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Year 4 Neurology and Special Senses > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

What is present in background diabetic retinpathy

A

Microaneurysms, blot hemorrhages, hard exudates, cotton wool spots

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2
Q

What questions should be asked when taking an opthalmic history?

A
  • Did the problem start suddenly or gradually?
  • Painful or painless?
  • Transient of persistent?
  • Unilateral or bilateral?
  • Is the vision blurred: centerally or both centerally and peripherally
  • Is there and associated distortion or double vision
  • Are the symptoms there all the time?
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3
Q

Causes of an acute red eye?

A

Conjuntivities
Scleritis
Keratitis
Anterior uveitis
Corneal forigen body
Episcleritis
Subconjunctival haemorrhage

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4
Q

An acute red eye is usually painful or uncomfotable, what might be the cause if it is not?

A

Subconjunctivial haemorrhage

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5
Q

Vision in conjunctivitis?

A

Normal

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6
Q

Vision in scleritis?

A

Either normal or reduced

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7
Q

Vision in keratitis?

A

Reduced

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8
Q

Vision in anterior uveitis?

A

Normal or reduced

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9
Q

Vision in episcleritis?

A

Normal

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10
Q

Will a corneal forigen body reduce vision?

A

Sometimes, depedning on where the FB is

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11
Q

Vision in subconjuncitival haemorrhage?

A

Normal

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12
Q

What might be the cause of reduced vision and red eye in a patient found to have normal IOP?

A

Corneal abrasion
Keratitis
Endophthalmitis

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13
Q

What might be the cause of reduced vision and red eye in a patient found to have increased IOP?

A

Acute glaucoma
Anterior uveitis

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14
Q

What might cause a sudden, painless loss of vision, of a few seconds of duration?

A

Unilateral:
Giant cell arteritis
Optic disc swelling (infectious, inflammatory)
Impending central retinal vein occlusion

Bilateral:
Disc swelling due to idiopathic intracranial hypertension (visual obscurations)

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15
Q

What might cause a sudden, painless loss of vision, of a few minuites of duration?

A

Unilateral:
Amaurosis fugax
Giant cell arteritis

Bilateral:
Vertebrobasilar artery insufficiency

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16
Q

How long might visual loss from migraine aura last?

A

Up to 1 hour

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17
Q

What is visual obscurations?

A

Disc swelling due to idiopathic intracranial hypertension

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18
Q

What might cause a painful sudden loss of vision?

A

CORNEAL ABNORMALITY - Keratitis
DISC ABNORMALITY - optic neuritis
UVEA ABNORMALITIY - anterior uveitis
NORMAL FUNDUS - retrobulbar optic neuritis

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19
Q

Generalised causes of gradual visual loss?

A

Refractive error
Cataract

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20
Q

Central causes of gradual visual loss?

A

Abnormal macula (e.g. age related macular degeneration, macula oedema, diabetic maculopathy)
Abnormal optic disc (optic neuritis)

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21
Q

Peripheral or pathy causes of gradual loss of vision?

A

Abnormal choroid/retina (e.g. posterior uveitis)
Abnormal optic disc (e.g. glaucoma)

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22
Q

Causes of monocular diplopia?

A

Due to pathology from affectsed eye

Abnormal refraction
Abnormal cornea
Abnormal lens
Abnormal iris
(Normal examination - not diplopia)

e.g. cataract, corneal abrasion, eyelid cyst

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23
Q

What might cause binocular diplopia?

A

Pathology in the nerves, neurmuscular junction or muscles

Intermittent/variable:

Myasthenia gravis (NMJ)
Intranuclear opthalmoplegia
Giant cell arteritis

Persistent:

Neurogenic - cranial nerve palsies
Myogenic - congenital (rare) or acquired (e.g. thyroid)

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24
Q

Ocular clinical features of myasthenia gravis?

