Glaucoma Review by Dr. Allen


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Glaucoma Review by Dr. Allen

  1. 1. Glaucoma Review Fritz Allen, MDVisionary Ophthalmology April 22th 2012
  2. 2. Overview of Content• Diagnostic Tests• Open-Angle Glaucomas• Angle-Closure Glaucomas• Medical Management of Glaucoma 2
  3. 3. Diagnostic Tests• Gonioscopy• Examination of the Optic Nerve• Standard Automated Static Perimetry• Corneal Pachymetry 3
  4. 4. Gonioscopy• Indications – Overcomes problem of total internal reflectivity to see angle structures – Indirect gonioscopy (e.g., Goldmann or four mirror lens) • Essential diagnostic tool in glaucoma (viewing the iridocorneal angle) – Most common cause of incorrect diagnosis is omission of gonioscopy – Omission causes overlooking secondary glaucomas and other glaucomas – Periodically performed can detect secondary emergence of mixed mechanism 4
  5. 5. Gonioscopy• Identification of angle recession, foreign bodies, abnormal pigmentation, tumors, angle neovascularization, angle synechiae• Glaucoma treatment in the angle – Laser trabeculoplasty – Goniosynechialysis – Treatment and evaluation of internal ostium of trabeculectomy site – Gonioplasty/iridoplasty 5
  6. 6. Gonioscopy• Contraindications – Inability of patient to cooperate – Corneal abrasion or disease precluding application of corneal lens• Pre-procedure evaluation• Indirect gonioscopy – View angle with slit-lamp using a gonioscopic lens• Technique – Indirect gonioscopy • Produces inverted image 180 away from origination • Two types of lenses are in common use 6
  7. 7. Gonioscopy– Goldmann type • Goldmann lens requires clear fluid to fill space between cornea and goniolens • Lens is brought toward patient’s eye and tipped forward quickly enough to trap the clear fluid– 4 mirror type • Rests solely on cornea / tear film • Requires only drop of anesthetic • Indentation gonioscopy can be performed • Technique to differentiateappositional and synechial angle-closure 7
  8. 8. Gonioscopy• Complications – Corneal abrasion • Prevention: moist cornea, topical anesthesia, minimize movement of lens on cornea• Considerations in interpretation – Normal angle landmarks (best viewed with parallelepiped method) • Anterior to posterior: cornea, Schwalbe’s line, non-pigmented trabecular meshwork, pigmented trabecular meshwork, scleral spur, ciliary band, iris root 8
  9. 9. Gonioscopy 9
  10. 10. Examination of Optic Nerve• Indications – To examine the optic nerve head for clinical signs of glaucoma or other optic neuropathy – To examine the macula and posterior pole• Contraindications – No absolute contraindications – Difficult to use in cases of very small pupils and dense media opacities – Poor patient cooperation 10
  11. 11. Examination of Optic Nerve• Pre-procedure evaluation – Evaluate pupil function – Evaluate anterior segment – Evaluate angle by gonioscopy if glaucoma suspected – Dilate pupil• Techniques – Handheld – Contact lens (center of a gonio lens) – Indirect ophthalmoscopy – Direct ophthalmoscopy – Hruby lens 11
  12. 12. Examination of Optic Nerve• Technique – Slit-lamp biomicroscope and indirect and direct ophthalmoscopy – used to provide illumination and magnification, enabling a sense of contour of the optic nerve – Binocular viewing is easier through a dilated pupil, but with experience one can see optic nerve through an undilated pupil though usually monoscopically – A fixation target helps to stabilize and to manipulate the position of the eye• Complications – Corneal abrasion (complication of contact lens use) – Complications of dilation 12
  13. 13. Examination of Optic Nerve• Considerations in interpretation – Look for signs of glaucoma • Generalized – Large optic cup – Asymmetry of the cups – Progressive enlargement of the cup • Focal – Narrowing (notching) of the rim – Vertical elongation of the cup – Cupping to the rim margin – Regional pallor – Splinter hemorrhage – Nerve fiber layer loss 13
  14. 14. Examination of Optic Nerve © 2005 G.A. Cioffi, MD. Used by permission. 14
  15. 15. Standard Automated Static Perimetry• Indications – Diagnosis of disease • Suspected diagnosis of glaucoma (suspicious disc, ocular hypertension) • Neurologic vision loss • Subjective VF loss • Macular/retinal disease – Monitoring of disease process • Interval follow-up of suspected or established VF loss 15
