Thanks to Dr. Garfield Miller, MD, FRCSC, Assistant Professor of Opthalmology, University of Ottawa, The Ottawa Eye Institute, The Ottawa Hospital, ON Canada, and Sadie Sattan, RN, BScN, MN, School of Nursing, Faculty of Health Sciences, McMaster University/Mohawk College, Hamilton, ON Canada for their expertise with the initial review of this topic.


A variety of conditions with a common feature of glaucomatous optic neuropathy (GON) characterized by loss of retinal nerve fibers and changes in the optic disc. Permanent damage ensues if left untreated and results in progressive loss of vision and irreversible blindness.

Increased intraocular pressure (IOP) is the most common causative risk factor but is not necessary for diagnosis.

Open and closed-angle glaucoma can be primary or secondary.

  • Primary glaucoma: Refers to conditions in which there are no other associated ocular or systemic cause
  • Secondary glaucoma: Refers to those conditions in which there is an associated ocular or systemic condition
  • Congenital or developmental glaucoma: Represent only a small percentage of the overall cases of glaucoma and are usually identified prior to 3-5 years of age

Note: Open angle glaucoma makes up ~90% of all primary glaucoma cases, while angle closure glaucoma makes up the other 10%, and its incidence increases with age.

Classification flow chart:

1) Open angle 2) Angel closure 3) Developmental


Primary and secondary glaucoma may be associated with increased intraocular pressure (IOP).

Putative mechanisms of elevated IOP include:

Obstruction to aqueous outflow from:

  1. Closure of iridocorneal drainage due to apposition of the trabecular meshwork and iris root (closed-angle) or obstruction to outflow through the drainage pathways of an open angle
  2. Obstruction to the venous drainage of the eye

Other potential causes of increased IOP include:

  • Trauma to outflow pathways
  • Metabolic factors related to aqueous production
  • Anatomic or physiologic features of the trabecular meshwork
  • Mutations in the myocilin gene (MYOC) have been identified. Myocilin is produced in the ciliary body and in the trabecular meshwork

Closed-angle glaucoma develops if the high IOP causes glaucomatous damage to the optic disc.

Open angle glaucoma occurs if damage to the disc is present in the face of an open angle.

Secondary causes that may lead to glaucoma include:

  • Pseudo-exfoliation syndrome
  • Pigment dispersion syndrome (pigmentary glaucoma)
  • Lens-induced glaucoma
  • Ocular inflammatory diseases
  • Intraocular tumors
  • Raised episcleral venous pressure (e.g. Sturge Weber syndrome, orbit tumor, carotid cavernous fistula)
  • Neovascularization of trabecular meshwork (diabetes, vascular occlusions, etc.)

Risk factors for glaucoma include

  • Age
  • Family history of glaucoma
  • Elevated eye pressure (IOP)
  • Nearsightedness (POAG)
  • Farsightedness (angle closure)
  • African, Hispanic or Asian ancestry
  • Diabetes mellitus
  • Previous eye injury
  • Thin cornea
  • Prolonged use of topical, periocular, inhaled, or systemic corticosteroids



  • Glaucoma is the leading cause of irreversible blindness
  • Approximately affects 300,000 Canadians, ~80% are >40 years of age, while ~50% of these are unaware of there diagnosis


  • Prevalence for primary open angle glaucoma POAG
    • In the adult US population over age 40 is 1.86%
    • In whites is 1.69%
    • Age-adjusted prevalence in blacks is three times higher than in whites


Approximately 3 million people are bilaterally blind from POAG.


  • Primary open angle glaucoma is 1.96%
  • Angle closure glaucoma is 0.69%

The incidence increases with age and is more prevalent among men.


Pathogenesis of open angle glaucoma

Although the exact mechanism is unknown, elevated IOP is often associated with the development of glaucoma.

