Glaukoma Sudut Terbuka

01Pathophysiology

The eye continuously produces aqueous humor from the ciliary body in the posterior chamber. This fluid flows through the pupil into the anterior chamber, where it drains primarily through the trabecular meshwork into the canal of Schlemm, and from there into the episcleral venous system. In open angle glaucoma, the anterior chamber angle remains anatomically open, but there is increased resistance to outflow at the level of the trabecular meshwork. This leads to a gradual elevation of intraocular pressure (IOP).

The elevated IOP transmits mechanical stress to the lamina cribrosa, a sieve-like structure at the optic nerve head through which retinal ganglion cell axons pass. Chronic compression and ischemia at this site cause progressive retinal ganglion cell apoptosis. Because the peripheral nerve fibers (which correspond to the arcuate bundle) are affected earliest, patients lose peripheral vision first while central acuity is preserved until late in the disease. This is why patients are unaware of their deficit for years.

The hallmark finding on fundoscopy is optic disc cupping, which represents the loss of neural tissue at the optic nerve head. As ganglion cell axons die, the neuroretinal rim thins and the cup enlarges relative to the disc. A cup-to-disc ratio greater than 0.5, or asymmetry of more than 0.2 between the two eyes, should raise concern.

It is critical to understand that IOP can be within the statistically normal range (< 21 mmHg) and the patient can still have glaucoma. This entity is called normal-tension glaucoma and represents a subset where the optic nerve is susceptible to damage at lower pressures. The diagnosis of open angle glaucoma is therefore made based on the combination of optic nerve changes and visual field loss, not on IOP alone.

02Classification and Clinical Manifestation

Classification by Stage

03Diagnostic Workup

Tonometry is the best initial test and the standard screening tool. It measures intraocular pressure. However, a single normal reading does not exclude glaucoma, because IOP fluctuates throughout the day and normal-tension glaucoma exists. If screening reveals elevated IOP, further workup is warranted.

Fundoscopic examination is where the diagnosis becomes apparent. The examiner evaluates the optic disc for cupping. An increased cup-to-disc ratio, especially if asymmetric between the two eyes, is the cardinal structural sign. Disc hemorrhages (Drance hemorrhages) are an ominous sign indicating active damage.

Visual field testing (perimetry) is the functional correlate. The classic pattern is an arcuate scotoma that follows the distribution of the arcuate nerve fiber bundle. A nasal step (asymmetric sensitivity across the horizontal midline in the nasal field) is another early finding. Perimetry is used both for diagnosis and for monitoring disease progression over time.

Gonioscopy is essential to confirm that the angle is open. This step distinguishes primary open angle glaucoma from angle-closure glaucoma, which has a fundamentally different mechanism and treatment. If gonioscopy is not performed, the diagnosis is incomplete.

OCT of the retinal nerve fiber layer has become a key tool because it can detect structural thinning before the patient develops measurable visual field loss. This makes it valuable for early detection and for following patients with ocular hypertension (elevated IOP without optic nerve damage yet).

The overall diagnostic logic: tonometry screens, fundoscopy and OCT identify structural damage, perimetry confirms functional loss, and gonioscopy classifies the type of glaucoma.

04Management and Treatment

First-line therapy is a topical prostaglandin analog, most commonly latanoprost, administered once nightly. Prostaglandin analogs reduce IOP by 25-30% and have the best efficacy-to-side-effect profile. The test-relevant side effects are iris color darkening (increased melanin in the iris stroma, permanent in some cases), eyelash lengthening, and periorbital fat atrophy (causing a sunken appearance around the eye).

If a prostaglandin analog alone is insufficient, topical timolol is typically added. Timolol reduces aqueous production and lowers IOP by roughly 20-25%. The contraindications to timolol are high-yield: it is a non-selective beta-blocker, so it must be avoided in patients with asthma, COPD, decompensated heart failure, second or third-degree heart block, and symptomatic bradycardia. Even topical application can produce systemic beta-blockade.

Brimonidine and dorzolamide serve as second or third-line adjuncts. Brimonidine is contraindicated in infants and young children due to the risk of crossing the blood-brain barrier and causing respiratory depression and apnea.

For patients who fail medical therapy, selective laser trabeculoplasty (SLT) can be offered. It is non-destructive and repeatable. If laser therapy also fails, trabeculectomy (a surgical filtering procedure) is the definitive intervention. The target in all cases is to lower IOP to a level that halts optic nerve damage, often defined as a target IOP reduction of at least 20-30% from baseline or an absolute target tailored to the severity of damage.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common trap with open angle glaucoma is confusing it with acute angle-closure glaucoma. If the vignette describes a patient with sudden, severe eye pain, a red eye, nausea, vomiting, and a mid-dilated non-reactive pupil, that is angle-closure. Open angle glaucoma is the opposite: the patient is asymptomatic, has no pain, no redness, and the vision loss is discovered incidentally or on screening. The moment you see "painless" and "gradual peripheral vision loss," think open angle.

A second trap involves normal-tension glaucoma. Students often dismiss glaucoma if the IOP is within normal range. If a vignette describes a patient with progressive cupping and arcuate visual field defects but a normal IOP, the answer is still glaucoma.

A third frequently tested concept is the contraindication of timolol in asthmatics. A vignette may present a patient with glaucoma and a history of asthma, then ask for the best medication. Timolol is the wrong answer; latanoprost or brimonidine would be appropriate.

Finally, understand that steroid use can cause or worsen open angle glaucoma. Any patient on chronic corticosteroids (topical ophthalmic, inhaled, or systemic) who develops elevated IOP should be evaluated for steroid-induced glaucoma. This is reversible if the steroid is discontinued early.

The core competency being tested is the ability to recognize a slowly progressive, painless optic neuropathy, to differentiate it from acute angle-closure and other causes of visual field loss, and to select appropriate pharmacotherapy while respecting contraindications.