  16. 16. Standard Automated Static Perimetry• Pre-procedure evaluation – Ensure patient can understand and follow instructions – Assess for refractive error – Ensure there are no physical limitations to performing test • Seat patient comfortably • Check head and eyelid position• Alternatives – Goldmann perimetry – Confrontation visual fields – Amsler grid (to test central VF) 16
  17. 17. Standard Automated Static Perimetry• Considerations in interpretation – Assess patient reliability – Review threshold values, global indices, total and pattern deviation plots – Correlate test results with anatomy • Optic disc and retina appearance should correspond to VF • Be aware of neurological defects 17
  18. 18. Standard Automated Static Perimetry– Rule-out artifactual field loss • Lens rim artifact • Incorrect refractive correction used for test– Compare to prior tests • Establish good baseline – Repeat testing takes into account learning effect – Establishes presence of scotomas and fluctuation level of patient’s responses 18
  19. 19. Automated Static Perimetry 19
  20. 20. Corneal Pachymetry• Indications – Measurement of central corneal thickness (CCT) – Known diagnosis of glaucoma, including normal-tension glaucoma – Glaucoma suspect and/or ocular hypertension• Considerations in interpretation – Thinner corneas underestimate IOP while thicker corneas overestimate IOP• Patient instructions – Explanation of how CCT could alter course20 of glaucoma treatment
  21. 21. Corneal PachymetryPhoto courtesy of Jeff Henderer, MD 21
  22. 22. Corneal pachymetry is important in the evaluation of which of the following diseases?A. Anterior basement membrane dystrophyB. Normal tension glaucomaC. Anterior uveitisD. Senile cataracts 22
  23. 23. Open-Angle Glaucomas• Primary open-angle glaucoma• Primary open-angle glaucoma suspect• Normal tension glaucoma• Secondary open-angle glaucomas• Post-traumatic or angle recession glauocma• Hyphema• Corticosteroid-induced glaucoma 23
  24. 24. Primary Open-Angle Glaucoma• Etiology – Elevated IOP is acknowledged as the principal etiologic risk factor• Epidemiology – Significant public health problem • Prevalence in African-Americans higher • Prevalence increases with age • Most frequent cause of blindness in Hispanic and African-Americans 24
  25. 25. Primary Open-Angle Glaucoma• History – Age – Race – Symptoms • Usually asymptomatic until late in disease – Family history – Cardiovascular disease, diabetes – Refractive state – Medications – Rule out secondary causes (i.e., corticosteroids) – Previous eye injury and surgery 25
  26. 26. Primary Open-Angle Glaucoma• Features – Usually insidious onset – Slowly progressive visual loss without symptoms – Painless – Usually bilateral, can be asymmetric – Central acuity unaffected until late in the disease – Elevated IOP • Can be intermittent (diurnal fluctuation) • Subset who never have high IOP (normal-tension glaucoma) – Consider corneal pachymetry measurement when assessing the accuracy of applanation tonometry – Open angle by gonioscopy 26
  27. 27. Primary Open-Angle Glaucoma– Optic disc appearance • Asymmetry of the neuroretinal rim area or cupping • Focal thinning or notching of the neuroretinal rim • Optic disc hemorrhage • Any acquired change in the disc rim area or the surrounding retinal nerve fiber layer • Large optic disc, large cup/disc ratio, peripapillary atrophy– Visual fields • Defects can precede visible optic nerve damage • VF defects may not be detectable by standard 27 perimetry
  28. 28. Primary Open-Angle Glaucoma– Typical glaucoma defects • Paracentral scotoma • Arcuate or Bjerrum scotoma • Nasal step • Altitudinal defect • Temporal wedge • Central island in far advanced cases 28
  29. 29. Primary Open-Angle Glaucoma• Testing – Visual fields • Automated static perimetry (most useful for glaucoma diagnosis) – Optic nerve photography or detailed drawing and description • Stereo photography particularly useful – Optic nerve head image analysis systems – Central corneal thickness measurement 29