The putative mechanism by which IOP initiates glaucomatous damage includes:

  • Mechanical Hypothesis: Elevated IOP causes a backward bowing of the lamina cribrosa, compressing the axons as they exit through the luminal pores, interfering with axoplasmic flow of trophic factors, triggering cell death
  • Vascular Hypothesis: Chronic hypoxia and ischemia leads to glaucomatous damage

Other potential mechanisms include:

  • Excitotoxic injury from excessive retinal glutamate
  • Deprivation of neuronal growth factors
  • Peroxynitrite toxicity from increased nitric oxide synthetase activity
  • Immune-mediated nerve damage, and oxidative stress

The above mentioned conditions lead to apoptotic cell death

Pathogenesis of acute angle closure glaucoma (AACG)

Apposition of the iris to the trabecular meshwork at the angle of the anterior chamber, obstructs aqueous outflow from the eye leading to increased IOP.

In primary angle closure glaucoma, this apposition is due to a mechanism called Pupil Block:

  • The normal flow of aqueous humour is from the posterior chamber, around the lens, through the pupil, into the anterior chamber, and out through the trabecular meshwork. In predisposed patients, the pupil margin touches the lens and can cause resistance to the normal flow through the pupil. Pressure builds in the posterior chamber causing the peripheral iris to bulge forward (iris bombe). If the peripheral iris covers the trabecular meshwork, outflow is obstructed

Note: Immediate treatment is required to prevent nerve damage and vision loss; symptoms are severe in sudden closure.

Pathogenesis of chronic angle closure glaucoma (CACG)

  • May occur when portions of the anterior chamber angle are closed permanently by peripheral anterior synechiae (PAS)

Note: Eyes with progressive peripheral anterior synechiae (PAS) formation eventually may develop AACG when pupillary block results in closure of the remaining portions of the angle unaffected by PAS.

Combined mechanism glaucoma

  • Carry both components of open and closed angle glaucoma

Common mechanisms IOP

Clinical Manifestations:

Open Angle Glaucoma:

History is crucial in the evaluation of open angle glaucoma as this condition is often asymptomatic until most of the vision is lost.

Acute Angle Closure Glaucoma:

Triggered by rapid elevation in IOP resulting in:

  • Decreased vision
  • Halos around lights
  • Headache
  • Severe eye pain
  • Nausea and vomiting

Chronic Angle Closure Glaucoma:

  • Patients remain asymptomatic for a long time due to slow elevation in IOP

Workup and Diagnosis

History should include:

  • Birth and developmental history
  • Family history
  • Episodes of eye pain/headache/nausea/blurred vision (acute glaucoma)
  • Halos around lights (acute glaucoma)
  • Cataract
  • Uveitis
  • Previous eye surgery/trauma
  • Systemic illnesses
    • Diabetes
    • Hypertension
    • Cardiovascular disease
    • Migraines
    • Raynaud’s disease
  • Use of medicines affecting intraocular pressure (steroids – systemic, ocular, inhaled)

Physical examination should include assessment of:

  • Pupil
  • Anterior segment
  • Central corneal thickness (CCT)
  • Gonioscopy
  • Optic nerve head and retinal nerve fibre layer evaluation
  • Visual field sensitivities
  • Intraocular pressure (IOP)

Normal intraocular pressure

  • Adult: 10-21 mmHg (16 mmHg ±2.5). Tends to increase with age
  • Children: Increases ~1 mmHg every 2 years till 12 years
    • At birth 6-8 mmHg
    • At 12 years 12 ±3 mmHg
  • Diurnal Variation: IOP often follows circadian rhythm
    • Maximum: Between 8 a.m. and 11 a.m.
    • Minimum: Between midnight and 2 a.m.
    • Variation: Between 3 and 5 mmHg

Tonometry (to measure IOP)

A Tonometer measures IOP in millimeters of mercury (mmHg)

  • Multiple readings from hour to hour are taken
  • IOP in both eyes are measured
  • Comparison with previous readings are done
  • Difference of 3 mmhg in both eyes is an indication for further investigation for glaucoma

Corneal Pachymetry

  • Used to check central corneal thickness (CCT)


