ACUTE ANGLE CLOSURE GLAUCOMA

SIGNS AND SYMPTOMS

Patients with angle closure glaucoma manifest symptoms of ocular and facial pain, unilateral blurring of
vision, 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.
PATHOPHYSIOLOGY
Angle closure occurs when the peripheral iris physically opposes the trabecular meshwor or corneal
endothelium and impedes a/ueous outflow. -everal mechanisms are possible. The most common etiology
of angle closure is pupillary bloc, whereby the flow of a/ueous from the posterior to anterior chamber is
inhibited, causing iris bomb. This may be simply due to genetic predisposition and anterior segment
anatomy ,primary pupil bloc., or from posterior synechiae, lenticular enlargement or displacement of the
lens or &'0 ,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 subse/uent closure during physiologic
or pharmacologic dilation. 'ther etiologies of angle closure without pupil bloc include neovascular
membranes inducing PA-, anterior uveal displacement ,such as in choroidal detachment. or, rarely,
posterior segment inflammation or tumors.
MANAGEMENT
The paramount concern in managing an angle closure attac is to lower &'P /uicly. 2our 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 a/ueous into
the trabeculum and temporarily opening the angle. &t may be necessary to use topical glycerin to clear the
cornea 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 carbonic
anhydrase inhibitor ,aceta8olamide 2 " 240mg tablets.. 2ou 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 are
again visible with gonioscopy. 9aintain the patient on the following medications: pilocarpine 25 ;&<,
prednisolone acetate 65 ;&<, timolol ,or e/uivalent. 0.45 =&<, and oral aceta8olamide 400mg =&<.
>hen the inflammation has diminished and the A? is /uiet, refer the patient for a peripheral iridotomy.
This provides a secondary outflow channel for a/ueous, 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 diagnosis
and prompt intervention. @irst distinguish between angle closure glaucoma and other acute open
angle 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 reduced
vision. 'ther possible symptoms are headache, abdominal pain, nausea and
vomiting. Acute glaucoma can be treated successfully, but it needs
immediate treatment to 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 Aacute angle closure glaucomaA or Aacute closed angle
glaucomaA. Another term sometimes used is Aprimary angle closure glaucomaA, 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 Aprimary open angle glaucomaA ,also called Achronic glaucomaA.. -ee separate leaflet on
'Glaucoma (Primary Open Angle'.. 'ther, less common types are Asecondary glaucomaA
and Acongenital glaucomaA. The rest of this leaflet deals only with acute glaucoma.
!at causes acute "laucoma#
To understand the cause, it helps to understand how fluids wor in the eye. The eye needs
to eep its shape so that light rays are focussed accurately onto the retina. -o, most of the
eye is filled with a substance lie !elly called the Avitreous humourA ,humour meaning
fluid.. The front of the eye is filled with a clear fluid called Aa/ueous humourA, which is
more watery.
The a/ueous humour is made continuously by cells called the Aciliary bodyA. The fluid
circulates through the front part of the eye, and then drains away through an area called
the Atrabecular meshworA, which is located near the base of the iris. -o, there is constant
production and drainage of fluid.
!at !a$$ens in acute an"le "laucoma#
&n acute glaucoma, there is a sudden blocage, so that a/ueous 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 more
fluid 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 Anarrow drainage angleA or
Ashallow anterior chamberA 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 for
controlling the si8e 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
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, for
the 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 before
starting 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 AtricyclicA or A--D&A types.
-ome of the medicines used to treat nausea, vomiting or schi8ophrenia ,a type
called Aphenothia8inesA..
&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.
0ying on your front ,for a long period. may also affect fluids in the eye, and can trigger
acute 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 AhaloesA ,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.
-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 ha8y ,AmilyA or AsteamyA..
As e"plained above, symptoms often begin in a situation of dim lighting, sudden
e"citement, with certain medications or after a general anaesthetic.
Are t!ere an' )arnin" s'm$toms#
Acute glaucoma can start Aout of the blueA with no warning. *owever, you may have
warning symptoms, which often are not recognised. These occur when pressure rises in
the 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"es
the 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 involves
measuring the pressure in the eye ,a /uic and easy test. and e"amining the eye using a
special light and magnifier called a Aslit lampA.
!at is t!e treatment (or acute "laucoma#
Initial treatment
Treatment is *er' ur"ent+ 2ou should be seen by an ophthalmologist ,eye specialist.
immediately. &f it will tae time getting to the ophthalmologist, treatment can be started
meanwhile.
The first treatment is medication to lower the pressure of fluid in the eye. There are
various types of medicine that reduce eye pressure. <ifferent combinations can be used,
depending on your medical history. The usual treatment is:
An intravenous in!ection of aceta8olamide.
Cye drops containing beta#blocer medication ,to reduce fluid in the eye. and
steroid ,to reduce inflammation..
'ther treatments which may be used initially are:
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 brin8olamide,
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 or
surgery 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.
0aser treatment is called Aperipheral iridotomyA. 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 removed
can be replaced by an artificial lens, or by using glasses.
$sually, laser or surgical treatment will be advised for the other eye at some stage. This is
to prevent acute glaucoma happening in the other eye. Also, eye drops may sometimes be
needed as long#term treatment, to help eep the eye pressure under control.
!at are t!e com$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 to
the front of the eye ,cornea.. This blocs the drainage area, so a Adrainage operationA is
needed. This operation creates a channel between the inside of the eye and the outside
,white 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.
&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 you
are a driver and have glaucoma in both eyes, the law says that you must inform the <river
and Behicle 0icensing Authority ,<B0A..
Ho) can acute "laucoma %e $re*ented#
-ome people have an increased ris of getting acute glaucoma, due to a narrowing of the
area where fluid normally drains from the eye. This is called a Ashallow anterior chamberA
or Anarrow drainage angleA. -ometimes a narrow drainage angle is noticed at a routine eye
e"amination. 2ou may be told about this and advised to be careful with certain
medications and eye drops ,as above..
&f you are at very high ris of acute glaucoma, you may be advised to have treatment such
as laser iridotomy ,above. to prevent it.
=e aware of the symptoms of acute glaucoma. Anyone who has a red eye with pain or
vomiting, or a red eye with reduced vision, should get medical advice immediately. &f
you tae a new medication or have eye drops to dilate the pupil, and then have symptoms
of acute glaucoma, get medical advice straightaway1 tell the doctor about the medication
and symptoms. This maes it easier for the problem to be recognised early.
Acute Glaucoma
A condition of the eyes wherein internal pressure suddenly rises, acute glaucoma is
characteri8ed by reduced vision, pain and redness. The said eye disorder also e"hibit
symptoms such as nausea, headache and abdominal pain. &f left untreated, it could result
to further eye damage.
Also called acute closed angle glaucoma, this eye disorder has two types: primary,
secondary and congenital glaucoma. Primary or chronic glaucoma is the most common
type.
Causes o( Acute Glaucoma
&n order to fully understand the aetiology of this eye condition, it is recommended that
you first understand the function of the eye fluid. &t is important for the eye to maintain
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 Fa/ueous humourG in the front portion of the eye
The a/ueous 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 eyeAs 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 a
football 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 involved
in 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
Phenothia8ines , 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

