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Clinical Opthalmology > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What conditions can cause secondary congenital glaucoma?

A
  • Aniridia
  • Sturge-Weber
  • Rubella
  • Anterior angle cleavage Syndrome
  • Micro cornea
  • Spherophakia
  • Persistent Hyper plastic Primary Viteous
  • Marfan’s
  • Homocystinuria
  • Neurofibromatosis
  • Retinopathy of Prematurity
  • Congenital Cataract
    –> most of these managed within hosp. when baby is born
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2
Q

Classification/mechanism of secondary glaucoma?

A

o Pre-trabecular: blockage in front of trab meshwork (ocular)
 Neovascular (diabetic ret), ICE syndrome (iridocorneal endothelial – corneal endo grows over trab & sometimes over iris), epithelial ingrowth (after injury or surgery, epithelial cells from conj or cornea)
o Trabecular: inside trab meshwork (ocular)
 Pigmentary glaucoma, red cell glaucoma, ghost cell glaucoma (RBCs lost blood), phacolytic glaucoma (advanced cataract can exude proteins, get trapped), hypertensive uveitis (cells from uveitis get stuck), pseudoexfoliative glaucoma (white particles stick in trab meshwork), oedema (inflammatory response – cells), scarring
o Post-trabecular: further towards brain
 Sturge-Weber syndrome (congenital manifestations w/ characteristic malformations observed in CNS, skin, & eyes; haemangiomas causing obstructions in outflow), carotid-cavernous fistulae (vascular communications between carotid artery & cavernous sinus), obstruction of superior venous cava

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3
Q

Describe Pseudoexfoliation Syndrome (PXE)?

A

Front surface of lens
White dots
Pupillary rough
Proteins released
Genetically predisposed
Cells under oxidative stress
Circular due to miosis/mydriasis of pupil  iris rubbing on lens  can gather on edge of pupil

PXE syndrome: proteins released due to oxidative stress – genetics involved, proteins are present in non-pigmented ciliary epithelial cells, trab endothelial cells & pre-equatorial lens epithelial cells
–> Material is released into extracellular space & deposited around cells that produced the material
–> Leads to altered metabolism, structure & function  Trab gets blocked

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4
Q

Describe Pigment Dispersion Syndrome?

A
  • Pigment on iris surface w/ ↑ pigmentation of trab meshwork
  • Pigment rubs off back of iris when surround structures rub agaisnt it – lens fibres
  • Clogs trab meshwork & pressure –> pigment in anterior chamber angle
  • Pigment dispersion: iris transillumination –> holes in iris where pigment released from –> perform this in pxs >40
  • Krukenberg Spindle: back surface of cornea, normally verical line of pigment in central cornea
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5
Q

When do pseudoexfoliation syndrome & pigment dispersion syndrome become pseudoexfoliation glaucoma & pigment dispersion glaucoma?

A

-Pseudoexfoliation (PXE) Syndrome (white dots but not optic nerve damage or VF changes) vs Pseudoexfoliation (PXE) glaucoma
-Pigment dispersion syndrome (see pigment (iris, angle, back surface of cornea) but normal VFs & discs) vs Pigment dispersion glaucoma

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6
Q

What is plateau iris?

A

Caused by narrowing of anterior chamber angle due to insertion of iris anteriorly on ciliary body or displacement of ciliary body anteriorly, which in turn alters position of peripheral iris in relation to trab meshwork (i.e. placing them in apposition)
Aqueous flows in fine but can’t get out

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7
Q

Secondary Closed Angle Glaucoma causes?

A
  • Swollen lens – mature cataract –> lens big/fat
  • Dislocated lens –> trauma/systemic condition causing weakness of lens fibres
  • Posterior synechiae (iritis) –> cells cause iris to stick to lens
  • Peripheral Anterior Synechiae
  • Rubeosis Iridis –> NV in iris –> NV scar tissue & can contract & close angle
  • Epithelial ingrowth/downgrowth –> any movement/contraction can cause angle to close
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8
Q

Glaucoma Previous Ocular History and family history?

A

o uveitis
o psuedoexfoliation
o pigment dispersion
o myopia

1st degree relative (mother/father/son/daughter/brother/sister)
o Ask who in H&S?

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9
Q

Glaucoma general health conditions & previous meds?

A

o Diabetes?
o High Blood Pressure?
o Peripheral Vascular disease
o Migraine
o Raynauds phenomenon
o Sleep Apnoea

o steroid use –> can ↑IOP

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10
Q

Glaucoma investigations to carry out?

A
  • Fundus: disc and nerve fibre layer (volk and imaging)
  • IOP
  • Visual fields
  • Corneal thickness
  • Angles
  • Gonioscopy
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11
Q

When to refer Glaucoma - IOP?

A
  • Irrespective of other signs of glaucoma, SIGN guidelines recommend referral when:
    o IOP is >26mmHg - irrespective of CCT (at risk of developing glaucoma in lifetime)
    o IOP 21-26, central corneal thickness is <555µm and patient is aged under 65
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12
Q

When to refer Glaucoma - Angles?

A
  • Irrespective of other signs of glaucoma, SIGN guidelines recommend referral when:
    o Risk of angle closure:
     Using Van Herricks technique, a peripheral angle with of less than a quarter of the corneal thickness (≤ Grade 2)
     Using Gonioscopy, when posterior trab meshwork is not visible for ≥ 270 degrees
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13
Q

When to refer Glaucoma - Fields?

