Painful red eye Flashcards
What are the differential diagnoses of a painful red eye?
Painful red eye:
- Scleritis
- Acute angle-closure glaucoma
- Anterior uveitis (acute iritis)
- Acute keratitis
- Corneal abrasion
- Corneal ulcer
- High-velocity FB, trauma e.g. penetrating eye injury, chemical injuries
- Neonatal conjunctivitis
a) . What is uvea?
b) . There are four types of uveitis. What are they?
c) . What structures are affected in each type?
a). The uvea is the middle layer of the eye comprising of the iris and ciliary body anteriorly and the choroid posteriorly.
_*Uveitis is inflammation of this uveal tract, with or without inflammation of nearby structures, such as the retina, the optic nerve, and the vitreous humor_
b). 3 types of uveitis:
-
Anterior uveitis (AKA ‘Iridocyclitis’ or ‘iritis’)
- The term ‘iritis’ is wrong as anterior uveitis often involves Iris + anterior part of the ciliary body (pars plicata)
-
Intermediate uveitis (AKA ‘pars planitis’ or ‘cyclitis’)
- Involves posterior part of the ciliary body (pars plana)+vitreous (vitritis) + peripheral part (outer edge) of the retina
-
Posterior uveitis
- Involves choroid + retina posterior to the vitreous base
-
Panuveitis
- Involves the entire uveal tract!
The ciliary body consists of 2 parts. What are they?
The ciliary body is a part of the eye that includes the ciliary muscle, which controls the shape of the lens, and the ciliary epithelium, which produces the aqueous humor. The ciliary body, the iris and the choroid together make up the uvea
- Pars plicata (anterior part of the ciliary body)
- Pars plana (posterior part of the ciliary body)
Which is the most common type of uveitis?
Anterior uveitis
Other than classifying uveitis based on the part of the eye being affected, another way of classifying it is by its course. It can be divided into acute, chronic and recurrent uveitis.
How do you define acute, chronic and recurrent uveitis?
Acute uveitis - sudden onset of inflammation which resolves within 3 months
Chronic uveitis - persistent inflammation lasting > 3 months, in which prompt relapse (within 3 hrs) occurs when treatment is discontinued
Recurrent uveitis (common) - repeated episodes, separated by periods of inactivity without treatment, for 3 months or more
What are the causes of uveitis?
Causes:
- Idiopathic in most cases
-
Systemic autoimmune disorders, such as:
- Seronegative spondyloarthropathies (RF-negative, HLA-B27)
- Ankylosing spondylitis
- Psoriatic arthritis
- Reactive arthritis (“Reiter syndrome”)
- Enteropathic arthritis e.g. IBD (Crohns, UC), coeliac disease
- Juvenile rheumatoid arthritis
- RF is positive in most adult RA but negative in most juvenile RA
- Sarcoidosis
- Behcet’s disease (may cause bilateral uveitis)
- Multiple sclerosis
- Seronegative spondyloarthropathies (RF-negative, HLA-B27)
-
Infection
- HSV (herpes simplex keratitis), HZV (herpes zoster ophthalmicus), CMV, toxoplasmosis, syphilis, TB
- Trauma
What conditions are associated with anterior uveitis?
Ankylosing spondylitis (The 6As) –> Anterior uveitis, Aortic regurgitation, Apical lung fibrosis, Amyloidosis, Aortitis, AV block, Atlanto-axial subluxation
Psoriatic arthritis
Reactive arthritis
Enteropathic arthritis (IBD, coeliac disease)
Sarcoidosis
Behcet’s disease (a type of vasculitis)
Give 3 risk factors for developing uveitis?
Personal Hx of uveitis
Age > 20 yrs old
Genetics - HLA-B27
What is the epidemiology of uveitis?
- Anterior uveitis is the most common type of uveitis (90% of all cases in primary care in Western countries), of which idiopathic anterior uveitis is the most common form. Posterior uveitis is less common, followed by intermediate uveitis
- Uveitis causes 10% of visual impairment worldwide
- Most common in people aged 20-50 yrs old
- Uncommon in children < 10 yrs old and adults > 70 yrs old
What are the clinical features of anterior uveitis?