  30. 30. Primary Open-Angle Glaucoma• Risk factors – Strongest evidence • Older age • Race (higher prevalence in African-Americans) • Elevated IOP • Positive family history• Differential diagnosis – Disc abnormalities – Other glaucomas • Secondary open-angle types • Angle-closure types • Normal tension glaucoma 30
  31. 31. Primary Open-Angle Glaucoma• Medical therapy – Beta-adrenergic antagonists – CAIs – Adrenergic agonists (sympathomimetics) – Prostaglandin analogues – Parasympathomimetic agents• Surgical therapy – Laser trabeculoplasty – Trabeculectomy (with or without antimetabolites) – Glaucoma drainage tube implants – Ciliary body ablation 31
  32. 32. Primary Open-Angle Glaucoma• Disease-related complications – Limitations due to VF loss – End stage glaucoma and blindness• Patient instructions – Discussion of medications and surgical treatments • Options, side effects, risk-benefit ratios • Instructions relating to compliance – Appropriate drop timing – Nasolacrimal occlusion, passive lid closure – Prevention of washout effect by spacing drop therapy – Discussion regarding quality of life issues • Support groups, career issues, financial issues regarding treatment – Importance of periodic follow-up 32
  33. 33. Primary Open-Angle Glaucoma 33
  34. 34. Primary Open-Angle Glaucoma Temporal pallor of the optic nerve 34
  35. 35. Primary Open-Angle Glaucoma Suspect• History – Previous history of elevated IOP – Family history of glaucoma – Age – Ethnicity of patient (e.g., African descent) – Previous history of vision loss – Previous medication history 35
  36. 36. Primary Open-Angle Glaucoma Suspect• Features – Optic disc or nerve fiber layer damage suggesting of glaucoma • Enlarged cup/disc ratio • Asymmetric cup/disc ratio • Notching or narrowing of the neural rim • Disc hemorrhage • Diffuse or local abnormality in the nerve fiber layer – Visual fields suspicious for early glaucomatous damage – IOP consistently above 21 mm Hg (i.e., ocular hypertension) – Normal open angle on gonioscopy with absence of secondary causes 36
  37. 37. Primary Open-Angle Glaucoma Suspect• Testing – Determination of central corneal thickness – Evaluation of optic nerve head and retinal nerve fiber layer – VF testing and analysis – Documentation of optic nerve head appearance 37
  38. 38. Primary Open-Angle Glaucoma Suspect• Risk factors – Elevated IOP – History of glaucoma – Advancing age – Race and ethnicity (e.g., African descent, Hispanics) – Associated disease states (systemic hypertension, cardiovascular disease, diabetes mellitus) – Vasospastic diseases (e.g. migraine, Raynauds) 38
  39. 39. Primary Open-Angle Glaucoma Suspect• Differential diagnosis – POAG (early) – Normal tension glaucoma (early) – Corticosteroid responder – Previous history of trauma (i.e., angle recession glaucoma) – Previous or current uveitis – Nonglaucomatous causes (e.g., compressive lesions, ischemic episodes)• Patient instructions – Need for periodic follow-up – Rationale for individualized therapy – Counseling / referral 39
  40. 40. Primary Open-Angle Glaucoma Suspect - Case 40 Photos courtesy of Jeffrey Henderer, MD
  41. 41. Primary Open-Angle Glaucoma Suspect - Case 41 Photos courtesy of Jeffrey Henderer, MD
  42. 42. Normal Tension Glaucoma• Definition – Characteristic features of POAG with IOP in normal range without treatment; also known as low-tension glaucoma• Features – No clear difference from optic nerve cupping seen in POAG 42
  43. 43. Normal Tension Glaucoma• Testing – Repetitive measurement of IOP – Automated VF – Gonioscopy – Stereoscopic optic disc evaluation – Measurement of corneal thickness (pachymetry) 43
  44. 44. Normal Tension Glaucoma• Differential diagnosis – Undetected high-pressure glaucoma • POAG with large diurnal pressure variation • Intermittent elevation of IOP caused by another type of glaucoma • Previous episode of elevated IOP – Decreased CCT – Nonglaucomatous optic nerve disease resembling glaucoma • Congenital anomalies • Compressive lesions of the optic nerve and chiasm • Arteritic ischemic optic neuropathy • Compromised ocular blood flow 44
  45. 45. Normal Tension Glaucoma 45
  46. 46. Secondary Open-Angle Glaucomas - Pseudoexfoliation• Etiology – Systemic disorder with widespread deposition of fibrillar material in many organs including the anterior segment of the eye 46
