A 58-year-old man from Delhi presents to the ophthalmology clinic for routine eye examination. He is asymptomatic and denies any visual complaints. On examination, visual acuity is 6/6 in both eyes. Intraocular pressure (IOP) measured by applanation tonometry is 24 mmHg OD and 22 mmHg OS. Gonioscopy reveals open angles (Shaffer grade III–IV) bilaterally. Optic disc examination shows a vertical cup-to-disc ratio of 0.7 OD and 0.6 OS with inferior neuroretinal rim thinning. Automated perimetry shows a superior arcuate defect in the right eye. What is the most likely diagnosis?

Explanation

## Clinical Diagnosis: Primary Open-Angle Glaucoma (POAG) ### Key Diagnostic Features Present **Key Point:** The patient meets the diagnostic triad for POAG: elevated IOP, open angles on gonioscopy, and glaucomatous optic neuropathy with corresponding visual field defect. ### Structural Findings | Feature | Finding | Significance | |---------|---------|---------------| | **IOP** | 24 mmHg OD, 22 mmHg OS | Above statistical normal (>21 mmHg) | | **Gonioscopy** | Open angles (Shaffer III–IV) | Rules out angle-closure; confirms open-angle disease | | **Cup-to-disc ratio** | 0.7 OD, 0.6 OS | Elevated; normal is <0.3 | | **Neuroretinal rim** | Inferior thinning | Characteristic pattern in POAG | | **Visual field** | Superior arcuate defect | Matches optic disc damage; arcuate defects are pathognomonic for glaucoma | ### Why This Is POAG and Not Ocular Hypertension **High-Yield:** Ocular hypertension is defined as elevated IOP (>21 mmHg) WITHOUT optic nerve damage or visual field loss. This patient has both optic disc cupping (C/D 0.7, 0.6) and a corresponding arcuate visual field defect—therefore, he has glaucomatous optic neuropathy, not mere ocular hypertension. ### Why Not Normal-Tension Glaucoma? **Clinical Pearl:** Normal-tension glaucoma (NTG) presents with glaucomatous optic neuropathy and visual field defects but IOP is consistently ≤21 mmHg. This patient's IOP of 24 and 22 mmHg exceeds the normal range, making POAG the diagnosis rather than NTG. ### Why Not Secondary Glaucoma? **Key Point:** Secondary glaucomas (pseudoexfoliation, pigment dispersion, uveitis) require identifiable secondary causes visible on examination. The stem provides no mention of pseudoexfoliative material, pigment dispersion, inflammation, or other secondary pathology—only primary open-angle disease. ### POAG Pathophysiology ```mermaid flowchart TD A[Increased resistance to aqueous outflow]:::action --> B[Elevated IOP] B --> C[Mechanical compression of axons]:::action C --> D[Optic nerve head ischemia]:::action D --> E[Axonal loss & apoptosis]:::action E --> F[Optic disc cupping & pallor]:::outcome E --> G[Visual field defect]:::outcome G --> H[Arcuate/nasal step/altitudinal patterns]:::outcome ``` ### Diagnostic Criteria Summary **Mnemonic: POAG = **I**OP + **O**pen angles + **N**europathy** - **I**OP: Elevated (typically >21 mmHg, but can be <21 in NTG) - **O**pen angles: Confirmed on gonioscopy - **N**europathy: Optic disc cupping + visual field loss [cite:Parson's Diseases of the Eye 22e Ch 11]