Patients Are Asking: What Should My Eye Pressure Be?

The answer is not as simple as you might think.

As glaucoma specialists, we encounter this question from patients frequently, and with good reason. It’s one of our “vital signs” of eye health, and for glaucoma patients, it’s the most scrutinized. How many of us communicate to the patient what our tonometer reading is? How many of our patients ask, “What was it today, Doc?” This is by far the easier of the almost universally 2-part question, the second being, “Well, what should it be?”

This question can be deceptively difficult for us to answer. We know that lowering intraocular pressure (IOP) is beneficial in reducing the risk of glaucoma development or progression. There are a number of randomized controlled trials that clearly identify elevated baseline IOP as a risk factor for glaucoma development, the Ocular Hypertension Treatment Study (OHTS) and the European Glaucoma Prevention Study (EGPS) to name a few.1,2 But on the other hand, if we dig into the details of these and other studies, we start to understand that IOP isn’t the only player on the field. The Collaborative Normal Tension Glaucoma Study (CNTGS) found no link between baseline IOP and glaucoma progression.3 And in the aforementioned OHTS study, some untreated patients never developed glaucoma, while some treated patients did. Other potential factors, such as corneal hysteresis,4 IOP fluctuation,5 translaminar pressure gradient, and low cerebrospinal fluid pressure6 are emerging as possible explanations. These are the details that muddy the water of the seemingly clear question from the patient in front of you.

There is no standard glaucoma management strategy to determine how low a patient’s pressure should be. Target IOP is defined by the American Academy of Ophthalmology as the upper limit of an IOP range “at which visual field loss is unlikely to significantly reduce a patient’s health-related quality of life over his or her lifetime.”7 But how do we determine what this pressure is? It could be a percentage reduction of baseline IOP, as in the OHTS (20% of baseline) or CNTGS (30% of baseline).2,3 This method of course depends on your confidence in establishing what a patient’s true baseline IOP is. After all, the range of IOP fluctuation is higher in glaucoma patients,5 and a single-visit IOP reading only represents the true 24-hour average about 40% of the time.8 Your target IOP could also be an absolute number that you aim to achieve with all glaucoma patients, as suggested by the mean IOP of 12.3 mmHg in patients from the Advanced Glaucoma Intervention Study (AGIS) who showed no progression.9 Still a different option could be a target IOP derived from a formula that takes visual function and disease stage into account,10 but to date, these are not widely used. As we learn more about other factors such as the biomechanical properties of the eye and translaminar pressure differences, I predict we will see a redux of the formula-based approach.

While the benefits of IOP reduction are irrefutable, it is important to emphasize to patients that the level at which IOP can be considered “controlled” is different for everyone, and that it often requires time and sequential examination (ie, whether progression has occurred) to determine. Patients who focus solely on attaining a single pressure (say, 12 or below) can develop “IOP obsession,”11 even if their current pressure is in fact adequate. Patients may also be dismayed when learning that the IOP target agreed upon at treatment outset is not preventing progression. It is our job to allay those concerns through patient education, discussing both what’s known and unknown about the connection between IOP and glaucoma, and this is best done early in the patient-doctor relationship.

As suggested in the Academy’s definition of target IOP, the ultimate goal is to reduce the impact of glaucoma on the patient’s quality of life. Each intervention we offer, whether adding a drop or scheduling a surgery, comes at some cost to the patient — it behooves us as physicians to help our patients make treatment decisions that balance their personal cost-to-benefit ratio.

So, what should your patient’s pressure be? Probably, the best answer is, “Monitored carefully, and here’s why …” GP


  1. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:701-713
  2. Miglor S, Torri V, Zeyen T, et al. Intercurrent factors associated with the development of open-angle glaucoma in the European glaucoma prevention study. Am J Ophthalmol. 2007;144:266-275
  3. Collaborative Normal-Tension Glaucoma Study Group (CNTGS). The effectiveness of intraocular pressure reduction in the treatment of normal-tension glaucoma. Am J Ophthalmol. 1998;126(4):498-505.
  4. Deol M, Taylor D, Radcliffe NM. Corneal hysteresis and its relevance to glaucoma. Curr Opin Ophthalmol. 2015;26(2):96-102.
  5. Mosaed S. Liu JH, Weinreb RN. Correlation between office and peak nocturnal intraocular pressures in healthy subjects and glaucoma patients. Am J Ophthalmol. 2005;139:320-324.
  6. Berdahl JP, Allingham RR, Johnson DH. Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma. Ophthalmology. 2008;115(5):763-768.
  7. American Academy of Ophthalmology Preferred Practice Pattern Glaucoma Panel. Primary Open-Angle PPP. 2015; p. 63.
  8. Fogagnolo P, Orzalesi N, Ferreras A, et al. The circadian curve of intraocular pressure: can we estimate its characteristics during office hours? Invest Ophthalmol Vis Sci. 2009;50:2209-2215.
  9. Nouri-Mahdavi K, Hoffman D, Coleman AL, et al. Predictive factors for glaucomatous visual field progression in the Advanced Glaucoma Intervention Study. Ophthalmology. 2004;111:1627-1635.
  10. Aquino MV. Suggested formula for setting target intraocular pressure. Asian J Ophthalmol. 2004;6:2-6.
  11. Clement CI, Bhartiya S, Shaarawy T. New perspectives on target intraocular pressure. Surv Ophthalmol. 2014;59:615-626.