Date post: | 16-Jul-2015 |
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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