A

Variable diplopia/pstosis - usually worsening towards evening/with exercise

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25
What determines IOP?
Balance of aqueous production and aqeous drainage
26
How is glaucoma treated?
Aim: stop or slow progression. Only option is aim to lower the pressure - by reducing production or increasing drainage 1. Drugs: topical or oral - production/drainage? 2. Laser (irodotomy) - production/drainage 3. Surgery: trabeculectomy (less common) -drainage NB. pressure is a risk factor not a given
27
What drugs can be used to decrease IOP in glaucoma and how do they act?
Drops: - Alpha agonists: reduce aqueous production and increase drainage - Beta blockers: reduce aqueous production only - Carbonic anhydrase inhibitors: reduce aqueous production only - Prostaglandin analogues: increase aqueous drainage only Tablets: Carbonic anhydrase inhibitors
28
What is a trabeculectomy and how is it utilised in glaucoma?
Sclera incised, new channel (bleb) through which aqueous fluid can drain is created. Restoring the eye's ability to drain aqeuous humour reduced IOP
29
How does acute angle closure glaucoma typically present?
Patients over 50, usually female Unilateral eye pain Watering eye Bad headache Typically starts in evening Progression to N&V Patients may report collapsing ''off legs'' Reduced vision Red eye Corneal odeama Fixed mid dilated pupil High IOP
30
What is the 7th cranial nerve responsible for?
Motor: Facial expression Sensory: taste and sensation in the mouth Parasympathetic: salivary & lacrimal glands
31
What will be effected in a proximal facial nerve palsy, at point of nerve root?
Motor, parasympathetic and sensory function Paralysis of nerves of facial expression Loss of taste and sensation in mouth Dry mouth and eyes
32
What will be affected in a facial nerve palsy just distal to the geniculate ganglion?
Chorda typania nevre paraysis - loss of taste on anterior two thirds of tounge Loss of parasympathetic innervation to the salivary glands - dry mouth Loss of motor innervation enterirely: facial muscle and stapedius muscle paralysis Intact: Sensory innervation to the soft palate (taste buds) (greater pretosal nerve), parasympathetic innervation to the lacrimal gland and glands of the nasal mucosa, sensory innervation to the skin of external ear (wuth vagus)
33
What will happen in a facial nerve palsy at the level of the stylomastoid foramen?
Paralysis of facia muscles (temporal zygomatic buccal mandibula and cervical branches compromised) Loss of sensation to skin of external ear Rest of sensory innervation and the paraysympathetics are intact (taste and sesnation in mout intact, salivary and lacrimal glands still inverated)
34
Causes of facial palsy?
Bells palsy (75%) Viral - HSV/VZV (VZV+ramsey hunt syndrome) Chronic otitis media Iatrogenic Tumour - cerbellopontine angle Cerebrovascular (brainstem or supranuclear) Rare; DM, MS, lyme disease
35
What is Ramsay Hunt syndrome?
An acute peripheral facial neuropathy that occurs as a complication of shingles. It causes hearing loss and facial paralysis.
36
Symptoms of Ramsay Hunt syndrome?
A painful red rash with fluid-filled blisters on, in and around one ear Facial weakness or paralysis on the same side as the affected ear Ear pain Heating loss Tinitus Difficulty closing one eye Vertigo Change or loss of taste Dry mouth Dry eyes
37
What are the opthalmic manefestations of Ramsay Hunt syndrome?
Lagophthalmos (can't close eye) Dry eye
38
What are the opthalmic manefestations of Ramsay Hunt syndrome?
Lagophthalmos (can't close eye) Dry eye
39
Symptoms of facial nerve palsay?
Unilateral facial weakness Rapid onset Dribbling from mouth Sore, red eye (Be suspicious if pain or other cranial nerves involved)
40
Opthalmic manefestations of facial nerve palasy?
Bell's phenomenon - rolling up of eye onclosure - present in 80% of population but detoriorates with age Lagophthalmos - failure of lids to meet on closure, can be measured in mm, needs to be assesed with Bell's phenomenon
41
What should be checked (in terms of the eye) in facial nerve palsay, to establish risk of corneal ulceration and scarring?
Corneal sensation - if absent this significantly increased the risk of corneal ulceration & scarring
42
How can acute eye protection be provided in management of facial nerve palsy?
Lubricant ointment: lacrilub or simple eye ointment Cross taping if needed (no patching)
43
When might you further investigate facial nerve palsy?
Worring features or slow recovery MRI brain, brainstem and facial nerve Electroneurography if available
44
How is facial nevre palsy managed?
Acute eye protection (drops, taping) Acyclovir PO for 7 days if ?viral aetiology Prednisolone Referral: eye casualty or OPD, ENT, facial nerve clinic
45
Recovery of Bells plasy?
85% recovery starts within 3 weeks 16% wil be left with a perminent deficity and &% with have a recurrent epidose
46
How is Ramsay-Hunt syndrome different in its presentation compared to other facial nerve palsies?
Pain is a prominent deature
47
Prognosis of Ramsay Hunt Syndrome
60% full recovery
48
Why should pathcing be avoided in facial nerve palsy?
Causes corneal alcers
49
Acute eye management in facial nerve palsy?
Copuous lubrucant ointment
50
What causes an afferent pupillary defect?
Complete potent nerve lesion
51
What is found in an afferent pupillary defect?
Affected pupil is stimulated neither eye reacts When the normal pupil stimulated both eyes react Involved eye is blind
52
What is RAPD
Relative afferent pupil defect/ Marcus Gunn pupil Defect caused by an incomplete optic nerve lesion
53
What is found in a relative afferent pupil defect
The affected side will react to light more Weasley when compared to the normal side The difference between the level of function between these nerves can be exploited by the swinging flashlight test
54
What is the normal reaction to swinging flashlight test?
Both pupils constrict when light shone into non-tested side Flashlight off both eye temporarily as swings - pupils start to dilate Light shone to the tested side - pupils constrict
55
What will happen in swinging flashlight test in RAPD
both pupils constrict when light shone into non tested eye Flashlight off both eye temporarily swings - pupils start to dilate Both pupils continue to dilate when swung to tested side
56
Causes of relative afferent pupillary defect?
Optic nerve aetiology: Optic neuritis Optic nerve tumours (glioma, meningioma) Trauma to optic nerve ie. Surgery Pressure on optic nerve (TED) Advanced unilateral glaucoma Retinal aetiology: Sever retinal pathology: retinal detachment, CRVO, CRAO
57
What is the action of the EOM lateral rectus, and which nerve is it innervated by?
aBduction CN 6 Abducens
58
What is the action of the EOM medial rectus, and which nerve is it innervated by?
ADuction CN3 occulomotor
59
What is the action of the EOM superior recuts, and which nerve is it innervated by?
Elevation (and aduction and intorsion) CN 3
60
What is the action of the EOM inferior rectus, and which nerve is it innervated by?
Depression (Aduction, extortion) CN3
61
What is the action of the EOM superior oblique, and which nerve is it innervated by?
Depression (abbduction, intorsion) CN4 trochlear
62
What is the action of the EOM inferior oblique, and which nerve is it innervated by?
Elevation (aBduction, extorsion) CN3 occulomotor
63
Which EOMs does the Abducens nerve, CN6, supply?
Lateral recuts
64
Which EOMs does the occulomotor nerve, CN3, supply?
Medial rectus Inferior rectus Superior rectus Inferior oblique
65
Which EOMs does the trochlear nerve, CN4, supply?
Superior oblique
66
What might be seen in a nerve palsy of CN6 (abducens)
Esotropia in primary postion Inability to aBduct the eye No issues with aDuction
67
Symptoms of CN6 (abducens) nerve palsy?
Binocular Diplopoda (images side by side) Worse in direction of impaired muscle Pt may turn their head into the direction of the impaired field
68
Causes of CN6 (abducens) nerve palsy?
Most common: microvascular: DM, HTN Stroke Acoustic neuroma Acute petrositis Raised cranial pressure
69
Differentials for CN6 (abducens) nerve palsy?
Medial wall # Myasthenia
70
Features of CN4 (trochlear) nerve palsy?
Vertical diplopia (difficulty walking downstairs, looking down and in) Left hypertropia WOOG - hypertropia worse on opposite gaze BOOT - better on opposite tilt
71
Causes of CN4 (trochlear) nerve palsy?
Common: vascular, trauma Uncommon: aneurysm, tumour
72
What does the occulomotor nerve (CN 3) innervate?
Ocular muscles (SR, IR, MR, IO) (all except LR and SO) Levator palpebrae superioris Spinchter pupillae (parasympathetic)
73
Symptoms of CN3, occulomotor nerve palsy?
Opthalmoplegia Affected eye down and out Pupil size (dilated) Lid droop Ptosis
74
Causes of dilated pupil?
Pupil involved - aneurysm (post communicating artery), tumour, cavernous sinus lesion, pituitary apoplexy Pupil sparing - ischemia micro vascular disease (common) GCA
75
Symptoms associated with papiloedema?
Transient visual field loss Enlarged blind spot Headaches n and v
76
What are the most important causes of papilodema to exclude?
Intracranial tumours Other masses - brain abscess Meningitis/encepahilitis
77
Most common cause of paipilodema?
Idiopathic intracranial hypertension
78
Risk/associated factors for IIH (idiopathic intracranial hypertension)
Obesity Weight gain Pregnancy OCP Tetracylcines
79
How is idiopathic intracranial hypertension diagnosed?
Normal MRI V INcreased opening pressure on lumbar puncture
80
How is IIH treated?
Diamox (acetylzolamide) Optic nerve decompression Neurosurgical shunts
81
How might optic neuritis present?
Unilateral gradual visual loss Loss colour vision Pain on extraocular movements
82
Causes of optic neuritis?
MS most common Viral infections Granulomatosis inflammation - TB sarcoidosis syphlis
83
What is internuclear ophthalmoplegia? (INO)
Weakness of aDuction of affected eye and horizontal jerk Nystagmus of aBducting other eye Caused by lesion in the medial longitudinal fasciculus (connects 3rd and 6th nerves on opposite sides) Most common cause is MS
84
What could cause loss of red reflex and leucokoria?
Cataracts Retinoblastoma Pseudoleukocoria Retinal detatchment ROP Coats disease Warrents urgent referral - retinoblastoma is fatal if mets, cataracts can cause amblyopia
85
What can cause cataracts in childhood?
Intrauterine infection - rubella, varicella Metabolic - galastosaemia, hypocalcaemia, diabetes Trauma Radiation Inherited - autosomal dominant, recessive or X-linked Chromosomal - trisomy 21, trisomy 13
86
How should childhood cataracts be investigated?
Urinalysis: for glucose and also urinary reducing substances in younger children Infants: blood calcium and glucose, test for galactokinase deficiency Referal to paediatricians and geneticists should be considered
87
What is coloboma?
Eye abnormality caused by failure of closure of optic fissure. Can occur in isolation or be associated with lens and retinal coloboma If optic disc coloboma involves macula area, vision is poor, nystagmus and strabismus may be present. Can also be associated with microphthalmos?
88
What causes ptosis in children?
Congenital (most common, due to dystrophy or dsygenesis of levator muscle) Neurogenic (third nerve palsy, marcus Gunn jaw-winking, Horner syndrome) Trauma Myogenic (progressive external opthalmoplegia, myasthenia gravis) Pseudoptosis (excess skin from resolving haemangioma, enophthalmos, hypotropic eye)
89
How can coloboma be managed in young adults?
Cosmetic contact lenses
90
When can congenital ptosis be managed surgically?
Once the child is able to cooporate with local anesthesia, as young as 9 or 10
91
What should be looked for in significant ptosis in children with congenital ptosis?
Early signs of amblyopia
92
Clinical features of Horners syndrome?
Miosis – anisocoria greatest in the dark (failure of dilator pupillae muscle) Ptosis – mild (1 to 2mm) Ipsilateral anhidrosis Heterochromia (light irides on affected side)
93
What will be found in pharmacological testing in horners syndrome with cocaine?
Normal pupil will be dilated by 10%, abnormal will not
94
Causes of horners syndrome in children?
Neuroblastoma Syringomyelia Trauma
95
What should all children with anisocoria which is not physiological undergo?
Urinary catecholamine analysis (VMA - vanilymandelic acid)
96
Causes of Horner syndrome in adults?
Pancoast tumour - lung apex Trauma Mets Internal carotid dissection
97
What are myelinated nerve fibres associated with?
Gorlin syndrome Retinal dystrophy with night blindness Limb deformities Extensive unilateral myelination can be associated with high myopia amblyopia
98
What is CHRPE?
Congenital hypertophy of retinal pigment epithelium Usually have no visual or systemic problems
99
What is important to exclude in patients with congenital hypertrophy of retinal pigment epithelium (CHRPE)?
Gardner syndrome (adenomatous polyposis of colon and extracolonic manifestations)
100
Ocular findings to exclude in congenital toxoplasmosis?
Microphthalmos, cataracts, panuveitis, optic atrophy
101
What can be associated with congenital toxoplasmosis?
Chorioretinitis Epilepsy Hydrocephalus Microcephaly Intracranial infection
102
How can you demonstrate a shallow anterior chamber?
Oblique flashlight test
103
What should be included in a history from a patient with a red eye?
Onset Location (unilateral/bilateral/sectoral) Pain/discomfort (gritty, FB sensation, itch, deep ache) Photosensitivity Watering +/- discharge Change in vision (blurring, halos) Trauma Contact lens wear Previous ocular history PMH
104
What might cause localized eyelid tenderness?
Hordeolum Chalazion
105
Opthalmic causes of photophobia?
Cornial abrasions Iritis Acute glaucoma
106
Causes of halo vision?
Corneal edema (acute glaucoma, contact lens overwear)
107
How to examine a patient with a opthalmic complaint?
► Inspect whole patient ► Visual acuity- each eye - WITH GLASSES/CONTACT LENSES TO MEAUSRE CORRECTED ACUITY (IF FOR DISTANCE) + pinhole ► Eye movement (ask about double vision) ►Visual fields (arms width apart max, level with pt eyeline) ► Symettry positions of eyballs (hypoglobus) ► Eyelids (lid retraction, ptosis, blepharitis, eczema, etc) ► Conjunctiva (bulbar and palpebral, diffuse or local redness, injection, haemorrhage) ► Cornea (clarity, staining with fluorescein, sensation, localised opacity) ► Anterior chamber (depth) - with slit lamp ► Pupils shape/ reaction to light / accomodation / RAPD ►Lense ►Vitreous ►Fundus - fundoscopy (retina) ►Optic nerve
108
What is ciliary flush and when might it be seen?
Injection of deep conjuncitval vessels and episcleral vessels surrounding the cornea Seen in iritis and acute glaucoma - not seen in simple conjuncitvits
109
What is conjunctival hyperemia?
Engorgement of more superficial vessels Nonspecific sign
110
Lid related causes of acute red eye?
blepharitis marginal keratitis trichiasis chalazion stye sub tardal foreign body dacrocystitits
111
Conjunctiva related causes of red eye?
bacterial conjuncitvitis gonococcal conjunctivitis chlamydial conjunctivitis viral conjunctivitis allergic conjunctivitis subconjuncitvital haemorrhage episcleritis vs scleritis
112
Cornea related causes of red eye?
bacterial keratitis herpetic keraitits forigen body
113
Anterior chamber related causes of red eye?
anterior uveitis/iritis vs viritis
114
What is blepharitis
Inflammation of the lid margin Characterized by: lid crusting, redness, telangectasia, misdirected lashes Styes and conjunctivitis are often associated Often caused by staphylococcus and other skin flora major causes Often meibomian gland abnormality Older patients may have dry eye
115
Symptoms of blepharitis?
Forigen body sensation/gritty Itching Redness Mild pain
116
How is blepharitis treated?
Lid hygiene Topical antibiotics Lubricants Doxycycline - meibomian gland disease and rosacea
117
What is marginal keratitis?
Hypersensitivity to staphylococcal exotoxins Associated with chronic stahplococcal blepharitis Subepithelial marginal infiltreate separated from the limbus by a clear zone FB sensation
118
How is marginal keratitis treated?
Short course of topical low dose steroids Treat associated blepharitis
119
What is trichiasis?
Inward turning lashes Idiopathic/secondary to chronic blepharitis/herpes zoster opthalmicus Presents with FB sensation and tearing Treated with lubricants epilation, electrolysis (few lashes), cryotherapy - many lashes
120
What is an internal hordeolum and how is it treated?
Acute chalazion Staphylococcal infection of the meibomian (tarsal) gland Tender nodule within the tarsal plate May be associated cellulititis Treated with hot compress, topical antibiotic ointment, incision and drainage once the infection subsides
121
What is an external hordeolum and how is it treated?
Stye or hordeolum Staphylococcal abscess of lash follicle and its associated glands of Zeiss or Moll Tender nodule in the lid margin pointing through the skin Treated with a hot compress, epilation of lash associated with the infected folicle and topical antibiotic ointment
122
How do you manage a subtarsal forigen body?
Evert eyelid while patient looks downwards and removed with cotton bud Stain with flourescein for abrasion +/- abx
123
Common causeative organisms bacterial conjuncitvitis?
Staph aureus Staph epidermis Strep pneumoniae Haemophilus influenzae
124
How is bacterial conjunctivitis aquired?
Direct contact with infected secretions
125
Symptoms of bacterial conjunctivitis?
Subacute onset Redness Grittiness Burning Mucopurulent discharge Often bilateral (No photophobia)
126
Signs of bacterial conjuncitivits?
Crusty lids Conjunctival hyperaemia Mild papillary reaction Lids and conjuncitiva may be odematous
127
How would you manage bacterial conjuncitvitis?
Swab if uncertain Topical antibiotics, effective in 2 to 7 days (except in very severe infections) Chloramphenicol or fusidic acid are a appropriate first line treatments
128
What is chlamydial conjunctivitis?
Veneral infection - chlamydia trachomatis serotypes D to K Sexually active patients Chronic with a mild keratitis
129
How does chlamydial conjunctivitis?
Usually unilateral FB sensation Lid crusting with sticky discharge Follicles No response with topical antibiotics
130
How is Chlamydial conjunctivitis managed?
Swab/smear: direct monoclonal flourescent antibody microscopy, PCR Treat with topical tetracycline/oral doxycycline/azithromycin Contact trace GUM referral
131
What causes viral conjunctivitis?
Most commonly adenoviral Adenovirus types 3, 4 and 7 - pharyngoconjunctival fever (PCF) Adenovirus types 8 and 9 -epidemic keratoconjunctivitis
132
Symptoms of viral conjunctivitis?
Acut onset Bilateral Watery discharge Grittiness Soreness, FB sensation Often no photophobia History of URTI Associated: follicles, haemorrhages, inflammatory membranes, lymphadenopathy (preauricular node), keratitis
133
How is viral conjunctivitis managed?
Self resolving up to two weeks Advice - very contagious Topical steroids for keratitis if risk of scarring
134
Symptoms/signs of allergic conjunctivitis?
Itchy Bilateral wattery discharge Chemosis (odema)- swollen conjunctive Papillae (can be giant cobblestone in chronic cases)
135
Viral vs allergic conjuncitvitis?
Viral not typically itchy
136
Management of allergic conjunctivitis?
► Investigation Exclude infection (generally viral is NOT itchy) IgE levels ? Patch testing ► Treatment (severity dependent) - cold compresses - remove (reduce) allergen - NSAIDS - antihistamines oral/ topical (olapatanol) - mast cell stabilizers (sodium cromoglycate) - topical corticosteroids - Immunosuppressants (cyclosporin) for steroids
137
How does spontaneous subconjunctival haemorrhage present and how is it managed?
Painless red eye w/o discharge VA not affected Clear borders Masks conjunctival vessels Check BP No treatment (lubricants) 10-14 days to ressolve Clotting and FBC to be done if recurrent
138
What is episcleritis, how does it present and how is it managed?
► Episcleral inflammation ► Localized (sectoral) or diffuse ► Symptoms/Signs: Often asymptomatic Mild tearing/ irritation Tender to touch but not particularly painful Vessels blanch with phenylephrine ► Self-limiting (may last for months) ► Treatment Lubricants NSAIDS (Froben po 100mg tds) Rarely low dose steroids (predsol)
