Classification of Glaucoma

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Classification of Glaucoma

  1. 1. CLASSIFICATION OF GLAUCOMA
  2. 2. CLASSIFICATION OF GLAUCOMA Factors to be considered in classification of Glaucoma 1. Why to Classify ? 2. Congenital/Acquired 3. Acute/Chronic 4. Primary/Secondary 5. Open angle/Close angle
  3. 3. CLASSIFICATION OF GLAUCOM A- Primary Congenital Glaucoma A1- Primary Congenital Glaucoma A2- Primary Infantile Glaucoma A3- Glaucoma associated with congenital anomalies
  4. 4. CLASSIFICATION OF GLAUCOMA Glaucoma associated with congenital anomalies             Aniridia Sturge Weber Syndrome Neurofibromatosis Marfan’s Syndrome Pierre Robin’s Syndrome Homocystinuria Lowe’s Syndrome Micro-spherophakia Micro-cornea Rubella Syndrome Chromosomal abnormalities PHPV (Persistent hyper plastic Primary Vitreous)
  5. 5. CLASSIFICATION OF GLAUCOMA B- Primary Open Angle Glaucoma (POAG) B1- Primary Juvenile Glaucoma B2- Primary Open Angle Glaucoma (POAG) B3- Normal Tension Glaucoma (NTG) (POAGNormal Pressure) B4- Ocular Hypertension
  6. 6. CLASSIFICATION OF GLAUCOMA C. Secondary Open Angle Glaucoma Caused By Ophthalmological Diseases C1. Pseudo-exfoliation Glaucoma C2. Pigmentary Glaucoma C3. Lens Induced Secondary Open Angle Glaucoma C4. Glaucoma Associated With Intraocular Hemorrhage C5. Uveitic Glaucoma C6. Glaucoma Due To Intraocular Tumors
  7. 7. CLASSIFICATION OF GLAUCOMA C8. Glaucoma Associated With Retinal Detachment C9. Open Angle Glaucoma Due To Trauma C10. Glaucoma Due To Corticosteroids Treatment C11. Secondary Open Angle Glaucoma Due To Ocular Surgery And Laser
  8. 8. CLASSIFICATION OF GLAUCOMA D. Primary Angle Closure Glaucoma D1. Acute Angle Closure Glaucoma D2. Intermittent Angle Closure Glaucoma D3. Chronic Angle Closure Glaucoma D4. Status Post Acute Closure Attack
  9. 9. CLASSIFICATION OF GLAUCOMA E. Secondary Angle Closure Glaucoma E1. Secondary angle closure glaucoma with pupillary block E2. Secondary angle closure glaucoma with anterior pulling mechanism without papillary block E3. Secondary angle closure glaucoma with posterior pushing mechanism without pupillary block
  10. 10. CLASSIFICATION OF GLAUCOMA Pathogenesis of PACG Mechanisms of primary angle closure  Angle-closure is defined on the basis of findings at Gonioscopy  It is always important to exclude secondary causes of angle-closure Pupillary block mechanism Plateau-iris mechanism Lens mechanism Creeping-angle closure mechanism Posterior aqueous misdirection mechanism Systemic drugs and angle closure  1. 2. 3. 4. 5. 6.
  11. 11. CLASSIFICATION OF GLAUCOMA Mechanisms of primary angle closure  Pupillary block mechanism – The flow of aqueous from PC through the pupil to the AC is impeded causing the pressure in the PC to become higher than the AC. As a result, the peripheral iris, which is thinner than the central iris, bows forward and comes into contact with the trabecular meshwork and Schwalbe’s line. – The prevalence of PAC is higher in hyperopia, in elderly patients, in diabetics, women and in some races
  12. 12. CLASSIFICATION OF GLAUCOMA Pupil block • Increase in physiological pupil block • Dilatation of pupil renders peripheral iris more flaccid Increased pressure in posterior chamber causes iris bombe • • Angle obstructed by peripheral iris and rise in IOP
  13. 13. CLASSIFICATION OF GLAUCOMA Mechanisms of primary angle closure  Plateau-iris mechanism The isolated plateau iris mechanism causes angleclosure by direct obliteration of the chamber angle recess, crowded by the iris base when the pupil is dilated. This can occur only with one or more of the following: 1. The tissue of the peripheral iris is thick (iris rolls) 2. The iris base inserts anteriorly, leaving only a very narrow ciliary band, or inserts at the scleral spur 3. The ciliary processes are displaced anteriorly in the posterior chamber and push the iris base into the chamber angle. 4. The iris profile is almost flat from the periphery to the far periphery, where it becomes very steep, creating and extremely narrow angle recess.