  • Used to determine if the angle is closed, open or abnormal


  • Direct ophthalmoscopy one that produces an upright, or unreversed, image of approximately 15 times magnification
  • Indirect ophthalmoscopy one that produces an inverted, or reversed, direct image of 2 to 5 times magnification
  • Findings:
    • Evidence of glaucomatous optic nerve damage
    • Thinning or notching of the disc rim
    • Retinal nerve fiber layer defects

Slit-lamp examination

  • Focus on cornea, anterior chamber, lens, optic nerve fibers, and fundus

Perimetry (visual fields)

  • It is the systematic measurement of visual field function, that is central and peripheral (side) vision


Routine labs are not routinely done, unless considering normal tension glaucoma or other optic neuropathies/infections.


Methods of measuring the optic disc and the nerve fiber layer:

  • Laser scanning polarimetry(e.g. GDx Nerve Fiber Analysis System)
    • Measures the thickness of the nerve fiber layer
  • Confocal laser ophthalmoscopy – (e.g. Heidelberg Retinal Tomography or HRT)
    • Scans layers of the retina to make quantitative measurements of the surface features of the optic nerve head and fundus
  • Optical coherence tomography (OCT)
    • OCT can create a contour map of the optic nerve, optic cup and measure the retinal nerve fiber thickness
    • New anterior segment OCT machines are helpful in the evaluation of angle closure
  • Stereo photographs
    • Used to determine the three-dimensional characteristics of the optic nerve head, and for following glaucomatous change of the optic nerve head over time
  • Ultrasound biomicroscopy (UBM) – (High resolution ultrasound technique)
    • Helpful to obtain a better view of the angle, iris, and ciliary body structures to rule out anatomical pathology and secondary causes of elevated IOP
RN/Medical Management:

Specific treatment goals:

  • Stop progression and maintain quality-of-life
  • Lower IOP to desired pressure; if causing damage
  • Identify and treat underlying causes


Indication for treatment:

  • Patients with high IOPs may or may not require treatment; the latter is based on evidence of ongoing damage, rather than a specific IOP
  • Some patients with normal IOP may require treatment, if there is evidence of ongoing injury and visual field loss
  • Target pressures should be set and achieved, but treatment is generally escalated until there is no more evidence of progression
  • Choice of therapeutic agents depends on patients disease status, target ocular pressure, medical history, pharmacoeconomics, and psychological factors

Medical therapy:

Alpha-agonists: Suppress aqueous inflow and include

  • Apraclonidine
  • Brimonidine

Red eye and ocular irritation are often associated with the use; caution required in pregnancy, contraindicated if the patient is taking monoamine oxidase inhibitors (MAO).

Beta-blockers: Suppress aqueous inflow and include

  • Betaxolol
  • Carteolol (only available in the US)
  • Levobunolol
  • Metipranolol (only available in the US)
  • Timolol

May cause some dry eyes, nonselective agents require caution in patients with obstructive airway diseases. Mask symptoms of hypoglycemia in individuals with diabetes.

Carbonic anhydrase inhibitors: Suppress aqueous inflow and include

  • Dorzolamide (topical)
  • Brinzolamide (topical)
  • Acetazolamide (oral)
  • Methazolamide (oral)

Prescribed when topical treatment is not effective.

May cause hypokalemia if sodium and potassium levels are depressed as in kidney or liver disease caution is advised.

Prostaglandin analogs: Increase outflow and include

  • Latanoprost
  • Travoprost
  • Bimatoprost
  • Tafluprost
  • Latanoprostene bunod

Discoloration of iris and foreign body sensation is a common complaint; caution advised on use during pregnancy.

Rho kinase inhibitor: suppressing the rho kinase enzymes responsible for fluid increase

  • Netarsudil

Conjunctival hyperemia is a common complaint.

Cholinergic agents: facilitate aqueous outflow

  • Pilocarpine
  • Carbachol

Headaches and dim vision is a common complaint.