139
What is scleritis, how does it present?
Scleral inflammation with maximal congestion in the deep vascular plexus RED EYE ► Symptoms/Signs: Pain (often severe boring) Significant ocular tenderness to movement and palpation Watering and photophobia Appearance bluish-red ► Localized ► Diffuse ► Nodular
140
What causes scleritis and what is it commonly associated?
Usually immune rather than infectious, most commonly with RA
141
How is scleritis managed?
Underlying condition managed NSAIDs Corticosteroids Immunosupression
142
What is pterygium?
Fibrovascular growth from the conjunctiva onto the cornea
143
How is pterygium managed?
Excision of pterygium - covering of defect with a conjunctival autograft or amniotic membrane Adjuvant mitomycin - reduce recurrence
144
Corneal abrasion/foreign presentation and management
History ► Severe pain esp with blinking ► Watering ++ ► Remove FB with cotton bud if able under topical anaesthetic ► Chloramphenicol ointment, cyclopentolate, double pad ► Abrasion crossing visual axis refer ► High impact history hammering/ grinding with out protective eye wear- exclude intraocular foreign body
145
Causative organisms of bacterial keratitis?
Staph aureus Strep pyogenes Strep pneumoniae Pseudomonas aeruginosa
146
Risk factors for bacterial keratitis?
Contact lense wear (extended, soft lenses) Pre existing chronic corneal disease e.g. neurotrophic keratopathy
147
Bacterial Keratitis: signs and symptoms
Ocular pain Watering discharge Foregin body sensation Descreased vision Photophobia Corneal lesion (ulcer) - can spread rapidyly Corneal oedema Hypopyon - pus level (sterile) seen in eye
148
How do you investigate bacterial keratitis?
Culture - blood agar, chocolate agar, sabran agar
149
How is bacterial keratitis managed?
Treated with ofloxacin Initially hourly, subequently 2 hrly (waking hours) Tapered Cyclopentolate tds Steroids when cultutres become sterile and evidence of improvement (7-10 days initiation of treatment)
150
What is herpes simplex keratitis?
Reactivation of laternt herpes simplex virus type 1 (which lies dormant in the trigeminal ganglion) Migrates down branch of the trigeminal nerve to cornea Form of corneal blindness Pts have a hx of cold sores, run down, stress
151
Signs/symptoms of HSV keratitis?
Tearing (epiphoria) Light sensitivity Pain hyperaemia Corneal sensation reduced Geographic amoeboid ulcer esp if incorrect use of steroid Under slit lamp examination with fluorescein applied, dendritic ulcers may be seen, which are pathogonomic of the infection
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How is herpes simplex keraititis managed?
Topical aciclovir ointment 5X/day 10-14 days Cyclopentolate Topical steroids to minimise scarring Aciclovir PO for up to a year Corneal scarring may cause blindness if untreated
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How does hepres zoster present and how is it treated?
► Reactivation ► Crusting and ulceration of skin innervated by 1st division of trigeminal nerve ► Lesions to tip of noseHutchinson’s sign, increased chance ocular involvement ► Tx 1. Oral aciclovir within 48hrs of onset of vesicles 800mg 5x day for 7 days (No effect if later) 2. Aciclovir ointment within 5/7 of onset of vesicles Ocular complications include conjunctivitis, uveitis, keratitis, scleritis, optic neuritis
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What is anterior uveitis (iritis)?
Inflammation of the anterior uveal tract Idiopathic (70%) Associated with systemic disease: sarcoid, ankylosing spondilitis, IBD, Reiter's syndrome, Psoriatic arthritis, Juvenile Chronic arthritis, HLA B27
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What can cause uveitis?
Idiopathic (70%) Infection: bacteria - TB syphillis, leprosy, viral: HSV, HZV, HIV, fungal (candida), protozoa: toxopasmosis, infestation (most vascular structure in the body hence why infection can cause uveuitus), Autoimmune: sarcoid, SLE, MS bechets, vogt koyanagi Drugs: Bisphiosphonates, rifabition, cidofovir (antiviral) Post-trauma: Sympathetic opthalmia Lens induced Post-op Retinoblastoma, lymphoma
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How does anterior uveitis (iritis) present?
Pain (ache) Photophobia - due to cillary muscle spasam Blurred vision Reduced visual acuity Floaters (cell clumps in vitreous body) Perilimbal conjunctival injection Pupil miotic/poorly reactive (sphincter muscle contraction constricts pupil) Lacrimation (excessive tear production) Abnormally shaped pupil due to posterior synechiae (adhesions) pulling the iris into abnormal shapes A hypopyon is a collection of white blood cells in the anterior chamber, seen as a yellowish fluid collection settled in front of the lower iris, with a fluid level Cillary flush
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Slit-lamp examination of anterior uveitis (iritis) - what is seen and why?
Flare (protein) in AC - (can't see beam in non inflamed eye) Cells in AC Keratic precipitates (WBC on the back of the cornea) Hypopyon - level of sterile pus vidable Iris inflammed Odema of iris leaky WBC leak anteriorly into aqueous humour (cells visable on slit lamp) Number of cells determines the severity
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How is anterior uveitis (iritis) managed?
Steroids (oral, topical or intravenous) May need sub conjunctival steroid if very severe. Initially topical steroids can be as often as half hourly in severe cases Cycloplegic-mydriatic medications such as cyclopentolate or atropine eye drops. Cycloplegic means paralysing the ciliary muscles. Mydriatic means dilating the pupils. Break synechiae, comfort. Cyclopentolate and atropine are antimuscarinic medications that blocks to the action of the iris sphincter muscles and ciliary body. These dilate the pupil and reduce pain associated with ciliary spasm by stopping the action of the ciliary body. Immunosuppressants such as DMARDS and TNF inhibitors Laser therapy, cryotherapy or surgery (vitrectomy) are also options in severe cases.
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How might you investigate repeated attacks of anterior uveitis?
CXR Lumbar XR Autoimmune serology HLA B27 Full blood count U and E LFT Q Gold Treponemal antibody Specific test based on aetiolofy (PCRs, HLA B27, MRI (MS), HLA b51 (bechets), Anti DsDNA (SLE) Satcoid - ACE, X ray, vitreous biopsy Bilateral or severe cases
160
Why is acute angle closure an opthalmic emergency?
Needs immediate treatment to prevent irreversible glaucomatous damage from raised intraocular pressure
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How is aqueous humour produced and drained?
Produced by the ciliary body in the posterior chamber of the eye It diffuses from the posterior chamber, through the pupil, and into the anterior chamber From the anterior chamber, the fluid is drained into the vascular system via the trabecular meshwork and Schlemm canal contained within the angle
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Aetiology of acute angle closure?
Peripheral iris blocking the outflow of aqueous humour
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What might predispose to acute angle closure?
Anatomical factors: relatively anterior location of iris-lens diaphragm (plateau iris), shallow anterior chamber, floppy iris Female (anterior chamber is shalloweer) Asian Hypermetropia Fhx Avg. age 60 years
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Signs and symptoms of acute angle closure?
Severe ocular pain Headache Nausea and vomiting Decreased vision Coloured haloes around lights Photophobia Semi-dilated non reactive pupil Cilary injection Corneal oedema Shallow AC Flare in AC Raised IOP Tense on palpation
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How is acute angle closure treated?
IF delay in admission: Lie patient on their back without a pillow Give pilocarpine eye drops (2% for blue, 4% for brown eyes) Give acetazolamide 500 mg orally Given analgesia and an antiemetic if required Medical: to lower the pressure IOP Topical steroid Iopidine Pilocarpine Acetazolamide (oral or IV) Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in the eye Timolol is a beta-blocker that reduces the production of aqueous humour Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour Brimonidine is a sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow Surgical: Laser iridotomy - curative, prophylactically to unaffected eye
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Pre-septal vs orbital cellulitis
Prespetal - infection of the subcutaneous tissues anterior to the orbital septum. CONFINED TO SOFT TISSUES ANTERIOR TO ORIBTAL SEPTUM Usually follows periorbital trauma or dermal infection Systemic illness rare Orbital - infection and inflammation within the orbital cavity producing orbital signs and symptoms Most commonly secondary to ethmoidal sinusitis Proptosis, chemosis, opthalmoplegia, decreased visual acuity (Both: bacterial infection usually resultss from local spread of adjacent URTI Erythema, induration, tenderness of eyelid Swelling so sevre pt cannot open eye)
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What is the orbital septum?
Fibrous membrane that originates from the orbital periosteum and inserts into the anterior surface of the tarsal plate of the eyelid Seperates the eyelid into preseptal and post septal areas
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Preseptal cellulitis caustive ogranisms
Staphylococcus aureus Staphylococcus epidermidis Streptococcus
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Orbital cellulitis causative organisms
Strep pneumoniae and pyogenes, Staph aureus Haemophilus influenzae, anaerobes
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What should be acertained in a history from a patient with either orbital cellulitis or preseptal cellulitis?
Recent URTI Trauma Sinus disease Recent dental work or infection Systemic symptoms - fever CNS symptoms - headache, neck stiffness
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How is pre-septal cellulitis managed?
Mild: augmentin or first generation cephalosporin, warm compress, topical antibiotics for concurrent conjunctivitis Failure to respond withing 48-72hrs conside iv abx
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How is orbital cellulits managed?
Immediate referral Admit for IV abx +/- imaging
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Risks associated with orbital cellulitis?
Raise intraocular pressure Endopthalmitis Optic neuropathy Meningitis Cavernous sinus thrombosis Superiosteal/orbital infections
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Different severities of ocular blunt trauma?
Mild to moderate: bruise ocular tissues, eyewall intact Moderate to severe - ruptured eye wall, severe consequences
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Types of ocular trauma?
Foreign bodies Corneal abrasions Disruption of globe Introcular FB Hyphemas Orbital wall fractures Chemical injury
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How is acid injury to the eye limited?
Damage occurs due to denaturation and coagulation of protein, but is often limited by neutralisation of the buffering action of the tissues, damage is limited to the area of contamination
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Why are alkaline injuries to the eye serious?
Penetrate ocular tissues rapidly and produce intense ocular reactions. Damage is widespread, uncontrolled and progressive Often results in epithelial loss, corneal opacification, scarring, severe dry eye, cataract, galucoma and blindness
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Management of chemical injury to the eye
Complete and copious irrigation, should be insitiuted within minuites Instil topical anestethic Use eye irrigation solutions and normal saline IV drip Squeeze copious amounts of solution into the eye and direct towards the temple, away from the unaffected eye Irrigate under the lids After several minuites or irrigation, check the pH of the eye by placing litmus paper into the inferior fornix Continue until pH neutralized, check pH after 30 mins as may rise again after irrigation stopped Remove any visable particulate mater and urgently refer to an opthalmologist
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What is hyphema?
Blood in anterior chamber of the eye Usually associated with trauma Requires urgent referal to an opthalmologist for treatment
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How is hyphaema treated?
Strict bedrest Topical steroids Topical cyloplegic agents Admit to hosptial if youn or concerned about follow-up/compliance Need exams for 5 days including mesaurement of IOP Sickle-cell prep (pts with sickle cell trait need more aggresive management of elevated IOP)
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What might follow a orbital floor fracture?
Muscle entrapment
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Common minor eye injuries?
Corneal abrasion Corneal foreign body Chemical splash Traumatic iritis
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What is the uvea?
Pigmented part of the eye Iris Ciliary body Choroid (most vascular part of the body)
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Why is uveitis sight threatenting
Retina is directly anterior to the choroid (part of uvea) - rods and cones get blood supply from choroid, so if effected when uvea inflamed, hence why uveitis is sight threatening.
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Types of uveitis by location?
Anterior - iritis - iris Intermediate: cyclitis - cillary body Posterior - choroiditis - choroid
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Why can dots be seen on the cornea in uveitis?
Keritic precipitates adhere to the cornea Granulomatous and non-granulomatous
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Signs in uveitis?
Keratic precifitates Cells in anterior chamber Fibrin in anterior chamber Posterior synechae (pupil has an abnormal shape), circumcorneal congestion - iris bludges forward (pushed forward by aqueous humour which is unable to flow out via pupil as lens is stuck) Cells in viteros Choroiditis lesions Macular odeama HIGH INTRAOCULAR PRESSURE
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Anatomical location of the iris?
Lens is posteior In close proximity to conjunctivia Cornea is anterior
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How can a posterior synachea be broken?
Cataract laser eye surgery Pupil dilation
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Symptoms of intermediate uveitis?
Blurring of vision Floaters
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Signs of intermediate uveitis
Cells in vitreous Snow balls (fundoscpoy) Snowbanking (fundoscopy) Sheating of blood vessels (seen on fundoscopy) Macula odeama (fudoscopy or OCT)
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How can TB cause uveitis?
1. Formation of granulomas 2. Immune reaction to TB protein
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Management of intermediate and posterior uveitis?
Local treatment: Periocular steroids Intravitreal steroid implants TOPICAL STEROIDS NOT SUITABLE Systemic treatment: Pulse therapy Oral steroids Immunosuppression Aetilogy specific antibiotic/antifungal/antiviral
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Infections associated with chronic anterior uveitis?
Sarcoidosis Syphilis Lyme disease Tuberculosis Herpes virus
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Side effects of topical steroids in opthalmology?
Cataracts Increased intraocular pressure (can lead to glaucoma and blindness)
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What is an Ozurdex implant?
Steroid implant (for the eye) Oral steroid sparing
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Anterior uveitis complications?
Posterior synechiae Pupillary Membrane Ocular HTN/glaucoma Hypotony (low IOP) - cillary body produces less aqeous humour - greater worry than high IOP Cataract Cystoid Macular Odema
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Complications of posterior uveitis?
Inflammation and infection in the posterior chamber may lead to retinal scarring and irreversible visual compromise
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Complications of posterior uveitis?
Inflammation and infection in the posterior chamber may lead to retinal scarring and irreversible visual compromise
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Complications of intermediate uveitis?
Glaucoma: A condition that can cause blindness due to higher intraocular pressure Cataracts: When the lens of the eye becomes clouded and cause vision loss Macular edema Retinal detachment: An eye condition wherein the retina gets separated from the eye structures that holds the retinal layers together Over time and due to a lack of proper treatment, the condition can affect other surrounding eye structures such as the lens, optic nerve, vitreous fluid, and retina
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In a patient with congenital absence of the zygomatic bone, what opthalmic abnormality would be present?
Proptosis, oulsitile
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Which muscle opens the eye and what nerve supplies it?
Levator palpabre superioris - elevates the upper eyelid Occularmotor nerve
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Where do the recti muscles
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What might a unilateral fixed dilated pupil in and injured (eye) patient?
Retrobulbar haemorrage, causing compatment syndrome
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Why is there only partial ptosis in Horners syndrome
Sympathetic innervation to superior tarsal muscle (Mullers muscle) only is compromised
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Where would a lesion cause non-axial proptosis?
Extra conal lesion
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Where would a lesion cause an axial proptosis?
Intra conal lesion (In muscle cone)
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Why are many patients with autoimmune conditions such as GPA and RA at risk of eyeball rupture?
Thinning of the sclera increased susceptibility to injury (blue sclera)
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Where is the blind spot in a healthy person and why?
Temporal visual field Optic nerve head as no photoreceptors here
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What is OCT?
Optical coherence tomography (OCT) is a non-invasive imaging test that uses light waves to take cross-section pictures of your retina Can view retina at cellular level
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Where would pathology likely arise from if a patient is complaining of an ache or pressure in their eye?
Pain from the orbit
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Where would pathology likely arise from if a patient is complaining of an itchiness or grittiness in their eye?
Surface of eye
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What is photopsia and how might it differ per cause?
Flashing lights Migraine: bilateral, may be coloured Retinal detachment or tare : unilateral, yellow or white
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Blephirits vs eczema
Both erythematous dry painful eyelid Blephritis involvement of eyelash, treat with warm compress Eczema look for skin thickening and fissures in other area, do not use warm compress
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Bacterial vs allergic bs viral conjunctivitis****
Bacterial: purulent discharge Viral: systemically unwell (fever, sore throat) haemorrhages visible, clear discharge Allergic: clear discharge
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Causes of unilateral photophobia
Corneal abrasion Corneal ulcer Anterior uveitis
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What might cause pressure sensation with nausea and vomiting
Acute angle closure glaucoma
