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PRIMARY OPEN ANGLE GLAUCOMA - Copy (2).pptx
- 1. APPROACH TO PRIMARY OPEN ANGLE GLAUCOMA Presenter : Dr. Divya Kesarwani
- 2. DEFINITION Primary open-angle glaucoma (POAG) can be considered as Chronic, progressive, anterior optic neuropathy Characteristic cupping and atrophy of the optic disc, Visual field loss, Open angles, No obvious causative ocular or systemic conditions IOP elevated above statistically ‘normal’ range in majority but not all cases.
- 3. Risk Factors • IOP • Age/Gender • Race • Refractive Error • Corneal Thickness • Heredity and Genetics • Systemic Factors
- 6. Dx: HISTORY Visual symptoms: Early stages mostly asymptomatic Late stages Tubular vision is retained, Temporal field loss central fixation loss. H/o myopia, trauma, inflammation, previous eye Sx/ refractive Sx. Family H/o of POAG / any other ocular ds.. T/t H/o steroids or oral B blockers. H/o smoking/alcohol/ any drug allergy. Past Medical H/o Asthma, heart ds, PVD CI’s to the use of B-blockers. Head injury, intracranial ds, stroke optic atrophy or visual field defects. Migraine and Raynaud phenomenon vasospasm Diabetes, HTN and CVS ds risk of POAG
- 7. EXAMINATION Visual acuity Pupils : RAPD SLE Tonometry Gonioscopy. Optic disc examination: intrapapillary changes Peripapillary changes : PPA, RNFL defects, Disc splinter H’ages, diameter of retinal arterioles.
- 8. Evaluationof opticnerve head The optic disk size and shape, Cup-to-disk (C:D) ratio in relation to the disk size, Configuration and depth of the optic cup, The configuration of the neuroretinal rim, Position of the exit of the central retinal vessel trunk, Presence and location of disk hemorrhage, RNFL defects, and Configuration and location of parapapillary chorioretinal atrophy
- 9. The Neuroretinal Rim • Most important parameter. • This is the ‘ISNT rule’ which helps to determine glaucomatous changes in the disc glaucoma. • On an average, the inferior rim is 18% thicker than the superior rim.* • The loss of NRR from the inner edge of the rim cardinal feature. • The sequence of loss is usually first in the inferotemporal and superotemporal disk regions. • *Arvind H, George R, Raju P, Ve RS, Mani B, Kannan P, Vijaya L. Neural rim characteristics of healthy South Indians: the Chennai Glaucoma Study. Invest Ophthalmol Vis Sci 2008 Aug;49(8): 3457-3464
- 11. Optic disc haemorrhage • Splinter or flame-shaped hemorrhage, with feathered edges, oriented radially and perpendicular to the disk margin. • Location: prelaminar area of the optic disk and in the adjacent superficial RNFL. • It is located within one disk diameter from the optic disk border
- 12. Retinal Nerve Fibre Layer • Red-free light is best for evaluation of the RNFL as the short wavelength light brings the anterior layer into better focus. • The classic localised defect of the RNFL associated with glaucoma is seen as a darkened wedge that extends from a corresponding thinning in the neuroretinal rim tissue
- 13. Peripapillary ChorioretinalAtrophy • The peripheral alpha zone : Irregular hypo- and hyperpigmentation, associated with thinning of the chorioretinal tissue layer. • Bthe cenral beta zone : marked atrophy of the RPE and choriocapillaris and thinning of the chorioretinal tissues with good visibility of the large choroidal vessels and sclera. • If both zones are present, the beta zone is always closer to the optic disc than the alpha zone.
- 15. INVESTIGATIONS • Pachymetry • Perimetry • Ocular coherence tomography(OCT): optic disc and peripapillar RNFL imaging • Fundus photograph
- 16. DIFFERENTIAL DIAGNOSIS Other causes of increased IOP Ocular hypertension Secondary open angle glaucoma Chronic angle closure glaucoma Other causes of cupping and field defects Physiological cupping Congenital optic nerve defects Anterior ischemic optic neuropathy Primary optic atophy
- 17. TREATMENT
- 18. INDICATIONS 1) Classic glaucoma triad or at high risk for same. 2) Progressive cupping without detectable field loss, 3) The development of visual field loss, 4) Episodes of corneal edema caused by elevated IOP, 5) Vascular occlusion associated increased IOP. 6) C/L eye in pts with asymmetric POAG treated aggressively 40% chance of v. field loss over a 5-year .
