Special Senses & Otolaryngology

Open-angle glaucoma: screening and management

Clinical Overview and When to Suspect Open-Angle Glaucoma

— Age >40, especially with positive family history (first-degree relative confers 4–9× risk)

— African or Hispanic ancestry

— Type 2 diabetes, hypertension, migraine, obstructive sleep apnea, high myopia

— Chronic corticosteroid use (topical, inhaled, intranasal, systemic)

— History of ocular trauma, uveitis, or pseudoexfoliation syndrome

— Incidental finding of elevated IOP or cup-to-disc ratio >0.5 on routine eye exam

Board pearl: Step 3 stems often describe a middle-aged Black patient with a father who "went blind from glaucoma" and an asymptomatic IOP of 24 mmHg on routine optometry — the answer is refer to ophthalmology for comprehensive evaluation, not start drops empirically. Primary care never initiates glaucoma therapy without optic nerve and visual field confirmation by an eye specialist.

Key distinction: POAG is painless and bilateral (often asymmetric); acute angle-closure is unilateral, painful, with red eye and halos — a true ocular emergency, not the same disease pathway.

Primary open-angle glaucoma (POAG) is a chronic, progressive optic neuropathy characterized by retinal ganglion cell loss, characteristic optic nerve head cupping, and corresponding visual field defects — typically in the setting of an open, normal-appearing anterior chamber angle.

Leading cause of irreversible blindness in the US; second leading cause overall after age-related macular degeneration. Disproportionately affects Black and Hispanic Americans, who develop it earlier and more aggressively.

Pathophysiology centers on trabecular meshwork outflow resistance → elevated intraocular pressure (IOP) → mechanical and vascular damage at the lamina cribrosa. However, up to one-third of POAG occurs at "normal" IOP (≤21 mmHg) — so-called normal-tension glaucoma.

When to suspect in primary care:

Symptoms are typically absent until late disease — peripheral visual field is lost first, central acuity preserved until end-stage. Patients rarely complain spontaneously; detection is screening-driven.

Presentation Patterns and Key History

— Bumping into doorframes, missing curbs, difficulty driving at night

— Trouble in dim restaurants or theaters (poor dark adaptation)

— "Missing" words while reading, frequent prescription changes

— Falls in the elderly — glaucoma roughly doubles fall risk

— Family history of glaucoma or blindness (first-degree relatives)

— Race/ethnicity — Black patients develop POAG ~10 years earlier and have 3–4× the prevalence of White patients

— Steroid exposure — inhaled fluticasone for asthma, intranasal sprays, joint injections, chronic prednisone, even dermatologic steroids near the eye

— Refractive history — high myopia is a POAG risk factor; high hyperopia is an angle-closure risk

— Cardiovascular: hypertension (especially nocturnal hypotension from overtreatment), diabetes, OSA, Raynaud/migraine (vasospastic phenotype suggests normal-tension glaucoma)

— Trauma, uveitis, prior intraocular surgery

— Sickle cell disease — alters management because beta-blocker drops and certain procedures carry risk

— Adherence barriers — cost, dexterity (arthritis), cognition, vision needed to instill drops

Step 3 management: When a patient on chronic inhaled corticosteroids reports new visual blurring, screen for steroid-induced ocular hypertension — refer for IOP measurement and optic disc evaluation. Do not stop the inhaler unilaterally; coordinate with pulmonology/allergy on the lowest effective dose while ophthalmology manages IOP.

Board pearl: Asymptomatic elevated IOP without nerve damage = ocular hypertension, not glaucoma — treatment is individualized based on the OHTS risk calculator, not automatic.

POAG is insidious and asymptomatic for years. Visual loss begins in the mid-peripheral arcuate (Bjerrum) area, progresses to nasal steps, then tunnel vision, and finally central loss.

Patients may report — usually only in moderate-to-advanced disease:

No pain, no redness, no halos, no acute vision change — those features should redirect you toward angle closure, uveitis, or optic neuritis.

Key history elements to elicit in a Step 3 ambulatory visit:

Physical Exam Findings and Office Assessment

— Visual acuity each eye with correction (Snellen at 20 feet or handheld card)

— Confrontation visual fields — gross test; insensitive but cheap. Asymmetric peripheral defects raise suspicion.

— Pupillary exam — a relative afferent pupillary defect (RAPD) in asymmetric glaucoma signals advanced optic nerve damage on the affected side

— External eye — quiet, white eye; no injection, no corneal edema (distinguishes from angle closure)

— Direct ophthalmoscopy through an undilated pupil — look at the optic disc:

– Cup-to-disc ratio >0.6, or asymmetry >0.2 between eyes

– Thinning or notching of the neuroretinal rim (especially inferotemporal/superotemporal — the ISNT rule is violated: normally Inferior ≥ Superior ≥ Nasal ≥ Temporal rim thickness)

– Disc hemorrhages (Drance hemorrhages) — splinter hemorrhages at the disc margin, highly specific for progressing glaucoma

– Bayoneting of vessels, nerve fiber layer defects, peripapillary atrophy

CCS pearl: On a CCS case of an asymptomatic 55-year-old Black man with a cupped disc on funduscopy, order "Ophthalmology consultation" and "Visual field testing" — do not order acetazolamide, pilocarpine, or laser iridotomy. Those belong to angle-closure pathways.

