GLAUCOMA

GROUP 4
MANALO  MARAMOT  MARQUEZ  PAPASI
N  PATITICO
 The glaucomas are a
group of ocular disorders
that lead to an optic
neuropathy characterized
by changes in the optic
nerve head (optic disk).
 TWO MAJOR TYPES:
– Open angle
– Closed angle
 Associated with loss of
visual sensitivity and
field.
 INCREASED Intraocular Pressure (IOP) is thought to play
an important role in the pathogenesis of glaucoma, but it is
not a diagnostic criterion for glaucoma.

 OCULAR HYPERTENSION – consistently high IOP (IOP

greater than 21 mmHg or 2.8kPa) without signs or
symptoms of glaucoma.

 GLAUCOMA SUSPECTS – consistently high IOP or

patients with clinical findings suspicious of early
glaucomatous changes
 Basic Concepts:
Aqueous Humor and Intraocular Pressure
 Aqueous humor in the anterior chamber leaves the eye by two routes:
- filtration through the trabecular meshwork (conventional outflow) to the Schlemm’s
canal (80% to 85%)
- through the ciliary body and the suprachoroidal space (uveoscleral outflow or
unconventional outflow).
 Cholinergic agents such as pilocarpine appear to increase outflow by
physically opening the meshwork pores secondary to ciliary muscle
contraction.

 Prostaglandins are thought to result in remodeling of extracellular

matrix in the meshwork, thereby increasing outflow.

 Novel adenosine receptor agonists - cannabinoids, serotonin agents,

and dopamine agonists also increase aqueous humor outflow and
reduce IOP.
The increased IOP in all types of glaucoma
results from the decreased facility for
aqueous humor outflow.
 This circadian variation results in a minimum IOP at
approximately 6 pm and a maximum IOP at awakening
 Although, some studies suggest that both healthy and glaucoma
patients may have their highest IOP at night after falling asleep.
 This circadian variation and the poor relationship of IOP with
visual loss make measurement of IOP a poor screening test for
glaucoma.
 Controlling circadian increases in IOP is thought to be important
in prevention of disease progression
 Prostaglandin analogs a
nd carbonic anhydrase i
nhibitors (CAIs) reduce n
octurnal IOP

 β-blockers and alpha-2 a

drenergic agents have m
inimal effects
 The risk of developing glaucoma increases with
older age, family history of glaucoma, lower ocular
perfusion pressure, lower blood pressure, thinner
central cornea, optic disk hemorrhage, larger cup-
to-disk ratio, and specific visual fields findings.
 Normal-tension Glaucoma
 Patients with glaucomatous visual field loss have an IOP
of less than 21 mm Hg (2.8 kPa)
Thus the absolute IOP is a less precise predictor of optic nerve
damage.
 Glaucoma medications that provide maximal reduction of
IOP over 24 hours and have minimal influence on blood
pressure may be advantageous in treating glaucoma
patients.
Optic Disk and Visu
al FieldS
 The optic disk is the portion of the optic nerve
ophthalmoscopically visible as it leaves the eye.
 The small depression within the disk is termed the
cup.
 A normal physiologic cup does not extend beyond
the optic nerve rim and has a varying diameter of
less than one-third to one-half that of the disk
Cup to disk ratio >0.5
Splinter hemorrhages
Pallor of the cup
Progression of visual field loss in
Glaucoma
Figure 24-4
Progression of visual field loss in
Glaucoma
Figure 24-4
 These methods offer the ability t
o assess the damage to the optic heidelberg retinal tomography

nerve quantitatively:
Scanning laser polarimetry (GDX),
Confocal laser ophthalmoscopy (H
eidelberg retinal tomography, or H
RT),
and optical coherence tomography
(OCT)

 The peripheral visual field is meas

ured using a visual field instrume Optical Coherence Tomography

nt called a perimeter.
 Epidemiology of
Open-Angle Glaucoma
 Epidemiology of Open-Angle Glaucoma

 Open-angle glaucoma is the second leading cause of

blindness affecting up to 70 million individuals worldwide
 The incidence of the disease for patients 80 years of age is 3%
in whites and 5% to 8% in blacks
 The risk of glaucoma increases with family history, thinner
central corneal thickness, lower ocular perfusion pressure,
type 2 diabetes, myopia, and certain genetic mutations
 In the Philippines, glaucoma was ranked as the third most
common cause of bilateral blindness, and the fifth most
common cause of low vision. (Philippine Journal of
Ophthalmology)
 Etiology of
Open-Angle Glaucoma
Etiology of Open-Angle Glaucoma
 Pressure-sensitive astrocytes and other cells in the optic disk
supportive matrix may produce changes and remodeling of
the disk, resulting in axonal death.

