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Duke Elder: Finals Ophthalmology (Alice) > Loss of vision > Flashcards

Loss of vision Flashcards

1
Q

What is the first most important question to ask in loss of vision?

A

Is it painless or painful

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2
Q

Why is it important to ask about pain in loss of vision?

A

important for localisation; painful means affecting structures with rich sensory innervation (iris, cornea, sclera) but painless suggests lens structures further back in eye e.g. retina, such as macular degeneration and retinal detachment, glaucoma

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3
Q

What type of cause of loss of vision is the exception to the anterior=painful, posterior=painless rule?

A

Optic nerve pathology: can and often does cause pain, but associated with ocular movements

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4
Q

What are 7 important questions to ask in a loss of vision history?

A
  1. painful or painless?
  2. Duration
  3. Degree of vision loss
  4. Permanent or transient
  5. Central or peripheral loss
  6. One or both eyes
  7. Associated symptoms
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5
Q

Why is it important to ask about duration in los of vision?

A

sudden reduction tends to be vascular or rarely neurological; chronic diseases of the retina tend to have slow course, gradual impairment of vision

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6
Q

Why is important to ask about the degree of vision loss?

A

if sudden and complete –> neurological or vascular insult, blurring or loss of ability to read fine print implies difficulty focusing light on retina, tends to be caused by media opacity and varies with ambient lighting levels. Unusual to get complete visual los - NPL (no perception of light)

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7
Q

What are usually the causes of NPL (no perception of light)?

A

Significant neurological or vascular problems

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8
Q

What are 2 common causes of transient visual loss?

A
  1. Amaurosis fugax in transient ischaemic attacks (TIAs): black curtain over vision in one eye at a time resolving within 24 hours
  2. Optic nerve pathology - transient visual obscurations, or complete NPL for second or two
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9
Q

What does permanent visual loss suggest?

A

Significant structural damage to other structures of the eye e.g. macular degeneration or glaucoma

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10
Q

Why is it important to ask about central or peripheral loss of vision?

A

Localising pathology: central implies macular disease, peripheral suggests retinal detachment or glaucoma, or could be problem with neurological pathways to occipital cortex

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11
Q

What does both eyes simultaneously experiencing loss of vision suggest?

A

Neurological pathway problem, or macular degeneration/ diabetic eye disease/ glaucoma occurring at different rates

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12
Q

What does it tell you if just one eye experiences visual loss?

A

Localised pathology to eyeball or section of optic nerve connecting eye to chiasm

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13
Q

What are 3 key systemic diseases that affect the eye, meaning associated symptoms are important?

A

HTN, DM, vasculitis (e.g. co-existent kidney disease)

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14
Q

What are 2 key important parts of examination in patients with visual loss and why?

A
  1. visual acuity: need to know baseline acuity

2. Swinging light for RAPD: to detect early damage to optic nerve by comparing pupils

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15
Q

When performing the swinging light test for RAPD, which part of the eye’s response are you looking for?

A

Dilation rather than constriction: comparing constriction between the two eyes; consensual constriction will be normal but direct will be reduced, so what you see is diminished constriction as affected eye can’t constrict quick enough when light is shone directly. Affected eye continues to dilate for a few seconds when moving back to it before impulses travel back to the brain to overcome dilation

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16
Q

Where is the cause of painless loss of vision usually?

A

Back of the eye i.e. lens backwards: lens, vitreous, retina, some causes of optic nerve damage (glaucoma, optic neuropathy)

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17
Q

What are 9 causes of SUDDEN, painless loss of vision?

A
  1. Branch retinal vein occlusion
  2. Central retinal vein occlusion
  3. Branch retinal arteriolar occlusion
  4. Central retinal arteriolar occlusion
  5. Anterior ischaemic optic neuropathy
  6. Proliferative diabetic retinopathy
  7. Vitreous haemorrhage
  8. Retinal detachment
  9. WET age-related macular degeneration
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18
Q

What is the fovea and where is it located?

A

Centre of macula and part of eye with highest density of cone photoreceptors, 2.5 disc diameters temporal to the optic disc

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19
Q

What is the macula?

A

part of the eye we use for most visual tasks, 2 disc diameters in radius from the centre of the fovea

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20
Q

On a photograph of the back of the eye, how is the fovea identified?

A

Using a fixation marker: patient asked to look at a point while photo is taken, marker casts black shadow that points to fovea

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21
Q

What are the 4 arcades that retinal vasculature is split into?

