxoplasmosis retinitis classically presents with white focal retinitis with overlying vitreous inflammation.
Cytomegalovirus retinitis classically has the appearance of a ‘pizza pie’, with retinal spots and flame haemorrhages.
Retinitis pigmentosa is an inherited condition which has bone-spicules on the retina.
Hypertensive retinopathy and diabetic retinopathy do not present with single lesions or vitreous inflammation.
Chorioretinitis
Causes
syphilis
cytomegalovirus
toxoplasmosis
sarcoidosis
tuberculosis
Infective conjunctivitis
Conjunctivitis is the most common eye problem presenting to primary care. It is characterised by sore, red eyes associated with a sticky discharge
Type
Features
Bacterial conjunctivitis
Purulent discharge
Eyes may be ‘stuck together’ in the morning)
Viral conjunctivitis
Serous discharge
Recent URTI
Preauricular lymph nodes
Bacterial or viral conjunctivitis may be associated with a purulent discharge and bilateral symptoms where as preauricular lymph nodes are only a feature of viral or Chlamydial conjunctivitis
Management of infective conjunctivitis
normally a self-limiting condition that usually settles without treatment within 1-2 weeks
topical antibiotic therapy is commonly offered to patients, e.g. Chloramphenicol. Chloramphenicol drops are given 2-3 hourly initially where as chloramphenicol ointment is given qds initially
topical fusidic acid is an alternative and should be used for pregnant women. Treatment is twice daily
contact lens should not be worn during an episode of conjunctivitis
advice should be given not to share towels
school exclusion is not necessary
Keratitis
Keratitis describes inflammation of the cornea. Microbial keratitis is not like conjunctivitis - it is potentially sight threatening and should therefore be urgently evaluated and treated.
Aetiology
Causes
bacterial
typically Staphylococcus aureus
Pseudomonas aeruginosa is seen in contact lens wearers
fungal
amoebic
acanthamoebic keratitis
accounts for around 5% of cases
increased incidence if eye exposure to soil or contaminated water
parasitic: onchocercal keratitis (‘river blindness’)
Remember, other factors may causes keratitis:
viral: herpes simplex keratitis
environmental
photokeratitis: e.g. welder’s arc eye
exposure keratitis
contact lens acute red eye (CLARE)
Clinical features
Features
red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen
Evaluation and management
Referral
contact lens wearers
assessing contact lens wearers who present with a painful red eye is difficult
an accurate diagnosis can only usually be made with a slit-lamp, meaning same-day referral to an eye specialist is usually required to rule out microbial keratitis
Management
stop using contact lens until the symptoms have fully resolved
topical antibiotics
typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate
Complications may include:
corneal scarring
perforation
endophthalmitis
visual loss
Herpes simplex keratitis
Herpes simplex keratitis most commonly presents with a dendritic corneal ulcer.
Features
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer
Management
immediate referral to an ophthalmologist
topical aciclovir
Lens dislocation
Lens dislocation
Causes
Marfan’s syndrome: upwards
homocystinuria: downwards
Ehlers-Danlos syndrome
trauma
uveal tumours
autosomal recessive ectopia lentis
Nasolacrimal duct obstruction
Nasolacrimal duct obstruction
Nasolacrimal duct obstruction is the most common cause of a persistent watery eye in an infant. It is caused by an imperforate membrane, usually at the lower end of the lacrimal duct. Around 1 in 10 infants have symptoms at around one month of age
Management
teach parents to massage the lacrimal duct
symptoms resolve in 95% by the age of one year. Unresolved cases should be referred to an ophthalmologist for consideration of probing, which is done under a light general anaesthetic
Optic neuritis
Causes
multiple sclerosis
diabetes
syphilis
Features
unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma
Management
high-dose steroids
recovery usually takes 4-6 weeks
Prognosis
MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%
Orbital cellulitis
Orbital cellulitis is the result of an infection affecting the fat and muscles posterior to the orbital septum, within the orbit but not involving the globe. It is usually caused by a spreading upper respiratory tract infection from the sinuses and carries a high mortality rate. Orbital cellulitis is a medical emergency requiring hospital admission and urgent senior review. Periorbital (preseptal) cellulitis is a less serious superficial infection anterior to the orbital septum, resulting from a superficial tissue injury (chalazion, insect bite etc…). Periorbital cellulitis can progress to orbital cellulitis.
Epidemiology
Mean age of hospitalisation 7-12 years.
