Acute Angle Closure Glaucoma

8/12/2019 Acute Angle Closure Glaucoma

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ACUTE ANGLE CLOSURE GLAUCOMA

SIGNS AND SYMPTOMSPatients with angle closure glaucoma manifest symptoms of ocular and facial pain, unilateral blurring ofvision, photopsiae in the form of colored haloes around lights, and occasionally nausea and vomiting.

Acuity may be reduced significantly in the involved eye, often to 20/80 or worse.

The hallmar signs of angle closure include significantly elevated intraocular pressure, a closed angle upon

gonioscopic evaluation, deep con!unctival and episcleral in!ection in a circumlimbal fashion, and a fi"ed,

mid#dilated pupil. $pon slit#lamp e"amination, you may also see an edematous or %steamy% cornea and

shallow anterior chamber.

Applanation tonometry may reveal &'P in the range of (0 to )0mm *g, or even higher in some cases.

+onioscopy, which may prove difficult because of microcystic corneal edema, reveals no visible angle

structures without indentation. There may be evidence of previous angle closure episodes in the form of

peripheral anterior synechiae PA- in the fellow eye.

PATHOPHYSIOLOGYAngle closure occurs when the peripheral iris physically opposes the trabecular meshwor or corneal

endothelium and impedes aueous outflow. -everal mechanisms are possible. The most common etiology

of angle closure is pupillary bloc, whereby the flow of aueous from the posterior to anterior chamber is

inhibited, causing iris bomb. This may be simply due to genetic predisposition and anterior segmentanatomy primary pupil bloc, or from posterior synechiae, lenticular enlargement or displacement of the

lens or &' secondary pupil bloc.

Another mechanism which may induce angle closure involves an abnormal configuration of the iris, the so#

called %plateau iris syndrome.% Patients with this presentation may boast a deep anterior chamber centrally1

however, the iris demonstrates an unusual la"ity, coming into close appro"imation with the angle

peripherally. These patients may be prone to %angle crowding% and subseuent closure during physiologic

or pharmacologic dilation. 'ther etiologies of angle closure without pupil bloc include neovascularmembranes inducing PA-, anterior uveal displacement such as in choroidal detachment or, rarely,

posterior segment inflammation or tumors.

MANAGEMENTThe paramount concern in managing an angle closure attac is to lower &'P uicly. our choice of

primary medication depends upon the pressure at presentation. As most miotics are ineffective at pressures

over 30mm *g due to iris ischemia, immediately treat such patients with a beta#blocer of 0.45

concentration and/or apraclonidine 65.

7e"t, perform corneal compression with a gonioprism to aid in lowering the &'P by forcing aueous into

the trabeculum and temporarily opening the angle. &t may be necessary to use topical glycerin to clear thecornea if there is significant edema. Perform tonometry every 64 minutes after initiating therapy.

&f the patient does not achieve significant reduction in &'P after 34 minutes, administer an oral carbonicanhydrase inhibitor acetaolamide 2 " 240mg tablets. ou may also wish to use a hyperosmotic agent

such as three to five ounces of oral glycerin or isosorbide over ice. 'nce the &'P is below 30mm *g, instill

pilocarpine 25 as well as prednisolone acetate 65 every 64 minutes to abate the attac and reopen the

angle. &t is safe to discontinue this regimen when the &'P is below (0mm *g and the angle structures areagain visible with gonioscopy. 9aintain the patient on the following medications: pilocarpine 25 ;&


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>hen the inflammation has diminished and the A? is uiet, refer the patient for a peripheral iridotomy.

This provides a secondary outflow channel for aueous, and commonly causes a permanent anatomical

%deepening% of the anterior chamber.

CLINICAL PEARLS

The most important consideration in handling an acute angle closure attac is accurate diagnosisand prompt intervention. @irst distinguish between angle closure glaucoma and other acute openangle conditions such as uveitic glaucoma, glaucomatocyclitic crisis and phacolytic glaucoma.