A

Superotemporal
Superonasal
Inferotemporal
Inferonasal

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22
Q

What does each arcade of the retinal vasculature consist of?

A

Vein (thicker, darker vessel) and arterial (thinner, lighter coloured)

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23
Q

How will the retina appear in branch retinal vein occlusion?

A

Haemorrhages confined to area drained by that retinal vein branch; haemorrhages, lipid exudate, fluid leaks into retina

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24
Q

What may be the symptoms of branch retinal vein occlusion?

A

may pass unnoticed by patient and seen as incidental finding, or patient may be aware of blurring in peripheral part of vision

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25
Q

When to patients with branch retinal vein occlusion tend to present?

A

When a section of the retina involved overlaps the macula region –> causes profound reduction in vision

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26
Q

How does central retinal vein occlusion compare with branch retinal vein occlusion?

A

much more dramatic - widespread haemorrhages for central, 360 degrees all the way to the periphery, as well as fluid leakage, exudate into the retina

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27
Q

What causes central retinal vein occlusion?

A

Blockage of vein beyond the optic disc causing increased back pressure through the entire venous drainage of the eye

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28
Q

What are key risk factors for central retain vein occlusion? What are 3 key management steps?

A

Cardiovascular risk factors; therefore need to (1) optimise blood pressure and (2) blood sugar, and in (3) rarer cases think about clotting screens (e.g. younger patient)

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29
Q

Look at a picture of central retinal vein occlusion. What are 2 key features?

A

swollen disc, haemorrhages throughout retina

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30
Q

Look at a picture of central retinal vein occlusion. What are 2 key features?

A

swollen disc, haemorrhages throughout retina

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31
Q

What may cause arteriolar retinal branch occlusion and how might this be spotted?

A

Fibrin embolus, may appear as area of whitening within the blood vessel

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32
Q

What is an example of a blood vessel that could contain an embolus leading to branch retinal arteriole occlusion?

A

Branch of superotemporal retinal arteriole (could also be inferotemporal, superonasal and inferonasal)

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33
Q

What is the appearance of a retina with branch retinal arteriole occlusion?

A

Distal to blockage is area of infarcted retina, appears very white - has lost transparency; in contrast, normal retina is transparent (for light to reach photoreceptors in deepest parts) so has orange-pink glow from underlying choroidal circulation

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34
Q

Within what time frame after onset of BRANCH retinal arteriole occlusion can good function be restored?

A

within 4 hours of onset

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35
Q

What is the risk of patients with prolonged branch retinal arteriole occlusion?

A

Blockage in arterial supply to retina can cause profound reduction in function of photoreceptors in that area

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36
Q

What is the key principle of treatment of branch retinal arteriole occlusion?

A

drop pressure in eye as much as you can

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37
Q

Within what time frame might it be worth trying to restore normal circulation in the eye in branch retinal arteriole occlusion?

A

up to 24 hours (but within 4 hours higher chance of getting vision back)

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38
Q

What are 3 options to treat branch retinal arteriole occlusion?

A
  1. medically drop pressure: acetazolamide, beta blockers, mannitol, apraclonidine
  2. remove fluid from anterior chamber via paracentesis to shift clot along and restore blood supply
  3. rebreathe into brown paper bag, increasing CO2 concentration to cause vessels to dilate and increase blood supply
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39
Q

What are the symptoms of branch retinal arteriole occlusion?

A

acute onset painless, monocular vision disturbance; focal loss of vision due to only one branch being affected

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40
Q

What is commonly the cause of branch retinal arteriole occlusion?

A

arteriolar emboli, commonly originating from carotid arteries or AF

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41
Q

What 2 things should be examined in branch retinal arteriole occlusion, due to arterial emboli being a common cause?

A

auscultate for carotid bruit, feel radial pulse for arrhythmia

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42
Q

What 2 things should be examined in branch retinal arteriole occlusion, due to arterial emboli being a common cause? What 2 types of treatment may be needed if certain underlying causes are present?

A

auscultate for carotid bruit, feel radial pulse for arrhythmia. carotid endarterectomy or anticoagulation may be needed

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43
Q

What should be investigated for in BRAO if not embolic cause is found?

A

Coagulopathies - screen with blood tests

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44
Q

What is most likely the cause of central retinal arteriolar occlusion and how does this contrast with BRAO?