  47. 47. Secondary Open-Angle Glaucomas - Pseudoexfoliation• Features – Deposits of exfoliative material (XFM) on anterior lens surface, pupillary margin, corneal endothelium, and zonules – Transillumination defects at pupillary margin – Pigment deposition on iris surface, endothelium – Patchy increased pigmentation of trabecular meshwork – Poor pupillary dilation – Higher incidence of narrow angles – +/- IOP elevation – Zonular weakness, phacodonesis 47
  48. 48. Secondary Open-AngleGlaucomas - Pseudoexfoliation 48
  49. 49. Secondary Open-Angle Glaucomas – Pigmentary• Etiology – Concave peripheral iris configuration, usually in myopic eye with deep AC • Posterior iris surface comes into contact with lens zonule and with physiologic dilation/constriction of pupil, packets of pigment rubbed free from iris and become dispersed in aqueous • Collection of pigment within angle/trabecular meshwork occurs during normal aqueous circulation and causes obstruction to outflow and chronic IOP elevation 49
  50. 50. Secondary Open-Angle Glaucomas – Pigmentary• Features – Classic triad of pigmentary glaucoma: Krukenberg spindle, heavy 360 degree pigmentation of the trabecular meshwork, and mid-peripheral iris transillumination defects. – Gonioscopy • Angle recess very wide, usually approx. 45 degrees • Heavy dark pigmentation of TM fairly well distributed throughout entire circumference 50 • May have pigmentation on or anterior to
  51. 51. Secondary Open-Angle Glaucomas – Pigmentary 51
  52. 52. Pigmentary Glaucoma Krukenberg spindle Photo courtesy of Eydie Miller, MDPhoto courtesy of Jeffrey Henderer, MD 52
  53. 53. Post-Traumatic or Angle Recession Glaucoma• History – History of blunt ocular trauma usually with hyphema – Traumatic event may occur monthsto years prior to development of glaucoma• Features – Elevated IOP – Optic nerve and VF findings consistent with glaucoma 53
  54. 54. Post-Traumatic or Angle Recession Glaucoma – Gonioscopy reveals: • Angle recession (compare to opposite eye - since some eyes have very wide angles that appear to be recessed but are normal) • Broad angle recess-wide ciliary body face • Absent or torn iris processes • White glistening scleral spur • Depression in the overlying TM • Localized PAS at the border ofthe recession - extensive PAS occasionally mask recession 54
  55. 55. Post-Traumatic or Angle Recession Glaucoma• Risk factors – History of blunt ocular trauma – Gonioscopic evidence of angle recession of 180 degrees or more – Predisposition to, or family history of, open angle glaucoma• Differential diagnosis – Unilateral chronic open angle glaucoma – ICE syndromes (Chandler syndrome particularly) – Contusion angle deformities (i.e., cyclodialysis cleft, which may look similar but has a different clinical course) – Normal anomalous appearing angles 55
  56. 56. Post-Traumatic or Angle Recession Glaucoma Angle recession 56 Photo courtesy of Jane Durcan, MD
  57. 57. Hyphema• Etiology – Trauma – blunt or lacerating – Intraocular surgery – Spontaneous hyphemas • Rubeosis iridis – diabetes, CRVO, carotid occlusive disease, chronic RD • Anterior uveitis• History – History of ocular trauma or surgery – History of ocular or systemic disorders associated with spontaneous hyphemas – Medication history 57
  58. 58. Hyphema• Features – Decreased visual acuity – Elevated IOP • Etiology of acute elevation – Occlusion of TM by clot, inflammatory cells, erythrocytic debris – Pupillary block secondary to clot occluding pupil • Late-onset glaucoma – Days to years after injury – Etiology – Damage to TM – PAS leading to secondary angle closure – Blood in AC: circulating RBCs, layered hyphema, total hyphema 58
  59. 59. Hyphema• Testing – Sickle cell hemoglobin screening in all African American patients – Coagulation studies where indicated• Risk factors – Risk of increased IOP is greater following rebleeding after a traumatic hyphema – Rebleeding usually occurs during the first week after initial hyphema – Larger hyphemas are associated with higher incidence of increased IOP – Sickle cell hemoglobinopathy associated with higher incidence of glaucoma and vascular occlusions 59
  60. 60. Hyphema• Medical therapy – Cycloplegics – Topical and/or systemic corticosteroids useful in treating inflammation – Topical or systemic IOP-lowering medications as needed – Cautious use of systemic CAIs in patients with sickle cell hemoglobinopathy 60
