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GLAUCOMA-3.pptx, pathophysiology and its management

Glaucoma refers to the increase in intraocular pressure leading to optic nerve damage and subsequent visual loss

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12/18/2025 1 GLAUCOMA Gifty Mamle DOKU Andrews Kwarteng Sarpong Mohammed Gyimah
12/18/2025 2 Introduction  Glaucoma, a group of optic neuropathies characterized by progressive degeneration of retinal ganglion cells.  Retinal ganglion cells are central nervous system neurons that have their cell bodies in the inner retina and axons in the optic nerve.  Degeneration of these nerves results in cupping, a characteristic appearance of the optic disc and visual loss.  The biological basis of glaucoma is poorly understood and the factors contributing to its progression have not been fully characterized
12/18/2025 3 Epidemiology According to the American Academy of Ophthalmology(2024), Glaucoma is the leading cause of irreversible blindness worldwide. Glaucoma affects more than 70 million people worldwide with approximately 10% being bilaterally blind, making it the leading cause of irreversible blindness in the world. In Ghana, about 900, 000 people were living with glaucoma as at 2020 and over 19 per cent of blindness in Ghana is due to glaucoma.
12/18/2025 4 EPIDERMIOLOGY CONT’D  Glaucoma can remain asymptomatic until it is severe, resulting in a high likelihood that the number of affected individuals is much higher than the number known to have it.  Population-level surveys suggest that only 10% to 50% of people with glaucoma are aware they have it.
12/18/2025 5 Classification Glaucoma can be classified into 2 broad categories: Primary Open angle glaucoma Angle closure glaucoma With pupillary block Without pupillary block Secondary Secondary glaucoma can result from trauma, certain medications such as corticosteroids, inflammation, tumor, or conditions such as pigment dispersion or pseudo-exfoliation.
12/18/2025 6 Anatomy of the eye
12/18/2025 7 DRAINAGE PATHWAY OF AQUEOUS HUMOUR Aqueous humour is produced by 3 mechanisms  Active secretion(independent on IOP levels)  Ultrafiltration(influenced by the level of IOP)  Passive diffusion of ions There are 2 routes of aqueous outflow  80-90% trabecular mesh into the schlems canal and into venous circulation by the aqueous veins.  Uveoscleral pathway accounting for only 10-20% describes the outflow of the aqueous humour through the ciliary body into the suprachoroidal space, finally leaving the eye through the sclera.
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12/18/2025 9 Pathophysiology of Primary Open-Angle Glaucoma (POAG)  Although the pathogenesis of glaucoma is not fully understood, the level of intraocular pressure is related to retinal ganglion cell death. The axons of the retinal ganglion cells passes through the retina and through the lamina cribrosa to form the optic nerve head.  Raised IOP causes deformation of the lamina cribrosa with damage to the retinal ganglion cells and subsequent cell death.  Other pressure independent factors such as impaired vascular supply, low CSF pressure also influence glaucomatous progression. These factors are more significant in Normal Tension Glaucoma.
12/18/2025 10 Pathophysiology of Primary Open-Angle Glaucoma (POAG)  In patients with open-angle glaucoma, there is increased resistance to aqueous outflow through the trabecular meshwork usually due to age related factors.  In contrast, the access to the drainage pathways is obstructed due to closure of the iridocorneal angle in patients with angle-closure glaucoma. It occurs in anatomically predisposed eyes with increased lens size, shallower anterior chamber and shorter axial length. The lens continues to grow throughout life, thereby bringing its anterior surface to the cornea.
12/18/2025 11 PATHOPHYSIOLOGY CONT’D…  optic nerve damage in POAG can occur at a wide range of IOPs, and the rate of progression is highly variable.  Patients may exhibit pressures in the 20 to 30 mmHg (2.7-4.0 kPa) range for years before any disease progression is noticed in the optic disk or visual fields.  That is why POAG is often referred to as the “sneak thief of sight.  Glaucomatous optic neuropathy can occur in individuals with intraocular pressures within the normal range.  In such patients, primary neural pathological processes may cause secondary neuro-degeneration of other retinal neurons and cells in the central visual pathway by altering their environment and increasing susceptibility to damage
12/18/2025 12 Risk factors • Older age >40 • Family history of glaucoma • African, Hispanics or Asian heritage • Use of systemic or topical corticosteroids • High intraocular pressure • Eye injury • Thin cornea in the center • Diabetics • Migraine • High blood pressure • Far sightedness or near sightedness.
