Glaucoma good


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  • And you thought glaucoma was a disease in which there was too much pressure in the eye! So did most ophthalmologists until several years ago.
  • But pressure certainly plays a role. Glaucoma is just too complicated to fit a nice simple definition.
  • The Advanced Glaucoma Intervention Study documented that pressure does play a crucial role in the visual field damage of many patients. Note that the greater the percentage of visits in which the pressure was below 28, the less visual field defects developed.
  • The three mainstays of glaucoma diagnosis are inadequate. The actual intra-ocular pressure is too imprecise, and the changes in the visual field and the optic nerve occur too late to prevent most of the damage.
  • Sobering facts!
  • Two standard deviations above the mean occurs at about 22-23 mmHg.
  • Large intra-day fluctuations as seen on the right are a risk factor for glaucoma
  • The aqueous humor is manufactured by the non-pigmented ciliary epithelium in the posterior chamber.
  • Iris Bombe with secluded pupil
  • Normal anatomy. The aqueous humor is made in the posterior chamber and escapes through the trabecular meshwork of the anterior chamber.
  • These techniques illustrate the two most common means of measuring intra-ocular pressures. Applanation is probably the most accurate method but requires a slit lamp to use it.
  • Is this island of vision seen from a right eye or a left eye?
  • No two disks are alike. Signs suggesting glaucoma as seen in the right photo include a large cup, nasalization of vessels, and pallor of the cup. Note the peripapilary depigmentation on the right which can make the true cup:disk ratio difficult to estimate.
  • In glaucoma of all types, if not controlled. There is progressive enlargement of the cup, increased pallor of the base of the cup, and nasalization of the disk vessels.
  • Whie there is lots of variation in glaucomatous disks, three common characteristics stand out: large cups, pale color and nasalization of the vessels.
  • Note how vessels can hide under the lip of the disk which helps explain the apparent loss of continuity of vessels clinically.
  • Note that eyes with the thinnest corneas and highest pressures are at the greatest risk for developing open angle glaucoma.
  • The thinnest corneas with the greatest vertical cup:disk ratios are the most likely to develop open angle glaucoma.
  • This lecture covers only congenital and adult varieties of glaucoma but it is important to realize there are many other causes.
  • Haab’s striae are found only in congenital glaucoma.
  • The right eye in each patient has congenital glaucoma.
  • The classical signs and symptoms of narrow angle glaucoma.
  • Anterior chamber angles vary widely. Only Grade I angles are occludable and might lead to an angle closure attack, similar to what a Grade 0 looks like.
  • When the trabecular meshwork is obstructed, outflow is impaired and pressure rises. This can occur due to congenitally narrowed angles, the development of synechiae (top right), or rubeosis with a flat chamber (bottom right).
  • Mid-dilated, fixed pupils and cloudy corneas during an angle closure attack.
  • The permanent surgical cure for narrow angle glaucoma.
  • Remember: most patients with open angle glaucoma have no symptoms. This is the best reason to have periodic eye examinations with pressure checks and optic nerve evaluations.
  • No treatment works all the time!
  • Mechanisms of drug action vary and many people require multiple medications.
  • These are the two most common surgical procedures for open angle glaucoma with success rates of 80+%.
  • Creating a path for the aqueous to escape into the sub-conjunctival space is the aim of filtration surgery.
  • Glaucoma good

    1. 1. GLAUCOMA Harold E. Cross M.D., Ph.D. (Contributions by Todd Altenbernd, MD) 10-06-09 v. 7.0
    2. 2. GLAUCOMA What is it? A disease of progressive optic neuropathy with loss of retinal neurons and the nerve fiber layer, resulting in blindness if left untreated.
    3. 3. GLAUCOMA “Glaucoma describes a group of diseases that kill retinal ganglion cells.” “High IOP is the strongest known risk factor for glaucoma but it is neither necessary nor sufficient to induce the neuropathy.” Libby, RT, et al: Annu Rev Genomics Hum Genet 6: 15, 2005
    4. 4. GLAUCOMA What causes it? There is a dose-response relationship between intraocular pressure and the risk of damage to the visual field.
    6. 6. GLAUCOMA How do we diagnose it?     IOP is not helpful diagnostically until it reaches approximately 40 mm Hg at which level the likelihood of damage is significant. Visual fields are also not helpful in the early stages of diagnosis because a considerable number of neurons must be lost before VF changes can be detected. Optic nerve damage in the early stages is difficult or impossible to recognize. 50% of people with glaucoma do not know it!
    7. 7. GLAUCOMA Intraocular pressure is not the only factor responsible for glaucoma!    95% of people with elevated IOP will never have the damage associated with glaucoma. One-third of patients with glaucoma do not have elevated IOP. Most of the ocular findings that occur in people with glaucoma also occur in people without glaucoma.