 Optic nerve damage results from insufficient blood flow to

the retina secondary to the increased perfusion pressure
required in the eye, dysregulated perfusion, or vessel wall
abnormalities, and results in degeneration of axonal fibers of
the retina.

 IOP may disrupt axoplasmal flow at the optic disk.

Risk Factors: Potential Risk Factors:
 High eye pressure HBP
 Family history of glaucoma Steroid use
 Thin cornea Diabetes
 Age
Additional Contributory Factors:
 Increased susceptibility of the optic nerve
to ischemia
 Excitotoxicity
 Autoimmune reactions
 Other abnormal physiologic processes
Pathophysiology of
Open-Angle Glaucoma
PRIMARY OPEN-ANGLE GLAUCOMA

 Chronic

 Slowly progressive

 Found primarily in patients older than 50 years of age

 “sneak thief of sight” – No symptoms

 Optic nerve damage can occur at a wide range of IOPs and rate of
progression is highly variable

 Patients may exhibit pressures in the 20 to 30 mm Hg (2.7 to 4.0 kPa)

range for years before any disease progression is noticed in the optic disk
or visual fields
Signs
POAG: Disk changes and visual field loss; IOP can be normal or
elevated (>21 mm Hg [>2.8 kPa])
Mild: Optic disk abnormalities with normal visual field with standard
perimetry
Moderate: Optic disk changes plus visual field abnormalities in one
hemifield that are not within 5 degrees of central visual fixation
Severe: Optic disk changes with visual field loss in both hemifields
and loss within 5 degrees of central fixation and abnormalities in at
least one hemifield
Clinical Presentation
Open-Angle
of
Glaucoma
 Primary Open-Angle Glaucoma
 Bilateral, often asymmetric
Increased IOP - not required for diagnosis
Symptoms do not present until substantial visual field constriction
occurs.
Central visual acuity typically is maintained even in the late stages
of the disease.
It may have greater IOP and progression and severity in one eye
Each eye is treated individually
 Detection and diagnosis involve:
 Evaluation of the optic disk and retinal nerve fiber layer
 Assessment of the visual fields
 Measurement of IOP

 The presence of characteristic disk changes and visual field

loss with or without increased IOP confirms the diagnosis of
glaucoma.
 Diagnosis and diagnosis
involve:
 IOP of less than 21 mm Hg (<21mm Hg [2.8 kPa]) with occurring disk
changes and field loss account for 20% to 30% of patients and is
referred to as normal-tension glaucoma.
 Elevated IOP (>21 mm Hg [>2.8 kPa]) without disk changes or visual
field loss is observed in 5% to 7% of individuals (glaucoma suspects)
and is referred to as OHT
Secondary Open-Angle Glaucoma
 Exfoliation syndrome
 Pigmentary glaucoma
 Systemic diseases
 Trauma
 Surgery
 Ocular inflammatory diseases
 Medications
 Secondary Open-Angle
Glaucoma
 Pretrabecular form – membrane over
trabeculum
 Trabecular forms – ‘clogging up’ of
trabeculum
 Posttrabecular forms – raised episcleral
venous pressure.
Open-Angle Glaucoma
Laboratory tests
–None other

Diagnostic tests
–Emerging tests include OCT,
–Retinal nerve fiber analyzers, and
–Confocal scanning laser tomography of the optic nerve
–Tonometry
–Gonioscopy
 Epidemiology of
Primary Angle Closure
Glucoma
 Epidemiology of Primary Angle Closure Glucoma

There is an incident rate of 1% to 4% of PACG

that varies by the ethnic group, with a higher
incidence in individuals of Inuit, Chinese, and
Asian-Indian descent.
Because of the high frequency of PACG in
populous Asia, PACG accounts for
approximately one-third of glaucoma worldwide.
The Third National Survey on Blindness in the
Philippines showed that glaucoma is the third
major cause of visual impairment, after cataract
and refractive error, with a prevalence of 3%.
 Etiology of
Primary Angle Closure
Glucoma
Etiology of primary angle closure Glaucoma