Risk factors
Childhood
Previous sinus infection
Lack of Haemophilus influenzae type b (Hib) vaccination
Recent eyelid infection/ insect bite on eyelid (Peri-orbital cellulitis)
Ear or facial infection
Presentation
Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema and ptosis
Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
Differentiating orbital from preseptal cellulitis
reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis
Investigations
Full blood count – WBC elevated, raised inflammatory markers.
Clinical examination involving complete ophthalmological assessment – Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema.
CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis.
Blood culture and microbiological swab to determine the organism. Most common bacterial causes – Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
Management
admission to hospital for IV antibiotics
Papilloedema
Papilloedema describes optic disc swelling that is caused by increased intracranial pressure. It is almost always bilateral.
The following features may be observed during fundoscopy:
venous engorgement: usually the first sign
loss of venous pulsation: although many normal patients do not have normal pulsation
blurring of the optic disc margin
elevation of optic disc
loss of the optic cup
Paton’s lines: concentric/radial retinal lines cascading from the optic disc
Causes of papilloedema
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
Rare causes include
hypoparathyroidism and hypocalcaemia
vitamin A toxicity
Primary open-angle glaucoma: management
Glaucomas are optic neuropathies associated with raised intraocular pressure (IOP). They can be classified based on whether the peripheral iris is covering the trabecular meshwork, which is important in the drainage of aqueous humour from the anterior chamber of the eye. In open-angle glaucoma, the iris is clear of the meshwork. The trabecular network functionally offers an increased resistance to aqueous outflow, causing increased IOP.
Epidemiology
affects 0.5% of people over the age of 40
the prevalence increases with age up to 10% over the age of 80 years
affects males and females equally
Causes
increasing age
genetics: first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease
Symptoms:
characterised by a slow rise in intraocular pressure: symptomless for a long period
typically present following an ocular pressure measurement during a routine examination by an optometrist
Signs:
increased intraocular pressure
visual field defect
pathological cupping of the optic disc1
Case finding:
optic nerve head damage visible under the slit lamp
visual field defect
IOP > 24 mmHg as measured by Goldmann-type applanation tonometry
if suspected full investigations are performed
Diagnosis:
Case finding and provisional diagnosis is done by an optometrist
Referral to the ophthalmologist is done via the GP
Final diagnosis is done by investigations as below
Investigations:
automated perimetry to assess visual field
slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline
applanation tonometry to measure IOP
central corneal thickness measurement
gonioscopy to assess peripheral anterior chamber configuration and depth
Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy
The majority of patients with primary open-angle glaucoma are managed with eye drops. These aim to lower intra-ocular pressure which in turn has been shown to prevent progressive loss of visual field.
NICE guidelines:
first line: prostaglandin analogue (PGA) eyedrop
second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
if more advanced: surgery or laser treatment can be tried2
Reassessment
important to exclude progression and visual field loss
needs to be done more frequently if: IOP uncontrolled, the patient is high risk, or there is progression
Primary open-angle
glaucoma Rx
NICE guidelines:
first line: prostaglandin analogue (PGA) eyedrop
second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
if more advanced: surgery or laser treatment can be tried2
Medication
Mode of action
Notes
Prostaglandin analogues (e.g. latanoprost)
Increases uveoscleral outflow
Once daily administration
Adverse effects include brown pigmentation of the iris, increased eyelash length
Beta-blockers (e.g. timolol, betaxolol)
Reduces aqueous production
Should be avoided in asthmatics and patients with heart block
Sympathomimetics (e.g. brimonidine, an alpha2-adrenoceptor agonist)
Reduces aqueous production and increases outflow
Avoid if taking MAOI or tricyclic antidepressants
Adverse effects include hyperaemia
Carbonic anhydrase inhibitors (e.g. Dorzolamide)
Reduces aqueous production
Systemic absorption may cause sulphonamide-like reactions
Miotics (e.g. pilocarpine, a muscarinic receptor agonist)
Increases uveoscleral outflow
Adverse effects included a constricted pupil, headache and blurred vision
Red eye
There are many possible causes of a red eye. It is important to be able to recognise the causes which require urgent referral to an ophthalmologist. Below is a brief summary of the key distinguishing features
Acute angle closure glaucoma
severe pain (may be ocular or headache)
decreased visual acuity, patient sees haloes
semi-dilated pupil
hazy cornea
Anterior uveitis
acute onset
pain
blurred vision and photophobia
small, fixed oval pupil, ciliary flush
Scleritis
severe pain (may be worse on movement) and tenderness
may be underlying autoimmune disease e.g. rheumatoid arthritis
Conjunctivitis
purulent discharge if bacterial, clear discharge if viral
Subconjunctival haemorrhage
history of trauma or coughing bouts
Endophthalmitis
typically red eye, pain and visual loss following intraocular surgery
Red eye - glaucoma or uveitis?
