Post on 30-May-2018
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Definition
Glaucoma is a disease caused byincreased intraocular pressure (IOP)resulting either from a malformation
or malfunction of the eyes drainagestructures.
Left untreated, an elevated IOP causesirreversible damage the optic nerveand retinal fibers resulting in aprogressive, permanent loss of vision.
However, early detection and treatment
can slow, or even halt the progressionof the disease.
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Glaucoma is often called "the sneakthief of sight." This is because, asalready mentioned, in most cases, theintraocular pressure can build up anddestroy sight without causing obvioussymptoms.
Thus, awareness and early detection ofglaucoma are extremely important
because this disease can besuccessfully treated when diagnosedearly.
While everyone is at risk for glaucoma,certain people are at a much higher
risk and need to be checked more
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Pathophysiology
The major risk factor for most glaucomas andfocus of treatment is increased intraocularpressure.
Intraocular pressure is a function of production of
liquid aqueous humor by the ciliary processesof the eye and its drainage through thetrabecular meshwork.
Aqueous humor flows from the ciliary processesinto the posterior chamber, boundedposteriorly by the lens and the zonules of Zinnand anteriorly by the iris.
It then flows through the pupil of the iris into theanterior chamber, bounded posteriorly by theiris and anteriorly by the cornea.
From here the trabecular meshwork drains
aqueous humor via Schlemm's canal intoscleral plexuses and general blood circulation.
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The pathophysiology ofglaucoma lies on theoverproduction of theaqueous humor, the clearfluid that fills the anterior
chamber (the spacebetween the cornea andiris) or a drainage problem.
Any imbalance between theproduction and drainage ofthe aqueous will lead to anincrease in intraocular
pressure.Normal IOPs of most people
falls between 8 and 21mmHg.
Some eyes can tolerate higherpressures than others.
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In most people, the filtering angles arewide open, although in someindividuals, they can be narrow. For
example, the usual filtering angle isabout 45 degrees, whereas a narrowangle is about 25 degrees or less.
After exiting through the trabecular
meshwork in the filtering angle, theaqueous fluid then drains into tinyblood vessels (capillaries) into themain bloodstream. The aqueoushumor should not be confused withtears, which are produced by a gland
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Also, if the sink's faucet is on toohigh, the water may overflow.Again, if this sink were a closed
system, the pressure within the sinkwould increase. Likewise, if too much fluid is being
produced within the eye, the
intraocular pressure may becometoo high. In either event, since theeye is a closed system, if it cannotremove the increased fluid, the
pressure builds up and nerve
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In open angle glaucoma there isreduced flow through the trabecularmeshwor
In angle closure glaucoma, the iris ispushed forward against thetrabecular meshwork, blocking fluid
from escaping.
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A. The drainage angleformed between thecornea and the iris iswide open to about 40.Aqueous fluid flows freely
to the trabecularmeshwork and out of theeye.
B. The drainage angle isclosed. The iris and thecornea are in contact (*)and block the flow ofaqueous fluid to thetrabecular meshwork.
The fluid is trapped in theeye causing intraocularpressure to rise.
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Causes
Ocular hypertension (increased pressurewithin the eye) is the largest riskfactor in most glaucomas, but in somepopulations only 50% of patients withprimary open angle glaucoma actuallyhave elevated ocular pressure.
Those of African descent are three timesmore likely to develop primary open
angle glaucoma. People who are older,have thinner corneal thickness, andmyopia also are at higher risk forprimary open angle glaucoma. Peoplewith a family history of glaucoma have
about a six percent chance ofdevelo in laucoma.
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Many East Asian groups are prone todeveloping angle closure glaucomadue to their shallower anterior
chamber depth, with the majority ofcases of glaucoma in this populationconsisting of some form of angleclosure.