12/18/2025 13 Clinical presentation General  Glaucoma can be detected in otherwise asymptomatic patients, or patients can present with characteristic symptoms, especially vision loss.  Primary open-angle Glaucoma (POAG) is a chronic, slowly progressive disease found primarily in patients older than 50 years of age, whereas primary angle-closure glaucoma (PACG) is more typically associated with symptomatic acute episodes or may be slowly progressive like POAG
12/18/2025 14 OPEN ANGLE GLAUCOMA Symptoms  Bilateral and often asymmetric  Elevated intraocular pressure*  Optic nerve damage  Vision loss Note: No symptoms until substantial visual field loss occurs. Signs  Disk changes and visual field loss; IOP can be normal or elevated (>21 mm Hg [2.8 kPa]) 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.
12/18/2025 15 Angle closure glaucoma Symptoms • Hazy or blurred vision • The appearance of rainbow-colored circles around bright lights • Severe eye and head pain • Nausea or vomiting (accompanying severe eye pain) • Sudden sight loss • In contrast with open-angle glaucoma, symptoms of acute angle-closure glaucoma are very noticeable and damage occurs quickly. Signs • Acute, hyperemic conjunctiva, • cloudy cornea, • shallow anterior chamber, • and occasionally an edematous and hyperemic optic disk; • IOP is generally elevated markedly (40-90 mm Hg [5.3-12.0 kPa]) when symptoms are present.
12/18/2025 16 Diagnosis  A Comprehensive Glaucoma Exam  To be safe and accurate, these factors should be checked before making a glaucoma diagnosis:  To be safe and accurate, five factors should be checked before making a glaucoma diagnosis: Name of Test Description Tonometry The inner eye pressure Ophthalmoscopy (dilated eye exam) The shape and color of the optic nerve (optic disk changes) Perimetry (visual field test) The complete field of vision Gonioscopy The angle in the eye where the iris meets the cornea Pachymetry Thickness of the cornea Optic coherence tomography and Optic coherence tomography angiography. It takes cross section pictures of the retina
12/18/2025 17 DIAGNOSIS CONT’D  The presence of characteristic disk changes and visual field loss with or without increased IOP confirms the diagnosis of glaucoma.  Typical disk changes and field loss occurring at an IOP of less than 21 mm Hg (2.8 kPa) account for 20% to 30% of patients and are 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 ocular hypertension.
12/18/2025 18 DIFFERENTIAL DIAGNOSIS  Angle-Recession glaucoma  Anterior ischemic optic neuropathy(AION)  Aphakic and pseudophakic glaucoma  Compressive optic neuropathy  Drug-induced glaucoma  Juvenile glaucoma  Low tension glaucoma etc.
12/18/2025 19 Management Goals of therapy  Reduction of intraocular pressure  Slowing disease progression  preservation of quality of life
12/18/2025 20 MANAGEMENT CONT’D  Reduction of intraocular pressure (IOP) is the only proven method to treat glaucoma.  Current management guidelines from the American Academy of Ophthalmology Preferred Practice Pattern recommend lowering the intraocular pressure toward a target level.  Target intraocular pressure levels for a particular eye are established from pretreatment pressure levels that were associated with retinal damage, the severity of damage, risk factors for progression, life expectancy, and potential for adverse effects from treatment.
12/18/2025  In general, the initial target aims for a 20% to 50% reduction in pressure; however, the target pressure needs to be continuously reassessed during patient follow-up, depending on the evolution of the disease  The target intraocular pressure should be achieved with the fewest medications and minimum adverse effects.  Medication choice may be influenced by cost, adverse effects, and dosing schedules.  Risk factors such as family history of glaucoma, black/Hispanic ethnicity, severe myopia, and patients with only one eye must also be taken into consideration when deciding which individuals need treatment. 21
12/18/2025 22 Pharmacotherapeutic Approach Medications most commonly used to treat glaucoma are  the prostaglandin analogs,  nonselective β-blockers,  α2 –Adrenergic agonist,  topical carbonic anhydrase inhibitors (CAIs), (Brinzolamide, dorzolamide)  Parasympathomimetics
12/18/2025 23 CLASSIFICATION OF THE THERAPEUTIC AGENTS ACCORDING TO DECREASE PRODUCTION AND INCREASE OUTFLOW OF AQUEOUS HUMOUR Increase aqueous humour outflow  Topical Prostaglandins analogues e.g. Latanoprost, tafluprost,travuprost  Topical Prostamides e.g. bimatoprost  Topical miotics  E.g. pilocarpine Nb;Alpha-2 adrenergic agonists have effect on both mechanisms by increasing aqueous humour outflow and decrease aqueous humour production Decrease aqueous humour production  Topical beta blockers Eg. Timolol, Betaxolol  Topical and Oral Carbonic Anhydrase Inhibitors Eg. Dorzolamide , brinzolamide, acetazolamide(oral)
12/18/2025 24  Recently introduced effective and acceptable safety profiles include latonoprostene bunod and netarsudil.  The prostaglandin analogs are often recommended as first-line therapy (American Academy of Ophthalmology, Nov 2024).  They offer once-daily dosing, better IOP reduction, better 24-hour IOP control, good tolerance, and availability of lower-cost generics.