A
  • Irrespective of IOP, pxs with one or more of the following findings should be referred to secondary eye care services:
    o A reproducible visual field defect consistent with glaucoma
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14
Q

When to refer Glaucoma - discs?

A
  • Irrespective of IOP, pxs with one or more of the following findings should be referred to secondary eye care services:
    o Optic disc signs consistent with glaucoma in either eye
    o Pxs with an optic disc hemorrhage
    o Pxs with cup to disc asymmetry – (difference in C:D of 0.2 or greater consider referral?)
    o Narrowest rim/disc ratios:
     Identify narrowest rim ratio
     OR estimate degrees of absent rim is completely lost
     Compare size of rim to size of disc
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15
Q

Disc evaluation in glaucoma - what to record for suspicious discs?

A
  • For suspicious discs, record:
    o C:D
    o Other disc features
    o Volk lens being used  important as mag changes & can influence C:D & rim:disc
    o Rim/disc ratio
    o Size of disc
    o DDLS score  disc damage likelihood score – likelihood disc will be damaged from glaucoma
  • Start from centre of disc (cup, edge of cup, NRR, edge of disc, sclera/retina)
    o Look for where BVs change direction
  • Ask self: Is this eye likely to have glaucoma? – consider age, ethnicity, FH, gender, results of other investigations
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16
Q

How to measure size of the optic disc?

A
  • Measure size of disc  bigger disc have naturally bigger cups
  • Volk Super 66 has a 1:1 ratio of size of what measured  Volk 90 is the measurement times 1.30
  • Beware of PPA & myopic crescents when estimating disc size
  • Reduce width of beam to 1-2mm
  • Set SL beam to height of disc
  • Small disc size: <1.5mm
  • Medium disc size: 1.5-2.0mm (will be 1.1-1.5mm when using a 90D lens)
  • Large disc size: >2.0mm
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17
Q

What are abnormal glaucomatous fundus signs?

A
  • Not following ISNT rule (DO NOT USE THIS IN ISOLATION)
  • ↑ C:D (consider disc size)
  • Pallor ≠ cupping; barred blood vessels
  • Disc haemorrhage
  • Peripapillary atrophy (PPA)
  • Altered appearance of RNFL
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18
Q

What is the definition of glaucoma?

A
  • Refers to a group of disorders in which there is eventual development of an optic neuropathy with characteristic changes at ONH. These changes are likely to lead to a depression of visual function and eventual loss of VF.
  • Raised IOP often appears to be a significant factor in its development.
  • Group of disorders
  • Characteristic optic neuropathy – characteristic changes at ONH w/ loss of retinal GC nerve fibres
  • VF defect w/ characteristic patterns  consistent w/ loss of nerve fibre layer GCs
  • IOP is often a factor in development/progression of the neuropathy
    o Other factors e.g. ischaemia in ONH & GC apoptosis also involved
    o Severity of glaucoma at presentation is major factor in development of glaucoma blindness
    o Socioeconomic deprivation has been linked w/ late presentation of glaucoma in UK
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19
Q

Genetic factors in Glaucoma - family hx, ethnicity?

A
  • Glaucoma associated w/ systemic/ocular syndromes
  • FH: 6-fold ↑ risk of developing POAG if 1st degree relative w/ glaucoma
  • Racial factors:
    o POAG – African descent
    o ACG – Asians, Chinese
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20
Q

What are the risk factors of glaucoma?

A
  • IOP
  • Age
  • Family history
  • Rx
  • Central Corneal Thickness
  • Pseudoexfoliation
  • Pigment dispersion
  • Shallow AC
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21
Q

What are systemic factors that may lead to/indicate glaucoma?

A

-Drug hx
-Migraine
-Raynauds
-Vascular hx

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22
Q

Classification of ocular hypertension?

A
  • Risk factor for POAG
  • IOP > 21mmHg in absence of disc or field damage
  • NOT glaucoma but risk factor for developing it
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23
Q

Classification of Primary Open Angle Glaucoma?

A
  • High pressure (POAG) – >21mmHg w/ damage to disc & field damage
  • Normal pressure (NTG) – damage to disc & field but normal IOP
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24
Q

Classification of Primary Angle Closure Glaucoma?

A
  • Anterior segment anatomical abnormality or variant that predisposes person to developing:
    o Acute angle closure glaucoma
    o Intermittent angle closure glaucoma
    o Chronic angle closure glaucoma (mixed mechanism)
  • Raised IOP w/ risk of disc & VF damage
  • Associated with aging process & changes that take place in anterior segment with age (relative ↑ in size of lens or development off cataract) & the position of the iris-lens diaphragm
  • Plateau iris synsdrome
  • PACS – Primary Angle Closure Suspect:
    o 3 quadrants or more of iridotrabecular contact (ITC) but no peripheral anterior synechiae (PAS), normal IOP, disc & field
  • PAC – Primary Angle Closure:
    o ITC as above but w/ ↑ IOP &/or PAS but normal disc & field
  • PACG – Primary Angle Closure Glaucoma:
    o 3 quadrants or more of ITC w/ raised IOP & disc/field damage
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25
Q

Classification of Secondary Open Angle Glaucoma?