Presentations:
Symptoms
- Usually unilateral + sudden onset
- If bilateral –> usually associated with systemic disease and more likely to become chronic
-
Pain/ dull ache that is worse when reading, due to contraction of the ciliary muscle at close vision as part of the accommodation reflex
- May extend to the surrounding orbit and maybe tender to palpation through the eyelid
- Red eye
- Reduced visual acuity (blurred vision) - due to the presence of inflammatory cells and flare in the anterior chamber
- Watering
-
Photophobia
- The iris is made of 2 muscles: the radial muscle (dilator papillae) and the circular muscle (sphincter papillae). Contraction of the sphincter papillae causes constriction of pupils under bright light while contraction of the dilator papillae causes dilatation of pupils under dim light. This can cause a lot of pain due to contraction of these inflamed iris muscle in anterior uveitis
Signs
- Circumciliary injection - redness (dilated inflamed bvs) confined to the limbus of the eye - see image
-
Inflammatory cells and flare on a slit lamp examination - see image
- These inflammatory cells appear as tiny white dots floating in the anterior chamber while the “flare” is the smoky appearance given by proteins that have leaked from inflamed blood vessels
- The two combined gives an appearance similar to the beam of a projector passing through smoke in a darkened room
-
Hypopyon - see image
- If inflammation is severe, inflammatory cells can settle at the bottom of the anterior chamber, giving a layer of ‘pus’ which covers the inferior part of the iris
-
Keratic precipitates - see image
- These are clumps of inflammatory cells on the corneal endothelium, usually found on the inferior half of the cornea
- The larger clumps are known as ‘mutton fat’ lesions, they are typically found in association with granulomatous inflammation
- These are clumps of inflammatory cells on the corneal endothelium, usually found on the inferior half of the cornea
-
Miosis
- Caused by spasm of the sphincter papillae of the iris
- Later, inflammatory adhesions can occur between iris and the anterior lens capsule (posterior synechiae) –> irregularly-shaped pupil
-
IOP can be raised, normal or low
- Low due to ciliary body inflammation resulting in a decrease in aqueous production
- Raised due to either resistance to aqueous outflow by inflammatory cells and proteins, inflamed trabecular meshwork, or as a response to steroid therapy
- Granulomatous uveitis seen in sarcoidosis, syphilis, sympathetic ophthalmitis
- Sympathetic ophthalmitis is a rare granulomatous panuveitis affecting both eyes occurring weeks to months after penetrating injury
What does the image below show?
Circumciliary injection
Dull pinkish area confined to the limbus, with some overlying bright red vessels
This patient with anterior uveitis presents with eye pain. You examine the patient using slit lamp and you found this. What does the image show you?
Inflammatory cells and flares
(looks like the beam of a projector passing through smoke in a darkened room)
You saw these on a slit lamp examination, what are these?
Keratic precipitates
The patient with anterior uveitis presents with this? What is this?
Posterior synechiae
*You can see that the iris is adhered to the lens capsule at the back
Give 4 differential diagnoses of anterior uveitis
Acute glaucoma
Keratitis
Scleritis
Ocular trauma e.g. embedded FB
Episcleritis
Infective conjunctivitis
What investigations would you carry out in a patient with suspected anterior uveitis?
- Clinical diagnosis
- Systemic investigation is not usually indicated in the case of a single (first) episode of unilateral acute non-granulomatous anterior uveitis in the absence of clues in the history and examination that suggest a systemic or infectious cause.
- Investigations are needed if:
- Recurrence
- Bilateral disease –> usually systemic disease-related
- Persistent/ chronic
- Resistance to standard therapy
- Granulomatous uveitis
(Ix includes FBC, U&Es, CRP, ESR, syphilis serology, serum ACE (raised in sarcoidosis), ANA (raised in JIA) , HLA-B27, RF, anti-CCP, anti-dsDNA, C3 and C4, c-ANCA, p-ANCA, CXR (check for TB or sarcoidosis))
How do you manage acute anterior uveitis?