Key distinction: A pale, atrophic disc with normal cup suggests optic neuropathy from another cause (ischemic, compressive, demyelinating). Glaucoma causes cupping with rim thinning — the disc tissue is excavated, not just pale.

The primary care exam in glaucoma is limited but purposeful — definitive diagnosis requires ophthalmology. Document:

Tonometry — Goldmann applanation is the gold standard (ophthalmology); primary care offices may use iCare rebound or Tono-Pen. Normal IOP 10–21 mmHg, but IOP varies diurnally by 3–6 mmHg and a single reading is insufficient.

Gonioscopy — performed only by eye care providers; confirms the angle is open (vs. closed/narrow), which is what defines POAG.

Diagnostic Workup — Initial Evaluation and Screening

— Baseline at age 40 for all adults

— Every 1–2 years after age 65

— Every 1–2 years starting at age 40 (or earlier) for high-risk groups: Black, Hispanic, family history, diabetes, chronic steroid use, high myopia, prior ocular trauma

— Goldmann applanation tonometry — IOP measured on multiple visits; account for central corneal thickness (CCT) — thin corneas underestimate true IOP and are an independent risk factor for progression

— Pachymetry — measures CCT; thin CCT (<555 µm) substantially increases POAG risk per the Ocular Hypertension Treatment Study (OHTS)

— Gonioscopy — confirms open angle, excludes secondary causes (pseudoexfoliation, pigment dispersion, neovascular)

— Dilated fundus exam with stereoscopic disc evaluation and disc photography for baseline

— Standard automated perimetry (Humphrey 24-2 or 30-2 visual field) — detects functional defects: nasal step, arcuate scotoma, paracentral defects, eventual tunnel vision

— Optical coherence tomography (OCT) of the retinal nerve fiber layer (RNFL) and ganglion cell complex — detects structural loss often before visual field changes

Board pearl: Diagnosis of POAG requires characteristic optic nerve damage + corresponding visual field defect + open angle on gonioscopy. IOP elevation supports but is not required — normal-tension glaucoma exists.

There is no recommended universal population glaucoma screening in primary care. The USPSTF (2022) concluded insufficient evidence (I statement) for screening asymptomatic adults for primary open-angle glaucoma — neither for nor against.

However, the American Academy of Ophthalmology recommends comprehensive eye exams based on age and risk:

Primary care role: risk-stratify and refer, not diagnose. A Step 3 question asking what you should order in clinic for a high-risk asymptomatic adult — the answer is referral for comprehensive ophthalmologic evaluation, not a lab panel.

Core diagnostic studies (performed by ophthalmology, but you should know them):

Diagnostic Workup — Advanced and Confirmatory Studies

— OCT RNFL thickness — quantifies axonal loss; serial scans track progression sensitively. Reduced inferotemporal and superotemporal RNFL correlate with arcuate field defects.

— OCT ganglion cell–inner plexiform layer (GCIPL) in the macula — detects early central involvement, especially useful in high myopes whose discs are hard to interpret

— Humphrey visual field perimetry — the Glaucoma Hemifield Test, mean deviation (MD), pattern standard deviation (PSD), and Visual Field Index (VFI) quantify damage. Two reliable abnormal fields are needed before declaring progression.

— Disc photography / fundus imaging — baseline reference for future comparison; detects disc hemorrhages

— 24-hour IOP monitoring or diurnal curve — in patients progressing despite "normal" office IOP, peaks often occur in early morning supine position

— Pachymetry — CCT integrated into risk calculators

— Anterior segment OCT or ultrasound biomicroscopy — if angle status is ambiguous

— Pseudoexfoliation — flaky material on lens capsule, pupil margin

— Pigmentary glaucoma — Krukenberg spindle on cornea, iris transillumination defects, typically myopic young men

— Steroid-induced — history-driven

— Uveitic, traumatic (angle recession), neovascular (diabetes, CRVO)

Key distinction: Structure (OCT) often precedes function (visual field) in early disease; function leads structure in advanced disease where the OCT "floors out." Use whichever is more sensitive at that stage.

Step 3 management: A 45-year-old with IOP 26, CCT 510 µm, cup-disc 0.7 → high-risk ocular hypertensive — ophthalmology will likely initiate prostaglandin analog even without field loss.

Once POAG is suspected, ophthalmology builds a structure–function correlation:

OHTS risk calculator — for ocular hypertensives (elevated IOP, normal nerve/field), estimates 5-year risk of conversion to POAG using: age, IOP, CCT, vertical cup-disc ratio, and PSD. Treatment is recommended when 5-year risk exceeds ~12–15%.

Rule out secondary open-angle glaucomas:

Risk Stratification and First-Line Management Logic

— Advanced disease

— Rapid progression

— Normal-tension glaucoma (where "normal" IOP is still too high for that nerve)

— Younger patients with longer life expectancy of vision loss

— Definite POAG (nerve damage + field loss): treat all

— Ocular hypertension: treat if 5-year conversion risk >12–15% (OHTS), or IOP >24–30 mmHg, or other compelling risk factors

— Glaucoma suspects (suspicious disc, normal field): individualized monitoring vs. treatment

— Topical prostaglandin analog (latanoprost, travoprost, bimatoprost, tafluprost) — historically the most common first choice

— Selective laser trabeculoplasty (SLT) — the LiGHT trial (2019) established SLT as an excellent first-line option, providing IOP control with fewer drops needed and good 6-year durability. Many guidelines now endorse SLT as first-line alternative to or alongside medication.

