Acute Painful Eye Flashcards

1
Q

Causes of a painful red eye

A

◦ Corneal abrasions
◦ Corneal ulcers
◦ Corneal foreign bodies
◦ Chemical injuries
◦ Acute anterior uveitis
◦ Anterior scleritis
◦ Acute angle-closure glaucoma
◦ Endophthalmitis
◦ Trauma
◦ Ectropion and entropion
◦ Trichiasis
- conjunctivitis

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2
Q

Causes of a painless red eye

A

Subconjunctival haemorrhage
Blepharitis
Episclertisi
Conjunctivitis
Dry eyes
Allergic conjunctivitis

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3
Q

What are the 2 parts of the conjunctiva?

A

the thin, transparent mucous membrane lining the anterior part of sclera = bulbar conjunctiva
and the under-surface of the eyelids = palpebral conjunctiva

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4
Q

What can cause conjunctivitis?

A

• allergies
• Infections
• Mechanical irritation
• Neoplasia
• Contact with toxic substances

Up to 80% of all cases of acute conjunctivitis are caused by viral infections.
But 50-75% of cases of infective conjunctivitis in children are thought to be bacterial
Most common viral - adenovirus. Others include herpes simplex, VZV, molluscum contagiosum, EBV, coxsackie, enteroviruses
Bacterial - step pneumoniae, staph aureus, H.influenza or moraxella catarrhalis in children

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5
Q

Whats the most common viral cause of conjunctivitis?

A

Adenovirus

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6
Q

What is acute. And chronic conjunctivitis?

A

Acute <4 weeks
Chronic >4 weeks

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7
Q

What is hyper acute conjunctivitis and what typically causes it?

A

rapidly developing severe conjunctivitis - typically neisseria gonorrhoeae

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8
Q

What is ophthalmia neonatorum?

A

Conjunctivitis occurring within the first 4 weeks of life
Can be infectious - neisseria gonorrhoeae or chlamydia
Or can be non infectious

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9
Q

What are the clinical features of conjunctivitis?

A

• acute onset conjunctival erythema
• Grittiness or burning or foreign body sensation
• Watering and discharge which may cause transient blurring of vision
• Purulent or Mucopurulent discharge with crusting of lids which may be stuck together on waking - bacterial
• Pre-auricular lymphadenopathy - often seen with hyperacute bacterial conjunctivitis
• Petechial Subconjunctival haemorrhages - viral
• URTI symptoms - viral
• Bilateral itching with associated swelling of eyelids and conjunctiva (chemosis) - allergic conjunctivitis!

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10
Q

How does herpes conjunctivitis typically present?

A

unilateral red eye with vesicular lesions visible on the eyelid and watery discharge

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11
Q

What is Hutchinson’s sign?

A

Herpes zoster lesions on tip of nose = ocular involvement
indicates involving of the nasociliary nerve

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12
Q

How does neisseria gonorrhoeae conjunctivitis typically present?

A

12-24 hours rapid onset with copious mucopurulent discharge, eyelid swelling and tender preauricular lymphadenaopthy

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13
Q

What investigation for ?ophthalmia neonatorum?

A

Swabs of the discharge urgently

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14
Q

How do we treat acute non-herpetic viral conjunctivitis?

A

self-limiting resolves in 1-2 weeks, self care e.g. clean eyelids with boiled and cooled water, cool compresses and avoid spreading it

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15
Q

Tx acute bacterial conjunctivitis?

A

self-limiting in 5-7 days.
If severe or circumstances required rapid relation then chloramphenicol drops 2-3 hrly, chloramphenicol ointment QDS or fusidic acid eye drops (mainly latter if pregnant)
Advice not to share towels

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16
Q

Moa chloramphenicol?

A

antimicrobial that inhibits proteins synthesis by binding 50s

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17
Q

How is management of conjunctivitis different in contact lens wearers?

A

You must advise them to Stop lens use until infection symptoms are completely gone
Same management but use topical fluorescein to identify any corneal staining

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18
Q

Tx allergic conjunctivitis?

A

Topical or systemic antihistamines
Reduce causative allergic

Topical mast cell stabilisers e.g. sodium cromoglicate can also be used

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19
Q

Prognosis of viral conjunctivitis, bacterial conjunctivitis and ophthalmia neonatorum?

A

Viral - resolves within 7 days
Bacterial - 5-10 days
Ophthalmia - Most cases are mild but untreated infections can lead to serious complications such as sight loss and mortality

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20
Q

What are some of the differentiating features of viral and bacterial conjunctivitis?

A

Bacterial - purulent discharge and eyes may be stuck together in the morning
Viral - serous discharge, recent URTI, preauricular lymphadenopathy

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21
Q

How should you manage bacterial conjunctivitis in women who are pregnant?

A

Topical fusidic acid twice daily

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22
Q

What is the episclera?

A

A thin vascular layer sandwiched between the superficial conjunctiva and deeper sclera; its the outermost layer of the sclera

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23
Q

What causes episcleritis?

A

Idiopathic in 70% of cases
related to IBD and RA

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24
Q

How often is episcleritis bilateral?

A

In 50%

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25
Q

Presentation of episcleritis?

A

• acute onset unilateral localised/diffuse redness
• No or very mild pain
- watering and mild photophobia may be present
• Dilated episcleral vessels (moveable with a swab as its superficial + it will blanch with topical phenylephrine)

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26
Q

How can we differentiate between scleritis and episcleritis?

A

Scleritis is painful and epi is not
Applying phenylephrine eye drops will call blanching of episcleral vessels but not sclera vessels

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27
Q

How do we manage episcleritis?

A

Conservative as self limiting in 1-2 weeks
Artificial tears may sometimes be used

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28
Q

What is scleritis?

A

Full thickness inflammation of the sclera (the outer layer of connective tissue surrounding most of the eye and forming the visible white part of the eye - continuous with the cornea)

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29
Q

What causes scleritis?

