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  • Glaucoma

    1. 1. Glaucoma Ocular Pathology & Microbiology Dr Ian Pacey UNIVERSITY OF BRADFORD
    2. 2. Definition <ul><li>Glaucoma (Greek: grey / opaque) </li></ul><ul><ul><li>‘ a group of progressive ocular diseases with various aetiologies that ultimately result in a rather consistent optic neuropathy’ </li></ul></ul><ul><ul><li>‘ usually with a characteristic loss of visual function’ </li></ul></ul>
    3. 3. Overview <ul><li>The next two lectures will cover basic </li></ul><ul><ul><li>pathophysiology </li></ul></ul><ul><ul><li>symptoms </li></ul></ul><ul><ul><li>signs </li></ul></ul><ul><ul><li>management of... </li></ul></ul>Primary Open Angle Glaucoma Angle-Closure Glaucoma
    4. 4. Background <ul><li>You should have revised your notes on: </li></ul><ul><li>Ocular Anatomy </li></ul><ul><ul><li>Anterior angle </li></ul></ul><ul><ul><li>The optic nerve head </li></ul></ul><ul><ul><li>Aqueous production & outflow </li></ul></ul><ul><li>V.O.A. </li></ul><ul><ul><li>Gonioscopy </li></ul></ul><ul><ul><li>Optic nerve head analysis </li></ul></ul><ul><ul><li>Tonometry </li></ul></ul><ul><ul><li>Perimetry </li></ul></ul>
    5. 5. Definition <ul><li>Primary Open Angle Glaucoma (POAG) </li></ul><ul><ul><li>adult onset </li></ul></ul><ul><ul><li>an open angle of normal appearance </li></ul></ul><ul><ul><li>glaucomatous optic nerve head damage </li></ul></ul><ul><ul><li>visual field loss </li></ul></ul><ul><ul><li>often associated with </li></ul></ul><ul><ul><li>raised intra-ocular pressure (IOP) </li></ul></ul>secondary = no more on angle POAG
    6. 6. Pathophysiology <ul><li>Traditionally: </li></ul><ul><ul><li> age =  resistance to aqueous outflow </li></ul></ul><ul><ul><li>= increased IOP </li></ul></ul><ul><ul><li>results in damage to ganglion cell axons at optic nerve head, by </li></ul></ul><ul><ul><ul><li>? mechanical: stretching of lamina cribrosa </li></ul></ul></ul><ul><ul><ul><li>? vascular:  perfusion pressure of disc BVs </li></ul></ul></ul>Effectively the ability of O 2 etc to go BV to nerve ? reduced prod of aqu but overall incr IOP
    7. 7. Pathophysiology <ul><li>However, </li></ul><ul><ul><li>NB current definition does not include IOP! </li></ul></ul><ul><li>Characteristic disc damage </li></ul><ul><ul><li>fibres in inferior (& superior) neuroretinal rim (NRR) </li></ul></ul><ul><ul><li>? larger axons affected first </li></ul></ul><ul><ul><li>? up to 40% nerve fibre loss before measurable visual function loss </li></ul></ul>i.e. NTG. But IOP still relevant ACG & >30 affects appearance of disc & visual field more later SWAP, motion
    8. 8. How relevant? <ul><li>Prevalence </li></ul><ul><ul><li>the proportion of the population with the disease at a point in time </li></ul></ul><ul><ul><li>Quigley (1996) </li></ul></ul><ul><ul><ul><li>67million people world-wide affected by 2000! </li></ul></ul></ul><ul><ul><li>Overall prevalence ~1.5 to 3% </li></ul></ul><ul><ul><li>not gender dependent </li></ul></ul>?true - not counted
    9. 9. How relevant? <ul><li>Race </li></ul><ul><ul><li>(prevalence) </li></ul></ul><ul><ul><li>Caucasians ~ 1.5 to 2% </li></ul></ul><ul><ul><li>Asian ~ 3 to 5% </li></ul></ul><ul><ul><li>Afro-Caribbean ~ 6 to 8% </li></ul></ul><ul><ul><ul><li>disease starts younger </li></ul></ul></ul><ul><ul><ul><li>higher presenting IOP </li></ul></ul></ul><ul><ul><ul><li>more severe disc changes </li></ul></ul></ul><ul><ul><ul><li>more resistant to Tx,  worse prognosis </li></ul></ul></ul>not great deal of data
    10. 10. How relevant? <ul><li>Age </li></ul><ul><ul><li>prevalence increases with age </li></ul></ul><ul><ul><li>>60 yrs SIX times more likely than <60 </li></ul></ul>from Baltimore study why this point? all dead?
