GLAUCOMA

Aqueous Humour Dynamics

The normal eye maintains a near globular shape with various optical components in perfect
alignment. The normal intraocular pressure (IOP) is very important in maintaining the optical
alignment and eye shape. The IOP is kept at a steady level by continuous aqueous secretion and
drainage.

Aqueous Secretion And Drainage

The aqueous humour is secreted by the ciliary body epithelium into the posterior chamber (PC)
from where it enters the anterior chamber (AC) through the pupil. It is estimated that
approximately 3 microliters of aqueous humour is secreted and drained per minute.

The aqueous humour exits from the anterior chamber through the trabecular meshwork into the
canal of Schlemm from where the aqueous humour drains into the vortex veins via scleral and
episcleral venous channels. This is called as conventional patheway and accounts up to 90% of
aqueous humour outflow. The episcleral venous pressure (8-11 mmHg) is normally less than the
IOP. Any rise in episcleral venous pressure can compromise the conventional aqueous outflow.

The remaining 5-20% of the aqueous humour drains through the ciliary body into the
suprachoroidal space. This is called uveoscleral outflow, also known as unconventional pathway.
This outflow is possible because of the pressure gradient-the pressure in the suprachoroidal space
is 2-4 mmHg lower than in the anterior chamber. It becomes the major drainage system in
congenital malformation of conventional pathway, e.g. congenital glaucoma. Prostaglandins
decrease the IOP by increasing the uveoscleral outflow.

The normal IOP is less than 20 mmHg and shows a diurnal variation that normally does not
exceed 5 mmHg.

Factors controlling IOP

 Continuous aqueous humour secretion and drainage

  Trabecular resistance to outflow
 Episcleral venous pressure
 Circadian rhythm
 Neural and hormonal influences

DEFINITION

The glaucomas are a syndrome complex wherein the IOP does not commensurate with normal
functioning of the optic nerve. The disease is characterized by optic nerve damage known as ”
glaucomatous optic neuropathy” which may be subsequent to high IOP or innate weakness of
optic nerve to withstand normal IOP.

It is a slowly progressive, insidious optic neuropathy that usually is associated with chronic
elevation of intraocular pressure.

The glaucoma tend to have a familial component; a glaucoma patient’s relatives are at a greater
risk of developing glaucoma. This may call for family screening for glaucoma. The condition is
also more common in diabetics and myopes.

Glaucoma is a major cause of irreversible blindness throughout the world. According to WHO
survey (1992), there are 22.5 million patient; worldwide with glaucoma blindness. In India, it
constitutes 1.7% of total economic blindness.

AETIOLOGY OF GLAUCOMA

Glaucoma can occur if ciliary processes secrete excess aqueous humour. This is known as
hypersecretory glaucoma and is rarely encountered. It is seen in epidemic dropsy, which is the
consequence of consuming the poisonous argemone mexicana seeds.

Glaucoma can also occur if venous drainage channels in the orbit or intracranial channels are
blocked. This is less common but is seen in orbital cellulitis, cavernous sinus thrombosis or even
in carotid cavernous fistula.
By far the most common raised IOP are:

(a) Obstruction to the flow of aqueous humour from the PC into AC at the pupil results in
pupillary block glaucoma.

(b) Alternatively blockage of the angle can also ensue if the peripheral iris bows forwards or
adheres to the peripheral corneoscleral junction. These adhesions are called peripheral anterior
synechiae (PAS) and are responsible for primary angle closure glaucoma (PACG).

( c ) Commoner than blockage at the pupil is blockage at the angle of the AC. This can be due to
sclerosis of the trabecular meshwork, which hinders aqueous outflow to the Canal of Schlemm.
This is the Operative cause in chronic open angle glaucoma (COAG) and steroid Induced
glaucoma.

Classification of glaucoma

Primary

 Congenital
 Open angle
 Angle closure

Secondary

 Steroid induced
 Neovascular
 Post-traumatic
 Lens induced, etc.

PRIMARY GLAUCOMA

Primary glaucoma occur in the absence of any ocular or systemic disorder. The early events that
produce obstruction of aqueous humour outflow in these glaucomas are confined to anterior
chamber angle or conventional outflow pathway. These are typically bilateral and probably have
a genetic predisposition.

