GLAUCOMA SUSPECTS AND NORMAL

PRESSURE GLAUCOMA

DR.PUSKAR GHOSH

PGT

DEPT. OF OPHTHALMOLOGY

BURDWAN MEDICAL COLLEGE

Ocular HypertensionDefinition:

It is defined as the CCT corrected IOP above the 97.5 percentile

in that population, with open angles on gonioscopy and no disc or

field changes.

In older age SD is greater than younger individual.So,the

‘normal’ IOP in elderly women range up to 24 mm Hg.

4-7% of the population over the age 40yrs have IOP˃21mmHg.

Without detectable glaucomatous changes. This is Ocular

Hypertension (OHT).

Epidemiology of OHT Mean IOP-16mmHg.

Normal Range-(mean±2SD):11-21 mmHg.

Gaussian distribution.

4-10%-age ˃40yrs.

18.4%-black African descent.

13.6%-Mixed race

4.6%-white peoples.

Ocular Hypertension Treatment

Study (OHTS)

16000 pt.

IOP:(24-32) mmHg.

No visual field defects

OBSERVATION

MEDICAL TREATMENT

(to lower IOP 20% of baseline)

9.5% 4.4%

OHTS (Contd.)

Dilemma

Early intervention

No symptoms

Thus, instituting treatment in all patients does not seem

reasonable

The current recommendation is that most ocular

hypertensive individuals do not require medical therapy.

Treatment- early damage and high risk for developing

glaucoma.

Risk factors: Multivariate analysis:

1. Increased Intra ocular pressure

2. Age

3. Central Corneal thickness

4. Cup Disc ratio

5. Pattermed standard deviation.

Univariate analysis:

1. Race-African-american

2. Gender

3. Heart Disease.

Others:

1. Myopia

2. Diabetes

3. Family history of glaucoma

Management:Age and life expectancy is

the key point to consider.

In general,only those with

higher risk should be

considered.

THE GLAUCOMA SUSPECTS Optic nerve or nerve fiber layer defects.

Visual Field abnormality consistent with glaucoma.

An elevated IOP ˃ 21 mmHg.

If 2 or more of these findings-

POAG Risk factors (for POAG):

Age˃50yrs

family history of glaucoma.

black race.

Normal open angle on gonioscopy

Progression rate to POAG of approximately 1% per year over 5 to 15

years.

Comprehensive Eye evaluation (AAO):

IOP

Optic nerve study

Visual Field study

High Risk glaucoma Suspects

IOP˃21 mmHg.*

CCT ˂ 555µm.*

African descent*

Older age.*

Family history of glaucoma.*

Large vertical or horizontal cup-disc ratio.*

Greater pattern standard deviation on Humphery Visual Field.*

Signs of pigment dispersion or pseudoexfoliation syn.

DM,HTN,CVS

disease,hypothyroidism,myopia,migraine,vasospasm.

Screening: Problems:

IOP value ˃ 21 mmHg.- more false positive or negative.

Optic nerve examination-not always practical.

Perimetry (Goldman kinetic or Humphrey Static)-when

detected,axonal loss has occurred.

Tools:

Short Wavelength Automated Perimetry (SWAP) - less efficient.

Standard Automated Perimetry.

Frequency Doubleed Perimetry (FDP)

Diagnostic Assessment: IOP and Pachymetry:

o Glaucoma Suspects-more corneal thickness (˃585µm)

Slit Lamp Biomicroscopy

Gonioscopy

Contd.-

Contd.-Fundus examination• Optic nerve head

• Disc Rim

• Cup Disc Ratio

• Nerve fiber layer (red free light)

Laser Polarimetry

Scanning Laser Ophthalmoscopy

Optic Coherence Tomography

Contd.-Visual Field:o24-2 SITA standard HFA II analyzer.

o24-2 Full Threshold White on white Humphrey perimetry or

equivalent programme.

oSWAP/FDP

Repeat-in abnormal readings.

Ocular Blood Flow

Lowered in superotemporal,the cup and inferotemporal rim.