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 ha8y or mily

Again, these symptoms usually appear after the acute glaucoma is triggered due to certain
lighting 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 to
immediately recogni8e 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 you
contact 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 condition
after a detailed e"amination using a slit lamp as well as a specific test that will measure
eye pressure.
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
Aceta8olamide in!ection

-econdary treatment will usually involve:
Painillers or anti#sicness drugs
9annitol H to reduce fluid build up
Cye drops ,brimonidine, brin8olamide or pilocarpine
0ying 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:
0aser 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 surgery
involved1 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 the
other 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 glaucoma
can 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 "laucoma
patients is /uite good. The affected eye can easily recover and even return to normal after
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 re/uires you to inform the <B0A ,<river and
Behicle 0icensing Authority..
Pre*ention o( Acute Glaucoma
&ndividuals who e"perience narrowing in the area wherein eye fluid usually drains are
more liely to suffer from acute glaucoma. -uch narrowing, referred to as narrow
drainage angle or shallow anterior chamber can be detected during standard eye
e"amination. 2our eye specialist will immediately inform you of the ris involved and
might advice you to be careful with eye drops and other medications.
&f you are considered to be at high ris for acute glaucoma, a laser surgery treatment may
be recommended to prevent the condition from worsening.
?onsidering the seriousness of this particular eye condition, all individuals should pay
attention to symptoms such as vomiting, red eye, reduced vision and eye pain.
C"periencing any of these symptoms can signal acute glaucoma and you should
immediately get checed. 9ae sure you tae note of the instance or situation when you
e"perienced the symptoms such as dim lightning or after taing certain medicationsI
&nform your eye doctor about this in order to identify the possible triggers and allow for
easier diagnosis.
ORIGINAL ARTICLE
Year : 6JJ8 K -olume : 3) K Issue : 6 K Pa"e : 24#2J

