Glaucoma

GLAUKOMA

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Definition of Glaucoma
Glaucoma is an optic disc neuropathy which is characterized by: High intra ocular pressure (IOP) > 21 mmHg, Optic nerve fibers death optic disc damage, Progressive visual field defect, Cause of third permanent blindness.

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Incidence
Primary glaucoma is:
hereditary female > male especially at age > 40 years

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Incidence
Congenital glaucoma since in the intrauterine Infantile glaucoma after birth until 2 years Juvenile glaucoma age 10 - 15 years Secondary glaucoma: glaucoma as a complication from other eye disease

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Aqueous humor secretion

80% is secreted by non pigmented ciliary epithelium via active metabolic process that depends on a number of enzymatic systems (carbonic anhydrase enzyme),

20% is produced by passive processes as ultrafiltration and diffusion.

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Aqueous outflow
AH fills posterior chamber Trabecular route Schlemms canal suprachoroidal space leaves the eye through episcleral vein
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pupil 90 % anterior chamber uveoscleral route (10%) ciliary body

venous system in the ciliary body

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Aqueous outflow
a. Uveal meshwork b. Corneoscleral meshwork c. Schwalbes line d. Schlemms canal e. Collector channels f. Ciliary body g. Scleral spur
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Aqueous outflows, influenced by:

High intra ocular pressure (IOP), High episcleral pressure, Aqueous viscosity: exudate, blood cell, Ciliary block, pupillary block, posterior synechia, Narrow / closed anterior chamber angle, Narrowing of trabecular meshwork pore, Macrophage, lens cell at the trabecular meshwork.
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Trabecular Meshwork
The TM is located at the anterior chamber angle, which consists:
Descemet membrane Sclera Iris Ciliary body Schwalbes line scleral spur iris processus angle recess

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Intra Ocular Pressure (IOP)

Normal IOP < 21 mm Hg, IOP > 21 mm Hg glaucoma suspect, Diurnal fluctuation of IOP in 24 hours:
IOP higher in the morning IOP lower in the afternoon and evening

Ocular hypertension: IOP > 21 mmHg without any nerve fiber damage, Normal tension glaucoma: normal IOP, but presenting glaucomatous signs.
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Pathogenesis of Glaucomatous Damage

There are two current theories:
The indirect ischaemic theory: IOP -- nerve fiber death + interfering micro circulation of the optic disc, Direct mechanical theory: IOP -- damage on retinal nerve fiber at the optic disc.

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Classification of the glaucomas

According to:
Outflow impairment: open angle and angle closure glaucoma, contributing factors to IOP : primary and secondary glaucoma, Age: congenital, infantile, juvenile, adult.

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Primary glaucomas
High IOP is not associated with any ocular disorder
Open angle Angle closure Congenital (developmental)

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Secondary glaucoma

Aqueous outflow alters by ocular / non ocular disorders IOP : Secondary open angle glaucoma: pretrabecular, trabecular and post-trabecular, Secondary angle closure glaucoma caused by apposition between the peripheral iris and trabeculum, 11/2/2013 Pathogenesis: anterior forces / posterior forces 15

Tonometry
Two main methods of measuring IOP:
applanation force to flatten the cornea indentation force to indent the cornea

The main types of tonometer:

The Schiotz tonometer uses a plunger with a preset weight to indent the cornea. The amount of indentation is converted into mmHg by use of Friedenwald tables.
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Tonometry
The main types of tonometer:
Goldmann tonometer consists of double prism with 3.06 mm in diameter, applanation, more accurate, Perkins tonometer, hand held, applanation, The air puff tonometer, non contact, applanation, jet of air to flatten the cornea. Tono-pen Gas Tonometer Electrical Tonometer
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Schiotz Tonometer
Portable, simple, low cost, Measure the depth of indentation of cornea by a plunger with specific weight (5 gr; 7,5 gr ; 10 gr) The indentation represented in Schiotz scale is converted into mmHg by Freidenwald table, Low accuracy because it is influenced by ocular rigidity (high myop, DM, corneal leucoma).
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Goldmanns Applanation Tonometer