1. Maximize first-line drug or repeat SLT

2. Add a second class (different mechanism)

3. Combination drops to reduce burden

4. Incisional surgery (trabeculectomy, tube shunt, MIGS) for refractory disease

Board pearl: The LiGHT trial changed practice — SLT as initial therapy is reasonable and may be preferred for patients with adherence concerns, cost barriers, or drop intolerance. Step 3 may test recognition that SLT is no longer "second-line."

Step 3 management: Counsel patients that treatment preserves remaining vision but does not restore lost vision — glaucoma damage is irreversible. This frames the importance of adherence and follow-up.

Treatment goal in POAG: lower IOP enough to halt or slow progression of optic nerve damage. There is no IOP target that fits all patients — therapy is individualized.

Target IOP setting — typically a 20–30% reduction from untreated baseline, with lower targets (40%+ reduction) for:

Who to treat:

First-line therapy options (per AAO Preferred Practice Pattern and EAGLE/LiGHT trials):

Stepwise escalation if monotherapy insufficient:

Pharmacotherapy — First-Line Topical Regimens

— Mechanism: increase uveoscleral outflow

— Dosing: once nightly (best 24-hour IOP control of any class)

— Efficacy: 25–33% IOP reduction — most potent single agent

— Side effects: iris hyperpigmentation (irreversible), eyelash growth, periorbital fat atrophy (PAP — prostaglandin-associated periorbitopathy), conjunctival hyperemia, cystoid macular edema (rare, more in pseudophakes/aphakes), reactivation of herpetic keratitis

— Caution: active uveitis (relative contraindication)

— Mechanism: decrease aqueous production

— Efficacy: ~20–25% IOP reduction

— Systemic side effects matter on Step 3: bradycardia, AV block, bronchospasm, masked hypoglycemia, fatigue, depression, erectile dysfunction

— Contraindicated in: asthma, COPD with reactive component, sinus bradycardia, 2nd/3rd-degree AV block, decompensated heart failure

— Teach nasolacrimal occlusion (finger pressure on medial canthus for 1–2 minutes after instillation) to reduce systemic absorption

— Decrease production + increase uveoscleral outflow

— Side effects: allergic conjunctivitis (common after months), fatigue, dry mouth

— Contraindicated in infants/young children — risk of CNS depression, apnea, hypotension, bradycardia (crosses BBB)

— Avoid with MAOIs

— Decrease aqueous production; ~15–20% IOP drop

— Side effects: bitter taste, stinging; avoid in sulfa allergy with caution, severe renal impairment

Board pearl: Timolol drops in a patient with asthma → bronchospasm hospitalization is a classic Step 3 stem. The answer: switch to a prostaglandin or non-selective avoidance; betaxolol (β1-selective) is safer but still not ideal.

Prostaglandin analogs (PGAs) — latanoprost, travoprost, bimatoprost, tafluprost, latanoprostene bunod

Beta-blockers — timolol 0.25–0.5% twice daily (or 0.5% gel once daily)

Alpha-2 agonists — brimonidine

Topical carbonic anhydrase inhibitors — dorzolamide, brinzolamide

Rho kinase inhibitors — netarsudil — increases trabecular outflow; common conjunctival hyperemia, corneal verticillata

Cholinergics (pilocarpine) — rarely used now; miosis, brow ache, retinal detachment risk

Procedural and Surgical Management

— Targets pigmented trabecular meshwork cells with a Q-switched Nd:YAG laser

— First-line or adjunct; per LiGHT trial, more patients achieved target IOP without drops and avoided incisional surgery

— IOP reduction ~20–30%, effect wanes over 3–5 years, repeatable

— Office procedure, topical anesthesia, low risk; transient IOP spike and mild inflammation are typical

— Especially valuable in: poor adherence, drop intolerance, pregnancy planning, cost constraints

— iStent, Hydrus microstent, Xen gel stent, goniotomy (Kahook, GATT), endoscopic cyclophotocoagulation

— Modest IOP lowering, excellent safety, faster recovery — used in mild-to-moderate disease

— Especially attractive when cataract surgery is already indicated

— Gold standard for moderate-to-severe or refractory POAG

— Creates a guarded fistula and subconjunctival bleb for aqueous drainage

— Augmented with antimetabolites (mitomycin C, 5-FU) to reduce scarring

— Complications: hypotony, bleb leak, bleb-related endophthalmitis (lifetime risk — patients must report red eye urgently), cataract progression, choroidal effusion

— For failed trabeculectomy, neovascular glaucoma, complex anterior segment, pediatric/uveitic cases

— Tube Versus Trabeculectomy (TVT) study: tubes had higher 5-year success and fewer reoperations

CCS pearl: A post-trabeculectomy patient presenting with sudden eye pain, redness, decreased vision, and hypopyon — order emergent ophthalmology consult for suspected bleb endophthalmitis; do not delay for outpatient workup. Lifelong vigilance is required.

