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I. DEFINITION
Glaucoma - refers not to a single disease entity, but rather to a group of diseases that have certain common features, including; 1. IOP to high for the continued health of the eye 2. optic head nerve changes, e.g. cupping, atrophy 3. visual field loss
2. Uveoscleral outflow: comprises 20% of the aqueous humor outflow posterior chamber Ciliary processes pupil Anterior chamber ciliary muscles supraciliary and suprachoroidal spaces venous system
V. CLINICAL EVALUATION
A. The IOP Normal range: 9-21mmHg. (mean +/- SD 16 +/2.5mmHg.)
Factors influencing IOP: time of the day season of the year blood pressure heartbeat respiration genetic influence age Measuring devices: indentation tonometer e.g. Schiotz * applanation tonometer e.g. Goldmann, pneumatic
B. The optic nerve head - composed of neural tissues, glial, and collagenous supportive tissues, and blood vessels. - contains of approximately 1.2 million axons whose cell bodies lie in the ganglion cell layer of the retina. - the average diameter of the intraocular portion is 1.5mm. - the arcuate fibers entering the superior and inferior portion of the disc are more susceptible to glaucomatous damage Blood supply: Central retinal artery
Histopathologic findings in glaucoma: loss of axons, blood vessels, and glial cells Theories of glaucomatous damage: 1. mechanical theory 2. ischemic theory Optic nerve head changes in glaucoma (ophthalmoscopic findings): generalized enlargement of the cup focal enlargement of the cup superficial splinter hemorrhages loss of nerve fiber layer asymmetry of cupping between the 2 eyes
C.The visual field An island hill of vision in a sea of darkness. Traquair Superiorly: 60 degrees Inferiorly: 75 degrees Nasally: 60 degrees Temporally: 100 degrees Perimeter - the instrument used to quantitatively measure the visual field.
Scotoma - a localized defect or depression in the visual field. 1. absolute - a VF defect that persists when the maximum stimulus of the testing apparatus is used. e.g. the normal blind spot 2. relative - a VF defect that is present to weak stimuli but disappears when tested with bright stimuli.
The glaucoma suspect: (+) family history of glaucoma Elevated IOP ( 21mmHg.) Suspicious appearing disc Normal tension glaucoma ( low-tension glaucoma) - resembles primary open-angle glaucoma in all aspect except that the IOP is not elevated. Theories: abnormal susceptibility of the optic nerve head to pressure poor perfusion of the optic nerve
2. secondary open-angle glaucoma a) Pseudoexfoliative glaucoma - characterized by the deposition of a characteristic fibrillar material in the anterior segment of the eye. - probably arises from multiple sources as a part of a generalized basement membrane disorder. - prognosis is worse - resistant to medical treatment Treatment: laser trabeculoplasty
b) Pigmentary glaucoma - the pigment dispersion syndrome consists of pigment deposition on the corneal endothelium in a vertical pattern, in the TM, and in the lens periphery. - Usually occurs in young myopic males between the age of 20-50 years. - Affected females tend to be older than affected males. Treatment: medical, laser trabeculoplsty, filtering surgery
c) Lens-induced glaucomas c.1. phacolytic glaucoma occurs as a result of a leakage of lens protein from a mature or hypermature cataract; the TM becomes blocked by macrophages and high molecular weight lens proteins. Treatment: cataract extraction c.2. lens particle glaucoma - may occur after acute penetrating lens injury or after ECCE with retained cortical materials. Treatment: medical (mydriatic, steroids, anti-glaucoma meds) surgical
c.3. phacoanaphylactic glaucoma - occurs after penetrating trauma or surgery; patient becomes sensitized to their own lens protein and develop a granulomatous reaction about the lens. Treatment: medical, surgical d) Intraocular tumors e) ocular inflammation f) drug-induced e.g. coticosteroids
B. Angle-closure glaucoma - develops because iris apposition to the trabecular meshwork blocks the drainage of the aqueous humor.
1. Primary acute-angle closure glaucoma - usually bilateral Manifestations: pain blurred vision rainbow-colored halos around light nausea and vomiting Signs: increased IOP mid-dilated, sluggish and often irregular pupil corneal epithelial edema congested episcleral and conjunctival blood vessels shallow anterior chamber mild aqueous cells and flare
Work-ups: gonioscopy perimetry funduscopy Treatment: laser iridotomy treatment of choice anti-glaucoma meds
2. Chronic angle-closure glaucoma - may develop after acute angle-closure glaucoma or when the anterior chamber angle gradually closes and the IOP rises slowly. - seen commonly in Black patients Characteristics: lacks subjective symptoms modest elevation of IOP progressive cupping of the optic nerve head characteristic visual field loss
3. Secondary angle-closure glaucoma a.) lens-induced glaucoma a.1. phacomorphic secondary to swollen lens a.2. dislocated lens a.3. microspherophakia b.) posterior synechiae c.) aphakia
Clinical Evaluation: history refraction external examination pupil examination biomicroscopy perimetry tonometry gonioscopy ophthalmoscopy
VII.MANAGEMENT OF GLAUCOMAS
A. Medical treatment Classifications: 1. Beta adrenergic antagonist MOA: lowers IOP by reducing aqueous humor formation e.g. timolol, betaxolol, levobunolol 2. Alpha adrenergic agonist MOA: lowers IOP by reducing aqueous humor formation e.g. brimonidine
3. Parasympathomimetic agents MOA: reduces IOP by causing contraction of the ciliary muscles 3.1 Direct-acting affects the motor end plates similar to acetylcholine e.g. pilocarpine 3.2 Indirect-acting inhibits the enzyme acetylcholinesterase e.g. echothiopate, demecarium bromide 3.3 Direct and indirect-acting e.g. carbachol
4. Carbonic Anhydrase inhibitors MOA: reduces aqueous humor formation by direct inhibition of Carbonic anhydrase enzyme in the ciliary body. e.g. acetazolamide, methazolamide, dorzolamide, brinzolamide 5. Hyperosmotic agents MOA: reduce vitreous volume e.g. mannitol, glycerine, urea, isosorbide
6. Prostaglandin F2a analogues MOA: increase uveo-scleral outflow e.g. latanoprost, travoprost, bimatoprost B. Surgical treatment 1. laser surgery 2. filtering procedures