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Juvinielle artheritis vs RA eye problems
Scleritis - RA Uveitis - Juvinielle arthritis
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Most important cause of nausea vommiting and pressure sensation in eye to exclude?
Acute angle glaucoma
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What sight threatening condition is jaw claudication indicative of?
GCA Differs from artheritis as more anterior and worsens with eating (rather than improving)
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Diplopia in 6th nerve palsy?
Horizontal
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Vision loss in papilodema?
Intermittent visual loss
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Conditions which may cause generalised eye blurring?
Usually means a reduction in the clarity of the entire field of vision Astigmatisim (reffractive error) Side effects of medications such as ORAL steroids Cataracts
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Causes of central visual blurring?
Age related macular degeneration (preceeded by complaints of distorion) Diabetic maculopathy Optic disc swelling
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How to tell difference between floaters and a scotoma (blind spot)
Floaters - can move into and out of view, 'slosh about with eye movements'. Suggest pathology in the vitreous e.g. posterior vitreous detatchment,vitritis, blood Scotoma- moves with vision. Suggests vascular occlusion or retinal detatchment.
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What might cause 'curtain vision' and how can you differentiate between the causes?
Retinal detachment - curtain constant - progressive Amaurosis fugax -curtain is transient Central retinal artery occlusion - sudden, may improve as associated swelling foes down Central retinal vein occlusion - comes on more gradually and progressive
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What might you see with an opthalmoscope in retinal detatchment?
Section of retina unable to focus on and section that you can
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Key questions in history (diplopia)
One or both eyes - Usually due to misalignment of eyes - Monocular (rare, catracts or corneal deformity), double vision remains when one eye covered
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What does red desaturation indicate?
Red desaturation - paler shade of red in eye of concern - suggestive of optic nerve disease
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What medical conditions can cause eye pathology?
Diabetes – retinopathy, cranial nerve palsies, infection, vascular occlusion Hypertension – hypertensive retinopathy, cranial nerve palsies, vascular occlusion Thyroid disease – lid retraction, lid lag, exophthalmos, dry eye, ocular motility restriction, optic neuropathy Ankylosing spondylitis- anterior uveitis and side effects from treatment e.g. oral steroids Arthritis – rheumatoid arthritis, reactive arthritis
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Which patients can be registered as blind or partially sighted?
Visual field defects in BOTH eyes with low visual acuity
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How is the fundus imaged?
Direct opthalmoscopy Indirect opthalmoscopy Slit lamp bimicroscopy Photography Optical coherence tomography Florescein angiography
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Clinical tests to asses opthalmology patient
Snellen visual acuity Near vison acuity test Amsler grid Ishihara Eye movement examination Cranial nerve examination
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What is glaucoma?
Group of conditions with characteristic progressive optic nerve damage associated with visual field damage +/- raised intraocular pressure
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V****ISUAL FIELD PATHWAY
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Pathophysiology of glaucoma?
In open-angle glaucoma, there is a gradual increase in resistance through the trabecular meshwork. This makes it more difficult for aqueous humour to flow through the meshwork and exit the eye. Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma. Acute angle-closure glaucoma occurs when the iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away. This leads to a continual build-up of pressure in the eye. The pressure builds up particularly in the posterior chamber, which causes pressure behind the iris and worsens the closure of the angle. Increased pressure in the eye causes cupping of the optic disc. In the centre of a normal optic disc is the optic cup. This is a small indent in the optic disc. It is usually less than half the size of the optic disc. When there is raised intraocular pressure, this indent becomes larger as the pressure in the eye puts pressure on that indent making it wider and deeper. This is called “cupping”. An optic cup greater than 0.5 the size of the optic disc is abnormal.
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Charcteristic pattern to loss of visual field in glaucoma
Rim of optic nerve becomes thinner as disc caves in and becomes more cupped
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Acute angle glaucoma vs Open angle glaucoma?
Acute angle: Painful red eye, blurred vision, halos around lights, headache, N&V Open angle: Peripheral vision loss, (It can present with gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time.)
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Normal intraocular pressure?
10-21(24)
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How is open-angle glaucoma managed?
Management of glaucoma aims to reduce the intraocular pressure. Treatment is usually started at an intraocular pressure of 24 mmHg or above. Patients are followed up closely to assess the response to treatment. Prostaglandin analogue eye drops (e.g. latanoprost) are first line. These increase uveoscleral outflow. Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning). Other options: Beta-blockers (e.g. timolol) reduce the production of aqueous humour Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour Sympathomimetics (e.g. brimonidine) reduce the production of aqueous fluid and increase uveoscleral outflow Trabeculectomy surgery may be required where eye drops are ineffective. This involves creating a new channel from the anterior chamber, through the sclera to a location under the conjunctiva. It causes a “bleb” under the conjunctiva where the aqueous humour drains. It is then reabsorbed from this bleb into the general circulation.
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How does iridotomy treat acute angle glaucoma?
Laser iridotomy is usually required as a definitive treatment. This involves using a laser to make a hole in the iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber. The relieves pressure that was pushing the iris against the cornea and allows the humour the drain.
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How can open angle glaucoma be diagnosed?
Goldmann applanation tonometry can be used to check the intraocular pressure. Fundoscopy assessment to check for optic disc cupping and optic nerve health. Visual field assessment to check for peripheral vision loss.
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Risk factors for open angle glaucoma
Increasing age Family history Black ethnic origin Nearsightedness (myopia)
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How is laser utilised to manage glaucoma?
Selective laser trabeculoplasty Cylodiode Peripheral laser irodtomy in angle closure glaucoma Goniotomy in congenital glaucoma
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Risk factors for open angle glaucoma?
Raised IOP Age African descent Family history Myopia
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Risk factors for angle closure gluacoma?
Raised IOP Hyperopia Increasing age Females are affected around 4 times more often than males Family history Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic origin. Shallow anterior chamber Medications:
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Risk factors for less common types of glaucoma?
Raised IOP Trauma Topical steroids Ocular inflammation Poor circulation
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Aetiology of refractive error (defocussed image on the retina causing blurred vision)
Average corneal power anomalous axial length Average axial length anomalous corneal power Physiological or pathological
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Types of refractive error?
Myopia (short sighted) -long axial length and avg cornea (or high power cornea average axial length, uncommon) CORRECTED WITH CONCAVE LENS Hypermetropia (long sighted) - short axial lenght, average cornea (or low power cornea avg axial length) CORRECTED WITH CONVEX LENS Astigmatism - not related to axial length, related to variation in cornea curvature
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How is intraocular pressure measured?
Non-contact tonometry is the commonly used machine for estimating intraocular pressure by opticians. It involves shooting a “puff of air” at the cornea and measuring the corneal response to that air. It is less accurate but gives a helpful estimate for general screening purposes. Goldmann applanation tonometry is the gold standard way to measure intraocular pressure. This involves a special device mounted on a slip lamp that makes contact with the cornea and applies different pressures to the front of the cornea to get an accurate measurement of what the intraocular pressure is.
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What size optic cup is abnormal?
An optic cup greater than 0.5 the size of the optic disc is abnormality
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What is presbyopia?
Declining amplitude of accommodation with age Patients will find it easier to move things they read away from them Managed with reading glasses/bifocals/varifocals
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What medications increase the risk of acute angle glaucoma?
Adrenergic medications such as noradrenalin Anticholinergic medications such as oxybutynin and solifenacin Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects
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Causes of forigen body sensation in the eye?
Forigen body Conjuncitvitis Blepharitis Eyelid cysts
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Causes of lid irritation?
Blepharitis Stye Chalazion Eczema
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What should you ask a patient complaining of visual disturbance?
Generalized blurring Central blurring Black spots, blob, curtain Photopsia Double vision - monocular or binocular Vertical or horiziontal Colour changes
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Common causes of colour changes to vision?
Cataract Optic nerve pathology (Ishihara colour vision testing is helpful)
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What type of complication is diabetic retinopathy?
Microvascular
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Risk factors for diabetic retinopathy?
Duration of diabetes Poor glycemic control HTN Pregnancy Nephropathy Smoking Obesity
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Pathogenisis of diabetic retionpathy?
1. Occlusion of capilaries - leading to ischemic shcnges: IRMA- intraretinal microvascular abnormalities (these can act as a shunt between the arterial and venous vessels in the retina.), cotton wool (nerve fibre damage) spots, irregular retinal veins, venous bleeding, new vessels). Basement membrane thikcening, endothelial damage, RBC changes, rouleuax. INcreased platelet stickiness and aggregation. 2. Leakage of capilaries - leading to haemorrhags, odema and lipid exudates - loss of pericyte
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Belphritis management
Management is with hot compresses and gentle cleaning of the eyelid margins to remove debris using cotton wool dipped in sterilised water and baby shampoo. Lubricating eye drops can be used to relieve symptoms: Hypromellose is the least viscous. The effect lasts around10 minutes. Polyvinyl alcohol is the middle viscous choice. It is worth starting with these. Carbomer is the most viscous and lasts 30 – 60 minutes.
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How is background diabetic retinopathy managed?
Observation
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What is CSMO (clinically significant macula odema)?
Retinal thickening at or within 500 microns of the centre of the macula Hard exudates at or within 500 microns of the centre of the macula if associated with adjacent retinal thikcening Retinal thickeness of >1 disc area, any part of which is within 1DD within the centre of the retina
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What are the stages of diabetic eye disease?
Background Preproliferative Proliferative Maculopathy
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What is preproliferative diabetic retinopathy?
Cotton wool spots (infarcts) - Haemorrhages (cluster of large blot haemorrhages) Venous beading IRMA Venous loop These are signs of retinal ischemia and therefore warrents specialist referral
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How is preproliferative diabetic retinopathy managed?
FU 4/12
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What is proliferative diabetic retionpathy?
Neovascularisatuion (new vessel formation, usually occuring at the optic disc) Warrents URGENT specialist refferal
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How is proliferative diabetic retinopathy treated?
Pan retinal photocoagulation within 2 weeks
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Classifications of diabetic maculopathy?
Focal Diffuse Ischemic Mixed CSMO Central involving
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In diabetic eye disease when should maculopathy be suspected?
Should be suspected if visual acuity drops (hard to see in early stages)
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What is focal diabetic maculopathy?
Well circumscribed area of leakage Full/part rings of exudates often surrounding a microaneurysm
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Management of diabetic maculopathy
Prompt laser, intravitreal steroids or anti-angiogenic agents may be needed
272
Treatment of focal diabetic maculopathy?
Focal laser
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What is diffuse diabetic maculopathy and how is it treated?
Diffuse retinal thickeness with cystoid oedema, MA Treated with grid laser
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What is ischeamic diabetic maculopathy?
Reduced VA Normal clinical appearance Macular ischemia on FFA Managed by observation
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Mixed vs central involving diabetic maculopathy?
MIXED: Combination of diffuse and ischemic CENTRAL INVOLVING : • Thickening involving the fovea centre >400 micron • Treatment: Anti VEGF therapies, • IV Iluvien for persistent DMO
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Opthalmic complications of diabetes?
Iridopathy (minor iris transillumination defects) Retinopathy Unstable refraction Orbital infection Ocular ischaemic syndrome Recurrent stye Accelerated senile Cataract NVG Ocular motor nerve palsies Reduced corneal sensitivity Papillopathy Tractional retinal detachment
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General principles of treatment in diabetic eye disease?
Retinopathy • Background : Annual screening , Systemic disease 9-12/12 hospital FU • Pre Proliferative: 4-6/12 FU • Proliferative/Active : Pan Retinal Photocoagulation(PRP) with in 2/52 • Proliferative /stable: 4-6/12 FU • Proliferative with DMO: Macular laser and PRP Maculopathy: • Focal: Focal laser, FU 3-4/12 • Diffuse: grid laser, FU 3-4/12 • Central involving: > 400 micron Anti VEGF • Ischaemic : observe • Persistent maculopathy: IV fluocinolone (Iluvein)
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What is vitreous hemorrhage?
Vitreous hemorrhage is the extravasation of blood into one of the several potential spaces formed within and around the vitreous body. This condition may result directly from retinal tears or neovascularization of the retina, or it may be related to bleeding from preexisting blood vessels in these structures. Managed by • View present : PRP same day or 2/52 • Persistent: vitrectomy+ endolaser+ anti VEGF
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What is Rubeosis?
Condition characterized by a new formation of vessels and connective tissue on the surface of the iris, frequently seen in diabetic patients. Management • Urgent PRP • Vit h’age: VITI+ Endolaser • Rubeotic glaucoma: PRP/ANTI VEGF,IOP reduction,Cyclodiode
280
What is diabetic retinopathy?
Diabetic retinopathy is a condition where the blood vessels in the retina are damaged by prolonged exposure to high blood sugar levels (hyperglycaemia) causing a progressive deterioration in the health of the retina.
281
Management of diabetic retinopathy?
Laser photocoagulation Anti-VEGF medications such as ranibizumab and bevacizumab Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease
282
Pathophysiology of diabetic eye disease?
Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells. Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages and the formation of hard exudates. Hard exudates are yellow/white deposits of lipids in the retina. Damage to the blood vessel walls leads to microaneurysms and venous beading. Microaneurysms are where weakness in the wall causes small bulges. Venous beading is where the walls of the veins are no longer straight and parallel and look more like a string of beads or sausages. Damage to nerve fibres in the retina causes fluffy white patches to form on the retina called cotton wool spots. Intraretinal microvascular abnormalities (IMRA) is where there are dilated and tortuous capillaries in the retina. These can act as a shunt between the arterial and venous vessels in the retina. Neovascularisation is when growth factors are released in the retina causing the development of new blood vessels.
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Types of stye?
Hordeolum externum is an infection of the glands of Zeis or glands of Moll. The glands of Moll are sweat glands at the base of the eyelashes. The glands of Zeis are sebaceous glands at the base of the eyelashes. A stye causes a tender red lump along the eyelid that may contain pus. Hordeolum internum is infection of the Meibomian glands. They are deeper, tend to be more painful and may point inwards towards the eyeball underneath the eyelid.
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How are styes treated?
Styes are treated with hot compresses and analgesia. Consider topic antibiotics (i.e. chloramphenicol) if it is associated with conjunctivitis or persistent.
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What is a chalazion and how is it treat?
A chalazion occurs when a Meibomian (tarsal) gland becomes blocked and swells up. It is often called a Meibomian cyst. It presents with a swelling in the eyelid that is typically not tender. It can be tender and red. Treatment is with hot compress and analgesia. Consider topic antibiotics (i.e. chloramphenicol) if acutely inflamed. Rarely if conservative management fails then surgical drainage may be required.
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What is an entropian, how is it managed and why?
Entropion is where the eyelid turns inwards with the lashes against the eyeball. This results in pain and can result in corneal damage and ulceration. Initial management is by taping the eyelid down to prevent it turning inwards. Definitive management is with surgical intervention. When the eyelid is taped down it is essential to prevent the eye drying out by using regular lubricating eye drops. A same-day referral to ophthalmology is required if there is a risk to sight.
287
What is an ectropian (eye), what can it lead to and how is it managed?