A

Most commonly idiopathic
Related to RA mostly. Other relations include SLE, sarcoidosis and granulomatosis with polyangiitis. 50% cases linked to systemic conditions
Less commonly can be infective cause

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30
Q

What is the most severe type of scleritis?

A

Necrositing scleritis which can lead to perforation of the sclera

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31
Q

How does scleritis present?

A

• red eye
• A boring pain with painful eye movements and tender to touch (in comparison to episcleritis)
• Watering and photophobia are common
• Gradual decrease in vision
• If recurrent there may be sclera thinning

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32
Q

How do we manage scleritis?

A

same-day assessment by an ophthalmologist

oral NSAIDs are typically used first-line
oral glucocorticoids may be used for more severe presentations
immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)

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33
Q

What is a subconjuntcival haemorrhage?

A

When small blood vessels within the conjunctiva rupture releasing blood into the space between the sclera and conjunctiva

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34
Q

What causes a subconjunctival haemorrhage?

A

Episodes of strenuous activity - heavy coughing, weight lifting, vomiting, straining in constipation
Trauma to the eye
Or idiopathic with risk factors such as hypertension, bleeding disorders, whooping cough, meds such as antiplatelets or NAI

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35
Q

How does a subconjuntival haemorrhage present?

A

A painless bright red blood patch covering the white of the eye
The haemorrhage will stop at the limbus! Will not affect vision!

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36
Q

what is the limbus?

A

Junction between cornea and conjunctiva

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37
Q

What investigations could we do when someone presents with a subconjuntival haemorrhage?

A

Check bp if idiopathic
Check INR if pt on warfarin

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38
Q

how do we manage a subconjuntival haemorrhage?

A

Harmless and will resolve spontaneously without treatment within 2 weeks

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39
Q

What is blepharitis?

A

Inflammation of the lid margins

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40
Q

How does blepharitis present?

A

symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur

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41
Q

What causes blepharitis?

A

It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).
Blepharitis is also more common in patients with rosacea

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42
Q

Whats the function of Meibomian glands?

A

Responsible for secreting meibum (oil) onto the surface of the eyes to prevent the rapid evaporation of the tear film

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43
Q

How do we manage blepharitis?

A

softening of the lid margin using hot compresses twice a day
‘lid hygiene’ - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film

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44
Q

What is a stye?

A

An infection of the glands of the eyelids

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45
Q

What are the types of stye?

A

Hordeolum externum: infection (usually staphylococcal) of the glands of Zeis or glands of Moll

Hordeolum internum: infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)

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46
Q

what are the glands of Zeis?

A

Sebaceous glands at the base of eyelashes

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47
Q

What are the glands of Moll?

A

Sweat glands at the base of eyelashes

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48
Q

What does a Hordeolum externum look like?

A

A red tender lump along the eyelid that will likely have a yellow head as it contains pus

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49
Q

What does a Hordeolum internum look like?

A

Deep painful lumps that may point inwards towards the eyeball underneath the eyelid

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50
Q

What is a Chalazion?

A

Aka a Meibomian cyst
It 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

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51
Q

How do we manage a stye?

A

Hot compress and analgesia
Only use topical antibiotics if associated with conjunctivitis

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52
Q

What is an entropion?

A

In turning of the eyelid with lashes pressed against the eye
This causes pain and can result in corneal damage/ulceration

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53
Q

How do we manage an entropion?

A

Tape the eyelids down and eye drops
Definitive management is surgical

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54
Q

what is an ectropion?

A

When the eyelid is turned outward exposing the inner aspect of the eye
It usually affects the bottom lid

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55
Q

What can an ectropion lead to?

A

Exposure keratopathy as the eyelid is exposed and not adequately lubricated and protected

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56
Q

How do we manage ectropion?

A

Mild cases may not require treatment other than regular lubricator eye drops to protect the eye surface
More significant cases may require surgery to correct the defect

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57
Q

What causes entropions and ectropions?

A

Ectropion is usually associated with ageing. It can happen as the tissues and muscles of the eyelids become weaker as you get older.

Less common causes of ectropion include:
- Bell’s palsy
- a lump, cyst or tumour on the eyelid
- damage to the skin around the eyelid as a result of an injury, a burn, a skin condition such as contact dermatitis, or previous surgery
Rarely, ectropion can be present from birth if the muscles under the eyelid do not develop properly.

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58
Q

What is trichiasis?

A

The inward growth of eyelashes which causes pain and can sometimes cause corneal damage

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59
Q

How do we manage trichiasis?

A

Remove the affected eyelashes
Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent re growth

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60
Q

What is herpes zoster ophthalmicus? what are the features?

A

The reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve

Features: vesicular rash around the eye which may or may not involve the eye, Hutchinson’s sigh

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61
Q

How do we manage herpes zoster ophthalmicus?

A

oral antiviral treatment for 7-10 days ideally started within 72 hours
IV antivirals may be given for very severe infection or if the patient is immunocompromised
topical corticosteroids may be used to treat any secondary inflammation of the eye

!!ocular involvement requires urgent ophthalmology review!!

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62
Q

What are complications of herpes zoster ophthalmicus?

A

Ocular - conjunctivitis, keratitis, episcleritis, anterior uveitis
Ptosis
Post-hermetic neuralgia

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63
Q

Why are annual eye exams recommended for rheumatoid arthritis patients?

A

Retinopathy can occur due to hydroxychloroquine use in rheumatoid arthritis

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64
Q

What can we use to determine if blurred vision is due to a refractive error?

A

pinhole occluders
if the blurring improves with a pinhole occluder then likely cause is a refractive error

It is a simple way to focus light, temporarily removing the effects of refractive errors such as myopia.

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65
Q

What is preseptal cellulitis?

A

Aka periorbital cellulitis
An infection of the soft tissues anterior to the orbital septum - eyelids, skin and subcutaneous tissue of the face (not contents of orbit!!)

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66
Q

What causes periorbital cellulitis?

A

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.

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67
Q

What age does preseptal cellulitis typicall affect?

A

Children - 80% of Pt are <10 and median age of presentation is 21 months

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68
Q

Why is orbital cellulitis more common in winter?