Inuit also have a twenty to forty timeshigher risk than Caucasians ofdeveloping primary angle closureglaucoma. Women are three timesmore likely than men to develop acuteangle-closure glaucoma due to their
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There is increasing evidence that ocularblood flow is involved in thepathogenesis of glaucoma. Current dataindicate that fluctuations in blood floware more harmful in glaucomatous opticneuropathy than steady reductions.Unstable blood pressure and dips arelinked to optic nerve head damage and
correlate with visual field deterioration. A number of studies also suggest a
possible correlation betweenhypertension and the development ofglaucoma. In normal tension glaucoma,nocturnal hypotension may play a
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There is no clear evidence that vitamindeficiencies cause glaucoma in humans. Itfollows then that oral vitamin supplementationis probably not useful in glaucoma treatment.
Various rare congenital/genetic eyemalformations are associated with glaucoma.Occasionally, failure of the normal thirdtrimester gestational atrophy of the hyaloidcanal and the tunica vasculosa lentis isassociated with other anomalies. Angle closure
induced ocular hypertension andglaucomatous optic neuropathy may alsooccur with these anomalies and modelled inmice.
Those at risk for glaucoma are advised to have adilated eye examination at least once a year.
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Classification of glaucoma
1. Primary glaucoma and its variants(H40.1-H40.2) Primary angle-closure glaucoma, also known
as primary closed-angle glaucoma,narrow-angle glaucoma, pupil-blockglaucoma, acute congestive glaucoma
Acute angle-closure glaucoma Chronic angle-closure glaucoma Intermittent angle-closure glaucoma Superimposed on chronic open-angle
closure glaucoma ("combinedmechanism" - uncommon)
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Primary open-angle glaucoma, alsoknown as chronic open-angleglaucoma, chronic simple glaucoma,
glaucoma simplex High-tension glaucoma Low-tension glaucoma
Variants of primary glaucoma Pigmentary glaucoma Exfoliation glaucoma, also known as
pseudoexfoliative glaucoma orglaucoma capsulare
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2. Developmental glaucoma(Q15.0)
Developmental glaucoma Primary congenital glaucoma Infantile glaucoma Glaucoma associated with hereditary
of familial diseases
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Drug-induced glaucoma Corticosteroid induced glaucoma Alpha-chymotrypsin glaucoma.
Postoperative ocular hypertension fromuse of alpha chymotrypsin.
Glaucoma of miscellaneous origin Associated with intraocular tumors Associated with retinal detachments Secondary to severe chemical burns of the
eye Associated with essential iris atrophy Toxic Glaucoma
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-rim a ry a n g le clo su reg la u co m a This is caused by contact between the iris
and trabecular meshwork, which in turnobstructs outflow of the aqueous humorfrom the eye.
This contact between iris and trabecularmeshwork (TM) may gradually damagethe function of the meshwork until it failsto keep pace with aqueous production,and the pressure rises.
In over half of all cases, prolonged contactbetween iris and TM causes theformation of synechiae (effectively"scars").
These cause permanent obstruction ofaqueous outflow.
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Diagnosis is made from physical signsand symptoms: pupils mid-dilated andunresponsive to light, corneaedematous (cloudy), reduced vision,redness, pain.
However, the majority of cases areasymptomatic.
Prior to very severe loss of vision, these
cases can only be identified byexamination, generally by an eye careprofessional.
Once any symptoms have beencontrolled, the first line (and oftendefinitive) treatment is laser iridotomy.
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The goal of treatment is to reverse,and prevent, contact between irisand trabecular meshwork.
In early to moderately advancedcases, iridotomy is successful inopening the angle in around 75% of
cases. In the other 25% laser iridoplasty,
medication (pilocarpine) orincisional surgery may be required.
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-rim a ry o p e n a n g leg la u co m a Optic nerve damage resulting in
progressive visual field loss. This is associated with increased
pressure in the eye. Not all people with primary open-
angle glaucoma have eye pressure
that is elevated beyond normal, butdecreasing the eye pressure furtherhas been shown to stop progressioneven in these cases.
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The increased pressure is caused bytrabecular blockage which is wherethe aqueous humor in the eye
drains out. Because the microscopic passage
ways are blocked, the pressure
builds up in the eye and causesimperceptible very gradual visionloss.
Peripheral vision is affected first buteventually the entire vision will be
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Diagnosis is made by looking for cupping of theoptic nerve.
Prostoglandin agonists work by openinguveoscleral passageways.
