Ophthalmology Flashcards
Stye
An acute infection of GLAND of Moll, Zeiss or eyelash follicle
Also known as external hordeolum - usually staphylococcal.
Hordeolum external is an abscess to infection in a lash follicle or glands of Moll (sweat glands) and of Zeis (sebum-producing glands attached directly to lash follicles)
(Glands of Moll and Zeiss - are modified sweat glands)
What is hordeolum internum?
An abscess of the Meiboimian glands.
Eyelids are supported by a tarsal plate (dense fibrous tissue) - contains tarsal (meibomian glands) – modified sebaceous gland secreting lipid which open at lid.
These ‘point’ inwards, opening on to conjunctiva, cause less local reaction but leave a residual swelling called a chalazion or a Melbomian cyst
when they subside. AKA internal hordeolum.
Vision may be reduced if corneal flattening occurs (rare)
Blepharitis- causes, features, diagnosis, treatment
Blepharitis - (inflammation of the eyelid MARGINS)- leads to a RED EYE
Causes:
- Due to MEIBOMIAN GLAND DYSFUNCTION - leads to DRYING of the eyes (as loss of oil secretion which prevented tear film evaporation) which leads to irritation - (posterior blepharitis; affecting meibomian glands – common)
- SEBORRHEIC DERMATITIS/ staphylococcal infection - (anterior blepharitis; affecting lashes – less common)
- Rosacea (more common in these patients)
Features:
- Eyes have ‘burning’ itching RED margins, with SCALES on the lashes.
- BILATERAL, GRITTINESS + discomfort (esp. around eyelid margins)
- Eyes may be sticky in morning/ worse in morning
- Eyelid margins are red
- Styes and chalazions are more common in blepharitis
- Swollen eyelids seen in staphylococcal blepharitis - therefore don’t have to be swollen
- 2° conjunctivitis may occur
Diagnosis:
On clinical examination
Inflammation of skin of eyelid –SCALING , flaking vesicles, telangiectasia & pustules
Loss of eyelashes –CRUSTING; scaling around lashes
Chalazion/STYE formation
Scarring may be seen on fluorescein staining
Entropion due to blepharitic changes can scratch cornea (lashes)
Treatment:
Poor tear film quality means eye is less protected
1) SOFTEN lid margin w/ hot compress 2x day 5-10 mins – mobilise oil from glands
2) mechanical removal of debris from lid margins – w/ baby shampoo/ warm water + lid massage - essential
3) artificial tears/ eye lubricant for symptom relief
4) topical Abx (e.g. chloramphenicol or fusidic acid) or short term steroids may give some benefit
5)oral doxycycline.
In children with blepharokeratitis, consider oral erythromycin too
What are the meibomian glands?
Meibomian glands (also called tarsal glands) are holocrine type exocrine glands, along the rims of the eyelid inside the tarsal plate. They produce meibum, an oily substance that prevents evaporation of the eye's tear film.
Entropian- causes , signs,mx
Lid INVERSION is typically due to degeneration of LOWER (rarely upper) lid fascial attachments and their muscles. It is rare if <40yrs old.
Causes:
- INVOLUTIONAL: common, inferior retractor dysfunction and tissue laxity.
- CICATRICIAL: chronic conjunctivitis, Trachoma, Ocular cicatricial pemphigoid, bullous disease, chemical injuries, RT, trauma and chronic blepharitis.
- CONGENITAL : Orientals, usually self resolving
Symptoms:
Irritation
Watering
Corneal ulcer - The inturned eyelashes IRRITATE the CORNEA.
Signs: Look for lid laxity Symblepharon Lower fornix height and depth Upper tarsal fibrosis in trachoma Corneal abrasion or ulcers
If left untreated patient can develop a corneal ulcer
Mx surgical
Lubricants & tape (to pull eyelid outwards can be used in mean time)
Taping the (lower) eyelids to the cheek, or botulinum toxin injection to the lower lid gives temporary relief; more last- ing relief needs surgery.
Cataract
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.
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
- Uveitis
- Down’s syndrome
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
HALO 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-normal fundus and optic nerve
Slit lamp examination- visible cataract
Classification:
NUCLEAR: change lens refractive index, common in old age.Involving lens nucleus. Yellowish- brown due to deposition of urochrome pigment.