A

Due to increased prevalence of RTIs

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69
Q

How does preseptal cellulitis present?

A

Red, swollen, painful eye of acute onset
Parital or complete ptosis of the eye due to swelling

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70
Q

Investigations s for preseptal cellulitis?

A

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

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71
Q

how do we manage preseptal cellulitis?

A

All cases should be referred to secondary care for assessment
Oral antibiotics are frequently sufficient - usually co-amoxiclav
Children may require admission for observation

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72
Q

Complication of preseptal cellulitis?

A

Bacterial infection. May spread into the orbit and evolve into orbital cellulitis

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73
Q

What is orbital cellulitis?

A

An infection affecting the fat and muscles posterior to the orbital septum
A medical emergency requiring hopsital admission and urgent senior review

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74
Q

What causes orbital cellulitis?

A

Spreading URTI from the sinuses usually

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75
Q

Risk factors for orbital cellulitis?

A

Childhood (Mean age of hospitalisation 7-12 years)
Previous sinus infection
Lack of Haemophilus influenzae type b (Hib) vaccination
Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
Ear or facial infection

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76
Q

How does orbital cellulitis present?

A

Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema and ptosis

Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)

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77
Q

How do we differentiate orbital from preseptal cellulitis?

A

reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis

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78
Q

How do we investigate orbital cellulitis?

A

Full blood count – WBC elevated, raised inflammatory markers.
Clinical examination involving complete ophthalmological assessment – Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema.
CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis.
Blood culture and microbiological swab to determine the organism.

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79
Q

Most common bacterial causes of orbital cellulitis?

A

Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.

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80
Q

How do we manage orbital cellulitis?

A

Admission to hospital for IV antibiotics

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81
Q

What are corneal abrasions?

A

Scratches or damage to the cornea

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82
Q

What causes corneal abrasions?

A

Damaged contacts
Finger nails
Foreign bodies
Makeup brushes
Entropion etc

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83
Q

How does corneal abrasion present?

A

a history of trauma followed by a painful red eye, photophobia, foreign body sensation, Epiphora, blurred vision.
The pain will typically be surface sympotms e.g. grittiness

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84
Q

How do we diagnose a corneal abrasion

A

Fluorescein stain - yellow-orange colour collects in abrasions of ulcers highlighting them under cobalt blue light

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85
Q

How do we manage a corneal abrasion?

A

Usually heals over in 2-3 days

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86
Q

What is a corneal ulcer?

A

A defect on the cornea, typically secondary to an infective cause

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87
Q

What are risk factors for a corneal ulcer?

A

Contact lens use
Vitamin A deficiency in the developing world

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88
Q

Causes of corneal ulcer?

A

bacterial keratitis
fungal keratitis
viral keratitis: herpes simplex, herpes zoster - may lead to a dendritic ulcer
Acanthamoeba keratitis: associated with tap water and contact lens use

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89
Q

Features of corneal ulcer?

A

eye pain
photophobia
watering of the eye
focal fluorescein staining of the cornea

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90
Q

What is a corneal ulcer also known as?

A

Microbial keratitis

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91
Q

How do we manage a corneal ulcer?

A

Topical antibiotics, antiviral sor antifungal
Corneal transplant for permenatn scarring and vision loss

Without treatment they can cause rapid, permenantsight loss!

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92
Q

What is an alkali chemical injury of the eye worse than an acid injury?

A

Acids have a lower pH than the eye so they precipitate tissue protein which creates a barrier preventing further ocular penetration
Alkalis are more severe as they penetrate deeper into ocular tissue

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93
Q

How do we manage a chemical injury to the eye?

A

Immediate irrigation of the eye until pH neutralises before conducting any further investigation
Control pain and nausea
Specialist referral!!

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94
Q

Typical clinical findings in a chemical injury to the eye?

A

• conjunctival hyperaemia
• Corneal haze with an impaired view of the underlying iris and pupil if severe
• Blanched blood vessels
• After instilling fluorescein 2% under blue light areas of corneal/conjunctival epithelial defect will glow green

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95
Q

What is the most common cause of abnormal tearing in infants and children in the first year of life?

A

Nasolacrimal duct obstruction

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96
Q

How does nasolacrimal duct obstruction present?

A

History of chronic or intermittent tearing and occasionally redness of the conjunctiva

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97
Q

Why do pt with orbital cellulitis require admission and IV antibiotics?

A

Due to the risk of cavernous sinus thrombosis and intracranial spread

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98
Q

What is anterior uveitis also known as?

A

Irititis

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99
Q

What is anterior uveitis?

A

Inflammation of the anterior portion of the urea - iris and ciliary body

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100
Q

What is the uvea?

A

Middle portion of the eye between the sclera and retina
It contains the iris, ciliary body (part of eye that helps lens focus) and and choroid (part of eye connecting retina to sclera)

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101
Q

What conditions are associated with anterior uveitis?

A

HLA-B27 related conditions:

ankylosing spondylitis
reactive arthritis
IBD
Behcet’s disease
sarcoidosis: bilateral disease may be seen

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102
Q

What are symptoms of anterior uveitis?

A

acute onset ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon
visual acuity initially normal → impaired

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103
Q

How do we manage anterior uveitis?

A

urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops

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104
Q

Examples of cycloplegics?

A

Atropine
Cyclopentolate

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105
Q

What is endophthalmitis?

A

An infection of the intraocular fluids (vitreous and aqueous) and internal eye tissues

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106
Q

What can cause endophthalmitis?

A

May be secondary to an exogenous source - recent cataract surgery or intravitreal injection
May be secondary to an endogenous source e.g. seeded from endocarditis or candida sepsis

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107
Q

Features of endophthalmitis?

A

Red eye - diffuse conjunctival injection
Severe Pain
Rapidly progressive visual loss
Photophobia
Floaters
Corneal haze
Hypopyon
RAPD

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108
Q

What is glaucoma?

A

A group of disorders characterised by optic neuropathy. In the majority of pt this is caused by a raised intraocular pressure

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109
Q

What is acute angle-closure glaucoma?