Beta blockers such as timolol, work bydecreasing aqueous formation. Carbonic anhydrase inhibitors decrease
bicarbonate formation from ciliary processes inthe eye, thus decreasing formation of Aqueoushumor.
Parasympathetic analogs are drugs that work onthe trabecular outflow by opening up thepassageway and constricting the pupil.
Alpha 2 agonists (brimonidine, apraclonidine)both decrease fluid production (via. inhibition
of AC) and increase drainage.
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eo vascu lar g lau co m a Neovascular glaucoma is an uncommon
type of glaucoma that is difficult ornearly impossible to treat.
This condition is often caused byproliferative diabetic retinopathy(PDR) or central retinal vein occlusion(CRVO).
It may also be triggered by otherconditions that result in ischemia ofthe retina or ciliary body.
Individuals with poor blood flow to the
eye are highly at risk for thiscondition.
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Neovascular glaucoma results whennew, abnormal vessels begindeveloping in the angle of the eye
that begin blocking the drainage. Patients with such condition begin to
rapidly lose their eyesight.
Sometimes, the disease appears veryrapidly, specially after cataractsurgery procedure.
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In neovascularglaucoma, the iris isoften covered by
new vessels(arrow).These vessels can
grow
and eventuallyblock the drainageof fluid through thetrabecularmeshwork.
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A new treatment for this disease, asfirst reported by Kahook andcolleagues, involves use of a novel
group of medications known as Anti-VEGF agents.
These injectable medications can
lead to a dramatic decrease in newvessel formation and, if injectedearly enough in the diseaseprocess, may lead to normalization
of intraocular pressure.
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Toxic glaucoma
Toxic glaucoma is open angleglaucoma with an unexplainedsignificant rise of intraocular
pressure following unknownpathogenesis.
Intraocular pressure can sometimes
reach 80 mmHg (11 kPa). It characteristically manifests as
ciliary body inflammation andmassive trabecular oedema that
sometimes extends to Schlemm's
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This condition is differentiated frommalignant glaucoma by thepresence of a deep and clear
anterior chamber and a lack ofaqueous misdirection.
Also, the corneal appearance is not as
hazy. A reduction in visual acuity can occur
followed neuroretinal breakdown.
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Associated factors include inflammation,drugs, trauma and intraocular surgery,including cataract surgery and
vitrectomy procedures. Gede Pardianto (2005) reports on fourpatients who had toxic glaucoma. Oneof them underwentphaecoemulsification with smallparticle nucleus drops. Some casescan be resolved with somemedication, vitrectomy procedures ortrabeculectomy. Valving procedures
can give some relief but further
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The major risk factors include:
Age over 45 years Family history of glaucoma Black racial ancestry Diabetes
History of elevated intraocular pressure Nearsightedness (high degree of myopia), which is
the inability to see distant objects clearly History of injury to the eye Use of cortisone (steroids), either in the eye or
systemically (orally or injected) Farsightedness (hyperopia), which is seeing distant
objects better than close ones (Farsighted peoplemay have narrow filtering angles, which predisposethem to acute (sudden) attacks of closed-angleglaucoma.)
Ri k F C S
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Risk Factor Category Score
Age younger than 50 years50-64 years65-74 yearsolder than 75 years
0123
Race Caucasian/other African American
02
Family History of Glaucoma Negative or positive in non-first degreerelativePositive for parentsPositive for siblings
012
Last Complete Eye Exam Within last two years2-5 years agomore than 5 years ago
012
Level of Glaucoma Risk (Total Score)
High 4 or greater
Moderate 3
Low 2 or less
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SYMPTOMS
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Diagnosis
Because glaucoma does not causesymptoms in most cases, those whoare 40 or older should have an annual
examination including a measurementof the intraocular pressure. Thosewho are glaucoma suspects may needadditional testing.
Screening for glaucoma is usuallyperformed as part of a standard eyeexamination performed byophthalmologists and optometrists.
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The doctor evaluates the optic nerveand grades its health by noting thecup to disc ratio. This is simply a
comparison of the cup (thedepressed area in the center of thenerve) to the entire diameter of theoptic nerve.
As glaucoma progresses, the area ofcupping, or depression, increases.