About 2% of the general population above the age of 40 years has primary glaucoma; hence the
importance of yearly check ups after that age.

The primary glaucomas are of three basic types;

 Primary angle closure glaucoma (PACG)

 Chronic open angle glaucoma (COAG), also known as primary open angle glaucoma
(POAG)
 Congenital glaucoma.

 Primary angle closure glaucoma

The eye affected with PACG is typically small with a shallow AC i.e. hypermetropic eyes.

As the depth of AC decreases with age (because of increasing thickness of lens), the prevalence
of PACG is more in older age groups (53-58 years).

Unlike primary open angle, PACG shows a female preponderance, which is attributed to high
prevalence of narrow AC angle in women.

It does not have a clear-cut genetic predisposition and thus family history is not very useful.

Clinical features: Five clinical stages are discernable in PACG, but it must be remembered that
initial presentation may be an acute attack of angle closure glaucoma with no antecedent history
of preceding stages. These stages are given below:

(a) Prodromal stage

(b) Chronic instability stage

(c) Acute ACG stage

(d) Chronic ACG stage

(e) Absolute glaucoma stage.

Prodromal stage: In the prodromal stage, the patient sees coloured haloes due to high IOP with
some obscuration of vision. These events occur occasionally and subside spontaneously. The
coloured haloes are seen because the raised tension causes epithelial and some stromal oedema,
which lead to light dispersion. The colours are distributed as in the light spectrum with red
outside and blue inside. These attacks are precipitated by events that lead to pupillary dilatation,
such as dim light or anxiety. The IOP may be 40 to 60 mmHg but the eye remains white. The
pupillary dilatation leads to more intimate contact of the iris against the lens causing a functional
pupillary block. The build up of aqueous humour in the posterior chamber causes forward
bowing of the iris (iris bombe) occluding the anterior chamber angle. This angle closure,
however is reversible.

Chronic instability stage: In this stage, the intermittency of the prodromal stage is replaced by
the regularity of attacks.

Acute ACG stage: This is the most dramatic Of all the stages. Typically the patient presents in
emergency with his hand covering the affected eye. The pain is very severe; the lid and
conjunctiva may be oedematous. The cornea looks steamy because of the oedema; circumciliary
congestion is present, anterior chamber is shallow, the pupil mid-dilated and often vertically
oval; the eye feels stony hard and fundus examination may not be possible. If the acute attack is
not relieved in time, permanent loss of vision may take place. The principal differential diagnosis
is that of iritis. In both, patient may present with sudden and painful visual loss and even tension
may be raised in iritis but in iritis or iridocyclitis keratic precipitates and anterior chamber flare
are present, the pupil is small and often irregular. Shallowness of the anterior chamber of fellow
eye and antecedent history of coloured haloes is of great help in reaching at the correct diagnosis;
this is vital because the management of these two conditions is diametrically different.

Chronic ACG stage: The recurrent attacks of angle closure eventually lead to peripheral
anterior synechiae that may permanently block the exit pathways. This stage of PACG is known
as chronic ACG. Unlike the previous stages, the angle closure is organic and not reversible. The
degree of angle closure is studied by examining the angle with a specialised instrument known as
“gonioscope” and this procedure is termed as “gonioscopy”. Chronic ACG presents as elevation
of IOP with shallow anterior chamber and synechial closure of the angle. The Optic disc changes
and field defects are akin to COAG.

Absolute glaucoma stage: It is the end result of untreated attacks of ACG or chronic ACG. It
results in a stony hard, painful, blind eye.

Treatment of PACG

It is vital that PACG be diagnosed early as definitive treatment has high rates of success. Perhaps
no other surgical procedure has as high a rate of success as laser therapy in ACG. In PACG
(even after an acute attack has occurred but before extensive peripheral anterior synechiae, that
is, before involvement of more than three quadrants of anterior chamber angle), the simple
expedient of creating a hole in the iris cures the condition forever; the hole in the iris creates an
alternative channel for the aqueous inflow into anterior chamber. This makes pupillary blockage
totally inconsequential. Before the advent of Nd: YAG laser, this was accomplished surgically
where a total or complete (now obsolete) or a peripheral iridectomy was performed .This type of
surgery was initiated by Von Graefe (a German ophthalmologist) in the middle of the 19th
century.

