The Glaucomas

July 10, 2018 | Author: Jk Flores | Category: Glaucoma, Vision, Ophthalmology, Eye, Medical Specialties
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THE GLAUCOMAS Department of EENT RTR Medical Foundation  Amelia C. Reyes, MD., DPBO, DPBO, FPAO FPAO

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


III. THE AQUEOUS HUMOR  A. Formation  Aqueous humor is produced by the ciliary processes by a combination of active transport, ultrafiltration, and diffusion. B. Outflow system 1. Classical outflow: comprises 80% of the aqueous humor outflow Ciliary processes

posterior chamber

trabecular meshwork


anterior chamber 

Schlemm s canal ’

collector channels (venous system)

2. Uveoscleral outflow: comprises 20% of the aqueous humor outflow Ciliary processes

posterior chamber 

 Anterior chamber 


ciliary muscles supraciliary and suprachoroidal spaces venous system

IV. DETERMINANTS OF IOP 1. the rate of aqueous humor formation 2. the resistance to aqueous humor outflow 3. the level of episcleral venous pressure ( 8-12mm.Hg )

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

Goldmann applanation tonometer 

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.

VI. THE CLASSIFICATION OF GLAUCOMAS  A. Open-angle glaucoma 1. Primary open-angle glaucoma Characteristics: • insidious in onset • slowly progressive • painless • usually bilateral and asymmetric  Associated disorders: • myopia • DM • Retinal vein occlusion

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.

Pupillary block – the most frequent cause of  angle-closure glaucoma

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

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