Glaucoma
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Transcript of Glaucoma
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GlaucomaOcular Pathology & Microbiology
Dr Ian Pacey
UNIVERSITY OF BRADFORD
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‘a group of progressive ocular diseases with various aetiologies that ultimately result in a rather consistent optic neuropathy’
‘usually with a characteristic loss of visual function’
DefinitionGlaucoma (Greek: grey / opaque)
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Primary Open Angle Glaucoma
Angle-Closure Glaucoma
Overview
The next two lectures will cover basic pathophysiology symptoms signs management of...
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Ocular Anatomy Anterior angle The optic nerve
head Aqueous
production & outflow
Background
You should have revised your notes on:
V.O.A. Gonioscopy Optic nerve head
analysis Tonometry Perimetry
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adult onset an open angle of normal appearance glaucomatous optic nerve head damage visual field loss
Definition
Primary Open Angle Glaucoma (POAG)
often associated with raised intra-ocular pressure (IOP)
secondary =secondary =
no more on angle POAG
no more on angle POAG
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age = resistance to aqueous outflow
= increased IOP
results in damage to ganglion cell axons at optic nerve head, by
? mechanical: stretching of lamina cribrosa
? vascular: perfusion pressure of disc BVs
Pathophysiology
Traditionally:
Effectively the ability of O2 etc to go BV to nerve
Effectively the ability of O2 etc to go BV to nerve
? reduced prod of aqu but overall incr IOP
? reduced prod of aqu but overall incr IOP
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Characteristic disc damage
fibres in inferior (& superior) neuroretinal rim (NRR)
? larger axons affected first
? up to 40% nerve fibre loss before measurable visual function loss
Pathophysiology
However, NB current definition does not include IOP!
i.e. NTG. But IOP still relevant ACG & >30
i.e. NTG. But IOP still relevant ACG & >30
affects appearance of disc & visual field
affects appearance of disc & visual field
more later SWAP, motion
more later SWAP, motion
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Quigley (1996)67million people world-wide affected by 2000!
Overall prevalence ~1.5 to 3%
not gender dependent
How relevant?
Prevalence the proportion of the population with the
disease at a point in time
?true - not counted?true - not counted
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How relevant?Race
(prevalence) Caucasians ~ 1.5 to 2% Asian ~ 3 to 5% Afro-Caribbean ~ 6 to 8%
disease starts youngerhigher presenting IOPmore severe disc changesmore resistant to Tx, worse prognosis
not great deal of datanot great deal of data
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How relevant?Age
prevalence increases with age >60 yrs SIX times more likely than <60
from Baltimore study
why this point? all dead?
from Baltimore study
why this point? all dead?
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OH: none really
? prev brought back for re-checks
high myopia - 2 to 3x more likelyperhaps ‘cos myopes have more eye exams?
(retinal vein occlusion)
The Case History
Symtoms: NONE! sometimes ‘something not right’sometimes ‘something not right’
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The Case History
FH: Definite genetic link
recently gene loci discovered
13-47% of POAG are familial 5 to 20x prevalence for +’ve FH Baltimore Eye Study (odds ratio)
siblings 3.69
parents 2.17
children 1.12
‘mum went blind’ - 4x risk of getting POAG
‘mum went blind’ - 4x risk of getting POAG
most quote 8-10x riskmost quote 8-10x risk
good ‘cos unbiased population study
good ‘cos unbiased population study
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The Case History
GH: Diabetes
previously 2.8x risk for POAG
?due to hospital based studies
No assoc. (Baltimore, Barbados, Beaver Dam)
Slight assoc. (Rotterdam, Blue Mountains)
Poor peripheral circulation (eg Reynauds)
Systemic hypertensionrise in BP = rise in IOP but not incr. risk of
POAG
Therefore probably <2.8 but still there
Therefore probably <2.8 but still there
cold hands/feet/nose/ears & migrainecold hands/feet/nose/ears & migraine
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The Case History
GH: Perfusion pressure (PP)
(diastolic) BP minus IOPLOW PP associated with prevalence of
POAG<30 mmHg have SIX TIMES risk >50 mmHg
‘nocturnal dippers’ at increased risk
<60yr & BP less risk POAG than age-match controls
>70yr & BP higher risk POAG controls
‘dippers’ those who’s BP drops dramatically at night. often recently Tx systemic hypertensives
‘dippers’ those who’s BP drops dramatically at night. often recently Tx systemic hypertensives
initially incr BP helps perfusion, but not when secondary vascular changes have occured
initially incr BP helps perfusion, but not when secondary vascular changes have occured
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Intra-Ocular Pressure
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?increases with agenot in Japanese!