  61. 61. Hyphema– Persistently elevated IOP, rebleeding or persistent hyphema may necessitate consideration for surgical therapy– Analgesics and antiemetic medications as needed– Rigid shield– Elevate head of bed– Limit activity 61
  62. 62. Hyphema• Complications – Complications associated with use of topical and systemic IOP-lowering medications. Avoid use where contraindicated – CAIs may increase sickling tendency in patients with sickle cell hemoglobinopathy• Patient instructions – Comply with prescribed medical regimen – Use eye shield – Quiet activity and/or bedrest – Avoid bending over; elevate head of bed – Provide safe home environment – Reliable follow-up – No aspirin or NSAIDs 62
  63. 63. Hyphema 63Photo courtesy of Marlene Moster, MD
  64. 64. Corticosteroid-induced Glaucoma• Etiology – Caused by a reduction in facility of outflow• History – May develop at any time during long-term corticosteroid administration, but IOP elevation typically occurs within a few weeks with potent corticosteroids, or in months with the weaker corticosteroids – Routes of administration • Topical corticosteroid therapy is more often associated with IOP rise than is the case with systemic administration 64
  65. 65. Corticosteroid-Induced Glaucoma • Intraocular and periocular injections are the most dangerous route of corticosteroid administration from the standpoint of corticosteroid-induced glaucoma – IOP elevation may occur in response to subconjunctival, sub-Tenon’s, intravitreal or retrobulbar injections of corticosteroid – Patient’s response to earlier topical corticosteroid therapy does not always predict how that individual will respond to periocular corticosteroids • Systemic administration (oral or intravenous) of corticosteroids is least likely to induce glaucoma – This response does not correlate with the dosage or duration of treatment, but is associated with the degree of pressure response to topical corticosteroids 65
  66. 66. Corticosteroid-Induced Glaucoma• Features – The clinical picture resembles that of POAG with an open, normal-appearing AC angle and absence of symptoms – Much less often, the condition may have an acute presentation, in which pressure rises have been observed within hours after corticosteroid administration 66
  67. 67. Corticosteroid-Induced Glaucoma• Risk factors – Individuals with POAG or a family history of the disease are more likely to respond to chronic corticosteroid therapy with a significant rise in IOP – High myopes, diabetics, and patients with connective tissue diseases have a similar predisposition to corticosteroid-induced glaucoma 67
  68. 68. Corticosteroid-Induced Glaucoma• Medical therapy options – Discontinuation of the corticosteroid – first treatment option; often all that is required – The chronic form of this disease is said to normalize in 1-4 weeks, while the acute form typically resolves within days of stopping the corticosteroid – In rare cases, the glaucoma may persist despite stopping all corticosteroids – Glaucoma medical therapy algorithm, as per treatment of POAG, although miotics and prostaglandin analogues should be avoided in cases of uveitis 68
  69. 69. Corticosteroid-Induced Glaucoma• Surgical therapy options – Laser trabeculoplasty – Filtration surgery 69
  70. 70. Corticosteroid-Induced Glaucoma (steroid glaucoma) 70 Photo courtesy of Herbert Fechter, MD
  71. 71. Angle-Closure Glaucomas• Acute Primary Angle-Closure Glaucomas• Neovascular Glaucoma 71
  72. 72. Acute Primary Angle-Closure Glaucoma• Etiology – Physiologic pupillary block • Excessive iris-lens apposition impedes flow of aqueous from PC to AC, elevating PC aqueous pressure • Secondary forward bowing of peripheral iris results in occlusion of the TM• Features – Symptoms • Acute onset of brow ache, eye pain • Blurred vision • Colored haloes around lights • Nausea and vomiting 72
  73. 73. Acute Primary-Angle Closure Glaucoma• Signs – High IOP – Mid dilated, sluggish pupil – Corneal epithelial edema – Congested episcleral and conjunctival vessels – Shallow AC – AC inflammation – Appositional angle-closure – Iris bombe – Glaukomflecken and sector iris atrophy – indicators of previous bouts of acute-closure glaucoma 73
