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
Cotton wool spot
Nerve fibre layer of the retina is infarcted/ischaemic
Cherry red spot
Fovea in central retinal artery occlusion as no overlying nerve fibre layer
fovea supplied by choroid vessels not retinal
Third nerve palsy
Ptosis
Mydriasis (dilation of pupil)- due to parasympathetics on the oculomotor to the sphincter pupilae
Eye is down and out
Diabetic retinopathy pathophysiology
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. NEOVASCULARISATION is thought to be caused by the production of growth factors in response to retinal ischaemia.
If someone has flashes and floaters - what are you thinking?
Vitreous/retinal detachment
Flashes and floaters are symptoms of vitreous detachment. The patient is at risk of retinal detachment and should be referred urgently to an ophthalmologist
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
Argyll-Robertson pupil
Argyll-Robertson pupil is one of the classic pupillary syndrome. It is sometimes seen in neurosyphilis and is often said to be the prostitute’s pupil - ACCOMMODATES but DOESN’T REACT. Another 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
Cause:
diabetes mellitus
syphilis
Mydriasis- causes
Causes of mydriasis (large pupil):
- third nerve palsy
- Holmes-Adie pupil
- traumatic iridoplegia - paralysis of the sphincter pupillae- may result in short term blurred vision
- phaeochromocytoma - tumour of the adrenal medulla - which causes irregular secretion of adrenaline.
- congenital
Drug causes of mydriasis:
- topical mydriatics: tropicamide, atropine
- sympathomimetic drugs: amphetamines, cocaine
- anticholinergic drugs: tricyclic antidepressants
Anisocoria may result in apparent mydriasis, due to the difference with the other pupil.
Squint - classification
Squints may be classified as to where the eye deviates TOWARD:
- the nose: esotropia
- temporally: exotropia
- superiorly: hypertropia
- inferiorly: hypotropia
Squint
Squint (strabismus) is characterised by misalignment of the visual axes.
Squints may be divided into CONCOMITANT (common) and PARALYTIC (rare).
Concomitant
Due to imbalance in extraocular muscles
CONVERGENT is more common than divergent
Paralytic
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- refer child with squint immediately to ophthalmology - needs to be reviewed by ophthalmologist and orthoptist
A mother brings her son in to surgery as she suspects he has a squint. She thinks his right eye is ‘turned inwards’. You perform a cover test to gather further information. Which one of the following findings would be consistent with a right esotropia?
On covering the left eye the right eye moves laterally from the nasal (esotropic) position to take up fixation.
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
What distinguishes scleritis from episcleritis?
The presence of pain in scleritis
Both cause an acutely red and watery eye.
In episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera. In scleritis, vessels are deeper, hence do not move
Allergic conjunctivitis
Allergic conjunctivitis may occur alone but is often seen in the context of hay fever (which is seasonal allergic conjunctivitis)
Features:
- BILATERAL symptoms conjunctival erythema, conjunctival swelling (chemosis)
- ITCH is prominent
- The eyelids may also be SWOLLEN
- May be 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
Acute angle closure glaucoma- predisposing factors, features, mx
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 DILATION
- 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
- HALOS 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
What is latanoprost used in tue management of
Latanoprost is a PROSTAGLANDIN ANALOG analog used in glaucoma. It works by INCREASING UVEOSCLERAL OUTFLOW
If someone has bilateral grittiness in their eyes - what are you thinking ?
Blepharitis
Causes of painLESS sudden loss of vision
Amaurosis fugax
Central retinal artery occlusion
Retinal detachment
Vitreous haemorrhage
Treatment of DRY ARMD
Stop smoking
Take antioxidant vitamins - A, C, and E. They reduce progression
Otherwise there aren’t any more medical therapies currently available
Periorbital cellulitis
PRESEPTAL cellulitis is sometimes also referred to as periorbital cellulitis. It is an infection of the soft tissues ANTERIOR to the orbital septum - this includes the eyelids, skin and subcutaneous tissue of the face, but NOT THE CONTENTS of the orbit.
Infection usually spreads to the structures surrounding the orbit from other nearby sites, most commonly from breaks in the skin or local infections such as sinusitis or other respiratory tract infections. The most frequently causative organisms are Staph. aureus, Staph. epidermidis, streptococci and anaerobic bacteria.
Epidemiology
Preseptal cellulitis occurs most commonly in children.
It is more common in the winter due to the increased prevalence of respiratory tract infections.
Symptoms
The patient presents with a RED , SWOLLEN, PAINFUL eye of ACUTE onset. They are likely to have symptoms associated with FEVER.
Signs
- Erythema and OEDEMA of the EYELIDS, which can spread onto the surrounding skin
- Partial or complete PTOSIS of the eye due to swelling
- Orbital signs (pain on movement of the eye, restriction of eye movements, proptosis, visual disturbance, chemosis, RAPD) must be ABSENT in preseptal cellulitis - their presence would indicate orbital cellulitis
Significant differentials
Orbital cellulitis
Allergic reaction
Investigations
Bloods - raised inflammatory markers
Swab of any discharge present
Contrast CT of the orbit may help to differentiate between preseptal and orbital cellulitis. It should be performed in all patients suspected to have orbital cellulitis
Management
All cases should be referred to secondary care for assessment
Oral antibiotics are frequently sufficient - usually co-amoxiclav
Children may require admission for observation
Complications
Bacterial infection may spread into the orbit and evolve into orbital cellulitis
Orbital cellulitis
Orbital cellulitis is an infection of the soft tissues BEHIND the orbital septum, and is a much more serious infection.
- Orbital signs (PAIN on MOVEMENT of the eye, restriction of eye movements, PROPTOSIS, VISUAL DISTURBANCE , chemosis, RAPD) - presence would indicate orbital cellulitis
Infective conjunctivitis
Characterised by SORE, RED eyes associated with a STICKY discharge
Bacterial conjunctivitis
- Purulent discharge
- Eyes may be ‘stuck together’ in the morning)
Viral conjunctivitis
- SEROUS discharge
- Recent URTI
- Preauricular lymph nodes
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
Traditional classification of diabetic retinopathy
Background retinopathy
- microaneurysms (dots)
- blot haemorrhages (<=3)
- hard exudates
Pre-proliferative retinopathy
- cotton wool spots (soft exudates; ischaemic nerve fibres)
- > 3 blot haemorrhages
- venous beading/looping
- deep/dark cluster haemorrhages
- more common in Type I DM, treat with laser photocoagulation
New classification of diabetic retinopathy
- 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 VITREOUS 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
Features of corneal ulcer
Corneal ulcers are more common in contact lens users
Features
- eye PAIN
- PHOTOPHOBIA
- WATERING of eye
- focal fluorescein staining of the cornea