diurnal variation 3-6 mmHg (>10 suspect) inter-ocular difference <5 mmHg IOP reduced by exercise, accommodation IOP increased by drinking, lying down
Intra-Ocular Pressure‘Normal’ IOP
mean = 16 mmHg distribution skewed towards higher IOP
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progression slowed by reducing IOP eye with higher IOP progresses faster
Intra-Ocular Pressure
Increased IOP is a risk factor for POAG prevalence increases with IOP
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Intra-Ocular Pressure
Problem overlap between
normal and POAG’s IOP
~50% of POAG have IOP <22mmHg
large no. have IOP with no POAG
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DO NOT use as diagnosis on its own
Intra-Ocular Pressure
measure on all pts: increase over time = suspect
measure on all pts: increase over time = suspect
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raised IOP in the absence of optic nerve head changes or visual field defects
Prevalence Framingham Study ~25% !
Conversion to POAG incidence 1% per year
Refer IOP > 30 mmHg (GOLDMANN)
Ocular Hypertension
Definition
made up?!made up?!
ie after 10 years 1/10th will have converted
ie after 10 years 1/10th will have converted
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Optic Nerve Head - normal
Disc size and shape size variation 1:7 in
normal Caucasians inner margin of
Elschnig’s Ring vertically oval
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Optic Nerve Head - normal
Disc size and shape
Afro-Caribbean higher prevalence of POAG due to larger discs & cups more susceptible to damage
Afro-Caribbean higher prevalence of POAG due to larger discs & cups more susceptible to damage
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Optic Nerve Head - normal
Neuroretinal Rim (NRR) size varies according to disc size shape = ISNT rule
I
S
NT
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Optic Nerve Head - normalOptic cup
3 dimensional pale depression in discusually horizontally oval
size varies according to disc size three main ‘normal’ types
dimple with small central cup
punched out with larger/deeper cup
sloping temporal wall
possibly absent in small discspossibly absent in small discs
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Optic Nerve Head - normal
Optic cup watch confusion
b/w pallor & cupping ?
many pallor=cupping. glauc cupping increases & pallor same (?ageing too). if pallor>cup suspect neurological lesion
many pallor=cupping. glauc cupping increases & pallor same (?ageing too). if pallor>cup suspect neurological lesion
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Optic Nerve Head - normal
Optic cup:disc ratio with Volk & S/L can use beam height
1.5mm
1mmC:D = ??
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Optic Nerve Head - normal
Optic cup:disc ratio C:D larger horizontally larger ratios in larger discs average is 0.3-0.4 less than 5% ‘normals’ have >0.65 asymmetry of <0.2 in 96% of ‘normals’
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Optic Nerve Head - normal
Peripapillary atrophy potential confusion for CD ratios
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Optic Nerve Head - POAG
Changes to NRR progressive thinning of NRR general enlargement of CD ratio
ISNT rule no longer applies
generally results in vertical elongation of cup
usually asymmetrical
focal
Increased depth of cupping ‘saucerisation’ in small discs Laminar Dot sign
weak diagnostic toolweak diagnostic tool
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Optic Nerve Head - POAG
General enlargement of CD ratio
PPA
nearly end stage
Not ISNT: Sup thinning?Not ISNT: Sup thinning?
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Optic Nerve Head - POAG
CD asymmetry
Not ISNT: Sup thinning?Not ISNT: Sup thinning?
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Optic Nerve Head - POAG
Loss of NRR (notching)
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Optic Nerve Head - POAG
Baring of blood vessels early specific sign of glaucoma
circumlinear vessel usually supported by NRR
elongation of cup leaves vessel hanging in ‘mid-air’
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Optic Nerve Head - POAG
Baring of blood vessels
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Optic Nerve Head - POAG
Nasal shift of disc vessels said to indicate
glaucomatous changes
can occur in large C:D’s!