Mx:
- Primary care:
- Urgent same-day referral to ophthalmology for people with severe eye pain and a significant reduction in vision
- Urgent referral for people with suspected uveitis (new presentations, and recurrent) for assessment within 24 hrs by an ophthalmologist
- Secondary care:
- If non-infectious
- Corticosteroids - reduce inflammation and prevents adhesions in the eye. Taper corticosteroids slowly over weeks because withdrawing them too quickly can cause rebound inflammation
- Cycloplegic-mydriatic drug (muscarinic receptor blockers) e.g.cyclopentolate 1% or atropine 1% to paralyse the ciliary body - relieves pain and prevents adhesions between the iris and lens
- If severe or chronic –> Immunosuppressive drugs e.g. methotrexate, TNF inhibitors e.g. adalimumab, laser phototherapy, cryotherapy, or vitrectomy (removal of the vitreous fluid)
- If non-infectious
- If infectious –> Abx + corticosteroids + cycloplegics
- Regular monitoring of IOP as IOP can raise as a result of anterior uveitis or by topical steroid use
What is glaucoma?
Glaucoma is a group of eye diseases with characteristic optic nerve head (optic disc) changes associated with corresponding visual field defects (scotomas), with or without raised IOP
Changes to the optic disc include increased cup-to-disc ratio, or as a late sign, pallor of the optic disc which indicates optic atrophy
a) . What is the normal range of intraocular pressure?
b) . What IOP is considered ocular hypertension?
c i). Glaucoma is high pressure in the eye - true or false
c ii). Glaucoma can be cured - true or false
c iii). Glaucoma always causes red & painful eyes - true or false
c IV). Only people with sight problems should get their eyes tested for glaucoma - true or false
a) . IOP 11-21 mmHg is considered normal
b) . Ocular hypertension is defined as consistently or recurrently raised IOP (> 21 mmHg) but with NO SIGNS of glaucoma
c i). False - some people develop glaucoma at a pressure < 21 mmHg (“normal tension glaucoma”), and some people have pressures well above this level without showing signs of glaucoma
c ii). False - glaucoma is the leading cause of IRREVERSIBLE blindness in the world so it’s NOT curable (but there are treatments to prevent or delay its progression)
c iii). False - Open-angled glaucoma is slowly progressive and most patients are asymptomatic. By the time they actually start developing visual field changes, it’s already too late. That’s why it’s important for EVERYONE to get their eyes checked for glaucoma
c IV). False - EVERYONE should get their eyes checked for glaucoma
Pathophysiology of open-angled glaucoma:
Describe how aqueous humour is drained in the anterior chamber and how the blockage of drainage can lead to open-angled glaucoma
Ciliary epithelium of the ciliary body –> produces aqueous humour in the posterior chamber (production is mediated by enzyme carbonic anhydrase) –> aqueous humour then flows through the pupil into the anterior chamber –> drained primarily through the trabecular meshwork that is situated in the apex of the anterior chamber angle –> canal of Schlemm
A small percentage of aqueous humour may drain via the ciliary muscle into the supraciliary and suprachoroidal spaces (the uveoscleral outflow)
Secretion of aqueous humour is increased by stimulation of beta-2 receptors and decreased by stimulation of alpha-2 receptors of the sympathetic nervous system that are located on cells of the ciliary body
If the drainage via the trabecular meshwork is blocked, aqueous humor builds up in the eye and causes raised IOP, this pushes the posterior segment of the eye towards the back compressing and damaging the optic nerve fibres. The increased pressure on the blood vessels can cause ischaemic damage to nerve fibres –> Open angle glaucoma (it develops painlessly and insidiously over time so it’s a chronic condition that’s difficult to pick up)
How many routes of outflow are there to drain aqueous humour?
