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{{Reflist|refs=
{{Reflist|refs=
<ref name=ao>{{cite book|last=Basic and clinical science course|title=Glaucoma|year=2011-2012|publisher=American Academy of Ophthalmology|isbn=978-1615251179}}</ref>
<ref name=ao>{{cite book|last=Basic and clinical science course|title=Glaucoma|year=2011–2012|publisher=American Academy of Ophthalmology|isbn=978-1615251179}}</ref>
<ref name=yanoff>{{cite book|last=Myron Yanoff, Jay S. Duker|title=Ophthalmology|year=2009|publisher=Mosby Elsevier|isbn=9780323043328|edition=3rd ed.}}</ref>
<ref name=yanoff>{{cite book|last=Myron Yanoff, Jay S. Duker|title=Ophthalmology|year=2009|publisher=Mosby Elsevier|isbn=9780323043328|edition=3rd}}</ref>
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Revision as of 03:56, 21 March 2014

The goal of currently available glaucoma therapy is to preserve visual function by lowering intraocular pressure (IOP) below a level that is likely to produce further damage to the nerve. The treatment regimen that achieves this goal with the lowest risk, fewest adverse effects, and least disruption of the patient's life, taking into account the cost implications of treatment, should be the one employed.

The more advanced the glaucomatous process on initial presentation, the lower the target range generally needs to be to prevent further progression. This more aggressive target is meant to minimize the risk of progressive glaucoma damage and vision loss. Once the optic nerve is damaged, it is more likely to incur more damage, and if severe visual loss is present, there is greater impact on the patient from any additional damage that may occur.

An initial reduction in the IOP of 20% from baseline is suggested. However, reduction of IOP to the target pressure range does not guarantee that progression will not occur. Therefore, the target pressure range needs to be constantly reassessed and changed as dictated by IOP fluctuations, optic nerve changes, and/or visual field progression.

Medications are divided into several groups based on chemical structure and pharmacologic action. Agents in common clinical use include:[1][2]

Name Other names Mechanism of action Dosage IOP decrease Side effects
Prostaglandin analogs
Latanoprost Xalatan Increased USO (uveoscleral outflow ) Once daily 25-32% pigmentation of eyelashes, eyelid skin pigmentation, hyperemia (red eye), flu-like symptoms (joint/muscle pain and headache)
Bimatoprost Lumigan Increased USO (uveoscleral outflow ) Once daily blurred vision, eyelid redness, eye discomfort, permanently darken iris, darken/thicken eyelashes
Travoprost Travatan Increased USO (uveoscleral outflow ) Once daily blurred vision, eyelid redness, eye discomfort, permanently darken iris, darken/thicken eyelashes
Beta blockers
Timolol Timoptic Decrease aqueous production Every 12 hours 20-30% bronchospams, bradycardia, depression, impotence
Betaxolol Betoptic Decrease aqueous production Every 12 hours 15-20% Fewer pulmonary complications due to selective Beta blockage
Adrenergic agents
Brimonidine Alphagan Decrease aqueous production, increase USO every 8–12 hours 20-30% blurring, foreign body sensation, eyelid edema, dryness, headache, fatigue, hypotension, depression,insomnia
Miotics
Pilocarpine Isoptocarpine, Pilocar Increase trabecular outflow Every 6–12 hours 15-25% posterior synechia, keratitis, miosis,brow ache,cataract,myopia,retinal tear,dermatitis,increased salivation
Carbonic anhydrase inhibitors
Dorzolamide Trusopt Decrease aqueous production Every 8–12 hours 15-20% eye irritation, bitter taste
Brinzolamide Azopt Decrease aqueous production Every 8–12 hours 15-20% eye irritation,bitter taste
Acetazolamide Diamox Decrease aqueous production 62.5–250 mg/every 6–12 hours 15-20% malaise, depression, weight loss, kidney stones

See also

References

  1. ^ Basic and clinical science course (2011–2012). Glaucoma. American Academy of Ophthalmology. ISBN 978-1615251179.
  2. ^ Myron Yanoff, Jay S. Duker (2009). Ophthalmology (3rd ed.). Mosby Elsevier. ISBN 9780323043328.