THE GLAUCOMAS 2

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THE GLAUCOMAS 2

  1. 1. THE GLAUCOMAS 2 Dr Russell J Watkins
  2. 2. Classification <ul><li>The diagnosis of glaucomatous optic neuropathy is based on ONH examination, and to some extent, VF analysis </li></ul><ul><li>All forms of glaucoma are classified into primary & secondary forms based on </li></ul><ul><ul><li>Gonioscopic findings </li></ul></ul><ul><ul><li>Associated ocular and extraocular findings </li></ul></ul><ul><li>Major risk factors </li></ul><ul><ul><li>IOP </li></ul></ul><ul><ul><li>Vascular risk factors </li></ul></ul><ul><ul><ul><li>Local </li></ul></ul></ul><ul><ul><ul><li>Systemic </li></ul></ul></ul><ul><ul><li>Race </li></ul></ul>
  3. 3. Classification <ul><li>Associated conditions </li></ul><ul><ul><li>Ocular </li></ul></ul><ul><ul><li>Extraocular </li></ul></ul><ul><li>Additional useful clinical data </li></ul><ul><ul><li>BP, pulse, blood glucose, blood lipids </li></ul></ul><ul><ul><li>Migraine, cold hands/raynaud’s </li></ul></ul><ul><ul><li>Thyroid disease, neurological diseases </li></ul></ul><ul><ul><li>History of blood loss, smoking </li></ul></ul><ul><ul><li>FOH +ve for visual loss </li></ul></ul><ul><ul><li>FOH +ve for glaucoma </li></ul></ul>
  4. 4. Classification <ul><li>Primary Congenital Forms </li></ul><ul><ul><li>Primary Congenital Glaucoma </li></ul></ul><ul><ul><li>Primary Infantile Glaucoma </li></ul></ul><ul><ul><li>Glaucoma associated with congenital anomalies </li></ul></ul>
  5. 5. Classification <ul><li>Primary Open Angle Glaucomas </li></ul><ul><ul><li>Primary juvenile glaucoma </li></ul></ul><ul><ul><li>Primary open angle glaucoma </li></ul></ul><ul><ul><li>Normal tension glaucoma </li></ul></ul><ul><ul><li>Ocular hypertension </li></ul></ul>
  6. 6. Classification <ul><li>Secondary Open Angle Glaucoma </li></ul><ul><ul><li>Pseudoexfoliation glaucoma </li></ul></ul><ul><ul><li>Pigmentary glaucoma </li></ul></ul><ul><ul><li>Lens-induced OAG </li></ul></ul><ul><ul><li>Glaucoma associated with intraocular haemorrhage </li></ul></ul><ul><ul><li>Uveitic glaucoma </li></ul></ul><ul><ul><li>et al ++ </li></ul></ul>
  7. 7. Classification <ul><li>Primary Angle Closure Glaucomas </li></ul><ul><ul><li>Pupillary block mechanism </li></ul></ul><ul><ul><li>Plateau iris mechanism </li></ul></ul><ul><ul><li>Chronic and intermittent ACG </li></ul></ul><ul><ul><li>Malignant glaucoma (some may class this as secondary) </li></ul></ul>
  8. 8. Classification <ul><li>Secondary Angle Closure Glaucomas </li></ul><ul><ul><li>Secondary ACG with pupil block </li></ul></ul><ul><ul><li>Secondary ACG due to “pulling” of AC </li></ul></ul><ul><ul><ul><li>NVG </li></ul></ul></ul><ul><ul><ul><li>Aniridia </li></ul></ul></ul><ul><ul><ul><li>Inflammatory membrane </li></ul></ul></ul><ul><ul><ul><li>et al++ </li></ul></ul></ul>
  9. 9. Primary ACG <ul><li>Multiple pathogeneses </li></ul><ul><li>Basically acute & chronic forms </li></ul><ul><li>Defined on the basis of findings on gonioscopy </li></ul><ul><ul><li>In acute angle closure, there is iridocorneal apposition that can be reversed </li></ul></ul><ul><ul><li>In chronic angle closure, angle closure is irreversible because of PAS </li></ul></ul><ul><ul><li>Angle is closed without a discernible cause </li></ul></ul><ul><li>Medical & surgical management differs with OAG so identification important </li></ul>