A

There is a rise in intraocular pressure secondary to an impairment of aqueous outflow
The iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining and leading to an increase in IOP. The pressure builds in the posterior chamber, pushing the iris foeward and exacerbating the angle closure

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110
Q

Risk factors for acute angle-closure glaucoma?

A

Hypermetropia
Pupillary dilatation
Lens growth associated with age
Certain meds - adrenergic meds, Anticholinergics, TCAs etc

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111
Q

Features of acute angle-closure glaucoma?

A

severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain

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112
Q

Investigations for acute angle-closure glaucoma?

A

Tonometry to assess for elevated IOP
Genioscopy - special lens for the slit lamp that allows visualisation of the angle

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113
Q

How do we manage acute angle-closure glaucoma?

A

Should prompt urgent referral to ophthalmology

Emergency medical treatment to lower IOP:
- eye drops - direct parasympathomimetics, beta blockers, alpha-2 agonists
- IV acetazolamide

Definitive surgical treatment:
- laser periperal iridotomy

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114
Q

what is laser peripheral iridotomy?

A

Creating a tiny hole in the peripheral iris so aqueous humour can flow to the angle

115
Q

Give examples of a direct parasympathomimetic eye drop you can use for acute angle-closure glaucoma? How does it work?

A

Pilocarpine
Causes contraction of ciliary muscles which opens the trabecular meshwork and increases the outflow of the aqueous humour

116
Q

Give examples of a beta blocker eye drop you can use for acute angle-closure glaucoma? How does it work? Side effects?

A

Timelol
Decreases aqueous humour production

117
Q

Give examples of a alpha-2 agonist eye drop you can use for acute angle-closure glaucoma? How does it work? Side effects?

A

Apraclonidine
Decreases aqueous humour production and increases uveoscleral outflow

118
Q

How does acetazolamide work for acute angle-closure glaucoma?

A

Blocks carbonic anhydrase which reduces the amount of aqueous secretions

119
Q

What is hyphema?

A

Blood in the anterior chamber of the eye most commonly caused by trauma

120
Q

Why does hyphema warrant urgent referral to ophthalmology?

A

As There’s a risk to sight from raised IOP which can develop due to blockage of the angle and trabecular meshwork with erythrocytes

121
Q

Management of hyphema?

A

Strict bed rest - excessive movement can re disperse blood that had settled
High-risk cases admitted
Daily ophthalmic review and pressure checks
Assessment for orbital compartment syndrome

122
Q

What are features of orbital compartment syndrome?

A

eye pain/swelling
proptosis
‘rock hard’ eyelids
relevant afferent pupillary defect

123
Q

Management of orbital compartment syndrome?

A

urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit

124
Q

What most commonly causes orbital compartment syndrome

A

A retrobulbar haematoma after blunt trauma or surgery

125
Q

What is optic neuritis?

A

Inflammation of the optic nerves

126
Q

What causes optic neuritis?

A

MS - most common
Diabetes - due to ischaemia
Syphilis
Can also be antibody-mediated, associated with sarcoidosis, Lyme disease or ethambutol

127
Q

How does MS cause optic neuritis?

A

T cells directed against CNS antigens which destroys the myelin sheath = inflammation of optic nerves

128
Q

What % of MS patients will have at least 1 episode of optic neuritis?

129
Q

Features of optic neuritis?

A

unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’ - as optic nerve carries these colour symptoms
pain worse on eye movement (when eye moves, inflamed optic nerve is pulled triggering discomfort)
relative afferent pupillary defect
central scotoma (as central area of optic nerve is more susceptible to damage in optic neuritis)

130
Q

Investigation of optic neuritis?

A

MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases

131
Q

How do we manage optic neuritis?

A

high-dose steroids
recovery usually takes 4-6 weeks

132
Q

How can MRI in optic neuritis help tel us the risk of the pt developing MS?

A

MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%

133
Q

What is a relative afferent pupillary defect?

A

Aka a Marcus Gunn pupil

The pupil will remain dilated despite exposure to bright lights and the individuals pupils may become different sizes
When a light is shone into the affected eye, it will not constrict as much as the unaffected eye

134
Q

What causes a relative afferent pupillary defect?

A

Optic neuritis
Retinal detachment
Severe glaucoma

135
Q

What is the most common cause of blindness in adults aged 35-65 years?

A

Diabetic retinopathy

136
Q

Pathophysiology of diabetic retinopathy

A

Hyperglycaemia causes increased retinal blood flow and abnormal metabolism in the retinal vessel walls -> damage to endothelial cells and pericytes
This endothelial dysfunction leads to increased vascular permeability = exudates
Pericytes dysfunction = predisposition to formation of microaneurysms
Retinal ischaemia leads to production of growth factors = Neovasculization

137
Q

What are blot haemorrhages seen in diabetic retinopathy caused by?

A

Increased vascular permeability

138
Q

What are hard exudates seen in diabetic retinopathy caused by?

A

Endothelial dysfunction causing increased vascular permeability = Deposits of lipids and proteins in the retina

139
Q

What are microaneurysms and venous beading seen in diabetic retinopathy caused by?

A

Damaged blood vessel walls

140
Q

What are cotton wool spots seen in diabetic retinopathy caused by?

A

Represents nerve fibre layer infarction and ischaemia
Also known as soft exudates

141
Q

How do we classify diabetic retinopathy?

A

Non-proliferative - microaneryssm, blot haemorrhages, hard exudates, cotton wool spots, venous beading, intraretinal micro vascular abnormalities. But NO neovascularisation

Proliferative diabetic retinopathy - retinal neovasculiration which may need to vitroeous haemorrhage - more common in type 1 diabetes

142
Q

What % of proliferative diabetic retinopathy will be blind in 5 years?

143
Q

What is maculopathy?

A

When diabetic retinopathy affects the macula - poor central vision
Known as diabetic macular oedema
Hard exudates and other ‘background’ changes on macula
More common in typ2 diabetes

144
Q

How do we manage all pt with diabetic retinopathy?