PACG results from mechanical blockage of the

trabecular meshwork by the peripheral iris.
Etiology of primary angle closure Glaucoma

 Between attacks of PACG, the IOP is usually

normal unless the patient has concomitant POAG
or nonreversible blockage of the meshwork with
synechiae (“creeping” angle closure) that
develops over time in the narrow-angle eye.
Etiology of primary angle closure Glaucoma

Two Major Types of Classic Reversible PACG:

PACG with pupillary block
 Results when the iris is in firm contact with the lens.
 This produces a relative block of aqueous flow through the pupil to
the anterior chamber (pupillary block), resulting in a bowing
forward of the iris, which blocks the trabecular meshwork.
PACG without pupillary block
 Occurs when a patients has an abnormality called a plateau iris.
 The ciliary processes in these cases are situated anteriorly, which
indent the iris forward and cause closure of the trabecular
meshwork, especially during mydriasis.
Etiology of primary angle closure Glaucoma

 The mydriasis produced by anticholinergic

drugs or any other drug results in
precipitation of both types of PACG
glaucoma, whereas drug-induced miosis
may produce pupillary block.
 Pathophysiology of
Primary Angle Closure Glucoma

It is caused by disorders of the iris, the lens, and retrolenticular structures.

Pupillary block is the most common mechanism of angle closure.
 Physical blockage of trabecular
meshwork is present, causing the
elevation of IOP

 Pupillary block causes pressure

gradient between posterior and the
anterior chamber

 Due to pressure gradient the peripheral

iris bows forward (iris bombe) against
the trabecular meshwork leading to
obstruction of aqueous outflow and rise
of IOP
 In many cases, single or multiple episodes of high IOP
that in some patients may exceed 40 mm Hg (5.3 kPa)
and result in optic nerve damage
 Very high IOP (>60 mm Hg [>8.0 kPa]) may result in
permanent loss of visual field within a matter of hours to
days.
 Clinical Presentation
Primary Angle of
Closure Glucoma
Primary Angle Closure Glaucoma
 More typically associated with symptomatic acute episodes or may be slowly
progressive as with POAG
 Symptoms are determined by the rapidity and degree of ↑IOP.

Symptoms:
 Chronic ACG: blurred or hazy vision with halos around lights that
is caused by a hazy, edematous cornea, and occasionally headache
 Acute ACG: cloudy, edematous cornea, ocular pain, or discomfort,
nausea, vomiting, abdominal pain, and diaphoresis
Laboratory tests
–None other

Diagnostic tests
–Emerging tests include OCT,
–Retinal nerve fiber analyzers, and
–Confocal scanning laser tomography of the optic nerve
–Tonometry
–Gonioscopy
Drug-Induced
Glaucoma
 Drug-Induced Glaucoma: poag
Patients with treated, controlled POAG are at minimal risk of induction of an
increase in IOP by systemic medications with anticholinergic properties or
vasodilators; however, for patients with untreated glaucoma or uncontrolled
POAG, the potential of these medications to increase IOP should be considered.

Topical anticholinergic agents,

Potent anticholinergic agents
Inhaled, nasal, topical, or systemic glucocorticoids
 Drug-Induced Glaucoma: poag

 Glucocorticoids reduce the facility of aqueous humor outflow through

the trabecular meshwork.

 The decreased facility of outflow appears to result from the

accumulation of extracellular material blocking the trabecula channels.
Drug-Induced Glaucoma: pacg

 Sulfa drugs

 Topical anticholinergics or sympathomimetic agents

 Systemic and inhaled anticholinergic and sympathomimetic agents

 potent miotic agents

 Treatment: Glaucoma Suspects and Ocular
Hypertension

 GOAL: Lower the IOP to a level associated with a decreased

risk of optic nerve damage, usually at least a 20%, if not a 25%
to 30% decrease from the baseline IOP.

 The Ocular Hypertensive Treatment Study (OHTS) helped to

identify risk factors for treatment. Patients with IOPs higher than
25 mm Hg (3.3 kPa)
 Vertical cup-to-disk ratio of more than 0.5

 Central corneal thickness of less than 555 μm

 Treatment: Glaucoma Suspects and Ocular
Hypertension

• Risk factors:
Family history of glaucoma
Black
Latino/Hispanic ethnicity
Severe myopia
• Patients without risk factors typically are not treated and are monitored for
the development of glaucomatous changes.
• The use of risk calculators has been suggested as a means of determining
who are at greatest risk in developing glaucoma.
 Treatment: Glaucoma Suspects and Ocular
Hypertension

 Patients with significant risk factors usually are treated with a

well-tolerated topical agent such as a prostaglandin
analog or β-blocking agent.