2 routes of outflow:
- Via the trabecular meshwork (main primary route)
- Via the uveoscleral outflow (only a small % of aqueous humour drains here)
Pathophysiology of acute angle closure glaucoma:
Acute angle closure glaucoma maybe primary (due to anatomical predisposition) or secondary (due to another eye pathology)
Describe the pathophysiology of primary and secondary acute angle closure glaucoma
Primary angle-closure glaucoma (far more common)
- Caused by anatomical predisposition - the lens is located more anteriorly than normal and presses against the iris –> ‘pupillary block’
- This interrupts the normal flow of aqueous humour from the posterior chamber to the anterior chamber, causing pressure to build up in the posterior chamber
- As the pressure builds up in the posterior chamber, the iris is pushed forward causing narrowing/ closure of the anterior chamber angle (iridocorneal angle). In addition, contact of the iris with the trabecular meshwork causes scar tissue formation (fibrosis) in the trabecular meshwork, further narrowing the angle and reducing drainage
Secondary angle-closure glaucoma (far less common)
- Caused by other eye pathologies, which can be divided into:
- Conditions that ‘push’ the iris/ ciliary body forward
- Space occupying lesion in the eye
- Conditions that ‘pull’ the iris causing deformity
- Neovascularisation of the iris (rubeosis iridis) –> neovascular glaucoma - most commonly caused by ischaemia (e.g. diabetic retinopathy, CRVO, ocular ischaemic syndrome), inflammation (e.g. chronic anterior uveitis, Behcet’s disease, endophthalmitis), and tumours
- Ischaemic, inflammatory, and carcinogenic tissues –> VEGF (angiogenic factor) –> passes into the anterior segment –> neovascularisation of the iris –> these abnormal new vessels have a surrounding contractile fibrovascular membrane which causes the iridocorneal angle to be pulled closed by peripheral anterior synechiae (see image) –> acute angle-closure glaucoma
- In addition, these new blood vessels are leaky, promoting secondary open-angle glaucoma
- Conditions that ‘push’ the iris/ ciliary body forward
What are the different types of glaucoma?
- Open-angle glaucoma (characterised by a normal iridocorneal angle)
- _*Primary open-angle glaucoma (POAG)_ - most common type of all glaucoma (idiopathic)
- _*Normal tension glaucoma_
- Suspected POAG
- When the appearance of the optic nerve head is suggestive of glaucoma but the visual fields appear normal, or the other way round, where a visual field defect exists but the optic nerve appears healthy
- Secondary open-angle glaucoma - uncommon
- Angle-closure glaucoma (characterised by a closing / narrowing of the iridocorneal angle)
- Primary angle closure glaucoma (PACG) - most common type of angle-closure glaucoma
- Secondary angle closure glaucoma - uncommon
Primary and secondary angle closure glaucoma can be further classified as acute and chronic:
- Acute: an ophthalmic emergency that presents with severe eye pain, visual loss, redness, headache, nausea and vomiting
- Chronic: insidious onset with visual loss only apparent in advanced disease. Normally pick up in otherwise asymptomatic patients on routine ophthalmic examination
- Ocular hypertension
* Defined as IOP > 21 mmHg but with NO SIGNS of glaucoma (i.e. no optic disc and visual field changes)
What’s the most common type of glaucoma?
Primary open angle glaucoma (POAC)
What’s the most common form of angle-closure glaucoma?
Primary angle-closure glaucoma (PACG)
What are the causes of secondary open angle glaucoma?
Causes of secondary open angle glaucoma:
Eye pathologies that make the drainage of aqueous humour difficult, including:
-
Pseudoexfoliative glaucoma
- The deposition of proteins within the anterior segment can block the trabecular meshwork resulting in aqueous outflow obstruction
- Seen in old people
- Cause unknown
-
Pigmentary glaucoma
- Pigment from the back of the iris deposited in the trabecular meshwork restricts outflow of the aqueous humor
-
Neovascular glaucoma
- New blood vessels formed in response to ischaemia (e.g. diabetic retinopathy or CRVO) block the outflow of aqueous humor through the trabecular meshwork
-
Uveitic glaucoma
- Inflammatory cells and proteins in the anterior chamber block the outflow through the trabecular meshwork
- **Note that the IOP can be low, normal or high in anterior uveitis
- _**Steroid-induced glaucoma_
- In susceptible people, corticosteroids increase the resistance to outflow of the aqueous humour by affecting the transport of aqueous humor by trabeculocytes in the trabecular meshwork
- Most commonly seen with eye drop preparations tho it may develop when steroids are administered by other routes
-
Angle-recession glaucoma
- Trauma to the drainage angle structures reduces outflow of the aqueous humor
Primary open angle glaucoma and primary angle closure glaucoma are idiopathic
A 30-year-old man has presented to the eye emergency department after being hit across the face with a baseball bat. On examination, the right eye has blood in the anterior chamber.