  10. 10. Primary ACG <ul><li>Pupillary block mechanism </li></ul><ul><ul><li>Pupil block is present in most cases of acute, intermittent & chronic primary ACG </li></ul></ul><ul><ul><li>The flow of aqueous from PC to AC is impeded </li></ul></ul><ul><ul><li>PC pressure  to be > AC </li></ul></ul><ul><ul><li>Peripheral iris bows forward to contact TM </li></ul></ul><ul><ul><li>Annular drainage obstruction results </li></ul></ul><ul><ul><li>IOP can  to 50-80 mmHg </li></ul></ul><ul><ul><li>If this occurs within a few hours, AACG results </li></ul></ul>
  11. 11. Primary ACG <ul><li>Pupillary block mechanism (cont.) </li></ul><ul><ul><li> resistance to transpupillary aqueous flow is caused by apposition of posterior iris to anterior lens </li></ul></ul><ul><ul><li>Pupil block mechanism may be precipitated during mid-dilatation of the pupil </li></ul></ul><ul><ul><ul><li>e.g. reading in poor light, mydriatic drug use </li></ul></ul></ul><ul><ul><li>Eye is usually predisposed </li></ul></ul><ul><ul><ul><li>Narrow AC </li></ul></ul></ul><ul><ul><ul><li>Hypermetropia/short axial length </li></ul></ul></ul><ul><ul><ul><li>Large lens </li></ul></ul></ul>
  12. 14. Primary ACG <ul><li>Plateau iris mechanism </li></ul><ul><ul><li>Rare mechanism compared with pupil block </li></ul></ul><ul><ul><li>Anatomical variation in angle causes block </li></ul></ul><ul><ul><ul><li>Anterior insertion of iris (even as far as scleral spur) </li></ul></ul></ul><ul><ul><ul><li>Ciliary processes displaced anteriorly, pushing iris base anteriorly </li></ul></ul></ul><ul><ul><li>Attack occurs if mydriasis </li></ul></ul>
  13. 17. Primary ACG <ul><li>Creeping angle closure mechanism </li></ul><ul><ul><li>Iris base “creeps” on to TM forming PAS </li></ul></ul><ul><ul><li>IOP usually rises when >50% of angle is occluded </li></ul></ul><ul><ul><li>More frequent in Asians </li></ul></ul>
  14. 20. Primary ACG <ul><li>Posterior aqueous misdirection mechanism (malignant glaucoma) </li></ul><ul><ul><li>Rare; usually seen after intraocular surgery </li></ul></ul><ul><ul><li>Aqueous misdirected into vitreous because of anatomical factors </li></ul></ul><ul><ul><li>Lens-iris complex pushed anteriorly, occluding angle </li></ul></ul><ul><ul><li>Narrow AC & hypermetropia are risk factors </li></ul></ul><ul><ul><li>F>M </li></ul></ul>
  15. 21. Primary ACG <ul><li>Risk factors for primary angle closure </li></ul><ul><ul><li>Female </li></ul></ul><ul><ul><li>+ve FOH </li></ul></ul><ul><ul><li>Use of sympathomimetics </li></ul></ul><ul><ul><li>Race: Eskimos, Asians (esp. Mongolians) </li></ul></ul><ul><li>Primary angle closure is divided into 3 subtypes </li></ul><ul><ul><li>AACG </li></ul></ul><ul><ul><li>IACG </li></ul></ul><ul><ul><li>CACG </li></ul></ul>
  16. 22. AACG <ul><li>Rapid & excessive increase in IOP due to circumferential iris apposition to TM </li></ul><ul><li>Does not resolve spontaneously </li></ul><ul><li>Pathomechanisms </li></ul><ul><ul><li>Usually pupil block </li></ul></ul><ul><ul><li>Occasionally plateau iris & posterior aqueous misdirection </li></ul></ul><ul><li>1 in 1000 people aged over 40yrs (rarer than OAG) </li></ul><ul><li>M<F (1:4) </li></ul>