During his lifetime Graefe was severely humiliated by his peers for advocating such a
supposedly silly treatment for a condition so dangerous and unpredictable as glaucoma. Presently
peripheral iridotomy is performed easily on an outpatient basis using Nd:YAG laser (In light
coloured irides it can alternatively be performed using argon laser).

Treatment of acute PACG

Acute PACG is a medical emergency and should be managed aggressively. The treatment is
aimed at reducing IOP rapidly and opening the angle. Careful history of symptoms related to
intermittent angle closure attacks in the fellow eye (the unaffected eye) and type of activity
preceding the attack should be taken.
Examination of both the affected and the fellow eye (the unaffected eye) with special attention to
central and peripheral anterior chamber depth and shape of the iris is noted. Indentation of the
central part of the cornea with Zeiss gonioscopic lens, cotton tip and muscle hook may open the
angle temporarily thereby decreasing the IOP. Similarly, shining the bright light of an
ophthalmoscope may cause enough miosis to abort an acute attack.

Systemic acetazolamide is the first line of treatment.

In case the patient has nausea or vomiting, IV administration of mannitol is the alternative.
Simultaneously, B-blockers are started to further lower the IOP.

Pilocarpine is not useful in acute stages because of ischaemia and paralysis of iris Sphincter.
Topical pilocarpine can be started once IOP is reduced, i.e. 30-40 minutes after the systemic
treatment.

Surgical management

A YAG laser iridotomy should be done in the affected eye as soon as the pressure normalises.
The fellow eye also has a high risk of an acute attack and thus, must undergo a prophylactic
peripheral iridotomy (P1). In case the PI is delayed, fellow eye should also be put on topical
pilocarpine to reduce the risk of acute attack.

A gonioscopic examination of the angle should be undertaken to assess the degree of peripheral
anterior synechiae (PAS). The IOP may not get controlled if there is more than 180° of PAS.
Such patients Will eventually need a filtration surgery.

Nd:YAG laser iridotomy is a safe procedure and has completely replaced surgical iridectomy.
The latter however may be indicated in cases with very shallow anterior chamber, corneal
oedema and in case of an uncooperative patient.
 Management of acute PACG

Acute congestive PACG

IV acetazolamide / oral acetazolamide / IV mannitol

Examine after 30 minutes

IOP not lowered IOP lowered

Hyperosmotic agents start pilocarpine 2%

IOP not controlled after 1 hr IOP controlled and angle opens

Argon laser iridoplasty continue medical treatment

Steroid drops laser in both eyes do PI using Nd: YAG

Treatment of chronic ACG

The treatment depends on the degree of synechial closure of angle of anterior chamber. In
patients with less than 180° of angle closure, a laser peripheral iridotomy may be adequate to
control IOP.

Topical antiglaucoma medication is started in cases where adequate control of IOP is not
achieved with P1 alone.
The above treatment however may not be effective in patients with more than 180° of angle
closure and filtration surgery may be required to prevent irreversible optic nerve damage.

Treatment of absolute glaucoma:

The painful blind eye is managed by lowering IOP by permanently destroying the ciliary
processes with external cryo application (cyclocryo) or laser (cyclophotocoagulation). A retro
bulbar injection of alcohol can also be given to alleviate pain. An intraocular tumour should
always be ruled as the aetiology of painful blind eye,

 Chronic open angle glaucoma

As the terminology indicates, the angle in COAG remains open and yet this is the site of
obstruction for aqueous humour .

Sclerosis or similar changes in the trabecular meshwork or its outflow channels or the defective
outflow mechanism cause the elevation of IOP.

The prevalence of COAG increases with age and most cases are seen after the age of 65 years.

Unlike PACG, it does not show any sex predisposition.

It has a strong genetic basis, most likely polygenic or multifactorial.

It is more common in myopes and diabetics.