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Optic Nerve Head - POAG
Bayonet sign vessel has ‘Z’
appearance at edge of cup
rarely seen in normals
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Optic Nerve Head - POAG
Splinter haemorrhages flame shaped at
margin mostly Inf Temp
& Sup Temp associated with
nerve fibre defect more in NTG?
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Optic Nerve Head - POAG
Focal changes to vasculature
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Nerve Fibre Layer (NFL)
Normal ganglion axons appear as silver striations easiest to see in young, darkly pigmented fundi,
using a bright ‘red-free’ light NFL defects seen in <3% normals
POAG defects seen easiest <2DD from edge of disc usually ‘wedge’ or ‘slit’ defects appear as dark bands radiating out
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Optic Nerve Head - normal
NFL defect
splinter haem
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Heidelberg Retinal Tomograph (HRT)
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HRT
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Problem Time consuming & subjective
But, often now ‘automated’ normal visual field less variable than discs used to gauge success of management
Visual Fields
‘Measures’ what trying to save!
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Visual FieldsThe basis
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patient reliability (False +’ve and -’ve responses & fixation errors)
ptosis, lens artefacts learning fatigue cataracts
Visual Fields
Problems for measurement
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Paracentral scotomas Arcuate scotomas (Bjerrum) Nasal steps Temporal wedges
Localised vs Diffuse the argument rages diffuse probably not due to glaucoma
Visual Fields
‘Typical’ defects
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Paracentral scotoma
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Arcuate scotoma (Bjerrum)
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Nasal step
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SWAP Short-wavelength Automated Perimetry POAG selective damage to SWS ‘pathway’
FDT Frequency Doubling Technology illusion based around M-pathway
Visual Fields
New techniques:
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When to treat? IOP > 30, irrespective of other risks
IOP > 24, if have other risks
Any IOP if evidence of optic nerve damage
Management
Following your referral Ophthalmologist confirms diagnosis!
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Medical Surgical
Both aim to
1. Reduce IOP
2. Prevent optic nerve damage
3. Preserve vision
4. Remain healthy!
Management
Then two potential courses of action
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Miotics (eg Pilocarpine, 4x day)Improve trabecular outflow
s/e: ciliary spasm, brow ache, VF constriction + others
Adrenaline (and pro-drugs, 2x day)aqueous inflow & trab outflow
s/e: elevated BP, tachycardia, arrhythmia, h/a, anxiety
stinging, hyperaemia, deposits, mydriasis, maculopathy
Medical Management
Eye drops of various types originaloriginal
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Carbonic anhydrase inhibitors (Dorzolamide, 3x)aqueous secretion
s/e: parasthesia, nausea, urinary frequency, diarrhoea, transient myopia
Medical Management Beta-blockers (eg Timolol, 2x day)
Mainstay for ~20 years, various types
IOP by reducing aqueous secretion
s/e: bradycardia, arrhythmia, BP, heart failure, asthma
dry eye syndrome
newernewer
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Future:Neuroprotection?
Medical Management Prostaglandin analogues
Latanoprost (Xalatan): 1x day at night
increase uveoscleral outflow
more potent than -blockers
s/e: mild conjunctival hyperaemia, mild punctate keratopathy, ocular irritation & increased iris pigmentation (about 20% of pts with mixed colour irides)
newernewer
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Argon Laser TrabeculoplastyLaser the trabecular meshwork (TM)
scars/contractions open TM
problem effect decreases over time
Trabeculectomyproduce a fistula to allow aqueous to drain into
subconjunctival space
seen as a ‘filtration bleb’
Surgical Management
Aim to facilitate aqueous outflow
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Surgical Management
Trabeculectomy
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CH: remember Age, Race, FH
Exam: need to measure IOP, do Fields and carefully examine the disc
Use ALL THREE to decide to refer
Counsel the Pt that it is usually a very slow progression
Summary
POAG is asymptomatic until late
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Hitchings (2000) Fundamentals of clinical ophthalmology: Glaucoma. BMJ Books. LIB:S617.74.007.681 HIT
Fingeret (2001) Primary care of the glaucomas. McGraw-Hill. LIB:S617.74.007.681 LEW
Kanski (1996) Glaucoma: a colour manual of diagnosis and treatment. Butterworth-Heinemann. LIB:S617.74.007.681 KAN
References
Web based case studieshttp://arapaho.nsuok.edu/~odce/htdocs/glaucoma/glaucoma_cases.html
+ numerous others+ numerous others