A

more commonly associated with inflammation, unlike BRAO which is often embolic

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45
Q

What could central retinal arteriolar occlusion be a presenting feature of?

A

Giant cell arteritis

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46
Q

What tests should always be performed in patients with CRAO?

A

inflammatory markers due to possibility of GCA

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47
Q

Look at a photograph of a retina showing central retinal arteriolar occlusion

A

white retina, cherry red spot at macula

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48
Q

What is the classical appearance of a retina with central retinal arteriolar occlusion?

A

ischaemic retina across a wider area than RAO with a cherry red macula temporally if soon after onset

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49
Q

What is a cherry red macula in CRAO a sign of?

A

early sign of central retinal artery occlusion

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50
Q

Why might a cherry red spot not be visible in CRAO?

A

it disappears soon after onset, as the retina tends to reperfuse and loses its whitish colour (however, no recovery of function if reperfuses)

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51
Q

if the retina is reperfused shortly after the onset of CRAO, does this mean there is recovery of function?

A

often not - can be cause of profound retinal pathology, e.g. causing NPL and RAPD

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52
Q

What is anterior ischaemic optic neuropathy?

A

blood supply to the optic nerve is lost

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53
Q

What are the two types of anterior ischaemic optic neuropathy?

A
  1. arteritic i.e. GCA

2. non-arteritic

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54
Q

What 2 types of risk factors can non-arteritic anterior ischaemic optic neuropathy be associated with?

A
  1. cardiovascular risk factors (like branch retinal vein occlusions)
  2. also sometimes seen in people with a small optic disc, where there isn’t much space for blood vessels so leads to mechanical obstruction of blood supply
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55
Q

What happens in vitreous haemorrhage?

A

blood pouring into vitreous cavity

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56
Q

What is the range of presentations like in retinal detachment?

A

Wide spectrum of presentation; can be innocuous flashers and floaters or quadrantanopic or hemianopic visual field loss in one eye (depends on extent of detachment)

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57
Q

What pathology occurs in anterior ischaemic optic neuropathy?

A

front part of the optic nerve loses its blood supply

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58
Q

What is the clinical appearance of the optic disc in AION?

A

instead of pink healthy appearance get pale, white, swollen optic disc with indistinct margins, blood vessels obscured as they pass through the edge of the nerve

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59
Q

What causes pallor of the optic disc in AION?

A

loss of blood supply

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60
Q

What key disease MUST be ruled out in AION?

A

Giant cell arteritis

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61
Q

What is usually the cause of AION if GCA can be ruled out?

A

same risk factors as other forms of stroke/vein occlusions - high blood pressure, high blood glucose

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62
Q

What are the symptoms of AION?

A

reduction or loss of vision

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63
Q

What occurs in proliferative diabetic retinopathy?

A

New vessels at the disc, lacy appearance over the disc

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64
Q

Look at an image of what anterior ischaemic optic neuropathy looks like in a retina.

A

pale, swollen optic disc, indisctinct margins, blood vessels obscured as passing through edge of nerve

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65
Q

Why does proliferative diabetic retinopathy occur?

A

response to hypoxia due to impaired blood supply –> compensation by upregulating pro-angiogenic signals to grow new blood vessels

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66
Q

What do the new blood vessels formed in proliferative diabetic retinopathy have a tendency to do?

A

often grow where they’re not wanted, can be leaky and result in haemorrhage. can also burst

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67
Q

What happens if blood vessels burst in proliferative diabetic retinopathy?

A

eye fills with blood, obscures path of light to the retina, causing a reduction in vision

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68
Q

What may be the consequence of a burst vessel in proliferative diabetic retinopathy?

A

can clear on its own but may take a long time; if actively bleeding, as blood starts to clear can bleed again

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69
Q

What may need to be done as treatment for a burst blood vessel in proliferative diabetic retinopathy if it doesn’t clear on its own/takes too long?

A

wash out back of eye to view what is causing the bleed and treat it

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70
Q

How common are vitreous floaters and what are they?

A

very common: areas of vitreous gel becoming solidified, casting shadow on retina as they move around

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71
Q

What is the most common cause of vitreous floaters and how serious is this?

A

posterior vitreous detachment; this is a normal age-related process as the vitreous jelly degenerates i the back of the eye, shrinks, collapses in on itself, forms black lines and dots

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72
Q

Why can vitreous floaters be more significant in a diabetic patient?