A
  • Anatomically like POAG w/ free access to trab meshwork but something causes malfunction of trab meshworks ability to drain aqueous at normal rate
    o Pseudoexfoliation syndrome/glaucoma
    o Pigment dispersion syndrome/ pigmentary glaucoma
    o Steroid induced glaucoma (topical, creams, systemic)
    o Phacolytic glaucoma – related to leakage of lens protein in mature cataract
    o Ghost cell glaucoma/Hyphaema – bleeding in eye either in vitreous or AC leading to blockage of trab meshwork by RBCs
    o Uveitis – can cause secondary open angle or closed angle glaucoma – sometimes steroids for it cause the glaucoma
    o Trauma – can result in damage to trab meshwork or inflammation of trab meshwork – can be chronic leading to damage to optic nerve & field over time
    o Raised episcleral venous pressure  causes back pressure of venous system in orbit, translates through into Schelmm’s canal & to trab meshwork making it more difficult for aqueous to get out  ↑IOP
     E.g. Sturge-Weber Syndrome (inherited)
     Dysthyroid Eye Disease (DED) – swelling in orbit & thickened muscles which leads to raised IOP & pressure on venous system
  • More than just these examples
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26
Q

Classification of Secondary Closed Angle Glaucoma?

A
  • Anatomically similar but not identical to PACGs – access to trab meshwork is retricted by some anatomical change secondary to usually another ocular disease or abnormality
    o Phacomorphic – swelling of lens over time, in pxs with already smaller angles e.g. hyperopic – can result in gradual closing and raise in IOP
    o Post-vitreoretinal or post-corneal graft surgery (mainly penetrating keratoplasty)
    o Ectopia lentis – displacement of lens in eye (due to Marfans, Ehlers Danlos, trauma)
    o Post segment tumours – can push iris-lens diaphragm forward
    o Aniridia – absence of iris or bunch up of iris can block angle
    o Aqueous misdirection syndrome – can happen following intraocular surgery
    o Uveitis – w/ chronic inflammation in eye, iris can gradually become adhered to trab meshwork & cause peripheral anterior synechiae & scar tissue formation, resulting in gradual closing up of angle
    o Rubeosis iridis – often secondary to ischaemia e.g. diabetic retinopathy, vein occlusions –> NV in iris & angle, gradually causes closing of angle & ↑IOP
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27
Q

Classification of congenital/developmental glaucomas?

A
  • Tend to arise from birth/infancy or in children & young adults
    o Congenital glaucoma – autosomal recessive inheritance
    o May see haab’s striae – linear cracks in Descemet’s membrane
    o Anterior segment dysgenesis syndrome like Iridocorneal Endothelial syndrome (ICE) or Axenfeld-Reiger syndrome
    o May see corectopia pupil
    o Juvenile Onset glaucomas
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28
Q

Signs & symptoms of POAG/NTG?

A
  • Signs:
    o Raised (POAG) or normal (NTG) IOP
    o Open angle or deep anterior chamber
    o Abnormal optic disc cupping
    o Abnormal VF (can often be normal in early stages when disc shows changes)
  • Symptoms:
    o None until advanced or paracentral VF defect (may then become aware)
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29
Q

Signs & symptoms of chronic angle closure glaucoma (CACG)?

A
  • Presentation v similar to POAG but anatomical clinical findings are v different yet sometimes subtle & can develop over time in pxs previously diagnosed w/ POAG or NTG
  • Signs:
    o Raised or normal IOP
    o Open but narrow angle or moderate/deep AC (can sometimes be shallow)
    o Abnormal optic disc cupping
    o Abnormal VF
    o Shallow AC
    o 3 plus Quadrants of ITC on gonioscopy
    o Hypermetropia – usually goes hand in hand with small eye & more crowded anterior segment
  • Symptoms:
    o None as per POAG
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30
Q

Signs & symptoms of intermittent angle closure glaucoma (ACG)?

A
  • Signs:
    o Raised or normal IOP
    o Narrow angle
    o +/- abnormal optic disc cupping
    o +/- abnormal VF
    o Shallow AC – narrow angle on Van Herick’s or gonioscopy
    o 3 plus quadrants ITC on gonioscopy
    o Hypermetropia
  • Symptoms:
    o Intermittent brow ache
    o Haloes
    o Often resolve after short period of time
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31
Q

Signs & symptoms of Acute Angle Closure Glaucoma (ACG)?

A
  • Signs:
    o Red eye
    o Fixed mid-dilated pupil
    o Hazy blue/green cornea – due to corneal oedema
    o Iritis – associated with high IOP
    o IOP>40mmHg
    o Shallow AC – hard to see with hazy cornea
  • Symptoms:
    o Blurred vision/haloes
    o Brow ache/headache
    o Nausea
  • Medial ophthalmic emergency as visual loss is rapid & condition must be referred EMERGENCY
  • Px generally unwell
  • Images show typical appearance of eye at risk or fellow eye & eye is affected
  • Gonioscopy shows closed/narrow angle in other eye or eye at risk & an anterior segment OCT
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32
Q

Mechanism of damage in glaucoma?

A

Loss of retinal GCs & their axons leading from optic nerve to brain
o Both glial & nerve cells are affected
* Ischaemic changes at ONH as well as raised IOP & development of inflammatory changes at ONH in form of release of free radicals (nitrous oxide & glutamate) which cause further neuronal loss
o Some of these changes may also be toxic changes where dying cells (due to ↑ IOP/ischaemia) release toxic substances which affect adjacent cells & cause them to become sick & eventually die
* Apoptosis – programmed cell death

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33
Q

Pathogenesis of Primary Angle Closure Glaucoma (PACG)?

