Painful red eye Flashcards

1
Q

What are the differential diagnoses of a painful red eye?

A

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
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2
Q

a) . What is uvea?
b) . There are four types of uveitis. What are they?
c) . What structures are affected in each type?

A

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!
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3
Q

The ciliary body consists of 2 parts. What are they?

A

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)
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4
Q

Which is the most common type of uveitis?

A

Anterior uveitis

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5
Q

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?

A

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

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6
Q

What are the causes of uveitis?

A

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
  • Infection
    • HSV (herpes simplex keratitis), HZV (herpes zoster ophthalmicus), CMV, toxoplasmosis, syphilis, TB
  • Trauma
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7
Q

What conditions are associated with anterior uveitis?

A

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)

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8
Q

Give 3 risk factors for developing uveitis?

A

Personal Hx of uveitis

Age > 20 yrs old

Genetics - HLA-B27

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9
Q

What is the epidemiology of uveitis?

A
  • 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
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10
Q

What are the clinical features of anterior uveitis?

A

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
  • 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
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11
Q

What does the image below show?

A

Circumciliary injection

Dull pinkish area confined to the limbus, with some overlying bright red vessels

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12
Q

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?

A

Inflammatory cells and flares

(looks like the beam of a projector passing through smoke in a darkened room)

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13
Q

You saw these on a slit lamp examination, what are these?

A

Keratic precipitates

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14
Q

The patient with anterior uveitis presents with this? What is this?

A

Posterior synechiae

*You can see that the iris is adhered to the lens capsule at the back

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15
Q

Give 4 differential diagnoses of anterior uveitis

A

Acute glaucoma

Keratitis

Scleritis

Ocular trauma e.g. embedded FB

Episcleritis

Infective conjunctivitis

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16
Q

What investigations would you carry out in a patient with suspected anterior uveitis?

A
  • 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))

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17
Q

How do you manage acute anterior uveitis?

A

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 infectious –> Abx + corticosteroids + cycloplegics
  • Regular monitoring of IOP as IOP can raise as a result of anterior uveitis or by topical steroid use
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18
Q

What is glaucoma?

A

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

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19
Q

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

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

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20
Q

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

A

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)

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21
Q

How many routes of outflow are there to drain aqueous humour?

A

2 routes of outflow:

  • Via the trabecular meshwork (main primary route)
  • Via the uveoscleral outflow (only a small % of aqueous humour drains here)
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22
Q

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

A

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
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23
Q

What are the different types of glaucoma?

A
  1. 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
  1. 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
  1. Ocular hypertension
    * Defined as IOP > 21 mmHg but with NO SIGNS of glaucoma (i.e. no optic disc and visual field changes)
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24
Q

What’s the most common type of glaucoma?

A

Primary open angle glaucoma (POAC)