Therefore, a patient with a higher
ratio has more damage.
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The above photos show progressiveoptic nerve damage (indicated bythe cup to disc ratio) caused by
glaucoma. Notice the paleappearance of the nerve with the0.9 cup as compared to the nervewith the 0.3 cup.
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The progression of glaucoma is monitoredwith a visual field test. This test mapsthe peripheral vision, allowing the doctorto determine the extent of vision loss
from glaucoma and a measure of theeffectiveness of the treatment. Thevisual field test is periodically repeated toverify that the intraocular pressure is
being adequately controlled. The structures in the front of the eye arenormally difficult to see without the helpof a special gonioscopy lens. This specialmirrored contact lens allows the doctor to
examine the anterior chamber and the
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Owing to the sensitivity of all methods oftonometry to corneal thickness, methodssuch as Goldmann tonometry should beaugmented with pachymetry to measure
central corneal thickness (CCT). A thicker-than-average cornea can result in
a pressure reading higher than the 'true'pressure, whereas a thinner-than-
average cornea can produce a pressurereading lower than the 'true' pressure. Because pressure measurement error can
be caused by more than just CCT (i.e,corneal hydration, elastic properties,etc.), it is impossible to 'adjust' pressure
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At St. Lukes, another test called theArden Screening Test is used toconfirm the diagnosis of glaucoma.
This color test may show vision
changes that occur before problemsappear on the visual field test. The Frequency Doubling Illusion can also
be used to detect glaucoma with the
use of a Frequency DoublingTechnology (FDT) perimeter. Examination for glaucoma also could be
assessed with more attention given tosex, race, history of drugs use,
refraction, inheritance and family
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M a n a g e m e n t
The modern goals of glaucoma management are toavoid glaucomatous damage, nerve damage,preserve visual field and total quality of life forpatients with minimal side effects.
This requires appropriate diagnostic techniques and
follow up examinations and judicious selection oftreatments for the individual patient. Although intraocular pressure is only one of the major
risk factors for glaucoma, lowering it via variouspharmaceuticals and/or surgical techniques iscurrently the mainstay of glaucoma treatment.
Vascular flow and neurodegenerative theories ofglaucomatous optic neuropathy have promptedstudies on various neuroprotective therapeuticstrategies including nutritional compounds some ofwhich may be regarded by clinicians as safe for usenow, while others are on trial.
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M e d ication
Intraocular pressure can be lowered withmedication, usually eye drops. There areseveral different classes of medicationsto treat glaucoma with several different
medications in each class. Each of these medicines may have local
and systemic side effects. Adherence tomedication protocol can be confusing
and expensive; if side effects occur, thepatient must be willing either to toleratethese, or to communicate with thetreating physician to improve the drugregimen. Initially, glaucoma drops may
reasonably be started in either one or in
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Poor compliance with medications andfollow-up visits is a major reason forvision loss in glaucoma patients. A2003 study of patients in an HMO
found that half failed to fill theirprescription the first time and one infour failed to refill their prescriptions asecond time.
Patient education and communicationmust be ongoing to sustain successfultreatment plans for this lifelongdisease with no early symptoms.
The possible neuroprotective effects of
various topical and systemic
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C om m o n ly u sed m ed ication s
Prostaglandin analogs like latanoprost(Xalatan), bimatoprost (Lumigan) andtravoprost (Travatan) increaseuveoscleral outflow of aqueous humor.
Bimatoprost also increases trabecularoutflow
Topical beta-adrenergic receptorantagonists such as timolol, levobunolol
(Betagan), and betaxolol decreaseaqueous humor production by the ciliarybody.
Alpha2-adrenergic agonists such asbrimonidine (Alphagan) work by a dualmechanism, decreasing aqueous
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Less-selective sympathomimetics likeepinephrine and dipivefrin (Propine)increase outflow of aqueous humorthrough trabecular meshwork and
possibly through uveoscleral outflowpathway, probably by a beta2-agonistaction.
Miotic agents (parasympathomimetics)like pilocarpine work by contraction ofthe ciliary muscle, tightening thetrabecular meshwork and allowingincreased outflow of the aqueoushumour. Ecothiopate is used in chronic
glaucoma.