'nce you have established angle closure as the cause, you must also differentiate the nature of the

attac, whether due to primary pupillary bloc, plateau iris, or secondary pupillary bloc. &f you

are uncertain of the etiology or if an inflammatory glaucoma is present, do not use a miotic, as this

will only e"acerbate the condition.

Acute Glaucoma

Acute glaucoma is an eye condition, where the pressure inside the eye rises

uicly. The usual symptoms are sudden eye pain, a red eye and reducedvision. 'ther possible symptoms are headache, abdominal pain, nausea and

vomiting. Acute glaucoma can be treated successfully, but it needsimmediate treatmentto relieve symptoms and to prevent damage to the

eye.

!at is acute "laucoma#

Acute glaucoma occurs when the pressure inside the eye gets high very uicly.

7ote: acute glaucoma is also called acute angle closure glaucoma or acute closed angleglaucoma. Another term sometimes used is primary angle closure glaucoma, which is a

similar situation that can lead to acute glaucoma.

There are other types of glaucoma, which occur more gradually. The most common type

is primary open angle glaucoma also called chronic glaucoma. -ee separate leaflet on

'Glaucoma (Primary Open Angle'. 'ther, less common types are secondary glaucoma

and congenital glaucoma. The rest of this leaflet deals only with acute glaucoma.

!at causes acute "laucoma#


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To understand the cause, it helps to understand how fluids wor in the eye. The eye needsto eep its shape so that light rays are focussed accurately onto the retina. -o, most of theeye is filled with a substance lie !elly called the vitreous humour humour meaning

fluid. The front of the eye is filled with a clear fluid called aueous humour, which is

more watery.

The aueous humour is made continuously by cells called the ciliary body. The fluid

circulates through the front part of the eye, and then drains away through an area called

the trabecular meshwor, which is located near the base of the iris. -o, there is constantproduction and drainage of fluid.

!at !a$$ens in acute an"le "laucoma#

&n acute glaucoma, there is a sudden blocage, so that aueous fluid cannot drain out of

the eye. This happens if the iris the coloured part of the eye gets too close to the lens.

@luid gets stuc behind the iris and maes it bulge forwards. This bulging then blocs the

drainage area the trabecular meshwor, so that fluid cannot leave the eye. =ut morefluid is still being made, so the pressure inside the eye starts to rise uicly.

!at causes t!e %loc&a"e#

$sually it is a combination of factors. &n some people, the area near the base of the iris is

very narrow, so it more easily gets bloced. &n other people, the lens of the eye may be

swollen, which has the same effect. This situation is called a narrow drainage angle orshallow anterior chamber and maes a person more susceptible to acute glaucoma.

The iris the coloured part of the eye is also involved. The iris muscle is responsible forcontrolling the sie of the pupil the blac area in the middle of the eye. >hen the iris

muscles enlarge the pupil, they tend to bulge, which can bloc the flow of fluid if the area

is already narrow. The pupil enlarges in conditions of dim light, sudden e"citement, or


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with certain medications. @or this reason, acute glaucoma is more liely to occur in the

evening, or in situations lie watching a football match on TB dim lighting and sudden

e"citement.

!at can tri""er acute "laucoma#

Barious medications can trigger acute glaucoma if you are susceptible to it. *owever, forthe population as a whole, the chance of getting acute glaucoma with these medicines is

very small # so they are commonly prescribed without too much worry. =ut if you have

been warned that you may be susceptible to acute glaucoma, tell your doctor beforestarting new medication or eye drops, especially if it is one of the ones listed below.

?ommonly used medicines which may trigger acute glaucoma are:

Cye drops used to dilate enlarge the pupil # they may be used for eye checups.

Antidepressants of the tricyclic or --D& types.

-ome of the medicines used to treat nausea, vomiting or schiophrenia a typecalled phenothiaines.

&pratropium used for asthma.

Topiramate.

-ome medicines used to treat allergies or stomach ulcers, such as

chlorpheniramine, cimetidine and ranitidine.