Interventional therapy

Laser therapy:

  • Laser trabeculoplasty
    • Increases aqueous outflow
    • The effect typically is not permanent
    • Laser can be repeated (especially Selective Laser Trabeculoplasty-SLT)
  • Cyclophotocoagulation
    • Diode laser applied directly through sclera targeting the ciliary body
    • Decreases aqueous production
    • Usually reserved for eyes with poor visual potential


  • Trabeculectomy: Creation of a filtration bleb to allow egress of aqueous humor from the eye. An artificial fistula is made between the anterior chamber and a formed space underneath the conjunctiva
  • Aqueous shunt: Small silicone tube implanted in the anterior chamber that leads to a baseplate placed underneath the conjunctiva. Shunts are typically used in patients who have failed conventional surgery or have an underlying diagnosis that increases the risk of surgical failure
  • Endocyclophotocoagulation: Endoscopic visualization and application of laser to the ciliary processes (where aqueous humour is produced.) Often done at the time of cataract surgery. Moderate IOP lowering

MICRO invasive glaucoma surgeries (minimally invasive glaucoma surgeries):

Newer surgical procedures, which may carry less risk and morbidity than traditional procedures. In general, these interventions do not lower IOP when compared with others, and often used for less advanced cases.

  • Schlemm’s canal procedures
    • iStent trabecular micro-bypass – smallest implant in the human body. L-shaped stent placed through the trabecular meshwork into Schlemm’s canal. Usually done in conjunction with cataract surgery
    • Trabectome – Electrocautery used to ablate trabecular meshwork, opening up Schlemm’s canal. Often done in conjunction with cataract surgery
    • Canaloplasty – Schlemm’s canal is approached externally with meticulous dissection. A fiber optic is used to canulate the canal 360 degrees, then a suture is left in the canal and tied with tension to expand it. The anterior chamber is not entered with this technique
  • Suprachoroidal procedures – Various procedures shunting aqueous humour from the anterior chamber into the suprachoroidal space. This space is found between the choroid and the sclera. These procedures have not yet achieved widespread use


Goal of treatment:

  • Prevention and reversal of angle closure
  • Control of intraocular pressure

Indications for treatment:

  • Patients with signs or symptoms suggesting possible acute angle closure should be referred for emergent assessment and treatment to prevent permanent damage

Treatment options:

In acute emergencies, treatment usually involves, combination of both topical and oral agents.

Topical Preparations

  • All classes of pressure lowering drops should be used
  • Topical steroid

Systemic therapy

  • Oral acetazolamide- 250 mg two tablets stat. The eye pressure should be checked 30 to 60 minutes after giving oral acetazolamide. Used mainly to temporize until definitive treatment (surgery) can be arranged or underlying cause removed (e.g. steroid effect)
  • IV mannitol
  • Oral glycerol or isosorbide

Laser peripheral iridotomy

  • Once the episode is controlled the treatment of choice is a laser peripheral iridotomy
  • This procedure creates a tiny hole in the peripheral iris allowing drainage of aqueous humor and equalizing the pressure between the anterior and posterior chambers, thus relieving pupil block
  • Reassess the IOP 30 to 120 minutes after the iridotomy
  • If it is not possible to perform laser iridotomies, surgical peripheral iridectomy may be necessary
  • Laser peripheral iridotomy is also indicated in the fellow eye as prophylaxis. It is recommended that all patients with narrow angles, symptomatic or not, should have prophylactic iridotomies performed

Complications of laser peripheral iridotomy

  • Increased IOP
  • Inflammation
  • Laser burns to the cornea, lens, or retina
  • Glare or “white line” in vision
  • Development of cataract
  • Need for repeat treatment if spontaneous closure occurs

Other surgical procedures

  • Goniosynechialysis: Mechanical lysis of peripheral anterior synechiae to restore drainage function
  • Phacoemulsification: Removing the lens that is crowding the angle and replacing it with a flat intraocular lens implant

Alpha-2 agonist, (ophthalmic)