Key distinction: SLT lowers IOP via outflow at the trabecular meshwork; laser peripheral iridotomy (LPI) is for angle closure, not POAG — they are not interchangeable on exam stems.

Selective laser trabeculoplasty (SLT)

Argon laser trabeculoplasty (ALT) — older, more thermal damage, largely replaced by SLT

Minimally invasive glaucoma surgery (MIGS) — performed often at time of cataract surgery

Trabeculectomy (filtering surgery)

Glaucoma drainage devices (tube shunts) — Ahmed, Baerveldt, Molteno

Cyclodestructive procedures — transscleral or endoscopic cyclophotocoagulation; reduce ciliary body aqueous production; refractory or end-stage eyes

Special Populations — Elderly and Renal/Hepatic Impairment

— Adherence challenges: arthritis (cannot squeeze bottles), tremor, poor aim, cognitive impairment, polypharmacy, drop-instillation literacy. Up to 50% of glaucoma patients are non-adherent.

— Practical aids: drop guides (Autodrop, Opticare), simplifying to once-daily PGA, fixed-dose combinations, family/caregiver assistance, voice-reminder apps, SLT as drop-sparing strategy

— Fall risk: glaucoma-related visual field loss roughly doubles falls; coordinate with PT/home safety evaluation, lighting, hazard removal

— Driving: state-specific visual field requirements; counsel on safety and report when legally required

— Beta-blocker drops in older adults: heightened risk of bradycardia, falls, depression, fatigue, masked hypoglycemia — use prostaglandins or SLT preferentially

— Topical drops generally have minimal systemic exposure, but oral acetazolamide (used short-term for IOP spikes or pre-op) — avoid in CrCl <10; cause metabolic acidosis, hypokalemia, nephrolithiasis, aplastic anemia (rare)

— Dorzolamide/brinzolamide (topical CAIs): systemic absorption is low but use caution in severe renal impairment (CrCl <30)

— Avoid beta-blocker drops in heart failure, sick sinus, AV block, severe asthma/COPD

— Avoid brimonidine with MAOIs and in those prone to orthostatic hypotension

— Overaggressive nocturnal BP lowering (especially with bedtime antihypertensives) may worsen optic nerve perfusion in normal-tension glaucoma — coordinate with primary care to avoid nocturnal hypotension

Step 3 management: For an 82-year-old with HFrEF, asthma, and POAG, first-line = latanoprost qHS (or SLT). Avoid timolol entirely; brimonidine causes fatigue. Reassess adherence at every visit.

Board pearl: Always ask "can you show me how you put in your drops?" — observation reveals non-adherence the chart never will.

Elderly patients — the dominant POAG demographic, with overlapping comorbidities that complicate management.

Renal impairment

Hepatic impairment — topical drops are largely safe; oral CAIs avoided in cirrhosis (risk of precipitating encephalopathy via metabolic acidosis and electrolyte shifts)

Cardiovascular comorbidity

Special Populations — Pregnancy, Pediatrics, and Other Subgroups

— Glaucoma medications cross into fetal circulation and breast milk; no agent is fully FDA Category A.

— Prostaglandin analogs: theoretical concern for uterine contractions (prostaglandins are oxytocic); generally avoided in pregnancy, especially third trimester, though human data are limited

— Beta-blockers (timolol): can cause fetal bradycardia, IUGR, neonatal hypoglycemia, apnea; use lowest dose with nasolacrimal occlusion if needed

— Brimonidine: contraindicated near term and during breastfeeding — risk of neonatal apnea and CNS depression; do not use in infants

— CAIs (oral acetazolamide): teratogenic in animal studies, avoid first trimester; topical dorzolamide preferred if a CAI is needed

— Preferred strategy: defer initiation if possible; SLT is the safest option during pregnancy — drug-free, durable

— Coordinate with maternal–fetal medicine and ophthalmology

— Presents with classic triad: epiphora, photophobia, blepharospasm, plus buphthalmos (enlarged eye), corneal haze, Haab striae

— Brimonidine is contraindicated in children <2 (apnea, bradycardia, hypotension, hypothermia, CNS depression); caution up to age 6

— Management is surgical: goniotomy or trabeculotomy as first-line

— Refer urgently to pediatric ophthalmology

— Higher prevalence, earlier onset, faster progression, worse outcomes

— Screen earlier (age 40 or with family history), treat more aggressively, ensure access — health equity is a Step 3 theme

— Up to 40% of population are "steroid responders"

— Inhaled, intranasal, topical, periocular, and systemic steroids all implicated

— Monitor IOP in chronic users; reduce steroid burden when possible

Key distinction: A neonate with tearing and a cloudy, enlarged cornea is congenital glaucoma until proven otherwise — not nasolacrimal duct obstruction (which has tearing but a clear, normal-size cornea).

Step 3 management: Pregnant patient with progressing POAG — refer for SLT rather than escalate drops.