  17. 23. AACG <ul><li>Patients present with </li></ul><ul><ul><li>Haloes around lights </li></ul></ul><ul><ul><li>Blurred vision </li></ul></ul><ul><ul><li>Ipsilateral frontal headache </li></ul></ul><ul><ul><li>Occasionally nausea & vomiting </li></ul></ul><ul><ul><li>Painful red eye </li></ul></ul>
  18. 24. AACG <ul><li>On examination </li></ul><ul><ul><li>Red eye (venous & ciliary injection) </li></ul></ul><ul><ul><li> VA </li></ul></ul><ul><ul><li>IOP elevated; often 50-80 mmHg </li></ul></ul><ul><ul><li>Corneal oedema </li></ul></ul><ul><ul><li>Shallow or flat AC ±cells & flare </li></ul></ul><ul><ul><li>Gonio: angle closed 360° </li></ul></ul><ul><ul><ul><li>Peripheral iris pushed forward to contact Schwalbe’s line </li></ul></ul></ul><ul><ul><ul><li>Check fellow eye - usually occludable angle </li></ul></ul></ul>
  19. 25. AACG <ul><li>On examination (cont.) </li></ul><ul><ul><li>Pupil mid-dilated with reduced or absent reactivity </li></ul></ul><ul><ul><li>Fundoscopy </li></ul></ul><ul><ul><ul><li>Fundus may be normal </li></ul></ul></ul><ul><ul><ul><li>May be disc oedema with venous congestion & haemorrhage </li></ul></ul></ul><ul><ul><ul><li>There may be glaucomatous excavation </li></ul></ul></ul><ul><ul><ul><li>Arterial pulsation with high pressure </li></ul></ul></ul>
  20. 28. IACG <ul><li>Aetiology is similar to AACG but is a milder manifestation </li></ul><ul><li>Resolves spontaneously </li></ul><ul><li>Pathomechanisms as AACG </li></ul><ul><li>Patients present with mild intermittent symptoms similar to AACG (esp haloes, frontal headache, episodic blurred vision) </li></ul><ul><li>On examination, signs vary according to amount of appositional angle closure </li></ul><ul><ul><li>Pupil is round & reactive or there may be APD </li></ul></ul><ul><ul><li>Optic disc may be normal or atrophic </li></ul></ul>
  21. 29. CACG <ul><li>CACG is permanent synechial closure of any extent of the angle less that 360° </li></ul><ul><li>Pathomechanism as previous – probably the end result of repeated IACG </li></ul><ul><li>Symptoms </li></ul><ul><ul><li>Visual disturbance - transient & intermittent </li></ul></ul><ul><ul><li>Usually painless, occasional discomfort </li></ul></ul><ul><ul><li>Occasionally transient haloes if IOP acutely  </li></ul></ul>
  22. 30. CACG <ul><li>Signs </li></ul><ul><ul><li>PAS of any degree at gonioscopy </li></ul></ul><ul><ul><li>IOP elevated to a variable degree </li></ul></ul><ul><ul><li>VA may be normal </li></ul></ul><ul><ul><li>ONH damage as OAG </li></ul></ul><ul><ul><li>“ Typical” OAG visual field defects </li></ul></ul><ul><ul><li>Superimposed IACG or AACG possible </li></ul></ul><ul><li>Treatment may be medical or surgical </li></ul>
  23. 31. Post AACG Attack <ul><li>Following an attack of AACG, there may be </li></ul><ul><ul><li>Poor vision </li></ul></ul><ul><ul><li>Patchy iris atrophy </li></ul></ul><ul><ul><li>Iris torsion </li></ul></ul><ul><ul><li>Pseudopolycoria </li></ul></ul><ul><ul><li>Posterior synechiae </li></ul></ul><ul><ul><li>Poorly or non-reactive pupil </li></ul></ul><ul><ul><li>Glaukomflecken </li></ul></ul><ul><ul><li>PAS on gonioscopy </li></ul></ul><ul><ul><li> Endothelial cell count  chronic corneal oedema </li></ul></ul>