    8. 8. GLAUCOMA Population distribution of IOP
    9. 9. GLAUCOMA IOP Variables Gender influences: Normal vs glaucoma:
    10. 10. GLAUCOMA Anatomy of anterior chamber angle
    11. 11. GLAUCOMA Iris bombé
    12. 12. GLAUCOMA Angle Anatomy
    13. 13. GLAUCOMA How do we measure IOP? Applanation Tonopen Schiotz Air Non-contact
    14. 14. GLAUCOMA Tonometry Applanation Schiotz
    15. 15. GLAUCOMA Goldmann applanation tonometer
    16. 16. GLAUCOMA Tonopen
    17. 17. GLAUCOMA The normal visual field: an island of vision in a sea of darkness:
    18. 18. GLAUCOMA Goldmann perimeter Glaucoma visual fields
    19. 19. THE VISUAL FIELD Humphrey automated perimetry
    20. 20. GLAUCOMA Visual fields in glaucoma Early Late
    21. 21. GLAUCOMA Cup-to-disk ratio
    22. 22. GLAUCOMA DISK CUPPING Normal Glaucoma
    23. 23. GLAUCOMA Glaucomatous cupping
    24. 24. GLAUCOMA The histology of glaucomatous optic nerve cupping: Glaucomatous: Normal:
    25. 25. GLAUCOMA Optic nerve signs of glaucoma progression  Increasing C:D ratio Development of disk pallor  Disc hemorrhage (60% will show progression of visual field damage)  Vessel displacement  Increased visibility of lamina cribosa 
    26. 26. GLAUCOMA Ocular hypertension treatment study (OHTS study) GOALS: To evaluate the effectiveness of topical ocular hypotensive medications in preventing or delaying visual field loss and/or optic nerve damage in subjects with ocular hypertension at moderate risk for developing open-angle glaucoma (POAG). POPULATION: 1636 participants aged 40-80 years with IOP 24-32 mm HG in one eye, and 21-32 in the other, randomly assigned to observation and treatment groups.
    27. 27. GLAUCOMA OHTS parameters    TREATMENT GOALS: Reduce pressure to less than or equal to 24 mm Hg with a minimum pressure reduction of 20% from the baseline. OUTCOME MEASURES: Development of reproducible visual field abnormality or development of optic disc deterioration. MEDICATIONS USED: beta-adrenergic antagonists, prostaglandin analogues, topical carbonic anhydrase inhibitors, alpha-2 agonists, parasympathomimetic agents, and epinephrine.
    28. 28. GLAUCOMA OHTS Conclusions At 60 months, the probability of developing glaucoma was: 9.5% in observation group 4.4% in treatment group
    29. 29. GLAUCOMA OHTS parameters that influence the risk of developing POAG IOP Age Cup-disk ratio Central corneal thickness
    30. 30. GLAUCOMA Percentage of OHTS participants in observation group who developed POAG (mean follow-up = 72 mo) IOP vs central corneal thickness
    31. 31. GLAUCOMA Normal central corneal thickness: 545 – 550 u Add or subtract 2.5 mmHg for each 50 u change in central corneal thickness
    32. 32. GLAUCOMA Types of glaucoma I. Primary: A. Congenital B. Hereditary C. Adult (common types) 1. Narrow angle 2. Open angle II. Secondary A. Inflammatory B. Traumatic C. Rubeotic D. Phacolytic etc.
    33. 33. Congenital Glaucoma Onset: antenatally to 2 years old Symptoms Irritability Photophobia Epiphora Poor vision Signs Elevated IOP Buphthalmos Haab’s striae Corneal clouding Glaucomatous cupping Field loss
    34. 34. Congenital Glaucoma Buphthalmos and cloudy corneas
    35. 35. Congenital Glaucoma Buphthalmos, glaucomatous cupping, and cloudy cornea OD Normal OS Haab’s striae
    36. 36. Narrow Angle Glaucoma Onset: 50+ years of age Symptoms Severe eye/headache pain Blurred vision Red eye Nausea and vomiting Halos around lights Intermittent eye ache at night Signs Red, teary eye Corneal edema Closed angle Shallow AC Mid-dilated, fixed pupil “Glaucomflecken” Iris atrophy AC inflammation
    37. 37. GLAUCOMA Angle anatomy Grade I Grade 0 Grade III Grade II
    38. 38. GLAUCOMA Anatomy of Angle Closure Glaucoma
    39. 39. Narrow Angle Glaucoma Mid-dilated, fixed pupil
    40. 40. Narrow Angle Glaucoma Treatment: Peripheral Iridotomy
    41. 41. Open Angle Glaucoma Aka: chronic simple glaucoma (CSG) and primary open angle glaucoma (POAG) Onset: 50+ years of age Symptoms Signs Usually none Elevated IOP May have loss of central Visual field loss and peripheral vision Glaucomatous disk changes late
    42. 42. Open Angle Glaucoma Risk factors HISTORY:  Positive family history  African American background  History of trauma  History of steroid use EXAMINATION: C/D 0.6 or greater Vertical elongation of disc Inf. rim thinner than sup. C/D 0.2 asymmetry >
    43. 43. GLAUCOMA Treatment Medical Miotics  Beta-blockers  Carbonic anhydrase inhibitors  Prostaglandin analogues  Alpha-2 agonists  Surgical Argon laser trabeculoplasty  Trabeculectomy  Filtering procedure  Cyclocryotherapy  Cyclolaser ablation  Iridotomy 
    44. 44. GLAUCOMA Treatment
    45. 45. GLAUCOMA Surgical treatment of glaucoma Argon laser trabeculoplasty Filtration procedures
    46. 46. GLAUCOMA Filtration blebs