 Other options include a α2-agonist (brimonidine) or a topical

CAI, depending on individual patient characteristics.
 Treatment: Glaucoma Suspects and Ocular
Hypertension

 Drug therapy measurement of IOP:

 examination of the optic disk
 assessment of the visual fields
 evaluation of the patient for drug adverse effects

 Partial responders may be treated with combinations of

well-tolerated topical medications (prostaglandins, β-
blockers, brimonidine or a CAI).
 Treatment: Open-Angle
Glaucoma
 GOAL: Prevent further visual loss.

 Target IOP: IOP reduction of 25-30%.

 Some controversy exists as to whether the initial therapy of glaucoma

should be surgical trabeculectomy (filtering procedure), argon or
selective laser trabeculectomy, or medical therapy.

 Patients with normal baseline IOPs (normal-tension glaucoma) may have

target IOPs of less than10 to 12 mm Hg (1.3 to 1.6 kPa)
 Treatment: Acute Angle Closure
Crisis (AACC)
 Goal of initial therapy: Rapid reduction of the IOP to preserve vision
and to avoid surgical or laser iridectomy on a hypertensive, congested
eye.

 Administration of one or more topical antiglaucoma medications

including miotics (eg, pilocarpine), secretory inhibitors (β-blockers, α2
-agonist, or topical/systemic CAIs), or a prostaglandin agonist.

 The aqueous secretory inhibitors and pilocarpine may not be effective

due to ischemia of the ciliary body and pupillary sphincter, respectively.
 Treatment: Acute Angle Closure Crisis
(AACC)
 A hyperosmotic agent such as mannitol or glycerin may be needed to
temporarily reduce IOP and restore response to the topical agents.

 Osmotic agents reduce IOP by withdrawing water from the eye

secondary to the osmotic gradient between the blood and the eye.

 Oral glycerin 1 to 2 g/kg can be used if an oral agent is tolerated; if not,

IV mannitol 1 to 2 g/kg should be used.

 Topical corticosteroids often are used to reduce the ocular inflammation

and reduce the development of synechiae in PACG eyes.
 Treatment: Acute Angle Closure Crisis
(AACC)
 Patients failing therapy altogether will require an emergency iridectomy.
 Iridectomy produces a hole in the iris that permits aqueous humor flow
to move directly from the posterior chamber to the anterior chamber,
opening up the block at the trabecular meshwork.
 Peripheral iridectomy essentially “cures” primary PACG without
significant synechiae.
 Pharmacotherapeutic approach is essentially identical to that for the
POAG patient, or laser or surgical procedures are performed.
 Pharmacotherapeutic Approach

Medications most commonly used to treat glaucoma:

 β-blockers
 Brimonidine (an α2-agonist)
 Topical CAIs
 Fixed combination products:
– timolol/dorzolamide
– timolol/brimonidine
– brimonidine/brinzolamide
– timolol/prostaglandins
 Pharmacotherapeutic Approach

 The prostaglandin analogs are often recommended as first-line

therapy.
 Once-daily dosing
 better IOP reduction
 better 24-hour IOP control
 good tolerance
 availability of lower-cost generics
 The topical β-blockers have a long history of successful use,
providing a combination of clinical efficacy and general tolerability.
 Brimonidine and topical CAIs are also well tolerated and effective
agents, but often considered second-line agents.
 Pharmacotherapeutic Approach

 Therapy optimally is started as a single agent, and may be started in

one to evaluate drug efficacy and tolerance, although response may
differ between contralateral eyes.
 Initial check for IOP response to therapy is typically done 4 to 6
weeks after the medication is started.
 More frequent monitoring is necessary if the IOP target is not
achieved, disease progression is noted, and after any change in drug
therapy.
 Pharmacotherapeutic Approach

 For patients failing to respond to an initial drug, a switch to an

alternative agent should be considered.
 Prostaglandin agonists, β-blockers, brimonidine, CAIs, and
pilocarpine may be used in various combinations.
 Using more than one drop per dose does not improve response but
rather increases the likelihood of adverse effects and the cost of
therapy.
 When using more than one medication, separation of drop instillation
of each agent by at least 5 minutes is suggested to provide optimal
ocular absorption.
 Pharmacotherapeutic Approach