Pregnancy and lactation

Pediatric glaucoma (primarily a different disease — primary congenital glaucoma)

Black and Hispanic patients

Steroid-induced ocular hypertension

Complications and Adverse Outcomes

— Irreversible vision loss — peripheral first, then central; end-stage glaucoma reaches "no light perception"

— Functional disability: difficulty driving, reading, navigating stairs; loss of independence

— Falls and fractures — visual field loss doubles fall risk; hip fractures carry high mortality in elderly

— Depression and reduced quality of life — chronic disease + vision loss

— Motor vehicle accidents — risk rises with bilateral field loss

— Acute IOP spikes — uncommon in pure POAG but can occur with pigment dispersion, pseudoexfoliation, post-laser, or steroid response

— Topical drops:

– Ocular surface disease — burning, dryness, allergy (especially with benzalkonium chloride preservative)

– PGAs: iris/periocular hyperpigmentation, eyelash hypertrichosis, PAP (sunken eye appearance), macular edema, herpetic reactivation

– Beta-blockers: systemic bradycardia, bronchospasm, depression, fatigue, ED

– Brimonidine: allergic conjunctivitis (common, often after months), fatigue, dry mouth, CNS depression in children

– CAIs: stinging, metallic taste; oral form — paresthesias, kidney stones, acidosis, hypokalemia, rare aplastic anemia

— SLT/ALT: transient IOP spike, mild inflammation, occasionally peripheral anterior synechiae

— Trabeculectomy: hypotony maculopathy, bleb leak, bleb-associated endophthalmitis (lifetime risk ~1% per year cumulatively), cataract, suprachoroidal hemorrhage, late bleb failure

— Tube shunts: tube erosion, corneal decompensation, diplopia from extraocular muscle restriction, hypotony

— Cyclophotocoagulation: hypotony, phthisis (rare), vision loss, inflammation

CCS pearl: Any post-trabeculectomy or post-tube patient with acute pain, redness, decreased vision, and discharge — assume endophthalmitis until proven otherwise. Immediate ophthalmology consultation, intravitreal antibiotics (vancomycin + ceftazidime), possible vitrectomy. Do not start oral antibiotics and send home.

Board pearl: Patients with filtering blebs should be counseled to never wear soft contact lenses in that eye and to report any red eye immediately — bleb integrity is a lifelong infection risk.

Disease-related complications

Treatment-related complications

When to Escalate Care — Consult, Referral, and Urgent Triage

— Asymptomatic patient with elevated IOP, suspicious disc, or family history meeting screening criteria

— Established POAG patient on stable therapy needing surveillance — every 3–12 months depending on severity

— New visual field defect on confrontation testing

— Disc hemorrhage detected on exam

— IOP markedly elevated (>30 mmHg) but eye is quiet and pain-free

— Glaucoma patient with progressing disease or new symptoms

— Steroid-responder needing IOP control coordination with the prescribing service

— Acute painful red eye with halos, nausea, fixed mid-dilated pupil, corneal haze, IOP >40 → acute angle-closure — not POAG, but you must distinguish. Initial management while awaiting ophthalmology: timolol, brimonidine, dorzolamide topically; acetazolamide 500 mg PO/IV; pilocarpine 1–2% once IOP drops below 40; definitive treatment is laser peripheral iridotomy

— Post-glaucoma surgery patient with red eye, pain, vision loss → suspected endophthalmitis

— Sudden vision loss in a glaucoma patient → consider CRVO, ischemic optic neuropathy, or hypotony — same-day evaluation

— Hyphema, trauma, or chemical injury in any patient — immediate

— Reinforce adherence; observe drop technique

— Monitor for systemic side effects of topical drops (especially beta-blockers)

— Coordinate steroid stewardship in pulmonary, rheumatologic, dermatologic patients

— Ensure annual or biannual ophthalmology follow-up; flag missed appointments

— Address fall prevention, driving safety, and depression screening

Step 3 management: A 70-year-old on chronic prednisone for PMR develops IOP 32 in clinic — call ophthalmology for same-week evaluation, start a topical agent only on their guidance, and discuss with rheumatology about minimizing steroid dose (consider steroid-sparing agents like methotrexate).

Board pearl: POAG itself is never an ED disease. If the eye hurts acutely, think angle closure, endophthalmitis, or another diagnosis — not POAG decompensation.

Routine ophthalmology referral (non-urgent, within weeks)

Semi-urgent referral (days to 1–2 weeks)

Emergent same-day referral

Primary care role in ongoing co-management

Key Differentials — Other Glaucoma Subtypes

— Painful, red eye, halos, nausea/vomiting, mid-dilated fixed pupil, corneal edema, IOP often 40–80

— Risk: hyperopia, Asian ancestry, advancing age, shallow anterior chamber, pupil-dilating medications (anticholinergics, sympathomimetics, some antidepressants)

— Treatment: emergent topical + oral IOP-lowering agents → laser peripheral iridotomy; prophylactic LPI in the fellow eye

— Classic POAG damage with IOP always ≤21 mmHg

— Associations: migraine, Raynaud, OSA, nocturnal hypotension, disc hemorrhages

— Treat by lowering IOP further (target 30% below baseline) — the Collaborative Normal-Tension Glaucoma Study confirmed IOP reduction slows progression

— Also address vascular dysregulation: caution with bedtime antihypertensives, treat OSA

— Most common identifiable cause of open-angle glaucoma worldwide

— Dandruff-like flakes on lens capsule, pupil margin, trabecular meshwork

— Higher IOP fluctuation, faster progression, increased cataract surgery complication risk (zonular weakness)

— Young, myopic men; Krukenberg spindle (pigment on corneal endothelium), iris transillumination defects

— Pigment liberation triggered by exercise

— Topical/inhaled/systemic/periocular steroids; IOP rise weeks to months after exposure; reversible if caught early

— Iris neovascularization from proliferative diabetic retinopathy, CRVO, ocular ischemic syndrome; aggressive — needs anti-VEGF and panretinal photocoagulation plus IOP lowering

Key distinction: POAG = open angle, painless, gradual, bilateral. Acute angle-closure = closed angle, painful, sudden, unilateral. The angle on gonioscopy is the defining feature, not the IOP number.