This can result in exposure keratopathy as the eyeball is exposed and not adequately lubricated and protected. Mild cases may not require treatment. Regular lubricating eye drops are used to protect the surface of the eye. More significant cases may require surgery to correct the defect. A same-day referral to ophthalmology is required if there is a risk to sight.
288
How might a corneal ulcer present?
Pain, photphobia Contact lense Recen injury or abrasion Recent coldsore Rash or vesicles Conjunctival injection, infiltrate
289
How is corneal ulceration managed?
Bacterial - Intensive abx drops (hourly) Viral - antivirals Less common fungal/acanthameba (increased risk with swimming showering or sleeping in contact lenses)- antifungal and anti amoebic intensice eye drops
290
What is panuveitis?
Uveitis across entire uvea, associated with inflammatory conditions: Bechets. SLE, PAN, Wegners, toxo Inflammation of anterior and post segments
291
What might cause conjunctivitis in infants?
Vertical transmission - chalmydial or gonorrheal
292
How is infantile conjunctivitis managed?
Requires management due to risk of sereous corneal disease or blindness Urgent swabs and treat appropriatley (topic abx drops) Admit under peads
293
Name the infection
294
What does punctuate staining on fluorescein staining suggest?
Dry eye disease, occular surface irriation
295
What are the potential of complications of cataract surgery
Endophthalmitis is the most dangerous complication and the first thing any doctor should rule out when presented with a patient complaining of visual symptoms following intraocular surgery. Patients typically present within days of surgery with severe pain, loss of vision and hyperaemia. They should be admitted and seen immediately by an ophthalmologist. Posterior lens capsule pacification is a relatively common complication of cataract surgery that usually occurs a few weeks following the operation. The typical patient complains of blurry vision as if their cataract has returned, and a white opacity may be visible on observation. The condition can be treated easily with a simple laser procedure which can be carried out as an outpatient. Other rare complications to be aware of are: • Retinal detachment Macular oedema Glaucoma • Corneal oedema
296
How is cataracts managed
Cataract surgery, sometimes referred to as pseudophakia, involves removing the lens that has developed a cataract, and replacing it with an artificial lens. The most common procedure used is phacoemulsification, which involves breaking down the existing lens with ultrasound waves before replacing it. It is a simple day case procedure which can be carried out under topical anaesthetic, general anaesthetic is reserved for special circumstances such as for use in children.
297
What is a cataract?
Lens opacification due to denatured proteins
298
Minimum VA driving standard?
6/12 Snellen 0.30 logMAR Both eyes
299
Perfect vision VA
6/6 Snellen 0.00 logMAR
300
Keeler Preferential Looking Cards
Testing VA ages 8 weeks to 12 months Tested using grating and objects behind to see if child looks, Tested at 0.38m
301
Cardiff Acuity Cards
Visual acuity testing 3-18 months. Simple picture located at top or bottom of the card. Test at 50cm or 1m. Examiner objectively observes if patient looks towards picture.
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Kay pictures
Visual acuity testing 2-4 years • Picture-based test (with matching card). • Crowded and uncrowded versions. • Test at 3m. • 4 optotypes on each line. Therefore each picture worth 0.025. • Recorded as LogMAR.
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LogMAR Keeler book
Visual acuity testing in children 4+ • Letter-based test (with matching card). • Crowded and uncrowded versions. • Test at 3m.
304
Symptoms of thyroid eye disease?
Gritty eyes / watery eyes Puffy eyelids Ocular pressure or pain Angry-looking eyes Bulging eyes Diplopia Visual loss (Field loss) (Dyschromatopsia – colour deficiency) Depression
305
What is almost always present in thyroid eye disease?
Lid retraction
306
What treatment for hyperthyroidism increases the risk of thyroid eye disease?
Radioiodine therapy
307
Cause of eye discharge?
Serous: viral conjunctivitis, secondary to FB Mucoid: allergic conjunctivitis Mucopurulent: bacterial conjunctivitis
308
What questions should you ask a patient presenting with blurred or decreased vision?
Laterallity Onset Duration Distance or near of both Peripheral or central vision Associated symptoms or signs (headaches, nausea, vomiting)
309
What is an amsler grid chart used to assess?
Visual distortion?
310
What should you ask a patient complaining of floaters or flashes about?
Cobweb Moves with eye movements Shower of black spots (retinal detachment/tare - ruptured blood vessels) Associated with the floaters True flashes or zigzag line Frequency Improving or worsening
311
How can the direction of diplopia suggest the aetiology?
Worse in direction of the palsied muscle
312
Relevant PMH for ophthalmic patients?
Lazy eye Squint (corrected in last?) Previous surgery Previous of current medication Diabetes HTN Collagen disease Asthma Autoimmune (RA, etc.)
313
What should be checked before examining the fundus?
Red reflex if absent - cataract will prevent anything being visible on fundoscopy
314
Fundus examination
Not for any media opacities While the patient is looking straight approach from the side at about 15 degrees Ap preach pupil maintain in centre of view Optic nerve surrounded by abudence of blood vessels - follow these to find Change lenses in ophthalmoscopee to focus Move to temporal side to visualise macula (lateral) Use same eye to examine patients eye, try to be at eye to eye level with pt
315
Subarachnoid haemorrhage
316
Investigations for acute angle closure glaucoma?
Gonioscopy (gold standard) Tonometry
317
Complications of acute angle closure glaucoma?
Sight loss Central retinal artery or vein occlusion Repeated episodes of AACG
318
What is a carotid cavernous fistula and how might it present
This a communication between the carotid artery and the cavernous sinus. All cranial nerves that run through the cavernous sinus may be affected which include (Ill, IV, V1, V2 and VI). The eye is usually proptosed with an injected conjunctiva and may be pulsatile.
319
What is Argyll-Robertson pupil?
Argyll-Robertson pupil refers to bilaterally small pupils that constrict on convergence but do not constrict in response to light. They are highly specific for neurosyphilis. Additionally, neurological examination elicits the typical signs of tabes dorsalis, also known as syphilitic myelopathy. This is another manifestation of late neurosyphilis.
320
What is the best investigation to confirm a diagnosis of orbital cellulitis?
CT sinus and orbits with contrast
321
Simple tests if VF is too low to perform with charts (even at a close distance)
Counting fingers Hand movements Perception of light No perception of light
322
Purpose of each type of cover test? What else might be observed?
Cover-uncover test - Manifest deviations Alternate cover test - lateral deviations Additional observations: Compensatory head posture (CHP) Ptosis Nystagmus Unequal pupils (Anisocoria)
323
What is esotropia?
Medial deviation of the eye (convergent)
324
What is inotropia?
Lateral deviation of the eye (divergent)
325
What is hypertropia?
Upwards deviation of the eye
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What is hypotropia?
Downwards deviation of the eye
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What is nystagmus?
Involuntary rhythmic oscillation of the eyes
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What type of cranial nerve palsy may cause a patient to adopt a CHP?
Fourth nerve palsy (TROCHLEAR)
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What is strabismus?
Also known as squint, a condition where the eyes point in different directions. One eye may turn inwards, outwards, upwards or downwards while the other eye looks forward.
330
What is the cover test method?
Use pen torch to observe corneal reflections (present and symettrical) Use and accomdative target (accomidation can affect the squint) Test 1/3m holding the target at eyelevel Test in the distance (6m) Test with and without glasses at all distances (refractive error can influence the squint) Test with and without a CHP at all distances
331
How is ocular motility graded
Between 0 and -4 0 Normal -4 eye cannot move past middle
332
At what age does the fovea fully develop?
4 to 6 months
333
Axial length in infants?
Shorter than adults
334
Up to what age does the visual cortex remain plastic?
Ages 7-9
335
What is amblyopia?
''Lazy eye'' Unilateral (less freq. bilateral) condition of reduced visual acuity in the absence of any obvious structual abnormality, a cortical adaption due to abnormal binocular environment
336
Causes of ambylopia?
Strabismus Amnisometropia High bilateral refractive error Stimulus deprivation - due to obscuration of the visual axis (ptosis, congenital, cataract) (ambylopia will persist even if problem resolves) High astigmatism
337
Most common causes of squints in children?
Refratcive error Family history prematurity Developmental delay Idiopathic
338
How should childhood squint be investigated?
VA, CT, OM, classification if posible Cycloplegic refraction (Cyclopentolate and tropicamide are drugs used to induce relaxation of the accomodation (focusing) system and mydriasis (pupil dilation) to allow for objective measurement of refractive error Fundus and media examination - to ensure strabismus is not the result of fundus of media pathology (2* strabismus), cataract, retinalblastoma
339
What investigations may be warrented if a child with strabismus presents unsually, there is evidence of paralytic strabismus, acommpanying red flag symptoms, e.g. severe headache, dizziness, nausea/vomitting?
CT/MRI to image head and orbits Blood test to assess for systemic conditions
340
Management of strabismus and amblyopia?
• A period of refractive adaptation is allowed for any glasses prescription issued (according to research 18-20 weeks). • Once refractive adaptation is complete it is essential to ensure that vision in either eye is equal. • If this is not the case a period of patching is undertaken to help improve the vision in the weaker eye. • Once vision is equal in either eye and the squint is still noticeable with a refractive correction the patient can then be considered for squint surgery should parents wish to pursue this. • It is important to note surgery is NOT a permanent fix and reoccurrence of the squint later on in life could occur. • However various studies have shown improved mental health and quality of life in patients who have had squint surgery as opposed to those patients who have not undergone squint surgery.
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Monocular double vision
Overlapping images with blurring Usually in one eye but can be both Will remain when one eye is covered Eyes will appear straight
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Horizontal binocular double vision
2 identical images seen next to each other Horizontal misalignment Occurs when the eyes become misaligned - nerve palsy, trauma Brain projects images from two different positions Resolves when one eye is converged
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Vertical binocular double vision
Two identical images on top of each other Vertical misalignment Occurs when the eyes become misaligned - nerve palsy, trauma Brain projects images from two different positions Resolves when one eye is converged
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Oblique binocular double vision
2 identical images at an angle to each other Diagonal misalignment Occurs when eyes are extorted/intorted
345
Why do patients with binocular diplopia have a higher risk of falls or accidents
Secondary confusing image Loss of depth perception
346
Why do people with childhood squints not have diplopia?
Retinal suppression. The image is never perceived consciously by suppressed area of the retina. Depending on whether the patient is esotropic or exotropic, either the nasal half or temporal half of the retina will be suppressed. Essentially making patients operate monocularly.
347
Classical features of occulomotor nerve palsy?
o Ptosis (complete or partial) o Eye depressed and abducted (down and out) o Pupil may be dilated and unreactive. o Diplopia (when ptosis lifted) diagonal (horizontal and vertical).
348
What is pupil involvement in a 3rd (occulomotor) nerve palsy?
Compressive aetiology
349
What does the superior branch of the occulomotor nerve supply?
LPS Superior rectus
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What does the inferior branch of the occulomotor nerve supply?
Medial rectus Inferior rectus Inferior oblique
351
Aetiologies of 3rd nerve palsy?
• Microvascular – Diabetes and hypertension risk factors • Posterior Communicating Artery (PCA) Aneurysm • Space occupying lesion • Trauma • Demyelinating disease • Infection • GCA • Congenital
352
What are the consequences of loss of innervation to LPS?
Ptosis Dilated pupil Unreactive pupil
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Implication of CN3 palsy on ocular movement
• Left complete upper lid ptosis. • Left exotropia (divergent eye). • Anisocoria – Left pupil larger than Right. • Pupil involvement indicating compressive aetiology.
354
What type of nerve palsy might a thromboses cavernous sinus aneurysm cause?
CN3 occulomotor
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Investigation and management of CN3 nerve palsy?
• Investigation: o Orthoptic: VA, CT, OM, Pupils o General: Blood tests, BP, scan (MRI, CT, MRA), biopsy • Treatment: • Treat underlying aetiology, microvascular likely to recover 6-9 months. • Prisms for diplopia. • Ptosis prop if only seeing eye. • Strabismus surgery if non-recovering to aid ocular alignment and alleviate diplopia.
356
Implications of trochlear nerve (CN4) palsy?
o Hypertropia (greater at near) slight esodeviation. o CHP Head tilt to unaffected side, chin depression (adaptation to correct diplopia) o Diplopia vertical (with torsional and horizontal components) o Torsion
357
When can prisms be utilised to correct diplopia?
Horizontal or vertical displacement Cannot alter tilt if torsional
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Causes of a trochlear nerve palsy?
Aetiologies: o Trauma (back of head) (susceptible as it leaves the brainstem backwards before curling around and projecting anteriorly) o Microvascular (DM, hypertension) o Demyelinating disease (MS) o Tumour o Aneurysm o Congenital
359
What tendon will be lax in congenital 4th nerve weakness?
SO tendon
360
Investigation and management of CN4 (trochlear) palsy?
Investigation: o Orthoptic: VA, CT, OM, pupils. o General: Image if unusual presentation, eg. young patient with no history of head trauma • Treatment: Monitor recovery, Prism, Surgery.
361
Implications of CN6 (abducens nerve) palsy?
o Esodeviation (larger in the distance). o CHP – Face turn towards affected side. o Horizontal diplopia (greater in distance and looking towards affected side, normal looking towards unaffected side) o Limited abduction. Esotropia in primary postion towards affected side
362
Abducens nerve palsy causes?
Exits the pins and runs over the oestrous temporal ridge, therefore susceptible to damage from raise ICP SOL Microvascular : diabetes, HTN Trauma Demyelinating lesions Infection
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Investigation and management of CN6 (abducens) never palsy?
• Investigation: o Orthoptic: VA, CT, OM, pupils, CV, PCT (prism cover test) measurements on side gaze o General: BP, bloods, scan (if non-recovering especially), ?LP (bilateral) • Treatment: • Treat underlying aetiology, • Monitor recovery – recovery likely in microvascular aetiology, usually 6-9 months. • Prisms for diplopia. • Surgery to aid ocular alignment and alleviate diplopia if non-recovering.
364
What type of thyroid disorder is thyroid eye disease (graves ortbitooathy) usually associated with?
Hyperthyroidism
365
What happens in thyroid eye disease?
Imflmmatory process affecting extraocular muscles and connnective tissues lasting months to years, then enters an inactive fibrotic phase
366
Features of graves orbitopathy?
o Proptosis – Finite space in bony orbit, EOM swelling forces globes forwards. o Optic neuropathy due to stretching and crushing (reduced VA, reduced CV, VF loss, pupil abnormality). o Upper lid retraction (corneal exposure). o Increased IOP. o Strabismus/restricted EOM (diplopia). Commonly the IR is first affected followed by MR
367
Management of thyroid eye disease?
Achieve euthyroid status (radiotherapy, anti thyroid medications, thyroidectomy) Smoking cessation can halt progression Steroids to help active inflammatory process Orbital decompression surgery Strabismus surgery or lid surgery in fibrotic stage
368
What is an orbital blow out fracture?
Break in orbital wall whilst orbital rim remind intact Secondary to assault of sporting injury, occuring as the orbital floor breaks acting as a crumple zone to protect the globe from rapid increase in intraocular pressure Orbital contents may drop downwards into the maxillary sinus May cause IR compression (trap door mechanism)
369
What might cause a unilateral proptosis?
An orbital mass or SOL, with associated ocular and orbital pain: Orbital tumour - optic nerve Glioma, schwannomas, sarcomas Retrobulbular haemorrhage Orbital pseudotumour
370
Management of unilateral proptosis?
• Prisms • Fresnel Prism – Temporary stick on prism • Incorporated Prism – Built into glasses • Occlusion • Eye patch • Occlusive contact lens • Blenderm – Translucent tape for glasses lens • Surgery • EOM surgery.
371
What is dysthyroid optic neuropathy?
Dysthyroid optic neuropathy (DON) is a sight-threatening complication of thyroid eye disease (TED), characterized by thyroid-related impairment of visual function, leading to permanent sight loss. To avoid blindness, prompt diagnosis and timely intervention are required. Hydraulic pressure causes optic nerve compression
372
What is CCF (carotid cavernous fistula)?
A carotid-cavernous fistula (CCF) is the result of an abnormal vascular connection between the internal carotid artery (ICA) or external carotid artery (ECA) and the venous channels of the cavernous sinus. May mimic other eye conditions such as thyroid eye disease, symptoms include: Bulging eyes. Swelling of the membranes that cover the outside of the eyes and line the eyelids. Forward displacement of the eyeballs. Deteriorating vision. Cranial nerve palsies. Nosebleed. Headache. Bruit (a blowing sound in the vessel that can be heard with a stethoscope)
373
If a patient is euthyroid but presenting thyroid antibodies what are they likely to have on blood test that is normal?
Raised autoantibodies
374
Which patients is typically affected by thyroid assosciated ophthalmopathy?
Patients aged 30-50 years More common in women but more often severe in men
375
Pathophysiology of thyroid associated opthalmopathy?
Autoimmune attack Antibody mediated reaction against the tsh receptor with orbital fibroblast modulation of T cell lymphocytes T cell lymphocytes are believed to react against thyroid follicular cells with shared antigenic epitopes infections the orbit
376
Relevance of ILGF1R in thyroid eye disease?
Insulin lie growth factor 1 receptor is an auto antigen that may be important in TAO Aberrant expression by TAO fibroblasts Promotion of T cell recruitment Circulating activating autoantibodies
377
In Graves disease, B and T lymphocyte-mediated autoimmunity are known to be directed at which well-known thyroid antigens?
Thyroglobulin Thyroid peroxidase Sodium iodide symporter Thyrotropin = TSH receptor (itself is the primary autoantigen of Graves’ disease and is responsible for hyperthyroidism)
378
What is the most common cause of unilateral and bilateral proptosis in adults, how does it present and how can it be identified?