 Benefits of Combination drugs:

reduce the number of daily doses,
improving adherence and preventing washout effect
reduces exposure to ophthalmic preservatives

 Because of the frequency of adverse effects, dipivefrin, carbachol,

topical cholinesterase inhibitors, and oral CAIs are considered last-
line agents to be used for patients who fail less-toxic combination
topical therapy.
Nonpharmacologic
Therapy:
Laser and Surgical
Procedures
 Nonpharmacologic Therapy: Laser and Surgical
Procedures
Laser trabeculoplasty is usually an intermediate step between drug therapy and
trabeculectomy. It uses a very focused beam of light to treat the drainage angle
of the eye.
- Argon Laser Trabeculoplasty (ALT)- The objective of the surgery is to help fluids drain
out of the eye, reducing intra-ocular pressure that can cause damage to the optic nerve and
loss of vision.

- Selective Laser Trabeculoplasty (SLT) is a new procedure performed to lower

intraocular pressure (IOP). SLT is an outpatient laser used to selectively target the
pigmented trabecular meshwork cells in the angle of the eye.
 Nonpharmacologic Therapy: Laser and
Surgical Procedures
Trabeculectomy (Filtration Surgery) involve the creation of a channel through
which aqueous humor can flow from the anterior chamber to the subconjunctival
space (filtering bleb), where it is reabsorbed by the vasculature.
Glaucoma surgery is still plagued with the shortcomings despite modifications and
improvements over the past century, including potentially vision-threatening
complications such as hypotony, wound leaks, and infections.
Minimally invasive glaucoma surgery (MIGS) uses microincisions and implants
that reduce IOP by targeting various areas of the outflow pathway.
 Nonpharmacologic Therapy: Laser and
Surgical Procedures
Modification of the healing process to maintain patency is possible with the use of
antiproliferative agents.

5-fluorouracil and mitomycin C are used for patients undergoing glaucoma-

filtering surgery to improve success rates by reducing fibroblast proliferation and
consequent scarring.

A standardized formulation of mitomycin C (MMC) that is prepacked in a kit with

a fixed dose and concentration was approved by FDA in 2012 and is commercially
available under the name “Mitosol.”
PHARMACOLOGIC
AGENTS USED IN
GLAUCOMA
 CAUTION IS
MECHANISM OF RECOMMENDED
SUBCLASS, DRUG EFFECTS ADVERSE EFFECTS
ACTION FOR PATIENTS
WITH

PROSTAGLANDIN
ANALOGS

 Latanoprost  induction of  reduce IOP  Hypertrichosis  ocular

metalloproteinases in  Hyperpigmentation inflammatory
 Travoprost the ciliary body, which  Loss of periorbital conditions
breakdown the fat
 Bimatoprost extracellular matrix
 Tafluprost
 increase the
uveoscleral and, to a
lesser extent,
trabecular outflow of
aqueous humor
 CAUTION IS
SUBCLASS, MECHANISM OF RECOMMENDED
EFFECTS ADVERSE EFFECTS
DRUG ACTION FOR PATIENTS
WITH
β-BLOCKING
DRUGS LOCAL:
 ocular  stinging on application  pulmonary diseases
 Timolol  decreasing the
production of hypotensive  dry eyes  sinus bradycardia
 Levobunolol aqueous humor by effects  second- or third-
 corneal anesthesia
the ciliary body  lower IOP degree heart block
 Metipranolol without producing  blepharitis
substantial effects  blurred vision  congestive heart
 Carteolol failure
on aqueous humor  
 Betaxolol outflow facility SYSTEMIC:  atherosclerosis
 decreased heart rate  diabetes
 reduced blood pressure  myasthenia gravis
 negative inotropic effects
 conduction defects
 Bronchospasm
 CNS effects
 CAUTION IS
MECHANISM OF RECOMMENDED
SUBCLASS, DRUG EFFECTS ADVERSE EFFECTS
ACTION FOR PATIENTS
WITH