Board pearl: A young myopic man whose IOP spikes after jogging → pigmentary glaucoma — counsel on exercise modification and refer.

Acute angle-closure glaucoma

Chronic angle-closure glaucoma — silent progressive angle closure with peripheral anterior synechiae; gonioscopy distinguishes from POAG

Normal-tension glaucoma (NTG)

Pseudoexfoliation glaucoma

Pigmentary glaucoma

Steroid-induced glaucoma

Neovascular glaucoma

Uveitic, traumatic (angle recession), lens-induced, ICE syndrome

Key Differentials — Non-Glaucomatous Optic Neuropathies and Vision Loss

— Non-arteritic AION: sudden painless vision loss, altitudinal field defect, swollen disc with hemorrhages; risk = HTN, DM, sleep apnea, "disc at risk" (small cup); manage vascular risk factors

— Arteritic AION (giant cell arteritis): age >50, jaw claudication, headache, scalp tenderness, elevated ESR/CRP, polymyalgia rheumatica — emergency: high-dose IV/PO steroids, temporal artery biopsy, then taper

— Young adult, painful vision loss worsened by eye movement, dyschromatopsia, RAPD, often associated with multiple sclerosis

— MRI of brain and orbits; high-dose IV methylprednisolone shortens recovery but does not change final acuity

— Pituitary adenoma, meningioma, thyroid eye disease — bitemporal hemianopia suggests chiasm; MRI

— Ethambutol, amiodarone, methanol, B12 deficiency — bilateral central scotomas, pale discs

— Retinitis pigmentosa: peripheral field loss mimicking glaucoma — but with bone-spicule pigmentation, nyctalopia, family history, abnormal ERG

— Branch retinal artery/vein occlusions, age-related macular degeneration, diabetic retinopathy

— Homonymous hemianopia from occipital/parietal stroke — respects the vertical midline; glaucoma defects respect the horizontal midline

Key distinction: A pale disc without cupping suggests a non-glaucomatous optic neuropathy — order MRI, GCA workup, and B12. Cupping with rim thinning and matching nasal/arcuate field defect = glaucoma.

Step 3 management: An older patient with new headache, jaw claudication, and acute monocular vision loss → start high-dose IV methylprednisolone immediately, then ESR/CRP and temporal artery biopsy within 1–2 weeks. Do not wait for biopsy results — the fellow eye can be lost within hours.

Ischemic optic neuropathy

Optic neuritis

Compressive optic neuropathy

Toxic/nutritional optic neuropathies

Retinal causes of field loss

Stroke-related visual field defects

Functional/psychogenic vision loss — incongruent findings, normal pupils and OCT

Long-Term Plan, Adherence, and Secondary Prevention

— Studies show 30–50% of glaucoma patients are non-adherent within the first year

— Predictors of non-adherence: cost, complex regimens, asymptomatic disease, side effects, poor dexterity, low health literacy, depression

— Interventions:

– Simplify — once-daily PGA is the easiest regimen; fixed-combination drops reduce bottle count

– Generic latanoprost is inexpensive — leverage for cost-constrained patients

– SLT as drop-sparing alternative

– Drop technique training, written instructions, alarms, caregiver involvement

– Open-ended questions: "Most people miss doses sometimes — how often do you?"

— Treat OSA (CPAP) — strong association with NTG progression

— Smoking cessation — modest evidence of progression risk

— Avoid unnecessary systemic corticosteroids; use lowest effective dose of inhaled/intranasal steroids

— Coordinate antihypertensive timing to avoid nocturnal hypotension in NTG

— Moderate aerobic exercise modestly lowers IOP — encourage, but counsel pigmentary glaucoma patients on iris-shaking exertion

Step 3 management: When ED-prescribed timolol drops appear on a new med list during med reconciliation, always check for asthma/COPD/HF and substitute prostaglandin if present — a quintessential transitions-of-care safety task.

Board pearl: "Adherence" includes persistence (still on therapy at 12 months) and execution (correct daily use). Both fail in glaucoma — measure both.

Lifelong therapy is the rule. POAG cannot be cured; treatment slows progression of an otherwise relentless disease.

Adherence is the single biggest determinant of outcome outside of pressure target attainment.