Patient becomes myopic due to increase refractive index of lens. Colours appear less well saturated and more yellow/brown
CORTICAL
Cortex of lens. Radial spokes in the periphery.
Give rise to astigmatic changes. Patients troubled more in dark when pupil dilates and exposes more of cataract.
SUBCAPSULAR: due to steroid use, just deep to the lens capsule, in the visual axis.Directly under the lens capsule. Granular or plaque like appearance.
Near vision affected more than distance as opacity at nodal point of eye.
POLAR: localised, commonly inherited, lie 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 (MYOPIC SPECTACLE LENS - as cataract alters lens’ refractive index) , 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.
Complications following surgery
Posterior capsule OPACIFICATION: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
ENDOPHTHALMITIS: inflammation of aqueous and/or vitreous humour
Primary open-angle glaucoma- causes, sx, ix,
Glaucomas are optic neuropathies associated with RAISED INTRAOCULAR PRESSURE (IOP).
In open-angle glaucoma, most common cause is increase in resistance to drainage in the trabecular meshwork, even though the drainage angle between the cornea and iris remains open- leading to an increased resistance to aqueous outflow, causing increased IOP.
Causes: increasing AGE GENETICS: first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease Black patients MYOPIA HTN DM Corticosteroids
Symptoms:
characterised by a SLOW RISE in intraocular pressure:
SYMPTOMLESS for a long period
PERIPHERAL visual field loss - nasal scotomas progressing to ‘TUNNEL VISION’
Decreased visual acuity
optic disc CUPPING
(associated with peripheral visual loss than blurry vision)
Fundoscopy signs of primary open-angle glaucoma (POAG):
- Optic disc CUPPING- cup-to-disc ratio >0.7 (normal = 0.4-0.7) - occurs as loss of disc substance makes optic cup widen and deepen
- Optic disc PALLOR- indicating optic atrophy
- Bayonetting of vessels - VESSELS have BREAKS as they disappear into the deep cup and re-appear at the base
- Additional features - Cup NOTCHING (usually inferior where vessels enter disc), Disc HAEMORRHAGE.
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
Cataract surgery
CATARACT SURGERY = phacoemulsification
Common technique performed as a day case under local anaesthetic & patient remains prone during procedure;
Can be with sub-tenon OR peribulbar injection or topical drops
Entry to eye is made via limbus (peripheral cornea) using a self-sealing incision (step wise incision of about 2.2mms) & viscoelastic is injected into anterior chamber to maintain eye shape during surgery & enlarges anterior chamber to ↓ risk of corneal endothelium damage
A circular incision is then made in the anterior lens capsule – capsulorrhexis. The cataractous lens is removed using high speed ultrasound cutting nucleus into tiny pieces which are then aspirated
Posterior capsule is retained and there is insertion of new artificial intraocular lens (can be silicone, acrylic or hydrogels) calculated to correct the patient’s refractive error.
Viscoelastic is then removed. No sutures inserted which ↓astigmatism & ↑ healing.
Treatment of glaucoma and its mode of action
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: B-BLOCKER, CARBONIC ANHYDRASE inhibitor, or sympathomimetic eyedrop
- if more advanced: surgery or laser treatment can be tried
Medication:
- Prostaglandin analogues (e.g. latanoprost)
- Increases uveoscleral outflow
- 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
Surgery in the form of a trabeculectomy may be considered in refractory cases.
What is a chalazion?
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
What are the different types of styes?
External (hordeolum externum)
Internal (hordeolum internum)
Episcleritis
- RED eye
- classically NOT PAINFUL (in comparison to scleritis), but mild pain may be present
- WATERING and MILD PHOTOPHOBIA may be present
- In episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera. In scleritis, vessels are deeper, hence do not move
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.
Is associated with Rheumatoid arthritis.
Management:
conservative
artificial tears may sometimes be used
It can be treated with non-steroidal anti-inflammatories or steroids in resistant cases.