9edication used during a general anaesthetic.

ying on your front for a long period may also affect fluids in the eye, and can triggeracute glaucoma. This can occur, for e"ample, during an operation on the spine.

!o "ets acute "laucoma#

Appro"imately 6 in 6000 people get acute glaucoma. &t is more liely in people over age

30 years, and most often happens at around age )0#E0 years. &t is more common in long#sighted people and women. &t is also more common in certain populations: -outheast

Asian and Csimo people.

!at are t!e s'm$toms o( acute "laucoma#

The symptoms usually start suddenly. They are:

-udden, severe pain in the eye.

Dedness of the eye.

Deduced vision, often with haloes circles seen around lights.

The pain may be spread around the head and be felt as a severe headache.

-ometimes, the pain may cause nausea, vomiting, or there may be abdominal pain

tummy pain as well.


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-ome people may not get eye pain, but instead have some of the other symptoms

listed here, such as headache or abdominal pain with a red eye or reduced vision.

The pupil blac part of the eye will loo large, and the clear part of the eye

loos hay mily or steamy.

As e"plained above, symptoms often begin in a situation of dim lighting, suddene"citement, with certain medications or after a general anaesthetic.

Are t!ere an' )arnin" s'm$toms#

Acute glaucoma can start out of the blue with no warning. *owever, you may have

warning symptoms, which often are not recognised. These occur when pressure rises inthe eye, and then improves by itself. The symptoms are: blurred vision, seeing haloes or

rainbows around lights, and eye pain. The warning symptoms can come and go # they

may start in the evening with dim light, and may settle after sleep because sleep rela"esthe iris muscles.

&f you have these symptoms you should see a doctor urgently, in case you need treatment

to prevent a more severe attac.

Ho) is acute "laucoma dia"nosed#

The diagnosis is made from the symptoms and the appearance of the eye. A provisional

diagnosis can be made by any doctor not necessarily an eye specialist. The diagnosis

can be confirmed by an e"amination done by an eye specialist. This usually involvesmeasuring the pressure in the eye a uic and easy test and e"amining the eye using a

special light and magnifier called a slit lamp.

!at is t!e treatment (or acute "laucoma#

Initial treatment

Treatment is *er' ur"ent+ou should be seen by an ophthalmologist eye specialist

immediately. &f it will tae time getting to the ophthalmologist, treatment can be startedmeanwhile.

The first treatment is medication to lower the pressure of fluid in the eye. There are

various types of medicine that reduce eye pressure.


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Painillers and anti#sicness medication, if needed.

$sually, it is recommended that you lie flat on your bac # this position may help

drain the trapped fluid.

'ther types of eye drops which reduce fluid in the eye, such as brinolamide,

brimonidine or pilocarpine.

'ther fluid#reducing medication such as intravenous mannitol.

,urt!er treatment

>hen the pressure in the eye has gone down, further treatment is needed in order to

prevent the acute glaucoma from coming bac. This involves using laser treatment orsurgery to mae a small hole in the iris. The hole allows fluid to flow freely around the

iris, which stops the iris bulging forwards and blocing the trabecular meshwor.

aser treatment is called peripheral iridotomy. This is the usual treatment, and the

preferred option, as it does not involve surgery to the eye. Two small holes are made in

the iris using a laser. The holes are almost unnoticeable to other people.

-urgical treatment is called surgical iridectomy. &t maes a small, triangular hole in the

iris. The hole is visible afterwards as a very small, blac triangle at the edge of the iris.

-ometimes, another type of surgery is used, which is similar to a cataract operation. This

operation removes the lens of the eye # which can help if a swollen lens was causing the

acute glaucoma in the first place. As with cataract operations, the lens which is removedcan be replaced by an artificial lens, or by using glasses.

$sually, laser or surgical treatment will be advised for the other eye at some stage. This is

to prevent acute glaucoma happening in the other eye. Also, eye drops may sometimes beneeded as long#term treatment, to help eep the eye pressure under control.