glaucoma: severe pain, haloes, ‘semi-dilated’ pupil
uveitis: small, fixed oval pupil, ciliary flush
Relative afferent pupillary defect
Relative afferent pupillary defect
Also known as the Marcus-Gunn pupil, a relative afferent pupillary defect is found by the ‘swinging light test’. It is caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina
Finding
the affected and normal eye appears to dilate when light is shone on the affected eye
Causes
retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis
Pathway of pupillary light reflex
afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
Retinitis pigmentosa
Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision
Features
night blindness is often the initial sign
tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Associated diseases
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport’s syndrome
Tunnel vision
Tunnel vision
Tunnel vision is the concentric diminution of the visual fields
Causes
papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
Scleritis
Features
red eye
classically painful (in comparison to episcleritis), but sometimes only mild pain/discomfort is present
watering and photophobia are common
gradual decrease in vision
Keratoconjunctivitis sicca is characterised by dry, burning and gritty eyes caused by decreased tear production
Rheumatoid arthritis: ocular manifestations
Ocular manifestations of rheumatoid arthritis are common, with 25% of patients having eye problems
Ocular manifestations
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
Iatrogenic
steroid-induced cataracts
chloroquine retinopathy
painful eye
Scleritis is the correct answer. This presents as a painful red eye with reduced visual acuity and blurred vision. It can be unilateral or bilateral and peak incidence is age 40-60. It is associated with systemic illness in 50% of cases such as SLE, rheumatoid arthritis, herpes zoster and other infections. Treatment is with steroids and urgent ophthalmology referral.
Episcleritis can be differentiated from scleritis by the absence of pain. It is also more commonly unilateral although a third of cases are bilateral. Treatment is with non-steroidal anti-inflammatories.
Anterior uveitis presents with a painful red eye with photophobia, blurred vision and reduced visual acuity. Its presentation differs from scleritis in that the affected pupil is often small and there may be pus in the anterior chamber (a hypopyon) on examination. Patients often have worsening pain on convergence as the pupil constricts. Anterior uveitis is associated with seronegative arthropathies such as ankylosing spondylitis in 30% of cases. If suspected patients should be urgently referred to ophthalmology.
Blepharitis is caused by inflammation of the lid margins often caused by ingrowing eyelashes. Patients report dry red uncomfortable eyes, however, no visual problems making this the incorrect answer. Treatment is conservative with regular eye care using hot cloth.
Conjunctivitis is another cause of red eye but would present with eye discharge and sticky eyes particularly on waking. There is also no effect on visual acuity in conjunctivitis.
Squint
Squint (strabismus) is characterised by misalignment of the visual axes. Squints may be divided into concomitant (common) and paralytic (rare)
Concomitant
Paralytic
Due to imbalance in extraocular muscles
Convergent is more common than divergent
Due to paralysis of extraocular muscles
Detection of a squint may be made by the corneal light reflection test - holding a light source 30cm from the child’s face to see if the light reflects symmetrically on the pupils
The cover test is used to identify the nature of the squint
ask the child to focus on a object
cover one eye
observe movement of uncovered eye
cover other eye and repeat test
Management
eye patches may help prevent amblyopia
referral to secondary care is appropriate
Intermittent squint in newborns less than 3 months is normal and does not need to be investigated. Intermittent squint in newborns under 3 months of age is normal due to underdeveloped eye muscles, as such the correct answer is 4. If the squint persists or there is concern regarding the newborns ability to see, then referral to secondary care is appropriate. Eye patches may be trialled in older children to prevent lazy eye.
Subconjunctival haemorrhage
Subconjunctival haemorrhages result from the bleeding of blood vessels into the subconjunctival space. The vessels that bleed are usually the ones responsible for supplying the conjunctiva or episclera. The cause is most commonly traumatic followed by spontaneous idiopathic cases, Valsalva manoeuvres and several systemic diseases. Subconjunctival haemorrhages can look dramatic and cause worry to patients, however they are rarely an indicator of anything sinister.