  14. 14. CLASSIFICATION OF GLAUCOMA Angle closure in the plateau iris syndrome
  15. 15. CLASSIFICATION OF GLAUCOMA Mechanisms of primary angle closure  Lens mechanism Large and/or anteriorly placed crystalline lens can predispose per se to angle-closure and be a factor in worsening pupillary block. It can also cause secondary angle-closure glaucoma
  16. 16. CLASSIFICATION OF GLAUCOMA Mechanisms of primary angle closure  Creeping angle-closure mechanism Some cases of chronic angle-closure glaucoma result from synechial closure of the chamber angle, caused by a previous acute angle-closure ‘attack’, while creeping angle-closure is probably a primary event. The iris base ‘creeps’ on to the trabecular meshwork forming irreversible peripheral anterior synechiae (PAS). The IOP usually rises when more than half of the angle is obstructed.
  17. 17. CLASSIFICATION OF GLAUCOMA Mechanisms of primary angle closure  Posterior aqueous misdirection mechanism In rare cases posterior aqueous misdirection can be the cause of primary angle-closure, mostly resulting in chronic IOP elevation. In these cases, usually younger or middle aged women, the ciliary processes come into contact with the lens equator,and/or a firm zonule/posterior capsule diaphragm, causing misdirection of aqueous into the vitreous. As a consequence, the lens/iris diaphragm is pushed forward and occludes the chamber angle. Eyes predisposed to posterior aqueous misdirection often have narrow anterior chamber (peripheral and axial) and hypermetropia. After iridotomy or iridectomy, the use of miotics raises the IOP, whereas the use of cycloplegics reduces the IOP. This ‘inverse’ or ‘paradoxical’ reaction To parasympathomimetics should be tested only after iridotomy has been performed.
  18. 18. CLASSIFICATION OF GLAUCOMA Mechanisms of primary angle closure  Systemic drugs and angle-closure Systemic drugs which may induce angle-closure in pre-disposed individuals are phenothiazines and their derivatives, tricyclic and non-tricyclic antidepressants, monoamine oxidase inhibitors, antihistamines, antiParkinson drugs, some minor tranquillisers, parasympatholytic and sympathomimetic agent.
  19. 19. CLASSIFICATION OF GLAUCOMA Pathogenesis of POAG   Still not well understood Two Aspects – Outflow Facility – Sclerosis of Trabecular Meshwork – Pinocytosis – Contractile element in Trabecular meshwork relaxed with NO and contracted with endothelin  Optic Nerve Damage – Mechanical – Vascular – Neurotoxic
  20. 20. CLASSIFICATION OF GLAUCOMA Pathogenesis of POAG  Mechanical Damage – Chronically elevated IOP causes direct damage to the nerve fibres as they bent 90° through lamina cribrosa  Directly damage nerve fibres  Compromised blood flow  Delivery of nutrients – Interrupt retrograde flow of neurogenic factors from Axons to the somata
  21. 21. CLASSIFICATION OF GLAUCOMA Pathogenesis of POAG  Vascular Damage – Direct damage through IOP but can not explain NTG – Disturbance of Auto-regulation – Role of NO And Endothelin – NTG more common in patients with Vaso-spastic phenomenon i.e. Migraine, Raynaude’s, Prinzametal angina
  22. 22. CLASSIFICATION OF GLAUCOMA Pathogenesis of POAG  Neurotoxin – Genetically determined programmed death of neuronal cells --- Apoptosis – Activation of NMDA receptors by glutamate – levels of glutamate in vitreous of POAG patients – M-Cells more susceptible
  23. 23. CLASSIFICATION OF GLAUCOMA Pathogenesis of PCG  Impaired aqueous outflow in PCG is caused by maldevelopment of the angle of the anterior chamber, unassociated with any other major ocualr anomalies (isolated trabeculodysgenesis). Clinically, trabeculodysgenesis is characterized by absence of the angle recess with the iris inserted directly into the surface of the trabeculum in one of two configurations: 1. Flat iris insertion. The iris inserts flatly and abruptly into the thickened trabeculum at or anterior to the scleral spur. 2. Concave iris insertion is less common. The superficial iris tissue sweeps over the iridotrabecular junction and the trabeculum. In contrast to a flat iris insertion, the angular structures are obscured by the overlying iris tissue, which is either sheet-like or consists of a dense arborizing meshwork.