!at are t!e com$lications o( acute "laucoma#

&f treatment is delayed, the high pressure in the eye can damage nerves and blood vessels.This can cause reduced vision, and in severe cases can cause blindness in the affected

eye.

Also, delayed treatment can lead to the the iris thecoloured part of the eye sticing tothe front of the eye cornea. This blocs the drainage area, so a drainage operation is

needed. This operation creates a channel between the inside of the eye and the outsidewhite part of the eye.

!at is t!e outloo& (or acute "laucoma#

The outloo is good if treatment is given promptly. The eye can recover, and laser

treatment or surgery can prevent the problem coming bac.


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&f the attac is severe or if treatment is delayed, there is a ris of complications

e"plained above.

Dri*in" and "laucoma

9any people will be allowed to drive after recovering from acute glaucoma. Cven if

vision is reduced in one eye, you may still be allowed to drive if your vision is good

enough in the other eye. *owever, you will need advice from your eye specialist. &f youare a driver and have glaucoma in both eyes, the law says that you must inform the


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its shape for the accurate focusing of light rays into the retina. This is actually

accomplished by a !elly#lie substance called Fvitreous humourG which fills most parts of

the eye and the watery Faueous humourG in the front portion of the eye

The aueous humour circulates through the eye front and drains via the trabecular

meshwor found at the iris base. This fluid production as well as drainage is continuous.

-udden blocage in the draining of the eye fluid could cause the increase in internal

pressure in the eye. As long as the fluid is not drained, the pressure continues to build up.The blocage can actually be attributed to the pro"imity of the iris to the eyes lens

resulting to the fluid getting stuc and maing the iris bulge forward.

As for the reason for the blocage, it can be due to the following:

Area near iris base is very narrow maing it easier to get bloced

-wollen lens which could result to a shallow anterior chamber or narrow drainage

angle. This will mae the person more at ris for glaucoma. &ris muscle causes pupil to enlarge and bulge which blocs the fluid flow

especially if the immediate area has narrowed.

Cnlargement of pupils due to sudden e"citement, medication and dim lights can

also result to fluid flow being bloced.

Acute Glaucoma Tri""ers

-ince it was mentioned that dim lighting can cause acute glaucoma, it is not surprising

that it occurs most commonly during the night time. A simple activity such as watching afootball game can trigger the symptoms due to combination of e"citement and dim lights.

&ndividuals who are at ris of acute glaucoma should also be cautious when taing certain

medications for it could trigger the onset of this eye condition. Although the ris involvedin suffering from this eye condition is relatively small, it certainly would not hurt to be

careful. Among the medications considered as triggers include:

Anti#depressants --D& or tri#cyclic types

Cye drops H dilates the pupils and usually used during routine checups

Topiramate

Phenothiaines for treatment of nausea and vomiting &pratropium for asthma treatment

?hlorpheniramine, ranitidine and cimetidine for stomach ulcers

'ther medications for allergy treatments and general anaesthetics


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Another possible trigger is lying face down, such as in spinal operations, for a prolonged

period for this could affect eye fluid.

Ris& ,actors (or Acute Galucoma

?ertain ris factors should be considered to now if you are at ris for acute glaucoma.

&ndividuals aged 30 years old and above

&ndividuals who are long#sighted

Csimo, -outheast Asian race

Common S'm$toms o( Acute Galucoma

$nfortunately, most of the symptoms associated with acute glaucoma start without

warning. They include:

-udden pain in your eyes usually severe

Dedness

Deduced vision accompanied by haloes round light sources

*eadache due to eye pain

7ausea and vomiting due to eye pain

Pupils appear larger than normal

?lear portion of the eye will loo hay or mily

Again, these symptoms usually appear after the acute glaucoma is triggered due to certainlighting conditions or medications. &f you e"perience any of the above symptoms, it is

important that you see medical attention to prevent worsening of the eye condition.

arnin" Si"ns o( Acute Glaucoma

&n most cases, acute glaucoma appears suddenly and you might not be able toimmediately recognie the danger signs. -uch symptoms that you should loo out for

include: seeing rainbows or haloes around lights, eye pain and blurred vision. They could

be e"perienced intermittently and could even disappear after sleep. 9ae sure youcontact your doctor at once to prevent further attacs.