12/18/2025 25 β-Adrenergic Blockers  Ophthalmic β-adrenergic antagonists block the β-adrenergic receptors in the ciliary epithelium of the eye and lower IOP primarily by decreasing aqueous humor production. On average, β-blockers decrease IOP by 20% to 35% depending on the strength used and the frequency of administration. Drug Dose Side effects Timolol 0.25% (Timoptic) 1 drop bid reduction of resting pulse rate , worsening of heart failure, and adverse pulmonary effects, uveitis and corneal anesthesia. Levobunolol (Betagan) 0.5% and 1% 1 drop bid Carteolol (Ocupress) 1% and 0.25% 1 drop bid Betaxolol (Betoptic)
12/18/2025 26 Prostaglandin Analogs  The prostaglandin analogs increase uveoscleral outflow of aqueous humor and, thereby, decrease IOP . 35 These agents often are prescribed as first-line agents for the treatment of POAG because they are at least as effective as the β-blockers, can be administered once a day, and are associated with minimal systemic adverse effects. Drug Dose Side effects Lantanoprost (xalatan) 0.005% 1 drop at bedtime eyelash thickening, pigmentation, and misdirected growth; hypertrichosis conjunctival hyperemia, ocular irritation; superficial punctate keratitis Travoprost (Travatan z)0.004% 1 drop at bedtime increased iris pigmentation and eyelash changes. Bimatoprost (Lumigan) 0.03% 1 drop od/bid conjunctiva hyperemia
12/18/2025 27 α2 -Adrenergic Agonists  α2 -Adrenergic agonists appear to lower IOP by reducing aqueous inflow via an a-mediated vasoconstriction in the ciliary body and increased outflow due to the dilation of the aqueous and episcleral veins.  Apraclonidine (Iopidine) and brimonidine (Alphagan) are selective α2 - adrenergic agonists similar to clonidine.  Apraclonidine is less lipophilic than clonidine and brimonidine, does not cross the blood–brain barrier as readily, and theoretically has fewer systemic side effects (e.g., hypotension, decreased pulse, dry mouth).  Brimonidine is more highly selective for α2 -adrenergic receptors than clonidine or apraclonidine and, theoretically, should be associated with fewer ocular side effects.
12/18/2025 28 α2 -Adrenergic Agonists Drug Dose Side effects Apraclonidine (Iopigan) 0.5%,1% 1drop preoperatively and postoperatively or 1 drop BID to TID burning, stinging, blurring, conjunctival follicles, hyperemia, pruritus, edema of the lid and conjunctiva, and foreign body sensation. Brimonidine (Alphagan) 0.5%,0.2% 1drop BID to TID dry nose and mouth, mild hypotension, decreased pulse, and lethargy
12/18/2025 29 Carbonic Anhydrase Inhibitors  Carbonic anhydrase occurs in high concentrations in the ciliary processes and retina of the eye. Carbonic anhydrase inhibitors (CAIs),I, II, IV are present in ocular tissues. In the ciliary epithelium, inhibition of CA-II slows the formation of bicarbonate ions and their secretion into the posterior chamber of the eye. This reduces bicarbonate, sodium, and water into the posterior chamber of the eye, resulting in a 40% to 60% decrease in aqueous humor secretion.  Topical CAIs are excellent alternatives to β-blockers in the initial management of elevated IOPs, and are effective as adjunctive agents.  Systemic CAIs(eg. Acetazolamide) are indicated for patients failing to respond to or tolerate maximum topical therapy.  Oral CAIs reduce aqueous humor inflow by 40% to 60% and IOP by 25% to 40%.
12/18/2025 30 Drug (Topical) Dose Side effects Brinzolamide (Azopt) 1% 1 drop TID Dorzolamide (Trusopt) 2% 1 drop TID Systemic and topical CAIs should not be used in combination because no data exist concerning improved IOP reduction, and the risk for systemic adverse effects is increased.