  24. 24. CLASSIFICATION OF GLAUCOMA Pathogenesis of PCG Flat iris insertion Concave iris insertion
  25. 25. Symptomatology in Glaucoma • • • • No complaints Glare/ photophobia /pain Redness / Watering Visual complaints 1. 2. 3. 4. 5. Haloes / Blurring / Loss of vision Accommodation difficulties Dark adaptation problems Fields defects Sudden loss of vision • Corneal enlargement / globe enlargement • Hazy cornea / corneal edema
  26. 26. Primary Congenital Glaucoma  Etiology  angle dysgenesis  Onset is from birth to Haloes / Blurring / Loss of vision  second year of life  2/3 of the patients are male, 2/3 of cases are bilateral.  2/3 of cases are non-hereditory  Presents with photophobia, tearing, blepharospasm and rubbing of eyes, big eyes, cloudy corneas  Examination under general anesthesia to measure IOP, corneal diameters, optic nerve head assessment and gonioscopy.
  27. 27.  Differential  Diagnosis Cloudy Cornea at birth • Birth trauma • Rubella Syndrome • Metabolic disorders  Large Cornea • Megalo-cornea  Lacrimation • Congenital blocked NLD • Keratitis • Uveitis
  28. 28.  Management  It is surgical which should be performed as early as possible. For a short period, drugs may be given.
  29. 29. Primary Infantile Glaucoma – Etiology  angle dysgenesis – Onset is from third to tenth year of life – Corneal diameters are within normal limits – On gonioscopy, open angle with poorly differentiated structures. – Cupping of optic nerve head and visual fields loss.
  30. 30. Primary Juvenile Glaucoma Etiology: Unknown Patho-mechanism: Decreased aqueous outflow Features  Onset tenth to 35th year of life  Heredity: family history may be present. Genes associated with primary juvenile glaucoma have been identified on chromosome 1 (1q21-q31) and TIGR  Signs and symptoms
  31. 31.  Asymptomatic  Peak IOP 24 mm Hg without treatment (diurnal curve)  Optic nerve head:  Optic nerve rim damage typical  Splinter hemorrhage  Nerve fiber layer: diffuse defects typical  Visual field: glaucomatous defects may be present  Gonioscopy: Open anterior chamber angle
  32. 32. Primary Open Angle Glaucoma (POAG) Etiology: Unknown Patho-mechanism: Decreased aqueous outflow Features: Onset: from 35th year of age onwards Signs and symptoms: Asymptomatic until field loss advanced IOP > 22 mm Hg without treatment (day curve) Optic nerve head: characteristic glaucomatous damage nerve fiber layer changes (diffuse or localized defects) Visual field: glaucomatous defects corresponding to the disc damage may be present Gonioscopy: open anterior chamber angle (not occludeno gonio-dysgenesis) and/or optic able,
  33. 33. Pathogenesis of POAG   Still not well understood Two Aspects – Outflow Facility – Sclerosis of Trabecular Meshwork – Pinocytosis – Contractile element in Trabecular meshwork relaxed with NO and contracted with endothelin  Optic Nerve Damage – Mechanical – Vascular – Neurotoxic
  34. 34. Pathogenesis of POAG  Mechanical Damage – Chronically elevated IOP causes direct damage to the nerve fibres as they bent 90° through lamina cribrosa  Directly damage nerve fibres  Compromised blood flow  Delivery of nutrients – Interrupt retrograde flow of neurogenic factors from Axons to the somata
  35. 35. Pathogenesis of POAG  Vascular Damage – Direct damage through IOP but can not explain NTG – Disturbance of Auto-regulation – Role of NO And Endothelin – NTG more common in patients with Vasospastic phenomenon i.e. Migraine, Raynaude’s, Prinzametal angina
  36. 36. Pathogenesis of POAG  Neurotoxin – Genetically determined programmed death of neuronal cells --- Apoptosis – Activation of NMDA receptors by glutamate – levels of glutamate in vitreous of POAG patients – M-Cells more susceptible
  37. 37. Normal Tension Glaucoma (NTG) (POAG-Normal Pressure) Etiology: Unknown Patho-mechanism: Unknown Features: Onset: from the 35th onwards Signs and symptoms: Asymptomatic until field loss advanced Peak IOP < 22 mm Hg without treatment (diurnal curve) Optic nerve head: damage typical of glaucoma Visual field defect: typical of glaucoma; common Para central defects Gonioscopy: open anterior chamber angle (not occlude-able) No history or signs of other eye disease or steroid use.