α2-ADRENERGIC
AGONISTS For Apraclonidine:
 cardiovascular
 Brimonidine  decreasing the rate of  reduce IOP  lid edema diseases
aqueous humor  eye discomfort
 Apraclonidine production.  foreign-object sensation  renal compromise
 Itching  cerebrovascular
 brimonidine known to  hyperemia disease
also increase  
For Brimonidine:  diabetes
uveoscleral outflow
 dizziness
 fatigue
 somnolence
 dry mouth
 slight reduction in blood
pressure and pulse
SUBCL CAUTION IS
MECHANISM OF
ASS, EFFECTS ADVERSE EFFECTS RECOMMENDED FOR
DRUG ACTION
PATIENTS WITH

 Increased  Reduce OCULAR:  cardiovascular diseases

aqueous humor IOP  tearing
 burning  cerebrovascular diseases
outflow
 ocular discomfort  aphakia
 brow ache
 conjunctival hyperemia  CAG
 punctate keratopathy
DIPIVEFRIN

 hyperthyroidism
 allergic blepharoconjunctivitis
 rare loss of eyelashes  diabetes mellitus
 stenosis of the nasolacrimal duct
 blurred vision
 
SYSTEMIC:
 headache
 faintness
 increased blood pressure
 tachycardia
 arrhythmias
 tremor
 pallor
 anxiety
 increased perspiration
 CAUTION IS
MECHANISM OF
SUBCLASS, DRUG EFFECTS ADVERSE EFFECTS RECOMMENDED
ACTION
FOR PATIENTS WITH

CARBONIC LOCAL:
ANHYDRASE
 sulfa allergies
 decreasing ciliary  reduce IOP  transient burning and
INHIBITORS
body aqueous humor stinging  sickle cell disease
TOPICAL AGENTS secretion  reduce  ocular discomfort and  respiratory acidosis
 Dorzolamide aqueous transient blurred  pulmonary disorders
 inhibit aqueous humor vision
 Brinzolamide  renal calculi
production by inflow  tearing
  blocking active  blurry vision  electrolyte imbalance
SYSTEMIC CAI secretion of sodium  hepatic disease
AGENTS and bicarbonate ions  renal calculi
from the ciliary body  increased uric acid  renal disease
 Acetazolamide to the aqueous  blood dyscrasias  diabetes mellitus
 Methazolamide humor  Diuresis
 Addison’s disease
 myopia
  asthma
PARASYMPATHOMI  increasing  reduce OCULAR:
 miosis  retinal detachments
METIC AGENTS aqueous IOP
humor  visual field constriction  narrow angles
 Pilocarpine  reduce
trabecular uveoscle  bradycardia
outflow SYSTEMIC:
 Carbachol ral  hypotension
 diaphoresis
outflow
 Echothiophate  nausea  heart failure
 vomiting  down’s syndrome
 diarrhea  epilepsy
 cramping  parkinsonism
 urinary frequency  peptic ulcer
 bronchospasm  ocular inflammation
 heart block
 retinal tears or detachment
 allergic reaction
 permanent miosis
 cataracts
 precipitation of CAG
 Future Drug Therapy
 Rho kinase inhibitors (ROCK), which induce changes in
the trabecular meshwork and reduce impedance to aqueous
outflow. They possess neuroprotective effects and produce an
increase in ocular blood flow.
 Future Drug Therapy
Other classes of drugs:
 Adenosine-1 receptor agonists
 Cannabinoids
 Serotonin agonists
 Dopamine agonists
 Nitric oxide/ Carbon dioxide modulators
 Hydroxysteroid dehydrogenase inhibitors.
 Future Drug Therapy
 Agents with dual ROCK inhibition and norepinephrine
transport inhibition are in later clinical phase trial.
 PATIENT
EDUCATION
 An important consideration for patients failing to respond to drug
therapy is adherence. Poor adherence or nonadherence occurs in 25% to
60% of glaucoma patients. A large percentage of patients also fail to use
topical ophthalmic drugs correctly. Patients should be taught the
following procedure:
1. Wash and dry the hands; shake the bottle if it contains a suspension.
2. With a forefinger, pull down the outer portion of the lower eyelid to form
a “pocket” to receive the drop.
3. Grasp the dropper bottle between the thumb and fingers with the hand
braced against the cheek or nose and the head held upward.
4. Place the dropper over the eye while looking at the tip of the bottle; then
look up and place a single drop in the eye.
5. The lids should be closed (but not squeezed or rubbed) for 5 minutes after
instillation. This increases the ocular availability of the drug and reduces
systemic absorption.
6. Recap bottle and store as instructed.