Clinical features

The course of chronic open angle glaucoma is entirely different from angle closure glaucoma.
The eye remains quiet (no congestion); symptoms, if any, are vague. The visual loss of COAG is
irreversible; it is so gradual that the patient hardly notices it till he is virtually blind.

The triad of the main features of COAG is:

(i) Raised intraocular pressure

(ii) Optic disc cupping
(iii) Visual field defects.
Raised IOP

It is the most important risk factor for development of COAG. A recording of two IOP readings
of more than 21 mmHg on two separate occasions is considered suspicious for COAG. Initially
the IOP may rise only at certain periods of the day While It may be normal at other times. If the
patient is suspected to have glaucoma, diurnal tension (three hourly IOP records for 24 hours)
recording must be undertaken. A diurnal IOP variability of 8 mmHg or more is abnormal even if
all the pressure recordings are within normal limits.

It should be understood that while the main feature of glaucoma is the raised IOP, much of the
visual damage is caused by optic nerve head ischaemia. The ischaemic process is accelerated by
raised tension but in susceptible eyes even normal tension may cause glaucoma like damage. The
latter condition is known as normal tension glaucoma.

Optic disc cupping

The normal cup disc ratio (CDR) is 0.3 or less. The retinal vessels arise from the centre of the
cup. The cup size varies in different individuals and some normal cups may exceed CD ratio of
0.3. This is known as “physiological cupping”. A physiologically large cup, however, is
symmetrical between the two eyes and has an intact neuroretinal rim, i.e. margins of the cup and
the disc run parallel to each other and do not change in size over time. Glaucomatous cupping on
the other hand may be asymmetrical between the two eyes and is progressive. An asymmetry of
more than 0.2 between the two eyes is considered abnormal.

In glaucomatous cupping the vessels shift with cupping, often nasally. The cupping in glaucoma
may first appear as a vertically oval cup, Which later becomes deep. This is well appreciated on
slit lamp examination With a contact/non-contact lens (This examination is known as ”indirect
biomicroscopy”). The progressive increase in size and depth of optic nerve cup is a definite sign
of progressive glaucomatous damage.

With increase in cupping, vessels seem to dip into the cup margin. Thus there appears an
apparent discontinuity of the vessels; this sign is called the bayonetting of the vessels.
The cupping essentially occurs because the raised tension stretches the lamina cribrosa through
which all the optic nerve fibres pass. The mechanical stress causes the death of nerve fibres and
thus the field defects. This is known as mechanical theory of glaucomatous cupping.

Another view is the ischaemia theory of glaucomatous cupping implicating ischaemia of the
nerve fibres to be vital in cupping. Ischaemia leads to the atrophy of the glial cells, which
support the optic nerve fibres resulting in cavernous Optic atrophy, Which is characteristic of
glaucoma

Visual field defects

The visual field may be described as an island of vision surrounded by an area of darkness. The
outer aspect of the visual field extends approximately 50° superiorly, 60° nasally, 70° inferiorly
and 90° temporally The optic nerve lacks any retinal tissue and hence is charted as a blind spot in
the visual field examination. It is located in the temporal field between 10° and 20°.

The ischaemia not only destroys the supporting glial tissue but also affects the Optic nerve fibres
at the optic disc. This leads to various field defects, detection of which is vital in arriving at the
diagnosis of COAG. The examination to chart the visual fields is called ”perimetry” and the
instrument used for the same is called a ”perimeter” .Highly sensitive automated perimeters are
available nowadays that can detect the visual field defects very early.

Because ischaemia affects the optic nerve fibres at the Optic disc head, the initial field defects
appear in the isopter of the optic nerve head. A scotoma is an area of visual loss surrounded by
vision. later these field defects may join the blind spot and form a sickle-shaped scotoma-the
Seidel’s sign. As the disease advances, this scotoma may reach the horizontal raphe that bisects
the macula horizontally. This field defect, which may encircle the macula above or below or
both, is a typical field defect of glaucoma. It is a nerve fibre bundle defect, also known by the
name of arcuate scotoma, Scimitar smtoma or Bjerrum scotoma. In addition to the scotomas, the
peripheral field constriction occurs, first in the upper nasal field. This forms a sharp border
known as Roenne’s step at the level of the horizontal raphe and represents a difference in
sensitivity between the superior and inferior halves along the horizontal midline in nasal field.

