Glaukoma Sudut Tertutup

01Pathophysiology

The eye constantly produces aqueous humor in the ciliary body of the posterior chamber. This fluid normally flows forward through the pupil into the anterior chamber, drains through the trabecular meshwork at the iridocorneal angle, and exits via the canal of Schlemm. Any process that blocks this circuit raises intraocular pressure.

In angle-closure glaucoma, anatomy is the problem. Patients tend to have a shallow anterior chamber and a short axial eye length, which is why hyperopia (farsightedness) is such a strong risk factor. When the pupil dilates to a mid-position (around 4 to 6 mm), the iris becomes thick and floppy at its periphery, and at the same time the lens pushes forward against the iris. The iris bows forward, contacts the lens, and aqueous can no longer pass through the pupil. This is pupillary block. Pressure builds in the posterior chamber and shoves the peripheral iris into the trabecular meshwork, closing the angle and shutting off drainage. Pressure rises within minutes to hours.

The clinical picture flows directly from this mechanism. The sharp pressure spike stretches ocular nerve endings and triggers the vagal reflex, producing severe pain, headache, nausea, and vomiting that can mimic an abdominal or neurologic emergency. Pressure forces fluid into the corneal stroma, producing corneal edema, which is why the cornea looks hazy and the patient sees halos around lights. The iris sphincter becomes ischemic at high pressure, leaving the pupil fixed and mid-dilated. Conjunctival vessels dilate, giving a ciliary flush, and the globe feels stony hard on gentle palpation through the closed lid. Without rapid treatment, sustained pressure causes optic nerve infarction and permanent vision loss, sometimes within hours.

The classic exam trigger deserves emphasis. Anything that produces a mid-dilated pupil can precipitate an attack in a susceptible eye: walking into a dim room, watching a movie, emotional excitement, or, most commonly tested, anticholinergic and sympathomimetic medications (antihistamines, tricyclic antidepressants, antipsychotics, scopolamine patches, nebulized ipratropium, and over-the-counter decongestants).

02Diagnostic Workup

The workup begins clinically. A patient with sudden unilateral eye pain, halos, a hazy cornea, and a fixed mid-dilated pupil is presumed to have angle closure until proven otherwise, and treatment must not wait for confirmatory imaging.

The best initial test is tonometry. Intraocular pressure of 40 mmHg or higher in the setting of the classic syndrome is essentially diagnostic. Goldmann applanation tonometry is preferred, but a Tono-Pen or iCare device works in the emergency setting. Be aware that severe corneal edema can make readings less reliable, in which case digital palpation comparing the two globes (the affected eye feels like a marble) supports the diagnosis.

The most accurate, confirmatory test is gonioscopy, which uses a mirrored lens at the slit lamp to visualize the iridocorneal angle directly. A closed angle confirms the mechanism and distinguishes angle closure from open-angle pressure spikes. Gonioscopy is also performed on the unaffected fellow eye, because angle anatomy is bilateral and the fellow eye is at high risk for an attack and will need prophylactic iridotomy.

Slit-lamp examination provides supporting findings: corneal microcystic edema, a shallow chamber graded by the van Herick technique, mild anterior chamber inflammation, and a poorly reactive pupil. Fundoscopy is often deferred because the cloudy cornea obscures the view, and dilating drops are contraindicated. Once pressure has been lowered, the optic disc is examined for glaucomatous cupping.

03Management and Treatment

The patient is an ophthalmologic emergency. The initial step is to lower intraocular pressure pharmacologically as fast as safely possible. The standard combination is a topical beta-blocker, a topical alpha-2 agonist, and a systemic carbonic anhydrase inhibitor, given essentially together. A practical bedside regimen for an adult is one drop of timolol 0.5%, one drop of apraclonidine 1% (or brimonidine 0.15 to 0.2%), and acetazolamide 500 mg intravenously or orally as the loading dose, followed by acetazolamide 250 mg every 6 hours. The drops can be repeated once after 30 minutes if pressure has not fallen. Intraocular pressure is rechecked every 15 to 30 minutes to gauge response.