A

may be vessels bleeding in the back of the eye

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73
Q

What should be done if a diabetic patient notices a sudden increase in floaters in the eye?

A

could be vitreous haemorrhage due to vessels bleeding, must get it checked straight away as may be leaky blood vessels –> needs to be treated before progresses to full vitreous haemorrhage

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74
Q

What can posterior vitreous detachment occasionally be associated with?

A

retinal tears and detachments

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75
Q

What causes retinal detachment to occur?

A

posterior vitreous detachment; in areas where the jelly is firmly adherent - in the most peripheral anterior portion and around nerve and fovea - can lift retina in rare cases during posterior vitreous detachment, and with it may causes a retinal tear

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76
Q

Why does vitreous detachment cause the odd flash of light?

A

stimulates photoreceptors which brain perceives as flash of light

77
Q

What causes posterior vitreous detachment?

A

as a result of jelly degenerating in the back of the eye, collapsing in on itself and casting shadows on the retina (may be odd flash of light as jelly pulls from retina)

78
Q

What happens immediately following a retinal tear, and what could this lead to?

A

allows fluid to track under the retina, which may lead to retinal detachment

79
Q

What are the symptoms of retinal detachment?

A

more floaters, more flashing light, potential reduction in vision

80
Q

Look at a picture showing what retinal detachment may look like when examining the retina

A

Normal retinal architecture blurred, blood vessels not crisp, retina coming towards you. Fluid tracked under, may or may not involve macula, visible tear.

81
Q

How reversible is the damage caused by retinal detachment?

A

even if detachment is repaired and the fovea is put back in position, damage to central part which is very sensitive is often irreversible

82
Q

Why is it good to try and spot retinal tears/detachment early?

A

if you can spot it before it progresses to the macula region, can often preserve central retinal function so that there’s no significant reduction in central vision, just very mild in periphery

83
Q

Look at a drawing of retinal detachment on a diagram.

A

may show U-shaped tear, which is what allows fluid to get behind the retina and stretch it away from the inside of the eye

84
Q

What is the treatment for retinal TEARS if spotted early?

A

can apply laser around the tear, to produce scar tissue to prevent progression to retinal detachment. can often operate to put retina back in position again with good restoration of vision

85
Q

What causes prognosis to fall greatly in retinal tears?

A

as soon as there is macula involvement

86
Q

What should be the course of action for any patient with flashes and floaters?

A

should be seen by ophthalmologist within 24 HOURS OF SYMPTOM ONSET (according to NICE, if signs of sight-threatening diseases such as visual field or acuity changes, fundoscopic signs/vitreous haemorrhage; otherwise, refer to practitioner competent in using slit lamp and indirect ophthalmoscopy)

87
Q

What should be the management of retinal detachment that doesn’t involve the MACULA?

A

OPERATED ON WITHIN 24 HOURS OF DIAGNOSIS

88
Q

What are 3 types of surgery for retinal detachment that doesn’t involve the macula, depending on position/number/size of tears?

A
  1. Vitrectomy: removes vitreous attached to the retinal breaks. then gas/oil bubble spans and closes break
  2. Scleral buckling: silicone buckle placed on scleral surface over retinal breaks, to close off breaks
  3. Pneumatic retinopexy: gas bubble injected into vitreous cavity to close retinal break (relies on patient positioning over following days)
89
Q

What are 6 causes of RECENT onset (not sudden) painless loss of vision?

A
  1. Cataract
  2. Age-related macular degeneration (wet)
  3. Retinal detachment - if starts peripherally
  4. Primary open-angle glaucoma
  5. Maculopathy - diabetic or uveitic
  6. Papilloedema
90
Q

What type of cataract cause can lead to a rapid cataract formation?

A

significant ocular trauma: blunt trauma e.g. squash ball or cricket ball injury, can occur in 30 seconds as normal clearing processes disrupted by trauma

91
Q

What lesions occur in dry age-related macular degeneration?

A

Circular area of pallor - geographic atrophy of retinal pigmental epithelium leading to loss of photoreceptors

92
Q

Can anything be done to treat dry AMD?

A

no known treatment to reverse damage, can only slow progression; stop smoking, eat diet rich in leafy green veg (can reassure and will only lose central vision, won’t go completely blind)

93
Q

What type of AMD can be progressive over days to weeks?