Thyroid associated opthalmopathy Unilateral proptosis of TAO usually reflects asymmetric muscle involvement Retropulsion is a useful test (decreased retropulsion in TAO) Exopthalmometry can be used to measure orbital profusion Lacrimal gland enlargement is not uncommon
379
What is Dalrymple?
Upper lid retraction often with temporal flare and scleral show - most common ocular sign of TAK
380
Possible causes of lid retraction
Loss of sympathetic innervation of tarsal muscles Upgaze restirction Levator fibrosis Proptosis
381
What is von Graefe sign?
Lid lag on downgaze, an important feature of TAO
382
When might pseudoptosis be observed?
Contralateral lid retraction is present
383
Lid signs in TAO?
Lid lag Lid oedema Glabellar furrows
384
Anterior segment problems/abnormalities that may occur in thyroid eye disease?
Superficial punctuate keratitis Superior limb ischemia keratoconjuncgivitis Conjunctival injection usually over the rectus muscle insertions Conjunctival chemosis/swollen caruncle With severe proptosis corneal exposure with frank corneal ulceration may occur
385
IOP in TAO
Glaucoma may result from decreased episcleral venous outflow Because of restrictive myopathy, intraocular pressure may rise more that 8mmHg on upgaze Choroidal folds may be seen with TAO
386
Strabismus is common in with TAO, how does it often present?
Hypotropia of Esotropia because the inferior rectus muscle and the medial rectus muscle are the most commonly involved extraocular muscles
387
Visible optic nerve odema in cases of compressive thyroid optic neuropathy?
Most cases of compressive thyroid optic neuropathy occur without visible optic nerve oedema
388
What are deep glabellar rhytids
Frown lines, have significant association with thyroid opthalmopathy
389
What are pretibial dermolathy and thyroid arcopachy signs of?
Dysthyroidism
390
Mourtis score
DON Corneal involvement Strabismus Proptosis
391
Examination of a patient with thyroid eye disease?
Visual acuity Ishihara colour vision assessment Exophalmometry Orbital tension Assess lid lag, lagophthalmos and lid retraction Corneal exposure Conjunctival venous flow Intraocular pressure in primary gaze and elevation Pupils and optic discs Orthoptic assessment (field of binocular single vision, field of uniocular fixation, Hess chart and visual field study) Photos - old and studio pictures
392
What clinical activity score indicates a patient with thyroid eye disease is likely to benefit from immunosupression?
CAS greater than of equal to 4, points awarded in the following categories: Pain Redness Swelling Impaired function
393
TAO type I vs type II
Type I is characterised by minimal inflammation and restrictive myopathy - mainly fat expansion Type II is characterised by significant orbital inflammation and restrictive myopathy
394
Relevant investigations for thyroid eye disease
Serum free thyroxine TSH Anti thyroid antibodies: anti-thyroid peroxisdase antibodies (TPO), anti-TSH receptor antibodies FBC/ parental and liver profile ESR TMOT weight and blood pressure measurement Urinalysis CXR Photography CXR and Sinus X ray may be indicated Orbital imaging: MRI (helps to identify high signals in active extra ocular muscles) and CT scan (aids the diagnosis and assists the surgeon during decompression)
395
What further step is essential to prevent when treating wet ARMD, and how can this be achieved?
Prevention of further neovascularisation - anti-VEGF agents such as Bevacizumab (which can be injected directly into the vitreous to increase its bioavailability to the choroid)
396
What feature seen under slit lamp examination with fluorescein applied is pathognomonic of herpes simplex keratitis?
Dendritic ulcer
397
What eye disorder is associated with ankylosing spondylitis?
Anterior uvetitis
398
What antibiotic topical eydrops should be used in bacterial conjuncitvitis when conservative management has failed?
Topical chloramphenicol eyedrops
399
Mild, Non-Proliferative Diabetic Retinopathy features?
Microaneurysms only
400
Contents of the optic tracts
Left optic tract – contains fibres from the left temporal (lateral) retina, and the right nasal (medial) retina. Right optic tract – contains fibres from the right temporal retina, and the left nasal retina.
401
episcleritis vs scleritis
Scleritis involves inflammation of the full thickness of the sclera. Episcleritis is benign and self-limiting inflammation of the episclera, the outermost layer of the sclera. The episclera is situated just underneath the conjunctiva. Scleritis is more serious than episcleritis. Like episcleritis, scleritis an inflammatory condition - It is not usually caused by infection. Both have links to AID - RA, IBD (both) and SLE sarcoidosis GPA (more so scleritis) but episcleritis more l Presenting features different Scleritis: Severe pain and pain with eye movement, deep boating pain Episcleritis: mild or no eye pain - more of grittiness/FB sensation S: photophobia (absent in E) Both eye watering S: can be bilateral (E usually unilateral) S: tenderness to palpation of the eye S:reduced visual acuity S: abnormal réaction to light S: diffuse red eye, E: segmental E: dilated episcleral vessels S: does NOT blanch with phenylephrine drops E does
402
How to describe a lesion on fundoscopy
Size of lesion in terms of disc Location of lesion Pigmentation (hypo/hyper) colour (ie. orange is red flag) Flare or no flare (flare is reassuring) - flare meaning you can see blood vessels
403
Which is episcleritis and which is scleritis
404
What is the most significant complication of scleritis?
The most severe type of scleritis is called necrotising scleritis. Most patients with necrotising scleritis have visual impairment but may not have pain. It can lead to perforation of the sclera. This is the most significant complication of scleritis.
405
Scleritis management?
Consider an underlying systemic condition NSAIDS (topical / systemic) Steroids (topical / systemic) Immunosuppression appropriate to the underlying systemic condition (e.g. methotrexate in rheumatoid arthritis)
406
Episcleritis management?
If in doubt about the diagnosis, refer to ophthalmology. Episcleritis is usually self limiting and will recover in 1-4 weeks. In mild cases no treatment is necessary. Lubricating eye drops can help symptoms. Simple analgesia, cold compresses and safetynet advice are appropriate. More severe cases may benefit from systemic NSAIDs (e.g. naproxen) or topical steroid eye drops.
407
What is the orbit and what are its borders and anatomical relations?
Orbit is the pyramidal cavity in the facial skeleton which contains the eyeball and its associated muscles, and a number of nerves and vessels. Roof/superior wall: frontal bone and lesser wing of sphenoid Floor: Maxilla, zygomatic and palatine bones Medial: Ethomid, maxilla, lacrimal and sphenoid bones Apex: Located at the opening to the optic canal, the optic foramen Base: opens out into the face, bounded by eyeball. Is also known as orbital rim.
408
What separates the anterior cranial fossa from the orbit?
Frontal bone
409
What separates the orbit from the underlying maxillary sinus?
Maxilla
410
What separates the ethmoid sinus from the orbit?
Ethmoid bone
411
Contents of the orbit?
Extra ocular muscles Eyelids cover anteriorly Cranial nerves: Optic, oculomotor, trochlear, tirgeminal and abducens nerves Blood vessels: Opthalmic artery and inferior ophthalmic veins Orbital fat fills all other space, cusions the eye, and stablises the extraocular muscles
412
The walls of the orbit are thin and may fracture as a result of direct trauma or blows, except for which wall?
Lateral wall (zygomatic bone+greater wing of the sphenoid)
413
What are the three main pathways into the orbit and what do they contain? What are the minor openings?
Optic canal (optic nerve and ophthalmic artery) Superior orbital fissure (lacrimal, frontal, trochlear, oculomotor, nasocillary and abducens nerves, superior opthalmic vein) Inferior orbital fissure: transmits the zygomatic branch of the maxillary nerve, the inferior ophthalmic vein and sympathetic nerves Minor openings: nasolacrimal canal (drains tears from eye to nasal cavity, supra orbital foramen, infraorbital canal)
414
What is an orbital rim fracture?
Fracture of the bones forming the outer rim of the bony orbit (maxilla zygomatic and frontal) usually along the sututres joining these three bones
415
What is this?
Orbital blowout fracture Partial herniation of the orbital contents through one of its walls. This usually occurs via blunt force trauma to the eye. The medial and inferior walls are the weakest with the contents heniating into the ethmoid and maxillary sinuses respectively.
416
Why does orbital fracture cause exophthalmos?
Raised intraorbital pressure
417
What clinical sign is this?
Exophthalmos
418
What is the periorbita?
Periosteum lining the bones of the orbit, forming a sheath of the eyeball. Continous at the optic canal and supraoribtal fissure with the periosteal layer of the dura matter, over the orbital margin and through the infraorbital fissure, it is continous with the periosteum covering the external surface of the cranium
419
Protective mechanisms of the eye?
Eyelids: protect cornea and eyeball from injury, keep cornea moist by covering it with tear film. Inner surface of eyelids: lined by palpebral conjunctiva that if reflected onto the eyeball (where it is continous with the bulbar conjunctiva overlying the anterior surface of the eye.
420
What muscles are responsible for moving the eye lids and what are their respective cranial nerves?
Obicularis oculi - facial nerve Levator papebrae superioris - occulomotor nerve
421
What is the tarsal plate and what does it contain?
Dense fibrous tissue supporting the eyelids Contains: Tarsal (meibomian glands) - modified sebaceous gland secreting lipid Tarsal glands open at the lid margin along with glands of Moll (modified sweat glands), glands of Zeiss (sebaceuous glands)
422
What is this
Stye/Hordeolum/External hordoleum - resulting from acut infection of a gland of Moll, Zeiss or he eyelash folicle.
423
What is this
Chalazion/Internal hordelum/Eyelid cyst Swelling involving tarsal (meibomian) gland
424
What does the lacrimal apparatus consist of?
Lacrimal glands Lacrimal ducts Lacrimal canaliculi
425
Blockage of the tarsal/meibomian gland?
Chalazion/Internal hordeolum
426
Blockage of the gland of Moli, Zeiss or eyelash follicle?
Stye/hordeolum/external hordeolum
427
What do the lacrimal glands produce and what is the pathway of this fluid?
Gland secretes one of the component of tears Lies in a fossa on the upper part of the orbit Lacrimal fluid entering the conjunctival sac through the lacrimal ducts passes into the lacrimal lake (at medial angle of eye) Lacrimal fluid drains from lacrimal lake to lacrimal sac Fluid passes through nasal cavity through the nasolacrimal duct Passes from nasolacrimal duct into the nasopharynx where it is swollowed
428
Why does any obstruction of the lacrimal appartus cause problems, and what problems might occur?
Epiphora (overflow of tears) or infection may occur due to stagnant tears There are no anastomotic pathways for the drainage of tears
429
What is the function of tear film and what are its components?
Provides a smooth ocular furface for light rays to be refracted uniformly Prevent friction between ocular surfaces on closing the eyes Tears possess antibacterial properties Prevent ocular surface from 'drying out' which would cause damage to the epithelial surface of the cornea and conjunctiva - grittiness Surface lipid layer - meibomian (tarsal glands) Middle aqueous layer - lacrimal gland and accessory lacrimal glands Inner mucus layer - secreted by the goblet cells of the conjunctiva and the epithelial cell surface
430
Role of lipid layer of tear film, and where is it produced?
Produced by the meibomian (tarsal glands) Prevents evaporation of the underlying aqueous component
431
Why might dry eyes occur?
Deficiency of the tarsal glands (i.e. chalazion) causing reduce production of the lipid layer of tear film and therefore increased evaporation of the aqueous layer Reduced tear production (autoimmune: Sjogren's, RA, medication: antihistamines)
432
Consequences of dry eyes?
Epithelial surface of the cornea and conjunctiva is damaged - grittieness Predisposition to infection
433
How can a facial nerve palsy lead to an ineffective lacrimal pump?
Paralysis of obicularis occuli prevents complete eyelid closure and therefore loss of protective blinking of the eye Cornea becomes dry and is left unprotected from dust and other small particulate material Irritation of the eyebal results in excessive tear production and failure of the blink results in an ineffective lacrimal pump
434
The three layers of the eyeball?
Outer, protective layer: Sclera and the cornea. Fibrous, provides attachments for the extra ocular muscles. Middle: Choroid, cillary body and iris. Rich network of vessels. Inner layer: retina, consisting of optic and non visual parts
435
What part of the middle coat of the eye is both muscular and vascular?
Cillary body
436
Which part of the eye secretes aqeous humour that fills the chambers of the eye?
CIllary body
437
What is the choroid?
Dark membrane sitting between the sclera and the retina, forming the largest vascular layer of the eyeball
438
What is the anterior chamber?
Space between cornea and iris
439
What is the posterior chamber?
Space between iris and lens
440
What is this iris?
Lies on anterior surface of lense Thin contractile diaphragm with a central apeture (pupil) to allow for transmission of light. Two musclrs (sphincter and dilator pupillae) control pupil size
441
What fills the cavity behind the lens?
vitreous humor, which supports the lens and holds the retina in place
442
Layers of the retina?
Neural (light receptive) Pigmented layer
443
Posterior part of the eye?
Termed the fundus Circular depressed area - optic disc, where the optic nerve enters the eyeball
444
What does the optic disc contain?
Nerve fibers and no photoreceptor
445
What area of the retina contains photoreceptor cells specialised for the acuity of vision?
Macula lutea, sits just latterally to optic disc
446
What is the fovea centralis?
Depression in center of the retina, area of most acute vision.
447
What are these, and when are they seen?
Microaneurysms Microaneurysms are localised outpouchings of capillaries that leak plasma constituents into the retina. They may be clinically indistinguishable from small dot and blot haemorrhages Seen in background diabetic retinopathy
448
What are these, and when are they seen?
Dot and blot haemorrhages Dot and blot haemorrhages arise from bleeding capillaries in the middle layers of the retina. They may look like microaneurysms if small enough. It is not particularly important to be able to distinguish between small haemorrhages and microaneurysms as they are both parts of background diabetic retinopathy.
449
What are these, and when are they seen?
Cotton wool spots appear as small, fluffy, whitish superficial lesions. They are accumulations of dead nerve cells from ischaemic damage. The presence of retinal ischaemia represents a progression from background diabetic retinopathy to the pre-proliferative stage.
450
What are these, and when are they seen?
NVE - Neovascularisation elsewhere Insufficient retinal perfusion results in the production of vascular endothelial growth factor (VEGF) which results in the development of new vessels on the retina (neovascularisation). Proliferative diabetic retinopathy
451
What are these, and when are they seen?
NVD- Neovascularisation at the disc Insufficient retinal perfusion results in the production of vascular endothelial growth factor (VEGF) which results in the development of new vessels on the retina (neovascularisation). Proliferative diabetic retinopathy
452
What is this and why might it be present?
Pan-retinal photocoagulation is the primary treatment for proliferative diabetic retinopathy. The rationale behind the treatment is to reduce the production of VEGF by reducing the oxygen demand from the peripheral retina. Clinically it is seen as clusters of burn marks on the retina which have been created by the laser used in the treatment process.
453
What are these and in which condition are they seen?
Hard exudates Hard exudates are waxy yellow lesions with relatively distinct margins arranged in clumps or rings, often surrounding leaking microaneurysms. They are called “hard exudates” to distinguish them from “soft exudates”, an older term for cotton wool spots They are seen in diabetic maculopathy
454
What is this and when is it seen?
AV nipping Grade 2/3 hypertensive retionpathy
455
What is this clinical sign and when is it seen?
The image shows extensive haemorrhages, cotton wool spots, optic disc swelling and a ring of exudates around the macula (macular star). Mallignant hypertension
456
How is hypertensive retinopathy graded?
Grade 1 disease: the changes of early hypertensive retinopathy are subtle, with generalised arteriolar narrowing. Grade 2 disease: development of areas of focal narrowing, and compression of venules at sites of arteriovenous crossing (AV nipping). Grade 3 disease: development of features similar to those of diabetic retinopathy, namely retinal haemorrhages, hard exudates and cotton wool spots.
457
What is seen her and what condition does it occur in?
Cupping - increased vertical cup-to-disc ratio Glaucoma results in irreversible loss of nerve fibres, leading to an appearance of “cupping” or an increased vertical cup-to-disc ratio (C/D ratio).
458
What is seen here
Papillodema/optic disc swelling Optic disc margins appear blurred and small haemorrhages may be noted.
459
Hypopyon, acute extremely painful eye and blurred vision after cataract surgery suggests what?
In the context of an intra-ocular procedure (cataract surgery in this case), endophthalmitis is the most likely diagnosis. This is inflammation of the interior of the eye. The slit lamp examination shows a hypopyon (collection of white cells and debris) in the anterior chamber. This is an ophthalmic emergency and requires immediate sampling and broad spectrum antibiotics
460
Hypopyon, blurred vision and acute severe eye pain suggests what following cataract surgery?
In the context of an intra-ocular procedure (cataract surgery in this case), endophthalmitis is the most likely diagnosis. This is inflammation of the interior of the eye. The slit lamp examination shows a hypopyon (collection of white cells and debris) in the anterior chamber. This is an ophthalmic emergency and requires immediate sampling and broad spectrum antibiotics
461
Typical pupil in acute angle glaucoma?
Fixed dilated
462
Chlaky, white patches visible on the tympanic membrane, but it does not appear inflamed and is not bulging - suggestive of what
Tympanosclerosis May present with hearing deterioration, history of grommets and recurrent otitis media
463
What is Acanthamoeba keratitis
This is a rare disease in which amoebae invade the cornea of the eye. Contact lens wearers become exposed to the organism through contaminated water. It is a potentially blinding condition and is characterised by pain out of proportion to the findings, which include eye redness and decreased visual acuity
464
When might radiograph of the orbit be appropriate when a patient presents with a forigen body in the eye?
Radiographs are sometimes required if metallic foreign bodies penetrate the eye at a high velocity such as during welding
465
In left homonymous hemianopia with macular sparing, where is the lesion?
classically seen when disease affects the calcarine sulcus of the occipital cortex
466
Where is the lesion - ipsilateral anopia / monocular blindness
Optic nerve
467
Where is the lesion - bitemporal hemianopia
Optic chiasm
468
Where is the lesion - homonymous hemianopia
Contralateral optic tract
469
Where is the lesion - homonymous quadrantanopia
Contralateral optic radiation
470
What is the likely diagnosis in a patient who reports the sensation of a curtain falling down covering the visual field of one eye, preceded by a shower of sparks and floaters, in the absence of eye pain?
Retinal detachment, warrants slit lamp examination
471
What is keratitis?