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25
What's the most common form of angle-closure glaucoma?
Primary angle-closure glaucoma (PACG)
26
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_**
27
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.
28
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... 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!
29
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_**
30
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_**
31
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
32
a) . Is primary angle closure glaucoma more common in men or women, or it affects both sexes equally? b) . Which race is more commonly affected by primary angle closure glaucoma? c) . Myopia increases the risk of developing primary angle closure glaucoma - true ot false
a) . Primary angle closure glaucoma affects women more b) . Asians, esp Chinese are more commonly affected by primary angle closure glaucoma c) . False! It's hyperopia (or hypermetropia) i.e. longer eyeball that increases the risk of developing primary angle closure glaucoma
33
Epidemiology of angle closure glaucoma: a) . Is primary or secondary angle closure glaucoma more common? b) . Which gender does PACG affect more? c) . Which ethnicity of people are more commonly affected by PACG? d) . Is it more common in elderly people or in the young?
a) . **_Primary angle closure glaucoma_** is more common b) . PACG affects **_women_** more c) . PACG affects **_asian population_** more, particularly the **_Chinese_** d) . **_The prevalence of PACG increases with increasing age_**. It affects 0.4% of people in the UK \> 40 yrs old and 0.95% in those \> 70 yrs old
34
Which autonomic nervous system causes increased production of aqueous humor? and which causes increased outflow (drainage)?
* Increased sympathetic nervous system activity increases production of aqueous humor * **_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 * Increased parasympathetic nervous system activity increases outflow (drainage)
35
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)
36
Which medication is contraindicated in acute angle closure glaucoma? and Why?
**_Antimuscarinic_** (e.g. atropine, tropicamide, TCA) and **_adrenergic_** medications (e.g. phenylephrine)
37
What are the clinical features of chronic primary angle closure glaucoma?
Presentations: * Insidious onset (just like primary open angle glaucoma) * **_Asymptomatic_** in most cases - usually picked up on routine ophthalmic examination * **_Raised IOP_** * **_Visual field defects_** * People are often unaware that they have a visual field defect, even when it's severe, as the visual fields of each eye overlap, and so a visual field defect in one eye may well be compensated for by the other eye until that too becomes affected * In addition, small visual field loss (scotoma) in glaucoma is usually compensated by the brain 'filling in these missing gaps/ information' so people often don't notice the visual field defect * **_Cupped optic disc_** * Signs of angle closure as detected by gonioscopy * A gonioscopy is often used together with a slit lamp to view the iridocorneal angle! (see image)
38
What investigations would you do in someone with suspected acute angle closure glaucoma?
Ix: * **_Clinical diagnosis_** - painful red eye, reduced visual acuity/ visual loss * **_Gonioscopy_** - should be performed in ALL PATIENTS with suspected angle-closure glaucoma - this allows assessment of the anterior chamber including the iridocorneal angle * **_Ophthlamoscopy/ slit lamp examination_** may show cupping of the optic disc i.e. an **_increased cup-to-disc ratio_** * **_Optical Coherence Tomograophy (OCT)_** to assess the retina * USS biomicroscopy
39
Although there is no official screening programme in place for glaucoma, NICE CKS advises 3 groups of patients to have their eyes checked by an optometrist as they are more at risk. What are the 3 groups of patients that need review by optometrists in an opportunistic testing?
Opportunistic testing * **_Elderly patients_** - people \>/= 60 yrs old should be examined every 2 yrs until they are 70 yrs of age, when they should be examined annually * Free examination through the NHS is available * **_FHx of glaucoma_** - people \> 40 yrs old with an affected 1st degree relative (parent, sibling, or child) should have their eyes checked annually * Free examination through the NHS is available. However, if they are stated by an ophthalmologist to be at high risk of glaucoma, then they are entitled to have free eye examinations * **_Ethicity_** - those of black African origin \> 40 yrs old should be examined annually * Free examination through the NHS is NOT available
40
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_** * 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_**
41
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
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What is the prognosis of acute angle-closure glaucoma?
If left untreated, it accounts for half of glaucoma-related blindness worldwide With early recognition and treatment, the prognosis is good
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Epidemiology of open angle glaucoma: a) . Does it affect men or women more, or it affects both sexes equally? b) . Is it common in people under age of 40? c) . How common is primary open angle glaucoma in the UK? d) . It's more commonly seen in Asians - true or false
a) . Affects both sexes equally b) . RARE in people under aged 40 yrs old (prevalence increases with age) c) . It affects 2% of adults over the age of 40 yrs old in the UK d) . FALSE ! It's more common in black ethnicity
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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
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What does the image below show?
Bayonetting of blood vessels --\> primary open angle glaucoma
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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
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How do you manage primary open angle glaucoma?