  38. 38. Ocular Hypertension Etiology: Unknown Patho-mechanism: Decreased aqueous outflow Features: Peak IOP > 21 mm Hg < 30 mm Hg without treatment (diurnal curve) Visual field: normal Optic disc and nerve fiber layer: normal Other risk factors: none
  39. 39. Pseudo-exfoliation Glaucoma Etiology: Pseudo-exfoliative material, an abnormal fibrillogranular protein, and pigment accumulate in the trabecular meshwork, where TM function decreases. Similar material has been identified in the conjunctiva and other body parts Patho-mechanism: reduction of the trabecular outflow owing to the pseudoexfoliative material Features: Onset: usually older than 60 years Frequency: large racial variations Asymptomatic until visual field loss advanced One or both eyes IOP: > 22 mm Hg, frequently higher than in average POAG cases
  40. 40. Visual field loss as in POAG; frequently severe at least in one eye Slit lamp examination: dandruff-like exfoliation material on the pupil border and on the surface of the anterior lens capsule except the central zone, better visualized after pupillary dilation. The pupillary collarette is irregular and typically has a moth-eaten appearance. Frequently associated with nuclear cataract, Pigmentary loss from the central or mid-iris pigment granules in the angle. When pigment accumulates along an undulating line anterior to Schwalbe’s line it is called Sampaolesi’s line. Loose zonules are frequent with occasional phacodonesis and lens subluxation. Narrow or closed angle is relatively common.
  41. 41. Pigmentary Glaucoma Etiology: Melanin granules accumulate in the trabecular meshwork, where TM function decreases. Patho-mechanism: Reduction of the trabecular outflow owing to melanin granules. According to the theory of ‘reverse papillary block’ the iris works as a valve resulting in IOP higher in the anterior chamber than in the posterior chamber, causing peripheral posterior bowing of the iris. Melanin granules are released from the iris as a result of rubbing between the zonules and the posterior surface of the iris. Features: Onset: typically third to fifth decades Frequency: 1-1.5% of the total glaucoma cases, mostly Caucasians, more in myopes, male. One or both eyes
  42. 42. Symptoms: uncommonly mild to moderate pain during acute episodes of IOP rise. Haloes around lights. IOP: > 21 mm Hg, characteristically with large variations. Significant increase may occur after exercise, pupillary dilation or blinking. Gradual decrease of IOP with age 60 years has been reported. Slit lamp examination: deep anterior chamber, midperipheral iris pigment epithelial atrophy with radial pattern especially well visible with retro-illumination. Pigment dispersed on the trabecular meshwork, the Schwalbe’s line, the iris surface, and the lens equator and on corneal endothelium, where often shapes as a central, vertical spindle (Krukenberg’s spindle).