  • Apraclonidine
  • Brimonidine


  • It is selective alpha2-receptors agonist with some binding to alpha1-receptors
  • Decreases aqueous humor formation
  • Produces local vasoconstriction and reduction in blood flow in the eye

Brimonidine (additional)

  • Increased uveoscleral outflow




  • 1-2 gtt 0.5% solution in the affected eye TID

Postsurgical intraocular pressure elevation

  • 1 gtt 1% solution in the operative eye 1 hour before surgery; Then 1 gtt immediately upon completion of a procedure


Glaucoma/Ocular hypertension

  • 0.2% (1 gtt) in affected eye twice daily

Beta-blockers (ophthalmic)

  • Timolol
  • Betaxolol
  • Levobunolol


  • Reduces the production of aqueous humor


  • Blocks both beta1– and beta2-adrenergic receptors

Betaxolol (additional)

  • Selectively blocks beta1-receptors antagonist, with little or no effect on beta2-receptors



Glaucoma/Elevated IOP

  • Solution: 1 gtt of 0.25% solution BID into affected eye(s); Max. 1 gtt of 0.5% solution BID
    • Note: Decrease to 1 gtt one daily if controlled.
  • Gel-forming solution: 1 gtt of either 0.25% or 0.5% once daily into affected eye(s)

Betaxolol, Levobunolol

Open-angle glaucoma/Elevated IOP

  • 0.5% solution: 1-2 gtt BID into affected eye(s)
  • 0.25% suspension: 1 gtt BID into affected eye(s)

Carbonic anhydrase inhibitors (ophthalmic)

  • Dorzolamide
  • Brinzolamide


  • Reversible inhibition of the carbonic anhydrase enzyme produces
    • Reduction of hydrogen ion secretion at renal tubule
    • Increased renal excretion of sodium, potassium, bicarbonate, and water to decrease production of aqueous humor
  • This results in decreased production of aqueous humor



Open-angle glaucoma / Ocular hypertension

  • 1 gtt of 2% solution TID in the affected eye(s)
  • Dose in Renal Impairment: Avoid use if CrCl <30


Open-angle glaucoma / Ocular hypertension

  • 1 gtt 1% suspension TID in affected eye(s)

Carbonic anhydrase inhibitors (Oral/IV)

  • Acetazolamide
  • Methazolamide


  • Reversible inhibition of the enzyme carbonic anhydrase resulting in
    • Reduction of hydrogen ion secretion at renal tubule
    • Self-limiting urinary excretion of sodium, potassium, bicarbonate, and water
  • Alkaline diuresis prevents precipitation of uric acid or cystine in the urinary tract
  • CNS inhibition of carbonic anhydrase and resultant diuresis may decrease abnormal discharge from CNS neurons
    • Methazolamide is not considered an effective anticonvulsant



Acute angle-closure glaucoma/Secondary glaucoma

  • 250 mg PO/IV every 4 hrs
  • In acute cases: initial 500 mg IV followed 125-250 mg every 4 hrs is preferable
  • Short-term therapy with 250 mg twice daily, some adults may respond to this as well

Chronic simple (open-angle)

  • 250 mg PO/IV once daily or in 2-4 divided doses up to 1g/day. Or 500 mg PO BID of Extended-release capsules

Dose in renal impairment:

  • If CrCl 10-50 mL/min give only 12 hourly
  • CrCl <10 avoid use


  • 50-100 mg PO BID or TID

Prostaglandin agonist, (ophthalmic)

  • Latanoprost
  • Travoprost
  • Bimatoprost
  • Tafluprost
  • Latanoprostene bunod


  • Exact mechanism is unknown
  • Possibly it decreases the IOP by increasing uveoscleral outflow of aqueous humor

Dose: In glaucoma and ocular hypertension


  • 1 gtt at night in the affected eye(s)


  • 1 gtt at night in the affected eye(s)


  • 1 gtt at night in the affected eye(s), do not exceed once daily dosing


  • 1 gtt at night in the affected eye(s)