Which of the following does the blood most put him at risk for?
a) . Cataract
b) . Ectopia lentis
c) . Endophthalmitis
d) . Glaucoma
e) . Uveitis
The answer is D - Glaucoma!
Blunt ocular trauma with associated hyphema is a high-risk scenario of raised IOP. This is due to the blood causing a blockage in the drainage of the aqueous humour.
What are the causes of secondary angle-closure glaucoma?
Causes of secondary angle closure glaucoma:
Eye pathologies that cause narrowing/ closing of the iridocorneal angle, which can be divided into:
- Conditions that ‘push’ the iris/ ciliary body towards the trabecular meshwork
- Space occupying lesion in the eye
- Conditions that ‘pull’ the iris towards the trabecular meshwork
- Things that cause neovascularisation of the iris (rubeosis iridis) which leads to neovascular glaucoma:
- Ischaemia (e.g. diabetic retinopathy, CRVO, ocular ischaemic syndrome)
- Inflammation (e.g. chronic anterior uveitis, Behcet’s disease, endophthalmitis)
- Tumours of the iris, ciliary body…
- Things that cause neovascularisation of the iris (rubeosis iridis) which leads to neovascular glaucoma:
Ischaemic, inflammatory, and carcinogenic tissues –> VEGF (angiogenic factor) –> passes into the anterior segment –> neovascularisation of the iris–> these abnormal new vessels have a surrounding contractile fibrovascular membrane which causes the iridocorneal angle to be pulled closed by peripheral anterior synechiae –> acute angle-closure glaucoma
In addition, these new blood vessels are leaky, so proteins and plasma can flow into the anterior chamber promoting secondary open-angle glaucoma. Blood vessels forming on top of the trabecular meshwork can block the drainage directly!
Give 5 risk factors for developing primary open angle glaucoma
Raised IOP
Age
FHx and genetics
Black ethnicity
Myopia (longer eyeball)
Corticosteroids
T2DM
HTN and cardiovascular disease
Give 5 risk factors for developing primary angle closure glaucoma (PACG)
- Age
- Women (as women tend to have shallower anterior chambers than men)
- Asians (esp Chinese)
- Hyperopia (shorter eyeball) - think about a sofa in a room. A sofa in a small room makes the room more crowded while a sofa in a big room makes it less crowded
- FHx and genetics
-
Anticholinergic (mydriatic) eye drops (e.g. atropine, tropicamide) or adrenergic eye drops (e.g. phenylephrine) –> Pupil dilation –> pushes the iris against the meshwork, blocking the outflow
- Doesn’t have to be an eye drop, can also be caused by medications administered via other routes e.g. oral TCA (antimuscarinic)
- Anything that causes pupil dilation can precipitate/ trigger acute angle-closure glaucoma e.g. watching TV in dim light, during stress (increases sympathetic activity which causes pupil dilation) or excitement, at night, or reading in a semi-prone position
- Systemic medications e.g. antimuscarinic or adrenergic medications
a) . Is primary open angle glaucoma more common in men or women or it affects both sexes equally?
b) . What ethnicity of people is more commonly affected by primary open angle glaucoma?
c) . Myopia increases the risk of primary open angle glaucoma - true or false
a) . Primary open angle glaucoma affects both sexes equally
b) . Black ethnicity are more commonly affected by primary open angle glaucoma
c) . True - myopia (shorter eyeball) increases the risk of primary open angle glaucoma
What are the clinical features of acute angle closure glaucoma?
Presentations:
Symptoms
- Severe eye pain, headache, N&V
- Red eye (usually unilateral)
- Reduced visual acuity (or vision loss) - due to corneal oedema
- Halos around lights - caused by a diffraction effect as light passes through the pupil (aperture)
- Photophobia - light makes the pain worse due to ischaemic iris caused by markedly elevated IOP
-
Symptoms worse with pupil dilation (e.g. watching a TV in a darkened room, feeling stressed or excited, reading in a semi-prone position, use of an adrenergic e.g. phenylephrine or antimuscarinic drug e.g. atropine or tropicamide eye drops)
- They usually happen at night time as light exposure decreases, resulting in pupil dilation and exacerbation of symptoms
- Symptoms usually get better when sleeping as increased parasympathetic activity causes pupil constriction!