A
  • Always involves ↑ IOP but many of other mechanisms e.g. ischaemia, neurodegeneration & apoptosis are probably also in play after initial high pressure insult
  • Limited access to trab meshwork is initially main cause followed over time by trab dysfunction even after successful tx of underlying anatomical issues of angle closure
  • Restricted access to trab meshwork:
    o Hypermetropia (e.g. +2.00)
    o Shallow anterior chamber
    o Small eyes (short axial length)
    o Anteriorly inserted iris
    o ↑ in lens size
    o Dilatation of pupil – can precipitate bunching up of iris in angle & lead to angle closure (happens physiologically when pupil dilates or pharmacologically when px is dilated)
    o Trab dysfunction –> may be able to open up drainage angle in eye by doing iridotomy but sometimes IOP will still be elevated & continue to climb
    o Narrow gonioscopic angle
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34
Q

Mechanism of Chronic Angle Closure (PACG)?

A

Iris slowly comes into contact w/ ↑ area of trab meshwork, resulting in trab meshwork dysfunction & gradual rise in IOP

35
Q

Mechanism of Intermittent Angle Closure (PACG)?

A

o Angle is narrow but open, but certain physiological states (producing dilation – e.g. dim light) lead to transient rises in IOP which resolve over variable periods of time (~20-30mins)
 Often produces transient symptoms of acute angle closure – experience headache/brow ache around eye or haloes then resolve
o Eventually this type of eye will develop either CACG or more acutely AACG
o Pupil block which occurs spontaneously resolves

36
Q

Mechanism of Acute Angle Closure (PACG)?

A

o Dilation of pupil (physiological or otherwise) leads to angle becoming closed
o Marked rise in IOP due to:
 Pupil block
 Peripheral iris tissue occluding angle
 (Often both present simultaneously)
o Similar to intermittent ACG but attack is permanent & can be devastating to site & subsequent successful management of px
o This type of attack can & freq occurs w/ no previous hx of IAC attacks
o Underlying mechanism in IACG and AACG attacks is something known as Pupil block
 Pupil is in a physiological mid dilated state & comes into contact with lens
 Temporarily in these px prevents aqueous from making its way from posterior chamber into the AC and to trab meshwork.
 Trapped aqueous pushes peripheral iris forward & further shallows peripheral AC and blocks access to the trab meshwork.
o Treatment of this condition requires relief of the pupil block and iridotomy is the definitive treatment

37
Q

Describe pupillary block?

A
  • Caused by iridolenticular contact
  • Usually relative but may be absolute as in the case of posterior synechiae
  • Usually asymptomatic but if appositional closure occurs w/o an acute rise of IOP then PAS may form leading to chronic angle closure
  • If pupillary block becomes absolute, IOP in posterior chamber rises pushing the peripheral iris forward to cover trab meshwork w/ an ensuing greater rise in IOP & acute ACG
  • In nearly all cases of ACG, some element of pupil block is present
38
Q

What is plateau iris and plateau iris syndrome?

A
  • Anatomical iris configuration
    o Anteriorly displaced ciliary body position
    o Anteriorly inserted or thicker iris
  • The central AC is usually not shallow, & the iris plane is flat or slightly convex
  • Angle appears narrow and crowded on gonioscopy
  • Gonioscopy shows a “double hump” sign
  • Hard to diagnose/detect as central AC is often normal depth
39
Q

What is plateau iris syndrome?

A

-ACG associated w/ plateau iris is usually cured by YAG laser Peripheral Iridoplasty (PI)
-Plateau iris syndrome is where post-PI, angle closure recurs w/ elevated IOP attacks
Requires different tx e.g. ALPI (argon laser peripheral irdoplasty), pilocarpine long term or lens extraction

40
Q

What to consider when think px may have glaucoma?

A
  • Take several systematic & clinical findings into account to arrive at correct diagnosis
    o Glaucoma refers to collective term for several different conditions w/ similar & related features
  • Take:
    o H&S
     Ocular & systemic
    o Family Hx
    o Refraction
     Myopic: more likely to get POAG
     Hyperopic: more likely to get ACG
    o IOP & CCT
    o Ant chamber & gonio (or Van Hericks)
    o Discs, VFs, OCT
41
Q

What looking at in an optic disc assessment?

A
  • ISNT rule – normal disc rim is thickest inferiorly then superiorly and then nasally then temporally  IF NOT FOLLOWED, DOES NOT MEAN PX HAS GLAUCOMA
  • Notice rim colour – pallor should correspond or be slightly less than cup
  • Tilted discs are difficult to interpret – common in myopes & astigmats
    o Look carefully for glaucomatous features and correlate VF  (SuperTemporal VF defects – tilted disc VF does not normally encroach on central (this would usually be due to cupping))
  • Note size of optic disc:
    o Disc size can be measured with normal disc being 1.5 to 2mm in vertical diameter or assessed in relation to the calibre of BVs which are fairly constant in size
    o Small discs in hyperopes apparently normal CD ratio may be misleading
    o Large discs have large cups - look at NRR

CANNOT RELY ON C:D ALONE

42
Q

What questions should you ask yourself if you think px has glaucoma?

A
  • Is there any definite evidence of glaucomatous nerve damage? E.g apon or notch
  • Is there any difference in appearance of 2 optic nerves – asymmetry often sign in glaucoma (>0.2C:D between eyes)
  • Is there a reason other than glaucoma for any apparent difference in appearance of the 2 optic nerves? E.g. px may be myopic in one eye & not other
  • Does appearance of optic nerve indicate any acquired change? Progressive? – PPA v common feature, but if see notch or haemorrhage this is a sign of change
43
Q

What are the 10 signs that a glaucomatous disc is likely to have?