In an untreated patient the Whole field is lost except for the central field and a small island of
temporal field. The important thing to note here is that the patient’s vision may be still normal
and he may be totally oblivious of the impending doom. Finally these remaining areas of vision
are also lost.

Diagnosis

The triad of findings, i.e. IOP of >21 mmHg on at least two occasions, optic disc cupping (>O.3
CDR or asymmetry of >02 between the two eyes) along With visual field defect in an eye with
an open anterior chamber angle confirm the diagnosis of COAG. A patient with raised IOP
without optic disc cupping and visual field defects is said to have Ocular hypertension

The patients with high IOP and a large optic disc cup in the absence of field defects are termed
as ”glaucoma suspects” and should be kept on longterm follow-up.

Sometimes optic nerve damage and visual field defects are encountered in patients with normal
IOP. These patients are said to have ”normal tension glaucoma” and should be thoroughly
investigated for any cardiovascular disease like anaemia, cardiac failure, transient ischaemic
attacks, cardiac arrhythmias, and other conditions that can compromise optic nerve perfusion.

Treatment of COAG

The primary management of COAG is medical. Only if the maximal medical therapy fails is the
surgery considered.

Once the diagnosis of COAG is confirmed, the patient is put on topical therapy. It may be
recalled that raised IOP is the most important risk factor in the development of glaucomatous
damage, but it is only a risk factor and not a disease. The goal of therapy is to prevent functional
visual loss for the remainder of the patient’s lifetime. This goal should preferably be achieved
with minimal number and strength 0f medications,
Ideally, initial treatment should be started in one eye only so that the fellow eye acts as a control.

The drug of first choice is B-blockers unless there is a specific systemic contraindication.

The patient is carefully followed to assess the drug response and side effects. In addition, the
visual fields are periodically monitored. The long standing stability of visual fields and optic
nerve head appearance determines the safe level of IOP.

Alternatively, a parasympathomimetic drug like pilocarpine can be started in place of a B-

blocker. Pilocarpine may be poorly tolerated because of brow ache and headache.

A combination therapy is recommended if single drug fails to control the IOP or stabilise the
visual fields.

Newer drugs like brimonidine, an alpha 2 agonist, not only lower the IOP but also provide
neuroprotection against further optic nerve damage. It is indicated as monotherapy or in
combination therapy in advanced glaucomas.

Prostaglandin analogues like latanoprost and bimatoprost are new drugs that can be prescribed in
a convenient once daily regimen. They are well tolerated and may well become the first choice
drug in future. However, they are costly and may produce irreversible pigmentation of iris.

When topical treatment fails, a systemic carbonic anhydrase inhibitor such as acetazolamide is
instituted. However, prolonged treatment With acetazolamide is clearly not feasible because of
numerous systemic side effects. This is the maximal medical therapy and if this fails or patient is
intolerant to such therapy, surgery is indicated though argon laser trabeculoplasty (ALT) remains
a short-term option.

It is commonly believed that vision loss in glaucoma is irreversible; it is so but the important
thing is that if diagnosed in time, the visual loss is largely preventable for glaucomas are
eminently treatable. The patient must understand that success of the therapy is determined by his
absolute compliance with the doctor’s instructions. The patient can be bluntly told that he can
miss his meals but not his eye drops. It is important for a COAG patient to realise that the
treatment once initiated has to be life long and careful follow-up remains a must.
Surgical treatment

It is indicated under the following conditions: If the maximal medical treatment fails to control
IOP, progressive deterioration of visual field defects, poor drug compliance and nonavailability
of drugs the surgical procedure of choice is trabeculectomy. This is a filtering surgery but
guarded by a superficial scleral flap. Over the years innumerable surgical manoeuvres have been
used where the basic idea was to obviate the trabecular meshwork and create an alternative
drainage pathway. Presently all such operations are obsolete because of their unpredictability and
higher risk of postoperative infection. The only filtering surgery procedure currently in use is
trabeculectomy.