12/18/2025 31 Parasympathomimetic Agents  The parasympathomimetic (cholinergic) agents reduce IOP by increasing aqueous humor trabecular outflow.  The increase in outflow is a thought to be a result of physically pulling open the trabecular meshwork secondary to ciliary muscle contraction, thereby reducing resistance to outflow. These agents may actually reduce uveoscleral outflow.  Their use as primary or even adjunctive agents in the treatment of glaucoma has decreased significantly because of local ocular adverse effects and/or frequent dosing requirements.  Pilocarpine, the parasympathomimetic agent of choice in POAG.
12/18/2025 32 Drug Dose Side effects Pilocarpine (Isopto Carpine)1%,2%,4% 1-2 drops TID or QID Carbachol (Isopto Carbachol) 1.5%, 3% 1-2 drops TID or QID Echothiophate iodide (phospholine iodide)0.125% 1 drop BID
12/18/2025 33  Initial IOP response does not predict long-term IOP control, as tachyphylaxis to IOP reduction and or disease progression may occur.  The value of an agent with which the patient has shown a drop in IOP following an initial response can be measured by discontinuing the medication completely and determining if an increase in IOP occurs.
12/18/2025 34  Patients responding to but intolerant of initial therapy may be switched to another drug. For patients failing to respond to an initial drug, a switch to an alternative agent should be considered.  If only a partial response occurs, addition of another topical drug to be used in combination is a possibility.  A number of drugs or drug combinations may need to be tried before an effective and well-tolerated regimen is identified.
12/18/2025 35  Prostaglandin agonists, beta blockers, brimonidine, CAI, and pilocarpine may be used in various combinations. • Brimonidine tartrate 0.2%/Timolol 0.5%(Combigan) • Dorzolamide 2%/Timolol 0.5% (Cosopt) • Brinzolamide 1%/ Brimonidine 0.2% (Simbrinza)  Generally adding a second drug results in a less than additive reduction in IOP. Using more than one drop per dose does not improve response, and it increases the likelihood of adverse effects and the cost of therapy.
12/18/2025 36  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.  Combination products reduce the number of daily doses, possibly improving adherence and preventing washout effect seen when a second medication is administered too soon after the initial medication.  Use of combination products also reduces exposure to ophthalmic preservatives.
12/18/2025 37  Ocular surface disease (OSD) secondary to glaucoma therapy will often manifest as superficial punctate keratitis, tear-film instability, or allergy  Patients with medication-related OSD may try treatment with artificial tears, anti- inflammatory therapy, or possibly preservative-free therapy if feasible.  The IOP response to ocular hypotensive medication may vary with corneal thickness.  The response might be better in those with normal or thin corneas than in those with thicker structures.  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.
12/18/2025 38 Algorithm for the pharmacotherapy of open-angle glaucoma(NICE Guidelines).
12/18/2025 39 Medical management (AAOO Guideline) 1st-line Therapy Prostaglandin analogues(PGA’S); Commonly used as first-line monotherapy Second-line therapy, given with beta blockers, topical CAIs or Brimonidine Alternative 1st -line therapy Alpha-2 selective adrenergic agonist; Brimonidine Alternative to beta blockers or PGAs as monotherapy Second-line therapy is given with beta blockers, Lantanoprost or topical CAIs lerance to side effects ach NLO to minimize stemic side effects if not being done witch to alternative ents within the drug class(eg Betaxolol, Brinzolamide) Therapeutic goal not achieved Access compliance Teach NLO to optimize therapeutic effect Alternative 1st -line therapy Topical carbonic anhydrase inhibitors; Dorzolamide or Brinzolamide Alternative to beta blockers or PGAs as monotherapy Second-line therapy is given with beta blockers ,sympathomimetics , lantanoprost and cholinergic agents. Change to fixed combination products Timolol/Dorzolarmides (Cosopt) Timolol/Brimonidine (combigan) Add a second topical agent PGAs/Lantanoprost, brimonidine, or topical carbonic anhydrase Pilocarpine/Carbacol Increase concentra tion Switch to alternative 1st -line agent If therapeutic goal is not achieved Increase concentration of the second topical agent Change pilocarpine/ carbachol to cholinersterase inhibitor If therapeutic dose is not achieved , increase the dose of thr cholinesterase inhibitor 1st -line therapy Betablockers; Commonly used as first line monotherapy Nonselective agents appear to be most effective to decrease IOP
12/18/2025 40 Nonpharmacologic Therapy: Laser and Surgical Procedures  laser trabeculoplasty (argon or selective) or  trabeculectomy (filtering procedure)  Laser trabeculoplasty is usually an intermediate step between drug therapy and trabeculectomy.  Recent studies have demonstrated good efficacy for this procedure in comparison with medical treatment options for POAG.
