Glaucoma

GlaucomaOcular Pathology & Microbiology

Dr Ian Pacey

UNIVERSITY OF BRADFORD

‘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)

Primary Open Angle Glaucoma

Angle-Closure Glaucoma

Overview

The next two lectures will cover basic pathophysiology symptoms signs management of...

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

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

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

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

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

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

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?

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’

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

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

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

Intra-Ocular Pressure

?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

progression slowed by reducing IOP eye with higher IOP progresses faster


Increased IOP is a risk factor for POAG prevalence increases with IOP


Problem overlap between

normal and POAG’s IOP

~50% of POAG have IOP <22mmHg

large no. have IOP with no POAG

DO NOT use as diagnosis on its own


measure on all pts: increase over time = suspect

measure on all pts: increase over time = suspect

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

Optic Nerve Head - normal

Disc size and shape size variation 1:7 in

normal Caucasians inner margin of

Elschnig’s Ring vertically oval


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


Neuroretinal Rim (NRR) size varies according to disc size shape = ISNT rule

I

S

NT

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


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


Optic cup:disc ratio with Volk & S/L can use beam height

1.5mm

1mmC:D = ??


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’


Peripapillary atrophy potential confusion for CD ratios

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


General enlargement of CD ratio

PPA

nearly end stage

Not ISNT: Sup thinning?Not ISNT: Sup thinning?


CD asymmetry

Not ISNT: Sup thinning?Not ISNT: Sup thinning?


Loss of NRR (notching)


Baring of blood vessels early specific sign of glaucoma

circumlinear vessel usually supported by NRR

elongation of cup leaves vessel hanging in ‘mid-air’


Baring of blood vessels


Nasal shift of disc vessels said to indicate

glaucomatous changes

can occur in large C:D’s!


Bayonet sign vessel has ‘Z’

appearance at edge of cup

rarely seen in normals


Splinter haemorrhages flame shaped at

margin mostly Inf Temp

& Sup Temp associated with

nerve fibre defect more in NTG?


Focal changes to vasculature

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


NFL defect

splinter haem

Heidelberg Retinal Tomograph (HRT)

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!

Visual FieldsThe basis

patient reliability (False +’ve and -’ve responses & fixation errors)

ptosis, lens artefacts learning fatigue cataracts

Visual Fields

Problems for measurement

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

Paracentral scotoma

Arcuate scotoma (Bjerrum)

Nasal step

SWAP Short-wavelength Automated Perimetry POAG selective damage to SWS ‘pathway’

FDT Frequency Doubling Technology illusion based around M-pathway

Visual Fields

New techniques:

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!

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

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

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

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

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

Surgical Management

Trabeculectomy

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

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

Glaucoma

Health & Medicine

Transcript of Glaucoma