  74. 74. Acute Primary Angle- Closure Glaucoma• Risk factors – Hyperopia – Family history of angle-closure – Older age – Female gender – Age-related cataract (lens swelling) – Asian ethnicity 74
  75. 75. Acute Primary Angle-Closure Glaucoma• Medical therapy options – To lower the IOP and allow clearing of corneal edema in preparation for laser iridotomy • Beta-adrenergic antagonists • Alpha2-adrenergic agonists • CAIs – topical, oral, IV • Miotics – 1-2% pilocarpine after IOP starts to normalize • Prostaglandin analogues • Hyperosmotic agents • Topical corticosteroids 75
  76. 76. Acute Primary Angle-Closure Glaucoma – Deformation of cornea with cotton tip applicator or Indentation gonioscopy occasionally opens the angle – Topical glycerin or epithelial removal may be necessary to enable visualization of the chamber angle• Surgical therapy – Laser peripheral iridotomy – Nd:YAG and/or argon 76
  77. 77. Acute Primary Angle-Closure Glaucoma• Complications – Complications of laser iridotomy – Posterior synechiae – Miotics, especially strong miotics, may increase pupillary block – Formation of PAS • Perform laser iridotomy as soon as possible 77
  78. 78. Acute Primary Angle-Closure Glaucoma• Disease-related complications – Residual stage of angle-closure glaucoma – Corneal decompensation – Sectoral iris atrophy – Posterior synechiae – Cataract formation – Optic nerve damage – Retinal vascular occlusion 78
  79. 79. Acute Primary Angle-Closure Glaucoma Glaukomflecken under the anterior lens capsule after an attack of acute angle closure. These lens changes are caused by necrosis of the lens epithelium. 79
  80. 80. Neovascular Glaucoma• History – Pain, photophobia (usual) – Markedly reduced vision (usual) – Diabetes – Hypertension, arteriosclerosis 80
  81. 81. Neovascular Glaucoma• Epidemiology – CRVO – PDR – Post cataract extraction, vitrectomy • Particularly with breached posterior capsule – Carotid occlusive disease • May have normal or low IOP – CRAO 81
  82. 82. Neovascular Glaucoma• Features: Early – Tufts of new vessels at pupillary margin – Fine vessels crossing scleral spur• Features: Late – Very high IOP – Conjunctival injection – Corneal edema – Florid iris neovascularization with ectropion uveae – Fibrovascular membrane over iris and angle structures – Variable synechial angle-closure – With total angle closure, there can be minimal neovascularization of iris, and with pigmented Schwalbes line, on gonioscopy can be mistaken for OAG – AC cells and flare 82
  83. 83. Neovascular Glaucoma• Risk factors – Retinal hypoxia• Disease-related complications – Absolute glaucoma with blindness – Intractable pain• Patient instructions – Medication and surgical discussion – Referral for PRP, surgical intervention, and/or cyclodestructive procedure 83
  84. 84. Neovascular Glaucoma Neovascularization of the iris and angle 84 Photo courtesy of Teresa Chen, MD
  85. 85. Glaucoma Medications – Side Effects and ContraindicationsBeta Blockers Corneal toxicity COPD Allergic reactions Asthma Congestive heart Emphysema failure Congestive heart Bronchospasm failure (relative) Bradycardia Bradycardia Depression Hypotension Impotence Greater than first degree heart block
  86. 86. Glaucoma Medications – Side Effects and ContraindicationsAlpha 2- Burning on Monoamineadrenergic instillation oxidase inhibitoragonists therapy Conjunctival injection Infants and Pupillary dilation children younger than 2 years old Allergic reactions due to apnea, bradycardia, and Increased blood dyspnea pressure Tachyarrhythmias Tremor, headache
  87. 87. Glaucoma Medications – Side Effects and ContraindicationsParasympatho- Increased myopia Neovascular,mimetics uveitic, or Eye or brow pain malignant glaucoma Decreased vision Cataract Periocular contact dermatitis Corneal toxicity Paradoxical angle closure
  88. 88. Glaucoma Medications – Side Effects and ContraindicationsCAIs Corneal toxicity Sulfa allergy Stevens-Johnson Kidney stones syndrome Aplastic anemia Malaise, anorexia, Thrombocytopeni depression a Serum electrolyte Sickle cell abnormalities, disease renal calculi Blood dyscrasias Metallic taste
  89. 89. Glaucoma Medications – SideEffects and Contraindications Changes in iris pigmentation 89