    11. 11. The Case History <ul><li>Symtoms: </li></ul><ul><ul><li>NONE! </li></ul></ul><ul><li>OH: </li></ul><ul><ul><li>none really </li></ul></ul><ul><ul><ul><li>? prev brought back for re-checks </li></ul></ul></ul><ul><ul><li>high myopia - 2 to 3x more likely </li></ul></ul><ul><ul><ul><li>perhaps ‘cos myopes have more eye exams? </li></ul></ul></ul><ul><ul><li>(retinal vein occlusion) </li></ul></ul>sometimes ‘something not right’
    12. 12. The Case History <ul><li>FH: </li></ul><ul><ul><li>Definite genetic link </li></ul></ul><ul><ul><ul><li>recently gene loci discovered </li></ul></ul></ul><ul><ul><li>13-47% of POAG are familial </li></ul></ul><ul><ul><li>5 to 20x prevalence for +’ve FH </li></ul></ul><ul><ul><li>Baltimore Eye Study (odds ratio) </li></ul></ul><ul><ul><ul><li>siblings 3.69 </li></ul></ul></ul><ul><ul><ul><li>parents 2.17 </li></ul></ul></ul><ul><ul><ul><li>children 1.12 </li></ul></ul></ul>‘ mum went blind’ - 4x risk of getting POAG most quote 8-10x risk good ‘cos unbiased population study
    13. 13. The Case History <ul><li>GH: </li></ul><ul><ul><li>Diabetes </li></ul></ul><ul><ul><ul><li>previously 2.8x risk for POAG </li></ul></ul></ul><ul><ul><ul><li>?due to hospital based studies </li></ul></ul></ul><ul><ul><ul><li>No assoc. (Baltimore, Barbados, Beaver Dam) </li></ul></ul></ul><ul><ul><ul><li>Slight assoc. (Rotterdam, Blue Mountains) </li></ul></ul></ul><ul><ul><li>Poor peripheral circulation (eg Reynauds) </li></ul></ul><ul><ul><li>Systemic hypertension </li></ul></ul><ul><ul><ul><li>rise in BP = rise in IOP but not incr. risk of POAG </li></ul></ul></ul>Therefore probably <2.8 but still there cold hands/feet/nose/ears & migraine
    14. 14. The Case History <ul><li>GH: </li></ul><ul><ul><li>Perfusion pressure (PP) </li></ul></ul><ul><ul><ul><li>(diastolic) BP minus IOP </li></ul></ul></ul><ul><ul><ul><li>LOW PP associated with prevalence of POAG </li></ul></ul></ul><ul><ul><ul><li><30 mmHg have SIX TIMES risk >50 mmHg </li></ul></ul></ul><ul><ul><ul><li>‘ nocturnal dippers’ at increased risk </li></ul></ul></ul><ul><ul><ul><li><60yr &  BP less risk POAG than age-match controls </li></ul></ul></ul><ul><ul><ul><li>>70yr &  BP higher risk POAG controls </li></ul></ul></ul>‘ 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
    15. 15. Intra-Ocular Pressure
    16. 16. Intra-Ocular Pressure <ul><li>‘ Normal’ IOP </li></ul><ul><ul><li>mean = 16 mmHg </li></ul></ul><ul><ul><li>distribution skewed towards higher IOP </li></ul></ul><ul><ul><li>?increases with age </li></ul></ul><ul><ul><ul><li>not in Japanese! </li></ul></ul></ul><ul><ul><li>diurnal variation 3-6 mmHg (>10 suspect) </li></ul></ul><ul><ul><li>inter-ocular difference <5 mmHg </li></ul></ul><ul><ul><li>IOP reduced by exercise, accommodation </li></ul></ul><ul><ul><li>IOP increased by drinking, lying down </li></ul></ul>
    17. 17. Intra-Ocular Pressure <ul><li>Increased IOP is a risk factor for POAG </li></ul><ul><ul><li>prevalence increases with IOP </li></ul></ul><ul><ul><li>progression slowed by reducing IOP </li></ul></ul><ul><ul><li>eye with higher IOP progresses faster </li></ul></ul>
    18. 18. Intra-Ocular Pressure <ul><li>Problem </li></ul><ul><ul><li>overlap between normal and POAG’s IOP </li></ul></ul><ul><ul><li>~50% of POAG have IOP <22mmHg </li></ul></ul><ul><ul><li>large no. have  IOP with no POAG </li></ul></ul>