- Previous episodes of attacks
Signs
-
Hazy cornea due to corneal oedema –> reduced visual acuity/ visual loss, loss of red reflex
- Normally, the endothelium of the cornea pumps fluid out of the cornea. This keeps your vision clear and your eyes working as they should. Raised IOP makes it hard for the fluid to be pumped out, so fluid accumulates in the cornea, causing corneal oedema –> haziness
- Semi-dilated, oval, fixed (non-reactive) pupil - due to ischaemia of the iris sphincter muscles which can no longer constrict the pupils
- A tender, hard eye on palpation
- Markedly raised IOP
- Hyperopia (risk factor for acute angle closure glaucoma)
How do you manage acute angle closure glaucoma?
Mx:
Acute angle-closure glaucoma is a MEDICAL EMERGENCY!
Initial Mx:
- Primary care
-
ADMIT IMMEDIATELY + URGENT REFERRAL TO AN OPHTHALMOLOGIST
- If immediate admission is not possible, start emergency treatment:
- Lie the person flat with their face up and head NOT supported by pillows, this will relieve some of the pressure on the angle
- Give a combination of eyedrops, including:
- Topical parasympathomimetic (e.g. pilocarpine –> contraction of ciliary muscles –> opening the trabecular meshwork –> increased drainage of the aqueous humour)
-
Carbonic anhydrase inhibitors (e.g. oral acetazolamide or topical brinzolamide) - reduces secretion of aqueous humour
- This can be given as IV in secondary care or if the patient is unable to swallow
- Topical beta-blocker (e.g. timolol) - blocks beta-2 adrenoceptors to reduce production of aqueous humour by the ciliary epithelium
- Topical alpha-2 agonist (e.g. apraclonidine, brimonidine tartrate) - reduces secretion of aqueous humour + increases uveoscleral outflow
- If all of the above fail –> hyperosmotic agents (e.g. mannitol) - reduces IOP by extracting fluid from the aqueous humour
- Analgesics and antiemetics
- If immediate admission is not possible, start emergency treatment:
-
ADMIT IMMEDIATELY + URGENT REFERRAL TO AN OPHTHALMOLOGIST
- Secondary care
- If initial medical management in primary care can’t immediately relieve the IOP –> anterior chamber paracentesis
Definitive Mx:
-
Laser peripheral iridotomy - creates a hole in the iris
- This allows aqueous humor to flow freely from the posterior chamber into the anterior chamber without having to go through the pupil. This equilibrises the pressure between the two chambers, freeing the angle and reducing IOP
- The unaffected eye is usually also treated preventively with laser iridotomy due to a high risk of developing acute angle closure in the future
How do you manage chronic angle closure glaucoma?
Mx:
-
Laser peripheral iridotomy to bypass the ‘pupillary block’ - this allows equilibrisation of pressure between the posterior and anterior chambers thereby preventing a buildup of pressure in the posterior chamber
- Pupillary block (see image) occurs when the flow of aqueous humour from the posterior chamber to the anterior chamber is obstructed by a functional block between the pupillary portion of the iris and the anterior part of the lens
- If treatment failure due to significant scarring of the trabecular meshwork from previous contact with the iris –> treat it as open-angle glaucoma
What are the clinical features of primary open angle glaucoma?
Presentations:
- Insidious onset!
- Asymptomatic in most cases until late stages of disease - diagnosis usually made on routine ophthalmic examination
- However, in those who are symptomatic:
-
Visual field loss (nasal scotomas –> ‘tunnel vision’ –> central vision loss (late stages)
- People are often unaware that they have a visual field defect, even when it is severe. This is because the visual fields of the eyes overlap, and so a visual field defect in one eye may be well compensated for by the other eye until that too becomes affected. Small visual field defect is hard to notice as the brain will try to “fill out the missing gaps’ in the visual field
- Decreased visual acuity
- Raised IOP
- Fundoscopy shows:
-
Optic disc cupping
- Cup-to-disc ratio > 0.7 (normal = 0.4-0.7)
- Optic disc pallor –> optic atrophy (due to raised IOP causing damage on the optic nerve)
- Bayonetting of blood vessels - this is when bvs bend or kink sharply when they pass over the edge of the cup
- Cup notching (usually on the inferior side where vessels enter disc), disc haemorrhages
-
Optic disc cupping
-
Visual field loss (nasal scotomas –> ‘tunnel vision’ –> central vision loss (late stages)
What does the image below show?