When to treat?Guideline for frequency of treatment and follow up (AAO):

Treatment Target IOP

achieved

High Risk Follow up interval (m)

Examination ONH/VF

evaluation

No N/A No 6-24 6-24

No N/A Yes 3-12 6-18

Yes Yes Yes 3-12 6-18

Yes No Yes ≤4 3-12

Approach to treatment:

Target Pressure:

IOP at which the sum of the health-related

quality of life (HRQOL) from preserved vision

and the HRQOL from not having side effects

from treatment is maximized.

It is the highest IOP in a given eye at which no

clinically apparent nerve damage occurs.

Range with upper limit unlikely to further

damage.

Individualized.

Contd.-

Topical agent

Laser trabeculoplasty-

controversial role.

Adjunct in lowering IOP 20-25%.

Surgery (trabeculectomy)-extreamly

high uncontrolled IOP

NORMAL PRESSURE GLAUCOMA

Characterized by

IOP ≤ 21 mmHg.

Optic Nerve damage (glaucomatic

pattern)

Open anterior chamber angle.

Visual field loss (consistent with

damage)

No features of secondary glaucoma or

non glaucomatous cause.

Pathogenesis:

Abnormalities in local optic nerve or peripapilary blood flow

Association with peripheral vasospasm,migraine.

Myppia,peripapilary atrophy deff of blood flow short post ciliary artery.

Nocturnal dips of BP lower pulse pressure of optic disc.

Systemic characteristic:

Abnormal immunoprotiens

Silent myocardial infarction.

Mutation in Optineurine gene:

E50K mutation-more severe

Polymorphism in OPA1 gene.

CCT-very low

Risk Factors:

Age-older than those with POAG.

Gender-females.

Race- Japanese.

Family history-greater in families of patients with

NPG.

CCT-lower

Abnormal vasoregulation- migraine and Ranaud’s

Phenomenon.

Systemic Hypotension-nocturnal blood pressure dips of

˃20%

Obstructive sleep apnoea syndrome.

Autoantibody levels.

Differencial Diagnosis:POAG

Spontaneously resolved pigmentary glaucoma

Previous episodes of raised IOP

Masking by systemic therapy

Progressive retinal nerve fiber damage not due to

glaucoma.

Neurological lesions causing optic nerve and

chiasmal compression.

Previous anterior ischemic optic neuropathy.

Previous acute optic nerve insult.

Ocular manifestations:

Nothing specific

Diagnosis:

HISTORY-

Migraine and Raynaud phenomenon

Episodes of shock

Head injury

Headache and other neurological symptom

(intracranial lesions)

Medications,such as systemic hypotensives (beta

blockers) or steroids.

Diagnosis (contd.): EXAMINATIONS-

IOP-is usually at the high teens.

Optic nerve Head-

May be larger in NPG than in POAG.

Glaucomatous cupping is similar.

Pits are more common.

Peripapilary atrophic changes are more prevalent.

Splinter haemorrhage is present.

Visual field defects-

Are essentially same as in POAG.

In probably half of the patient,the field changes are non progressive over a period of

5 yrars,even without treatment.

Other Investigations-

Assesment of systemic vascular risk factors.

24 hrs ambulatory BP monitoring

Blood tests for non-glaucomatous optic neuropathy

Cranial MR.

Nail fold capillaroscopy with cold provocation

Management: Regular assessment including perimetry : 4-6 months interval.

IOP reduces by 30% from baseline,80% stabilizes,20% shows progression.

MEDICAL TREATMENT:

Beta Blockers (Betaxolol)

Prostaglandin derivatives

FILTRATION SURGERY- Argon Laser Trabeculoplasty .

SURGICAL THERAPY- Full thickness filtration surgery like Trabeculectomy with adjunct 5-

FU or Mitomycine C

Fellow eye - filtration in the future.

Risk factors for progression

Diabetes Melitus,

positive family history,

female gender,

disc heamorrhage

prolonged cold recovery.

OTHER TREATMENT

The serotonin antagonist (Naftidrofuryl.)

Calcium channel blockers -Brovincamine or nimodepine

Monitoring:

The younger the patient at diagnosis, the is the possibility of

clinically significant visual loss in their lifetime.

All patients require repeat visual field testing to identify

progression

Outcome:

• Slow disease progression-no visual change.

• Rapid Progression and - severe visual loss

• No progression has been seen in some patients monitored for 10

years or more

• The identification of change- IOP must be lowered.

• Neuroprotective agents.

THANK YOU