Profile of the subtypes of angle closure glaucoma in a tertiary hospital in 7orth &ndia
D -ihota, *? Agarwal
<r. Da!endra Prasad ?entre for 'phthalmic -ciences, All &nstitute of 9edical -ciences,
7ew <elhi, &ndia
Corres$ondence Address:
D -ihota
<r. Da!endra Prasad ?entre for 'phthalmic -ciences, All &nstitute of 9edical -ciences,
7ew <elhi
&ndia
Source o( Su$$ort. 7one, Con(lict o( Interest. 7one
PMID. JE0E833

Abstract
A prospective study of 400 consecutive patients of primary angle closure glaucoma was
undertaen to study the clinical profile of the three subtypes: acute, subacute, and
chronic. 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 subtypes
of angle closure glaucoma was carried out using the chi#s/uare 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 46.35
of 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 2A+ iridotomy alone or with topical medication
controlled the intraocular pressure in 38.(5 of acute angle closure glaucoma, E8.85 of
subacutes, 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.aspP6JJ8/3)/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 high
incidence of angle closure glaucoma ,A?+. in &ndia, which forms almost half of all adult
primary glaucomas seen.N2O,N(O There is however a paucity of literature available about
the presentations and relative incidence of the subtypes of angle closure glaucoma.
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 individualAs symptoms, clinical e"amination for anterior
chamber depth and optic nerve head status, intraocular pressure ,&'P. recordings, single
or 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 their
records. 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 of
headache.
>e e"cluded patients in whom no subtypical classification of angle closure glaucoma
was possible, for e"ample, suspects, those with aphaia, pseudophaia or previous
filtering surgery.
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 observers
who did not now the patientAs history or decide the patientAs 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 narrow
angle 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?+, the
eye with more advanced optic nerve head changes was reviewed, to prevent observer
bias. The patients all underwent a 2A+ 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 or
diurnal 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 additional
topical medication was re/uired 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 had
to be employed because the *umphrey perimeter was out of order for almost a year.
-tatistical analysis was performed using the chi#s/uare test, overall and between the
subtypes.
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. <uring the same period, there were 488 primary open angle glaucomas ,'A+., a
ratio of A?+:'A+ 3):43.
&n the A?+ group as a whole there were 23( ,38.)5. males and 24E ,46.35. females.
@emales predominated in the acute subgroup, JJ of 623 ,EJ.85., and in the subacute
group 603 of 64) ,)).E5.. 9ales were more commonly involved in the chronic subtype,
6)) of 220 ,E4.35.. There was no significant difference in the occurence of A?+
between males and females in the various age groups NTable # 6O.
A?+ occurred between (0#80 years with the ma"imally affected decade being the si"th.
Analysing the subtypes of A?+ vis#a#vis age, by the chi#s/uare 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 fifth
decades ,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. A
nonspecific 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, but
in 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 acute
A?+ 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, by
the -haffer system,N4O the 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 of
subacute 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
techni/ues, such as indentation gonioscopy and asing the patient to loo towards the
gonioscope mirror, were performed in all patients to confirm the presence of peripheral
anterior synechiae but their e"tent and nature was not recorded in all patients especially
in acute A?+, and have therefore not been discussed. Post 2A+ iridotomy, gonioscopy
was repeated only to confirm the presence of peripheral anterior synechiae. All patients
underwent a 7d#2A+ 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 additionally
re/uired 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 re/uired a trabeculectomy, as against 46.)5
in acute A?+ and 26.65 among the subacute glaucoma eyes.
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 field
analyser, 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 to
indicate 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 e/uivalent 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 generali8ed 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. The
difference between acute and subacute was less significant ,pL0.06..
C"amination of the contralateral eye was recorded simultaneously. This was used to
determine the fre/uency 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 the
subacute 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 acute
A?+, )2.65 NTable # 8O. -ome second eyes had other subtypes of A?+ but all had
potentially occludable angles.
<iscussion
>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 the
chronic 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?+
presents as a spectrum of symptoms and signs because of dissimilar pathogenic
mechanisms. @urther wor is re/uired to determine if the apparent similarities between
the acute and subacute subtypes as compared to chronic A?+, could be traced to
disparate anatomic or pathophysiological factors.
Acnowledgement
The authors than B.R. ?habra for his assistance with statistical analysis.

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