A

Wet form; newly vascular membranes growing deep to the retina cause fibrosis and bleeding into macula, can cause sudden deterioration in vision

94
Q

Is wet AMD treatable and if so how?

A

Yes if caught early; use vascular endothelial growth factor (VEGF) inhibitors e.g. Lucentic, Eylea, Levastin which switch off drive to produce VEGF and reverse formation of vascular membranes.

95
Q

How frequent are VEGF inhibitor injections to treat wet AMD?

A

Monthly until happy vascular membrane is regressing

96
Q

What is vital in the treatment of wet AMD?

A

recognise and refer appropriately for early treatment

97
Q

What are the typical symptoms of wet AMD?

A

central visual loss, blind spots or areas of distortion (metamorphosia, problems reading words). Can also have dense central scotoma (problems with recognising faces, reading bus numbers, watching TV)

98
Q

What does a normal optic disc look like? (Look at a picture)

A

Round with clearly distinct margins, can see blood vessels clearly as they pass over the margin, with an area of pallor in the centre (cup)

99
Q

What is the cup in an optic disc?

A

dead space in a nerve, where axons are travelling forward through the nerve as they enter the eye. as they turn out and spread over the retina you can see the rim of the disc, the pink healthy part which is the nerve fibres spreading outwards

100
Q

What is the normal cup:disc ratio in a healthy person?

A

<0.3

101
Q

What causes the cup: disc ratio to increase in pathology?

A

if there is damage to the optic nerve, there is a loss of healthy axons, meaning the rim of peripheral healthy tissue reduces and pale dead space increases (typical of glaucoma, 0.8 ratio)

102
Q

Why does glaucoma cause the cup:disc ratio to increase?

A

raised pressure within the eye leads to damage of the optic nerve, which limits peripheral vision. tends to be asymptomatic until advanced

103
Q

What features are typical of diabetic maculopathy?

A

exudate, dot and blot haemorrhages across the macula; oedema at macula, leakage of fluid in addition to blood and exudate –> limits vision

104
Q

Look at a picture of diabetic maculopathy

A

key features are exudate, dot and blot haemorrhages

105
Q

What was the old treatment of diabetic maculopathy?

A

for diabetic RETINopathy use laser treatment to burn retinal pigment epithelium, causing scarring. this is still used in maculopathy but the laser is inherently destructive, damaging retina overlying the macula (archaic treatment)

106
Q

What is now the treatment of diabetic maculopathy?

A

VEGF inhibitors

107
Q

What is cystoid macula oedema?

A

intraretinal oedema contained in honeycomb-like (cystoid) spaces filled with clear fluid. retinal cells displaced by cysts. usually self limiting. common endpoint to many insults to macular area

108
Q

What are 7 causes of cystoid macular oedema?

A
  1. ocular inflammatory diseases e.g. uveitis, pars planitis, Behcet’s syndrome
  2. postoperative following cataract surgery aka Irvine Gass syndrome
  3. central and branch retinal vein occlusions
  4. retinal vascular diseases and retinal dystrophies
  5. drug-induced
  6. injury
  7. choroidal tumours
109
Q

What are the symptoms of cystoid macular oedema?

A

scotoma, impaired acuity, visual distortion, reduced colour sensitivity

110
Q

What is the treatment for cystoid macular oedema?

A

steroids: injected into or around eye, to reduce swelling

111
Q

What should papilloedema only be used to describe?

A

bilateral swelling of optic discs due to increased intracranial pressure

112
Q

How can you tell an optic nerve is swollen? Look at pictures.

A

loses normal pink healthy appearance, lose clearly distinct margin, hard to see where nerve starts. blood vessels crossing disc margin have areas where they disappear as swollen part of optic nerve wraps around and obscures. exudate over surface, cotton wool spots flame haemorrhages

113
Q

What does papilloedema imply the presence of?

A

space occupying lesion in brain until proven otherwise

114
Q

What are examples of space-occupying lesions that could cause papilloedema?

A

suprasellar meningioma, other pituitary pathology pressing on optic chiasm

115
Q

What action should be taken in any case of bilateral optic disc swelling?

A

order neuro-imaging to exclude space-occupying lesion as may be life-threatening that need neurosurgery - save patient life and vision in one go

116
Q

What can cause papilloedema if not SOL?

A

Idiopathic intracranial hypertension (IIH)

117
Q

What will IIH lead to over time?

A

visual loss - constriction of peripheral vision

118
Q

What are the symptoms of IIH?