A
  1. CD ratio: vertical height of cup to vertical height of disc – 0.5 C:D is potentially suspect but have to think where position of cup is & if it is a large nerve or not
  2. BV Position: BVs can give clue to where edge of cup is in glaucoma – if see BV bayoneting over edge of contour then suggests that’s where edge of cup is
    o BVs tend to come out of nasal side of cup – as lose nerve fibre layer & rim, BVs tend to fall away with loss of tissue – see change in position of BVs over time
    o BV contrast important: “baring of BVs” – when BV overlies NRR, NRR usually pink & BV red so not lot of contrast  as NRR disappears &dies away, red BV outline starker against paler background of cup
  3. Rim Thickness: shows where deficit is in NRR – if v thin then NOTE this
  4. Pallor: of NRR can be sign of glaucoma or other optic neuropathies
  5. Peri-papillary atrophy (PPA): where get loss of NRR, get more PPA in that area – WEAK sign as v common
  6. APON: acquired pit of optic nerve – areas of highly focal loss of tissue – seen mainly in pxs w/ NTG – often associated w/ paracentral VF defects
  7. Optic disc haemorrhages: strong correlation w/ glaucoma (~40% of pxs) – not exclusive though (e.g. PVD, systemic hypertenstion)
  8. Nerve fibre layer defects: see on volk & red-free light – hard to see though – use photos/OCT
  9. Notch: highly focal loss of tissue – gradual shelving & loss of nerve fibre layer
  10. Laminar (cribosa) dots: often seen in base of notch, normal to see in central part of cup – round – if see them more peripherally in optic nerve (appear more oval) – sign suggests loss of NRR
44
Q

What are signs of change that can be used in detection of glaucoma?

A
  • Shift in position of BVs
  • Thinning of NRR
  • Developing notch (strong sign)
  • Haemorrhage crossing disc rim
  • Developing focal pallor – often develops in pxs w/ v high IOP
  • Change in peripapillary atrophy – does occur naturally overtime
45
Q

What is the Disc Damage Likelihood Scale (DDLS)?

A
  • Based on:
    o 1. Size of disc – measure & state if small, medium, large – use graticule on SL & volk
    o 2. Thinning of NRR (inverse of CD ratio) in thinnest areas & degrees of involvement
46
Q

Correction factors when measuring optic disc size (muliply measurement by these numbers)?

A
  • Volk:
    66D-1.0
    60D-0.88
    78D-1.2
    90D-1.33
47
Q

Disc damage likelihood scale & referral?

A
  • DDLS stage 4 or more: refer
  • Medium size disc: stage 4: NRR of 0.1 to 0.19 in thinnest area –> suspect glaucoma for referral
  • Small optic disc measuring <1.25mm  stage 4: NRR of 0.2 to 0.29 –> suspect glaucoma
  • Large disc: <0.1 NRR thickness
  • Look at all sign of glaucoma
48
Q

Describe concentric enlargement - glaucoma?

A
  • Say cup:disc starts at C:D ~0.3 –> increasing as px develops glaucoma (e.g. C:D~0.5) –> then becomes e.g. C:D~0.8 w/ v thin rim inferotemporally, temporally & slightly superotemorally
  • Difficult to say if px has glaucoma in early stages
  • If saw 1st disc probs wouldn’t say had glaucoma but if px returned 2yrs later w/ 2nd disc then you would see the CHANGE
  • If saw 3rd disc as presentation: would almost certainly say it is glaucoma
49
Q

Describe temporal unfolding - glaucoma?

A

Variant of concentric cupping – principal loss of NRR on temporal side

50
Q

Describe vertical extension - glaucoma?

A
  • Common pattern seen in glaucomatous optic nerve development
  • Start with small, central cup – enlarges superiorly or inferiorly
51
Q

Describe notching - glaucoma?

A
  • Like vertical extension but w/ v highly focal loss of tissue in that region either inferiorly or temporally
  • May see lamina cribosa dots extending into periphery & v oval
52
Q

Describe Acquired Pit of Optic Nerve (APON) - glaucoma?

A
  • Highly focal loss of tissue like notch, develops generally at inferotemporal or superotemporal part of optic disc
  • May see little BVs disappearing into pits & popping out again on other side
  • More common in NTG than POAG
  • A congenital Pit: occur on central or temporal part of optic disc, tend to be larger than APON
53
Q

Describe nasal cupping - glaucoma?

A
  • Variant of concentric cupping – preferential loss of NRR on nasal side
  • Nasalisation of BVs
  • May see BVs in central trunk fall away to nasal side as no NRR left
54
Q

Describe senile sclerosis - glaucoma?

A
  • Type of glaucomatous change seen in v elderly pxs (90s)
  • Don’t see lots of signs of obvious cupping but see gradual saucerisation of optic disc
  • Will also see development of pallor across whole nerve due to ischaemic changes of age
  • Development of generalised PPA
  • Disc may appear like saucer, generalised gradual concentric cupping occurs w/ extreme pallor
55
Q

Describe generalised pallor?

A

Sometimes see in glaucoma but occurs in other conditions/optic neuropathies which may be more important/serious than glaucoma

56
Q

Describe the differential diagnosis of glaucoma?