Keratitis is a serious, potentially blinding condition resulting from bacterial, viral, fungal or protozoal infection of the cornea. Major risk factors include contact lens wearing, ocular trauma, dry eyes, blepharitis, immunosuppression and living in warm tropical climates. Symptoms typical of keratitis include severe eye pain, photophobia, foreign body sensation and loss/reduction of vision. Keratitis may present with the following signs: A red eye Corneal ulcer White corneal infiltrates Hypopyon (seen as a white fluid level)
472
Thyroid eye disease causes symptoms relating to eye movement (e.g. diplopia, dizziness, falls), proptosis (bulging of the eyes) and rarely visual loss - why
Autoimmune destruction of the extraocular muscles
473
What is a history of a central scotoma and the initial loss of ability to read small print suggestive of?
Macular degeneration
474
Periorbital vs orbital cellulitis features?
475
How does retinitis pigmentosa present?
Patients typically present with tunnel vision (reduced peripheral vision) and night vision problems. Eventually, retinitis pigmentosa leads to loss of all peripheral vision then central vision is affected. Occasionally, retinitis pigmentosa may present as part of a syndrome with non-ocular features including deafness associated with Usher’s syndrome and renal dysfunction associated with Bardet-Biedl syndrome. Fundoscopy shows characteristic dark brown, star-shaped aggregations all over the retina creating a mottled appearance.
476
What is AG indicative of
indicative of transient retinal ischemia
477
Fundoscopy findings in retinitis pigmentosa?
Characteristic fundoscopy findings include peripheral bone-spicule pigmentation, optic disc pallor and retinal vessel attenuation.
478
Fundoscopy findings in retinitis pigmentosa
Characteristic fundoscopy findings include peripheral bone-spicule pigmentation, optic disc pallor and retinal vessel attenuation.
479
Carotid artery bruit is a clinical finding associated with which ophthalmic complaint
Central retinal artery occlusion (often thromboembolic in nature originating form the carotid artery)
480
The description of a 'curtain rolling up/down' in the vision is classically associated with what?
retinal detatchment
481
First line treatment of glaucoma and common non harmful side effects?
latanoprost eye changing colour thickening and darkening of eyelashes
482
Patient presenting with dry side of face, eyelid droop and miosis
This is the classic description of Horner's syndrome. A significant cause of which is a tumour in the apex of the lungs (Pancoast's tumour). The tumour causes a pre-ganglionic Horner's syndrome, thus resulting in ptosis, miosis, and anhidrosis (loss of sweating)
483
Consequence of not correcting a childhood squint
pt will develop amblyopia
484
What is leukocoria
Leukocoria refers to a white pupillary reflex and can be caused by several conditions, one of which being retinoblastoma
485
Age related macula degeneration is the leading causes of blindness in the UK, what key finding appears in fundoscopy in both wet and dry ARMD? What other features do both have i. common?
A key finding associated with macular degeneration is drusen seen during fundoscopy. Atrophy of the retinal pigment epithelium Degeneration of the photoreceptors
486
Which type of ARMD is more common and which carried the worse prognosis
Dey 90%, wet carries worst prognosis (bleeding caused damage to the retina leading to fibrosis
487
Layers of the macula
The macula is made of four key layers. At the bottom, there is the choroid layer, which contains blood vessels that provide the blood supply to the macula. Above that is Bruch’s membrane. Above Bruch’s membrane there is the retinal pigment epithelium and above that are the photoreceptors.
488
What are these called and when are they seen?
Drusen are yellow deposits of proteins and lipids that appear between the retinal pigment epithelium and Bruch’s membrane. Some drusen can be normal. Normal drusen are small (< 63 micrometres) and hard. Larger and greater numbers of drusen can be an early sign of macular degeneration. They are common to both wet and dry AMD.
489
Wet AMD pathophysiology
In wet AMD there is the development of new vessels growing from the choroid layer into the retina. These vessels can leak fluid or blood and cause oedema and more rapid loss of vision. A key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF) and this is the target of medications to treat wet AMD.
490
Risk factors for AMD?
Age Smoking White or Chinese ethnic origin Family history Cardiovascular disease
491
Présentation of AMD?
Gradual worsening central visual field loss Reduced visual acuity Crooked or wavy appearance to straight lines NOTE wet AMD presents more acutely
492
Wet AMD course of disease
Wet age-related macular degeneration presents more acutely. It can present with a loss of vision over days and progress to full loss of vision over 2-3 years. It often progresses to bilateral disease.
493
Examination and diagnosis of AMD
Reduced acuity using a Snellen chart Scotoma (a central patch of vision loss) Amsler grid test can be used to assess the distortion of straight lines Fundoscopy. Drusen are the key finding. Slit-lamp biomicroscopic fundus examination by a specialist can be used to diagnose AMD. Optical coherence tomography is a technique used to gain a cross-sectional view of the layers of the retina. It can be used to diagnose wet AMD. Subretinal/intra retinal fluid loss and retinal fibrosis observed Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to look in detail at the blood supply to the retina. It is useful to show up any oedema and neovascularisation. It is used second line to diagnose wet AMD if optical coherence tomography does not exclude wet AMD.
494
Management of dry AMD
There is no specific treatment for dry age-related macular degeneration. Management focuses on lifestyle measure that may slow the progression: Avoid smoking Control blood pressure Vitamin supplementation has some evidence in slowing progression
495
Management of wet AMD?
Anti-VEGF medications are used to treat wet age-related macular degeneration. Vascular endothelial growth factor is involved in the development of new blood vessels in the retina. Medications such as ranibizumab, bevacizumab and pegaptanib block VEGF and slow the development of new vessels. They are injected directly into the vitreous chamber of the eye once a month. They slow and even reverse the progression of the disease. They typically need to be started within 3 months to be beneficial.
496
How does the choroid attach to the retina
The choroid attaches to the retina by way of a basement membrane known as Bruch’s membrane. This is important in the pathophysiology of Age Related Macular Degeneration
497
How does the choroid attatch to the retaina?
The choroid attaches to the retina by way of a basement membrane known as Bruch’s membrane. This is important in the pathophysiology of Age Related Macular Degeneration
498
What is the choroids rich layer of the capillary bed called and what does it supply?
choriocapillaris. It is this layer that supplies the outer half of the retina.
499
Where is the choroid found and what is it’s function?
The choroid is found lining the posterior part of the eye, extending from the ciliary body to the optic nerve lying between the retina and the sclera. As with the iris and ciliary body it too is a pigmented structure. The choroid has several important functions: 1. Allows nerves and vessels to reach the anterior eye by passing through the choroid 2. Removes waste product from the outer retina (area closest to choroid) 3. Supplies essential nutrients to the outer half of the retina 4. Absorbs any light passing through the retina, thus preventing it from reflecting back and interfering with vision
500
Most common method of cataract surgery and basic outline of what is done
Phacoemulsification is the most common technique for cataract surgery in the United Kingdom. It is usually performed under local anaesthetic and the patient must be prone. Entry to the eye is made via the limbus (peripheral cornea) using a self-sealing incision. A circular incision is made in the anterior lens capsule – capsulorrhexis. The cataractous lens is removed using ultrasound and replaced with a plastic lens calculated to correct the patients’ refractive error.
501
Main types of lenses implants for cataract surgery ?
Monofocal lens. These are the standard types of IOL implants used for patients who are having cataract removal. ... Toric lens. Toric lens are designed to correct the for nearsightedness with astigmatism or farsightedness with astigmatism. ... Multifocal and Accommodating lenses
502
Scleritis signs
Signs for this condition include violaceous discolouration of the sclera, decreased visual acuity and deep episcleral congestion on slit-lamp examination
503
Colour changes in graves obritopathy
colours appear 'washed out', and on further questioning, she finds that the colour red is most desaturated
504
For what ophthalmic complain is sublingual isosorbide dinitrate and apparopriate therapy to initiate?
Central retinal artery occlusion - sublingual isosorbide dinitrate is the most appropriate therapy to initiate, as it leads to the relaxation of smooth muscle cells and causes vasodilation, thus helping to increase blood oxygen content to the retina.
505
Sudden painless complete monocular loss of vision and pale retina
CRAO central retinal artery occlusion
506
Most important investigations in acute angle closure glaucoma
gonioscopy (gold standard investigation for assessing the angle between the iris and the cornea (iridocorneal angle) and is the definitive test for diagnosing angle-closure) tonometry (intra ocular pressure)
507
What is meant by IOP?
Aqueous humour is responsible for maintaining an adequate pressure in the eye. IOP is a balance between the rate of production of aqueous and the rate of drainage.
508
How is IOP controlled autonomically?
This is via adrenergic receptors. Cholinergic mechanisms have little direct effect on aqueous production. Alpha 2 receptors – stimulation reduces IOP by reducing aqueous production and may increase uveoscleral outflow Beta 2 receptors – stimulation increases IOP by increasing aqueous production
509
Drugs targeting IOP?
BETA BLOCKERS Timolol, Carteolol OD-BD Reduce production of aqueous ALPHA AGONISTS Apraclonidine, Brimonidine BD Reduce production and small increase in drainage of aqueous PROSTAGLANDIN ANALOGUES Latanoprost, Bimataprost ON Increase uveoscleral outflow of aqueous CARBONIC ANHYDRASE INHIBITORS Dorzolamide, Brinzolamide TDS Reduces production of aqueou PARASYMPATHOMETIC Pilocarpine QDS (when used as monotherapy) Increases outflow of aqueous by ciliary muscle contraction opening trabecular meshwork
510
Normal IOP
The ‘normal’ range of IOP is 11-21 mmHg. Above 21 is considered to be ocular hypertension.
511
Pathway of aqueous humour?
Aqueous is produced by the ciliary processes of the ciliary body. It then flows up between the iris and anterior surface of the lens and through the pupil. After passing through the pupil it flows out through the drainage angle of the eye, between the cornea and the peripheral iris, through the trabecular meshwork then into the Canal of Schlemm. Aqueous then drains into the episcleral vessels and finally into the systemic venous circulation. However, about 10-20% of aqueous is drained via an ‘unconventional’ or ‘uveoscleral’ route. Here, instead of aqueous passing into the trabecular meshwork it passes into the root of the iris and/or ciliary muscle before draining into the scleral vascular system.
512
Chambers of the eye
513
Chambers of the eye
514
Chambers of the eye
515
Examination of a patient with acute angle glaucoma might reveal what?
Red-eye Teary Hazy cornea Decreased visual acuity Dilatation of the affected pupil Fixed pupil size Firm eyeball on palpation
516
Mild vs moderate vs severe diabetic retinopathy
Mild: microaneurysms Moderate: microaneurysms, blot haemorhages, hard exudates, cotton wool spots and venous beading Severe: blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrates, intraretinal microvascular abnormality (IMRA) in any quadrant
517
Complications of diabetic reintopathy
Retinal detachment Vitreous haemorrhage (bleeding in to the vitreous humour) Rebeosis iridis (new blood vessel formation in the iris) Optic neuropathy Cataracts
518
Two basic features of diabetic maculopathy?
Macular oedema Ischaemic maculopathy
519
Clinical signs in hypertensive retinopathy
Silver wiring or copper wiring is where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light. Arteriovenous nipping is where the arterioles cause compression of the veins where they cross. This is again due to sclerosis and hardening of the arterioles. Cotton wool spots are caused by ischaemia and infarction in the retina causing damage to nerve fibres. Hard exudates are caused by damaged vessels leaking lipids into the retina. Retinal haemorrhages are caused by damaged vessels rupturing and releasing blood into the retina. Papilloedema is caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins.
520
Keith-Wagener Classification of hypertensive retionpathy
Stage 1: Mild narrowing of the arterioles Stage 2: Focal constriction of blood vessels and AV nicking Stage 3: Cotton-wool patches, exudates and haemorrhages Stage 4: Papilloedema
521
Presentation of cataracts
Symptoms are usually asymmetrical as both eyes are affected separately. It presents with: Very slow reduction in vision Progressive blurring of vision Change of colour of vision with colours becoming more brown or yellow “Starbursts” can appear around lights, particularly at night time A key sign for cataracts is the loss of the red reflex. The lens can appear grey or white when testing the red reflex. This might show up on photographs taken with a flash.
522
What are cataracts?
Cataracts are where the lens in the eye becomes cloudy and opaque. This reduces visual acuity by reducing the light that enters the eye.
523
Cataract risk factors
Increasing age Smoking Alcohol Diabetes Steroids Hypocalcaemia
524
Symptoms that can distinguish the causes of visual problems: cataracts vs MD vs glaucoma
Cataracts cause a generalised reduction in visual acuity with starbursts around lights. Glaucoma causes a peripheral loss of vision with halos around lights. Macular degeneration causes a central loss of vision with a crooked or wavy appearance to straight lines.
525
Causes of an abnormally shaped pupil?
Trauma to the sphincter muscles in the iris can cause an irregular pupil. This could be caused by cataract surgery and other eye operations. Anterior uveitis can cause adhesions (scar tissue) in the iris that make the pupils misshapen. Acute angle closure glaucoma can cause ischaemic damage to the muscles of the iris causing an abnormal pupil shape, usually a vertical oval. Rubeosis iridis (neovascularisation in the iris) can distort the shape of the iris and pupil. This is usually associated with poorly controlled diabetes and diabetic retinopathy. Coloboma is a congenital malformation in the eye. This can cause a hole in the iris causing an irregular pupil shape. Tadpole pupil is where there is spasm in a segment of the iris causing a misshapen pupil. This is usually temporary and associated with migraines.
526
Pupil constriction
There are circular muscles in the iris that cause pupil constriction. They are stimulated by the parasympathetic nervous system using acetylcholine as a neurotransmitter. The fibres of the parasympathetic system innervating the eye travel along the oculomotor (third cranial) nerve.
527
Pupil dilation
The dilator muscles of the pupil arranged like spokes on a bicycle wheel travelling straight from the inside to the outside of the iris. They are stimulated by the sympathetic nervous system using adrenalin as a neurotransmitter.
528
Causes of mydriasis (dilated pupil)
Third nerve palsy Holmes-Adie syndrome Raised intracranial pressure Congenital Trauma Stimulants such as cocaine Anticholinergics
529
Causes of miosis (constricted pupil)
Horners syndrome Cluster headaches Argyll-Robertson pupil (in neurosyphilis) Opiates Nicotine Pilocarpine
530
What does a CN3 nerve palsy with pupil sparing suggest as the underlying cause?
A third nerve palsy with sparing of the pupil suggests a microvascular cause as the parasympathetic fibres are spared. This may be due to: Diabetes Hypertension Ischaemia
531
What does a CN3 nerve palsy without pupil sparing suggest as the underlying cause?
A full third nerve palsy is caused by compression of the nerve, including the parasympathetic fibres. This is called a “surgical third” due to the physical compression: Idiopathic Tumour Trauma Cavernous sinus thrombosis Posterior communicating artery aneurysm Raised intracranial pressure
532
Caauses of Horners syndrome
The causes can be remembered as the 4 Ss, 4 Ts and 4 Cs. S for Sentral, T for Torso (pre-ganglionic) and C for Cervical (post-ganglionic). Central lesions (4 Ss): S – Stroke S – Multiple Sclerosis S – Swelling (tumours) S – Syringomyelia (cyst in the spinal cord) Pre-ganglionic lesions (4 Ts): T – Tumour (Pancoast’s tumour) T – Trauma T – Thyroidectomy T – Top rib (a cervical rib growing above the first rib above the clavicle) Post-ganglionic lesion (4 Cs): C – Carotid aneurysm C – Carotid artery dissection C – Cavernous sinus thrombosis C – Cluster headache
533
What problems does a third nerve plasy cause and why?
A third nerve palsy causes: Ptosis (drooping upper eyelid) Dilated non-reactive pupil Divergent strabismus (squint) in the affected eye. It causes a “down and out” position of the eye. The third cranial nerve is the oculomotor nerve. It supplies all of the extraocular muscles except the lateral rectus and superior oblique. Therefore when these muscles are no longer getting signals from the oculomotor nerve, the eyes moves outward and downward due to the effects of the lateral rectus and superior oblique still functioning without resistance. It also supplies the levator palpebrae superioris, which is responsible for lifting the upper eyelid. Therefore third nerve palsy causes a ptosis. The oculomotor nerve also contains parasympathetic fibres that innervate the sphincter muscle of the iris. Therefore third nerve palsy causes a dilated fixed pupil. The oculomotor nerve travels directly from the brainstem to the eye in a straight line. It travels through the cavernous sinus and close to the posterior communicating artery. Therefore, cavernous sinus thrombosis and a posterior communicating artery aneurysm can cause compression of the nerve and a third nerve palsy.
534
The location of the Horner syndrome can be determined by which feature?
The location of the Horner syndrome can be determined by the anhidrosis. Central lesions cause anhidrosis of the arm and trunk as well as the face. Pre-ganglionic lesions cause anhidrosis of the face. Post-ganglionic lesions do not cause anhidrosis.
535
What are the signs and symptoms of horners syndrome?
Horner syndrome is a triad of: Ptosis Miosis Anhidrosis (loss of sweating) They may also have enopthalmos, which is a sunken eye. Light and accommodation reflexes are not affected.
536
What can be used to test for Horner's syndrome?
Cocaine eye drops can be used to test for Horner syndrome. Cocaine acts on the eye to stop noradrenalin re-uptake at the neuromuscular junction. This causes a normal eye to dilate because there is more noradrenalin stimulating the dilator muscles of the iris. In Horner syndrome, the nerves are not releasing noradrenalin to start with so blocking re-uptake does not make a difference and there is no reaction of the pupil. Alternatively, a low concentration adrenalin eye drop (0.1%) won’t dilate a normal pupil but will dilate a Horner syndrome pupil.
537
What congenital syndrome is associated with hetrochromia
Congenital Horner syndrome is associated with heterochromia, which is a difference in the colour of the iris on the affected side.
538
What is a Holmes Adie pupil?
A Holmes Adie pupil is a unilateral dilated pupil that is sluggish to react to light with slow dilation of the pupil following constriction. Over time the pupil will get smaller. This is caused by damage to the post-ganglionic parasympathetic fibres. The exact cause is unknown but may be viral. Holmes Adie Syndrome is where there is a Holmes Adie pupil with absent ankle and knee reflexes.
