Glaucoma suspects and normal pressure glaucoma

This is a PPT of Normal pressure glaucoma and glaucoma suspects.

1. GLAUCOMA SUSPECTS AND NORMAL PRESSURE GLAUCOMA DR.PUSKAR GHOSH PGT DEPT. OF OPHTHALMOLOGY BURDWAN MEDICAL COLLEGE

2. Ocular Hypertension Definition :  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).

3. 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.

4. Ocular Hypertension Treatment Study (OHTS) 9.5% 4.4%

5. OHTS (Contd.) 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.

6. Risk factors : Multivariate analysis: Increased Intra ocular pressure Age Central Corneal thickness Cup Disc ratio Pattermed standard deviation. Univariate analysis: Race-African- american Gender Heart Disease. Others: Myopia Diabetes 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.

7. THE GLAUCOMA SUSPECTS Optic nerve or nerve fiber layer defects. Visual Field abnormality consistent with glaucoma. An elevated IOP ˃ 21 mmHg.

8. 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 P rogression rate to POAG of approximately 1% per year over 5 to 15 years . Comprehensive Eye evaluation (AAO): IOP Optic nerve study Visual Field study

9. 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 H umphery Visual Field.* Signs of pigment dispersion or pseudoexfoliation syn. DM,HTN,CVS disease,hypothyroidism,myopia,migraine,vasospasm .

10. 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)

11. Diagnostic Assessment: IOP and Pachymetry : Glaucoma Suspects-more corneal thickness (˃585µm)

12. Slit Lamp Biomicroscopy Gonioscopy Contd.-

13. 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

14. Contd.- Visual Field: 24-2 SITA standard HFA II analyzer. 24-2 Full Threshold White on white Humphrey perimetry or equivalent programme . SWAP/FDP Repeat -in abnormal readings. Ocular Blood Flow Lowered in superotemporal,the cup and inferotemporal rim.

15. 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

16. 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.

17. Contd.- Topical agent Laser trabeculoplasty - controversial role. Adjunct in lowering IOP 20-25%. Surgery ( trabeculectomy )- extreamly high uncontrolled IOP

18. 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.

19. 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

20. 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.

21. 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.

22. 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.  

23. 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

24. 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 F ellow 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 ( N aftidrofuryl .) Calcium channel blockers - Brovincamine or nimodepine

25. 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 : S low 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. N europrotective agents .

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