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Carbonic anhydrase inhibitors likedorzolamide (Trusopt), brinzolamide(Azopt), acetazolamide (Diamox)
lower secretion of aqueous humorby inhibiting carbonic anhydrase inthe ciliary body.
Physostigmine is also used to treatglaucoma and delayed gastricemptying
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Surgery
Conventional surgery to treat glaucomamakes a new opening in themeshwork. This new opening helpsfluid to leave the eye and lowersintraocular pressure.
Both laser and conventional surgeriesare performed to treat glaucoma.
Surgery is the primary therapy for thosewith congenital glaucoma. Generally, these operations are a
temporary solution, as there is not yet
a cure for glaucoma
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Canaloplasty
Canaloplasty is a nonpenetrating procedure utilizingmicrocatheter technology.
To perform a canaloplasty, an incision is made intothe eye to gain access to Schlemm's canal in asimilar fashion to a viscocanalostomy.
A microcatheter will circumnavigate the canal aroundthe iris, enlarging the main drainage channel andits smaller collector channels through the injectionof a sterile, gel-like material called viscoelastic.
The catheter is then removed and a suture is placedwithin the canal and tightened.
By opening the canal, the pressure inside the eyemay be relieved, although the reason is unclearsince the canal (of Schlemm) does not have anysignificant fluid resistance in glaucoma or healthyeyes. Long-term results are not available.
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Laser surgery
Laser trabeculoplasty may be used to treat open angleglaucoma.
It is a temporary solution, not a cure. A 50 m argon laser spot is aimed at the trabecular
meshwork to stimulate opening of the mesh to allow
more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty utilizes a thermal argon
laser. The procedure is called Argon LaserTrabeculoplasty or ALT.
A newer type of laser trabeculoplasty exists that uses a
"cold" (non-thermal) laser to stimulate drainage in thetrabecular meshwork. This newer procedure which uses a 532 nm frequency-
doubled, Q-switched Nd:YAG laser which selectivelytargets melanin pigment in the trabecular meshworkcells, called Selective Laser Trabeculoplasty or SLT.
Studies show that SLT is as effective as ALT at lowering eyepressure.
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Trabeculectomy
The most common conventional surgeryperformed for glaucoma is the trabeculectomy.
Here, a partial thickness flap is made in thescleral wall of the eye, and a window openingmade under the flap to remove a portion of thetrabecular meshwork.
The scleral flap is then sutured loosely back inplace.
This allows fluid to flow out of the eye throughthis opening, resulting in lowered intraocular
pressure and the formation of a bleb or fluidbubble on the surface of the eye. Scarring can occur around or over the flap
opening, causing it to become less effective orlose effectiveness altogether.
One person can have multiple surgicalrocedures of the same or different t es.
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Glaucoma drainageimplants There are also several different glaucoma drainage
implants. These include the original Molteno implant (1966), the
Baerveldt tube shunt, or the valved implants, such as theAhmed glaucoma valve implant or the ExPress MiniShunt and the later generation pressure ridge Molteno
implants. These are indicated for glaucoma patients not responding
to maximal medical therapy, with previous failedguarded filtering surgery (trabeculectomy).
The flow tube is inserted into the anterior chamber of theeye and the plate is implanted underneath the
conjunctiva to allow flow of aqueous fluid out of the eyeinto a chamber called a bleb. The first-generation Molteno and other non-valved implants
sometimes require the ligation of the tube until the blebformed is mildly fibrosed and water-tight
This is done to reduce postoperative hypotonysuddendrops in postoperative intraocular pressure (IOP).
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Valved implants such as the Ahmedglaucoma valve attempt to controlpostoperative hypotony by using amechanical valve.
The ongoing scarring over the conjunctivaldissipation segment of the shunt maybecome too thick for the aqueous humorto filter through. This may require
preventive measures using anti-fibroticmedication like 5-fluorouracil (5-FU) ormitomycin-C (during the procedure), oradditional surgery. And for Glaucomatouspainful Blind Eye and some cases of
Glaucoma, Cyclocryotherapy for ciliary
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THANKZ!!!!