Glaucoma

Definition
acquired chronic optic neuropathy characterized by optic disk cupping and visual field loss. characterized by:
Raised IOP, >21 mmHg Abnormal optic disc
Cup-disc ratio asymmetry Large cup-disc ratio for disc size Disc hemorrhage Vessel bayoneting/ nasally displaced Peripapillary atropy (B-zone) Thinning of the (inferior superior nasal - temporal rule) neuroretinal rim

Visual field defect

Aqueous Humor Dynamics

Aqueous humor is actively secreted, 2-3 microliters per minute, by the cilliary processes, which are highly folded, making a considerable large area of 6 square cms in each eye.

Starts from
Sodioum ions are actively transported between the epithelial cells, pulling chloride and bicarbonate ions to sustain electrical neutrality. Hence, causing water osmosis from the blood capillaries into the same epithelial spaces. The resulting solution flows into the anterior chamber of the eye.
Other substances: amino acids, ascorbic acid, and glucose are also actively transported, or through facilitated diffusion.

Aqueous Humor Dynamics

extraocular veins

TM minute openings: 2-3 micrometers as the pressure rises, the flows of fluid into the canal is increased. At approximately 15 mmHg, outflow fluid through the canal of Schlemm is about 2.5 microliters per minute, = inflow of aqueous humor from the ciliary body. The average: 15 mmHg, a range from 12 to 20 mmHg

Defense mechanism
phagocytic cells on the surface of TM outside the canal of Schlemm is a layer of interstitial gel that contains reticuloendothelial cells surfaces of the iris and other surfaces behind the iris are covered by an epithelium capable to phagocytoze proteins and small particles.

Aqueous Humor and Its relation to Glaucoma

20 to 30 mmHg can cause loss of vision if it is not treated 60 to 70 mmHg, extremely high loss of vision in days or even hours High pressure compressed optic nerve at the optic disc. blockage of the axonal flow to the optic fibers leading to the brain inadequate nutrition and consequently death of fibers. Another cause the retinal artery might be compressed precipitate the neuronal damage.

How to Diagnose
Triad Tonometry Gonioscopy Optic Disc Examination

Gonoscopy
open-angle, or angle-closure glaucoma? Narrow? oblique illumination with pen-light or by slitlamp observation of the depth of the peripheral anterior chamber BEST: GONOSCOPY

pen-light

Gonoscopy

Schwalbes line or a small portion of the trabecular meshwork is seen means that the angle is narrow; full trabecular meshwork, scleral spur, and the iris processes are seen means the angle is open; unable to see Schwalbes line means that the angle is closed

Optic Disk Examination

normal range: 0.2 to 0.5

Classification
open-angle glaucoma increased resistance to aqueous outflow in open angle high IOP MYOC gene! Characteristics of primary open-angle glaucoma:
IOP greater than 21 mmHg An open chamber angle Characteristic disk cupping with visual field defects Absence of a known secondary cause of glaucoma

Classification
primary angle-closure glaucoma Acute PACG: two different mechanisms.
papillary block mechanism, where the apposition of the iris to the lens blocks aqueous flows to the anterior chamber. Therefore, causing a buildup pressure behind the iris, anterior bowing of the peripheral iris, and angle closure. The second mechanism is plateu iris mechanism where the peripheral iris bunches up and block the TM directily.

Sign and symptoms are severe pain, redness, and blurring of vision. Subacute PACG incomplete closure of the angle episodes of increased IOP that spontaneously resolves blurred vision, halos, and red eye. Chronic PACG
synechial closure, an asymptomatic or repeated episodes of acute or subacute angle closure a POAG-like mechanism, where there is a trabecular dysfunction in narrow, but clinically open angles.

POAG Treatment Algorithm

POAG

Pharmaco Treatment
Suppression of Aqueous Production Facilitation of Aqueous Outflow Reduction of Vitreous Volume Miotics, Mydriatics, and Cycloplegics

Pharmaco Treatment
Suppression of Aqueous Production Beta-blockers topically It blocks beta2 receptors on the ciliary body decreasing the production of aqueous humor timolol maleate, betaxolol hydrochloride, carteolol hydrochloride, levobunolol hydrochloride, metipranolol.

Pharmaco Treatment
Suppression of Aqueous Production Beta-blockers topically systemic >> local decreased heart rate, reduced blood pressure, conduction defects, CNS effects, alteration of serum lipids, and may block the symptoms of hypoglycemia. These effects are not elicited by B1 specific agents.

Pharmaco Treatment
Suppression of Aqueous Production Beta-blockers topically caution in patients with pulmonary diseases, sinus bradycardia, second or third degree heart block, congestive heart failure, atherosclerosis, diabetes, and myasthenia gravis, and also in patients receiving oral beta-blockers. To avoid systemic effects, use of nasolacrimal occlusion technique during administration may be done. It can also optimize the response. Beta-blockers are usually well tolerated in most patients.