    19. 19. Intra-Ocular Pressure DO NOT use as diagnosis on its own measure on all pts: increase over time = suspect
    20. 20. Ocular Hypertension <ul><li>Definition </li></ul><ul><ul><li>raised IOP in the absence of optic nerve head changes or visual field defects </li></ul></ul><ul><li>Prevalence </li></ul><ul><ul><li>Framingham Study ~25% ! </li></ul></ul><ul><li>Conversion to POAG </li></ul><ul><ul><li>incidence 1% per year </li></ul></ul><ul><li>Refer IOP > 30 mmHg (GOLDMANN) </li></ul>made up?! ie after 10 years 1/10th will have converted
    21. 21. Optic Nerve Head - normal <ul><li>Disc size and shape </li></ul><ul><ul><li>size variation 1:7 in normal Caucasians </li></ul></ul><ul><ul><li>inner margin of Elschnig’s Ring </li></ul></ul><ul><ul><li>vertically oval </li></ul></ul>
    22. 22. Optic Nerve Head - normal <ul><li>Disc size and shape </li></ul>Afro-Caribbean higher prevalence of POAG due to larger discs & cups  more susceptible to damage
    23. 23. Optic Nerve Head - normal <ul><li>Neuroretinal Rim (NRR) </li></ul><ul><ul><li>size varies according to disc size </li></ul></ul><ul><ul><li>shape = ISNT rule </li></ul></ul>I S N T
    24. 24. Optic Nerve Head - normal <ul><li>Optic cup </li></ul><ul><ul><li>3 dimensional pale depression in disc </li></ul></ul><ul><ul><ul><li>usually horizontally oval </li></ul></ul></ul><ul><ul><li>size varies according to disc size </li></ul></ul><ul><ul><li>three main ‘normal’ types </li></ul></ul><ul><ul><ul><li>dimple with small central cup </li></ul></ul></ul><ul><ul><ul><li>punched out with larger/deeper cup </li></ul></ul></ul><ul><ul><ul><li>sloping temporal wall </li></ul></ul></ul>possibly absent in small discs
    25. 25. Optic Nerve Head - normal <ul><li>Optic cup </li></ul><ul><ul><li>watch confusion b/w pallor & cupping </li></ul></ul>many pallor=cupping. glauc cupping increases & pallor same (?ageing too). if pallor>cup suspect neurological lesion ?
    26. 26. Optic Nerve Head - normal <ul><li>Optic cup:disc ratio </li></ul><ul><ul><li>with Volk & S/L can use beam height </li></ul></ul>C:D = ?? 1.5mm 1mm
    27. 27. Optic Nerve Head - normal <ul><li>Optic cup:disc ratio </li></ul><ul><ul><li>C:D larger horizontally </li></ul></ul><ul><ul><li>larger ratios in larger discs </li></ul></ul><ul><ul><li>average is 0.3-0.4 </li></ul></ul><ul><ul><li>less than 5% ‘normals’ have >0.65 </li></ul></ul><ul><ul><li>asymmetry of <0.2 in 96% of ‘normals’ </li></ul></ul>
    28. 28. Optic Nerve Head - normal <ul><li>Peripapillary atrophy </li></ul><ul><ul><li>potential confusion for CD ratios </li></ul></ul>
    29. 29. Optic Nerve Head - POAG <ul><li>Changes to NRR </li></ul><ul><ul><li>progressive thinning of NRR </li></ul></ul><ul><ul><li>general enlargement of CD ratio </li></ul></ul><ul><ul><ul><li>ISNT rule no longer applies </li></ul></ul></ul><ul><ul><ul><li>generally results in vertical elongation of cup </li></ul></ul></ul><ul><ul><ul><li>usually asymmetrical </li></ul></ul></ul><ul><ul><li>focal </li></ul></ul><ul><li>Increased depth of cupping </li></ul><ul><ul><li>‘ saucerisation’ in small discs </li></ul></ul><ul><ul><li>Laminar Dot sign </li></ul></ul>weak diagnostic tool
    30. 30. Optic Nerve Head - POAG <ul><li>General enlargement of CD ratio </li></ul>nearly end stage Not ISNT: Sup thinning? PPA
    31. 31. Optic Nerve Head - POAG <ul><li>CD asymmetry </li></ul>Not ISNT: Sup thinning?