A common test point concerns the timing of pilocarpine. Pilocarpine is a miotic that pulls the peripheral iris away from the trabecular meshwork, and it sounds intuitive to give it first. However, when intraocular pressure is very high (over 40 to 50 mmHg), the iris sphincter is ischemic and unresponsive to cholinergic stimulation, and pilocarpine does not work and may worsen pupillary block by increasing iris-lens contact. The correct sequence is to lower pressure first with the agents above, and once pressure begins to drop (generally below 40 mmHg) add pilocarpine 1 to 2%, one drop every 15 minutes for two doses, then every 6 hours. Pilocarpine is also instilled in the fellow eye at a lower concentration (typically 1%) for prophylaxis until iridotomy is performed.

If pressure does not respond within about an hour, hyperosmotic agents are added. Intravenous mannitol 20% is the next step at 1 to 2 g/kg infused over 30 to 45 minutes. Oral glycerol 50% at 1 to 1.5 g/kg is an alternative when intravenous access is unavailable, but must be used cautiously in diabetic patients because of the sugar load. Hyperosmotics pull fluid from the vitreous and reduce ocular volume within 30 to 60 minutes. Topical prednisolone acetate 1%, one drop every 15 to 30 minutes for four doses then hourly, is added to suppress the secondary inflammation that accompanies pressure-induced ischemia.

Important contraindications and pitfalls to remember. Acetazolamide is a sulfonamide derivative and should be avoided in sulfa-allergic patients, in sickle cell disease (it can worsen sickling and cause irreversible vision loss when used with hyperosmotics), and in significant renal impairment; the dose is reduced when creatinine clearance is below 30 mL/min. Topical beta-blockers must be used carefully or avoided in severe asthma, chronic obstructive pulmonary disease, decompensated heart failure, sinus bradycardia, and second or third-degree heart block. Mannitol is contraindicated in heart failure, pulmonary edema, and anuric renal failure because of the rapid intravascular volume shift, and serum osmolality and electrolytes should be monitored. Brimonidine is avoided in infants and used cautiously in patients on monoamine oxidase inhibitors. Crucially, never give mydriatic (pupil-dilating) drops in this setting; they will worsen the attack.

The definitive treatment is laser peripheral iridotomy, in which a small hole is created in the peripheral iris with a YAG laser. This bypasses pupillary block by allowing aqueous to flow directly from the posterior to the anterior chamber. It is performed once the cornea clears enough for the laser to penetrate, generally within 24 to 48 hours. The fellow eye must also receive prophylactic laser iridotomy because anatomic predisposition is bilateral. If laser cannot be performed, surgical iridectomy or lens extraction (the lens is a major contributor to the crowded anterior segment) is the alternative. Long-term follow-up with an ophthalmologist is required to monitor for residual chronic angle closure or optic nerve damage.

04Differential Diagnosis and Distractors

05Traps and High-Yield Pearls

The classic trap is misattribution of symptoms to a non-ocular cause. The patient presents with headache, nausea, and vomiting, and the test-writer hides the eye findings deep in the vignette or buries them after a sentence about a recent emergency department workup for migraine, gastroenteritis, or even acute abdomen. Always reread the vignette for visual symptoms, halos, or unilateral eye pain before locking in a neurologic or gastrointestinal diagnosis. A second classic trap is the medication trigger: a vignette mentions an elderly patient started on diphenhydramine for sleep, a tricyclic antidepressant, a scopolamine patch for motion sickness, or a nebulizer with ipratropium, and then develops eye pain. The test is asking you to connect anticholinergic-induced mydriasis with an attack of angle closure.

A third trap concerns sequencing of management. Students often pick pilocarpine as the initial step because it logically opens the angle. The correct sequence is to first reduce aqueous production with timolol, apraclonidine, and acetazolamide, and only add pilocarpine once pressure is falling, because the ischemic iris will not respond to a miotic at very high pressure. Likewise, the question may distinguish between the initial test (tonometry) and the gold standard (gonioscopy), or between acute medical therapy and definitive laser iridotomy, and you must keep these tiers separate.

Finally, do not forget the fellow eye. The unaffected eye shares the same shallow anterior chamber anatomy and is at high risk of an attack within months. Prophylactic laser peripheral iridotomy of the contralateral eye is a frequently tested management point that students miss.

The core competency under examination is recognizing a vision-threatening emergency from a deceptively systemic presentation, applying the correct sequence of tests (tonometry, then gonioscopy), and ordering acute therapy in the right order before moving to definitive laser iridotomy with bilateral protection.