A

May go unnoticed by patient, but could have raised ICP symptoms such as headaches worse when lying down, transient visual obscurations, nausea and vomiting, tinnitus –> prompt to look at optic nerves

119
Q

What are 5 possible associated symptoms with painless loss of vision to ask about?

A
  1. misty vision/glare - cataract
  2. distortion/central scotoma - macular
  3. flashes and floaters - vitreous/retina
  4. asymptomatic- if POAG
  5. peripheral hemianopic - visual pathway lesion
120
Q

What are 4 types of TRANSIENT painless visual loss?

A
  1. amaurosis fugax = fleeting blindness
  2. Giant cell arteritis or optic nerve pathology
  3. Embolic: carotids or AF
  4. Unilateral = eye, bilateral = brain (visual pthway or occipital cortex)
121
Q

What is amaurosis fugax?

A

painless temporary loss of vision, fleeting blindness which may last up to 24 hours but in transient visual obscuration (as in optic nerve pathology) occurs for seconds at a time

122
Q

In what way is giant cell arteritis painful?

A

painful but not in eye itself- temporal tenderness, jaw claudication, pain brushing hair

123
Q

Who is the typical GCA patient?

A

age 50 or over

124
Q

What kind of visual changes are often reported in GCA?

A

transient visual obscurations over days or weeks, or sudden painless loss of vision in one eye

125
Q

What systemic symptoms may GCA be associated with?

A

fatigue, weight loss, night sweats, loss of appetitie

126
Q

What disease is GCA strongly associated with and what are its symptoms?

A

Polymyalgia rheumatica: shoulder girdle pain, weakness in upper arms

127
Q

What will the superficial temporal artery appearance be like on examination in GCA?

A

prominent, tender to touch, pulseless, feel cord like (rather than soft and spongy)

128
Q

Why is it important to make an early diagnosis in GCA?

A

can cause strokes and heart attacks so can be rapidly fatal; can also cause rapid, painless irreversible visual field loss in one eye. if undiagnosed/untreated can quickly involve other eye

129
Q

How is diagnosis of GCA made?

A

one or combination of symptoms (rarely textbook findings), inflammatory markers ESR, CRP, FBC and elevated platelets

130
Q

What is the treatment for GCA?

A

high dose IV steroids

131
Q

What investigation can be performed to confirm diagnosis of GCA AFTER starting treatment?

A

temporal artery biopsy

132
Q

Who manages GCA without ophthalmic features?

A

general medical teams (most commonly rheumatologists) - if painless visual loss, ophthalmologists

133
Q

What are 5 causes of painful loss of vision?

A
  1. Keratitis
  2. Uveitis
  3. Angle closure glaucoma
  4. Optic neuritis (specifically retrobulbaroptic neuritis at back of eye, worse on eye movements)
  5. Trauma
134
Q

What is keratitis?

A

inflammation of the cornea

135
Q

What are 3 types of keratitis?

A
  1. Bacterial
  2. Viral - herpes SIMPLEX
  3. Acanthamoeba
136
Q

Look at a picture of what typical bacterial keratitis looks like

A

white infiltrate in centre of cornea, some surrounding haze, hypopyon

137
Q

What is the definition of hypopyon?

A

inflammatory debris in inferior part of anterior chamber

138
Q

What are 4 symptoms of bacterial keratitis?

A
  1. patient has few day history of eye feeling gritty,
  2. painful
  3. photophobic in bright sunlight
  4. reduced vision (due to haze in centre)- blurring of vision, inability to read as far down Snellen chart but overall vision reasonably functional
139
Q

What is the most common predisposing cause of bacterial keratitis?

A

contact lens misuse e.g. sleeping with in when shouldn’t, not paying proper attention to hand hygiene, washing in water not sterile solutions

140
Q

Why do contact lens issues commonly cause keratitis?

A

traps bacteria and other organisms on surface of eye in warm, moist environment, perfect place to proliferate, protected from tear film which usually prevents infection

141
Q

What is the viral cause of keratitis?

A

herpes simplex

142
Q

What are 4 symptoms of herpes simplex keratitis?

A
  1. Gritty foreign body sensation
  2. Vision problems - less blurring than bacterial keratitis but not quite right
  3. Red eye
  4. Lacrimation
143
Q

How can herpes simplex keratitis be diagnosed?