- 19. GOALS To preserve good visual function for the patient’s lifetime. To preserve a reasonable quality of life and comfort. Minimizing the side effects from the treatment, the risk of vision loss and, in many cases, the costs associated with treatment.
- 20. TARGET PRESSURE Definition : The pressure level (range) below which further damage to the optic nerve is unlikely to occur. Choice of target IOP: It is usually 20-30 % reduction of baseline IOP but it should be individualized for each patient based on 1.Initial untreated IOP. 2.Degree of existing damage.(Optic nerve cupping, visual field loss and RNFL thickness) 3. Age of the patient (life expectancy)
- 21. Follow-up and Resetting target IOP Target IOP is a dynamic value. The initial efficacy of therapy is determined by its effect on IOP, but long-term efficacy must be determined by the analysis of damage (visual field, the optic nerve head, retinal nerve fiber thickness). Deterioration in any of these more aggressive T/t (i.e. to Re-set the Target intraocular pressure at a lower level) taking into consideration the other risk factors
- 23. THANK YOU
Editor's Notes
- In the majority, but by no means all, cases the intraocular pressure (IOP) is elevated above the statistically ‘normal’ range, reflecting a reduced aqueous humor outflow facility. Although elevated IOP is not the cause of all damage in POAG, it is the major risk factor.
- Because many individuals with ‘elevated’ IOP never develop glaucoma, and because many people with glaucoma have ‘normal’ IOPs, IOP obviously cannot be the only risk factorThere is general agreement that IOP is the most important known risk factor for open-angle glaucoma development Conflicting information exists. In several studies, males had a higher prevalence of glaucoma. In the Barbados study, POAG was associated with older men, high IOP, positive family history. The prevalence of POAG increases with age. Although it occurs in children and young adults as well. After compensating the relationship between increasing age and increasing IOP, POAG does increase in prevalence with age Risk factor ; ocular hypertension open-angle glaucoma. Even in normal-pressure glaucoma, asymmetric IOP has been noted to correlate with asymmetric cupping and field loss, with the greater damage most often occurring on the side with higher pressure. Among those with elevated IOP without evidence of glaucomatous damage (ocular hypertensives), the OHTS study shows that the higher the IOP, the more likely that glaucomatous damage will develop. . Myopia has been associated with POAG in many studies. Myopia direct influence on the prevalence of the disease known associations with increased IOP and larger cup-to-disc ratios. A Thin cornea risk factor for ocular hypertension POAG is a marker and possible risk factor for advanced glaucoma on diagnosis. underestimate the IOP on GAT. marker for increased susceptibility of the optic nerve Genetic or familial component. Autosomal dominant, autosomal recessive, and sex-linked inheritance patterns. Polygenic or multifactorial transmission. 5–50% hereditary, 4-16% risk first degree relative. 13% monozygotic and dizygotic twin inheritance Diabetes mellitus: affects the small blood vessels supplying the optic nerve more susceptible to glaucomatous damage. Thyroid disease, corticosteroid function, systemic vascular disease and sleep apnea.
- On a routine examination a patient's intraocular pressure is found to be high. A single IOP recording of more than 21 mm Hg does not always indicate glaucoma. If the second reading is normal, and if gonioscopy, disc examination and the visual field examination are normal, then there is no evidence of glaucoma. If a repeat IOP is also high, the next step is to determine whether the pressure is raised due to angle closure glaucoma or is associated with open angles. Anytime a high IOP is recorded (including a first measurement), a gonioscopy should be done immediately. If the patient with a raised pressure has a closed angle i.e. trabecular meshwork is not visible, then a diagnosis of angle closure glaucoma is made and the treatment proceeds appropriately. If on gonioscopy the central anterior depth is found normal, but the iris has a plateau configuration, the treatment follows the flow chart for angle closure. Gonioscopy may be, however inconclusive. The angle may look suspicious but not closed, i.e. the raised IOP may (or may not) be due to closure. Angle closure is an absolute phenomenon, and may be intermittent and/or partial. Alternatively the angle may be narrow and closable, but open, in which case this may represent a combined mechanism. If the IOP is raised and the angles on gonioscopy are open, the patient should be evaluated for POAG, and the patient slots into that flow chart.