Latanoprostene bunod

  • 1 gtt at night in the affected eye(s), do not exceed once daily dosing

Rho kinase inhibitor:

  • Netarsudil


  • Exact mechanism is unknown
  • Suppress the rho kinase enzymes responsible for fluid increase
  • May reduce IOP by increasing the outflow of aqueous humor through the trabecular meshwork route

Dose: In open-angle glaucoma


  • 1 gtt 0.02% solution at night in the affected eye(s)

Cholinergic agents, (ophthalmic)

  • Pilocarpine
  • Carbachol


Directly stimulates cholinergic receptors in the eye causing

  • Constriction of the pupil by contracting the iris sphincter
  • Loss of accommodation by contracting the ciliary muscle
  • Lower the intraocular pressure and facilitates aqueous humor outflow



Open-angle glaucoma

  • 1-2 gtt of 1-4% solution 6 times a day
  • 0.5 inch strip of 4% gel into lower conjunctival sac at bedtime

Acute angle-closure glaucoma

  • 1 gtt of 2% solution in the affected eye every 5-10 mins for 3-6 doses, followed by 1 drop every 1-3 hours until pressure is controlled


Open-angle glaucoma

  • 1-2 gtt of 1.5-3% solution 3 times a day

Diuretic, osmotic

  • Mannitol


  • Increases the osmotic pressure of glomerular filtrate, which inhibits tubular reabsorption of water and solutes and increases urinary output
  • It increases the excretion of Sodium, Potassium, Chloride, Calcium, Phosphorus, Lithium, Magnesium, Urea, and Uric acid



Reduction of intraocular pressure

  • 1.5-2 g/kg IV as a 15-25% solution over 30-60 minutes

Laxative, Osmotic

  • Glycerol


  • Osmotic dehydrating agent increases osmotic pressure
  • It draws fluid into lumen and also from the extravascular spaces into intravascular compartment
  • It also irritates luminal mucosa and increases peristalsis



Reduction of intraocular pressure

  • 1-1.8 g/kg PO1-11/2 hours preoperatively; may administer additional doses at 5 hour intervals

Fixed-combination preparations, (ophthalmic)


  • Dorzolamide/Timolol
    • 1 gtt BID into affected eye(s)
  • Brinzolamide/Timolol
    • 1 gtt BID into affected eye(s)
  • Latanoprost/Timolol
    • 1 gtt daily into affected eye(s)
  • Travoprost/Timolol
    • 1 gtt once every morning into affected eye(s)
  • Brimonidine/Timolol
    • 1 gtt BID into affected eye(s)
Diagnosis and Goals:
  • Incomplete information about the disease and treatment/procedures
  • Acute pain related to increased IOP
  • Post-procedure pain and erythema
  • Fear related to pain and potential loss of vision
  • Non-compliance
  • Risk of injury
  • Self-care deficits


    • Maintain eye comfort lower the intraocular pressure (IOP) to the target level
    • The target value is based on the degree of advancement of the disease
    • No progression of visual impairment
    • Prevent, or slow progressive visual loss
    • Preserve the structure and function of the optic nerve
  • Patient understands disease process and rationale for therapy
  • Eliminate pain and improve vision in acute forms
  • Prevent central retinal artery occlusion
  • Achieve maximum effect with the minimum required drugs
  • Patient’s complies with all aspects of therapy
Nursing Intervention:

Once the diagnosis is confirmed, regular follow up to review the changes within the eye is required.