  43. 43. Lens Induced Secondary Open Angle Glaucoma Etiology: Obstruction of the trabecular meshwork by lens proteins and/or inflammatory cells induced by lens proteins. Patho-mechanism: Lens proteins from a mature or hyper mature cataract with intact capsule (phacolytic glaucoma) Lens particles from a traumatically or surgically injured lens (lens particle glaucoma) Granulomatous inflammation of the trabecular meshwork after uneventful ECCE when the fellow eye was already operated and the lens proteins has sensitized the immune system (phaco-anaphylatic glaucoma)
  44. 44. Features: Age of onset and acute or chronic course depend on the pathomechanism Often painful with redness and inflammation IOP > 22 mm Hg Slit lamp examination: injured lens and /or cataract or after ECCE, with or without iritis
  45. 45. Glaucoma Associated With Intraocular Hemorrhage Etiology: Obstruction of the trabecular meshwork by rigid red blood cells (ghost cell glaucoma, sickle cell disease) or by a large quantity of normal red blood cells (hyphaema). Pathomechanism: Red blood cells (ghost cells) from an old vitreous hemorrhage, via a ruptured anterior hyaloid face, or from the iris (for example trauma and intraocular surgery) obstruct the trabecular meshwork Features: Pain, redness, recurrences possible IOP > 22 mm Hg
  46. 46. Uveitic Glaucoma Etiology: Several forms of anterior and intermediate uveitis can cause unilateral or bilateral obstruction of the trabecular meshwork. The most frequent conditions are           Juvenile rheumatoid arthritis Fuchs’ heterochromic inidocyclitis Posner-Schlossman syndrome (glaucomatocyclitic crisis) Herpes simplex Herpes zoster Syphilis Sarcoidosis Behcet’s disease Sympathetic ophthalmitis Pars planitis
  47. 47. Pathomechanism: Obstruction and edema of the trabecular meshwork caused by inflammatory cells, precipitates, debris, secondary scarring and neovascularization of the chamber angle. Secondary angle closure glaucoma due to synechiae can also develop. Features: Onset depends on underlying condition. Any age Pain, redness, photophobia, decreased vision are possible. IOP > 22 mm Hg. Some forms are associated with wide oscillations or periodic rise of IOP.
  48. 48. Glaucoma Due To Intraocular Tumors Etiology: Reduced aqueous humour outflow due to primary or secondary intraocular (anterior segment) tumors Pathomechanism: Compression or tumor extension to the trabecular meshwork and/or outflow channels. Trabecular meshwork obstruction due to tumor related inflammation, tumor necrosis, hemorrhage and pigment dispersion. (Secondary angle-closure glaucoma may also develop) Features: IOP > 22 mm Hg Onset and clinical picture highly variable, combining evidence for both the tumor and the glaucoma
  49. 49. Glaucoma Associated With Retinal Etiology: Although retinalDetachment associated with lower detachment is usually than normal IOP, the same disease processes can also cause both reduced trabecular outflow and retinal detachment Pathomechanism: Neovascularization, proliferative retinopathy, scarring, pigment dispersion and inflammation (e.g. photoreceptor sensitization). Cases in which surgery for retinal detachment causes glaucoma are discussed in the section of secondary angle closure glaucoma. Features: IOP > 22 mm Hg Redness and pain is possible Retinal detachment is present Note: In general, retinal detachment is associated with lower than normal IOP. Surgeries for retinal detachment can cause glaucoma.
  50. 50. Open Angle Glaucoma Due To Trauma Note: Ocular trauma leads to glaucoma by several different mechanisms. The secondary traumatic glaucomas can be caused by both open angle and angle closure pathomechanisms. To identify the etiology one must carefully evaluate all traumatic damage to the eye. Etiology: Reduced trabecular outflow due to traumatic changes of the trabecular meshwork Pathomechanism: Scarring and inflammation of the trabecular meshwork, obstruction by red blood cells and debris, lens induced glaucoma, angle recession Features: Highly variable Redness, pain, decreased vision, or no symptoms IOP > 22 mm Hg. Elevated intraocular pressure can be present immediately, but slow elevation occurring months, or up to decades later are also possible. Slit lamp examination: chemical burns, hyphema, traumatic cataract, swollen lens, uveitis, angle recession, ruptured iris sphincter.
