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1.
Indian J Ophthalmol ; 2018 Apr; 66(4): 495-505
Article | IMSEAR | ID: sea-196690

ABSTRACT

Lowering of intraocular pressure is currently the only therapeutic measure for Glaucoma management. Many longterm, randomized trials have shown the efficacy of lowering IOP, either by a percentage of baseline, or to a specified level. This has lead to the concept of 'Target” IOP, a range of IOP on therapy, that would stabilize the Glaucoma/prevent further visual field loss, without significantly affecting a patient's quality of life. A clinical staging of Glaucoma by optic nerve head evaluation and perimetric parameters, allows a patient's eye to be categorized as having – mild, moderate or severe Glaucomatous damage. An initial attempt should be made to achieve the following IOP range for both POAG or PACG after an iridotomy. In mild glaucoma the initial target IOP range could be kept as 15-17 mmHg, for moderate glaucoma 12-15 mmHg and in the severe stage of glaucomatous damage 10-12 mmHg. Factoring in baseline IOP, age, vascular perfusion parameters, and change on perimetry or imaging during follow up, this range may be reassessed over 6 months to a year. “Target” IOP requires further lowering when the patient continues to progress or develops a systemic disease such as a TIA. Conversely, in the event of a very elderly or sick patient with stable nerve and visual field over time, the target IOP could be raised and medications reduced. An appropriate use of medications/laser/surgery to achieve such a “Target” IOP range in POAG or PACG can maintain visual fields and quality of life, preventing Glaucoma blindness.

2.
Indian J Ophthalmol ; 2011 Jan; 59 (Suppl1): 97-101
Article in English | IMSEAR | ID: sea-136259

ABSTRACT

Glaucoma is now considered an abnormal physiology in the optic nerve head that interacts with the level of intraocular pressure (IOP), with the degree and rate of damage depending on the IOP and presumably the degree of abnormal physiology. Diagnosis of normal-tension glaucoma (NTG), defined as glaucoma without a clearly abnormal IOP, depends on recognizing symptoms and signs associated with optic nerve vulnerability, in addition to absence of other explanations for disc abnormality and visual field loss. Among the findings are a halo or crescent of absence of retinal pigment epithelium around the disc, bilateral pre-chiasmal visual field defects, splinter hemorrhages at the disc margin, vascular dysregulation (low blood pressure, cold hands and feet, migraine headache with aura, and the like), or a family history of glaucoma. Possibly relevant, is a history of hemodynamic crisis, arterial obstructive disease, or sleep apnea. Neurological evaluation with imaging is needed only for atypical cases or ones that progress unexpectedly. Management follows the same principle of other chronic glaucomas, to lower the IOP by a substantial amount, enough to prevent disabling visual loss. However, many NTG cases are non-progressive. Therefore, it may often be wisein mild cases to determine whether the case is progressive and the rate of progression before deciding on how aggressivene to be with therapy. Efforts at neuroprotection and improvement in blood flow have not yet been shown effective.


Subject(s)
Diagnosis, Differential , Diagnostic Techniques, Ophthalmological , Disease Progression , Humans , Intraocular Pressure , Low Tension Glaucoma/complications , Low Tension Glaucoma/diagnosis , Low Tension Glaucoma/etiology , Low Tension Glaucoma/therapy , Medical Records , Neurologic Examination , Ophthalmoscopy , Optic Disk/pathology , Optic Disk/physiopathology , Vision Disorders/etiology , Visual Fields
3.
Indian J Ophthalmol ; 2011 Jan; 59 (Suppl1): 88-92
Article in English | IMSEAR | ID: sea-136257

ABSTRACT

Glaucoma care is more an art than science. The introduction of several new classes of glaucoma medications and the completion of many large randomized clinical trials have not changed this fact. While we now have better choices when initiating glaucoma therapy relative to our predecessors, the principles of glaucoma therapy have not changed much during this period. Debates continue regarding the utility of concepts such as “the monocular therapeutic trial,” “target intraocular pressure (IOP),” and “maximal medical therapy.” Our tools for detecting and following glaucomatous disease have improved but are not precise enough for us to prospectively predict which patients will do better or worse than others. Much attention has been given to disease stage, rate of progression, and compliance with medications but regular patient follow-up, an area that has received little attention, may be among the most important predictors of patient outcomes.


Subject(s)
Adrenergic alpha-Antagonists/therapeutic use , Adrenergic beta-Antagonists/adverse effects , Adrenergic beta-Antagonists/therapeutic use , Antihypertensive Agents/therapeutic use , Carbonic Anhydrase Inhibitors/therapeutic use , Disease Progression , Follow-Up Studies , Glaucoma/drug therapy , Glaucoma/physiopathology , Goals , Humans , Intraocular Pressure/drug effects , Parasympathomimetics/therapeutic use , Prostaglandins/adverse effects , Prostaglandins/therapeutic use
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