A

optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology

145
Q

How do we manage maculopathy?

A

If there is a change in visual acuity then intravitreal VEGF inhibitors

146
Q

How do we manage non-proliferative diabetic retinopathy?

A

regular observation
if severe/very severe consider panretinal laser photocoagulation

147
Q

How do we manage proliferative diabetic retinopathy?

A

panretinal laser photocoagulation

intravitreal VEGF inhibitors - often now used in combination with panretinal laser photocoagulation. E.g. ranibizumab

if severe or vitreous haemorrhage: vitreoretinal surgery

148
Q

What are the complications of panretinal laser photocoagulation?

A

50% of pt will develop a noticeable reduction in their visual fields due to scarring of peripheral retinal tissue
Decrease in night vision - most rods are in peripheral retina and these are responsible for vision
General decrease in visual acuity
Macular oedema

149
Q

What is the important of detection and management of diabetic eye disease?

A

Can result in severe vision impairment and even blindness
Early detection saves vision as we can catch it in early stages to allow for timely intervention
With proper management we can prevent progression
Vision loss can significantly impact on an indiviual’s quality of life
Diabetic eye disease can serve as an indicator of other complications related to diabetes e.g. heart disease

150
Q

Outline screening in the UK for diabetic eye disease?

A

Every over 12 with diabetes is entitles to NHS diabetic eye screening at least once every 2 years (at first it will be annually and this will change dependant on results)

151
Q

What is a vitreous haemorrhage?

A

Bleeding into vitreous humour
One of the most common causes of sudden painless loss of visual

152
Q

What causes a vitreous haemorrhage?

A

50% is proliferative diabetic retinopathy
Posterior vitreous detachment
Ocular trauma - most common cause in children

153
Q

How does a vitreous haemorrhage present?

A

painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision
Visual field defects if severe haemorrhage

154
Q

What will you see on slit lamp examination in a vitreous haemorrhage?

A

RBCs in anterior vitreous

155
Q

Why do we use USS on vitreous haemorrhage?

A

To rule out retinal tear or detachment and if haemorrhage obscures the retina

156
Q

What investigations for vitreous haemorrhage?

A

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

157
Q

What is hypertensive retinopathy?

A

Damage to small blood vessels in the retina relating to hypertension
These changes can happen slowly with chronic hypertension or quickly in response to malignant hypertension

158
Q

What are the features of hypertensive retinopathy?

A

• silver or copped wiring - walls of arteries become thickened and sclerosed and reflect more light on examination
• Arteriovenous nipping - atterioles causing compression of the veins where they cross due to sclerosis and hardening of the arterioles
• Cotton wool spots - ischaemia and infarction in the retina causing damage to nerve fibres
• Hard exudates - damaged vessels leaking lipids onto the retina
• Retinal haemorrhages - damaged vessels rupturing and releasing blood in the retina - dot, blot and flame
• Papilloedema - ischaemia to optic nerve causing oedema

159
Q

What classification system for hypertensive retinopathy?

A

Keith-Waganer classification

Stage 1 : mild narrowing of atterioles and silver wiring
Stage 2 : AV nipping
Stage 3 : cotton wool patches, exudates and haemorrhages - haemorrhages may collect around fovea resulting in a ‘macula star’
Stage 4 : papilloedema

160
Q

How do we manage hypertensive retinopathy/

A

Control bp and risk fatcors

161
Q

What is papilloedema?

A

Optic disc swelling caused by increased ICP
Almost always bilateral

162
Q

Fundoscopy signs of papilloedema?

A

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

163
Q

What are the causes of papilloedema?

A

space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia

Rare causes include:
hypoparathyroidism and hypocalcaemia
vitamin A toxicity

164
Q

What is the Hirschberg test?

A

Corneal light reflection test - shining a light into pt eyes and observing the reflection on their corneas. If reflections are symmetrical it suggests normal alignament of eyes. If asymmetrical it may indicate a squint.

165
Q

What are cataracts?

A

Common eye condition where the lens of the eye gradually opacifies making it more difficult for light to reach the retina and thus causing reduced or blurred vision

166
Q

What is the leading cause of curable blindness worldwide?

167
Q

What causes cataracts?

A

Normal ageing process is the most common cause - 30% of pt over 65 have one

Other possible causes: smoking, alcohol, trauma, DM, long term steroids, radiation exposure, myotonic dystrophy, hypocalcaemia

168
Q

How do cataracts present?

A

Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights
Defect in red reflex

169
Q

Investigations for cataracts?

A

Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract

170
Q

Management of Cataracts?

A

Non-surgical: In the early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/contact lens, or by encouraging the use of brighter lighting. These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed.

Surgery 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.

171
Q

Complications following surgery of cataracts?

A

Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour

172
Q

Pathophysiology of primary open-angle glaucoma?

A

A gradual increase in resistance to flow through trabecular meshwork causing increased IOP

173
Q

Risk factors for primary open-angle glaucoma?

A

increasing age
genetics (first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease)
Afro Caribbean ethnicity
myopia
hypertension
diabetes mellitus
corticosteroids

174
Q

How does primary open-angle glaucoma present?

A

May present insidiously so is often detected during routine optometry appointments!
Peripheral visual field loss - nasal scotomas progressing to tunnel vision
Decreased visual acuity

175
Q

Fundoscopy findings in primary open-angle glaucoma?

A

Optic disc cupping - cup-to-disc ratio >0.7
Optic disc pallor indicating optic atrophy
Bayoneting of vessels
Cup notching and disc haemorrhages

176
Q

Investigations for primary open-angle glaucoma?

A

automated perimetry to assess visual field
slit lamp examination with pupil dilatation to assess optic nerve 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

177
Q

Management primary open-angle glaucoma?