  51. 51. Glaucoma Due To Corticosteroids Treatment Etiology: Reduced trabecular outflow due to trabecular changes caused by corticosteroids (TIGR gene) Pathomechanism: Topical as well as high dose and long-term systemic corticosteroids therapy induces changes in the trabecular extracellualr material (glycoproteins) that leads to decreased outflow facility. Usually pressure elevation is reversible if the corticosteroids stopped. Features: Individual, hereditary susceptibility can occur. Myopic, diabetic subjects and POAG patients may be more susceptible No pain, no redness, corneal edema is possible IOP > 22 mm Hg Typical glaucomatous optic nerve head and field damage if the disease is long-standing
  52. 52. Secondary Open Angle Glaucoma Due To Ocular Surgery And Laser Ocular surgery can cause secondary open-angle glaucoma by some of the mechanisms discussed above Pigmentary loss from uveal tissue, lens material, hemorrhage, uveitis and trauma. Etiology: Reduced trabecular outflow Pathomechanism: Visco-elastic materials, inflammatory, debris, intra-operative application of alpha-chymotrypsin, lens particles, vitreous in the anterior chamber after cataract surgery, prostaglandin. IOP elevation is usually transient. Acute onset secondary IOP elevation after Nd: YAG laser iridotomy, capsulotomy and argon laser trabeculoplasty. Usually transient, within the first 24 hours, most frequent in the first 4 hours after treatment
  53. 53. Silicone oil emulsion implanted intravitreally enters the anterior chamber and is partially phagocytosed by macrophages and accumulates in the trabecular meshwork (especially in the upper quadrant) Uveitis-glaucoma-hyphema (UGH) syndrome. Episodic onset, associated with anterior chamber pseudophakia. IOP elevation is induced by recurrent iris root bleeding and anterior uveitis. Features: Pain, redness, corneal edema are possible IOP > 22 mm Hg Visual field loss when IOP elevation is sufficient
  54. 54. PRIMARY ANGLE CLOSURE GLAUCOMA Mechanisms of primary angle closure  Pupillary block mechanism  Plateau iris mechanism  Creeping angle closure  Posterior aqueous misdirection
  55. 55. Acute Angle Closure Glaucoma          Peripheral iris apposition to trabecular meshwork causes rapid and severe rise in IOP. Decreased visual acuity Corneal edema Shallow anterior chamber Gonioscopy, closed angle 360 degrees Mid dilated, non reacting pupil Ciliary congestion Disc edema with or without glaucomatous excavation Symptoms of pain, Haloes, nausea and vomiting
  56. 56. Differential Diagnosis;  Secondary acute angle closure glaucoma  Neo-vascular glaucoma  Glaucomatico Cyclitic crisis  Other causes of acute headache
  57. 57. Management;  Immediate Treatment  Control pain  Bring down the intraocular pressure Pilocarpine  Beta-blocker  Steroids  Acetazolamide  Hyper-osmotic agents   Late treatment  Laser iridotomy  Surgical Iridotomy  Trabeculectomy
  58. 58. Intermittent Angle Closure Glaucoma  Manifestations are similar to acute angle closure but less severe and resolve spontaneously  Signs vary according to the amount of angle closure  Optic disc may show atrophy
  59. 59. Chronic Angle Closure Glaucoma  Caused by permanent angle closure by synechiae  IOP is variable, depending upon the amount of angle closure present  Optic disc cupping and visual field defects typical of glaucoma are present  Superimposed acute or intermittent angle closure may be present  Usually there is no pain but some discomfort may be present
  60. 60. Status Post Acute Closure Attack  Patchy iris atrophy  Iris torsion  Posterior synechiae  Pupil poorly reacting  Glaukomflecken  PAS on gonioscopy
  61. 61. Secondary angle closure glaucoma with pupillary block Clinical examples Swollen lens, Anterior dislocation of lens, Seclusio or occlusive pupillae. Pupil block due to herniating vitreous or an air bubble or silicon oil.
  62. 62. Secondary angle closure glaucoma with anterior pulling mechanism without papillary block Clinical examples Neovascular glaucoma, Irido-corneo-endothelial syndromes, Epithelial or fibrous in growth, Argon Laser Trabeculoplasty (ALT).
  63. 63. Secondary angle closure glaucoma with posterior pushing mechanism without papillary block Ciliary body and iris rotating forwards cause the angle closure. Clinical examples Malignant glaucoma, Iris and ciliary body cysts Intraocular tumors

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