  24. 36. The Occludable Angle <ul><li>High risk of closure by aforementioned mechanisms </li></ul><ul><li>Fellow eye of AACG/IACG/CACG </li></ul><ul><li>IOP elevation may or may not be present </li></ul>
  25. 37. Secondary ACG <ul><li>Pupil block can develop due to </li></ul><ul><ul><li>Swollen lens (cataract, trauma) </li></ul></ul><ul><ul><li>Anterior lens dislocation </li></ul></ul><ul><ul><li>PS  seclusio pupillae & iris bombé </li></ul></ul><ul><ul><li>Miotic use (lens moves forward, also) </li></ul></ul><ul><ul><li>IOL-induced (ACL; anterior dislocation of PCIOL) </li></ul></ul>
  26. 38. Secondary ACG <ul><li>An anterior “pulling” mechanism can obstruct TM, either by iris tissue or membrane </li></ul><ul><ul><li>NVG </li></ul></ul><ul><ul><li>Following trauma or intraocular surgery </li></ul></ul><ul><ul><li>Inflammatory membrane </li></ul></ul><ul><ul><li>Aniridia </li></ul></ul>
  27. 39. Secondary ACG <ul><li>A posterior “pushing” mechanism can obstruct TM, because ciliary body & iris rotate forward </li></ul><ul><ul><li>Abnormally large lens (phacomorphic glaucoma) </li></ul></ul><ul><ul><li>Aqueous misdirection following PCIOL insertion </li></ul></ul><ul><ul><li>Iris/ciliary body cysts & tumours </li></ul></ul><ul><ul><li>Uveal effusion </li></ul></ul><ul><ul><ul><li>Inflammatory (scleritis, uveitis), increased choroidal venous pressure (PRP, CRVO, scleral buckling), tumour </li></ul></ul></ul><ul><ul><li>ROP </li></ul></ul>
  28. 48. What is “IOP”?
  29. 49. Risk Factors for OAG <ul><li>IOP </li></ul><ul><li>Race </li></ul><ul><li>Age </li></ul><ul><li>Gender </li></ul><ul><li>Myopia </li></ul><ul><li>FOH of glaucoma OR visual loss </li></ul><ul><li>Optic nerve head ‘structure’ </li></ul><ul><li>Vascular disease </li></ul><ul><ul><li>Hypotension </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Vasospasm </li></ul></ul><ul><ul><li>Rheological abnormalities </li></ul></ul><ul><ul><li>Disc haemorrhage </li></ul></ul><ul><ul><li>?Diabetes mellitus </li></ul></ul><ul><li>Cigarette smoking </li></ul><ul><li>Hypothyroidism </li></ul>
  30. 50. % of Population Developing Glaucomatous Damage IOP (mmHg)
  31. 51. Rate Of Visual Loss & IOP in POAG <ul><li>21-25 mmHg </li></ul><ul><li>26-30 mmHg </li></ul><ul><li>>30 mmHg </li></ul><ul><li>14yrs </li></ul><ul><li>6yrs </li></ul><ul><li>3yrs </li></ul>
  32. 52. Loss of Central Vision & IOP in POAG <ul><li><18 mmHg </li></ul><ul><li>18-22 mmHg </li></ul><ul><li>>22 mmHg </li></ul><ul><li>4% </li></ul><ul><li>19% </li></ul><ul><li>29% </li></ul>
  33. 54. OHT <ul><li>Unknown aetiology & pathomechanism </li></ul><ul><li>IOP >21mmHg </li></ul><ul><li>ONH normal </li></ul><ul><li>VF normal </li></ul><ul><li>No other risk factors </li></ul>