12/18/2025 41 Acute Angle-Closure Crisis (AACC)  The goal of initial therapy for AACC with high IOP is rapid reduction of the IOP to preserve vision and to avoid surgical or laser iridectomy on a hypertensive, congested eye.  Iridectomy (laser or surgical) is the definitive treatment of PACG  Drug therapy of an AACC typically involves 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.
12/18/2025 42  The miosis produced by pilocarpine pulls the peripheral iris away from the meshwork. However, miotics may worsen angle closure by increasing pupillary block and producing anterior movement of the lens because of drug-induced accommodation.  The aqueous secretory inhibitors and pilocarpine may not be effective due to ischemia of the ciliary body and pupillary sphincter, respectively.
12/18/2025 43  A hyperosmotic agent such as mannitol or glycerin may be needed to temporarily reduce IOP and restore response to the topical agents.  An osmotic agent also is commonly administered because these drugs produce the most rapid decrease in IOP.  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.  Osmotic agents reduce IOP by withdrawing water from the eye secondary to the osmotic gradient between the blood and the eye.
12/18/2025 44  These drugs are among the first-line agents in the short-term treatment of an AACC or other forms of acute very high IOP elevations.  Topical corticosteroids often are used to reduce the ocular inflammation and reduce the development of synechiae in PACG eyes.  Patients failing therapy altogether will require an emergency iridectomy. Once the IOP is controlled, iridectomy is performed on the affected eye as well as the contralateral eye (if narrow angles are present).
12/18/2025 45  Peripheral iridectomy essentially “cures” PACG without significant synechiae.  Long-term drug therapy is not used unless IOP remains high because of the presence of synechiae blocking the trabecular meshwork or concurrent POAG.  In such cases, the pharmacotherapeutic approach is essentially identical to that for the POAG patient, or laser or surgical procedures are performed.
12/18/2025 46 Patient counseling Patients should be taught the following procedure:  Wash and dry the hands;  shake the bottle if it contains a suspension.  With a forefinger, pull down the outer portion of the lower eyelid to form a “pocket” to receive the drop.  Grasp the dropper bottle between the thumb and fingers with the hand braced against the cheek or nose and the head held upward.  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.  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.  Recap bottle and store as instructed
12/18/2025 47  Use of more than one drop per dose increases costs, does not improve response significantly, and may increase adverse effects.  When two drugs are to be administered, instillations should be separated by at least 5 minutes (preferably 10 minutes) to prevent the drug administered first from being washed out.  The patient should be taught not to touch the dropper bottle tip with eye, hands, or any surface.  Eyelid closure (ELC) also should be used to improve ocular bioavailability and reduce systemic absorption.  The patient induces ELC for 5 minutes by gently closing the eyes. ELC decreases nasolacrimal drainage of drug, thereby decreasing the amount of drug available for systemic absorption by the nasopharyngeal mucosa.  The use of ELC may improve drug response significantly, reduce adverse effects, and allow less- frequent dosing intervals and the use of lower drug concentrations
12/18/2025 48 REFERENCES  Kelvin McKinney, Anju Goyal et al , understanding Glaucoma, symptoms ,causes, treatment. American Academy of Ophthalmology (2024).  Rakofsky SI et al. A comparison of the ocular hypotensive efficacy of once-daily and twice-daily levobunolol treatment. Ophthalmology. 1989;96:8. Berson FG et al. Levobunolol compared with timolol for the long-term control of elevated intraocular pressure. Arch Ophthalmol. 1985;103:379.  American Academy of Ophthalmology. Primary open-angle glaucoma, preferred practice pattern. San Francisco, CA: American Academy of Ophthalmology, 2024. http://www.aao.org/ppp.  National Institute for Health and Care Excellence, management of ocular hypertention 2022.  Riordan-Eva P, Whitcher JP, eds. Vaughan and Ashbury’s General Ophthalmology. 18th ed. New York, NY: McGraw-Hill Professional; 20011.  Tham YC et al. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta- analysis. Ophthalmology. 2022;121(11):2081–2090.  Glaucoma Facts and Stats. Glaucoma Research Foundation. May 5, 2015. http://www.glaucoma.org/glaucoma/glaucoma-facts-and-stats.php. Accessed December 2015.  Gordon MO et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:714.  Battershill PE, Sorkin EM. Ocular metipranolol: a preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in glaucoma and ocular hypertension. Drugs. 1988;36:601.
12/18/2025 49 THANK YOU