More accurate, not influenced by ocular rigidity The foot plate is smaller (3.06 mm) Disadvantages: cannot be applied to
Corneal edema Keratitis, corneal ulcer Keratokonus High astigmatism
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Tonography
To estimate outflow facility of HA, Principle: to express the fluid flow from the eye by continuous pressing to the eye Place Schiotz tonometer for 2-4 minutes, Compare IOP at 0 to 4 minutes outflow facility (C), Normal C > 0.18.
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Provocation Test
Water drinking test, dark room test, midriatic test, steroid test, Positive if IOP at the end of the tests are more than 8 mmHg, Indications:
Narrow / closed angle glaucoma Normal tension glaucoma Bias IOP
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Gonioscopy
Three main purposes of gonioscopy:
To Identify the abnormal angle structure, To Estimate the width of the chamber angle, To Visualize the angle during these following procedures: goniotomy, laser trabeculoplasty.

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Identification of angle structures

Schwalbes line (an opaque line) is a peripheral termination of Descemet membrane,
Trabecular meshwork has a ground glass appearance stretching from Schwalbes line to scleral spur. Consists of two parts: The anterior: nonfunctional, non pigmented part, whitish color, The posterior: functional, pigmented part, greyish-blue translucent.
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Identification of angle structures

Schlemms canal: slightly darker line, behind the posterior trabeculum, Scleral spurs: anterior of sclera, narrow, dense, often shiny, whitish band. As a landmark for laser trabeculoplasty.

Ciliary body stands behind the scleral spur as dull

brown band. The width depends on iris insertion. Curve of the corner at the margin of the ciliary body

Iris processes
Iris processes, small extension of the anterior surface \ of the iris, inserted at the level of scleral spur.
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Angle classification by Shaffer

Grade IV III II I Grade 0 : 45 degrees angle : 20 - 25 degrees angle : 20 degrees angle closed : 10 degrees angle closed : closed angle, iridocorneal contact.

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Ophthalmoscopy of the optic disc

1.2 million axons passes across the retina and enter the optic disc, Fibers from the macula papillomacular bundle, straight to the optic disc, most resistant, Fibers from temporal of macula an arcuate path around the papillomacular bundle supero and inferotemporal of the optic disc, vulnerable to glaucomatous damage.

Nerve fiber layer anatomy

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Ophthalmoscopy of the optic disc

Normal nerve fiber layer

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Diffuse nerve fiber atrophy

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Ophthalmoscopy of the optic disc

The optic cup, pale depression in the center of the optic cup, absent of nerve fiber, The neuroretinal rim, tissue between the outer edge of the cup and the outer margin of the disc, the color is pinkish orange, uniform width, contains nerve fibers, Nerve fibers death thinning of retinal rim, High IOP posterior bowing of lamina cribrosa, nasalisation of central retinal vessels.

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Ophthalmoscopy of the optic disc

The cup-disc ratio: fraction of vertical and horizontal diameter cup and diameter of the disc, normal c/d ratio is 0.3 or less.

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Optic disc changes in glaucoma

Normal disc with small cup

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Optic disc changes in glaucoma

Cup and disc ratio > 0.6, Peripapillary atrophy at temporal region, Splinter-shaped hemorrhage on the disc margin.

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Optic disc changes in glaucoma

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Normal Visual Field Examination

Nasally : 60 degrees Temporally : 95 degrees Superiorly : 50 degrees Inferiorly : 70 degrees The blind spot is located temporally 10-20 degrees Visual field is an island of vision surrounded by the sea of darkness, the sharpest is at the top of the island.