Lastly, it needs to be remembered that all treatment modalities used in glaucoma only lower the
IOP but they do not ensure that Optic nerve damage will not continue. These facts mandate very
careful follow-up of all operated patients of COAG and it needs to be kept in mind that even
after surgery for COAG, the medical therapy may still be needed and be of help.

SECONDARY GLAUCOMAS

In secondary glaucomas ocular, orbital or even cranial pathology which results in elevated IOP is
obvious.

The pathological condition may be unilateral or bilateral and some of them have a genetic basis
while others are acquired. The common causes of secondary glaucoma include drugs such as
steroids, uveitis, trauma, lens induced, etc.

Treatment

It should be remembered that whatever the ocular cause of secondary glaucoma, the blockage to
aqueous flow takes place at the pupil or at the anterior chamber angle. IOP lowering therapy
though useful, the treatment should be directed towards the cause.

The aetiology and treatment of a few secondary glaucomas is described below:

Steroid induced glaucoma

Topical as well as systemic steroids can cause glaucoma but the typical clinical presentation is
seen with topical steroid therapy (The systemic steroids cause cataract more often than
glaucoma).

The rise in IOP results from obstruction to outflow at the angle subsequent to sclerosis of
trabecular meshwork. Thus any patient receiving long-term steroids should have his eyes
examined periodically. Whenever the patient is prescribed topical steroids, he must be
forewarned not to use them for longer duration than prescribed. It may so happen that a patient of
allergic conjunctivitis may find relief with topical steroids and next time when he gets an attack
of allergic conjunctivitis, he resorts to the use of same steroid drops on his own without a
medical consultation such cases are all too common. Hence, the physician must form a habit of
advising the patient never to use steroid drops longer than prescribed.

Treatment of steroid induced glaucoma is similar to chronic open angle glaucoma. The rise of
IOP is reversible and the discontinuation of the offending steroid is all that is required.

Lens induced glaucoma:

It may be caused by lens swelling leading to pupillary block (phacomorphic glaucoma) or by the
leaking proteins that block the trabecular meshwork (phacolytic glaucoma). The former is seen
with intumescent senile cataract while the latter is the complication of hypermature cataract. The
definitive treatment of both these conditions is cataract surgery.

Neovascular glaucoma: It occurs subsequent to rubeosis iridis (formation of new vessels at the
iris). This occurs after central retinal vein occlusion and in proliferative diabetic retinopathy. The
new vessels form strong peripheral anterior synechiae, which lead to one of the most severe and
recalcitrant glaucomas. The definitive treatment consists of ablating the retina with argon or
diode laser.

Glaucoma due to uveitis: intraocular pressure may raise in both acute and chronic uveitis.
Medical management is with corticosteroids.
Traumatic glaucoma: a blunt injury to the eye can cause a tear in the anterior face of the ciliary
body and recession of the angle of the anterior chamber. medical management is by miotic,
epinephrine, carbonic anhydrase inhibitors. In severe cases infiltration surgery may be done.

Glaucoma associated with intraocular tumours: melanoma and retinoblastoma may cause
glaucoma.

Glaucoma associated with retinal surgery: the injection of air and exxpansile gases and silicon oil
may result in angle closure glaucoma

Glaucoma associated with intraocular hemmorrhage: Traumatic hyphema is a common cause.

Larger the hyphema higher is the rise in IOP results in obstruction of trabecular meshwork

Congenital glaucomas: Congenital glaucomas result from a developmental anomaly of the

anterior chamber angle that produces aqueous outflow obstruction. This is due to the failure of
embryonal mesenchymal cells to become rearranged into normal trabecular meshwork. A glassy
membrane covering the anterior chamber angle may be evident on gonioscopy. Congenital
glaucoma differs from adult glaucoma as the eyes in children are stretchable unlike adults. Hence
with raised IOP, the eye becomes larger.