Pharmaco Treatment
Suppression of Aqueous Production Alpha adrenoreceptor agonis can also reduce the aqueous humor formation. The mechanism is the agonism of alpha-2 receptors on the ciliary body, and/or alpha-1 (vasoconstrictors) receptor in cilliary vessels.

Pharmaco Treatment
Suppression of Aqueous Production Carbonic anhidydrase inhibitors systemically it helps to converse carbon dioxide and water to carbonic acid (bicarbonate). The production of aqueous humor depends on the active transport of bicarbonate and Na+ ions. reducing the activity of carbonic anhydrase decrease of aqueous humor production. acetazolamide, or dichlorpheamide, or dorzolamide.

Pharmaco Treatment
Facilitation of Aqueous Outflow Prostaglandin analogs, such as bimatoprost 0.003%, latanoprost 0.005%, and travoprost 0.004% solutions (each once daily at night), and unoprostone 0.15% solution (twice daily) increasing the uveoscleral and to a lesser extent, trabecular outflow of aqueous humor decrease IOP It is well tolerated and produce fewer systemic adverse effects than timolol. Prostaglandin can be used in combination with other agents for additional IOP control. It can be used as first-line therapy for primary open-angle glaucoma (POAG).

Pharmaco Treatment
Facilitation of Aqueous Outflow Parasympathomimetic agents contracting cilliary muscle opening the trabecular meshwork reducing resistance to outflow increasing aqueous humor trabecular outflow reduce IOP However it may reduce uveoscleral outflow. Their use as a primary or adjunctive agent in glaucoma treatment has decreased, due to its ocular side effects and/or frequent dosing requirements.

Pharmaco Treatment
Facilitation of Aqueous Outflow Epinephrine mechanism is not fully know, beta-2 receptor-mediated increase in outflow facility through the trabecular meshwork and the uveoscleral route appears to be its mechanism, althought its activity to reduce IOP is less compared to beta-blockers or miotics.

Epinephrine 0,25 to 2 % instilled once or twice daily is infrequently used today, due to advances in better tolerated and more efficacious agent. Prodrug of epinephrine is dipivefrin, these drugs cannot be used in eyes with narrow anterior chamber angles.

Pharmaco Treatment
Reduction of Vitreous Volume Hyperosmotic agents can cause the reduction of vitreous volume by making the blood hypertonic, therefore drawing the water out of the vitreous and causing it to shrink. Moreover, it also decrease aqueous production. This agent is important in the treatment of acute angle closure glaucoma and in secondary angle-closure glaucoma.

Pharmaco Treatment
Miotics, Mydriatics, and Cycloplegics The use of Miotics is usefull to activate muscarinic receptors on the iris and ciliary body, causing pupil constriction and ciliary muscle contraction, thus improving the uveoscleral outflow. Carbachol and pilocarpine may assist the drainage of aqueous humor. side effect: permanent accommodative spasm blurred vision and headache.

These occur in all patients, but wears off in older patients. To minimize these effects, the use of slow-release formulation of miotics may be optional.

Surgical and Laser Treatment

Peripheral Iridotomy, Iridectomy, and Iridoplasty Laser Trabeculoplasty Glaucoma Drainage Surgery Cyclodestructive Procedures

References
1. Vaughan. Vaughan & Asburys: General ophthalmology. 17th ed. Lange; 2007. 2. Schlote T, Rohrbach J, Grueb M, Mielke J. Pocket atlas of ophthalmology. Thieme; 2006. 3. Guyton AC, Hall JE. Textbook of medical physiology. 11th ed. Elsevier; 2006. 4. Kumar V, Abbas AK, Fausto N, Aster JC. Robbins & cotran: pathologic basis of disease. 8th ed.Saunders; 2010. 5. Tsai JC, Denniston AKO, Murray PI, et al. Oxford American handbook of ophthalmology. NY: Oxford University Press, Inc; 2011. 6. McKay D, ODjay J, Swann P. Glaucoma vascular and nerve fibre layer signs: glaucomatous optic neuropathy signs. Available from: URL:http://www.opticianonline.net/assets/getAsset.aspx?ItemID=2265 7. Page CP, Curtis MJ, Sutter MC, et al. Integrated pharmacology. London: Mosby. 8. Dipiro JT, Talbert RL, Yee GC. Pharmacotherapy: a pathophysiologic approach.7th ed. USA: The McGraw-Hill Companies, Inc. 9. Garg A, Melamed S, Mortense JN, et al. Mastering the techniques of glaucoma diagnosis & management. India: Jaypee Brothers Medical Publishers Ltd; 2006.