Ocular Hypertension & Glaucoma Suspect

Intraocular pressure reflects the balance between aqueous humor production by the ciliary body and its outflow, primarily through the trabecular meshwork at the iridocorneal angle into Schlemm's canal (conventional outflow), with a smaller uveoscleral (unconventional) pathway. Ocular hypertension (OHT) is elevated IOP without glaucomatous optic nerve or visual field damage; "glaucoma suspect" more broadly includes patients with suspicious disc features or risk factors even at normal IOP. Both represent a spectrum of risk, not a diagnosis of glaucoma itself.

Elevated IOP reflects an imbalance between aqueous production and outflow resistance, typically at the trabecular meshwork. Whether elevated IOP causes clinically significant glaucomatous damage in a given individual depends on additional factors, including corneal biomechanics — thinner central corneal thickness (CCT) is associated with underestimated true IOP on applanation tonometry and independently predicts conversion — plus optic nerve structural vulnerability and possibly vascular factors.¹

OHT and glaucoma suspect status are virtually always asymptomatic, identified incidentally on routine exam. There are no symptoms to guide diagnosis, making objective testing (IOP, CCT, disc exam, OCT, visual fields) essential.

Differential diagnosis includes early primary open-angle glaucoma (established damage, distinguishing it from OHT), normal-tension glaucoma (damage at statistically normal IOP — the converse scenario), physiologically large but stable cup-disc ratio, and secondary causes of elevated IOP (steroid response, pigmentary or pseudoexfoliative glaucoma, uveitic glaucoma) that must be excluded before labeling a patient as primary OHT.

The OHTS risk calculator (age, IOP, CCT, cup-disc ratio, visual field pattern standard deviation) estimates an individual's 5-year conversion risk to glaucoma. In a large UK cohort of over 9,000 OHT patients, 16.9% converted to glaucoma over 5 years, and an updated/refitted version of the OHTS-EGPS model showed modest but useful discriminative ability (c-index improving from 0.61 to 0.67).² CCT measurement is essential both for IOP measurement accuracy and independent risk stratification.

Management is individualized based on calculated risk. OHTS demonstrated that treating OHT with topical IOP-lowering medication reduces the 5-year conversion rate to glaucoma to less than half that of untreated, monitored patients.¹ Higher-risk patients (older age, higher IOP, thin CCT, larger cup-disc ratio, suspicious visual field indices) are generally offered treatment; lower-risk patients may reasonably be monitored without treatment, with regular follow-up including IOP checks, disc/RNFL imaging, and visual field testing to detect any conversion early.

• Roughly 1 in 6 OHT patients converts to glaucoma over 5 years in real-world data — most do not, supporting individualized rather than universal treatment
• Treating OHT roughly halves the 5-year conversion rate to glaucoma compared with observation alone
• Thinner CCT is both a source of IOP measurement error and an independent risk factor for conversion — always measure it
• Common pitfall: treating all patients with elevated IOP uniformly without individualized risk assessment
• Common pitfall: overlooking secondary/reversible causes of elevated IOP (e.g., steroid use) that would change management