Clinical features: Congenital glaucoma is typically bilateral and presents at birth or shortly
thereafter. The child presents With tearing, photophobia and blepharospasm. Photophobia occurs
due to corneal oedema and is seen as child’s aversion to bright light. The elevation of IOP causes
distension of the globe known as buphthalmos. Stretching of the corneoscleral junction results in
enlargement of the cornea. Progressive enlargement of cornea causes horizontal ruptures of
Descemet’s membrane Which are called Haab’s striae. In untreated cases, the cornea becomes
opacified.

Treatment

The only definitive treatment of congenital glaucoma is surgery.

Medical therapy is used as a temporary measure to control IOP in case of pending surgical
intervention or in cases of repeated surgical failure. The surgery consists of incising the glossy
membrane stretching across the anterior chamber angle (goniotomy) If this fails standard
filtering surgery (trabeculectomy) may be indicated.
GLAUCOMA PROVOCATIVE TESTS

Water Drinking Test (WDT)

It is done to confirm COAG in individuals in whom the diagnosis is doubted on history and/ or
clinical examination.

Patient is kept fasting for 8 hours, preferably overnight.

A baseline IOP is recorded just before WDT.

Patient drinks 1 litre of water (15-20 ml /kg body Weight) in about 4-5 minutes.

IOP is measured every 15 minutes for 1 hour.

An IOP rise of less than 6 mmHg over the baseline is normal, 6-8 mmHg rise in IOP is
considered suspicious while 8 mmHg or more of IOP rise indicates COAG.

ANTIGLAUCOMA DRUGS

Antiglaucoma drugs form the mainstay of therapy in glaucoma and can be categorised into the
following

(a) beta -adrenergic antagonists ( timolol)

(b) Cholinergics (pilocarpine)

(c) Adrenergic agonists (epinephrine)

(d) Prostaglandin analogues (lanoprost, bimatoprost)

(e) Carbonic anhydrase inhibitors ( acetazolamide)

(f) Hyperosmotic agents (oral – glycerol, IV- mannitol)

(g) Ca++ channel blockers ( nifedipine, verapamil)

 Beta-adrenergic antagonists

B-blockers reduce IOP by reducing the aqueous humour production. They act on ciliary
processes, either on non-pigmented epithelium to decrease secretion or on local capillary
perfusion to reduce ultrafiltration.

Maximum IOP lowering effect occurs 2 hours after administration and lasts for about 24 hours.
B-blockers are useful in all types of glaucoma and are the first line drug in POAG.

Side effects

Local ocular toxicity is not commonly encountered, though toxic and allergic reactions have
been reported. The other side effects seen are blurred Vision, red eye, subepithelial punctate
keratopathy and corneal anaesthesia. Chronic treatment with timolol can damage the corneal
ocular surface, especially mucous layer of tear film. The adverse effects are due to systemic
absorption of the drug and are more often encountered than local ocular reactions.

Cholinergic Agonists

The principal mode of intraocular pressure reduction is by increasing the aqueous outflow
through the trabecular meshwork. This is achieved by contraction of the longitudinal muscle of
the ciliary body that pulls the scleral spur, thereby opening up the trabecular meshwork. The
miotic effect of cholinergic agonists opens up the angle by pulling the peripheral iris away from
the trabeculum. This makes them the drug of choice in PACG.

Side effects

 Ocular

Miosis

Impairment of night vision

Decrease in vision in patients with axial lens opacities

Generalized constriction of fields

Spasm of accommodation
Induced myopia

Brow ache

Redness/watering

Retinal detachment

 Systemic

Abdominal pain/diarrhoea

Breathlessness '

Marked salivation and perspiration

 Sympathomimetics

Sympathomimetics are alpha and beta adrenergic agonists. They increase aqueous outflow
through their beta -agonist action and decrease aqueous inflow through their Beta agonist
activity.

Side effects

 Local side effects

Stinging

Rebound conjunctival injection

Allergic blepharoconjunctivitis

Nasolacrimal duct obstruction

Pigmented conjunctival deposits

Mydriasis

Cystoid macular oedema

 Systemic

Palpitation/myocardial infarction
Nervousness

Faintness

Tremors

Skin blanching

Dipivefrin is a prodrug, which gets converted into adrenalin after absorption into the eye. It
causes fewer local and systemic side-effects and thus can be prescribed in patients intolerant to
adrenalin. Bromonidine is a selective alpha 2 agonist that lowers IOP by decreasing the aqueous
flow and increasing the uveoscleral outflow. In addition, it has a neuro protective effect and is a
useful adjunctive drug in advanced glaucoma.