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Visual Fields in Glaucoma

Baring of the blind spot Localized paracentral scotoma at 10 - 20 degrees of fixation at superior and inferior quadrant extension to the blind spot Byerrum scotoma ring scotoma with nasal step of Roenne,

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Visual Fields in Glaucoma

Peripheral scotoma that spreads and coalesces to the paracentral scotoma Leaving central island and accompanying temporal island, even if the central vision is still normal Temporal island total blindness

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Classification
Primary open-angle glaucoma Secondary open-angle glaucoma Primary closed-angle glaucoma Secondary closed-angle glaucoma Primary congenital glaucoma Secondary congenital glaucoma
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Primary Open-Angle Glaucoma (Simple Glaucoma)

Bilaterally, not necessarily symmetrical, absence of secondary causes of high IOP, Glaucomatous optic nerve damage, Open and normal angle, IOP > 21 mmHg, Adult onset, hereditary, steroid responsiveness, Glaucomatous visual field defects, central tunnel vision, Minimal clinical signs.
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Management of Primary Open Angle Glaucoma

Initial therapy is usually medical, except in advanced cases, Argon laser trabeculoplasty (ALT) if IOP is uncontrolled despite maximal tolerated medical therapy, Trabeculectomy with / without antimetabolic drug in refractory glaucoma, Artificial filtering shunt: Achmed valve, Molteno tube, Krupin- Denver valve.
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Surgical Indications for Simple Glaucoma

Uncontrolled IOP by maximal medical treatment Progressive disc damage and visual field defect Drugs intolerance Unable to buy the drugs Poor compliance Unable to do the regular control
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Primary Closed-Angle Glaucoma

Obstruction of aqueous outflow as a result of closure of the angle by the peripheral iris Anatomically predisposed, bilateral, Predisposition: Crowded anterior segment Relatively anterior location iris lens diaphragm, Shallow anterior chamber, Narrow entrance to the chamber angle.
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PACG stage
Five overlapping stages:
Latent Intermittent (sub acute) Acute (congestive and post congestive) Chronic Absolute

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Latent angle-closure glaucoma

Shallow anterior chamber, convex-shape iris lens diaphragm, close iris to cornea, normal IOP, occludable angle, Treatment:
Good fellow eye without treatment, follow up, PACG fellow eye laser iridotomy.

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Intermittent angle-closure glaucoma

Rapid partial closure anterior chamber angle and reopening of the angle after some rest, Precipitating factors: physiological mydriasis, watching TV in dark room, prone position, reading, sewing, emotion, stress, Transient blurring of vision, halo, headache, Recovery after some rest.
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Acute congestive angle-closure glaucoma

Presentation:
Rapidly progressive impairment of vision, sometimes the vision 1/300 0, Eye ache and frontal headache, Congestion, nausea, vomiting.

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Acute congestive angle-closure glaucoma

Examination
Ciliary and conjunctival injection IOP > 50 mmHg, dilated pupil, unreactive. Cornea: epithelial edema, KP(+), vesicle Ant chamber: shallow PAS, flare / cell (+),
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Acute congestive angle-closure glaucoma

Wide pupil, slow / negative light reflex, Papilla edema, retinal edema,

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Acute congestive angle-closure glaucoma

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Acute congestive angle-closure glaucoma

Differential diagnosis:
Red eyes:
conjunctivitis, iridocyclitis

Silent eyes:
simple glaucoma, ocular hypertension

Glaucomatous visual field defect:

anomaly of the optic nerve and retina

Papillary atrophy:
anomaly at optic nerve

Congenital megalocornea without high IOP

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Acute congestive angle-closure glaucoma

Treatment:
Immediately decrease IOP with maximal drugs, Wait for 24 hours evaluation, Normal IOP, deep AC, open angle iridectomy, High IOP, permanent AC closure > 50% trabeculectomy, The fellow eye: preventive iridectomy.
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Postcongestive angle-closure glaucoma

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Chronic closed-angle glaucoma

Clinical features of chronic CAG are similar as POAG except gonioscopy of the angle is closed, There are three mechanism of CCAG:
Creeping PAS laser iridotomy / trabeculectomy After intermittent and laser iridotomy drug > Combination of POAG with narrow angle laser iridotomy + medical trabeculectomy

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Chronic closed-angle glaucoma

Signs and therapy are similar as simple glaucoma:
Trabeculectomy, Laser iridoplasty to make an angle, Argon Laser Trabeculopasty (ALT)

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Primary Congenital Glaucoma

65% of patients are male, 1: 10.000, Inheritance is autosomal recessive, bilateral, Maldevelopment of the trabeculum and iridotrabecular junction, abscent of angle recess, trabeculodysgenesis, The iris insertion can be flat or concave, Poor prognosis.