Epidemiology:
Subconjunctival haemorrhages are more common in women than in men when there has been no history of trauma
The annual incidence of non-traumatic subconjunctival haemorrhages is 0.6%, the risk increases with age as the risk factors are more common in elderly patients. Newborns are also more susceptible
The incidence of both traumatic and non-traumatic subconjunctival haemorrhages is 2.6%
Risk factors:
Trauma and contact lens usage (68%): these are the most common causes generally, as well as being often the sole risk factor in younger patients
Idiopathic
Valsalva manoeuvre e.g. coughing, straining
Hypertension
Bleeding disorders
Drugs such as aspirin, NSAIDs and anticoagulants
Diabetes
Arterial disease and hyperlipidaemia
Symptoms:
Red-eye, usually unilateral
Subconjunctival haemorrhages are mostly asymptomatic, however mild irritation may be present
Signs:
Flat, red patch on the conjunctiva. It will have well-defined edges and normal conjunctiva surrounding it. Patches can vary in size depending on the size of the bleed, and can involve the whole conjunctiva
Traumatic haemorrhages are most common in the temporal region (40.5%), with the inferior conjunctiva as the next most commonly affected area
Vision should be normal, including acuity, visual fields and range of eye movements
On examination, the fundus should be normal
Investigations:
The diagnosis of a subconjunctival haemorrhage is a clinical one
If there is no obvious traumatic cause, check the patient’s blood pressure. If raised, refer the patient appropriately
If the patient is taking warfarin, check the INR. If raised, refer for appropriate adjustments to the dose to bring the INR back into the target range
If you cannot see the whole border of the haemorrhage i.e. the full extent of the haemorrhage is unclear, it may be associated with an intracranial bleed or an orbital roof fracture. This is often corroborated with a history of trauma and a black eye. Further appropriate investigations should then be done, including a full cranial nerve exam looking for neurological signs as well as a CT head, after discussion with a senior
Recurrent or spontaneous, bilateral subconjunctival haemorrhages warrant investigations for bleeding disorders or other pathology
Management:
Reassure the patient that whilst a subconjunctival haemorrhage may look alarming, it is a benign condition that will resolve on its own in 2 to 3 weeks. If the patient presents to services immediately after the haemorrhage occurs, it can spread over a couple of days until it begins to resolve. The colour of the patch may change to yellow/ green, like a bruise, but preparing the patient for this will prevent any alarm if this happens.
If the cause is traumatic consider a referral to the ophthalmologist to ensure no other damage has been caused to the eye
Advise the patient to consult their GP if this happens again because, as previously mentioned, recurrent subconjunctival haemorrhages warrant investigations for bleeding disorders or other potential pathology
Artificial tears can be used for a couple of weeks if there is any mild irritation
Prognosis:
This is a mild, self-limiting illness and should resolve on it’s own in 2-3 weeks
Sudden loss of vision
Sudden loss is a frightening symptom for patients. It may represent an ongoing issue or only be temporary. The term transient monocular visual loss (TVML) describes a sudden, transient loss of vision that lasts less than 24 hours.
The most common causes of a sudden painless loss of vision are as follows:
ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery
vitreous haemorrhage
retinal detachment
retinal migraine
Ischaemic/vascular
often referred to as ‘amaurosis fugax’
wide differential including large artery disease (atherothrombosis, embolus, dissection), small artery occlusive disease (anterior ischemic optic neuropathy, vasculitis e.g. temporal arteritis), venous disease and hypoperfusion
may represent a form of transient ischaemic attack (TIA). It should therefore be treated in a similar fashion, with aspirin 300mg being given
altitudinal field defects are often seen: ‘curtain coming down’
ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve
Central retinal vein occlusion
incidence increases with age, more common than arterial occlusion
causes: glaucoma, polycythaemia, hypertension
severe retinal haemorrhages are usually seen on fundoscopy
Central retinal artery occlusion
due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
features include afferent pupillary defect, ‘cherry red’ spot on a pale retina
Vitreous haemorrhage
causes: diabetes, bleeding disorders, anticoagulants
features may include sudden visual loss, dark spots
Retinal detachment
features of vitreous detachment, which may precede retinal detachment, include flashes of light or floaters (see below)
Vision Loss
Differentiating posterior vitreous detachment, retinal detachment and vitreous haemorrhage
Posterior vitreous detachment
Retinal detachment
Vitreous haemorrhage
Flashes of light (photopsia) - in the peripheral field of vision
Floaters, often on the temporal side of the central vision
Dense shadow that starts peripherally progresses towards the central vision
A veil or curtain over the field of vision
Straight lines appear curved
Central visual loss
Large bleeds cause sudden visual loss
Moderate bleeds may be described as numerous dark spots
Small bleeds may cause floaters