Prostaglandin Analogues

These are PGF 2alpha agonists, which lower IOP by increasing the uveoscleral outflow. They are
extremely potent ocular hypotensive drugs that can lower the IOP below episcleral venous
pressure. Their most peculiar side effect is increased pigmentation of iris and eye lashes.

Side effects

 Local

Burning and stinging

Foreign body sensation

Conjunctival hyperaemia

Blurred vision

Iridial pigmentation

Hypertrichosis

HyperPigmentation of eye lashes

 Systemic

Headache
Facial rash

Musculoskeletal pain

G1 disturbance

Carbonic Anhydrase Inhibitors (CAI)

Carbonic anhydrase inhibitors lower IOP by reducing aqueous production. They are primarily
used for short-term control of IOP because of their numerous metabolic side effects.
Dorzolamide a topical CAI, is devoid of the systemic side effects.

Side effects

 Systemic CAI

Metallic taste

Paresthesia

Malaise symptom complex

Metabolic acidosis

GI symptoms :cramps and nausea

Increase urinary stones

Stevens-Johnson syndrome

Bone marrow suppression

 Topical CAI

Burning and stinging

Allergic conjunctivitis

Superficial punctate keratitis

Bitter taste

Corneal decompensation
 Hyperosmotic agents

These lower IOP by deturgescence of vitreous. They are extremely useful in ocular hypertensive
emergencies like acute ACG.

Side effects

Nausea, Hyperglycaemia (glycerol),

Lethargy, Seizure ,Coma

Vomiting, Dehydration,

Thrombophlebitis

Cardiac overload, Hyperglycaemia (glycerol),

Lethargy, Seizure,

Coma.

References

1. Harrison’s. principles of internal medicine. 18 edition volume 1 . pg 226

2. Sharma Rag Yog,, Sudan. Concise textbook of ophthalmology. 2007. Elsevier
publications. Pg. 115-136
3. Nema nithin.textbook of ophthalmology.ed 4. 2008. Jaypee brothers medical publishers.
New Delhi. Pg 214 – 249
4. Jogi Renu. Basic ophthalmology. Ed 3. 2013. Jaypee brothers medical publishers. New
Delhi.pg 246 - 279
Presence and Risk Factors for Glaucoma in Patients with
Diabetes
Brian J. Song, MD,1 Lloyd Paul Aiello, MD, PhD,2 and Louis R. Pasquale, MD1,3

Abstract
Diabetes mellitus represents a growing international public health issue with a near quadrupling
in its worldwide prevalence since 1980. Though it has many known microvascular
complications, vision loss from diabetic retinopathy is one of the most devastating for affected
individuals. In addition, there is increasing evidence to suggest that diabetic patients have a
greater risk for glaucoma as well. Though the pathophysiology of glaucoma is not completely
understood, both diabetes and glaucoma appear to share some common risk factors and
pathophysiologic similarities with studies also reporting that the presence of diabetes and
elevated fasting glucose levels are associated with elevated intraocular pressure – the primary
risk factor for glaucomatous optic neuropathy. While no study has completely addressed the
possibility of detection bias, most recent epidemiologic evidence suggests that diabetic
populations are likely enriched with glaucoma patients. As the association between diabetes and
glaucoma becomes better-defined, routine evaluation for glaucoma in diabetic patients,
particularly in the telemedicine setting, may become a reasonable consideration to reduce the risk
of vision loss in these patients.

Keywords: Glaucoma, Diabetes Mellitus, Diabetic Retinopathy, Epidemiology, Risk Factors

MEDICAL SURGICAL NURSIING

SEMINAR ON

GLAUCOMA

Submitted to, submitted by,

Mrs.Sheeba Mathew, Yashly Varghese,

Assistant Proffessor, 2nd year MSc Nursing

Govt. College Of Nursing, Govt. College Of Nursing,

Thrissur. Thrissur.