Mx: * 1st line: * **_Topical prostaglandin analogue (e.g. Latanoprost)_**, OR * 1st line if patient has a **_Hx of asthma_**! * Mechanism of action - increases uveoscleral outflow * ADRs - brown pigmentation of the iris, increased eyelash length, and periocular pigmentation (bilateral dark circles/ rings on the infraorbital regions) * **_Topical beta-blocker (e.g. Timolol)_** * **_​_**Mechanism of action - reduces aqueous production * ADRs - non-selective side effects --\> bradycardia, bronchoconstriction, diarrhoea, peripheral coldness, confusion (from hypotension), heart failure * Contraindications - asthmatics, COPD, heart block * 2nd line treatment options may include: * Switch to a drug in the other 1st line drug class (e.g. if latanoprost doesn't work, give timolol, vice versa), OR * Combine a topical prostaglandin analogue with a topical beta-blocker, OR * Switching to, or adding in, a 2nd line drug, which are: * **_Topical sympathomimetic (alpha-2 agonist) e.g. brimonidine tartrate_** * **_​_**Mechanism of action - reduces aqueous production and increases uveoscleral outflow * ADRs - hyperaemia of the skin, dry mouth, headache, dizziness, unpleasant taste * Avoid if taking MAOI or TCA * Contraindications - pregnancy, breastfeeding * **_Topical carbonic anhydrase inhibitor e.g. brinzolamide or dorzolamide_** * **_​_**Mechanism of action - reduces aqueous production * ADRs - eye discomfort, altered taste, vision disorders, systemic absorption of brinzolamide can produce sulphonamide-like reactions * **_Topical miotic (muscarinic receptor agonist) e.g. pilocarpine_** * **_​_**Mechanism of action - increases uveoscleral outflow * ADRs - excessively constricted pupil, headache, blurred vision, diarrhoea, hypersalivation, hyperhidrosis * If more advanced/ refractory cases --\> **_surgery (trabeculectomy)_** OR **_laser treatment (selective laser trabeculoplasty)_**
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What is scleritis?
Inflammation of the sclera with maximal congestion in the **_deep vascular plexus_**
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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 **_c_****_onjunctival 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**_ * 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!_**
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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
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What are the causes of scleritis?
Usually **_systemic inflammatory diseases_** (50% of cases) rather than infectious Autoimmune-related: * _**\*Rheumatoid arthritis (most common)**_ * SLE * IBD * Sjogren's syndrome * Wegener's granulomatosis (Rarely, it can occur secondary to ocular surgery or infections e.g. TB, current or previous herpes zoster ophthalmicus)
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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_**
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What is the management for scleritis?
Mx: * Primary care * **_Urgent referral to an ophthalmologist for same-day assessment_** * **_Treat underlying cause_** * Rheumatoid arthritis (most common) * cDMARD monotherapy (methotrexate/ leflunomide/ sulfasalazine) +/- a short course of bridging prednisolone * Offer additional cDMARD * For flares --\> Oral/ IM corticosteroids * Infections (rare) * Abx (e.g. RHZE if TB) * NSAIDs * Corticosteroids * Immunosuppression
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Is scleritis more common or episcleritis more common?
**_Episcleritis_** is extremely common! | (Scleritis is rare)
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What is episcleritis? How common is episcleritis? Which age group does it most commonly affect? (Note that episcleritis is a differential of **_PAINLESS_** red eye, it's **_NOT sight-threatening_**)
Episclera inflammation (non-infective) with maximal congestion in **_superficial episcleral plexus_**. It's **_extremely common_**, particularly in **_young adults_**! Half of the cases are bilateral!
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What are the causes of episcleritis?
**_No obvious precipitants_** for episcleritis, though symptoms tend to recur Rarely a manifestation of a systemic disease
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What are the symptoms and signs of episcleritis?
Presentations: Symptoms * **_NOT painful_** (mild discomfort at most) - patients are often **_asymptomatic_** * Mild tearing/ irritation * **_Red eye: localised (sectoral) or diffuse hyperaemia_**, with **_dilated bright red vessels running superficially ("subconjunctival injection")_** * **_​_**Episclera is located beneath the conjunctiva, hence "subconjunctival" * Watering and mild photophobia may be present * No discharge and not sight-threatening Signs * Tender to touch * **_Vessels are mobile when gentle pressure is applied on the sclera using a swab (and topical anaesthesia)_** * This helps distinguish episcleritis from scleritis, as the vessels in scleritis are deeper so they do not move * **_Vessels blanch with phenylephrine eye drops (vasoconstrictor) leading to an improvement in eye redness_** * This helps distinguish episcleritis from scleritis, as phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels (too deep for the medication to reach)
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What is the management for episcleritis?
Mx: * **_Self-limiting_** * Simple analgesia (NSAIDs) * Topical lubricants * Rarely, low dose steroids
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How is scleritis different from episcleritis?
See image
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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
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What is the main innervation of the cornea? What are the afferent and efferent limbs of the corneal reflex?
CNV1 - ophthalmic division of the trigeminal nerve (The density of pain receptors in the cornea is 300-600 times greater than skin and 20-40 times greater than dental pulp, making any injury to the structure excruciatingly painful!) Corneal reflex: Afferent limb - CNV1 (ophthalmic of trigeminal) Efferent limb - CN7 (facial)
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What is keratitis? Is keratitis serious?
**_Keratitis is inflammation of the cornea_** **_Microbial keratitis_** (bacterial, fungal, amoebic, parasitic) are **_sight-threatening_** so they must be urgently evaluated and treated! (Don't confuse keratitis with conjunctivitis. Conjunctivitis is inflammation of the conjunctiva and is rarely serious)
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What are the causes of keratitis?