Dia"nosis and Treatment

-ince acute glaucoma may be e"perienced without warning, diagnosis is usually made

after the appearance of the symptoms. An eye specialist will confirm the eye conditionafter a detailed e"amination using a slit lamp as well as a specific test that will measure

eye pressure.


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After confirmation, the eye specialist will immediately try to lower the pressure and

reduce fluid build up by using:

Cye drops with beta#blocer and steroids

Acetaolamide in!ection

-econdary treatment will usually involve:

Painillers or anti#sicness drugs

9annitol H to reduce fluid build up

Cye drops brimonidine, brinolamide or pilocarpine

ying on bac to encourage fluid drainage

@urther treatment for prevention is recommended in order to ensure that the eye condition

will not come bac. Possible treatments include:

aser treatment or peripheral iridotomy H creation of two small holes near the iris

to promote fluid drainage1 usually the preferred treatment there is no eye surgeryinvolved1 holes will remain unnoticeable

-urgical treatment or surgical iridectomy H creation of triangular holes in the iris

for fluid drainage1 holes will be uite visible and will appear lie a blac triangle

at the iris edge Another surgery similar to cataract operation H removal of the eye lens and

replaced by artificial lens

9ost eye specialist will recommend any of the surgical treatment in order to prevent theother eye from getting acute glaucoma. -ome patients will be prescribed eye drops as a

part of their long#term treatment to ensure that eye pressure is ept in control.

Com$lications o( Acute Glaucoma

>ithout proper management and treatment, individuals diagnosed with acute glaucomacan e"perience blood vessel and nerve damage in their eyes due to the high pressure. This

could liely lead to reduced vision or, in some e"treme cases, even blindness.

Outloo& o( Acute Glaucoma Patients

>ith immediate treatment and proper management, the outloo for acute "laucomapatients is uite good. The affected eye can easily recover and even return to normal after


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laser surgery treatment. -ome individuals are even allowed to drive after recovery even if

vision is permanently reduced in the affected eye. @or those who were diagnosed with

acute glaucoma on both eyes, the law reuires you to inform the


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Abstract

A prospective study of 400 consecutive patients of primary angle closure glaucoma wasundertaen to study the clinical profile of the three subtypes: acute, subacute, andchronic. A record of age and se" distributions, symptomatology, the best corrected visual

acuity, gonioscopy, visual fields, methods of control of intraocular pressure, and status of

the second eye was maintained. -tatistical analysis of these parameters and the subtypesof angle closure glaucoma was carried out using the chi#suare test. Angle closure

glaucoma constituted 34.J5 of all primary adult glaucomas seen. 23.85 of these had

acute angle closure glaucoma, (6.25 subacute, and 335 chronic glaucoma. Angle

closure glaucoma occurred ma"imally in the si"th decade and females constituted 46.35of those affected. The difference in symptoms among the subtypes was significant

pL0.006. 9ore than 805 of the chronic eyes had no significant symptoms. Bisual field

defects specific for glaucoma were seen in only 64.65 of chronic glaucoma eyes.=ilaterality was commonest in subacute angle closure glaucoma J4.45 and least in

acute angle closure (4.45. 7d A+ iridotomy alone or with topical medication

controlled the intraocular pressure in 38.(5 of acute angle closure glaucoma, E8.85 ofsubacutes, and (05 of chronic eyes. -tatistically, each parameter reviewed was

significantly different among the subtypes. There are considerable differences as well as

an overlap of clinical features in the subtypes of angle closure glaucoma, which suggest

some anatomical differences or dissimilar pathogenic mechanisms in these eyes.