A
  • Excavated Disc Abnormalities:
    o Optic nerve coloboma
    o Congenital optic nerve pit
    o Morning glory syndrome
    o Tilted disc syndrome
    o Peri-papillary staphyloma – can sometimes be mistaken for disc cupping
  • Pale Optic Discs:
    o AION – anterior ischaemic optic neuropathy
    o CRAO
    o Heredofamilial optic atrophies like dominant optic atrophy
    o Other optic neuropathies (inflammatory, infectious, toxic, nutritional, compressive e.g. due to pituitary tumour or optic nerve tumour)
  • When see pallor, need to exclude these through history & other examinative tests

Papilloedema
Pituitary tumour (NRR v pale & almost yellow in colour, C:D normal)

57
Q

Considerations to make if think px has glaucoma?

A
  • Disease of change (slow) – with normal IOPs – start follow-up and watch for signs of change (particularly in pxs w/ normal IOPs)
  • Perform disc photography and store on computer or case records
  • Never in isolation - consider risk factors (age, fam Hx, IOP, myopia, central corneal thickness, VFs)
58
Q

What is the normal extent of the visual field?

A

90-100° temporally & 60° nasally
Superiorly ~60° & inferiorly ~75°

59
Q

Describe VFs in glaucoma - where do they normally occur?

A
  • Most defects occur within central 30 degrees but peripheral VF often involved
  • VF loss may be focal or generalised or both
  • Retinal GC axons follow an arcuate path to ONH. Field defects are direct result of axonal damage at level of ONH  Axonal damage will always respect horizontal midline
  • VF loss pattern is characteristic & tends to correlate w/ typical ONH excavation seen in glaucomatous optic neuropathy
60
Q

VFs in glaucoma - describe Bjerrumm’s Area Defect?

A

Frequent in early glaucoma & may account for 70% of early VF defects usually in superior VF between 10-20°

61
Q

VFs in glaucoma - describe Arcuate Defects?

A

Slightly more advanced than paracentral defects & occur in arcuate or Bjerrum’s area usually superior > inferior

62
Q

VFs in glaucoma - describe Paracentral Defects?

A

o Highly suggestive of glaucomatous aetiology
o Defined as within 10° of fixation
o More common in NTG
o Significant AMD can also produce a similar result

63
Q

VFs in glaucoma - describe Nasal Step?

A

Up to 40% of pxs w/ glaucomatous loss have nasal steps (usually superior)

64
Q

VFs in glaucoma - describe Temporal Wedge?

A

Uncommon – tend to be correlated with significant nasal cupping

65
Q

VFs in glaucoma - describe enlargement of blind spot?

A

Many different causes from neurological to ocular (including PPA) but in glaucoma may manifest as elongation (in superior or inferior direction) of blind spot in an arcuate fashion

66
Q

VFs in glaucoma - describe overall depression?

A

o Due to ↓sensitivity of retina secondary to diffuse loss of nerve fibres throughout optic nerve
o Accounts for up to 38% of VF defects
o Generalised depression especially nasally
o ↓mean deviation scores
o Can be due to media opacities e.g. cataract

67
Q

What to look for when assessing the VFs?

A
  • Check px data (refraction, pupil)
  • Check reliability indices – make sure px doesn’t have too many fixation losses or false +ves
  • Look at grayscale (overall impression)
  • Rule out possible artefacts (ptosis, lens, lens rim artefacts, px factors)
  • Observe numerical graph – look at dB values
  • Analyse total deviation probability plot (looking for diffuse loss of sensitivity – could be due to glaucoma or due to lens opacities)
  • Look at Pattern deviation plot (localised)
  • Analyse global indices – mean deviation & pattern standard deviation (confirm depth & extent of VF loss)
  • Check GHT (glaucoma hemifield test) – looks at asymmetry between superior & inferior VF
  • Compare VF to clinical info to see if it correlates
68
Q

When do you know a VF defect is due to glaucoma?

A
  • VF abnormalities should be repeatable before being considered as real & true defect
  • Changes at optic disc will commonly present before any VF defect manifests in early glaucoma  correlate any VF defect seen to other info for e.g. if have thinning of NRR in optic disc inferiorly then expect to see a superior VF defect  also look at retina for other abnormalities that may be causing the VF defect
  • VF defects should be considered as possible glaucomatous if they fit w/ appearances of optic disc neuropathy & have characteristic patterns
  • Any VF defect that is not typical of glaucoma & does not correlate w/ optic disc abnormalities should prompt a search for other ocular (retinal) or visual pathway pathology –> e.g. look for VF defect respecting vertical midline which may suggest it is of neurological origin & px may need to be referred for neuorophthalmic assessment & possibly scanning of brain
69
Q

Which IOP to aim for when px’s have different stages of glaucoma?

A
  • If have pxs w/ early disease, can achieve quite significant reduction in pxs progressing by a smaller reduction in IOP.
  • If have pxs w/ v advanced disease, need to achieve much lower target IOPs in order to keep them stable.
  • If need v low target pressures, surgery may be preferable over medical tx. Even w/ medical tx, if get pressure low enough, pxs can do v well.
  • With ocular hypertension, reducing IOP is important mainly in pxs in high-risk category for progression.
  • With all factors; IOP, CCT, age –> can stratify pxs into:
    * High risk for progression & treat them
    * Low risk can discharge
    * Medium risk can monitor
70
Q

Referral guidelines for glaucoma?

A

SAME DAY: acute red-eye & high IOP (acute glaucoma)
URGENT: IOP >30mmHg
ROUTINE: IOP <30mmHg w/ suspicious disc/fields
OHT w/ IOP>22mmHg as per NICE guidelines

IOP must be by contract tonometry
Referral on fields alone must be repeatbale

All glaucoma referrals must include: IOP + FIelds + Disc assessment

71
Q

What are the general principles of glaucoma treatment?