  34. 55. Definition of OAG <ul><li>“ The open angle glaucomas are a group of chronic, progressive optic neuropathies that have in common characteristic morphological changes at the optic nerve head & retinal nerve fibre layer in the absence of other ocular disease or congenital anomalies. Progressive retinal ganglion cell death & visual field loss are associated with these changes.” European Glaucoma Society, 1998. </li></ul>
  35. 56. OAG <ul><li>Primary open angle glaucoma </li></ul><ul><li>Normal tension glaucoma </li></ul><ul><li>Ocular hypertension </li></ul>
  36. 57. POAG <ul><li>Unknown aetiology </li></ul><ul><li>Unknown pathomechanism </li></ul><ul><li>Asymptomatic until field loss advanced </li></ul><ul><li>IOP>21mmHg without treatment </li></ul><ul><li>ONH suffers characteristic damage </li></ul><ul><li>Visual field shows corresponding damage </li></ul><ul><li>Gonioscopy shows open angle; not occludable; no goniodysgenesis </li></ul>
  37. 58. POAG <ul><li>POAG suspect </li></ul><ul><ul><li>ONH & VF normal or suspicious </li></ul></ul><ul><ul><li>Peak IOP >21mmHg but <30mmHg without treatment </li></ul></ul><ul><ul><li>IOP difference >4mmHg between the two eyes </li></ul></ul><ul><ul><li>Concurrent vascular risk factors </li></ul></ul><ul><ul><li>POAG in fellow eye </li></ul></ul><ul><ul><li>AION in fellow eye </li></ul></ul>
  38. 59. NTG <ul><li>Unknown aetiology </li></ul><ul><li>Unknown pathomechanism though vascular factors thought to be important </li></ul><ul><li>Asymptomatic until field loss advanced </li></ul><ul><li>Peak IOP <21mmHg without treatment (phased) </li></ul><ul><li>ONH damage as POAG </li></ul><ul><li>VF damage as POAG; paracentral defects are more common </li></ul><ul><li>Gonioscopy: open, unoccludable angle </li></ul>
  39. 60. Nocturnal Hypotension
  40. 61. NTG <ul><li>NTG suspect </li></ul><ul><ul><li>Normal or suspicious VF &/or ONH </li></ul></ul><ul><ul><li>IOP as NTG </li></ul></ul><ul><ul><li>IOP difference >4mmHg between eyes </li></ul></ul><ul><ul><li>Vascular risk factors </li></ul></ul><ul><ul><li>NTG in fellow eye </li></ul></ul>
  41. 62. IOP in NTG <ul><li>Diagnosis of NTG can only be made after IOP phasing </li></ul><ul><li>A reduction of IOP of 30% in NTG eyes prevents progression in 80% of eyes </li></ul><ul><li>A 30% reduction of IOP in NTG is possible in 50% of NTG eyes </li></ul><ul><li>If NTG remains untreated, 50-60% of eyes DO NOT show progression </li></ul>
  42. 63. NTG & HTG
  43. 64. NTG & HTG
  44. 65. IOP  Mechanical damage Perfusion pressure  Blood pressure  Vascular resistance  Blood flow 
  45. 66. ONH Autoregulation IOP Perfusion Rheology Other factors Structural factors
  46. 67. 2° OAG <ul><li>Elevated IOP causing progressive typical glaucomatous damage to ONH & VF caused by ocular or extraocular disease(s) or drugs </li></ul><ul><ul><li>Pseudoexfoliation syndrome </li></ul></ul><ul><ul><li>Pigmentary glaucoma </li></ul></ul><ul><ul><li>Phacolytic glaucoma </li></ul></ul><ul><ul><li>Ghost cell glaucoma </li></ul></ul><ul><ul><li>Uveitic glaucoma </li></ul></ul><ul><ul><li>Glaucoma due to intraocular tumours </li></ul></ul><ul><ul><li>Glaucoma associated with retinal detachment </li></ul></ul>
  47. 68. 2° OAG <ul><li>[Classification continued] </li></ul><ul><ul><li>Glaucoma secondary to ocular trauma </li></ul></ul><ul><ul><li>Glaucoma due to corticosteroid treatment </li></ul></ul><ul><ul><li>Glaucoma due to ocular surgery & laser </li></ul></ul><ul><ul><li>Glaucoma caused by increased episcleral venous pressure </li></ul></ul>