/e')ords.Angle closure glaucoma, subtypes, symptoms, signs, management

Ho) to cite t!is article.

-ihota D, Agarwal *?. Profile of the subtypes of angle closure glaucoma in a tertiary

hospital in 7orth &ndia. &ndian M 'phthalmol 6JJ813):24#J

Ho) to cite t!is URL.

-ihota D, Agarwal *?. Profile of the subtypes of angle closure glaucoma in a tertiary

hospital in 7orth &ndia. &ndian M 'phthalmol Nserial onlineO 6JJ8 Ncited 2060 Apr

28O13):24#J. Available from:http://www.i!o.in/te"t.asp6JJ8/3)/6/24/63J86

Angle closure glaucoma is a protean disease with a differing incidence, indeterminate

initial stages, and a varied presentation in difference races. There is a significantly highincidence of angle closure glaucoma A?+ in &ndia, which forms almost half of all adult

primary glaucomas seen.N2O,N(OThere is however a paucity of literature available about

the presentations and relative incidence of the subtypes of angle closure glaucoma.
http://www.ijo.in/text.asp?1998/46/1/25/14981http://www.ijo.in/text.asp?1998/46/1/25/14981http://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#ref2http://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#ref2http://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#ref3http://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#ref3http://www.copyright.com/ccc/openurl.do?sid=Medknow&issn=0301-4738&servicename=all&WT.mc_id=Medknowhttp://www.ijo.in/text.asp?1998/46/1/25/14981http://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#ref2http://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#ref3


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A prospective study of 400 consecutive patients of primary angle closure glaucoma,

routinely referred to the +laucoma -ervice of our hospital, was undertaen, to present a

profile of the subtypes of angle closure glaucoma.

9ethods

All patients suspected or diagnosed to have glaucoma in the general out patient

department of our hospital are sent for management to the +laucoma -ervice. The

referrals are based on an individuals symptoms, clinical e"amination for anterior

chamber depth and optic nerve head status, intraocular pressure &'P recordings, singleor a diurnal variation, a visual field, and occasionally a provocative test. -ome cases of

acute angle closure glaucoma were initially e"amined and treated by the ophthalmologist

on emergency duty and were then referred to the +laucoma -ervice together with theirrecords. There was no standard protocol followed for referral and a prior gonioscopy was

only performed in certain cases such as the acute A?+s.

'f the cases referred, 400 consecutive patients diagnosed to have a definitive primary

angle closure glaucoma were prospectively studied with respect to the three subtypes of

angle closure glaucoma: acute, subacute and chronic as defined by ?lemmesen.N3O

6. i -ubacute or intermittent A?+: defined as intermittent observed pressure

elevations accompanied by prodromal symptoms, headache, haloes, and vision,but with normal tension in the inter paro"ysmal period, in patients with an

occludable angle.

2. ii Acute A?+: patients with severe attacs of angle closure accompanied by

pain and the other usual symptoms.

(. iii ?hronic A?+: patients with partially occluded angles and constant &'P

elevation. -ome patients have no symptoms creeping A?+, others complain ofheadache.

>e e"cluded patients in whom no subtypical classification of angle closure glaucomawas possible, for e"ample, suspects, those with aphaia, pseudophaia or previous

filtering surgery.
http://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#ref4http://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#tophttp://www.ijo.in/article.asp?issn=0301-4738;year=1998;volume=46;issue=1;spage=25;epage=29;aulast=Sihota#ref4