539
WHat is an Argyll-Robertson pupil
An Argyll-Robertson pupil is a specific finding in neurosyphilis. It is a constricted pupil that accommodates when focusing on a near object but does not react to light. They are often irregularly shaped. It is commonly called “prostitutes pupil” due to the relation to neurosyphilis and because “it accommodates but does not react“.
540
Conjunctivits presentation
Conjunctivitis presents with: Unilateral or bilateral Red eyes Bloodshot Itchy or gritty sensation Discharge from the eye Conjunctivitis does not cause pain, photophobia or reduced visual acuity. Vision may be blurry when the eye is covered with discharge, however when the discharge is cleared the acuity should be normal. Bacterial conjunctivitis presents with a purulent discharge and an inflamed conjunctiva. It is typically worse in the morning when the eyes may be stuck together. It usually starts in one eye and then can spread to the other. It is highly contagious. Viral conjunctivitis is common and usually presents with a clear discharge. It is often associated with other symptoms of a viral infection such as dry cough, sore throat and blocked nose. You may find tender preauricular lymph nodes (in front of the ears). It is also contagious.
541
Painless vs painful red eye
Painless Red Eye Conjunctivitis Episcleritis Subconjunctival Haemorrhage Painful Red Eye Glaucoma Anterior uveitis Scleritis Corneal abrasions or ulceration Keratitis Foreign body Traumatic or chemical injury
542
Why do neonates with conjunctivitis require urgent ophthalmology review?
Patients under the age of 1 month of age with conjunctivitis need urgent ophthalmology review as neonatal conjunctivitis can be associated gonococcal infection and can cause loss of sight and more severe complications such as pneumonia.
543
What should patients with allergic conjunctivitis using Topical mast-cell stabilisers to manage chronic seasonal symptoms be adviseed?
May take several weeks before benefit shown
544
Common causes of corneal abrasion?
Contact lenses Foreign bodies Fingernails Eyelashes Entropion (inward turning eyelid)
545
When might you be concerned about infection in a patient presenting with corneal abrasion?
If the abrasion is associated with the use of contact lenses there may be infection with pseudomonas.
546
How does corneal abrasion tend to present?
History of contact lenses or foreign body Painful red eye Foreign body sensation Watering eye Blurring vision Photophobia
547
Management of corneal abrasion?
Management options include: Removing foreign bodies Simple analgesia (e.g. paracetamol) Lubricating eye drops Antibiotic eye drops (i.e. chloramphenicol) Follow-up after 24 hours Cyclopentolate eye drops dilate the pupil (they are mydriatics – causing mydriasis, meaning pupil dilation). They may be considered to help relieve symptoms, although evidence is lacking for their use in uncomplicated abrasions. Chemical abrasions require immediate irrigation for 20-30 minutes and urgent referral to ophthalmology. Uncomplicated corneal abrasions usually heal over 2-3 days.
548
How can corneal abrasions be diagnosed?
A fluorescein stain is applied to the eye to diagnose a corneal abrasion. This is a yellow-orange colour. The stain collects in abrasions or ulcers, highlighting them. Slit lamp examination may be used in more significant abrasions.
549
What is keratitis and what might cause it?
Keratitis is inflammation of the cornea. There are a number of causes of keratitis: Viral infection with herpes simplex Bacterial infection with pseudomonas or staphylococcus Fungal infection with candida or aspergillus Contact lens acute red eye (CLARE) Exposure keratitis is caused by inadequate eyelid coverage (e.g. eyelid ectropion)
550
Important differential for corneal abrasion?
?HSV keratitis
551
Herpes simplex keratitis is the most common form, what layers tend to be affected?
Herpes keratitis usually affects only the epithelial layer of the cornea. If there is inflammation of the stroma (the layer between the epithelium and endothelium), this is called stromal keratitis. This is associated with complications such as stromal necrosis, vascularisation and scarring and can lead to corneal blindness.
552
How does herpes keraitits present?
Painful red eye Photophobia Vesicles around the eye Foreign body sensation Watering eye Reduced visual acuity. This can vary from subtle to significant.
553
Investigating keratitis?
Staining with fluorescein will show a dendritic corneal ulcer. Dendritic describes the appearance of branching and spreading of the ulcer. Slit-lamp examination is required to find and diagnose keratitis. Corneal swabs or scrapings can be used to isolate the virus using a viral culture or PCR.
554
Management of herpes keratitis?
NICE Clinical Knowledge Summaries on red-eye say patients with potentially sight-threatening causes of red eye should be referred for same-day assessment by an ophthalmologist. Management options in secondary care: Aciclovir (topical or oral) Ganciclovir eye gel Topical steroids may be used alongside antivirals to treat stromal keratitis A corneal transplant may be required after the infection has resolved to treat corneal scarring caused by stromal keratitis.
555
What is subconjunctival haemorrhage?
Subconjunctival haemorrhages are a relatively common condition where one of the small blood vessels within the conjunctiva ruptures and release blood into the space between the sclera and the conjunctiva. They often appear after episodes of strenuous activity such as heavy coughing, weight lifting or straining when constipated. It can also be caused by trauma to the eye. A subconjunctival haemorrhage appears as a patch of bright red blood underneath the conjunctiva and in front of the sclera covering the white of the eye. It is painless and does not affect vision. There may be a history of a precipitating event such as a coughing fit or heavy lifting. They can be confidently diagnosed based on a simple history and examination.
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Why might subconjunctival haemorrhage occur?
Most cases are idiopathic and the patient is otherwise healthy, however there are a number of conditions that may have predisposed them to developing a subconjunctival haemorrhage. When a patient turns up with a subconjunctival haemorrhage use it as a clue to think about other conditions that may have contributed: Hypertension Bleeding disorders (e.g thrombocytopenia) Whooping cough Medications (warfarin, NOACs, antiplatelets) Non-accidental injury A subconjunctival haemorrhage appears as a patch of bright red blood underneath the conjunctiva and in front of the sclera covering the white of the eye. It is painless and does not affect vision. There may be a history of a precipitating event such as a coughing fit or heavy lifting. They can be confidently diagnosed based on a simple history and examination.
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Management of patients with subconjunctival haemorrhage?
Subconjunctival haemorrhages are harmless and will resolve spontaneously without any treatment. This usually takes around 2 weeks. Think about the possible causes such as hypertension and bleeding disorders. These may need investigating further. If there is a foreign body sensation lubricating eye drops can help with symptoms.
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What is posterior viterous detatchment?
The vitreous body is the gel inside the eye that maintains the structure of the eyeball and keeps the retina pressed on the choroid. The vitreous body is made up of collagen and water. With age it becomes less firm and less able to maintain its shape. Posterior vitreous detachment is a condition is where the vitreous gel comes away from the retina. It is very common, particularly in older patients.
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Presentation and management of posterior viterous detatchment?
Posterior vitreous detachment is a painless condition. It may be completely asymptomatic or patients may present with symptoms of: Painless Spots of vision loss Floaters Flashing lights No treatment is necessary. Over time the symptoms will improve as the brain adjusts. Posterior vitreous detachment can predispose patients to developing retinal tears and retinal detachment. They can also present very similarly. It is essential to exclude and assess the risk of a retinal tear or detachment with a thorough assessment of the retina. This is usually done by an optometrist or ophthalmologist.
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What does posterior vitreous detatchment predispose to?
Posterior vitreous detachment can predispose patients to developing retinal tears and retinal detachment. They can also present very similarly. It is essential to exclude and assess the risk of a retinal tear or detachment with a thorough assessment of the retina. This is usually done by an optometrist or ophthalmologist.
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What is retinal detatchment?
Retinal detachment is where the retina separates from the choroid underneath. This is usually due to a retinal tear that allows vitreous fluid to get under the retina and fill the space between the retina and the choroid. The outer retina relies on the blood vessels of the choroid for its blood supply. This makes retinal detachment a sight-threatening emergency unless quickly recognised and treated.
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Risk factors for retinal detatchment
Posterior vitreous detachment Diabetic retinopathy Trauma to the eye Retinal malignancy Older age Family history
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Retinal detachment presentation
Retinal detachment is a painless condition that can present with: Peripheral vision loss. This is often sudden and like a shadow coming across the vision. Blurred or distorted vision Flashes and floaters
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Retinal tare management
Management of retinal tears aims to create adhesions between the retina and the choroid to prevent detachment. This can be done using: Laser therapy Cryotherapy
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Retinal detatchment management
Management of retinal detachment aims to reattach the retina and reduce any traction or pressure that may cause it to detach again. This needs to be followed by treating retinal tears (laser therapy or cryotherapy). Reattaching the retina can be done using one of three options: Vitrectomy involves removing the relevant parts of the vitreous body and replacing it with oil or gas. Scleral buckling involves using a silicone “buckle” to put pressure on the outside of the eye (the sclera) so that the outer eye indents to bring the choroid inwards and into contact with the detached retina. Pneumatic retinopexy involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble creates pressure that flattens the retina against the choroid and close the detachment.
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Central retinal vein occlusion pathophysiology
Central retinal vein occlusion occurs when a blood clot (thrombus) forms in the retinal veins and blocks the drainage of blood from the retina. The central retinal vein runs through the optic nerve and is responsible for draining blood from the retina. There are four branched veins that come together to form the central retinal vein. Blockage of one of the branch veins causes problems in the area drained by that branch whereas blockage in the central vein causes problems with the whole retina. Blockage of a retinal vein causes pooling of blood in the retina. This results in leakage of fluid and blood causing macular oedema and retinal haemorrhages. This results in damage to the tissue in the retina and loss of vision. It also leads to the release of VEGF, which stimulates the development of new blood vessels (neovascularisation).
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How does central retinal vein occlusion present?
Sudden painless loss of vision
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CRVO risk factors
Hypertension High cholesterol Diabetes Smoking Glaucoma Systemic inflammatory conditions such as systemic lupus erythematosus
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What might be seen on examination in CRVO?
Fundoscopy examination is diagnostic of retinal vein occlusion. It give characteristic findings: Flame and blot haemorrhages Optic disc oedema Macula oedema
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Examination and investigation of central retinal vein occlusion
Fundoscopy examination is diagnostic of retinal vein occlusion. It give characteristic findings: Flame and blot haemorrhages Optic disc oedema Macula oedema Other Tests The Royal College of Ophthalmologists guidelines from 2015 suggest checking for possible associated conditions in patients presenting with retinal vein occlusion: Full medical history FBC for leukaemia ESR for inflammatory disorders Blood pressure for hypertension Serum glucose for diabetes
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Central retinal vein occlusion management
Patients with suspected retinal vein occlusion should be referred immediately to an ophthalmologist for assessment and management. Management in secondary care aims to treat macular oedema and prevent complications such as neovascularisation of the retina and iris and glaucoma. The options for this are: Laser photocoagulation Intravitreal steroids (e.g. a dexamethasone intravitreal implant) Anti-VEGF therapies (e.g. ranibizumab, aflibercept or bevacizumab)
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Central retinal artery occlusion aetiology
Central retinal artery occlusion occurs where something blocks the flow of blood through the central retinal artery. The central retinal artery supplies the blood to the retina. It is a branch of the ophthalmic artery, which is a branch of the internal carotid artery. The most common cause of occlusion of the retinal artery is atherosclerosis. It can also be caused by giant cell arteritis, where vasculitis affecting the ophthalmic or central retinal artery causes reduced blood flow.
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CRAO risk factors
Risk factors for retinal artery occlusion by atherosclerosis are the same as for other cardiovascular diseases: Older age Family history Smoking Alcohol consumption Hypertension Diabetes Poor diet Inactivity Obesity Those at higher risk for retinal artery occlusion secondary to giant cell arteritis are white patients over 50 years of age, particularly females and those already affected by giant cell arteritis or polymyalgia rheumatica.
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How does CRAO present?
Blockage of the central retinal artery causes sudden painless loss of vision. There will be a relative afferent pupillary defect. This is where the pupil in the affected eye constricts more when light is shone in the other eye compared when it is shone in the affected eye. This occurs because the input is not being sensed by the ischaemic retina when testing the direct light reflex but is being sensed by the normal retina during the consensual light reflex. Fundoscopy will show a pale retina with a cherry-red spot. The retina is pale due to a lack of perfusion with blood. The cherry-red spot is the macula, which has a thinner surface that shows the red coloured choroid below and contrasts with the pale retina.
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CRAO management
Patients with suspected central retinal artery occlusion should be referred immediately to an ophthalmologist for assessment and management. Giant cell arteritis is an important potentially reversible cause. Therefore older patients are tested and treated for this if suspected. Testing involves an ESR and temporal artery biopsy and treatment is with high dose steroids (i.e. prednisolone 60mg). Immediate Management If the patient presents shortly after symptoms develop then there are certain things that can be tried to attempt and dislodge the thrombus. None of these have a strong evidence base. Some examples are: -Ocular massage -Removing fluid from the anterior chamber to reduce intraocular pressure. -Inhaling carbogen (a mixture of 5% carbon dioxide and 95% oxygen) to dilate the artery -Sublingual isosorbide dinitrate to dilate the artery Long Term Management Long term management involves treating reversible risk factors and secondary prevention of cardiovascular disease.
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Night blindness is often the first symptom in retinitis pigmentosa - why?
Retinitis pigmentosa is a congenital inherited condition where there is degeneration of the rods and cones in the retina. Rods lost before cones in most genetic cases.
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Retinitis pigmentosa - management
General management involves: Referral to an ophthalmologist for assessment and diagnosis Genetic counselling Vision aids Sunglasses to protect the retina from accelerated damage Driving limitations and informing the DVLA Regular follow up to assess vision and check for other potentially reversible conditions that may worsen the vision such as cataracts There isn’t a huge amount of evidence supporting options to slow the disease process. Some options that may be considered by a specialist in certain scenarios include: Vitamin and antioxidant supplements Oral acetazolamide Topical dorzolamide Steroid injections Anti-VEGF injections Gene therapy is a potential future treatment that could alter the disease process and lead to better outcomes.
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Medical conditions that increase the risk of glaucoma
diabetes, migraines, high blood pressure and sickle cell anemia.
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Eye abnormalities in a CN3 palsy
adduction, elevation and depression whilst the eye is held in primary gaze is mediated by the medial rectus, superior rectus and inferior rectus respectively. The oblique muscles only elevate and depression the eye when the eye is held in adduction. If the pupil is also abnormally dilated, it is termed 'surgical'. Within the third nerve, the fibres to the pupil lie peripherally and those to the muscles centrally. Thus, dilation implies external compression, most classically from a posterior communicating artery aneurysm, which is treated surgically
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DEFINITIVE TREATMENT of primary angle closure glaucoma
Bilateral peripheral laser iridotomy
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Anisocoria worse in bright light implies what
Anisocoria worse in bright light implies a problem with the dilated pupil e.g. Adie's tonic pupil
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Scleritis vs episcleritis: pain
Scleritis is painful, episcleritis is not painful
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Anisocoria worse in bright light implies a problem with which pupil?
Anisocoria worse in bright light implies a problem with the dilated pupil
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What is the most common cause of amaurosis fugax?
Atherosclerosis of the ipsilateral internal carotid artery is by far the most common cause of amaurosis fugax
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HTN retinopathy grading
SAVE 1. Silvering ( retinal arteriole tortuosity ) 2. Arterio nipping 3. Venous haemorrhages 4. Edema
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What organsism should be suspected in contact lens associated keratitis?
Pseudomonas aeruginosa
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Advice for contact lens wearers weith conjuctivitis
Do not wear contact lenses until symptoms have resolved. Clean the eyelids with a wet cloth and apply a cold compress as needed to relieve symptoms

Year 4 Neurology and Special Senses (24 decks)

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