- The patient may be a suspect because of a raised IOP, suspicious discs, or occassionally on the basis of suspicious fields alone. If the IOP is high, the patient's disc and visual fields are evaluated. If these show glaucomatous changes, the patient has POAG. If the disc and fields are normal, and the IOP is raised, the patient fits into the "ocular hypertensive" category. Without going into the controversies surrounding this term, we prefer to call them glaucoma suspects. If the IOP is normal and the patient is a glaucoma suspect for whatever reason, a diurnal variation of IOP (DVT) is recorded. If this shows a high peak or a large variation, the patient's disc and fields need evaluation. If the DVT is negative, the patient was probably a suspect due to disc and field criteria, and these need to be critically reevaluated. A patient with normal IOP may be a POAG suspect due to the appearance of his discs and/or visual fields. A DVT, therefore, is desirable. If the discs and fields show characteristic changes of POAG, and the IOP is normal, the diagnosis is "normotensive" glaucoma . Subsequent DVT may reveal a raised TOP, which confirms POAG. If, with a normal IOP, the disc and field show no glaucomatous changes, the diagnosis of POAG can be excluded As usual we come to our equivocal category - the disc and the visual field look suspicious, but we are not convinced. In this instance, the disc and field examination are repeated and if the same indecision prevails, additional information is needed. If the patient has risk factors for POAG, the patient is followed up and the entire work up is repeated. If we are suspicious enough we may decide to follow up those without risk factors also.
- Temporal vision loss of fixation lost.
- Visual acuity is likely to be normal except in advanced glaucoma. Disc changes: EarlyRnFL defects, focal notching, vertical elongation of cup, Baring of circum linear vessels, splinter h’ages, assymetry of cup btwn 2 eyes Late concentric elongation, NRR thinning, increased cupping, vertical elong, peripapillary atrophy, nasal shifting of vessels, bayonetting sign, laminar dot sign. 2 Pupils. Exclude a relative afferent pupillary defect (RAPD); if absent then subsequently develops this constitutes an indicator of substantial progression. 3 Colour vision assessment such as Ishihara chart testing if there is any suggestion of an optic neuropathy other than glaucoma. 4 Slit-lamp examination. Exclude features of secondary glaucomas such as pigmentary and pseudoexfoliative. 5 Tonometry, prior to pachymetry, noting the time of day. 6 Pachymetry for CCT. 7 Gonioscopy. 8 Optic disc examination should always be performed with the pupils dilated, provided gonioscopy does not show critically narrow angles. Red-free light can be used to detect RNFL defects. 9 Perimetry should usually be performed prior to clinical examination. 10 Optic disc or peripapillary RNFL imaging as described above
- Some are round and blotchy because they are situated in deeper parts of the disk and, occasionally, when the cup is large, a hemorrhage can be seen on the lamina cribrosa itself. and one should rule out presence of optic disk edema, papillitis, diabetic retinopathy, central or branch retinal vein occlusion, or any other retinal disease associated with hemorrhage
- Diffuse RNFL defects can also be seen in glaucoma, although they are difficult to detect with biomicroscopy
- Occurs more often in glaucomatous eyes than in normal eyes, or in eyes with ocular hypertension. More often seen in glaucomatous eyes with shallow cupping than in glaucomatous eyes with deep and steep excavation The alpha zone and beta zone have to be differentiated from the scleral crescent in eyes with high myopia and from the inferior scleral crescent in eyes with tilted optic discs
- Physiological cupping horizontally oval, symmetry btwn 2 eyes , Follows ISNT rule, cup & NRR config( both margins runs parallel) Glaucomatous cupping vertically oval, asymmetry btwn eyes, progressive cup enlargement, saucerization of cup, PPA, RNFL defects Neurological cupping NRR pallor more than obliteration, AION ( disc edema, splinter h’age), non progressive, Va and field defects out of proportion to cupping, Red green color vision lost.