Bayonetting of blood vessels –> primary open angle glaucoma
What investigations would you like to carry out for primary open angle glaucoma?
Diagnosis is usually made during ophthalmic examination at optometrists:
- Ophthalmoscopy - shows cupping of optic disc, pale optic disc (optic atrophy), bayonetting of bvs
- Visual field assessment
- Check IOP - usually raised, however, some patients can develop glaucoma with a normal IOP
- Gonioscopy - check anterior chamber, the internal drainage system and the iridocorneal angle
- Pachymetry (see image) to assess corneal thickness - IOP readings vary depending on corneal thickness. Those with a thicker corneal thickness may show a higher reading of IOP than actually exists
To understand the pathophysiology of scleritis and episcleritis, you first need to understand the anatomy of the sclera and its position relative to the conjunctiva
The sclera is divided into 3 layers. What are these three layers called?
- Conjunctiva
- Lies on top of the 3 layers of sclera
- Contains conjunctival plexus
- No particular pattern
- Freely mobile
- _*In conjunctivitis - they appear bright red when inflamed_
From outer to innermost, the 3 layers of the sclera are:
- Episclera (see image)
- Contains the superficial episcleral plexus
- Lies within the superficial episclera
- Radial configuration
- Mobile over deeper layers
- _*In episcleritis - they appear salmon pink when inflamed_
- Contains the deep vascular plexus
- Lies deep to tenon’s capsule and directly over the scleral stroma
- Criss-cross pattern
- Immobile
- _*In scleritis - they appear violaceous (bluish red) when inflamed_
- Contains the superficial episcleral plexus
- Stroma
- Avascular middle layer and is made of type 1 collage
- Lamina fusca
- Anchors the sclera to the underlying choroid
So in episcleritis, it’s the superficial episcleral plexus that gets inflamed while in scleritis it’s the deep vascular plexus that gets inflamed!
This is a super simplified anatomical depiction of the conjunctiva, episclera, and scleral stroma, and the approximate location of the conjunctival, superficial episcleral, and deep vascular plexi
See image
What are the symptoms and signs of scleritis?
Presentations:
Symptoms
- Severe boring pain + painful eye movement
- Headaches
-
Red eye (bluish red/ violaceous/ dull pink), may have overlying bright red vessels
- Localised
- Diffuse
- Nodular
- Watering and photophobia
- Reduced visual acuity (late sign in severe scleritis)
- Clinical features of rheumatoid arthritis
Signs
- Very tender to touch
- Recurring scleritis can result in scleral thinning, exposing the underlying choroid –> giving the sclera a blue appearance (see image). It can also cause corneal thinning
How is scleritis different from episcleritis?
See image
To understand the pathophysiology of keratitis, it’s helpful to first understand the anatomy of the cornea
What are the different layers of the cornea?
From outer to innermost, the layers of the cornea are:
-
Corneal epithelium
- Thin and multicellular
- Non-keratinised stratified squamous epithelium - made of 6 layers of cells which are shed constantly on the exposed layer and are regenerated by multiplication in the basal layer
-
Bowman’s layer
- A tough layer composed of mainly type 1 collagen and other fibres
- Protects the underlying corneal stroma
-
Corneal stroma
- A thick transparent middle layer, consisting of regularly arranged type 1 collagen fibres along with sparsely distributed interconnected keratocytes, which are the cells for repair and maintenance
-
Descemet’s membrane
- Thin and acellular
- Serves as the basement membrane of the corneal endothelium
- Composed of type IV collagen
-
Corneal endothelium
- Simple squamous monolayer
- Role - regulates fluid and solute transport between the aqueous and corneal stromal compartments
- Bathed by aqueous humour, not by blood or lymph
- Unlike the corneal epithelium, the cells of the endothelium do not regenerate. Instead, they stretch to compensate for dead cells which reduces the overall cell density of the endothelium, which affects fluid regulation. If the endothelium can no longer maintain a proper fluid balance, stromal swelling due to excess fluids and subsequent loss of transparency will occur and this may cause corneal edema and interference with the transparency of the cornea and thus impairing the image formed
What are the symptoms and signs of bacterial keratitis?