    32. 32. Optic Nerve Head - POAG <ul><li>Loss of NRR (notching) </li></ul>
    33. 33. Optic Nerve Head - POAG <ul><li>Baring of blood vessels </li></ul><ul><ul><li>early specific sign of glaucoma </li></ul></ul><ul><ul><li>circumlinear vessel usually supported by NRR </li></ul></ul><ul><ul><li>elongation of cup leaves vessel hanging in ‘mid-air’ </li></ul></ul>
    34. 34. Optic Nerve Head - POAG <ul><li>Baring of blood vessels </li></ul>
    35. 35. Optic Nerve Head - POAG <ul><li>Nasal shift of disc vessels </li></ul><ul><ul><li>said to indicate glaucomatous changes </li></ul></ul><ul><ul><li>can occur in large C:D’s! </li></ul></ul>
    36. 36. Optic Nerve Head - POAG <ul><li>Bayonet sign </li></ul><ul><ul><li>vessel has ‘Z’ appearance at edge of cup </li></ul></ul><ul><ul><li>rarely seen in normals </li></ul></ul>
    37. 37. Optic Nerve Head - POAG <ul><li>Splinter haemorrhages </li></ul><ul><ul><li>flame shaped at margin </li></ul></ul><ul><ul><li>mostly Inf Temp & Sup Temp </li></ul></ul><ul><ul><li>associated with nerve fibre defect </li></ul></ul><ul><ul><li>more in NTG? </li></ul></ul>
    38. 38. Optic Nerve Head - POAG <ul><li>Focal changes to vasculature </li></ul>
    39. 39. Nerve Fibre Layer (NFL) <ul><li>Normal </li></ul><ul><ul><li>ganglion axons appear as silver striations </li></ul></ul><ul><ul><li>easiest to see in young, darkly pigmented fundi, using a bright ‘red-free’ light </li></ul></ul><ul><ul><li>NFL defects seen in <3% normals </li></ul></ul><ul><li>POAG </li></ul><ul><ul><li>defects seen easiest <2DD from edge of disc </li></ul></ul><ul><ul><li>usually ‘wedge’ or ‘slit’ defects </li></ul></ul><ul><ul><li>appear as dark bands radiating out </li></ul></ul>
    40. 40. Optic Nerve Head - normal <ul><li>NFL defect </li></ul>splinter haem
    41. 41. Heidelberg Retinal Tomograph (HRT)
    42. 42. HRT
    43. 43. Visual Fields <ul><li>‘ Measures’ what trying to save! </li></ul><ul><li>Problem </li></ul><ul><ul><li>Time consuming & subjective </li></ul></ul><ul><li>But, </li></ul><ul><ul><li>often now ‘automated’ </li></ul></ul><ul><ul><li>normal visual field less variable than discs </li></ul></ul><ul><ul><li>used to gauge success of management </li></ul></ul>
    44. 44. Visual Fields <ul><li>The basis </li></ul>
    45. 45. Visual Fields <ul><li>Problems for measurement </li></ul><ul><ul><li>patient reliability (False +’ve and -’ve responses & fixation errors) </li></ul></ul><ul><ul><li>ptosis, lens artefacts </li></ul></ul><ul><ul><li>learning </li></ul></ul><ul><ul><li>fatigue </li></ul></ul><ul><ul><li>cataracts </li></ul></ul>
    46. 46. Visual Fields <ul><li>‘ Typical’ defects </li></ul><ul><ul><li>Paracentral scotomas </li></ul></ul><ul><ul><li>Arcuate scotomas (Bjerrum) </li></ul></ul><ul><ul><li>Nasal steps </li></ul></ul><ul><ul><li>Temporal wedges </li></ul></ul><ul><li>Localised vs Diffuse </li></ul><ul><ul><li>the argument rages </li></ul></ul><ul><ul><li>diffuse probably not due to glaucoma </li></ul></ul>
    47. 47. <ul><li>Paracentral scotoma </li></ul>
    48. 48. <ul><li>Arcuate scotoma (Bjerrum) </li></ul>
    49. 49. <ul><li>Nasal step </li></ul>
    50. 50. Visual Fields <ul><li>New techniques: </li></ul><ul><li>SWAP </li></ul><ul><ul><li>Short-wavelength Automated Perimetry </li></ul></ul><ul><ul><li>POAG selective damage to SWS ‘pathway’ </li></ul></ul><ul><li>FDT </li></ul><ul><ul><li>Frequency Doubling Technology </li></ul></ul><ul><ul><li>illusion based around M-pathway </li></ul></ul>