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A detailed history and ophthalmic e"amination of the presenting eye was undertaen. At

this point an indentation gonioscopy was performed on each patient by mased observerswho did not now the patients history or decide the patients final diagnosis. An

applanation tonometry, detailed e"amination of the anterior segment, disc and fundus

were recorded. -ubacute A?+ was diagnosed if there was a significant history, a narrowangle recess with some synechiae or increased pigmentation, a record of raised &'P or a

positive dar room prone provocative test. The final diagnosis in all cases was made by

only two glaucoma specialists D-, *?A. &f both eyes had the same subtype of A?+, theeye with more advanced optic nerve head changes was reviewed, to prevent observer

bias. The patients all underwent a A+ iridotomy in both eyes. Cyes with pressures of

more than 26 mm*g were then advised the use of either or both, pilocarpine 25 drops

and timolol maleate 0.45 drops to control the intraocular pressure. A diurnal variation ordiurnal control of &'P was done 2 wees after the iridotomy and the gonioscopy was

repeated at this time, again by mased observers. &f the intraocular pressure was

uncontrolled despite topical medications, the patient underwent a trabeculectomy.

The results of surgery at a minimum follow up of three months, were classified as a

success if the &'P was L20 mm*g without medication, a ualified success if additionaltopical medication was reuired to control the &'P, and a failure if systemic medication

or surgery was needed.

Bisual fields are nown to be altered by alterations in the level of &'P. To allow a

comparison of the perimetry among the eyes studied, the visual field was charted with the

+oldmann perimeter or the *umphrey visual field analyser, after control of the

intraocular pressure medically or post surgery. Two different methods for perimetry hadto be employed because the *umphrey perimeter was out of order for almost a year.

-tatistical analysis was performed using the chi#suare test, overall and between thesubtypes.

Desults

400 patients diagnosed at our +laucoma -ervice to definitively have a primary angle

closure glaucoma were included in this study, out of a total of 6,44( patients seen at the

clinic.


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Analysing the subtypes of A?+ vis#a#vis age, by the chi#suare test, there was a

significant difference in the distribution of subtypes in a comparison between the third

and fourth decade pL0.06 when the acute predominated and between the fourth and fifthdecades pL0.04 when subacute cases were more common NTable # 2O.At the older ages,

the distribution of the subtypes was not significantly different.

The presenting complaints of the patients are detailed in NTable # (O. ?oloured haloes

were seen most often by patients having an acute attac )3.45.

'nly (4.(5 of those having subacute attacs complained of haloes and 68.25 of patients

having chronic angle closure. 'cular pain was most common in the acute and subacute

groups, )2.65 and 34.45 respectively. Associated vomiting occurred in (4.45 of acute

cases, and 6J.J5 of the subacutes and was negligible in chronic angle closure. Anonspecific headache and a diminution of vision were commonly encountered in all

subtypes of glaucoma. The difference in symptoms among the three subtypes of

glaucoma was highly significant pL0.006. ?omparing the occurrence of the symptoms

between the se"es, in acute and subacute types this was statistically non#significant, butin the chronic variety the females were more symptomatic pL0.04.

An absolute eye was most often seen with chronic angle closure glaucoma, (2.(5, and

following an acute attac, 64.(5. 7inety absolute eyes were present in the series overall,

that is 685, of which (4 E5 were bilateral. 'nly 8.J5 of patients who had an acuteA?+ achieved a vision of )/62 or better. The best corrected visual acuity was significant

different between the subtypes pL0.006 NTable # 3O.

+rading the angle of the anterior chamber prior to therapy and without manipulations, bythe -haffer system,N4Othe ma!ority of eyes were found to have a closed 0 angle in acute

cases. A closed angle was also seen in (8.25 of chronic A?+s and only (.25 of

subacutes. A slit lie opening with no angle structures visible was present in ))5 ofsubacute eyes, 38.)5 of chronic A?+ eyes, and 36.65 of those having acute A?+.

+rade & angles were seen in 2(.E5 of subacute eyes and 6(.25 of those having chronic

A?+ NTable # 4O.