Presentations:
Symptoms
- Severe eye pain + red eye
- Purulent conjunctivitis –> discharge
- Watering and photophobia
- FB, gritty sensation
- Reduced visual acuity
Signs
- Corneal ulcer
- Corneal oedema –> haziness
- In severe case –> hypopyon, which is a sign of intraocular infection (endophthalmitis) –> blindness
What is the pathophysiology of viral keratitis? (In other words, how does HSV1 and VZV cause viral keratitis)
HSV1:
- Primary infection usually occurs subclinically in childhood but can cause a blepharoconjunctivitis and a dendritic corneal ulcer. The virus then lies dormant in the trigeminal ganglion
- Secondary infection occurs when the virus reactivates and travels along the ophthalmic division of the trigeminal nerve to the cornea of the eye, causing a dendritic ulcer - this corneal involvement of the HSV infection is called herpes simplex keratitis. HSV1 can also travel along the maxillary or mandibular division of the trigeminal nerve to cause cold sores in upper and lower lips
- Reactivation is usually due to weakened immune system e.g. old age, immunosuppression (steroids, chemo, diabetes)
VZV:
- Primary infection (chickenpox) may cause a conjunctivitis and, rarely, a dendritic ulcer. The virus then lies dormant in the trigeminal ganglion
- Secondary infection occurs when the latent virus in the trigeminal ganglion reactivates and travels along the trigeminal nerve (ophthalmic division) to the ophthalmic area to cause shingles –> herpes zoster ophthalmicus (accounts for 10% of all cases of shingles)
- If the cornea is involved in herpes zoster ophthalmicus, it can result in a pseudodendritic ulcer - this corneal involvement of VZV infection is called herpes zoster keratitis
What are the clinical features of Herpes Simplex Keratitis?
Presentations
- Red, painful eye
- Watering (epiphora) and photophobia
- Reduced visual acuity
- Fluorescein staining under cobalt blue light shows dendritic corneal ulcer
- Decreased corneal sensation
- Recurrent cold sores
- Hx of illness, stress, run down, sunlight exposure, menstrual period
-
Steroid use in dendritic ulcer –> geographical ulcer
- Branches of dendritic ulcer enlarges and coalesces to form ‘amoeboid’ or ‘geographical’ configuration
- *‘Do not apply steroids to the undiagnosed red eye’. This is because applying steroid to a herpes simplex keratitis will likely result in a ‘geographic ulcer’, or a very large, irregular epithelial defect (as you have impaired the body’s immune response).
If the infection is confined to the corneal epithelium, healing occurs without scarring. However, if it affects the corneal stroma, it will cause scarring of the cornea +/- anterior uveitis
What is the management for herpes simplex keratitis?
Mx:
- Primary care
- Urgent same-day referral to an ophthalmologist to anyone with corneal ulcer
- Topical aciclovir
- Cyclopentolate for pain relief
- Oral aciclovir can be given long term as prophylaxis against recurrent disease
- Topical steroids to minimise scarring, esp when treating stromal disease and anterior uveitis. However, they can ONLY be given after healing of corneal ulcer
- Topical steroids applied to a herpetic corneal ulcer will cause a geographical/ amoeboid ulcer (fucking massive!), which is slow to heal and very hard to treat
What are the clinical features of herpes zoster ophthalmicus?
Presentations:
-
Vesicular rash (crusting and ulceration of skin) in ophthalmic (CNV1) territory - may or may not involve the cornea
- If cornea is involved –> pseudodendritic ulcer (herpes zoster keratitis)
- The skin rash is dermatomal, involving the forehead to occiput and the upper lid, tending to spare the lower lid but usually affecting the side of the nose
- Hutchinson’s sign - rash on the tip or side of the nose. This indicates nasociliary involvement and is a strong risk factor for ocular involvement