    51. 51. Management <ul><li>Following your referral </li></ul><ul><ul><li>Ophthalmologist confirms diagnosis! </li></ul></ul><ul><li>When to treat? </li></ul><ul><ul><li>IOP > 30, irrespective of other risks </li></ul></ul><ul><ul><li>IOP > 24, if have other risks </li></ul></ul><ul><ul><li>Any IOP if evidence of optic nerve damage </li></ul></ul>
    52. 52. Management <ul><li>Then two potential courses of action </li></ul><ul><ul><li>Medical </li></ul></ul><ul><ul><li>Surgical </li></ul></ul><ul><li>Both aim to </li></ul><ul><ul><li>Reduce IOP </li></ul></ul><ul><ul><li>Prevent optic nerve damage </li></ul></ul><ul><ul><li>Preserve vision </li></ul></ul><ul><ul><li>Remain healthy! </li></ul></ul>
    53. 53. Medical Management <ul><li>Eye drops of various types </li></ul><ul><ul><li>Miotics (eg Pilocarpine, 4x day) </li></ul></ul><ul><ul><ul><li>Improve trabecular outflow </li></ul></ul></ul><ul><ul><ul><li>s/e: ciliary spasm, brow ache, VF constriction + others </li></ul></ul></ul><ul><ul><li>Adrenaline (and pro-drugs, 2x day) </li></ul></ul><ul><ul><ul><li> aqueous inflow &  trab outflow </li></ul></ul></ul><ul><ul><ul><li>s/e: elevated BP, tachycardia, arrhythmia, h/a, anxiety </li></ul></ul></ul><ul><ul><ul><li>stinging, hyperaemia, deposits, mydriasis, maculopathy </li></ul></ul></ul>original
    54. 54. Medical Management <ul><ul><li>Beta-blockers (eg Timolol, 2x day) </li></ul></ul><ul><ul><ul><li>Mainstay for ~20 years, various types </li></ul></ul></ul><ul><ul><ul><li> IOP by reducing aqueous secretion </li></ul></ul></ul><ul><ul><ul><li>s/e: bradycardia, arrhythmia,  BP, heart failure, asthma </li></ul></ul></ul><ul><ul><ul><li>dry eye syndrome </li></ul></ul></ul><ul><ul><li>Carbonic anhydrase inhibitors (Dorzolamide, 3x) </li></ul></ul><ul><ul><ul><li> aqueous secretion </li></ul></ul></ul><ul><ul><ul><li>s/e: parasthesia, nausea, urinary frequency, diarrhoea, transient myopia </li></ul></ul></ul>newer
    55. 55. Medical Management <ul><ul><li>Prostaglandin analogues </li></ul></ul><ul><ul><ul><li>Latanoprost (Xalatan): 1x day at night </li></ul></ul></ul><ul><ul><ul><li>increase uveoscleral outflow </li></ul></ul></ul><ul><ul><ul><li>more potent than  -blockers </li></ul></ul></ul><ul><ul><ul><li>s/e: mild conjunctival hyperaemia, mild punctate keratopathy, ocular irritation & increased iris pigmentation (about 20% of pts with mixed colour irides) </li></ul></ul></ul><ul><ul><li>Future: </li></ul></ul><ul><ul><ul><li>Neuroprotection? </li></ul></ul></ul>newer
    56. 56. Surgical Management <ul><li>Aim to facilitate aqueous outflow </li></ul><ul><ul><li>Argon Laser Trabeculoplasty </li></ul></ul><ul><ul><ul><li>Laser the trabecular meshwork (TM) </li></ul></ul></ul><ul><ul><ul><li>scars/contractions open TM </li></ul></ul></ul><ul><ul><ul><li>problem effect decreases over time </li></ul></ul></ul><ul><ul><li>Trabeculectomy </li></ul></ul><ul><ul><ul><li>produce a fistula to allow aqueous to drain into subconjunctival space </li></ul></ul></ul><ul><ul><ul><li>seen as a ‘filtration bleb’ </li></ul></ul></ul>
    57. 57. Surgical Management <ul><li>Trabeculectomy </li></ul>
    58. 58. Summary <ul><li>POAG is asymptomatic until late </li></ul>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
    59. 59. References <ul><li>Web based case studies </li></ul><ul><li> </li></ul><ul><li>Hitchings (2000) Fundamentals of clinical ophthalmology: Glaucoma. BMJ Books. </li></ul><ul><ul><li>LIB:S617.74.007.681 HIT </li></ul></ul><ul><li>Fingeret (2001) Primary care of the glaucomas. McGraw-Hill . </li></ul><ul><ul><li>LIB:S617.74.007.681 LEW </li></ul></ul><ul><li>Kanski (1996) Glaucoma: a colour manual of diagnosis and treatment. Butterworth-Heinemann . </li></ul><ul><ul><li>LIB:S617.74.007.681 KAN </li></ul></ul>+ numerous others