  48. 69. 2° OAG <ul><li>Pseudoexfoliation glaucoma </li></ul><ul><ul><li>Pseudoexfoliative material = abnormal fibrillo-granular protein; accumulates in TM </li></ul></ul><ul><ul><li>Syndrome also involves pigment accumulation in TM </li></ul></ul><ul><ul><li>Similar material has been identified at extraocular sites </li></ul></ul><ul><ul><li> Aqueous outflow </li></ul></ul><ul><ul><li>Onset usually after age 60yrs </li></ul></ul>
  49. 70. 2° OAG <ul><li>Pseudoexfoliation glaucoma (cont.) </li></ul><ul><ul><li>IOP >21mmHg, often in the 40s </li></ul></ul><ul><ul><li>ONH & VF loss as in POAG </li></ul></ul><ul><ul><li>Dandruff-like material on pupil margin & anterior lens capsule </li></ul></ul><ul><ul><li>Pupillary collarette appears motheaten </li></ul></ul><ul><ul><li>Often associated with NS, narrow angle, phacodonesis </li></ul></ul><ul><ul><li>Pigment deposition anterior to Schwalbe’s line is termed Sampaolesi’s line </li></ul></ul>
  50. 74. 2° OAG <ul><li>Pigmentary glaucoma </li></ul><ul><ul><li>Melanin granules accumulate in the TM   aqueous outflow </li></ul></ul><ul><ul><li>“ Reverse pupillary block” theory </li></ul></ul><ul><ul><ul><li>Iris acts as valve </li></ul></ul></ul><ul><ul><ul><li>AC IOP > PC IOP pushing peripheral iris membrane posteriorly </li></ul></ul></ul><ul><ul><ul><li>Melanin granules released because iris rubs on zonules </li></ul></ul></ul>
  51. 75. 2° OAG <ul><li>Pigmentary glaucoma (cont.) </li></ul><ul><ul><li>Onset typically third - fifth decades (i.e. under 40!) </li></ul></ul><ul><ul><li>1-2% of the total glaucoma cases </li></ul></ul><ul><ul><li>White myopic males esp </li></ul></ul><ul><ul><li>Unilateral or bilateral </li></ul></ul><ul><ul><li>IOP can rise acutely  ACG symptoms </li></ul></ul><ul><ul><li>IOP usually >21mmHg with large variations esp. after exercise, blinking, mydriasis </li></ul></ul><ul><ul><li>Deep AC, iris transillumination, pigmented TM, Schwalbe’s line, iris surface, Krukenberg’s spindle </li></ul></ul>
  52. 80. 2° OAG <ul><li>Lens induced open angle glaucoma </li></ul><ul><ul><li>3 mechanisms </li></ul></ul><ul><ul><ul><li>Phacolytic </li></ul></ul></ul><ul><ul><ul><li>Traumatic </li></ul></ul></ul><ul><ul><ul><li>Phacoanaphylactic </li></ul></ul></ul><ul><ul><li>Age of onset depends on pathomechanism </li></ul></ul><ul><ul><li>Often painful with inflammatory response </li></ul></ul><ul><ul><li>IOP >21mmHg </li></ul></ul><ul><ul><li>Injured lens or cataract; AAU; phakic state of fellow eye </li></ul></ul>
  53. 84. 2° OAG <ul><li>Ghost cell glaucoma </li></ul><ul><ul><li>Follows intraocular haemorrhage </li></ul></ul><ul><ul><ul><li>Anterior chamber </li></ul></ul></ul><ul><ul><ul><li>Vitreous chamber </li></ul></ul></ul><ul><ul><li>Effete ghost cells are more rigid than viable RBCs & block TM </li></ul></ul><ul><ul><li>Often painful </li></ul></ul><ul><ul><li>TM can also be blocked following hyphaema </li></ul></ul>