A

Drop of fluoroscein in eye, characteristic branching pattern with terminal bulbs at ends of branches: DENDRITIC ULCER of herpes simplex keratitis

144
Q

What associated symptom may be present in herpes simplex keratitis?

A

anyone who has had cold sore in past - virus may act in trigeminal ganglia but travel down ophthalmic division of nerve rather than mandibular to cause this appearance

145
Q

How does herpes simplex keratitis compare in terms of severity to bacterial keratitis?

A

appearance and presentation less severe in herpes simplex than bacterial

146
Q

In a patient who wears contact lenses, what type of keratitis should you always assume is the cause?

A

Acanthamoeba

147
Q

What is key to remember in acanthamoeba keratitis about the clinical signs in relation to symptoms?

A

symptoms are disproportionate to signs, in a lot more pain and light sensitive. often first misdiagnosed as herpes simplex keratitis

148
Q

How does treatment of acanthamoeba keratitis compare to herpes simplex keratitis/bacterial keratitis?

A

very different treatment, more difficult to treat, is more damaging to the eye and leads to horrible complications

149
Q

How is acanthamoeba keratitis diagnosed?

A

slit lamp, corneal scrape and culture or swab and PCR; sometimes detected with confocal microscope scanner: can show acanthamoeba cysts within various layers of the cornea

150
Q

How is acanthamoeba keratitis treated?

A

topical antimicrobial drops such as PHMB, chlorhexidine, brolene, hexamidine. every hour for first few days including over night, reduce to 2 hourly by day only, then less frequently. Anti-inflammatories, painkillers, dilating drop for painful spasms

151
Q

What is the uvea?

A

middle layer of eye between sclera and retina, consisting of iris anteriorly, ciliary body (intermediate) and choroid (posterior)

152
Q

What is the function of the ciliary body?

A

produces aqueous humour and hyaluronic acid for vitreous humour; also holds zonules in place and involved in accommodation

153
Q

What is uveitis usually referred to as?

A

acute anterior uveitis/ iritis

154
Q

What are 3 groups of causes of acute anterior uveitis and examples of each?

A
  1. trauma/surgery
  2. infection: bacterial e.g. TB, herpes zoster virus, toxoplasmosis
  3. Autoimmune: sarcoidosis, ankylosis spondylitis, Crohn’s disease/ulcerative colitis
155
Q

What are 5 symptoms of acute anterior uveitis?

A
  1. red eye
  2. aching pain in the eye
  3. blurred vision (rather than complete loss)
  4. photophobia, glare from bright lights
  5. irregular pupil
156
Q

What are 5 complications of acute anterior uveitis?

A
  1. cataract
  2. glaucoma
  3. optic nerve damage
  4. retinal detachment
  5. permanent visual loss
157
Q

What genetic correlation is there in acute anterior uveitis?

A

50% of all patients are HLA-B27 positive

158
Q

What is the range of percentage chance of patients with ankylosis spondylitis of getting acute anterior uveitis?

A

25-40% chance

159
Q

What are 2 examples of key clinical signs on examination of acute anterior uveitis?

A
  1. posterior synechiae

2. hypopyon

160
Q

What are posterior synechiae?

A

leakage of inflammatory exudate from vessels in the iris make the aqueous more sticky than usual, allowing adhesions between the iris and anterior surface of the lens –> may cause clover leaf pupil when dilating drops put in as tethered at the posterior synechiae

161
Q

What is a hypopyon?

A

Collection of inflammatory exudate in inferior aspect of anterior chamber under gravity, as cells infiltrate aqueous humour due to inflammation. settles at bottom and may be visible

162
Q

In which type of eyes is acute angle closure glaucoma commoner in and why?

A

hypermetropes (long-sighted), short eye ball so structures at the front of the eye are closer together, more likely to get occlusion of anterior chamber drainage angle

163
Q

At what time of day is acute angle closure glaucoma worse and why?

A

evening, due to ambient light level low so naturally more dilated pupils, more iris in the periphery of anterior chamber, more tissue which could drop outflow of aqueous fluid into the drainage angle

164
Q

What are 5 key symptoms of acute angle closure glaucoma?

A
  1. painful eye
  2. red eye
  3. sudden monocular vision loss
  4. blurriness of vision (due to corneal oedema/scattering of light, haze)
  5. haloes around lights
  6. nausea and vomiting, may be associated mallory-weiss tears - very unwell
165
Q

What is the clinical appearance of the eye in AACG?