A

First line - 360 degree selective laser trabeculoplasty for pt with IOP >=24

Second line - prostaglandin analogue eye drops

Third line - beta blocker, carbonic anhydrase inhibitor or sympathomimetic eye drops

In refractory cases - trabeculectomy surgery

178
Q

Give example, MOA and SE of prostaglandin analogues for treatment of primary open-angle glaucoma

A

Latanoprost
Increases uveoscleral outflow
Brown pigmentation of iris and increased eyelash length

179
Q

Give example, MOA of beta blocker eye drops for treatment of primary open-angle glaucoma

A

Timolol or betaxolol
Reduces aqueous production

180
Q

Give example, MOA and SE of sympathomimetic eye drops for treatment of primary open-angle glaucoma

A

Brimonidine - alpha 2 adrenoreceptor agonist
Reduces aqueous production and increased outflow
Hyperaemia

181
Q

Give example, MOA and SE of carbonic anhydrase inhibitors for treatment of primary open-angle glaucoma

A

Dorzolamide
Reduces aqueous production
Sulphonamide-like reactions if systemic absorption

182
Q

Give example, MOA and SE of miotics for treatment of primary open-angle glaucoma

A

Pilocarpine - muscarinic receptor agonist
Increases uveoscleral outflow
Constricted pupil, headache, blurred vision

183
Q

What is retinal detachment?

A

When neurosensory layer of the retina comes away from its underlying pigment epithelium attaching to the choroid

184
Q

What causes retinal detachment?

A

Usually due to a retinal tear allowing vitreous fluid to get under the neurosensory layer of the retina and fill this space

185
Q

What % of those pt with untreated symptmatic retinal breaks will progress to retinal detachment?

186
Q

Risk factors for retinal detachment?

A

Diabetes - retinal breajs due to traction by vitreous humour
Myopia - increases risk of posterior vitreous detachment and peripheral retina may be thinned and more likely to tear
Age
Previous cataract surgery accelerates posterior vitreous detachment
Eye trauma e.g. boxing

187
Q

What is rhegmatogenous retinal detachment?

A

Most common type of retinal detachment
A retinal tear causing fluid to enter the subretinal space causing retinal detachment

188
Q

What is exudative retinal detachment?

A

When fluid builds up in the subretinal space but there aren’t any tears in the retina
This can be caused by inflammation in the eye

189
Q

What is tractional retinal detachment?

A

When scar tissue on the retina pulls your retina away from the back of your eye

Most commonly seen in pt with proliferative diabetic retinopathy - damaged blood vessels scar retina

190
Q

Features of retinal detachment?

A

new onset floaters or flashes, as these indicate pigment cells entering the vitreous space or traction on the retina respectively
sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery should also raise suspicion of detachment
if the macula is involved, central visual acuity and visual outcomes become much worse
peripheral visual fields may be reduced, and central acuity may be reduced to hand movements if the macula is detached
the swinging light test may highlight a relative afferent pupillary defect if the optic nerve is involved
fundoscopy
the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms
if the break is small, however, it may appear normal.

191
Q

Who should you refer to ophthalmology for ?retinal detachment?

A

Any pt with new onset flashes or floaters - within 24 hours
Visual field loss, changes in visual acuity or fundoscopic sigs of retinal detachment - immediate

192
Q

How do we manage retinal tears?

A

Laser therapy or cryotherapy to create a scar adhesions between retina and retinal pigment epithelium to seal the hole and prevent more fluid accessing the subretinal space

193
Q

How do we manage retinal detachment?

A

Virectomy
Sclera buckling
Pneumatic retinopexy

194
Q

What is virectomy?

A

keyhole surgery on the eye. relieves traction by removing the vitreous attached to the retinal breaks. A gas or oil bubble is then used to span and close the retinal break until a scar develops
Used in retinal detachment

195
Q

What is sclera buckling?

A

a silicone buckle is places on the sclera surface over retinal breaks; this puts pressure on the sclera from outside the eye, squashing the eye inwards to reconnect the layers of the retina
Used In retinal detachment

196
Q

What is pneumatic retinopexy?

A

injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble presses the separated
Used in retinal detachment

197
Q

What is the most common cause of blindness in the UK?

A

Age-related macular degeneration

198
Q

What is age-related macular degeneration

A

Degeneration of the macula (central retina) - degeneration of retinal photoreceptors that results in formation of drusen
Usually bilateral

199
Q

Risk factors for age-related macular degeneration?

A

Advancing age is the greatest ris factors
Smokers are twice as likely
FHx - first degree relatives are 4x more likely
RF for ischaemic CVD

200
Q

2 forms of macular degeneration?

A

Dry macular degeneration - 90% of causes
Wet macular degeneration - 10%

201
Q

What is dry macular degeneration also known as and what is it characterised by?

A

Atrophic
Drusen - yellow round spots in Bruch’s membrane

202
Q

What is wet macular degeneration also known as and what is it characterised by?

A

Exudative or neovascular macular degeneration
Characterised by choroidal neovasculiarisation
Carries worst prognosis as can cause rapid loss of vision

203
Q

Clinical features of macular degeneration?

A

Reduction in visual acuity, particuarly for near field objects - over years in dry or more rapid in wet ARMD
Deterioration in night vision
Photopsia (flickering or flashing lights)
Glare around objects
Visual hallucinations may occur = Charles-bonnet syndrome
Distortion of line perception on Amsler grid testing

204
Q

What is Amsler grid testing?

A

It’s a grid of straight lines
Hold it at ~12-14 inches away from face, cover 1 eye and focus on black dot in the middle of grid
Cover the other eye and repeate

205
Q

What would you see on fundoscopy in macular degeneration?

A

Drusen - yellow areas of pigment deposition in macular area
In wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage

206
Q

Investigations for age-related macular degeneration?

A

Slit-lamp microscopy - initial investigation of choice to identify any pigmentary, exudative or haemorrhage changes
Fluorescein angiography is neovascular ARMD is suspected as this can guide intervention with anti-VEGF therapy
Optical coherence tomography to visualise retina in 3D to reveal areas of disease which aren’t visible on microscopy alone

207
Q

Management of dry age-related macular degeneration?

A

Zinc with anti-oxidant vitamin A, C and E - reduces progression

208
Q

Management of wet age-related macular degeneration?