A
  • Topical hypotensives (monotherapy (1 agent) to maximal therapy (as required))
  • YAG iridotomy if narrow angles (ITC) – may also require topical hypotensives afterwards
  • Selective Laser Trabeculoplasty (SLT) – as long as angle is wide enough that can treat trab meshwork  used if px not controlled on drops or intolerant to drops
  • Trabeculectomy/Deep Sclerectomy – if not controlled w/ drops & laser & is still progressing then tend to proceed towards surgery – some pxs not suitable for surgery or in short term before have surgery may need stronger IOP lowering agents
  • Oral Acetazolamide – carbonic anhydrase inhibitor – tend to have side-effects & long-term effects on px’s health  generally not used except in short-term
  • Angle Surgery (Phaco, istent, trabectome, canaloplasty) – to try & improve drainage through trab meshwork
  • Cyclodiode Laser Ciliary Ablation
  • Tube or valve surgery – put in silicone tube/valve into eye, drains into reservoir or base-plate which sits under the conjunctiva & on surface of sclera –> reserved for pxs w/ more complex glaucomas where trabeculectomy is likely to fail or pxs who have had previous surgery already w/ trabeculectomy which has failed & there is significant scar tissue
72
Q

Which order should you give px drug types in glaucoma treatment?

A
  • 1st Line: Prostaglandin analogue (most effective in terms of % IOP reduction) or Beta-Blocker
    o Uniocular trials – some pxs – if other eye is not much at risk – start tx in worse eye to see what effect is compared to other eye, if makes difference then tx other eye too
  • 2nd Line: Prostaglandin analogue or Beta-Blocker  add in which ever didn’t start the 1st time so px on 2 meds
  • 3rd Line: Carbonic anhydrase inhibitor (less side-effects) or alpha 2 agonist (more side-effects)
  • 4th Line: Rarely as 3 above or pilocarpine
73
Q

Give examples of prostaglandin analogues, the mechanism of action and the most common side effects?

A
  • Latanoprost (Xalatan, Generic, Monopost) od
  • Travoprost (Travatan) od
  • Bimatoprost 0.01/0.03% (Lumigan) od
  • Tafluprost (Saflutan) od
  • Increased uveoscleral outflow by ciliary muscle relaxation
  • 30-35% reduction in IOP

o Mild conjunctival hyperaemia –> particularly 1st few weeks then decreases over time
o Mild punctate keratopathy
o Foreign body sensation
o Ocular irritation
o Lengthening of eyelashes – most pxs don’t mind this – some pxs end up w/ them rubbing on back of spectacles (trim lashes)
o Cystoid macular oedema (pseudo or aphakic pxs) – may need to stop txs if doing cataract surgery or where CMO develops
o Very rarely exacerbation of asthma – prostaglandin analogues are tx of choice in pxs w/ asthma as avoiding using a beta-blocker – if get exacerbation, need to stop tx

74
Q

Give examples of beta-blockers, the mechanism of action and the most common side effects?

A
  • Timolol
  • Levobunolol
  • Betaxolol
  • Decreased aqueous production from ciliary epithelium
  • 25-30% reduction in IOP
  • Suffer from tachyphylaxis – over period of time may become less effective

o Ocular Side Effects (these may be due to the preservatives in the drops):
 Corneal hypaesthesia
 Punctate keratopathy
 Dry eye syndromes
 Burning/stinging
 Pseudopemphigoid

  • Systemic Side effects:
  • Severe bradycardia
  • Arrhythmia
  • Heart failure – can exacerbate ability of heart to pump
  • Dyspnoea
  • Exacerbation of asthma
  • Anxiety
  • Hallucinations
  • Disorientation
  • Some pxs MUST NOT be prescribed beta-blockers – specifically if pxs have arrythmia or problems w/ heart rate
75
Q

Give examples of carbonic anhydrase inhibitors (CAIs), the mechanism of action and the most common side effects?

A
  • Dorzolamide (trusopt) tds
  • Brinzolamide (azopt) bd
  • 18% reduction in IOP – act as adjunct to other drops
  • Reduce aqueous secretion from ciliary epithelium
  • Possible improved optic nerve perfusion due to local vasodilatation
  • Side Effects:
    o Transient burning/stinging (33%)
    o Bitter taste (26%) – due to agent going down nasolacrimal duct through puncta & into nasopharynx
    o Ocular allergy – compared to timolol & prostaglandins which have v low rates of allergy
    o Superficial punctate keratitis (10%) – gives rise to dry-eye type symptoms
    o Blurred vision
    o Dryness
    o Hair loss – particularly woman on Brinzolamide – if caught early & stopped often reverses – can sometimes be stopped but not reversed
  • Systemic Side Effects:
     Rare and more relevant to systemic CAIs like acetazolamide
    o Sulphonamide hypersensitivity
    o Stevens-Johnson syndrome
    o Toxic epidermal necrosis
    o Aplastic anaemia
     These 4 conditions can potentially be fatal
76
Q

Give examples of alpha-2-agonists, the mechanism of action and the most common side effects?