Address modifiable risk factors

Vaccinations and general health — standard preventive care; influenza and COVID vaccines do not affect glaucoma

Document baseline and target IOP, share with patient — empowers self-advocacy at follow-up visits

Low vision rehabilitation — refer when functional impairment develops (magnifiers, lighting, mobility training, occupational therapy)

Driving — assess visual fields per state DMV requirements; counsel cessation when unsafe

Follow-Up, Monitoring, and Counseling

— Stable, mild POAG at target IOP: every 6–12 months with IOP check; OCT and visual fields annually

— Moderate POAG: every 3–6 months; fields and OCT every 6–12 months

— Severe or progressing POAG: every 1–3 months; more frequent imaging

— New therapy or surgery: 1 day, 1 week, 1 month, then per stability

— Suspect/ocular hypertension under observation: every 6–12 months

— IOP trends — single readings are noisy; trajectory matters

— Visual field progression — Guided Progression Analysis (GPA) flags statistically significant change over baseline

— OCT RNFL/GCIPL — serial thinning beyond age-expected rates indicates progression

— Disc photos — for hemorrhage, rim notching, peripapillary atrophy expansion

— Adherence and side effects at every visit

— Blood pressure (especially nocturnal patterns in NTG) — coordinate with primary care

— "Treatment preserves remaining vision but cannot restore lost vision."

— "Glaucoma is lifelong — even when your eye feels normal, the disease is active."

— "Never stop drops without telling your eye doctor."

— Family screening: first-degree relatives should begin eye exams by age 40 (or 10 years before the affected family member's diagnosis age)

— Driving safety, fall prevention, lighting at home

— Avoid eye-rubbing, well-fitting eyewear, UV protection (general eye health)

— Update PCP with target IOP, current regimen, and progression status

— Flag patients on inhaled or systemic steroids for IOP surveillance

— Encourage influenza and pneumococcal vaccination in chronically ill elderly with glaucoma

Step 3 management: New POAG diagnosis → counsel about first-degree relative screening at the index visit — a classic preventive medicine touchpoint that exam writers love.

Board pearl: When OCT plateaus in advanced disease, rely on visual fields for progression — and vice versa in early disease.

Follow-up cadence (set by ophthalmology, but coordinated by primary care)

Monitoring parameters

Counseling points to deliver and document

Coordinated care notes

Ethical, Legal, and Patient Safety Considerations

— Glaucoma treatment requires lifelong daily drops or laser/surgery for a patient who feels fine. Robust informed consent is essential: explain that adherence prevents future blindness, side effects exist, and follow-up is non-negotiable.

— For SLT or trabeculectomy: discuss alternatives, success rates, complication profiles (including lifetime endophthalmitis risk with blebs), and that surgery may not eliminate drops.

— Most states define legal driving based on acuity and visual field thresholds (commonly 20/40 best-corrected and 140° horizontal field). Glaucoma-related field loss may disqualify.

— Mandatory reporting laws vary by state — California, Oregon, Pennsylvania, and several others require physicians to report visually impaired drivers; most states allow but don't require reporting.

— Document the driving discussion and DMV referral when appropriate. The duty to warn the patient and, where mandated, the licensing authority — balanced against confidentiality — is a Step 3 ethics scenario.

— Hospitalized glaucoma patients frequently miss drops; nursing administration must be ordered explicitly. Missed PGA doses for days can cause IOP spikes.

— When discharging a patient newly on inhaled corticosteroids or oral steroids, document the need for ophthalmology surveillance if therapy will be prolonged.

— Anesthesia and ophthalmology should coordinate before non-ocular surgery: anticholinergics and prone positioning can affect IOP; avoid sudden drop discontinuation perioperatively.

— Black and Hispanic patients face higher prevalence, later diagnosis, and worse outcomes. Reduced access to comprehensive eye care, insurance limitations on optometry/ophthalmology coverage, and medication cost barriers contribute.

— Generic latanoprost, manufacturer assistance, and SLT (one-time procedure) help bridge access gaps.

— Bleb endophthalmitis warning cards; ID-style alert if any urgent care visit

— Caution patients on brimonidine about driving while fatigued

Step 3 management: A glaucoma patient with advancing field loss who insists on driving — counsel cessation, document the conversation, offer DMV-mediated evaluation, and report if state law mandates while preserving the therapeutic relationship.

Board pearl: Glaucoma drops are routinely omitted on hospital admission — explicitly order them.

Informed consent for chronic asymptomatic therapy

Driving and visual disability

Transitions of care and med reconciliation

Health equity and access

Patient safety pearls

High-Yield Associations and Rapid-Fire Facts

Board pearl: Bilateral, painless, peripheral-first vision loss with cupped optic discs in a Black 55-year-old with affected father = POAG — refer, don't initiate.

Risk factors (memorize): age >40, Black/Hispanic ancestry, family history, elevated IOP, thin central cornea, large cup-disc ratio, myopia, diabetes, hypertension, OSA, migraine, chronic steroid use

OHTS identified five baseline predictors of conversion from ocular hypertension to POAG: age, IOP, vertical C/D ratio, CCT, and pattern standard deviation

LiGHT trial — SLT first-line is non-inferior or superior to drops for IOP control, with fewer surgeries needed

CNTGS (Collaborative Normal-Tension Glaucoma Study) — 30% IOP reduction slows progression in NTG

EMGT (Early Manifest Glaucoma Trial) — each 1 mmHg IOP reduction → ~10% lower progression risk

AGIS (Advanced Glaucoma Intervention Study) — patients with IOP consistently <18 had minimal field progression

CIGTS — initial medical vs surgical therapy: similar long-term field outcomes

Normal IOP 10–21 mmHg; diurnal variation 3–6 (higher in glaucoma)