  54. 86. 2° OAG <ul><li>Uveitic glaucoma </li></ul><ul><ul><li>Anterior & intermediate uveitides </li></ul></ul><ul><ul><ul><li>JCA, FUS, Posner-Schlossman syndrome, HSV, VZV, sarcoidosis, Behçet’s disease, sympathetic ophthalmia, pars planitis </li></ul></ul></ul><ul><ul><li>TM blocked by oedema, inflammatory cells & debris, scarring, neovascularisation </li></ul></ul><ul><ul><li>Pupil block 2° to PS can also form </li></ul></ul><ul><ul><li>Onset depends on pathomechanism </li></ul></ul>
  55. 87. 2° OAG <ul><li>Glaucoma due to intraocular tumours </li></ul><ul><ul><li> Aqueous outflow due to primary or metastatic anterior segment tumour </li></ul></ul><ul><ul><li>TM may be compressed or invaded by tumour </li></ul></ul><ul><ul><li>Also tumour related inflammation, tumour necrosis, haemorrhage & pigment dispersion </li></ul></ul><ul><ul><li>Secondary ACG may also develop </li></ul></ul><ul><ul><li>Onset & clinical picture highly variable </li></ul></ul>
  56. 88. 2° OAG <ul><li>Glaucoma associated with retinal detachment </li></ul><ul><ul><li>RD usually associated with lower IOP </li></ul></ul><ul><ul><li>TM can be blocked by proliferative processes, pigment, scarring, inflammation </li></ul></ul>
  57. 89. 2° OAG <ul><li>OAG due to ocular trauma </li></ul><ul><ul><li>Several mechanisms </li></ul></ul><ul><ul><ul><li>Open angle & closed angle mechanisms </li></ul></ul></ul><ul><ul><li>Trauma can cause </li></ul></ul><ul><ul><ul><li>Scarring, inflammation, obstruction by RBC & debris, release of lens proteins, angle recession </li></ul></ul></ul><ul><ul><li>Varies from painful & red to asymptomatic </li></ul></ul><ul><ul><li>IOP can be normal at presentation & climb slowly over the years </li></ul></ul>
  58. 92. 2° OAG <ul><li>Corticosteroid induced OAG </li></ul><ul><ul><li>TIGR gene implicated </li></ul></ul><ul><ul><li>Tendency in myopes, diabetics & POAG </li></ul></ul><ul><ul><li>Blockage of TM by mucopolysaccharide with topical steroid </li></ul></ul><ul><ul><li>Increased aqueous production with systemic steroids </li></ul></ul><ul><ul><li>IOP elevation is usually reversible on cessation of steroid </li></ul></ul>
  59. 93. 2° OAG <ul><li>OAG secondary to intraocular surgery & laser </li></ul><ul><ul><li>Pigmentary loss, lens material, haemorrhage, inflammation & trauma are possible mechanisms </li></ul></ul><ul><ul><li>Alternative pathomechanisms are </li></ul></ul><ul><ul><ul><li>Viscoelastic materials, vitreous in AC, prostaglandin release (IOP spike transient) </li></ul></ul></ul><ul><ul><ul><li>IOP transient spike following YAG capsulotomy, YAG iridotomy, ALT </li></ul></ul></ul><ul><ul><ul><li>Macrophages take up silicone oil & block TM </li></ul></ul></ul><ul><ul><ul><li>ACIOL can induce chronic uveitis & bleeding of iris root </li></ul></ul></ul>
  60. 94. 2° OAG <ul><li>Glaucoma secondary to increased episcleral venous pressure </li></ul><ul><ul><li>Reduced aqueous outflow via schlemm’s canal </li></ul></ul><ul><ul><li>Episcleral, orbital & general causes </li></ul></ul><ul><ul><ul><li>Dural shunts, toxic or thermal damage to episcleral veins, TED, retrobulbar orbital tumour, AV fistula, Sturge-Weber syndrome et al++ </li></ul></ul></ul>
  61. 95. Next lecture……………

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