Horners syndrome
Features UNILATERAL miosis (small pupil) ptosis enophthalmos* (sunken eye) with or without anhidrosis (loss of sweating one side)
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
The affected and normal eye appears to dilate when light is shone on the affected
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
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 - high co2 Rare causes include: hypoparathyroidism and hypocalcaemia vitamin A toxicity
Stages of hypertensive retinopathy
Keith-Wagener classification
I - Arteriolar narrowing and tortuosity , increased light reflex - silver wiring
II - Arteriovenous nipping ( a small artery (arteriole) is seen crossing a small vein (venule), which results in the compression of the vein with bulging on either side of the crossing.)
III - Cotton-wool exudates, Flame and blot haemorrhages
IV - Papilloedema
Sudden loss of vision - causes
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
Age related macular degeneration- types,sx,signs,ix, tx
Age-related macular degeneration is the most common cause of blindness in the UK. The commonest cause of VISUAL LOSS in elderly persons in the developed world.
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)
Risk factors:
Advancing age
Smoking is another key risk factor in the development of ARMD
Family history
Other include:
Those associated with increased risk of ischaemic cardiovascular disease, such as HTN, dyslipidaemia and DM.
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 DRUSEN 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 - pigmentary, exudative or haemorrhagic changes affecting the retina
Colour fundus photography - so that changes can be identified over time.
Fluorescein angiography - if neovascular ARMD- 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 - 3D view of retina
Treatment:
- A combination of zinc with anti-oxidant vitamins A,C and E reduced progression - 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 - can limit progression of wet ARMD and stabilise or reverse visual loss. Examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib.
- 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.
Ischaemic/vascular sudden vision loss
often referred to as ‘amaurosis fugax’
Wide differential including large artery disease (atherothrombosis, embolus, dissection), small artery occlusive disease (anterior ischaemic optic neuropathy, vasculitis e.g. temporal arteritis), venous disease and hypo-perfusion.
May represent a form of transient ischaemic attack (TIA) - transient so WON’T LAST FOR LONG.
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
Sudden loss of vision
Incidence increases with age, more common than arterial occlusion
2 types : ischaemic (with has RAPD) and non ischaemic
Causes: glaucoma, polycythaemia, hypertension
Severe retinal HAEMORRHAGES are usually seen on fundoscopy
Central retinal artery occlusion
Sudden loss of vision
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
Vitreous haemorrhage is BLEEDING INTO THE VITREOUS HUMOUR. It is one of the most common causes of SUDDEN PAINLESS loss of vision. It causes disruption to vision to a variable degree, ranging from floaters to complete visual loss.
The source of bleeding can be from disruption of any vessel in the retina as well as the extension through the retina from other areas. Once the bleeding stops, the blood is typically cleared from the retina at an approximate rate of 1% per day.
Common causes (collectively account for 90% of cases):
- PROLIFERATIVE DIABETIC RETINOPATHY (over 50%)
- posterior vitreous detachment
- ocular trauma: the most common cause in children and young adults
- blood thinners would predispose
Patients typically present with an acute or subacute onset of:
- painless visual loss or haze (commonest)
- RED HUE in the vision
- FLOATERS or shadows/dark spots in the vision
Signs:
- decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
- visual field defect if severe haemorrhage
Investigations:
- dilated fundoscopy: may show haemorrhage in the vitreous cavity
- slit-lamp examination: red blood cells in the anterior vitreous
- ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
- fluorescein angiography: to identify neovascularization
- orbital CT: used if open globe injury
Sudden loss of vision
Causes: DIABETES , bleeding disorders, anticoagulants
- Features may include sudden visual loss, DARK spots, floaters
(Proliferative diabetic retinopathy is a risk factor for VH because the new vessels grow into the vitreous and are fragile, so they bleed easily).
Retinal detachment- features
Sudden loss of vision
Features of vitreous detachment, which may precede retinal detachment, include flashes of light or floaters
Classically presents as a CURTAIN COMING DOWN over the eye
Differentiating posterior vitreous detachment, retinal detachment and vitreous haemorrhage
POSTERIOR VITREOUS DETACHMENT
FLASHES of light (photopsia) - in the peripheral field of vision
FLOATERS, often on the temporal side of the central vision
RETINAL DETACHMENT
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
VITREOUS HAEMORRAHAGE
Large bleeds cause sudden visual loss
Moderate bleeds may be described as numerous dark spots