Aetiology: * _**\*Bacterial**_ * **_Staphylococcus aureus (most common)_** * Staphylococcus epidermidis * **_Pseudomonas aeruginosa (contact lens wearers) - most aggressive as it contains enzymes that can digest the cornea_** * Streptococcus pyogenes, streptococcus pneumoniae * Fungal * Aspergillus fumigatus * Candida albicans * Amoebic * Acanthamoeba (contact lens wearers) * Parasitic: onchocercal keratitis ('river blindness') - follows Onchocerca volvulus infection by infected blackfly bite. These blackfly usually dwell near fast-flowing African streams, hence the name "river blindness" * _**\*Viral**_ * **_Herpes simplex keratitis (HSV)_** * **_H_****_erpes zoster keratitis (VZV)_** * Environmental * Photokeratitis e.g. welder's arc eye - painful eye caused by exposure of insufficiently protected eye to the UV rays from either natural (e.g. intense sunlight) or artificial (e.g. the electric arc during welding) sources * Exposure keratitis * Contact lens acute red eye (CLARE)
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What are the common bacteria associated with bacterial keratitis?
Common bacteria: * Staphylococcus aureus * Staphylococcus epidermidis * Pseudomonas aeruginosa * Streptococcus pyogenes, Streptococcus pneumoniae
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Which bacterium is the most common cause of bacterial keratitis?
**_Staphylococcus aureus_**
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Which bacterium most commonly causes bacterial keratitis in contact lenses wearer?
**_Pseudomonas aeruginosa_** ## Footnote **(It causes a particularly aggressive infection as it contains enzymes that can digest the cornea)**
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Give 5 risk factors of developing bacterial keratitis
Risk factors: * **_Contact lens wear (usually soft lenses with extended use; rare with hard lenses)_** * Corneal trauma (including abrasion by eyelashes due to entropion) * A chronically compromised ocular surface e.g. dry eye, blepharitis, and bullous keratopathy (endothelial failure) * Herpetic keratitis * Corneal expsure (facial nerve palsy, proptosis) * Facial nerve palsy --\> impaired corneal reflex --\> eyes unable to blink when foreign material irritates the eye * Proptosis - more eye surface exposed to air * Corneal anaesthesia (neurotrophic keratopathy) - a rare degenerative disease of the cornea characterised by reduction/ loss of corneal sensitivity * Immunosuppression, including topical steroid use
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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
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What investigations would you consider for someone with suspected bacterial keratitis?
Ix: * Culture of conjunctival and corneal samples * Blood agar (for most fungi and bacteria except Neisseria) * Chocolate agar (for Neisseria and Moraxella) * Sabouraud agar (for fungi)
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How do you manage bacterial keratitis?
Mx: * Primary care * **_Urgent same-day referral to an ophthalmologist for anyone with a red eye who wears contact lenses_** * Assessing contact lens wearers who present with a painful red eye is difficult, an accurate diagnosis can only be made with a slit-lamp, hence the need for an urgent referral * Stop using contact lens until symptoms have fully resolved * Broad-spectrum topical Abx * 1st line - **_quinolones (topical ofloxacin)_** * Initially - administer hourly * Subsequently 2 hourly (waking hours) * Tapered * Cycloplegic (**_cyclopentolate_**) for pain relief * **_Topical steroids_** are only used when cultures become sterile (indicating resolution of the infection) with evidence of improvement (7-10 days after initiation of treatment)
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What are the 2 most common viruses associated with viral keratitis?
Viruses: * Herpes Simplex Virus type 1 (HSV1) * Varicella-zoster virus (VZV)
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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_**
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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
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How would you investigate for herpes simplex keratitis?
Ix: * Confirm the diagnosis by identification of the virus from cells scraped from the ulcer edge * This is important particularly because infection maybe recurrent and may mimic many other types of corneal infection and inflammation
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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
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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
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Give 5 complications of herpes zoster ophthalmicus
* Ocular complications: viral conjunctivitis, keratitis, anterior uveitis, scleritis, episcleritis, optic neuritis, ptosis * Post-herpetic neuralgia
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How would you manage herpes zoster ophthalmicus?
Mx: * Primary care * Urgent same-day referral to an ophthalmologist for anyone with a corneal ulcer (ocular involvement) * Oral aciclovir for 7-10 days, ideally started within 72 hrs of onset of vesicles * IV aciclovir maybe given for very severe infection or if the patient is immunocompromised * Topical aciclovir is NOT given in HZO * Topical corticosteroids maybe used to treat any secondary inflammation of the eye
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A 22-year-old woman presents with a red painful eye. She describes the pain as tearing. When asked to scale the degree of pain, she gave a score of 7 out of 10. She also reported that she uses contact lenses frequently. What is the most appropriate next step? a) . Aciclovir b) . Advice on stopping wearing contact lenses permanently c) . Reassurance d) . Same-day ophthalmology referral e) . Urgent 'two-week wait' ophthalmology referral
The answer is d! **_Contact lens wearers who present with a red painful eye_** should be referred to eye casualty to exclude microbial keratitis and corneal ulcer