Nursing management and assessment

  • Assess client’s ability to understand and comply with treatment
  • Assess client’s psychological reaction to sight-threatening disorder
  • Assess family for client care
  • Assess visual acuity, visual fields, IOP

Providing information about glaucoma:

  • Asymptomatic patients may have increased IOP and damage to the eye, so treatment and follow up visits are essential
  • Proper administration techniques of eyes drops should be taught – encourage to follow therapeutic regimen and follow-up recommendations
  • Information about purpose, frequency, and technique for administration of prescribed antiglaucoma agents
  • Provide both verbal and written instructions
  • Discuss the visual defects, and ways to compensate in daily routine
  • Inform patient that blindness is irreversible, and the treatment is aimed to stop disease progression – provide information about the disease process and treatment options, including rationales
  • Health promotion
    • Teach client and family risks of glaucoma
    • Stress importance of early detection
    • Ophthalmological examination
  • Surgery is done on outpatient basis and recovery is quick, with no prolonged restrictions
    • Patient should be informed of head elevation to 30 degrees is required to promote drainage after trabeculectomy
    • Patient should know that additional medications will be advised, including topical steroids and cycloplegics to decrease inflammation and to dilate the pupils
  • In acute angle closure glaucoma pain related to increased IOP and potential loss vision within 2-3hrs to days is an acute ophthalmic emergency which patient should be aware of.

Relieving pain:

  • Immediately notify pain to the physician, if severe go to the ER
  • Acute Intervention
  • Darken the environment
  • Apply cool compresses
  • Provide quiet space
  • Opioids with antiemetics and other medications as directed are given immediately
  • Patient should know that reduction in IOP is the main goal as quickly as possible
  • If procedures are advised, those should be explained and discussed with the patient
  • Reassure the patient in terms of reduction of IOP, pain and relieve of other signs and symptoms
  • Explain the side effects of mannitol, acetazolamide, and pilocarpine, as mentioned above

Relieving fear:

  • Provide assurance and calm patient to reduce the anxiety and fear
  • Prepare patient for surgery if required
  • Describe the procedure and cautions to be taken after surgery
    • Patch will be worn for several hours
    • Sunglasses would be advised (photophobia)
    • Vision would be blurred for a few days after surgery
    • Frequent follow-ups with Tonometry to make sure the pressure is in control would be necessary
    • Medications are to be discussed in detail post-procedure

Patient education and health maintenance:

  • Patient should always remember glaucoma cannot be cured but controlled
  • Stress the importance of long term medication use
  • Stress on being compliant with the drugs and follow up visits – encourage the client to follow therapy
  • Demonstrate and teach the technique of installation of all medications and ointments
  • Instruct patient to seek immediate medical attention if experience
    • Severe eye pain
    • Photophobia
    • Excessive lacrimation
  • Teach the patient the action, dosage, and side effects of all medications.
    • Timolol and betaxolol may cause irritation, decreased corneal sensitivity, and blurred vision. Gentle handling of the eye is recommended. Headaches, palpitation, hypotension are other effects which may occur
    • Pilocarpine, causes poor vision, and may cause hypertension and tachycardia
    • Acetazolamide and methazolamide, patient should be aware of and take a lot of fluids, it causes drowsiness, anorexia and upset stomach, in rare cases kidney and liver dysfunction may ensue
  • Patient should:
    • Know the desired measurement of their IOP
    • Be aware of the extent of optic nerve damage and vision loss
    • Maintain record of IOP and monitor progress
    • Have the dosing schedule and the medication information written to keep a check
    • Always review all the medications with the physician in every follow-up
  • Avoid use of medication that may increase IOP, by informing all the other health care providers
  • Avoid emotional upsets like worry, fear, and anger
  • Avoid exertion like snow shoveling, pushing and lifting heavy objects
  • Maintenance of regular bowel
  • Wearing medical identification tag that indicates the patient has glaucoma

Evaluation: Expected patient outcomes

  • Pain is decreased
  • No pain from disease and surgery
  • No further loss of vision
  • Comply with recommended therapy
  • Safely function in environment
  • Have a clear knowledge of treatment and expresses less disease fear
  • Demonstrate proper installation of ophthalmic medication
  • Have knowledge of adverse effects
Nursing Alerts:
  • Acute angle closure glaucoma is a medical emergency and requires immediate treatment, if left untreated causes irreversible blindness in less than a week
  • Dilatation is avoided if the anterior chamber is shallow
  • Developing asymptomatic glaucoma is not unusual, so recommending patients of all ages to have an eye examination that includes measurement of IOP (tonometry) to facilitate early detection is encouraged
  • Monitor for the risk of developing bradycardia (by checking vital signs), if the patient is already on beta-blockers for cardiovascular disease and has also been prescribed the same medication for topical use in glaucoma