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Primary Congenital Glaucoma

Clinical signs:
Depends on the age of the onset and the level of IOP, According to the age of the onset there are 3 types:
True congenital glaucoma (40%). IOP elevated since in the intrauterine buphthalmos, Infantile glaucoma (55%) manifesting after birth, Juvenile glaucoma: IOP at 10-35 years of age, with clinical manifestation same as POAG.
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Primary Congenital Glaucoma

Examinations: Corneal haze, lacrimation, photophobia and blepharospasm, Buphthalmos if IOP before the age of 3 usually associated with axial myop, subluxated lens, Break of Descemet membrane, endothelial decompensation permanent stromal edema, Reversible glaucomatous cupping.

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Primary Congenital Glaucoma

Treatments: Initial drug treatment, Goniotomy if cornea is still clear, Trabeculotomy at corneal clouding, Trabeculectomy and trabeculotomy, Trabeculectomy with antimetabolic agent, --Outcome of the operation is poor.

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Secondary Glaucoma
Inflammation and residual inflammation of the uveal tissue: iridocyclitis, posterior synechia, Immature cataract, hipermature cataract, Lens luxation, lens subluxation, Ischemic retina, Sub choroidal bleeding, Congenital anomaly of the eye
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Secondary Glaucoma
Pigmentary gl. - Neovascular gl. Inflammatory gl. - Phacolytic glaucoma Red cell gl. - Ghost cell glaucoma Angle recession glaucoma Iridocorneal endothelial syndrome Pseudoexfoliative glaucoma
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Therapy
Nerve fiber damage caused by glaucoma is irreversible, Principle of the therapy is to decrease IOP medically or surgically to maintain the current condition, The purpose of decreasing the IOP is to reduce progressivity of the nerve fiber damage and visual field defect, Early findings.
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Indications of Medical Treatment

Simple glaucoma Acute / chronic closed angle glaucoma Maintain the diurnal IOP Lower IOP before operation

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Reducing aqueous production

Carbonic anhydrase inhibitor
acetazolamide 250 mg qid orally, dorzolamide eye drop tid,

Beta-adrenergic antagonist:
beta-blocker (timolol maleat 0.25-0.5%) bid, betaxolol 0.25% - 0.5% bid.

Adrenergic agonist:
depefeprine 0.5% - 2% bid.
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Other antiglaucoma drugs

Parasympathomimetic agents:
pilocarpin eye drop 2-4%, 2-6 x / day carbachol 0.75% used after cataract operation

Increase the latanoprost uveoscleral flow Hyperosmotic fluid

glycerol 50% 1-2 ml/kg body weight, drink all at once, manitol 20% swift infusion preoperative, 1.5-3 ml/kg body weight.

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Surgical treatment
Peripheral iridectomy:
Acute attack glaucoma, with good trabecular meshwork, Preventive treatment from acute attack for the fellow eye.

Trabeculectomy for all types of glaucoma, Goniotomy for congenital glaucoma if the cornea is still clear, Trabeculotomy for congenital glaucoma if the cornea is edema.
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Surgical treatment
Treatment for absolute glaucoma:
cyclocryo coagulation destroys the ciliary body to decrease HA production, enucleation if all treatment is not successful.

Laser treatment:
iridotomy gonioplasty trabeculoplasty
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Good Prognosis
Early and right diagnosis, Adequate control of IOP by medical / surgical treatment, Compliance of the patients to check their IOP and use medical treatment, Case finding among glaucoma family.

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