A

Anti-VEGF intravitreal injections every 4 weeks
Laser photocoagulation can slow progression where there is new vessels but risk of acute visual loss

209
Q

Examples of anti-VEGF agents?

A

Ranibizumab
Bevacizumab
Pegaptanib

210
Q

What is squint also known as?

A

Strabismus

211
Q

What is strabismus?

A

Misalignment of the visual axes

212
Q

What is concomitant squint?

A

Due to an imbalance in extraocular muscles

213
Q

What is paralytic squint?

A

Due to paralysis of extraocular muscles

214
Q

What are the different names for the types of squint?

A

Esotropia - eye towards nose
Exotropia - eye towards ear
Hypertropia - eye up
Hypotropia - eye down

215
Q

Why is it important to detect and correct a squint?

A

As untreated they can lead to amblyopia - Bain fails to fully process inputs from the eye with the squint so favours the other eye causing visual acuity issues

216
Q

How can we detect a squint?

A

Using a corneal light reflection test
Cover test is used to identify the nature of the squint

217
Q

What can help prevent amblyopia in a child with a squint?

A

An eye patch

218
Q

Whats the leading cause of visual loss globally?

219
Q

What is a congruous visual field defect?

A

When there is a complete or symmetrical visual field loss

220
Q

What is an incongruous visual field defect?

A

When there is an incomplete or asymmetric visual field loss

221
Q

Where is the lesion in an incongruous defect of Homonymous haemianopia?

A

Optic tract

222
Q

Where is the lesion in an congruous defect of Homonymous haemianopia?

A

Optic radiation or occipital cortex

223
Q

Where is the lesion in a superior Homonymous quadrantanopia?
And in the inferior?

A

Superior -> lesion is in the Inferior optic radiation’s in temporal lobe

Inferior -> lesions of the superior optic radiations in parietal lobe

PITS parietal inferior temporal superior

(Note this is very much an exam answer as most research suggests the majority of quadrantanopias are caused by occipital love lesions)

224
Q

Where is the lesion in bitemporal haemianopia?

A

In the optic chiasm

225
Q

What causes a central scotoma?

A

Macula degeneration

226
Q

What causes a constricted visual field?

A

Glaucoma
Retinitis pigmentosa

227
Q

What should you do with contact lens wearers who present with a red painful eye as only symptoms?

A

Always refer to the eye clinic to exclude microbial keratitis

228
Q

What is central retinal vein occlusion?

A

A relatively rare cause of sudden painless, unilateral visual loss
Obstruction to blood flow through central retinal artery

229
Q

What causes central retinal arterial occlusion?

A

Thromboembolism from atherosclerosis or arteritis e.g. temporal arteritis

Both cause obstruction to blood flow through central retinal artery

230
Q

Risk factors for central arterial occlusion

A

• CVD risk factors which increase the risk of atherosclerosis causing central retinal aretry occlusion
• White ethnicity, older age, female, poly myalgia rheumatica - risk factors for temporal arteritis

231
Q

Features of central retinal arterial occlusion?

A

Sudden unilateral painless visual loss “a curtain coming down”
Relative afferent pupillary defect - this is because the input is not sensed by the ischaemic retina when testing the direct light reflex but is sensed during the consensual light reflex

232
Q

Fundoscopy findings central retinal artery occlusion?

A

Cherry red spot on a pale retina
(Retina is pale due to lack of perfusion and the cherry red spot is the fovea which has a thin surface so shows the red-coloured choriod)

233
Q

Management of central retinal arterial occlusion?

A

Identify and treat underlying conditions e.g. ESR and temporal artery biopsy for temporal arteritis

If pt attained acutely then intraarterial thrombolysis can be artrempted but trials show mixed results

234
Q

What % of patients with Graves’ disease have thyroid eye disease?

235
Q

Risk factors for thyroid eye disease?

A

Smoking
Radioiodine treatment

236
Q

Features of thyroid eye disease?q

A

• exophthalmos
• Conjunctival oedema
• Optic disc swelling
• Opthalmoplegia
• Inability to close the eyelids which may lead to sore, dry eyes. If severe and left untreated, pt can be at risk of exposure keratopathy

237
Q

Circular muscles in iris:
Function?
Which nervous system stimulates?
Neurotransmitter?

A

Pupil constriction
PNS
Acetylcholine

238
Q

Radial muscles in iris:
Function?
Which nervous system stimulates?
Neurotransmitter?

A

Pupil dilatation
SNS
Adrenalin

239
Q

What can cause abnormal pupil shapes?

A

• trauma to sphincter muscles e.g. During cataract surgery
• Anterior uveitis - can cause adhesions in iris
• Acute angle-closure glaucoma - can cause ischaemic damage to iris muscles and abnormal pupil shape, usually a vertical oval
• Rubeosis iridis (neovascularisation of the iris) - associated with poorly controlled diabetes and diabetic retinopathy
• Coloboma - a congenital malformation that causes a hole in the iris and an irregular shaped pupil
• Tadpole pupils - muscle spasms in part of the dilation muscle. Temporary and associated with migraines and Horner syndrome.

240
Q

What is a Coloboma?

A

A congenital malformation that causes a hole in the iris

241
Q

What causes a tadpole pupil?

A

Migraines or Horner syndrome

242
Q

What causes miosis?

A

• Horner syndrome
• Cluster headahces
• Opiates
• Nicotine
• Pilocarpine
• Argyll-Robertson pupil

243
Q

Features of occulomotor nerve palsy?

A

Ptosis
Dilated non-reactive pupil
Divergent strabismus - down and out in affected eye

244
Q

Why does occulomotor nerve palsy cause a divergent strabismus?

A

As palsy of all eye muscles except lateral rectus and superior oblique = eye pulled down and out

245
Q

Why does 3rd nerve palsy cause ptosis?

A

As occulomotor nerve usually supplies the levator palpebrae superioris which is responsible for lifting the upper eye lid so palsy = droop

246
Q

Why does 3rd nerve palsy cause dilated non-reactive pupil?