Core Resources:

  • Allingham RR, Damji KF, Freedman S, et al (2005) Shields’ Textbook of Glaucoma (5thed.) Philadelphia: Lippincott Williams & Wilkins
  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist Association. Toronto: Webcom Inc. 2012
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  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th ed. Toronto: Webcom Inc. 2011
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  • Kopczynski CC, Heah T; Netarsudil ophthalmic solution 0.02% for the treatment of patients with open-angle glaucoma or ocular hypertension; drugs Today (Barc). 2018;54(8):467-478. doi: 10.1358/dot.2018.54.8.2849627
  • Leary KA, Lin K‐T, Steibel JP, et al. Safety and efficacy of topically administered netarsudil (Rhopressa™) in normal and glaucomatous dogs with ADAMTS10‐open‐angle glaucoma (ADAMTS10‐OAG). Vet Ophthalmol. 2019; 00: 1– 12.
  • Liu Y, Mao W. Tafluprost once daily for treatment of elevated intraocular pressure in patients with open-angle glaucoma. Clin Ophthalmol. 2013;7:7‐14. doi:10.2147/OPTH.S30951
  • Longo D, Fauci A, Kasper D, et al (eds). Harrison’s Principles of Internal Medicine. 18thed. New York: McGraw-Hill; 2011
  • McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th ed. New York: McGraw-Hill; 2010
  • Ney JJ. Glaucoma Diagnosis and Treatment: The Role of the Ophthalmic Nurse. Insight. 2016;41(1):13-17
  • Pagana KD, Pagana TJ eds. Mosby’s Diagnostic and Laboratory Test Reference. 9th ed. St. Louis: Elsevier-Mosby; 2009
  • Rafuse PE, Buys YM, Damji KF, et al. Canadian Ophthalmological Society Glaucoma Clinical Practice Guideline Expert Committee. Canadian Ophthalmological Society Glaucoma Clinical Practice Guideline for the management of glaucoma in the adult eye. Can J Ophthalmol 2009;44:S7-93
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Online Pharmacological Resources:

  • e-therapeutics
  • Lexicomp
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Journals/Clinical Trials:

  • Chauhan BC, Mikelberg FS, Balaszi AG, et al; Canadian Glaucoma Study Group. Canadian Glaucoma Study: 2. Risk factors for the progression of open-angle glaucoma Arch Ophthalmol. 2008 Aug; 126(8):1030-6
  • Francis BA, Singh K, Lin SC, et al. Novelglaucoma procedures: a report by the American Academy of Ophthalmology. Ophthalmology 2011; 118: 1466-80
  • Greco A, Rizzo MI, De Virgilio A, et al. Emerging Concepts in Glaucoma and Review of the Literature. The American Journal of Medicine. 2016;129(9):1000.e7-1000.e13. doi: 10.1016/j.amjmed.2016.03.038
  • Heijl A, Peters D, Leske MC, et al. Am J Ophthalmol.2011; 152: 842-8
  • Iyigun E, Tastan S, Ayhan H, et al. Life Experiences of Patients With Glaucoma: A Phenomenological Study. J Nurs Res. 2017;25(5):336-343. doi:10.1097/JNR.0000000000000172
  • Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002; 120:701-13
  • Van Buskirk EM, Weinreb RN, Berry DP, et al. Betaxolol in patients with glaucoma and asthma. Am J Ophthalmol. 1986 May 15;101:531-4
  • Waterman H, Bull S, Shaw M, et al. Group-based patient education delivered by nurses to meet a clinical standard for glaucoma information provision: the G-TRAIN feasibility study. Pilot and Feasibility Studies 4, 121 (2018).