A
  • Apraclonidine (used as short-term adjunct to control IOP before px receives surgery) and Brimonidine (used more long-term)
  • Reduction in aqueous production
  • 25% reduction in IOP (more effective than CAIs but bad SIDE-EFFECTS)
  • Side Effects:
    o High rate of allergy (15-25% for brimonidine – can be in initial stages or can be months later)
    o Conjunctival hyperaemia or blanching
    o Follicular conjunctivitis (10%) – can give rise to itchy & uncomfortable eyes & red eyes
    o Systemic blood pressure reduction (never use in children)
    o Avoid with mono amine oxidase inhibitors or anti-depressants (depression)
77
Q

Give examples of cholinergic agents (parasympathomimetics & miotics), the mechanism of action and the most common side effects?

A
  • ↑ trabecular outflow via ciliary muscle contraction plus some minor ↓ in aqueous inflow
  • Pilocarpine 1-4% qds
    o ~ 20% reduction in IOP from baseline
  • ↑ trabecular outflow via ciliary muscle contraction plus some minor ↓ in aqueous inflow
  • Pilocarpine 1-4% qds
    o ~ 20% reduction in IOP from baseline

SIDE EFFECTS OF PILOCARPINE:
o Only really used to treat ACG in short term & v rarely used as a long-term tx
* Ciliary muscle spasm
* Brow ache
* Accommodative myopia
* Miosis with constriction of VFs – significant in pxs who have already visual loss due to macular disease or advanced glaucoma
* Increased risk of retinal detachment
* Bradycardia, nausea, sweating, diarrhoea, bronchospasm – if px is elderly & over-dosed on pilocarpine
* Acute or chronic angle closure – even though used in ACG, pilocarpine can facilitate pupil block & acute or chronic angle closure

78
Q

Give some examples of combined preparations for treatment of glaucoma?

A
  • Cosopt (Timolol and Dorzolamide)
  • Xalacom (Timolol and Latanoprost)
  • Combigan (Timolol and Brimonidine)
  • Duotrav (Timolol and Travoprost)
  • Ganfort (Timolol and Bimatoprost)
  • Azarga (Timolol and Brinzolamide)
  • Simbrinza (Brimonidine and Brinzolamide) (alpha-agonist & CAI)
  • Taptiqom (Timolol and Tafluprost)
79
Q

What are the principles of tx compliance with patients?

A
  • Simpler tx regimens – use combined preparation where possible, minimal amount of drop tx is required
  • Use agents w/ least side-effects
  • Educate px on why they are receiving the tx as most pxs w/ glaucoma are asymptomatic & are not aware they have a visual problem – px may feel side-effects from drops that they previously didn’t have
  • Reinforcement when px returns to clinic that their tx is working
  • Regular review & reassurance – so they understand importance of coming back for check ups
  • Realistic expectations of tx – sometimes pxs return after starting tx saying they stopped the tx because they didn’t notice any improvement in their eyesight – px has to understand that the tx is ↓ IOP & preserving their glaucoma from deteriorating over long period of time rather than improving their sight
80
Q

List more side effects and efficacy issues relating to drugs used for glaucoma treatment?

A
  • Preservative related (Irritation, redness, dryness)
  • Idiosyncratic – px may come with additional problem or side-effect that is not common – individual reactions that others don’t have
  • Remember nasolacrimal duct occlusion – if px reports bitter taste in their mouth or if want to minimise absorption of beta-blocker into the system –> can press on medial side of lower lid to occlude puncta (& thus nasolacrimal duct) to stop the drops draining into throat –> do for ~1min after applying the drops
  • Vaseline to lids – for dryness & excoriation – put on before putting drops in, acts as barrier to stop drops from irritating skin
  • Drops at least 5 mins apart (ideally 10-15mins apart) – if px on multiple drops – prevents one drop washing other drop out or diluting it
  • Close eyes for 1 to 3 mins after drop – helps w/ absorption & efficacy
  • Avoid dabbing eyes with tissue immediately after putting drop in as this can result in tissue taking medication out of eye  dab skin if spills onto skin but not eye
81
Q

What do preservatives do to the eye and why?

A
  • Preservatives e.g. Benzalkonium Chloride are harmful in long term to ocular surface
  • Intolerance/irritation – particularly in elderly pxs who have ocular surface disease anyway
  • Allergy – so pxs who are allergic to multiple drops are often allergic to the preservative rather than the medical agent
  • Exacerbates dryness especially in susceptible pxs & those on multiple drops
  • Vogue for prescribing preservative free glaucoma meds (long-term)
82
Q

Give some examples of preservative-free preparations of glaucoma drugs?

A
  • Timolol (MSD and Thea -Tiopex 0.1%, Eysano-Aspire)
  • Monopost (Latanoprost pres free)
  • Tafluprost (Saflutan)/Taptiqom (saflutan and timolol)
  • Lumigan UD/ Ganfort UD (Bimatoprost/Timolol)
  • Eyreida (bimatoprost 0.3%)
  • Travatan (BAK free – Polyquad)
  • Cosopt and Eylamdo (dorzolamide/timolol) Dorzolamide (Eydelto)
  • Pilocarpine 2%
  • Apraclonidine (Iopidine 0.5% and 1%)
83
Q

What do you have to remember about medications?

A

All medications have side effects but if those are tolerable, not causing harm, & medication is effective then px should continue w/ that treatment

84
Q

What are the differential diagnosis signs for Glaucoma?

A
  • Different types of glaucoma
  • Red eye
  • Different types of open angle
  • Different types of closed angle
  • Secondary glaucoma
  • Lens related glaucoma
  • Glaucoma w/ raised IOP
  • Glaucoma w/ normal IOP

Clinical Opthalmology (65 decks)

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