There was a highly significant difference between the subtypes pL0.006. 9anipulative

techniues, such as indentation gonioscopy and asing the patient to loo towards the

gonioscope mirror, were performed in all patients to confirm the presence of peripheralanterior synechiae but their e"tent and nature was not recorded in all patients especially

in acute A?+, and have therefore not been discussed. Post A+ iridotomy, gonioscopy

was repeated only to confirm the presence of peripheral anterior synechiae. All patientsunderwent a 7d#A+ iridotomy in both eyes, following which the &'P control was

recorded NTable # )O.&ridotomy alone controlled the &'P in )).E5 of subacute eyes and

62.J5 of the acute. 9edical therapy, that is pilocarpine and/or timolol, was additionallyreuired for (4.45 of the acute eyes, 62.65 of the subacute, and (0.05 of the chronic

cases. E0.05 of eyes in the chronic subgroup reuired a trabeculectomy, as against 46.)5

in acute A?+ and 26.65 among the subacute glaucoma eyes.
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The success rate of the surgery at ( months was ma"imal in subacute eyes and was the

lowest in the chronic group. The difference between the subtypes was significant

pL0.006. (0 patients were lost to follow#up.

Bisual fields were possible in only those patients with a vision of )/)0 and above, that is,

280 eyes and were unreliable in 23. 606 were performed on the *umphrey visual fieldanalyser, and the rest on the +oldmann perimeter. A cluster of Q2 central points

depressed by Q4 d= compared with surrounding points, a single point depressed by Q60

d= or difference of Q4 d= across the nasal meridian at Q2 contiguous points were taen toindicate an early glaucomatous damage. &f the +laucoma *emifield Test was %within

normal limits%, none of the focal changes enumerated above were present but the 9< had

a pL25, the field was considered as euivalent to a generalised constriction as seen on

+oldmann perimetry. The other scotomas were diagnosed by their position and e"tent.Acute and subacute glaucoma eyes had normal fields in )6.65 and E2.45 of eyes.

?hronic angle closure eyes showed a generalied constriction of the field in E).35 and

residual temporal and/or central islands of vision in 6(.25 NTable # EO.There was a

highly significant difference between the chronic versus acute/subacute subtypes. Thedifference between acute and subacute was less significant pL0.06.

C"amination of the contralateral eye was recorded simultaneously. This was used to

determine the freuency of bilaterality among the subtypes of A?+, or the presence of a

%fellow% or unaffected eye. There was no difference when the se"es were analysed in thesubacute and chronic subgroups, but there was a significantly higher incidence of

bilaterality in females having acute angle closure glaucoma pL0.04. =ilaterally affected

eyes were seen in J4.45 of subacute A?+, )3.65 of chronics, and only (4.45 of acute

A?+. Deciprocally, fellow or unaffected eyes were commonest in patients with acuteA?+, )2.65 NTable # 8O. -ome second eyes had other subtypes of A?+ but all had

potentially occludable angles.

e have characterised the three subtypes of angle closure glaucoma seen in a large

referral hospital in north &ndia on the basis of age, se", symptomatology, e"amination,and management. C"clusion of patients having undergone a prior cataract or glaucoma

surgery may have altered the data to a certain e"tent, but was necessary to identify the

subtypes.

&ridotomy alone or with topical medication was sufficient to control the intraocular

pressure in about half the acute eyes, three fourth of the subacute, but only (05 of thechronic sub group. *owever we have been doing it in all cases of angle closure glaucoma

and have had some surprising successes despite the prelaser gonioscopic picture. 'ther

studies have documented impressive results following a surgical iridectomy.NJO,N60O

>e have attempted to separate the three acnowledged subtypes of A?+ into identifiable

entities, but found a considerable overlap of clinical features. &t may be that A?+
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presents as a spectrum of symptoms and signs because of dissimilar pathogenic

mechanisms. @urther wor is reuired to determine if the apparent similarities between

the acute and subacute subtypes as compared to chronic A?+, could be traced todisparate anatomic or pathophysiological factors.

Acnowledgement

The authors than B.R. ?habra for his assistance with statistical analysis.

Deferences

6. ?ongdon 7, >ang @, Tielsch M9. &ssues in the epidemiology and population basedscreening of primary angle clsoure glaucoma. Surv Ophthalmol6JJ21():366#2(.

NP$=9C

Acute Angle Closure Glaucoma

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