A

As the occulomotor nerve carries the parasympathetic fibres that innervate the circular muscles of the iris so palsy = dilated non-reactive

247
Q

Causes of 3rd nerve palsy

A

Idiopathic
Compression of nerve - tumour, trauma, cavernous sinus thrombosis, posterior communicating artery aneurysm, raised ICP

248
Q

What are the features of Horner syndrome?

A

Ptosis
Miosis
Anhidrosis
Enopthalmos

249
Q

What generally causes Horner syndrome?

A

Damage to the symaoethtic nervous system. These nerves arse from the spinal cord in the chest and the post-ganglion is nerves travel to the head alongside the internal carotid artery

250
Q

Outline the specific causes of Horner syndrome?

A

4S, 4Ts, 4Cs for sentral, torso (pre-ganglionic) and cervical (post-ganglionic)

Central lesions:
Stroke
MS
Swelling - tumour
Syringomyelia (cyst in spinal cord)

Pre-ganglionic:
Tumour pancoast
Trauma
Thyroidectomy
Top rib/cervical rib

Post-ganglionic:
Carotid aneurysm
Cartotid artery dissection
Cavernous sinus thrombosis
Cluster headache

251
Q

How can you tell where a lesion is in horners syndrome from the symptoms?

A

Central lesions - causes anhidrosis of arm, trunk and face
Pre-ganglion lesiosn cause anhidrosis only on face
Post-ganglion lesions dont cause anhidrosis

252
Q

What is a distinguishing features of congenital Horner syndrome?

A

Heterochromia (difference in iris colour on affected side)

253
Q

What is a Holmes-Adie pupil?

A

A benign condition mostly seen in women

A dilated pupil that is sluggish to react to light
normal accommodation but slow to dilate following constriction “tonic pupil”

254
Q

What is Holmes-Adie syndrome?

A

A Holmes-Adie pupil with absent ankle and knee reflexes

255
Q

What is a Argyll-Robertson pupil?

A

A specific findings in neurosyphilis
A constricted pupil that accommodates but doesnt react to light
Often irregularly shaped

Accommodation Reflex Present but Pupillary Reflex Absent

256
Q

What is posterior vitreous detachment?

A

Separation of the vitreous membrane from the retina
This occurs due to natural changes to the vitreous fluid of the eye with ageing

257
Q

Epidemiology of posterior vitreous detachment?

A

> 75% of people over 65

258
Q

What must you rule out in posterior vitreous detachment?

A

Retinal tears or retinal detachment as these can result in permenant loss of vision

259
Q

Risk factors posterior vitreous detachment?

A

Age - vitreous fluid becomes les svsicous as we age and doesnt hold its shape as well so it pulls it away from the retina
Highly myopic people - myopic eye has a longer axial length

260
Q

Features of posterior vitreous detachment?

A

The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)

261
Q

Ophthalmoscopy findings in posterior vitreous detachment?

A

Weiss ring - detachment of vitreous membrane around the optic nerve to form a. Ring-shaped floater

262
Q

Referral for posterior vitreous detachment?

A

All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.

263
Q

Tx of posterior vitreous detachment

A

Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.

264
Q

What is central retinal vein occlusion?

A

When a thrombus forms in the retinal vein, blocking drainage of blood from the retina

265
Q

2 types of retinal vein occlusion?

A

Central retinal vein occlusion - causes problems with entire retina
Branch retinal vein occlusion - affects smaller area which was drained by that branch

266
Q

Risk factors central retinal vein occlusion?

A

increasing age
hypertension
cardiovascular disease
glaucoma
Diabetes
polycythaemia

267
Q

Features of central retinal vein occlusion?

A

sudden, painless reduction or loss of visual acuity, usually unilaterally

268
Q

Fundoscopy findings in central retinal vein occlusion?

A

widespread hyperaemia
severe retinal haemorrhages - ‘stormy sunset’

269
Q

Management of central retinal vein occlusion?

A

Majority managed conservatively

Indications for treatment:
- macular oedema
- retinal neovascularisation

Treat macular oedema with intravitreal VEGF agents
Treat retinal neovascularisation with laser photocoagulation

270
Q

What is retinitis pigmentosa?

A

A genetic condition that causes degeneration of photoreceptors in the retina, particuarly the rods, causing loss of vision

271
Q

Features of retinitis pigmentosa?

A

Night blindness is often the initial sign
Tunnel vision due to loss of peripheral retina
(These symptoms occur first as rods degenerate more than the cones and these are responsible for light and peripheral vision)

272
Q

Fundoscopy findings in retinitis pigmentosa?

A

black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium

273
Q

Retinitis pigmentosa associated conditions?

A

Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport’s syndrome

274
Q

What systemic diseases are related to scleritis?

A

RA
SLE
Sarcoidosis
Granulomatoss with polyangiitis

275
Q

What systemic diseases are related to episcleritis?

276
Q

What systemic diseases are related to uveitis?

A

Ankylysing spondylsos
Reactive arthritis
IBD
Behçet’s disease
Sarcoidosis

277
Q

What is anisocoria?

A

Difference in size of pupils

278
Q

Causes of a pale optic disc?

A

Glaucoma
Retinitis pigmentosa
Choroiditis
Centralretinal artery occlusion
MS
Leber’s optic atrophy
Syphilis

279
Q

What does sixth nerve palsy look like?

A

Double vision as convergent strabismus due to lack of function from lateral rectus muscle

280
Q

What is Leber optic neuropathy?

A

A rare mitochondrial disorder that typically presents in young males with progressive visual loss due to optic neuropathy

281
Q

Causes of sudden loss of vision?

A

Occlusion of central retinal vein or artery
Vitreous haemorrhage
Retinal detachment
Amaurosis fugax

282
Q

What is transient monocular visual loss?

A

Sudden, transient loss of vision that lasts less than 24 hours

283
Q

Screening for open angle glaucoma?

A

First relative with glaucoma then screen them from age of 40 annually

284
Q

Who do we refer to ophthalmology for suspected strabismus?

A

Any child under age of 4