A

fixed mid-dilated pupil, minimally reactive to light, red eye, corneal haze due to oedema

166
Q

Look at a picture of an eye with AACG

A

very red eye, very dilated pupil, haziness in cornea due to oedema

167
Q

What causes glare/haloes from bright lights in AACG?

A

as pressure goes high, normal mechanisms in cornea keeping it clear start to fail, so cornea becomes swollen and oedematous causing scattering of light, haloes around bright lights e.g. street lamps in evening

168
Q

What does reduction in vision in AACG tend to involve?

A

BLURRING –> SIGNIFICANT VISUAL LOSS –> NPL
At first tends to be blurring due to scattering of light as it moves through cornea;
Pressure remains high and progresses to a level sufficient to cause compression of nerve and blood vessels at back of eye, so develop secondary optic nerve problems or retinal artery occlusions leading to more significant visual loss.
Can rapidly lead to NPL in affected eye if untreated

169
Q

What is the management of AACG?

A

patients admitted, rapid medication to lower pressure in eye usually IV acetazolamide (diuretic) and range of topical agents

170
Q

What is the typical age range of patients with optic neuritis?

A

<30 years

171
Q

What is the typical presentation of optic neuritis?

A

Usually unilateral, often recurrent/ may be history of similar episodes in that or other eye previously. Pain on eye movement, reduced vision

172
Q

Why is there characteristic pain on eye movement in optic neuritis?

A

Nerve to the eye is swollen, every time eye moves around the nerve is moved, which, if swollen is painful

173
Q

What are 8 features of optic neuritis?

A
  1. unilateral
  2. recurrent
  3. pain on eye movement
  4. reduced vision
  5. RAPD often present
  6. central scotoma/altitudinal visual field defect (same as AION)
  7. reduced colour vision
  8. red desaturation
174
Q

What might patients with optic neuritis say about reduced colour vision?

A

this is rarely reported but if directly questioned, may say colours appear dimmer in one eye - if hold red pen in front, look with one then other eye

175
Q

What might the appearance of the optic disc be in optic neuritis?

A

may look normal; sometimes inflammation purely in stretch behind eyeball, sometimes subtle swelling, occasional haemorrhage at disc

176
Q

Does optic neuritis usually recover?

A

yes, usually recovers but never completely; usually worsens over two weeks, reaches lowest stage then gradual improvement over 6-8 weeks. in some cases, vision doesn’t return and have permanent impairment of vision e.g. permanent colour defect with normal acuity

177
Q

What proportion of patients with optic neuritis will get MS over the following 15 years?

A

up to 75%

178
Q

What is a common question asked by patients with optic neuritis?

A

does it mean i have multiple sclerosis - up to 75% may get in following 15 years. MS characterised by recurrent episodes varying in time and location

179
Q

What do the statistics for those patients that have optic neuritis that go on to have MS vary with?

A

whether there are white matter lesions on the MRI scan

180
Q

What should you be suspicious of if you see a significant injury to the eye?

A

be suspicious of injury elsewhere around the head and neck; also be aware patients with signiicant trauma may often also sustain ocular injury

181
Q

What type of trauma to the eye is more commonly missed?

A

chemical injury

182
Q

Why are alkali chemical injuries to the eye more dangerous than acid?

A

can penetrate intact cornea but acid tends to cause scarring at site of contact which limits penetrations

183
Q

How do patients tend to present with chemical injuries to the eye?

A

tend to know the injury has happened but may present days later as eye feels gritty, sore, vision blurred, red eye

184
Q

How should you be aware that intraocular foreign bodies can present?

A

may be painles aiwth minimal signs and vision of 6/6

185
Q

Why might there be few symptoms of IOFB?

A

eye has property that means small lacerations tend to self-seal, unless something directly in visual axis, small foregin bodies may go unnoticed

186
Q

Why is the mechanism of injury in IOFB key?

A

if patient involved in high velocity foreign body injury, important to examine thoroughly to make sure nothing has gone into eye

187
Q

Why do patients present early with minor injuries in form of bit of metal or foreign body on eye’s surface?

A

exquisitely painful, definite foreign body sensation and blurring of vision

188
Q

What is key in locating and dealing with eye foreign bodies?

A

good history of event and good examination to exclude more serious pathology

Duke Elder: Finals Ophthalmology (Alice) (20 decks)

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