ISNT rule for healthy disc rim thickness: Inferior ≥ Superior ≥ Nasal ≥ Temporal

Drance hemorrhages = disc-margin splinter hemorrhages = progression marker

PAP (prostaglandin-associated periorbitopathy) = sunken-eye look from periorbital fat atrophy with PGA use

Krukenberg spindle → pigmentary glaucoma

Pseudoexfoliation → flaky lens deposits, most common identifiable secondary cause

Buphthalmos + tearing + photophobia in infant → primary congenital glaucoma

Brimonidine in children <2 → contraindicated (apnea/CNS depression)

Timolol in asthma/COPD/AV block → avoid

Acetazolamide → metabolic acidosis, hypokalemia, kidney stones, sulfa cross-reactivity caution

Bleb-related endophthalmitis → lifelong post-trabeculectomy risk; red eye = ER

Field defect respects horizontal meridian → glaucoma; vertical meridian → chiasmal/retrochiasmal

First-degree relatives screened starting age 40 (or 10 years earlier than affected member)

USPSTF: insufficient evidence for general adult glaucoma screening (I statement)

AAO: baseline eye exam at age 40, more frequent with risk factors

Board Question Stem Patterns

"55-year-old Black man, father went blind from glaucoma, IOP 24 OU, cup-disc 0.7, normal acuity, asymptomatic."

→ Best next step: referral to ophthalmology for comprehensive evaluation (visual fields, OCT, gonioscopy, pachymetry). Not empiric drops. Not acetazolamide.

"68-year-old with asthma started on timolol drops, now wheezing and bradycardic."

→ Discontinue timolol, switch to prostaglandin analog (or SLT). Avoid all topical beta-blockers in reactive airway disease.

"45-year-old with atopic dermatitis on potent topical steroids near eyes for months; IOP 30."

→ Refer to ophthalmology, taper steroids with dermatology, initiate IOP-lowering therapy as directed.

"Eye pain, halos, headache, vomiting, fixed mid-dilated pupil, IOP 55."

→ Not POAG. Emergent topical timolol/brimonidine/dorzolamide + oral acetazolamide → laser peripheral iridotomy.

"Migraines, Raynaud, OSA, progressive field loss with IOP 17."

→ Lower IOP further (30% reduction target), treat OSA, avoid bedtime antihypertensives.

"Infant with tearing, photophobia, cloudy enlarged corneas."

→ Pediatric ophthalmology emergency; goniotomy/trabeculotomy. Not nasolacrimal duct obstruction.

"Patient with prior glaucoma surgery, now red eye, hypopyon, vision loss."

→ Immediate ophthalmology consult; intravitreal antibiotics.

"Newly diagnosed POAG; siblings ask when they should be checked."

→ Comprehensive eye exam now (and at minimum by age 40), then every 1–2 years.

"Field loss progressing despite three drops; admits 'sometimes forgets.'"

→ Simplify regimen, observe drop technique, consider SLT.

"Should we screen all adults for glaucoma?"

→ USPSTF: insufficient evidence (I). AAO recommends risk-based comprehensive eye exams.

Step 3 management: When in doubt on a POAG stem, the answer is rarely "start a drug" — it's almost always refer, confirm, then treat with prostaglandin or SLT as first-line.

Pattern 1 — The asymptomatic high-risk patient

Pattern 2 — The drop side effect

Pattern 3 — Steroid-induced

Pattern 4 — Acute angle-closure distractor

Pattern 5 — Normal-tension glaucoma

Pattern 6 — Congenital

Pattern 7 — Post-trabeculectomy endophthalmitis

Pattern 8 — Family screening

Pattern 9 — Adherence

Pattern 10 — USPSTF

One-Line Recap

Primary open-angle glaucoma is a chronic, painless, bilateral optic neuropathy whose diagnosis requires characteristic cupping plus matching visual field loss in an open angle — managed lifelong by lowering IOP 20–30% with a prostaglandin analog or selective laser trabeculoplasty as first-line, with primary care responsible for risk-based referral, adherence support, steroid stewardship, and avoidance of unsafe drop choices.

Board pearl: If the stem describes a painless, gradual, peripheral field loss with a cupped disc — pick ophthalmology referral, then prostaglandin or SLT. If it's painful, red, and acute — pivot to angle closure or endophthalmitis. The angle on gonioscopy, not the IOP number, defines the disease.

Screen by risk, not population: USPSTF says insufficient evidence; AAO recommends comprehensive eye exam at 40, earlier and more often for Black/Hispanic ancestry, family history, diabetes, steroid use, or high myopia.

Diagnose by structure + function in an open angle: cup-disc asymmetry, rim thinning (ISNT violated), Drance hemorrhages, OCT RNFL thinning, and corresponding nasal step or arcuate field defects on Humphrey perimetry. IOP need not be elevated — normal-tension glaucoma is real.

Treat with PGA qHS or SLT first-line (LiGHT trial); avoid timolol in asthma/COPD/HF/AV block; avoid brimonidine in young children and near term in pregnancy; SLT is the safest option in pregnancy and for adherence-challenged patients.

Surveillance and safety: lifelong follow-up every 3–12 months by severity; counsel that drops preserve but never restore vision; screen first-degree relatives at 40; flag patients on chronic inhaled/systemic steroids for IOP monitoring; reconcile glaucoma drops on every hospital admission and discharge.